You are on page 1of 3533

Spear’s

Surgery
of the Breast
PRINCIPLES AND ART

Fourth Edition

Allen Gabriel, MD, FACS


Clinical Professor of Surgery
Loma Linda University Medical Center
Plastic Surgery
Private Practice
Vancouver, Washington

Maurice Y. Nahabedian, MD, FACS


Professor of Plastic Surgery
VCU School of Medicine—Inova Campus
National Center for Plastic Surgery
McLean, Virginia
G. Patrick Maxwell, MD, FACS
Clinical Professor of Surgery
Department Plastic Surgery
Loma Linda University Medical Center
Loma Linda, California

Toni Storm, MD
Co-Director, Compass Oncology Breast Specialists
Medical Director, Surgical Services,
Kearney Breast Center, PeaceHealth
Vancouver, Washington
Executive Editor: Brian Brown
Senior Development Editor: Ashley Fischer
Editorial Coordinator: John Larkin
Senior Production Project Manager: Alicia Jackson
Manager, Graphic Arts & Design: Steve Druding
Artist/Illustrator: Jonathan Dimes
Senior Manufacturing Coordinator: Beth Welsh
Prepress Vendor: Aptara, Inc.
Copyright © 2021 Wolters Kluwer
Copyright ©1999, 2005, 2011 Wolters Kluwer/Lippincott Williams & Wilkins
All rights reserved. This book is protected by copyright. No part of this book may be reproduced or
transmitted in any form or by any means, including as photocopies or scanned-in or other electronic
copies, or utilized by any information storage and retrieval system without written permission from the
copyright owner, except for brief quotations embodied in critical articles and reviews. Materials
appearing in this book prepared by individuals as part of their official duties as U.S. government
employees are not covered by the above-mentioned copyright. To request permission, please contact
Wolters Kluwer at Two Commerce Square, 2001 Market Street, Philadelphia, PA 19103, via email at
permissions@lww.com, or via our website at shop.lww.com (products and services).
987654321
Printed in China
Library of Congress Cataloging-in-Publication Data
Names: Gabriel, Allen, editor.
Title: Surgery of the breast : principles and art / [edited by] Allen Gabriel.
Other titles: Surgery of the breast (Spear)
Description: Fourth edition. | Philadelphia, PA : Wolters Kluwer, [2021] |
Includes bibliographical references and index. | Summary: “As mentioned,
with the many changes in breast surgery during the last two decades and
the increasing need for interspecialty collaboration and cooperation,
the seeds of this book were thus sown. I saw an opportunity to write and
edit a unifying text/atlas that embraced the plastic surgery principles
as espoused by Gilles and Millard and yet span the entire breadth of
this discipline from breast oncology to breast augmentation. At the same
time, in the Millard tradition, my goal is to show others that beautiful
or normal-looking results are not only obtainable but critical for this
important area. This book is thus written for plastic surgeons, general
surgeons, gynecologists, oncologists, or anyone else who is looking for
a unified source of information for practical and principled surgical
management of the breast. Although the section dealing with oncology is
primary text in nature, most of the remaining chapters are in atlas
format, thus allowing the reader to pursue the surgical approach
espoused within the text. In total, there are over 130 chapters with
over 150 contributing authors. In order to have the most expertise in as
many areas as possible, we chose a multiauthored approach to the subject
rather than a single-authored text”– Provided by publisher.
Identifiers: LCCN 2020022994 | ISBN 9781496397027
Subjects: MESH: Breast–surgery | Mammaplasty–methods |
Mastectomy–methods | Breast Neoplasms–surgery
Classification: LCC RD539.8 | NLM WP 910 | DDC 618.1/90592–dc23
LC record available at https://lccn.loc.gov/2020022994
This work is provided “as is,” and the publisher disclaims any and all warranties, express or implied,
including any warranties as to accuracy, comprehensiveness, or currency of the content of this work.
This work is no substitute for individual patient assessment based upon healthcare professionals’
examination of each patient and consideration of, among other things, age, weight, gender, current or
prior medical conditions, medication history, laboratory data and other factors unique to the
patient. The publisher does not provide medical advice or guidance and this work is merely a reference
tool. Healthcare professionals, and not the publisher, are solely responsible for the use of this work
including all medical judgments and for any resulting diagnosis and treatments.
Given continuous, rapid advances in medical science and health information, independent professional
verification of medical diagnoses, indications, appropriate pharmaceutical selections and dosages, and
treatment options should be made and healthcare professionals should consult a variety of sources.
When prescribing medication, healthcare professionals are advised to consult the product information
sheet (the manufacturer’s package insert) accompanying each drug to verify, among other things,
conditions of use, warnings and side effects and identify any changes in dosage schedule or
contraindications, particularly if the medication to be administered is new, infrequently used or has a
narrow therapeutic range. To the maximum extent permitted under applicable law, no responsibility is
assumed by the publisher for any injury and/or damage to persons or property, as a matter of products
liability, negligence law or otherwise, or from any reference to or use by any person of this work.
shop.lww.com
Contributing Authors
William P. Adams Jr, MD
Program Director, UT Southwestern Aesthetic Surgery Fellowship
Associate Professor, UT Southwestern Department of Plastic Surgery
Dallas, Texas

Jayant P. Agarwal, MD
Professor of Surgery
Surgery, Division of Plastic Surgery
University of Utah School of Medicine
Salt Lake City, Utah

Brandon Alba, MD, MPH


Resident Physician
Division of Plastic and Reconstructive Surgery
Rush University Medical Center
Chicago, Iillinois

Amanda Amin, MD
Assistant Professor of Surgery
Breast and Surgical Oncology
University of Kansas Medical Center
Kansas City, Kansas

Lauren Antognoli, MD
General Surgery Resident
Anne Arundel Medical Center
Annapolis, Maryland

Anuja K. Antony, MD, MPH, MBA, FACS


Professor and Vice Chair of Surgery
Chief of Breast Reconstruction | Co-Director, Breast Cancer Service Line
Medical Director of Plastic Surgery
Department of Surgery
Rush University Cancer Center
Division of Plastic and Reconstructive Surgery
Rush University Medical Center
Chicago, Illinois

John G. Apostolides, MD, FACS


Medical Director
DEFY Plastic and Reconstructive Surgery
San Diego, California

Gary Arishita, MD
PRMA Plastic Surgery
San Antonio, Texas

Seth Z. Aschen, MD
Department of Surgery
Division of Plastic Surgery
New York Presbyterian Hospital
New York, New York

Yoav Barnea, MD
Professor of Plastic Surgery
Head, Plastic and Reconstructive Breast Surgery Unit
Tel Aviv Medical Center
Tel Aviv, Israel

Ibrahim Al Bassam, MD
Research fellow
Plastic Surgery Department
Brussels University Hospital—Vrij Universiteit Brussel (VUB)
Brussels, Belgium

Bradley Bengtson, MD, FACS


Founder and CEO
Bengtson Center for Aesthetics and Plastic Surgery
Grand Rapids, Michigan

Susana Benitez, MD
Department of Plastic Surgery
Clínica Las Condes
Santiago, Chile

Tiffany Berry, MD, MBA


Norton Breast Surgery
Norton Healthcare
Louisville KY

Gaurav Bharti, MD, FACS


Plastic Surgeon
Private Practice
Hunstad Kortesis Bharti Cosmetic Surgery
Charlotte, North Carolina

Brian Biggerstaff, MD
Former Chief Resident
Department of Plastic Surgery
The University of California, Irvine
Irvine, California

Joshua A. Bloom, MD
General Surgery Resident
Department of Surgery
Tufts Medical Center
Boston, Massachusetts

Rachel Bluebond-Langner, MD
Laura and Isaac Perlmutter Associate Professor of Plastic Surgery
Hansjörg Wyss Department of Plastic Surgery
NYU Grossman School of Medicine
New York, New York

Christopher A. Bobbitt, MD
Department of Plastic Surgery
Loma Linda University
Loma Linda, California

Jarrod T. Bogue, MD
Department of Surgery
Division of Plastic Surgery
New York Presbyterian Hospital
New York, New York

Kristen P. Broderick, MD
Assistant Professor of Plastic and Reconstructive Surgery
Plastic and Reconstructive Surgery
Johns Hopkins University School of Medicine
Baltimore, Maryland, USA

Ernesto Maria Buccheri


Founder of MedicinaPlastica Private Clinic
Plastic Surgery Unit of MedicinaPlastica
MedicinaPlastica Center, Rome
Rome, Italy

Patrick J. Buchanan, MD
CEO and Senior Plastic Surgeon
The Georgia Institute for Plastic Surgery
Savannah, Georgia

Edward Buchel, MD, FACS


Provincial Specialty Lead, Surgery, Shared Health
Professor and Head, Department of Surgery
Rady Faculty of Health Sciences, Max Rady College of Medicine, University
of Manitoba
Surgery Site Director, Health Sciences Centre
Section Head and Regional Leader, Section of Plastic Surgery, University of
Manitoba and WRHA
Program Director, University of Manitoba, Microvascular Reconstructive
Fellowship
Department of Surgery
Rady Faculty of Health Sciences, Max Rady College of Medicine, University
of Manitoba
Winnipeg, Manitoba, Canada

M. Bradley Calobrace, MD, FACS


Director, CaloAesthetics Aesthetic Surgery Fellowship
Private Practice, CaloAesthetics Plastic Surgery
Clinical Faculty, Department of Surgery, Division of Plastic Surgery
University of Louisville and University of Kentucky
Louisville and Lexington, Kentucky

Lisa Cassileth, MD, FACS


Plastic and Reconstructive Surgeon
Department of Plastic Surgery
Assistant Professor, UCLA
Founder, Cassileth Plastic Surgery
Beverly Hills, California

Giuseppe Catanuto, MD, PhD


Oncoplastic Breast Surgeon
G.RE.T.A. Group for Reconstructive and Therapeutic Advancements
Milan, Naples, and Catania, Italy
Multidisciplinary Breast Unit
Azienda Ospedaliera Cannizzaro
Catania, Italy

Shiliang Chang, MD, FACS


Assistant Professor
Department of Surgery
Division of Plastic and Reconstructive Surgery
Oregon Health and Science University
Portland, Oregon

Serena Chase, MBA


Chase Advocate Consulting, LLC
Co-Founder—Plastic Surgery Imaging
Cocoa Beach, Florida

Abhishek Chatterjee, MD, MBA, FACS


Associate Professor of Surgery
Chief, Division of Plastic Surgery
Tufts Medical Center
Boston, Massachusetts

Obaid Chaudhry, MD
Attending
Plastic Surgery
Private Practice, Be That Beautiful Plastic Surgery
Beverly Hills, California

Salman Chaudry, MD
General Surgery Resident
Anne Arundel Medical Center
Annapolis, Maryland

Angela Cheng, MD
Associate Professor
Division of Plastic Surgery
Emory University Hospital
Atlanta, Georgia

Jeremy Chidester, MD
Plastic and Hand Surgery
Draper, Utah

Minas Chrysopoulo, MD, FACS


President
PRMA Plastic Surgery
San Antonio, Texas

Mark W. Clemens, MD, FACS


Associate Professor Plastic Surgery
Plastic and Reconstructive Surgery
The University of Texas MD Anderson Cancer Center
Houston, Texas

Costanza Cocilovo, MD
Medical Director, Inova Breast Care Program
Breast Surgery
Inova Schar Cancer Institute
Fairfax, Virginia

Hiram S. Cody III, MD


Professor of Surgery
Department of Surgery
Breast Service
Memorial Sloan-Kettering Cancer Center
New York, New York

Robert Cohen, MD, FACS


Medical Director
Aesthetic Plastic Surgery
Scottsdale Center for Plastic Surgery
Paradise Valley, Arizona

Amy S. Colwell, MD
Associate Professor of Plastic Surgery
Surgery
Massachusetts General Hospital, Harvard Medical School
Boston, Massachusetts

Jonathan Cook, MD
Plastic Surgeon
Private Practice
Sanctuary Plastic Surgery
Boca Raton, Florida

Samuel G. Coulson, MBChB, MRCS(Ed), PGCert(Med Ed)


Speciality Registrar in Burns and Plastic Surgery
Department of Plastic and Reconstructive Surgery
Addenbrooke’s Hospital, Cambridge University Hospitals NHS Foundation
Trust
Cambridge, United Kingdom

Joseph H. Dayan, MD
Associate Professor of Plastic Surgery
Co-Director, Lymphatic Surgery and Research
Memorial Sloan-Kettering Cancer Center
New York, New York

Charles Deguzman, BS
Loma Linda University
School of Medicine
Loma Linda, California

Michael DeLong, MD
Resident in Plastic and Reconstructive Surgery
Department of Surgery
University of California, Los Angeles
Los Angeles, California

Sarah M. DeSnyder, MD, FACS, CMQ


Associate Professor of Breast Surgical Oncology
The University of Texas MD Anderson Cancer Center
Houston, Texas

Roberto Diaz, MD, PhD


Section Head for Breast Oncology and Senior Member
Department of Radiation Oncology
Moffitt Cancer Center
Tampa, Florida

Jill R. Dietz, MD, FACS


Associate Professor of Surgery
Seidman Cancer Center
Case western Reserve School of Medicine
Cleveland, Ohio

Tassos Dionisopoulos, MD, CM, FACS, FRCSC


Chief, Division of Plastic Surgery
Jewish General Hospital
Assistant Professor, Department of Surgery
McGill University
Montreal, Quebec, Canada

Joseph J. Disa, MD
Attending Surgeon, Memorial Sloan-Kettering Cancer Center
Professor of Surgery, Weill Medical College of Cornell University
Plastic and Reconstructive Surgery Service, Department of Surgery
Memorial Sloan-Kettering Cancer Center
New York, New York

Risal Djohan, MD, MBA


Vice Chairman
Department of Plastic Surgery
Cleveland Clinic
Cleveland, Ohio

Cassandra Drew, BSMLS


Medical Student
Loma Linda University
Loma Linda, California

James M. Economides, MD
Private Practice
Washington, DC and Arlington, Virginia

Kirsten Edmiston, MD, FACS


Breast Surgery Medical Director, Inova Schar Cancer Institute-Fair Oaks
Vice President, Surgical Safety and Operations, Inova Fair Oaks Hospital
Fairfax, Virginia
Dana Egozi, MD, PhD
Doctor of Plastic and Reconstructive Surgery
Plastic Surgery Department
Kaplan Medical Center
Rehovot, Israel

Francesco M. Egro, MBChB, MSc, MRCS


Resident Physician
Department of Plastic Surgery
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Asim Ejaz, PhD


Research Assistant Professor
Department of Plastic Surgery
University of Pittsburgh
School of Medicine
Pittsburgh, Pennsylvania

Omar Elfanagely, MD
Surgical House Staff, PGY 3
General Surgery
Rutgers Robert Wood Johnson Medical School
New Brunswick, New Jersey

Dora Evangelidou, MD, MSc


Plastic Surgery Consultant
Plastic Surgery
CosmeSurge Hospital
Dubai, United Arab Emirates

Gregory R. D. Evans, MD, FACS


Professor of Plastic Surgery and Biomedical Engineering
Founding Chair, Department of Plastic Surgery
The University of California, Irvine
Irvine, California
Past President, American Society Plastic Surgeons
Orange, California

Alexander Facque, MD
Fellow, Gender Confirmation Surgery
Plastic Surgery
Weiss Memorial Hospital and The Center for Gender Confirmation Surgery
Chicago, Illinois

Reuben A. Falola, MD, MPH


Division of Plastic and Reconstructive Surgery
Baylor Scott & White Medical Center
Temple, Texas

Jian Farhadi, MD, FMH(Plast), EBOPRAS


Professor of Plastic and Reconstructive Surgery
Guys and St Thomas’ NHS Foundation Trust
London, United Kingdom
School of Medicine, University of Basel
Switzerland

Giusy Fatigato, MD
Research Fellow
Plastic Surgery Department
Brussels University Hospital—Vrij Universiteit Brussel (VUB)
Brussels, Belgium

Sarah E. Ferenz
MD Candidate
Chicago Medical School at Rosalind Franklin University
North Chicago, Illinois

John P. Fischer, MD, MPH, FACS


Associate Professor of Surgery (Plastic Surgery)
Director of Clinical Research Program
Perelman School of Medicine, University of Pennsylvania
Philadelphia, Pennsylvania
Megan Fracol, MD
Resident Physician
Division of Plastic Surgery
Northwestern Memorial Hospital
Chicago, Illinois

Jordan D. Frey, MD
Plastic Surgeon
Erie County Medical Center
Buffalo, New York

Allen Gabriel, MD, FACS


Clinical Professor of Surgery
Department Plastic Surgery
Loma Linda University Medical Center
Loma Linda, California

Jennifer R. Garreau, MD
Surgical Oncologist
Legacy Cancer Institute
Portland, Oregon

Ramon Garza, MD
PRMA Plastic Surgery
San Antonio, Texas

Niv Gelerman, MD
Plastic Surgery Department
Tel Aviv Medical Center
Tel Aviv, Israel

Mohiedean Ghofrani, MD, MBA


PeaceHealth System Medical Director for Laboratory Services
Director, Cytopathology and Women’s Health
PeaceHealth Southwest Medical Center
Vancouver, Washington
Caroline A. Glicksman, MD, MSJ
Clinical Assistant Professor, Hackensack Meridian School of Medicine at
Seton Hall
Department of Surgery
Glicksman Plastic Surgery
Sea Girt, New Jersey

James D. Goggin, MD
Plastic Surgeon
Partners in Plastic Surgery
Grand Rapids, Michigan

Daniel J. Gould, MD, PhD


Associate Surgeon
Plastic Surgery
Marina Plastic Surgery Associates
Marina Del Rey, California

Dael Govreen-Segal, MSc


Senior Director, Research and Development
Polytech Health & Aesthetics GmbH
Haifa, Israel

Jacky Govrin-Yehudain, MD
Plastic Surgeon, Inventor of Lightweight Breast Implants
Beit Harofim Medical Center
Haifa, Israel

Orel Govrin-Yehudain, MD
Resident of Plastic and Reconstructive Surgery
Division of Reconstructive and Aesthetic Surgery
Tel Aviv Sourasky Medical Center
Tel Aviv, Israel

Richard J. Greco, MD
CEO and Senior Plastic Surgeon
The Georgia Institute for Plastic Surgery
Savannah, Georgia

Stephen R. Grobmyer, MD, FACS


Professor and Chairman
Oncology Institute
Cleveland Clinic Abu Dhabi
Abu Dhabi, United Arab Emirates

Yoav Gronovich, MD, MBA


Board Certified Plastic Surgeon
Head, Plastic Surgery Department
Shaare Zedek Medical Center, Affiliated with the Hebrew University School
of Medicine
Jerusalem, Israel

Subhas C. Gupta, MD, CM, PhD, FRCSC, FACS


Professor and Chairman of Plastic Surgery
Department of Plastic Surgery
Loma Linda University
Loma Linda, California

Elizabeth J. Hall-Findlay, MD, FRCSC


Plastic Surgeon, Private Practice
Banff Plastic Surgery
Banff, Alberta, Canada

Moustapha Hamdi, MD, PhD


Professor and Chairman
Plastic Surgery Department
Brussels University Hospital—Vrij Universiteit Brussel (VUB)
Brussels, Belgium

Dennis C. Hammond, MD
Associate Program Director
Plastic Surgery
Spectrum Health, Integrated Plastic Surgery Residency
Grand Rapids, Michigan
Neal Handel, MD, FACS
Clinical Professor
Division of Plastic Surgery
David Geffen School of Medicine at UCLA
Los Angeles, California

Juliana E. Hansen, MD
Professor and Chief
Plastic and Reconstructive Surgery, Department of Surgery
Oregon Health and Science University Hospital, OHSU
Portland, Oregon

Per Hedén, MD, PhD


Associate Professor in Plastic Surgery, Karolinska Institute
Founder, Akademikliniken Hospital Group
Stockholm, Sweden

John Hijjawi, MD, FACS


Associate Medical Director
One Intermountain Plastic Surgery
Intermountain Healthcare
Salt Lake City, Utah

Dennis R. Holmes, MD, FACS


Associate Professor of Surgery
John Wayne Cancer Institute
Santa Monica, California

Kathleen A. Holoyda, MD
Plastic Surgery Resident
Surgery, Division of Plastic Surgery
University of Utah School of Medicine
Salt Lake City, Utah

Luther H. Holton III, MD


Chief of Plastic Surgery
Anne Arundel Medical Center
Annapolis, Maryland

Christopher Homsy, MD
Assistant Professor of Surgery
Department of Surgery
Division of Plastic Surgery
Tufts Medical Center
Boston, Massachusetts

Anna C. Howell, MD
Resident Physician
Division of Plastic and Reconstructive Surgery
University of Southern California
Los Angeles, California

Michelle Lee Hsia, OTD, OTR/L, CLT


Associate Professor of Clinical Occupational Therapy
Occupational Therapy
Keck School of Medicine of the University of Southern California
USC Norris Comprehensive Cancer Center
Los Angeles, California

Matthew H. Isakson, MD
Aesthetic Plastic Surgery Fellow
Hunstad Kortesis Bharti Plastic Surgery
Charlotte, North Carolina

Kasia Kania, MD, MPH


Division of Plastic Surgery
Michael E. DeBakey Department of Surgery
Baylor College of Medicine
Houston, Texas

Nolan S. Karp, MD
Vice Chair of Clinical Operations
Professor of Plastic Surgery
Board of Directors, American Society for Aesthetic Plastic Surgery
Hansjörg Wyss Department of Plastic Surgery
NYU Grossman School of Medicine
New York, New York

Nima Khavanin, MD
Resident Physician
Plastic and Reconstructive Surgery
Johns Hopkins University School of Medicine
Baltimore, Maryland

Roger Khouri, MD
Miami Breast Center
Key Biscayne, Florida

Kimberly S. Khouri, MD
Resident, PGY 2
Harvard Plastic Surgery
Boston, Massachusetts

John Vincent Kiluk, MD


Associate Member, Breast Oncology Department
Moffitt Cancer Center
Tampa, Florida

Esther A. Kim, MD, FACS


Assistant Professor of Plastic and Reconstructive Surgery
Division of Plastic and Reconstructive Surgery
University of California, San Francisco
San Francisco, California

Hahns Y. Kim, MD, FACS


Associate Professor of Plastic Surgery
Department of Plastic Surgery
Loma Linda University
Loma Linda, California
John Y. S. Kim, MD, FACS
Professor of Surgery
Division of Plastic Surgery
Northwestern Memorial Hospital
Chicago, Illinois

Rebecca Knackstedt, MD, PhD


Plastic Surgery Resident
Plastic Surgery
Cleveland Clinic
Cleveland, Ohio

Lauren E. Kokai, PhD


Co-Director, Adipose Stem Cell Center
Assistant Professor of Plastic Surgery
Department of Plastic Surgery
University of Pittsburgh
Pittsburgh, Pennsylvania

George Kokosis, MD
Assistant Professor
Plastic and Reconstructive Surgery
Rush University Medical Center
Chicago, Illinois

Bill G. Kortesis, MD, FACS


Plastic Surgeon, Private Practice
Hunstad Kortesis Bharti Plastic Surgery
Charlotte, North Carolina

Alvin C. Kwok, MD, MPH


Assistant Professor of Surgery
Surgery, Division of Plastic Surgery
University of Utah School of Medicine
Salt Lake City, Utah

Ethan E. Larson, MD
Larson Plastic Surgery
Tucson, Arizona

Gustavo Jimenez Muñoz Ledo, MD


Plastic Surgeon
Phi Aesthetics
Leon, Mexico

Peter Ledoux, MD
PRMA Plastic Surgery
San Antonio, Texas

Chanel Lee, BA
Medical Student
Loma Linda University
Loma Linda, California

Michele L. B. Ley, MD, FACS


Breast Surgical Oncology
Arizona Oncology
Tucson, Arizona

Pamela Li, MD, FACS


Breast Surgeon
Department of Surgery
University Hospitals
Cleveland, Ohio

Kristin Limbach, MD
Surgical resident
Oregon Health and Science University
Portland, Oregon

Albert Losken, MD, FACS


Professor, Emory Plastic Surgery
Emory University School of Medicine
Atlanta, Georgia
Adi Maisel Lotan, MD
Department of Plastic and
Reconstructive Surgery
Shaare Zedek Medical Center
Affiliated with the Hebrew University School of Medicine
Jerusalem, Israel

Douglas R. Macmillan, MBChB, MD, FRCS


Oncoplastic Breast Surgeon
Nottingham Breast Institute
City Hospital
Nottingham, United Kingdom

Alexandra Maertens, MD
Doctor
Plastic Surgery
Institut Gustave Roussy
Villejuif, France

Charles M. Malata, BSc(HB), MBChB, MRCS LRCP, FRCS(Glasg),


FRCS(Plast)
Consultant Plastic Surgeon and Visiting Professor of Anglia Ruskin
University School of Medicine
Department of Plastic and Reconstructive Surgery
Addenbrooke’s Hospital, Cambridge University Hospitals NHS Foundation
Trust
Cambridge, United Kingdom

Anita Mamtani, MD
Assistant Attending Surgeon
Breast Service, Department of Surgery
Memorial Sloan Kettering-Cancer Center
New York, New York

Kacey G. Marra, PhD


Professor, Departments of Plastic Surgery and Bioengineering
Vice Chair of Research, Department of Plastic Surgery
University of Pittsburgh
Pittsburgh, Pennsylvania

Patrícia Martínez-Jaimez, RN, MSN


Lymphedema Nurse Navigator
Clínica Planas
Barcelona, Spain

Andres Mascaro, MD
Department of Plastic and Reconstructive Surgery
Cleveland Clinic Florida
Weston, Florida

Jaume Masià, MD, PhD, MSc


Professor and Chief of Plastic Surgery Department
Hospital de Sant Pau/Clínica Planas/Universitat Autonoma de Barcelona
Barcelona, Spain

G. Patrick Maxwell, MD, FACS


Clinical Professor of Surgery
Department Plastic Surgery
Loma Linda University Medical Center
Loma Linda, California

Chet Mays, MD
Co-Director, CaloAesthetics Aesthetic Surgery Fellowship
Private Practice, CaloAesthetics Plastic Surgery
Clinical Faculty, Department of Surgery, Division of Plastic Surgery
University of Louisville School of Medicine
Louisville, Kentucky

Stephen J. McCulley, MBChB, FCS(SA), FRCS


Plastic Surgeon
City Hospital
Nottingham, United Kingdom
Patricia McGuire, MD, FACS
Founder CEO
Parkcrest Plastic Surgery
St. Louis, Missouri

Alex N. Mesbahi, MD, FACS


Assistant Clinical Professor of Plastic Surgery
Georgetown University
National Center for Plastic Surgery
McLean, Virginia

Christina A. Minami, MD, MS


Associate Surgeon
Department of Surgery, Division of Breast Surgery
Dana-Farber/Brigham and Women’s Cancer Center
Boston, Massachusetts

Melissa Mitchell, MD, PhD


Associate Professor
Breast Radiation Oncology
MD Anderson Cancer Center at the University of Texas
Houston, Texas

Sunny Mitchell, MD
Director of Breast Surgery
Medical Director of the Breast Center
Montefiore Nyack Hospital
Nyack, New York

Anita T. Mohan, MRCS, MBBS, PhD


Division of Plastic and Reconstructive Surgery
Mayo Clinic
Rochester, Minnesota

Blaise P. Mooney, MD
Breast Imaging Fellowship Director
Medical Director, McKinley Outpatient Center
Associate Member, Diagnostic and Interventional Radiology
Moffitt Cancer Center
Tampa, Florida

Saba Motakef, MD
Plastic Surgery Resident
Department of Plastic Surgery
Loma Linda University
Loma Linda, California

Maurice Y. Nahabedian, MD, FACS


Professor of Plastic Surgery
VCU School of Medicine—Inova Campus
National Center for Plastic Surgery
McLean, Virginia

Chet Nastala, MD
PRMA Plastic Surgery
San Antonio, Texas

Maurizio Bruno Nava, MD


Oncoplastic Breast Surgeon
G.RE.T.A. Group for Reconstructive and Therapeutic Advancements
Milan, Naples, Catania, Italy

Anne M. Nickodem, MD, FACS


Private Practice
Annandale, Virginia

Oscar Ochoa, MD, FACS


Reconstructive Microsurgeon
Reconstructive Breast Surgery
PRMA Plastic Surgery
San Antonio, Texas

Ketan M. Patel, MD
Associate Professor of Surgery
Surgery, Plastic and Reconstructive
Keck School of Medicine of the University of Southern California
Los Angeles, California

Lauren Patty, MD, MS


Department of Plastic Surgery
The University of California, Irvine
Irvine, California

Anne Peled-Warren, MD
Co-Director, Sutter Health CPMC Breast Cancer Program
Private Practice, Breast and Plastic Surgery
San Francisco, California

J. Peter Rubin, MD, MBA, FACS


Chair, Department of Plastic Surgery
UPMC Endowed Professor of Plastic Surgery
Director, UPMC Wound Healing Services
Professor of Bioengineering
University of Pittsburgh
Pittsburgh, Pennsylvania

Brian Pettitt-Schieber, BHA


Medical Student, Emory University
School of Medicine
Atlanta, Georgia

Christopher Pham, MD
University of Southern California
Los Angles, California

Melissa L. Pilewskie, MD, FACS


Associate Attending
Department of Surgery
Memorial Sloan-Kettering Cancer Center
New York, New York
Steven Pisano, MD
PRMA Plastic Surgery
San Antonio, Texas

Troy A. Pittman, MD, FACS


Plastic and Reconstructive Surgeon
Private Practice
Washington, DC

Cristhian D. Pomata, MD, MSc


Attending Plastic Surgeon
Breast Reconstruction, Lymphedema
Clínica Planas
Barcelona, Spain

Stefano Pompei, MD
Consultant Plastic Surgeon and Head of Plastic Surgery Department
Plastic surgery
Medstar Healthcare LLC
Dubai, United Arab Emirates

Jason N. Pozner, MD
Adjunct Clinical Faculty
Plastic Surgery
Cleveland Clinic Florida
Weston, Florida

Jennifer L. Pretz, MD
Instructor in Radiation Oncology
Radiation Oncology
Dana-Farber/Brigham and Women’s Cancer Center
Boston, Massachusetts

Ali A. Qureshi, MD
Aesthetic Surgery Fellow
Marina Plastic Surgery
Marina del Rey, California
Alberto O. Rancati, MD, PhD
Professor of Surgery
Chief Surgery Department
Instituto Oncológico Henry Moore
Universidad de Buenos Aires.
Buenos Aires, Argentina

Agustin Rancati, MD
Staff surgeon
Surgery Department
Instituto Oncológico Henry Moore
Universidad de Buenos Aires.
Buenos Aires, Argentina

Bharat Ranganath, MD
Assistant Professor of Plastic Surgery
Department of Surgery
The George Washington University
Washington, DC

Neal R. Reisman, MD, JD, FACS


Clinical Professor of Plastic Surgery
Baylor College of Medicine
Attorney at Law
Houston, Texas

Chantal Reyna, MD, FACS


Assistant Professor of Surgery
Surgical Oncology
University of Cincinnati College of Medicine
Cincinnati, Ohio

Heather Richardson, MD, FACS


Breast Surgeon
Bedford Breast Center
Beverly Hills, California
Nicola Rocco, MD, PhD
Oncoplastic Breast Surgeon
G.RE.T.A. Group for Reconstructive and Therapeutic Advancements
Milan, Naples, Catania, Italy

Stacey Roddick, BS, ADN


Medical Student
Loma Linda University
Loma Linda, California

Abigail Rodriguez, MD
Division of Plastic and Reconstructive Surgery
Baylor Scott & White Medical Center
Temple, Texas

Rod J. Rohrich, MD, FACS


Clinical Professor of Plastic Surgery
Baylor College of Medicine
Houston, Texas
Founding Partner
Dallas Plastic Surgery Institute
Dallas, Texas

Jason Roostaeian, MD
Associate Clinical Professor in Plastic and Reconstructive Surgery
Department of Surgery
University of California, Los Angeles
Los Angeles, California

Barry S. Rosen, MD
Assistant Professor of Surgery, University of Illinois College of Medicine
Medical Director, Breast Center, Advocate Good Shepherd Hospital
Barrington, Illinois

Justin M. Sacks, MD, MBA


Division Chief of Plastic and Reconstructive Surgery
Department of Surgery
Washington University School of Medicine
St. Louis, Missouri

Tyler Safran, MD
Plastic and Reconstructive Surgery
McGill University Health Center
Montreal, Quebec, Canada

Michel Saint-Cyr, MD, FRCSC


Director, Division of Plastic Surgery
Vice Chairman, Surgical Services
Wigley Professor in Plastic Surgery
Clinical Professor (Affiliated), Texas A&M College of Medicine
Division of Plastic Surgery
Baylor Scott & White Medical Center
Temple, Texas

Ara A. Salibian, MD
Resident Physician
Hansjörg Wyss Department of Plastic Surgery
NYU Grossman School of Medicine
New York, New York

Benjamin Sarfati, MD, MSc


Senior Consultant in Plastic Surgery
Plastic Surgery Department
Gustave Roussy
Paris, France

Hani Sbitany, MD
Associate Professor of Surgery
Plastic and Reconstructive Surgery
Mount Sinai Medical Center
New York, New York

Mark Schafer, PhD, FAIUM, FASA


Co-Founder and Chief Technology Officer, Plastic Surgery Imaging
Sonic Tech, Inc
Ambler, Pennsylvania

Loren S. Schechter, MD
Clinical Professor of Surgery, University of Illinois at Chicago
Plastic Surgery
Attending Surgeon, Rush University Medical Center
Director, The Center for Gender Confirmation Surgery, Weiss Memorial
Hospital
Chicago, Illinois

Michael Scheflan, MD
Private Reconstructive and Aesthetic Plastic Surgeon
Plastic Surgery
Assuta & Atidim Medical Centers
Tel Aviv, Israel

Jaime S. Schwartz, MD, FACS


Diplomate, American Board of Plastic Surgery
Fellow, American College of Surgeons
Associate Clinical Professor of Surgery
Keck School of Medicine of the University of Southern California
Division of Plastic and Reconstructive Surgery
Beverly Hills, California

Michele A. Shermak, MD, FACS


Associate Professor of Plastic Surgery
Department of Plastic and Reconstructive Surgery
The Johns Hopkins University School of Medicine
Baltimore, Maryland
Private Practice in Plastic Surgery
Lutherville, Maryland

Hope Shin, MD
Division of Plastic and Reconstructive Surgery
Baylor Scott & White Medical Center
Temple, Texas

David A. Sieber, MD
Private Practice
Sieber Plastic Surgery
San Francisco, California

Noemi Makkai Sigalove, MD, FACS


Breast Surgeon
Comprehensive Breast Center of Arizona
Arizona Center for Cancer Care
Scottsdale, Arizona

Steven R. Sigalove, MD, FACS


Scottsdale Center for Plastic Surgery
Paradise Valley, Arizona

Devinder Singh, MD
Chief of Plastic Surgery
University of Miami Miller School of Medicine
Miami, Florida

Aseel Sleiwah, MRCS(Ed), MSc


Senior Clinical Fellow
Department of Plastic and Reconstructive Surgery
Guys and St Thomas’ NHS Foundation Trust
London, United Kingdom

Hatem Soliman, MD
Associate Member, Breast Oncology and Immunology Departments
Medical Director, Clinical Trials Office
Moffitt Cancer Center
Tampa, Florida

Magdolna Solti, MD, MS


Director of Survivorship Program
Compass Oncology
Vancouver, Washington

Aldona J. Spiegel, MD
Associate Professor, Weill Medical College of Cornell University
Institute for Reconstructive Surgery
Houston Methodist Hospital
Houston, Texas

Dhivya R. Srinivasa, MD
Faculty, Plastic and Reconstructive Surgery
Surgery
Cedars-Sinai
Los Angeles, California

W. Grant Stevens, MD, FACS


Clinical Professor of Surgery
Division of Plastic Surgery
Keck School of Medicine of the University of Southern California
Marina Plastic Surgery Associates
Marina del Rey, California
Director, USC Aesthetic Surgery Fellowship
Past President, American Society of Aesthetic Plastic Surgery
Co-Founder and CMO, Orange Twist

Toni Storm, MD
Co-Director, Compass Oncology Breast Specialists
Medical Director, Surgical Services, Kearney Breast Center, PeaceHealth
Vancouver, Washington

Louis L. Strock, MD
Clinical Assistant Professor
Department of Plastic Surgery
UT Southwestern Medical Center
Dallas, Texas

Seema Sugandh, BS
CEO and Founder
PlasticSurgeryRecoveryGuide.com
Beverly Hills, California

Jeffrey A. Sugandi, MD, PharmD


Chief Resident
General Surgery
University of Arizona
Tucson, Arizona

Susie X. Sun, MS, MD, CMQ


Assistant Professor of Breast Surgical Oncology
The University of Texas MD Anderson Cancer Center
Houston, Texas

Mia Talmor, MD, FACS


Professor of Plastic Surgery
Weill Cornell Medical College
Attending Surgeon
New York Presbyterian Hospital
New York, New York

Erin M. Taylor, MD
Division of Plastic and Reconstructive Surgery
Massachusetts General Hospital/Harvard Medical School
Boston, Massachusetts

Steven Teitelbaum, MD, FACS


Associate Clinical Professor of Plastic Surgery
David Geffen School of Medicine at UCLA
Los Angeles, California

Chad M. Teven, MD
Assistant Professor and Vice Chair of Research
Division of Plastic and Reconstructive Surgery
Mayo Clinic
Phoenix, Arizona
Brian P. Thornton, MD, PhD, MBA
ThorntonMD Plastic Surgery
Louisville, Kentucky

Laura Tobing, BSN


Medical Student
Loma Linda University
Loma Linda, California

Elizabeth Turner, PA-C


ThorntonMD Plastic Surgery
Louisville, Kentucky

Stephanie A. Valente, DO, FACS


Associate Professor of Surgery, Cleveland Clinic Lerner College of Medicine
and Case Western
Reserve University
Breast Surgeon, Department of General Surgery
Cleveland Clinic
Cleveland, Ohio

Vasileios Vasilakis, MD
Aesthetic Plastic Surgery Fellow
Hunstad Kortesis Bharti Plastic Surgery
Charlotte, North Carolina

Mark L. Venturi, MD, FACS


Clinical Associate Professor of Surgery
Department of Surgery
VCU School of Medicine—Inova Campus
National Center for Plastic Surgery
McLean, Virginia

Amedeo Villanucci, MD
Clinical Fellow
Plastic Reconstructive Surgery Department
Regina Elena Cancer Institute of Rome
Rome, Italy

Sheri S. Wang, MD
Resident Physician
Department of Anesthesiology and Perioperative Medicine
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania

Laura E. G. Warren, MD, EdM


Instructor in Radiation Oncology
Radiation Oncology
Dana-Farber/Brigham and Women’s Cancer Center
Boston, Massachusetts

Drew Welk, MD
Private Practice of Plastic Surgery
The Polyclinic Plastic Surgery
Seattle, Washington

Amy S. Xue, MD
Division of Plastic Surgery
Baylor College of Medicine
Houston, Texas

Louisa Yemc, PA-C


National Center for Plastic Surgery
Mclean, Virginia

Giovanni Zoccali, MSc, MD, PhD


Consultant Plastic Surgeon
Department of Plastic and Reconstructive Surgery
Queen Elizabeth Hospital
East Grinstead, United Kingdom

Roy de Vita, MD
Chief, Plastic and Reconstructive Surgery Department
Regina Elena Cancer Institute of Rome
Rome, Italy

Daniel Del Vecchio, MD


Instructor in Surgery/Attending
Plastic Surgery
Manhattan Eye, Ear, and Throat Hospital/Massachusetts General
Hospital/Private Practice, Uptown Body Contouring
New York, New York/Boston, Massachusetts
Foreword
I first met Scott Spear at the Senior Resident’s meeting in Dallas, TX in
1979, as we were each finishing our plastic surgery training: he at the
University of Miami while I was at Johns Hopkins. Despite our geographical
separation in residency and in practice that followed, we became hard and
fast friends for nearly 40 years, in no small part due to our common interests
in both breast surgery and golf! In addition to his many academic
accomplishments, Scott was a man of kindness, generosity, and compassion.
He had a passion for life, family, knowledge, and education. His sudden
passing in 2016 left a void that will not be easily filled, yet his legacy and
influence lives on, and will be further enhanced by this fourth edition of this
book he created, and has been appropriately “renamed” in his honor: Spear’s
Surgery of the Breast: Principles and Art.
The foreword to the first edition of this text, written by Scott’s esteemed
plastic surgical Professor, Dr D. Ralph Millard, the professor’s challenge to
his student as to why he was writing this book? “As one of your trainees and
a descendent of the Gilles-Millard School of plastic surgery, I have wanted
to, hoped to, and tried to play my part in passing on to the present and future
plastic surgeons the importance of key principles … and as only a handful of
plastic surgeons can combine principles and art … the same focus as your
books. I borrowed the title from your book, The Principles and Art of Plastic
Surgery, (bringing these) into play in a broadly aimed textbook on surgery of
the breast, in an attempt to help surgeons do their best job and ultimately help
patients get better results.” Undoubtedly, the student succeeded in his goal!
Dr Millard further cited in Dr Spear’s response as to why he wanted to
write this book: “I have been struck that the field of breast surgery needed a
textbook, which could cover the whole gamut of breast surgery from a
surgical point of view. What is currently available in the bookstore is focused
either on purely cosmetic surgery, reconstructive surgery, or ablative surgery.
No one has tied these three together; so we have oncologic surgeons who do
not understand aesthetic principles, we have aesthetic surgeons who do not
understand oncologic or reconstructive principles, and we have reconstructive
surgeons who do not understand aesthetic or oncologic principles. I expect
that, in the future, breast surgery will become more and more of a specialty
by itself. I see this textbook, therefore, as the fundamental text for this next
generation of breast surgeons.” Again, the student’s prediction was accurate,
and his goals accomplished! I am certain Dr Millard took great pride in the
transmission of “the principles and art” he taught his students, being
conveyed by them (here, by Dr Spear) into increasingly specialized areas of
plastic surgery, which was then transmitted to, and further refined by, future
generations!
Dr Spear’s predictions cited in this first forward have certainly come true,
as “breast surgery” has mushroomed in its scope, advances, and refinements.
The integration of aesthetic, reconstructive, and oncologic disciplines has
merged in collaboration and “mindset.” The surgical techniques in
therapeutic and risk-reducing breast cancer treatment have been refined to
allow for “aesthetic mastectomy” consideration, with immediate
reconstruction now the norm. “Onco-plastic” breast surgery has evolved with
breast preserving cancer treatment options. With the increasing importance of
“self-image health” and well-being, radiation and medical oncologic
treatments now take “breast appearance” into consideration. Technical
advances in minimally invasive surgery, “flap” surgery, microsurgery,
regenerative constructs as ADM’s, fat grafting, and stem cells, advances in
the safety and refinements in breast implants and tissue expanders … are
examples of the ongoing developments that have refined outcomes. Dr Spear
and I shared the podium together multiple times a year at regional, national,
and international venues, as well as in small group “think tanks” and in
publications sharing our experiences in all of these breast surgery
advancements.
No longer do we, as “life-long students” of breast surgery, have to go to
the “bookstore” to seek information on these advances or connect “by mail”
with our colleagues, as internet communication has brought the transmission
of information and global communication into a virtual and instantaneous
reality. Thus the importance continues of bringing all “breast-related”
disciplines together to contribute to this “single textbook,” now available
both in print and electronically.
I first met Dr Allen Gabriel at a plastic surgery meeting in Las Vegas in
2006 (almost 30 years later), when he was a senior Resident in plastic surgery
training. After interviewing him there at that meeting, I accepted him for the
2007–2008 postgraduate fellowship position in our training program in
Nashville. It was a time of incremental advances in “breast surgery” in the
United States with fourth-generation silicone gel implants having been
recently received FDA approval and fifth-generation, form stable implants, in
the last stages of clinical trials. We had embarked upon the “Team Up”
concept in breast reconstruction, working hand in hand with oncologic breast
surgeons, advancing nipple-sparing mastectomy approaches and introducing
the concept of “bio-engineered breasts” (combination of cohesive gel
implants, scaffles [ADM] and cells [fat]) which was the keystone to the
return of prepectoral breast reconstruction. In fact in June 2008, as Dr Gabriel
was finishing his fellowship, we (he and I, together) performed the first back
table assembly (wrap) of ADM affixed to a tissue expander, inserted into the
prepectoral pocket following nipple-sparing mastectomy. (completing 2
months later with expander removal, implant placement, and fat grafting).
When Dr Gabriel first began his fellowship, he asked me why I did not
follow up of all of my concepts and presentations with scientific
“publications”? It was an interesting question, which caused me to pause, as I
had to admit that I had moved away from scientific publications into more
technique and product development publications which followed the
generation of patented medical devices I had designed by partnering with
industry. He said “Let’s change that!,” and did we ever, by scientifically
documented all of our laboratory and clinical work in the peer-reviewed
scientific literature. Invigorated by Dr Gabriel’s enthusiasm, I reprioritized
my efforts not only toward “presenting” our clinical activities and outcomes,
but toward publishing them in the scientific literature (obviously via the work
ethic and penmanship of Dr Gabriel).
In January 2015, I was honored to present the Hartrampf Lectureship at the
Atlanta Breast Symposium. Later that year, Scott Spear was asked to give the
2016 Hartrampf Lectureship. As in everything he did, Scott wanted to give
his best effort in that presentation, and stated working on it months in
advance. We always communicated frequently, but especially in 2015 as he
shared with me some of his initial thoughts on his Hartrampf presentation,
asking my opinion. We each reflected on our careers and discussed other
current matters during this time frame, and one day he said: “It is time for the
next edition of my book, but it is also time to pass on the torch. I have
watched and been impressed by the early career advancements of your former
fellow, Dr Allen Gabriel. I believe he has the skillset, enthusiasm, and work
ethics to take on the editorship of the next edition. Do you think he would
have an interest?” I responded that I would give him a call, but that I thought
he would be honored and thrilled at the possibility. “The rest, as they say, is
history. Dr Gabriel took on the challenge of the creation of this fourth edition
with the vigor and enthusiasm which he applies to everything he does. Do not
be misled, however, by the four editors listed on the cover of this edition.
While all certainly contributed along with the numerous expert authors, this
is clearly the work product of Allen Gabriel, and only his modesty prevented
this from edition being titled: Gabriel’s: Spear’s Surgery of the Breast:
Principles and Art.
Referring back to Dr Millard’s Foreword to the first edition of this book, as
“the professor” challenging Dr Spear, his “student,” on why he would want to
write this book, were I (as the professor) to ask Dr Gabriel (as the student)
why he wanted to write this book, I would expect him to respond in a similar
vein (paraphrasing from the first edition):

“As one of your and Dr Spear’s trainees (descendants of the Gilles-


Millard and Johns Hopkins Schools of plastic surgery), I want to, hope to,
and am trying to play my part in passing on to the present and future plastic
surgeons, the importance of key principles … and as only a handful of plastic
surgeons can combine principles and art … the same focus you both have
taught … while maintaining the title from your book, Spear’s Surgery of the
Breast: Principles and Art,… updating and hoping to add to the legacy of this
great textbook on surgery of the breast, thus attempting to continue to help
surgeons do their best job resulting in patients getting increasingly better
results, and improving women’s health globally.”

G. Patrick Maxwell, MD, FACS


Clinical Professor, Plastic Surgery, Loma Linda School of Medicine
Associate Professor, Plastic Surgery, Vanderbilt University Medical Center
Preface
The field of cosmetic and reconstructive breast surgery continues to evolve
and has now entered the realm where the two share similar principles and
concepts. Reconstructive breast surgery is facilitated by understanding
aesthetic principles and aesthetic breast surgery is facilitated by
understanding reconstructive principles. The gradual evolution of these
concepts was recognized by one of the thoughtful leaders in plastic and
reconstructive surgery, Scott L. Spear, MD, to serve as the principal editor of
the first three editions of his masterful textbook, Surgery of the Breast:
Principles and Art. The third edition was published in 2011 and was state of
the art; however, over the past decade, there have been multiple
advancements that have continued to advance our understanding of the
principles and practice of aesthetic and reconstructive breast surgery. This
new and revitalized fourth edition incorporates the latest and most important
innovations that have occurred with regard to aesthetic and reconstructive
breast surgery. The practice of aesthetic breast surgery has seen a resurgence
with the use of autologous fat for volume and contour enhancement, less use
of textured surface and anatomic shaped implants, and increased emphasis on
proper counseling of patients before and after breast augmentation surgery.
Reconstructive surgery has been revolutionized with prepectoral placement of
implants, enhanced recovery after surgery pathways, and with the possibility
of improving sensation following autologous reconstruction.
As with the previous editions, this fourth edition is structured to provide
the reader with a detailed approach to a multitude of surgical procedures with
the goal of improving surgical outcomes. The new edition has been highly
illustrated with clinical pearls that should be useful to those who perform
aesthetic and reconstructive breast operations. Many of the chapters include
an audiovisual component that is intended to take the reader step-by-step
through an operation. We feel that the combination of written and audiovisual
material sets the new standard for the highest-quality print education
available and should facilitate ones’ ability to perform these operations at a
higher level of understanding and ability.
The book is intended for all surgeons interested in breast surgery to review
many of the essential principles, concepts, techniques, and case examples
associated with cosmetic and reconstructive breast surgery and to provide
insight as well as clinical pearls that will facilitate one’s ability to better
master these procedures. The contributors for each chapter were selected
based on talent, ability, reputation, and a commitment to the educational
process. Thus, some of the most renowned aesthetic and reconstructive breast
surgeons who have dedicated their careers to their craft have been invited to
contribute. The final product represents a compendium of breast operations
that the plastic surgeon should be able to perform and master.
There are several individuals that we would like to thank for without them,
completion of the text would not have been possible. The first is Scott L.
Spear, MD, who set the standard to excellent breast education and who laid
the foundation for this textbook. All of the editors are forever indebted to
Scott for his honesty, candor, and enthusiasm when it comes to education and
mentorship. He will be forever missed. Next, we would like to acknowledge
and thank G. Patrick Maxwell, MD, for all of his immense contributions to
the field of reconstructive and aesthetic breast surgery. He too has raised the
bar for all of us to become better breast surgeons and improve patient
outcomes. We would also like to thank the staff at Wolters Kluwer for their
hard work and commitment toward publishing this truly outstanding fourth
edition. Finally, we would like to thank our families for their support,
patience, and understanding during the many hours spent in preparation of
this work.

Maurice Y. Nahabedian, MD, FACS


Allen Gabriel, MD, FACS
Contents

Contributing Authors
Foreword
Preface

SECTION I
Breast Surgery and oncology
1 Epidemiology of Breast Cancer: Incidence and Risk
Factor
JILL R. DIETZ | CHANTAL REYNA

2 Breast Cancer Screening and Diagnosis, Including the


Surgically Altered Breast
TONI STORM | ALLEN GABRIEL

3 Molecular Pathology of the Breast


MOHIEDEAN GHOFRANI

4 Defining and Managing the High-Risk Patient


NOEMI MAKKAI SIGALOVE

5 Heredity and Breast Cancer: Risk Assessment, Genetic


Testing, and Management Options
MAGDOLNA SOLTI

6 Patient Selection for Breast-Conservation Therapy


MICHELE L. B. LEY | JEFFREY A. SUGANDI

7 Axillary Nodal Recurrence


KRISTIN LIMBACH | JENNIFER R. GARREAU

8 Role of Nonsurgical Management of Breast Cancer:


Endocrine Therapy and Tumor Ablation
DENNIS R. HOLMES

9 Oncoplastic Approach to Maximizing the Lumpectomy-


Level I
PAMELA LI | JILL R. DIETZ

10 Oncoplastic Approach to Maximizing the Lumpectomy-


Level II
BARRY S. ROSEN | ANNE PELED-WARREN |
TONI STORM

11 Breast Conservation Failure: When to Do a Completion


Mastectomy
ANITA MAMTANI | HIRAM S. CODY III

12 Radiation Therapy Following Breast-Conserving Surgery


JENNIFER L. PRETZ | LAURA E. G. WARREN
13 The Surgical Management of Locally Advanced and
Stage IV Breast Cancer
SUSIE X. SUN | SARAH M. DESNYDER

14 Neoadjuvant and Adjuvant Systemic Therapy


MAGDOLNA SOLTI

15 Breast Cancer Diagnosis, Prognosis, and Treatment in


Augmented Women
NEAL HANDEL

16 Guidelines and Patient Selection Criteria for Nipple and


Skin-Sparing Mastectomy
COSTANZA COCILOVO | MAURICE Y. NAHABEDIAN

17 Invasive Carcinoma: Radiation Therapy After


Mastectomy
LAURA E. G. WARREN

18 Optimizing Mastectomy Flaps Based on Breast Anatomy


NOLAN S. KARP | JORDAN D. FREY | ARA A. SALIBIAN

19 Male Breast Cancer: Surgery of the Breast


JOHN VINCENT KILUK | BLAISE P. MOONEY | HATEM
SOLIMAN | ROBERTO DIAZ

20 Breast Cancer Recurrence—Strategies for Risk


Reduction
KIRSTEN EDMISTON
21 Disease of the Breast, Benign to Premalignant;
Hyperplasia to DCIS
MICHELE L. B. LEY | JEFFREY A. SUGANDI

22 Breast Cancer Screening and Management in the


Transgender Patient
DHIVYA R. SRINIVASA | ESTHER A. KIM

23 Shared Decision Making: Patient Choice and Satisfaction


SUNNY MITCHELL

24 Team Approach to Nipple-Sparing Mastectomy


ALLEN GABRIEL | MAURICE Y. NAHABEDIAN | TONI
STORM | G. PATRICK MAXWELL

SECTION II
The Axilla and Lymphedema
25 Basic Science and Management of Postsurgical
Lymphedema and Vascularized Lymph Node Transplant
JOSEPH H. DAYAN

26 Sentinel Node Biopsy and Axillary Dissection


HIRAM S. CODY III

27 Postneoadjuvant Axillary Assessment and Management


CHRISTINA A. MINAMI | MELISSA L. PILEWSKIE
28 Alternative Methods for Axillary Sentinel Lymph Node
Dissection
STEPHANIE A. VALENTE | STEPHEN R. GROBMYER

29 Axillary Surgery Versus Radiation as Treatment of


Regional Nodes: AMAROS Trial and Beyond
AMANDA AMIN | MELISSA MITCHELL

30 Conservative Management of Postsurgical Lymphedema


MICHELLE LEE HSIA | CHRISTOPHER PHAM | KETAN M.
PATEL

31 Selection of Vascularized Lymph Node Donor Sites for


Upper Extremity Lymphedema Surgery and Strategies to
Minimizing Complications
ANNA C. HOWELL | DANIEL J. GOULD | KETAN M. PATEL

32 Liposuction as a Viable Treatment for End-Stage Upper


Extremity Lymphedema
JAUME MASIÀ | CRISTHIAN D. POMATA |
PATRíCIA MARTíNEZ-JAIMEZ

SECTION III
Oncoplastic Techniques and Breast
Reduction
33 Oncoplastic Breast Surgery and Shared Decision Making
MAURIZIO BRUNO NAVA | NICOLA ROCCO | GIUSEPPE
CATANUTO

34 Oncoplastic Techniques in Breast Conservation Therapy


—The Plastic Surgeon’s Perspective
ALBERT LOSKEN | BRIAN PETTITT-SCHIEBER

35 Local Flaps for Partial Mastectomy Defects


MOUSTAPHA HAMDI | IBRAHIM AL BASSAM

36 Local Flaps for Breast-Conserving Surgery Defects


DOUGLAS R. MACMILLAN | STEPHEN J. MCCULLEY

37 Avoiding Pitfalls in Symmetry Procedures Following


Unilateral Autologous Versus Implant-Based
Reconstruction
MICHELE A. SHERMAK

38 Breast Reduction and Mastopexy After Massive Weight


Loss
FRANCESCO M. EGRO | J. PETER RUBIN

39 Vertical Breast Reduction and Rereduction


ELIZABETH J. HALL-FINDLAY | GUSTAVO JIMENEZ MUñOZ
LEDO

40 Reduction Mammoplasty With Inverted-T Incision


ETHAN E. LARSON | MAURICE Y. NAHABEDIAN |
SHILIANG CHANG
41 Secondary Breast Reduction
PATRICK J. BUCHANAN | RICHARD J. GRECO

42 Management of Complications in Breast Reduction: The


Displaced NAC
NOLAN S. KARP | ARA A. SALIBIAN | JORDAN D. FREY

43 Male Breast Reduction: Liposuction Versus Excision


CHARLES M. MALATA | SAMUEL G. COULSON

SECTION IV
Implant Based Reconstruction
44 Evolution of Breast Surgery and the Bioengineered
Concept
ALLEN GABRIEL | G. PATRICK MAXWELL | MAURICE Y.
NAHABEDIAN

45 Overview of Indications and Consideration for


Prepectoral Versus Subpectoral Reconstruction
GEORGE KOKOSIS | MAURICE Y. NAHABEDIAN

46 Patient Selection for One-Stage Subpectoral


Reconstruction
AMY S. COLWELL | ERIN M. TAYLOR

47 Patient Selection for One-Stage Reconstruction


Prepectoral
ROY DE VITA | ERNESTO MARIA BUCCHERI

48 Breast Reconstruction With Form-Stable Implants


MAURIZIO BRUNO NAVA | GIUSEPPE CATANUTO |
NICOLA ROCCO

49 Management of Ptotic Patient Desiring Nipple-Sparing


Mastectomy With Implant-Based Reconstruction
ANNE M. NICKODEM

50 Two-Staged Nipple-Sparing Mastectomy for Preservation


of the Nipple Areolar Complex in the Large or Ptotic
Breast: Reconstructive Algorithm and Approach
TROY A. PITTMAN | JAMES M. ECONOMIDES

51 Can We Identify Risky Patients for NSM?


ALBERTO O. RANCATI | AGUSTIN RANCATI

52 Implant-Based Reconstruction in High-BMI Patients


ALLEN GABRIEL | MAURICE Y. NAHABEDIAN |
G. PATRICK MAXWELL

53 When Is Delayed Breast Reconstruction Indicated?


CHRISTOPHER A. BOBBITT | HAHNS Y. KIM

54 Immediate Two-Stage Breast Reconstruction Using a


Tissue Expander and Implant
MARK L. VENTURI
55 Delayed Expander/Implant Sequenced Breast
Reconstruction
DREW WELK

56 Prepectoral Direct-to-Implant Reconstruction: What Is


the Role for Dermal Substitutes?
TYLER SAFRAN | TASSOS DIONISOPOULOS

57 Role of Acellular Dermal Matrix in Breast


Reconstruction
MAURICE Y. NAHABEDIAN

58 Use of Meshed Acellular Dermal Matrix in Breast


Reconstruction
MICHAEL SCHEFLAN | ADI MAISEL LOTAN

59 Role of Implant Reconstruction in Previously Radiated


Patients
ANGELA CHENG | ALBERT LOSKEN

60 Management and Prevention of Nipple and Mastectomy


Skin Necrosis
BRIAN P. THORNTON | ELIZABETH TURNER | TIFFANY
BERRY

61 Management of the Exposed Implant


MEGAN FRACOL | JOHN Y. S. KIM

62 Management of Animation Deformity in Implant-Based


Reconstruction
ALLEN GABRIEL | STEVEN R. SIGALOVE | G. PATRICK
MAXWELL

63 Symmetry Procedures Following Unilateral Implant


Breast Reconstruction
MICHAEL SCHEFLAN | YOAV GRONOVICH

64 Implant-Based Breast Reconstruction After Unilateral


Mastectomy
CHAD M. TEVEN | BHARAT RANGANATH | JOSEPH J. DISA

65 Patient Satisfaction in Unilateral Versus Bilateral


Mastectomy With Reconstruction
HANI SBITANY

66 Surgical Treatment of Nipple Malposition in Nipple-


Sparing Mastectomy
SETH Z. ASCHEN | JARROD T. BOGUE | MIA TALMOR

67 Salvage of the Contracted Radiated Implant: Radiation


Sequelae and Evolving Strategies in Prevention and
Reconstruction
BRANDON ALBA | ANUJA K. ANTONY

68 Reconstruction of Previously Augmented Patients


Undergoing Mastectomy: Options for Implant-Based
Reconstruction
MICHAEL SCHEFLAN | YOAV GRONOVICH

69 Latissimus Dorsi Musculocutaneous Flap Breast


Reconstruction
DENNIS C. HAMMOND | JAMES D. GOGGIN

70 Radiating Implants Versus Expanders: Plastic Surgeon’s


Perspective and Experience
JAMES M. ECONOMIDES | TROY A. PITTMAN

71 Perioperative Pain Management: ERAS Protocols,


Blocks, and the Role of Pharmacogenomics
KIRSTEN EDMISTON

SECTION V
Autologous Based Reconstruction
72 Tips and Tricks to Achieve Best Result in Autologous-
Based Reconstruction: Shaping Flaps in Delayed Versus
Immediate Reconstruction
REUBEN A. FALOLA | HOPE SHIN | ABIGAIL RODRIGUEZ |
MICHEL SAINT-CYR

73 Efficiency in Autologous Breast Reconstruction


EDWARD BUCHEL

74 Management of the Unilateral Reconstruction and Timing


of Matching
YOAV BARNEA | NIV GELERMAN

75 Pedicle TRAM and Free TRAM


DANA EGOZI

76 Superior Gluteal Artery Perforator Flap (SGAP)


ASEEL SLEIWAH | GIOVANNI ZOCCALI | JIAN FARHADI

77 DIEP Flap Breast Reconstruction With Sensory


Neurotization
MINAS CHRYSOPOULO | OSCAR OCHOA |
STEVEN PISANO | PETER LEDOUX | GARY ARISHITA |
RAMON GARZA | CHET NASTALA

78 Profunda Artery Perforator Flaps


ANITA T. MOHAN | REUBEN A. FALOLA | MICHEL SAINT-
CYR

79 Transverse Upper Gracilis Flaps


ANITA T. MOHAN | REUBEN A. FALOLA | MICHEL SAINT-
CYR

80 The Lumbar Artery Perforator Flap: An Alternative to


DIEAP Flap for Breast Reconstruction
MOUSTAPHA HAMDI | GIUSY FATIGATO

81 Goldilocks Mastectomy for Immediate Reconstruction


Without Implants
LISA CASSILETH | HEATHER RICHARDSON

82 Neurotization of the Autologous Flap


KASIA KANIA | ALDONA J. SPIEGEL
83 Management of the Failed Free Flap
MAURICE Y. NAHABEDIAN

84 Management of Donor-Site Complications


DEVINDER SINGH | LUTHER H. HOLTON III | LAUREN
ANTOGNOLI | SALMAN CHAUDRY

85 Secondary Procedures for the Autologous Reconstructed


Breast
JAUME MASIà | CRISTHIAN D. POMATA

86 Radiation and Autologous Breast Reconstruction: The


Role of Delayed-Immediate Reconstruction
KATHLEEN A. HOLOYDA | ALVIN C. KWOK | JAYANT P.
AGARWAL

87 Abdominal-Based Breast Reconstruction—Optimizing


Aesthetic Results
ANDRES MASCARO | SUSANA BENITEZ

88 Autologous Tissue Breast Reconstruction in the Thin


Patient
REBECCA KNACKSTEDT | RISAL DJOHAN

89 Enhancing Volume in Autologous Reconstruction


ALEXANDRA MAERTENS | BENJAMIN SARFATI

SECTION VI
Fat Grafting
90 Does Fat Grafting Increase the Risk of Breast Cancer?
SHERI S. WANG | FRANCESCO M. EGRO | ASIM EJAZ |
KACEY G. MARRA | LAUREN E. KOKAI | J. PETER RUBIN

91 Indications and Controversies in Fat Grafting of the


Partial Mastectomy Defect
MAURICE Y. NAHABEDIAN | ALLEN GABRIEL

92 Fat Grafting in Implant-Based Breast Reconstruction


JOHN HIJJAWI

93 Fat Grafting in Autologous Breast Reconstruction


NIMA KHAVANIN | KRISTEN P. BRODERICK | JUSTIN M.
SACKS

94 Total Breast Reconstruction With Autologous Fat


Grafting and Tissue Expansion
KIMBERLY S. KHOURI | ROGER KHOURI

SECTION VII
Augmentation & Augmentation Mastopexy
& Revisionary Augmentation
95 Augmentation Mammaplasty: General Considerations
ALLEN GABRIEL | G. PATRICK MAXWELL
96 Augmentation in Patient With Congenital Breast
Deformity
GAURAV BHARTI | BILL G. KORTESIS | VASILEIOS
VASILAKIS | MATTHEW H. ISAKSON

97 Patient Education in Breast Augmentation


CAROLINE A. GLICKSMAN | SARAH E. FERENZ

98 Inframammary Approach to Breast Augmentation


M. BRADLEY CALOBRACE | CHET MAYS

99 The Periareolar Approach to Augmentation


Mammaplasty
JULIANA E. HANSEN

100 Transaxillary Breast Augmentation


LOUIS L. STROCK

101 Subfascial Breast Augmentation


ALEX N. MESBAHI | LOUISA YEMC

102 The Inframammary Approach to Augmentation


Mammaplasty
STEVEN TEITELBAUM | ALLEN GABRIEL | G. PATRICK
MAXWELL

103 Shaped Implant in Breast Augmentation


PER HEDéN
104 Light-Weight Implants in Breast Augmentation
MICHAEL SCHEFLAN | OREL GOVRIN-YEHUDAIN | DAEL
GOVREEN-SEGAL | JACKY GOVRIN-YEHUDAIN

105 Polyurethane Implants in Aesthetic Breast Surgery


STEFANO POMPEI | DORA EVANGELIDOU

106 Augmentation Mastopexy: General Considerations


ROBERT COHEN

107 Breast Augmentation Mastopexy—Safe and Simplified


ROD J. ROHRICH | AMY S. XUE

108 Augmentation-Mastopexy With Shaped or Round


Implants, Is There a Difference?
ROY DE VITA | ERNESTO MARIA BUCCHERI | AMEDEO
VILLANUCCI

109 Avoiding Pitfalls With Mastopexy–Augmentation


ALI A. QURESHI | W. GRANT STEVENS

110 Management of Recurrent Ptosis Following


Augmentation Mastopexy
M. BRADLEY CALOBRACE | CHET MAYS

111 Liposuction Mastopexy


JAIME S. SCHWARTZ

112 Neopectoral Technique for Implant Malposition


ALLEN GABRIEL | MAURICE Y. NAHABEDIAN |
G. PATRICK MAXWELL

113 Subpectoral “Dual-plane” Conversion for Treating


Aesthetic Concerns After Breast Augmentation
JONATHAN COOK | JASON N. POZNER

114 Secondary Revision of the Augmented Breast


DAVID A. SIEBER

115 Combining Lipofill and Small Implants for Breast


Augmentation
OBAID CHAUDHRY | DANIEL DEL VECCHIO

116 Breast Revisionary Surgery and the Role of Acellular


Dermal Matrix and Bioabsorbable Mesh
ALLEN GABRIEL | MAURICE Y. NAHABEDIAN |
G. PATRICK MAXWELL | STEVEN R. SIGALOVE

SECTION VIII
General Considerations in Aesthetic and
Reconstructive Surgery
117 Chest Masculinization for the Transmasculine Individual
ARA A. SALIBIAN | RACHEL BLUEBOND-LANGNER

118 Aesthetic Breast Surgery in Transgender Patients:


Feminization
LOREN S. SCHECHTER | ALEXANDER FACQUE

119 Tuberous Breast: Correction With and Without Implants


NIMA KHAVANIN | MAURICE Y. NAHABEDIAN

120 Effect of Smoking on Breast Plastic Surgery


BRIAN BIGGERSTAFF | LAUREN PATTY | GREGORY R. D.
EVANS

121 Should Elective Surgery Be Offered to High-BMI


Patients?
OMAR ELFANAGELY | JOHN P. FISCHER

122 Breast Implant–Associated Anaplastic Large Cell


Lymphoma
MARK W. CLEMENS

123 Proactive Approach to Capsular Contracture Prevention


MICHAEL DELONG | JASON ROOSTAEIAN |
WILLIAM P. ADAMS JR

124 Diagnosing, Treating, and Preventing Biofilms in


Implant-based Breast Surgery
SUBHAS C. GUPTA | CASSANDRA DREW | CHARLES
DEGUZMAN | CHANEL LEE

125 Breast Implant Illness: What We Know Now?


STEVEN TEITELBAUM | PATRICIA MCGUIRE | ALLEN
GABRIEL
126 Avoiding and Managing Patient Dissatisfaction
CHRISTOPHER HOMSY | JOSHUA A. BLOOM | ABHISHEK
CHATTERJEE

SECTION IX
Final Considerations
127 Informed Consent: Medicolegal Considerations in Breast
Surgery
NEAL R. REISMAN

128 Social Media for the Aesthetic and Reconstructive Breast


Surgeon
SUBHAS C. GUPTA | SABA MOTAKEF | JEREMY CHIDESTER
| SEEMA SUGANDH | CASSANDRA DREW | CHANEL LEE |
STACEY RODDICK | LAURA TOBING

129 Integrating High-Resolution Ultrasound Into Your


Practice Including Background, Ultrasound Basics,
Current Studies, and Clinical Applications
BRADLEY BENGTSON | MARK SCHAFER | SERENA CHASE |
PATRICIA MCGUIRE

130 Perioperative Principles in Breast Surgery


JOHN G. APOSTOLIDES

Index
SECTION I

Breast Surgery and Oncology


1 Epidemiology of Breast Cancer: Incidence and Risk Factor
2 Breast Cancer Screening and Diagnosis, Including the Surgically
Altered Breast
3 Molecular Pathology of the Breast
4 Defining and Managing the High-Risk Patient
5 Heredity and Breast Cancer: Risk Assessment, Genetic Testing, and
Management Options
6 Patient Selection for Breast-Conservation Therapy
7 Axillary Nodal Recurrence
8 Role of Nonsurgical Management of Breast Cancer: Endocrine Therapy
and Tumor Ablation
9 Oncoplastic Approach to Maximizing the Lumpectomy-Level I
10 Oncoplastic Approach to Maximizing the Lumpectomy-Level II
11 Breast Conservation Failure: When to Do a Completion Mastectomy
12 Radiation Therapy Following Breast-Conserving Surgery
13 The Surgical Management of Locally Advanced and Stage IV Breast
Cancer
14 Neoadjuvant and Adjuvant Systemic Therapy
15 Breast Cancer Diagnosis, Prognosis, and Treatment in Augmented
Women
16 Guidelines and Patient Selection Criteria for Nipple and Skin-Sparing
Mastectomy
17 Invasive Carcinoma: Radiation Therapy After Mastectomy
18 Optimizing Mastectomy Flaps Based on Breast Anatomy
19 Male Breast Cancer: Surgery of the Breast
20 Breast Cancer Recurrence—Strategies for Risk Reduction
21 Disease of the Breast, Benign to Premalignant; Hyperplasia to DCIS
22 Breast Cancer Screening and Management in the Transgender Patient
23 Shared Decision Making: Patient Choice and Satisfaction
24 Team Approach to Nipple-Sparing Mastectomy
CHAPTER 1

Epidemiology of Breast Cancer:


Incidence and Risk Factor
JILL R. DIETZ | CHANTAL REYNA
INCIDENCE, MORTALITY, AND SURVIVAL
Breast cancer is the second most common cause of cancer globally and the
most common cause of cancer in women, accounting for 12.3% of total
cancers (1). When specifically looking at women, breast cancer has the
highest incidence, accounting for 25.4% of new cancer diagnosis in the
female population (2). In 2018, there were over 2 million new breast cancers
diagnosed globally (1). Incidence ranges from 27 per 100,000 in Africa and
Asia to 92 per 100,000 in the United States, a threefold difference between
the lowest and highest countries. Although breast cancer is the 5th most
common cancer death worldwide, it remains the most common cause of
cancer mortality in less developed countries at 14.3% (3).
In the United States specifically, the average lifetime risk of breast cancer
is 12.4%. Excluding skin cancer, breast cancer remains the most common
cancer in females and responsible for the second highest cancer deaths. It
accounts for 15.3% of new cancer cases. In 2018, there were 266,120 newly
diagnosed invasive breast cancers with an additional 63,960 newly diagnosed
carcinoma in situ (4,5). It is estimated that the new cases of breast cancer will
rise to 271,270 in 2019. Although the mortality rates have decreased 39%
from 1989 to 2015, a woman still has a 2.6% chance of dying from breast
cancer. There were still 40,920 deaths from breast cancer in 2018 and 6.7%
of all cancer deaths (4,6). Rates have been declining in older women and
have remained steady in women younger than 50 years old (6).
There are over 3 million survivors in the Unites States, including those
undergoing treatment and post treatment. According to the American Cancer
Society, the relative 5-year survival from 2008 to 2014 for female breast
cancer was 90% for all stages. A recent study confirmed that the 5-year
survival was 90.2% in the United States, 89.5% in Australia, but only 66.1%
in India when looking at cases from 2010 to 2014 worldwide (7). In the
United States, survival rate for stage 0 or 1 breast cancer is near 100%
compared to stage 3 which is 72% or stage 4 which is 22%. When evaluating
for whether local, regional, or distant disease was present at diagnosis the
rates look slightly improved (99%, 85%, and 27%, respectively) (6).
Changing Trends and Migration
While breast cancer incidence is stable or slightly increasing, the mortality
rates are decreasing in high-income countries, mainly in Northern/Western
European countries. In certain areas including France, Italy, Israel, Norway,
and Spain, both incidence and mortality of breast cancer is decreasing.
However, in other countries (Colombia, Ecuador, and Japan) incidence and
mortality rates are climbing. There are some areas where mortality rates are
rising such as in Brazil, Egypt, Guatemala, Mexico, and Moldova (8).
Incidence, mortality, and survival rates vary across the world and the
trends are also changing. These changes can also be seen within individual
migration. Individuals who move from a low-risk to a high-risk country
change the risk of breast cancer within one or two generations. Specifically,
Asian women who moved to the United States had increase breast cancer
incidence after one or two generations (9). This suggests there may be some
environmental factors contributing to the increased risk.
RISK FACTORS

Gender, Age, and Race


Breast cancer is 100 times more likely to be found in women than men. As a
result, most research is based on women. However, male breast cancer makes
up 1% of cases in the United States (10). In the United States, the incidence
of male breast cancer has increased 0.8% per year, with 1.3 new cases per
100,000 from 2008 to 2012. Although both female and male breast cancer
have increased incidence with age, male breast cancer does not show any
difference of incidence based on race, and it presents at a more advance
stage, with a decreasing mortality rate (11). The rest of the chapter will focus
primarily on female breast cancer in the United States.
It has been shown that breast cancer incidence increases with age in both
men and women. The median age of diagnosis for female breast cancer is 62
years old. When looking at age ranges, 46.3% of cases are diagnosed between
the ages of 45 to 64 years old, with the highest number of cases found from
55 to 64 years old (5). The lowest number of cases are found from 20 to 43
years old. The median age of death is 68 years old, with the majority of
deaths occurring at 65+ years old (5).
Incidence and mortality rates as well as other characteristics vary with
race. Non-Hispanic white women have higher rates of breast cancer with
Korean Americans having the lowest rates (Fig. 1-1) (4). African Americans
have the highest incidence of breast cancer in the 40 to 50 year age group.
The incidence rate in African American women has increase 0.3% annually
whereas in has remained fairly stable in non-Hispanic white women (6).
African Americans also have the highest 5-year mortality at 28.9 deaths per
100,000 persons and Asian Pacific Islanders have the lowest at 11.4 deaths
per 100,000 persons (4,6,10). This can be partly explained as African
Americans present with more advanced stages and disparities to health care
access. However, when correcting for disparities, African Americans still
have the highest mortality suggesting there are additional contributing factors
(12,13).
FIGURE 1-1 Breast cancer incidence and death rates in the United States by race.
(Data from Noone AM, Howlader N, Krapcho M, et al., eds. SEER Cancer Statistics
Review, 1975–2015. Bethesda, MD: National Cancer Institute.
https://seer.cancer.gov/csr/1975_2015/, based on November 2017 SEER data submission,
posted to the SEER web site, April 2018.)

Early Life Events


During developmental periods (fetal, childhood, and adolescence), breast
tissue may be more vulnerable to carcinogenesis (14,15).
Exposure in utero to diethylstilbestrol (DES), the first synthetic female
hormone has been shown to have an increased risk for breast cancer,
particularly after the age of 40 (16). While a European study did not show a
difference between those exposed to DES in utero and those who were
unexposed, a more recent 2011 study confirmed previous results that showed
there was a risk of breast cancer after 40 years of age (17). Daughters of
women who took DES while pregnant should be informed of their risks in the
future.
Other in utero events have been associated with elevated risks of breast
cancer. Twin pregnancy has shown a 1.2 times increase risk compared to a
single live birth (18). Meanwhile, preeclampsia and eclampsia have also been
associated with a lower risk of breast cancer (19–22).
Some studies have demonstrated that increased birth weight has increased
the relative risk of breast cancer. Two meta-analyses showed that increased
birth weight has an increased risk of breast cancer with one study showing up
to 23% (19,23). In the United States, a more recent study meta-analysis of 34
studies Park et al. confirmed that that birth weight did increase risk of breast
cancer, about 18% for those in the heaviest category (18). A Swedish study
showed that increased birth weight for gestational age had an increased risk
of breast cancer for those under 50 years old (24). Premenopausal risk for
breast cancer has been shown to have increased with higher birth weights
with a 5% increased risk per 500 g, but this was now shown to increase
postmenopausal breast cancer risk (25–27). It is theorized that circulating
maternal estrogens and IGF-1 may be responsible for the elevated risk. This
has been documented in animal models (28,29).
Radiation exposure is a known risk factor for primary breast cancer.
Ionizing radiation even at low doses increases the development of breast
cancer (30,31). There is a higher risk of breast cancer when the age of
exposure is less than 20 years old and less for older than 40 years old, and the
risk lasts a lifetime (32,33). Based on the fact that both low-dose cumulative
effect seen in atomic bomb and diagnostic radiation and high-dose effect with
high cumulative doses seen in Hodgkin lymphoma have been shown to
increase the risk of breast cancer, this has led to a theory where there is linear
increase for low-dose cumulative dose up to 10 Gy where it flattens out, and
then no or minimal increase at 40 Gy (34). Although ionizing radiation does
increase the risk of primary breast cancers, adjuvant radiation therapy for de
novo breast cancers treated after 45 years old of age is not associated with an
elevated risk for a second primary breast cancer (34). Overall, younger age of
radiation exposure, higher radiation dose, and longer follow-up demonstrate
increases breast cancer risk.

Age of Menarche
It has been known that the age of menarche is linked to the risk of breast
cancer. However, early menarche is associated with several other risk factors
such as parity, age at first birth, adult height, and BMI which may confound
the absolute risk (35). It has been shown that menarche at a young age
increases breast cancer risk with a relative risk of 1.05 per year younger than
the age of 13 (36). Ma et al. found that late menarche decreased the risk of
both hormone receptor positive and negative breast cancers, but was more
protective against hormone receptor positive cancer (37). Menstrual age was
more associated with lobular rather than ductal carcinoma (35,38).
Unfortunately, the age of menarche is decreasing. However, the prostate,
lung, colorectal, and ovarian (PLCO) cancer screening trial has shown that
menstrual age is becoming a less important risk factor and may have other
influences as previously mentioned (35,39).

Age of Menopause
The age of menopause has been shown to influence the risk of breast cancer.
There was no difference in risk where it was a surgically induced or natural
menopause (35). The risk of breast cancer doubles each decade until
menopause and then stabilizes, although it is still more common in
postmenopausal women (40). PLCO trial demonstrated a relative risk of 1.29
for breast cancer in women who had menopause older than 55 years old
compared to those less than 45 years old, with less than 45 years appearing to
be protective (39). The risk increases 1.029 times for each year older than
mean age of natural menopause (49.3 years); it doubles for every decrease
after menopause. This is particularly true for estrogen-positive breast cancer
and lobular carcinoma (39).

Reproductive History and Parity


Reproductive history and parity are standard portions of risk assessment for
breast cancer. Early parity appears to be protective as individuals who had
their first child prior to the age of 25 had a lower risk for breast cancer than
those where were older than 30 years old and nulliparous (36). This
association is seen only in hormone-positive breast cancer and ranges from
11% to 36% reduced risk (37,41). Later parity however increased risk of
breast cancer up to 27% as well as increased the risk of hormone receptor
negative breast cancer. Younger parity with additional births was protective
against hormone-positive breast cancer regardless of breastfeeding, but later
parity with additional births and no breastfeeding showed an increase risk of
breast cancer (41). Although most studies show a decreased risk of breast
cancer with parity in the long term, there is an interval increase in the
peripartum risk and some data suggesting increased risk based on timing of
multiple parity. There is a short-term increased risk associated with
pregnancy, but postpartum there is a 5- to 10-year period of protection
(42–44). One study even found that having more than one birth decreased the
risk of cancer (45). However race and intervals between births may place a
factor. Increased parity was shown to have increased risk for breast cancer in
African American women younger than 45 years old, but a reduced risk for
those older than 45 years old (46). In relation to intervals between births, a
Finnish study evaluated the timing between pregnancy and number of
pregnancies to find that having more than five children within 1-year
intervals increased the risk of breast cancer compared to 3-year intervals. In
terms of parity and abortion, a meta-analysis showed there was no risk of
breast cancer as a result of abortion whether it was spontaneous or induced
(47). This was further supported by the Committee of Gynecologic Practice,
which stated no increased risk of breast cancer associated with abortion (48).

Breastfeeding
Breastfeeding has been shown to decrease the risk of breast cancer (25).
Breastfeeding for at least a year has been shown to decrease risk of breast
cancer, both for hormone-positive and hormone-negative subtypes (49).
Some studies have shown that there is a 2% decrease in risk per 5 months of
breastfeeding (25,50). Additionally, some studies suggest that a total year of
breastfeeding either with a single birth or over several children, decreases the
risk of breast cancer 4.3% (50,51). In a recent meta-analysis, breastfeeding
was shown to be protective in estrogen receptor (ER)-negative and triple-
negative breast cancer (50). The protection of breastfeeding from cancer is
theorized to be influenced by alternating hormonal patterns, decreasing
menstrual cycles, and inducing amenorrhea. This can decrease exposures to
sex hormones which have been shown to increase breast cancer risk (52).
Furthermore, it is believed that lactation exfoliates the breast and ductal tissue
which can purge defective cells and induce apoptosis in potentially
premalignant cells with damaged DNA at the end of lactation (25).
Nutritional Factors
Nonstarchy Vegetables
Although previous studies have eluded to a preventive factor with non-starch
vegetables with high consumption, other studies have shown no association
between starch consumption with breast cancer overall (25,53–55). When
looking at dose-related intake, a meta-analysis has confirmed no significant
association with 200 g intake per day and breast cancer risk in both pre- and
postmenopausal women (25). Although the Nurse’s Health Study did not
show any association between nonstarchy vegetables and ER-negative breast
cancer, several other studies have (55,56). When stratified for hormone
receptor status, several studies showed a decrease risk for ER-negative PR-
negative breast cancer (55,57,58). When looking at total amount of
vegetables, a pooling project of cohort studies showed that an intake of more
than 300 g a day decreased the risk of breast cancer by 12% (55). It is thought
that the phytochemicals in vegetables reduce epidermal growth factor (EGF),
thus reducing ER-negative breast cancer which has higher amounts of EGF
(55).

Dairy
A pooled analysis of several cohort studies did not show any association
between dairy fluids or solids for 100 g per day intake and breast cancer, but
more recent studies have found a protective factor of dairy products in
premenopausal women (59). It has been shown that there is 5% decrease in
risk of premenopausal breast cancer per 200 g intake of dairy products per
day (25). Dong et al. performed a meta-analysis of 18 publications which also
has demonstrated a decreased risk of premenopausal breast cancer when
comparing higher to lower intake of total dairy products (60). Zang et al.
performed a more recent and larger meta-analysis of 22 prospective cohorts
in Western and Asian women and has found high dairy intake (>600 g/day)
significantly reduced the risk of premenopausal breast cancer. It also has
shown that yogurt and low-fat dairy products were the more significant
dietary foods (61). However, there is no association seen between dairy
products and the risk of postmenopausal breast cancer.

Carotenoids
It has been suggested that carotenoids decrease the risk of breast cancer.
Clear evidence has demonstrated that higher levels of certain carotenoids
such as circulating beta carotene, total carotenoids, and lutein have a
protective benefit against breast cancer. Alpha carotene, beta cryptoxanthin,
and lycopene have some evidence which suggests a decreased risk of breast
cancer (62). This relationship appears to be more closely associated with ER-
negative breast cancer. Several studies have shown that dietary beta carotene,
diet alpha carotene dietary lutein/zeaxanthin, and circulating alpha carotene
decrease risk of ER-negative breast cancer (62–66). A recent study, the EPIC
study, has shown circulating alpha and beta carotene decrease the risk of ER-
negative breast cancer and circulating lutein was protective for ER-positive
breast cancer (64). It is suggested that carotenoids affect breast cancer risk
through cell differentiation and apoptosis. They have antioxidant properties
which help protect cells from DNA damage (67).

Calcium
Calcium rich diets are protective against pre- and postmenopausal breast
cancer. Several studies have confirmed that high-calcium diets when
compared to lower calcium diets decrease the risk of premenopausal breast
cancer (68–72). There is a 13% decreased risk per 300 mg of calcium per day
in premenopausal women and 4% in postmenopausal women (25). Calcium is
a second messenger in cellular pathways affecting cell proliferation and
apoptosis (73,74). It has been shown in rodents that calcium decreases fat-
induced mammary proliferation which may decrease cancer cell proliferation
(74).
ALCOHOL
Although not previously demonstrated, multiple studies have now shown an
association between increased alcohol consumption and breast cancer
(75–79). There is suggestion that it is a risk factor for premenopausal breast
cancer, but a clear risk for postmenopausal breast cancer (80). When
investigating dose-related alcohol use and breast cancer, there appears to be a
significant risk factor in the United States for premenopausal breast cancer
and a significant factor in Europe and North American in postmenopausal
women. In fact, a 5% increase in the risk for premenopausal breast cancer has
been found when consuming more than 10 g of alcohol per day with beer
being a higher risk factor than wine or spirits. In the postmenopausal
population, a 9% increase of risk has been shown per 10 g of alcohol per day
with wine being more of a risk factor (25,80). Additional findings support
that alcohol was associated with ER-positive cancer in postmenopausal breast
cancer (76,80–82). A pooled analysis has demonstrated increase in risk for
ER-positive and PR-positive breast cancers with greater than 15 g of alcohol
per day (80). A study by Schonfeld et al. shows that seven alcoholic drinks
per week compared to no alcohol intake increased risk of postmenopausal
women with relative risk increase based on parity (Table 1-1) (83). Research
theorizes heavy alcohol use can lead to malnutrition and susceptibility to
carcinogenesis. Rodent studies show alcohol can affect carotenoid
metabolism and create free oxygen radicals, an already established protective
factor for breast cancer (84).

TABLE 1-1 Postmenopausal Breast Cancer Risk and Alcohol Based on


Parity
Parity Relative Risk
Nulliparous 1.3
Parity <25 yrs old 1.22
Parity >25 yrs old 1.33
SMOKING
A clear relationship between tobacco and breast cancer has not been reliable
previously due to many cofounding factors, particularly alcohol. In 2002, a
meta-analysis found no association between smoking and breast cancer (85).
However, Catsburg et al. showed a relationship between smoking duration,
amount smoked, and cumulative exposure and breast cancer risk (86).
Recently NSABP P-1 has clearly shown an increased risk of breast cancer in
women who smoked when compared to nonsmokers (75).
BODY MASS INDEX AND TOTAL BODY FAT
Obesity is increasing in the United States, with body mass index (BMI) a tool
to measure it. It has previously been reported that age-specific incidence of
breast cancer is higher for obese women than lean women (87). BMI >25
differs on breast cancer risk depending on menopausal status with
premenopausal women having less breast cancer risk than postmenopausal
women. BMI also has different effects on risk depending on age (35).
For young adults between the ages of 18 and 30, higher BMI protects
against pre-and postmenopausal breast cancer (25,88,89). Several studies
showed that there is a decreased risk of premenopausal breast cancer per 5
kg/m2 with a meta-analysis having an 18% decrease (25,88,89). Animal
models show that fat induces early breast differentiation which might make it
less vulnerable to tumogenesis (90). In addition, BMI slows growth and
lowers IGF-1 levels, both associated with increased breast cancer risks
(91–93).
Total body fat indicated by BMI has an influence on the risk of both pre-
and postmenopausal breast cancer. Several pooled analyses show that higher
BMI protects against premenopausal breast cancer, with a 7% decreased risk
per 5 kg/m2 (94). For postmenopausal cancer, higher BMI has been
associated with increased breast cancer risk, 12% per 5 kg/m2 and mainly
with ER-positive and PR-positive breast cancer (25). In addition to BMI, two
meta-analyses have demonstrated increased weight gain was associated with
increased breast cancer risk and joint hormone status (ER positive PR
positive and ER negative PR negative) (95,96).
For protection against premenopausal breast cancer, adipose-induced
estrogens affect mammary differentiation decreasing susceptibility to the
development of breast cancer (97). Nutritional status can also affect attained
adult height which can influence the risk of breast cancer (see attained adult
section). Body fat influences hormones such as insulin, IGF, and leptin which
can promote growth of cancer cells (98). Obesity also leads to a low chronic
inflammatory state with elevated levels of TNF-alpha, interleukin 6, and C-
reactive protein which can also increase carcinogenesis (99).
PHYSICAL ACTIVITY
Physical activity influences the risk of breast cancer. A meta-analysis showed
that increased physical activity decreased the relative risk of premenopausal
breast cancer (100). This was supported by a recent meta-analysis that found
a decrease of 7% when comparing the highest to lowest amounts of total
physical activity (25). When evaluating for vigorous activity, the same meta-
analysis showed a 17% risk reduction for premenopausal breast cancer.
The Women’s Health initiative cohort studied 74,171 postmenopausal
females ranging from the ages of 50 to 79 years old with 6 years of follow-
up. It has been shown that exercise influences the relative risk of breast
cancer for strenuous exercise more than 4 hours per week, 1.25 to 2.5 hours
per week, or brisk walking 10 hours per week (RR 0.9, 0.82, 0.79,
respectively) (101). Several studies have shown that increased activity is
protective against postmenopausal breast cancer, with a 13% risk reduction
(25,100). Similar to the reduction of premenopausal breast cancer, vigorous
activity reduced the risk of postmenopausal but to less of an extent around
10% (25,100). The association between physical activity and breast cancer
risk can be understood by recognizing that lowering overall body fat can
affect endocrine function. Physical activity decreases fasting insulin levels
and C-peptide levels, increases insulin sensitivity, and decreases levels of
estrogen and androgens in postmenopausal women which may help decrease
the risk of breast cancer (102). The immunomodulatory effects of physical
activity enhances the innate and acquired immune system which may aid in
cancer surveillance (102,103).
BENIGN BREAST DISEASE
Several benign breast lesions are associated with an increased risk of breast
cancer (104,105). These have been categorized as nonproliferative lesions,
proliferative lesions without atypia, and atypical hyperplasia, each associated
with its own risk for breast cancer. Nonproliferative lesions, such as cysts,
have no or little increased risk of breast cancer; proliferative lesions such as
papillomas and adenosis, have 1.5- to 1.9-fold increased risk; whereas
atypical lesions confers a 3- to 5-fold risk of breast cancer (104–107). Flat
epithelial atypia is considered a part of atypical lesions although it does not
have any hyperplasia and only confers a 2-fold increased risk (104). Atypical
lobular hyperplasia is associated with a higher risk than atypical ductal
hyperplasia, with lobular carcinoma in situ having the highest risk up to 8 to
10 times (Table 1-2) (104,105,108). There is a higher likelihood of an
ipsilateral breast event, typically occurring within the first 5 years of
diagnosis (105,108). These lesions are clearly an indicator for a higher risk of
breast cancer.
BREAST DENSITY
Breast density on mammography is determined by the relative amounts of
radiolucent adipose tissue and radiopaque connective tissue (109). Almost
half of the population has dense breast tissue, but breast density decreases
with advancing age (110–112). One study has shown that breast density
decreases with BMI and parity, but remains dense with alcohol use and
hormone replacement therapy (113). Heterogeneously dense breast tissue has
a 1.2 relative risk of breast cancer compared to 2.1 times risk for extremely
dense breast (109). When evaluating the Breast Cancer Surveillance
Consortium cohort, Barlow et al. found the risk even higher for extremely
dense breasts, about two to four times (114). Additional studies have shown
that dense breast tissue can be associated with 2 to 6× the risk of breast
cancer (111,115,116). It is known that breast density can make detection
more challenging which can lead to interval breast cancers being found
between routine imaging (117–119). However, masking effect is not the only
explanation. A meta-analysis confirmed breast density as an independent risk
factor. When compared to breast tissue density <10%, breast density of 50%
to 74% and ≥75% had relative risk of 2.92 and 4.64, respectively (115).
Several studies also have shown there is still an association with breast
density and cancer risk even after 10 years of screening (116,120,121).
Further evidence has been reported by the International Breast Cancer
Intervention Study which demonstrated women taking Tamoxifen who had
decreased breast density had more risk reduction than those who did not
decrease to the same amount (122). Breast density not only has a masking
effect but is also an independent risk factor for breast cancer, but to an
unknown quantity.

TABLE 1-2 High-Risk Breast Lesions and Associated Risk for Developing
Breast Cancer
Category Lesion Risk
Nonproliferative Lesion Simple cyst No
Complicated cyst Little
Proliferative Lesion Without Adenosis 1.5–
Atypia Intraductal papilloma 1.9×
Atypical Lesions Atypical ductal/lobular 4–5×
hyperplasia
Lobular carcinoma in situ 8–10×
Flat epithelial atypia 2×
GROWTH FACTORS AND ADULT HEIGHT
Unlike previously believed, in more recent studies, insulin-like growth factor
(IGF) has been shown to be associated with a higher risk of breast cancer.
One of the earliest studies which showed the association was more seen in
premenopausal women (123). A more recent analysis has shown that there is
a relationship between IGF-1 and ER-positive breast cancer, regardless of
menopausal status, which was supported by additional findings (124,125).
Kaaks et al. found increased risk in both pre- and postmenopausal women.
BRCA gene carriers in Italy were found to higher risk for cancer with
elevated IGF-1 levels (126). Although there are mixed reports in the past
between IGF and breast cancer risk, more recent studies are showing an
association.
Adult attained height is considered a risk factor for breast cancer. A large
meta-analysis has demonstrated a significant association between adult height
and breast cancer, in addition to colon cancer, ovarian cancer, and melanoma.
This association with breast cancer remained when adjusting for birth weight
(127). Adult height has been shown to be associated with pre- and
postmenopausal breast cancer. Several studies have demonstrated an
increased risk of premenopausal breast cancer in individuals with increased
height compared to low height individuals, with most significance North
American and Asian studies (25,128–132). A meta-analysis showed that there
is a 6% increase per 5 cm of height, with an additional study showing an
elevated risk per 10 cm of height in both pre- and postmenopausal women
(130,133). The risk has been also seen in postmenopausal breast cancer, with
a 9% increased risk per 5 cm in height and seen in geographic areas of
Europe and North America (25,39,129,132,134–137). Taller postmenopausal
BRCA mutation carriers were found to have 1.7-fold increase risk of breast
cancer compared to BRCA mutation carriers shorter than 5.75 inches (128).
A recent meta-analysis of prospective trials showed a relative risk of 1.17 and
confirmed an association of ER-positive breast cancer (133). Since height is
influenced by genetics, hormonal statues, and nutritional status, attained adult
height may act as an indicator of other known risk factors.
EXOGENOUS HORMONES

Hormonal Contraceptives
Previously there had been only a weak suggestion of oral contraception
(OCP) and breast cancer risk. The Collaborative Group on Hormonal Factors
in Breast Cancer has shown a 24% increased risk for breast cancer in women
who used OCP compared to nonusers. After cessation of OCP, the relative
risk decreases to 1.15 after 1 to 4 years of cessation and 1.01 after more than
10 years (138). The use of oral contraceptives coupled with duration of use
and age at first use have been associated with ER negative premenopausal
breast cancer (139). In addition, an association was found between oral
contraception and both ER negative and ER positive breast cancer (139).
Most recently, the Norwegian Women and Cancer Study (NOWAC) has
demonstrated the association between OCP and premenopausal breast cancer
risk. This study evaluated 74,862 women and the role of progestin-only
contraception (POC) and combined oral contraception (COC) on the risk of
premenopausal breast cancer (139). POC use for more than 5 years was found
to be associated with ER-positive and ER/PR+ breast cancer but not with
hormone receptor negative cancer. COC, on the other hand, was associated
with ER-negative and ER/PR- cancer (139).
Hormone Replacement Therapy
Consensus about hormone replacement therapy and the risk of breast cancer
has been changing over the last two decades. Several studies have shown that
estrogen alone and estrogen with progesterone increase the risk of breast
cancer 1.3 to 2.0 fold (87,140,141). The risk increased at a rate of 2.3% per
year of use and a relative risk of 1.35 for greater than 5 years of use, but
decreases after 5 years of cessation (138). Chen et al. showed that estrogen
plus progesterone use increases the breast cancer risk by 24%, but the use of
estrogen alone does not (142). The Women’s Health Initiative evaluated
conjugated equine estrogen (CEE) versus placebo in 10,739 postmenopausal
females with hysterectomies. It was stopped early for increased risk of stroke
but did not find an increased risk of breast cancer (143). Later follow-up
showed that CEE did increase the number of mammographic abnormalities
and short-term imaging follow-ups (144). Chlebowski et al. then compared
estrogen with progesterone versus placebo and found increased risk for breast
cancer with more nodal involvement and higher mortality (145). Several
studies have shown that CEE may decrease the risk of invasive breast cancer
in patients who have received prior hormonal therapy (144,146).
FAMILY HISTORY AND GENETICS

Family History
Approximately 10% of breast cancer patients have a family history of breast
cancer (147). There is evidence that females with first-degree relatives with
breast cancer have a higher age-specific incidence (87). Having a first-degree
relative, mother or sister, with breast cancer increases breast cancer risk about
two times and changes with the number of relatives affected (147,148).
Relative risk increases with each family member affected with a relative risk
of 1.8 for one family member, 2.93 for two family members, and 3.9 for three
or more family members (147). A family history with early-onset breast
cancer, bilateral breast cancer, or male breast cancer also increases the risk
for breast cancer (148).
Genetics
Several genes have now been shown to create a predisposition to breast
cancer. Some of these are high-penetrance genes which have a relative risk
≥10, some are moderate-penetrance (1.5 to 5.0), low-penetrance genes (≤1.5),
and others still require further investigation (Fig. 1-2).

High-Penetrance Genes
Most commonly recognized high-penetrance genes associated with breast
cancer are BRCA 1 and BRCA 2, tumor suppressor genes which help repair
DNA. Of the 10% hereditary breast cancer, about half are attributed to BRCA
1 and BRCA 2 (149). In the United States, approximately 1 in 300 to 500
women carry BRCA 1 or BRCA 2, with a higher rate of 1 in 40 in the
Ashkenazi Jewish population (150,151). The risk for breast cancer in BRCA
1 and BRCA 2 mutation has been found to be 46% to 72% and 38% to 69%,
respectively (152,153). The risk of a second breast cancer after 10 years of
the first diagnosis is 23% to 43% and 13% to 35%, respectively. Males with
BRCA 1 mutation have 1.2% chance of breast cancer and males with BRCA
2 have a risk of 8% (152,153).
FIGURE 1-2 National Cancer Institute chances of developing breast cancer by age of
70. (Data from National Cancer Institute at
https://www.cancer.gov/research/progress/discovery/brca-cancer-risk-infographic.)

Another high-penetrance gene is PTEN, a phosphatase. PTEN has been


shown to have a 20% to 30% risk of breast cancer (154). It is also responsible
for Cowden syndrome characterized by ovarian cancer, thyroid adenoma, or
follicular cell carcinomas, polyps, and gastrointestinal adenocarcinomas. In
addition, Li–Fraumeni syndrome is associated with TP53 mutations, resulting
in <0.1% of breast cancers. However, the presence of a TP53 mutation
increases the risk of breast cancer 18 to 60 times in those younger than 45
years old (154,155).

Moderate-Penetrance Genes
There are a several genes considered moderate-penetrance genes which have
a relative risk of cancer between 1.5 and 5: ATM, CHEK2, PALB2, BARD1,
BRIP1, and NF1. For ATM, the relative risk of breast cancer has been found
to be 3.0 with a lifetime risk up to 27% to 38% (156). CHEK2 has a lifetime
risk of 20%, but the risk increases depending on the number of relatives
affected. One affected first-degree relative increases the lifetime risk to 34%,
and the risk increases to 44% when there are first- and second-degree
relatives affected. The risk, however, decreases with increasing age (157).
PALB2 has been shown to have a lifetime risk of about 35%, but with two
first-degree relatives affected, that risk increases the lifetime risk to 58%
(158). BARD1 has recently been shown to have an increased risk for breast
cancer (149). BRIP1 has a relative risk of 2.0 for breast cancer (159). NF1
has been shown to have a lifetime risk of 59.6%, but only before the age of
50. In patients beyond 50, the risk decreases to that of the general population
(160,161).

Other Genes
RAD51C and RAD51D have an unclear effect on breast cancer risk. Several
studies have shown a wide variety of odds ratios from 0.88 to 8.33 and thus
have insufficient evidence to treat these mutations differently. Lynch-
associated genes (MLH1, MSH2, MSH6) also do not have enough evidence
and are continued to be treated as average risk (149,162).

REFERENCES

1. Bray F, Ferlay J, Soerjomataram I, et al. Global cancer statistics 2018:


GLOBOCAN estimates of incidence and mortality worldwide for 36
cancers in 185 countries. CA Cancer J Clin 2018;68(6):394–424.
2. GLOBOCAN 2018 Database. Available online at http://gco.iarc.fr/.
Accessed January 14, 2019.
3. Ferlay J, Colombet M, Soerjomataram I, et al. Estimating the global
cancer incidence and mortality in 2018: GLOBOCAN sources and
methods. Int J Cancer 2019;144(8):1941–1953.
4. National Cancer Institute (U.S.). Cancer Statistics Branch. In: SEER
Cancer Statistics Review. Bethesda, MD: National Cancer Institute.
http://purl.access.gpo.gov/GPO/LPS3349.
5. Noone AM HN, Krapcho M, Miller D, et al., eds. SEER Cancer
Statistics Review, 1975–2015. Bethesda, MD: National Cancer Institute.
https://seer.cancer.gov/csr/1975_2015/, based on November 2017 SEER
data submission, posted to the SEER web site, April 2018.
6. American Cancer Society. Cancer Facts and Figures 2018. American
Cancer Society: Atlanta GACS.
7. Allemani C, Matsuda T, Di Carlo V, et al. Global surveillance of trends
in cancer survival 2000–14 (CONCORD-3): analysis of individual
records for 37 513 025 patients diagnosed with one of 18 cancers from
322 population-based registries in 71 countries. Lancet
2018;391(10125):1023–1075.
8. DeSantis CE, Bray F, Ferlay J, et al. International variation in female
breast cancer incidence and mortality rates. Cancer Epidemiol
Biomarkers Prev 2015;24(10):1495–1506.
9. Ziegler RG, Hoover RN, Pike MC, et al. Migration patterns and breast
cancer risk in Asian-American women. J Natl Cancer Inst
1993;85(22):1819–1827.
10. Surveillance EaERSPw, seer.cancer.gov) SEER*Stat Database:
NAACCR Incidence—CiNA Analytic File -, for NHIAv2 Origin,
Custom File With County, ACS, Facts and Figures Projection Project
NAAo, Registries CC.
11. Atlanta: ACSBCFF-, American Cancer Society I.
12. Newman LA, Griffith KA, Jatoi I, et al. Meta-analysis of survival in
African American and white American patients with breast cancer:
ethnicity compared with socioeconomic status. J Clin Oncol
2006;24(9):1342–1349.
13. Chlebowski RT, Chen Z, Anderson GL, et al. Ethnicity and breast
cancer: factors influencing differences in incidence and outcome. J Natl
Cancer Inst 2005;97(6):439–448.
14. Troisi R, Potischman N, Hoover RN. Exploring the underlying
hormonal mechanisms of prenatal risk factors for breast cancer: a review
and commentary. Cancer Epidemiol Biomarkers Prev 2007;16(9):1700–
1712.
15. Ruder EH, Dorgan JF, Kranz S, et al. Examining breast cancer growth
and lifestyle risk factors: early life, childhood, and adolescence. Clin
Breast Cancer 2008;8(4):334–342.
16. Palmer JR, Wise LA, Hatch EE, et al. Prenatal diethylstilbestrol
exposure and risk of breast cancer. Cancer Epidemiol Biomarkers Prev
2006;15(8):1509–1514.
17. Hoover RN, Hyer M, Pfeiffer RM, et al. Adverse health outcomes in
women exposed in utero to diethylstilbestrol. N Engl J Med
2011;365(14):1304–1314.
18. Park SK, Kang D, McGlynn KA, et al. Intrauterine environments and
breast cancer risk: meta-analysis and systematic review. Breast Cancer
Res 2008;10(1):R8.
19. Xue F, Michels KB. Intrauterine factors and risk of breast cancer: a
systematic review and meta-analysis of current evidence. Lancet Oncol
2007;8(12):1088–1100.
20. Troisi R, Innes KE, Roberts JM, et al. Preeclampsia and maternal breast
cancer risk by offspring gender: do elevated androgen concentrations
play a role? Br J Cancer 2007;97(5):688–690.
21. Terry MB, Perrin M, Salafia CM, et al. Preeclampsia, pregnancy-related
hypertension, and breast cancer risk. Am J Epidemiol
2007;165(9):1007–1014.
22. Nechuta S, Paneth N, Velie EM. Pregnancy characteristics and maternal
breast cancer risk: a review of the epidemiologic literature. Cancer
Causes Control 2010;21(7):967–989.
23. Troisi R, Hatch EE, Titus-Ernstoff L, et al. Birth weight and breast
cancer risk. Br J Cancer 2006;94(11):1734–1737.
24. McCormack VA, dos Santos Silva I, Koupil I, et al. Birth characteristics
and adult cancer incidence: Swedish cohort of over 11,000 men and
women. Int J Cancer 2005;115(4):611–617.
25. World Cancer Research Fund/American Institute for Cancer Research.
Continuous Update Project Report: Diet N, Physical Activity and Breast
Cancer. WCRF/ACIR; 2017.
26. Michels KB, Xue F, Terry KL, et al. Longitudinal study of birthweight
and the incidence of breast cancer in adulthood. Carcinogenesis
2006;27(12):2464–2468.
27. Silva Idos S, De Stavola B, McCormack V; Collaborative Group on Pre-
Natal Risk Factor, Subsequent Risk of Breast Cancer. Birth size and
breast cancer risk: re-analysis of individual participant data from 32
studies. PLoS Med 2008;5(9):e193.
28. Innes K, Byers T, Schymura M. Birth characteristics and subsequent risk
for breast cancer in very young women. Am J Epidemiol
2000;152(12):1121–1128.
29. Hilakivi-Clarke L. Mechanisms by which high maternal fat intake
during pregnancy increases breast cancer risk in female rodent offspring.
Breast Cancer Res Treat 1997;46(2–3):199–214.
30. Modan B, Chetrit A, Alfandary E, et al. Increased risk of breast cancer
after low-dose irradiation. Lancet 1989;1(8639):629–631.
31. Ronckers CM, Erdmann CA, Land CE. Radiation and breast cancer: a
review of current evidence. Breast Cancer Res 2005;7(1):21–32.
32. John EM, Kelsey JL. Radiation and other environmental exposures and
breast cancer. Epidemiol Rev 1993;15(1):157–162.
33. Preston DL, Mattsson A, Holmberg E, et al. Radiation effects on breast
cancer risk: a pooled analysis of eight cohorts. Radiat Res
2002;158(2):220–235.
34. Drooger JC, Hooning MJ, Seynaeve CM, et al. Diagnostic and
therapeutic ionizing radiation and the risk of a first and second primary
breast cancer, with special attention for BRCA1 and BRCA2 mutation
carriers: a critical review of the literature. Cancer Treat Rev
2015;41(2):187–196.
35. Collaborative Group on Hormonal Factors in Breast Cancer. Menarche,
menopause, and breast cancer risk: individual participant meta-analysis,
including 118 964 women with breast cancer from 117 epidemiological
studies. Lancet Oncol 2012;13(11):1141–1151.
36. Kelsey JL, Gammon MD, John EM. Reproductive factors and breast
cancer. Epidemiol Rev 1993;15(1):36–47.
37. Ma H, Bernstein L, Pike MC, et al. Reproductive factors and breast
cancer risk according to joint estrogen and progesterone receptor status:
a meta-analysis of epidemiological studies. Breast Cancer Res
2006;8(4):R43.
38. Willett WC TR, Hankinson SE, Hazra A, et al. Chapter 18: nongenetic
factors in the causation of breast cancer. In: Harris JR, Lippman ME,
Morrow M, et al., eds. Diseases of the Breast. 5th ed. Philadelphia, PA:
Lippincott Williams & Wilkins; 2014.
39. Lacey JV Jr, Kreimer AR, Buys SS, et al. Breast cancer epidemiology
according to recognized breast cancer risk factors in the Prostate, Lung,
Colorectal and Ovarian (PLCO) Cancer Screening Trial Cohort. BMC
Cancer 2009;9:84.
40. McPherson K, Steel CM, Dixon JM. ABC of breast diseases. Breast
cancer-epidemiology, risk factors, and genetics. BMJ
2000;321(7261):624–628.
41. Lord SJ, Bernstein L, Johnson KA, et al. Breast cancer risk and hormone
receptor status in older women by parity, age of first birth, and
breastfeeding: a case-control study. Cancer Epidemiol Biomarkers Prev
2008;17(7):1723–1730.
42. Pike MC, Krailo MD, Henderson BE, et al. ‘Hormonal’ risk factors,
‘breast tissue age’ and the age-incidence of breast cancer. Nature
1983;303(5920):767–770.
43. Kauppila A, Kyyronen P, Hinkula M, et al. Birth intervals and breast
cancer risk. Br J Cancer 2009;101(7):1213–1217.
44. Dickson RB PR, Lippman ME. Cancer of the breast. In: DeVita VT Jr.,
Hellman S, Rosenberg SA, eds. Cancer: Principles and Practice of
Oncology. Vol. 1 and 2. 7th ed. Philadelphia, PA: Lippincott Williams &
Wilkins; 2004.
45. Lambe M, Hsieh CC, Chan HW, et al. Parity, age at first and last birth,
and risk of breast cancer: a population-based study in Sweden. Breast
Cancer Res Treat 1996;38(3):305–311.
46. Palmer JR, Wise LA, Horton NJ, et al. Dual effect of parity on breast
cancer risk in African-American women. J Natl Cancer Inst
2003;95(6):478–483.
47. Beral V, Bull D, Doll R, et al; Collaborative Group on Hormonal
Factors in Breast Cancer. Breast cancer and abortion: collaborative
reanalysis of data from 53 epidemiological studies, including 83000
women with breast cancer from 16 countries. Lancet
2004;363(9414):1007–1016.
48. Committee on Gynecologic Practice. ACOG Committee Opinion No.
434: induced abortion and breast cancer risk. Obstet Gynecol
2009;113(6):1417–1418.
49. Collaborative Group on Hormonal Factors in Breast Cancer. Breast
cancer and breastfeeding: collaborative reanalysis of individual data
from 47 epidemiological studies in 30 countries i, 302 women with
breast cancer and 96,973 women without the disease. Lancet
2002;360(9328):187–195.
50. Islami F, Liu Y, Jemal A, et al. Breastfeeding and breast cancer risk by
receptor status–a systematic review and meta-analysis. Ann Oncol
2015;26(12):2398–2407.
51. Zhou Y, Chen J, Li Q, et al. Association between breastfeeding and
breast cancer risk: evidence from a meta-analysis. Breastfeed Med
2015;10(3):175–182.
52. Key T, Appleby P, Barnes I, et al; Endogenous Hormones and Breast
Cancer Collaborative Group. Endogenous sex hormones and breast
cancer in postmenopausal women: reanalysis of nine prospective
studies. J Natl Cancer Inst 2002;94(8):606–616.
53. Buckland G, Ros MM, Roswall N, et al. Adherence to the
Mediterranean diet and risk of bladder cancer in the EPIC cohort study.
Int J Cancer 2014;134(10):2504–2511.
54. Smith-Warner SA, Spiegelman D, Yaun SS, et al. Intake of fruits and
vegetables and risk of breast cancer: a pooled analysis of cohort studies.
JAMA 2001;285(6):769–776.
55. Jung SS, Spiegelman D, Baglietto L, et al. Fruit and vegetable intake
and risk of breast cancer by hormone receptor status. J Natl Cancer Inst
2013;105:219–236.
56. Fung TT, Chiuve SE, Willett WC, et al. Intake of specific fruits and
vegetables in relation to risk of estrogen receptor-negative breast cancer
among postmenopausal women. Breast Cancer Res Treat
2013;138(3):925–930.
57. Brasky TM, Lampe JW, Potter JD, et al. Specialty supplements and
breast cancer risk in the VITamins And Lifestyle (VITAL) Cohort.
Cancer Epidemiol Biomarkers Prev 2010;19(7):1696–1708.
58. Lof M, Sandin S, Lagiou P, et al. Fruit and vegetable intake and risk of
cancer in the Swedish women’s lifestyle and health cohort. Cancer
Causes Control 2011;22(2):283–289.
59. Missmer SA, Smith-Warner SA, Spiegelman D, et al. Meat and dairy
food consumption and breast cancer: a pooled analysis of cohort studies.
Int J Epidemiol 2002;31(1):78–85.
60. Dong JY, Zhang L, He K, et al. Dairy consumption and risk of breast
cancer: a meta-analysis of prospective cohort studies. Breast Cancer Res
Treat 2011;127(1):23–31.
61. Zang J, Shen M, Du S, et al. The association between dairy intake and
breast cancer in western and Asian populations: a systematic review and
meta-analysis. J Breast Cancer 2015;18(4):313–322.
62. Zhang X, Spiegelman D, Baglietto L, et al. Carotenoid intakes and risk
of breast cancer defined by estrogen receptor and progesterone receptor
status: a pooled analysis of 18 prospective cohort studies. Am J Clin
Nutr 2012;95(3):713–725.
63. Eliassen AH, Hendrickson SJ, Brinton LA, et al. Circulating carotenoids
and risk of breast cancer: pooled analysis of eight prospective studies. J
Natl Cancer Inst 2012;104(24):1905–1916.
64. Bakker MF, Peeters PH, Klaasen VM, et al. Plasma carotenoids, vitamin
C, tocopherols, and retinol and the risk of breast cancer in the European
prospective investigation into cancer and nutrition cohort. Am J Clin
Nutr 2016;103(2):454–464.
65. Sisti JS, Lindstrom S, Kraft P, et al. Premenopausal plasma carotenoids,
fluorescent oxidation products, and subsequent breast cancer risk in the
nurses’ health studies. Breast Cancer Res Treat 2015;151(2):415–425.
66. Eliassen AH, Liao X, Rosner B, et al. Plasma carotenoids and risk of
breast cancer over 20 y of follow-up. Am J Clin Nutr 2015;101(6):1197–
1205.
67. Elliott R. Mechanisms of genomic and non-genomic actions of
carotenoids. Biochim Biophys Acta 2005;1740(2):147–154.
68. Kesse E, Bertrais S, Astorg P, et al. Dairy products, calcium and
phosphorus intake, and the risk of prostate cancer: results of the French
prospective SU.VI.MAX (Supplementation en Vitamines et Mineraux
Antioxydants) study. Br J Nutr 2006;95(3):539–545.
69. Lin J, Manson JE, Lee IM, et al. Intakes of calcium and vitamin D and
breast cancer risk in women. Arch Intern Med 2007;167(10):1050–1059.
70. Hjartaker A, Thoresen M, Engeset D, et al. Dairy consumption and
calcium intake and risk of breast cancer in a prospective cohort: the
Norwegian Women and Cancer study. Cancer Causes Control
2010;21(11):1875–1885.
71. Larsson SC, Bergkvist L, Wolk A. Long-term dietary calcium intake and
breast cancer risk in a prospective cohort of women. Am J Clin Nutr
2009;89(1):277–282.
72. Abbas S, Linseisen J, Rohrmann S, et al. Dietary intake of vitamin D
and calcium and breast cancer risk in the European prospective
investigation into cancer and nutrition. Nutr Cancer 2013;65(2):178–
187.
73. Cui Y, Rohan TE. Vitamin D, calcium, and breast cancer risk: a review.
Cancer Epidemiol Biomarkers Prev 2006;15(8):1427–1437.
74. Jacobson EA, James KA, Newmark HL, et al. Effects of dietary fat,
calcium, and vitamin D on growth and mammary tumorigenesis induced
by 7,12-dimethylbenz(a)anthracene in female Sprague-Dawley rats.
Cancer Res 1989;49(22):6300–6303.
75. Land SR, Liu Q, Wickerham DL, et al. Cigarette smoking, physical
activity, and alcohol consumption as predictors of cancer incidence
among women at high risk of breast cancer in the NSABP P-1 trial.
Cancer Epidemiol Biomarkers Prev 2014;23(5):823–832.
76. Fagherazzi G, Vilier A, Boutron-Ruault MC, et al. Alcohol consumption
and breast cancer risk subtypes in the E3N-EPIC cohort. Eur J Cancer
Prev 2015;24(3):209–214.
77. Couto E, Sandin S, Lof M, et al. Mediterranean dietary pattern and risk
of breast cancer. PloS One 2013;8(2):e55374.
78. Zhang SM, Lee IM, Manson JE, et al. Alcohol consumption and breast
cancer risk in the Women’s Health Study. Am J Epidemiol
2007;165(6):667–676.
79. Chen WY, Rosner B, Hankinson SE, et al. Moderate alcohol
consumption during adult life, drinking patterns, and breast cancer risk.
JAMA 2011;306(17):1884–1890.
80. Jung S, Wang M, Anderson K, et al. Alcohol consumption and breast
cancer risk by estrogen receptor status: in a pooled analysis of 20
studies. Int J Epidemiol 2016;45(3):916–928.
81. Falk RT, Maas P, Schairer C, et al. Alcohol and risk of breast cancer in
postmenopausal women: an analysis of etiological heterogeneity by
multiple tumor characteristics. Am J Epidemiol 2014;180(7):705–717.
82. Romieu I, Scoccianti C, Chajes V, et al. Alcohol intake and breast
cancer in the European prospective investigation into cancer and
nutrition. Int J Cancer 2015;137(8):1921–1930.
83. Schonfeld SJ, Pfeiffer RM, Lacey JV Jr, et al. Hormone-related risk
factors and postmenopausal breast cancer among nulliparous versus
parous women: an aggregated study. Am J Epidemiol 2011;173(5):509–
517.
84. Dumitrescu RG, Shields PG. The etiology of alcohol-induced breast
cancer. Alcohol 2005;35(3):213–225.
85. Hamajima N, Hirose K, Tajima K, et al. Alcohol, tobacco and breast
cancer—collaborative reanalysis of individual data from 53
epidemiological studies, including 58,515 women with breast cancer and
95,067 women without the disease. Br J Cancer 2002;87(11):1234–
1245.
86. Catsburg C, Miller AB, Rohan TE. Active cigarette smoking and risk of
breast cancer. Int J Cancer 2015;136(9):2204–2209.
87. Colditz GA, Rosner B. Cumulative risk of breast cancer to age 70 years
according to risk factor status: data from the Nurses’ Health Study. Am J
Epidemiol 2000;152(10):950–964.
88. Suzuki R, Iwasaki M, Inoue M, et al. Body weight at age 20 years,
subsequent weight change and breast cancer risk defined by estrogen
and progesterone receptor status—the Japan public health center-based
prospective study. Int J Cancer 2011;129(5):1214–1224.
89. Catsburg C, Kirsh VA, Soskolne CL, et al. Associations between
anthropometric characteristics, physical activity, and breast cancer risk
in a Canadian cohort. Breast Cancer Res Treat 2014;145(2):545–552.
90. Grubbs CJ, Farnell DR, Hill DL, et al. Chemoprevention of N-nitroso-
N-methyl6urea-induced mammary cancers by pretreatment with 17 beta-
estradiol and progesterone. J Natl Cancer Inst 1985;74(4):927–931.
91. Berkey CS, Frazier AL, Gardner JD, et al. Adolescence and breast
carcinoma risk. Cancer 1999;85(11):2400–2409.
92. Bjorge T, Lukanova A, Jonsson H, et al. Metabolic syndrome and breast
cancer in the me-can (metabolic syndrome and cancer) project. Cancer
Epidemiol Biomarkers Prev 2010;19(7):1737–1745.
93. van den Brandt PA, Spiegelman D, Yaun SS, et al. Pooled analysis of
prospective cohort studies on height, weight, and breast cancer risk. Am
J Epidemiol 2000;152(6):514–527.
94. Bandera EV, Chandran U, Hong CC, et al. Obesity, body fat
distribution, and risk of breast cancer subtypes in African American
women participating in the AMBER Consortium. Breast Cancer Res
Treat 2015;150(3):655–666.
95. Keum N, Greenwood DC, Lee DH, et al. Adult weight gain and
adiposity-related cancers: a dose-response meta-analysis of prospective
observational studies. J Natl Cancer Inst 2015;107(3):dju428.
96. Vrieling A, Buck K, Kaaks R, et al. Adult weight gain in relation to
breast cancer risk by estrogen and progesterone receptor status: a meta-
analysis. Breast Cancer Res Treat 2010;123(3):641–649.
97. Hilakivi-Clarke L, Forsen T, Eriksson JG, et al. Tallness and overweight
during childhood have opposing effects on breast cancer risk. Br J
Cancer 2001;85(11):1680–1684.
98. De Pergola G, Silvestris F. Obesity as a major risk factor for cancer. J
Obes 2013;2013:291546.
99. Calle EE, Kaaks R. Overweight, obesity and cancer: epidemiological
evidence and proposed mechanisms. Nat Rev Cancer 2004;4(8):579–
591.
100. Wu Y, Zhang D, Kang S. Physical activity and risk of breast cancer: a
meta-analysis of prospective studies. Breast Cancer Res Treat
2013;137(3):869–882.
101. McTiernan A, Kooperberg C, White E, et al. Recreational physical
activity and the risk of breast cancer in postmenopausal women: the
Women’s Health Initiative Cohort Study. JAMA 2003;290(10):1331–
1336.
102. McTiernan A. Mechanisms linking physical activity with cancer. Nat
Rev Cancer 2008;8(3):205–211.
103. Friedenreich CM, Neilson HK, Lynch BM. State of the epidemiological
evidence on physical activity and cancer prevention. Eur J Cancer
2010;46(14):2593–2604.
104. Amersi F, Calhoun K (eds.). Atypical breast proliferative lesions and
benign breast disease. Springer 2018. ISBN 978-3-319-92657-5
105. Hartmann LC, Sellers TA, Frost MH, et al. Benign breast disease and
the risk of breast cancer. N Engl J Med 2005;353(3):229–237.
106. Dupont WD, Page DL. Risk factors for breast cancer in women with
proliferative breast disease. New Engl J Med 1985;312(3):146–151.
107. Bodian CA. Benign breast diseases, carcinoma in situ, and breast cancer
risk. Epidemiol Rev 1993;15(1):177–187.
108. Collins LC, Baer HJ, Tamimi RM, et al. Magnitude and laterality of
breast cancer risk according to histologic type of atypical hyperplasia:
results from the Nurses’ Health Study. Cancer 2007;109(2):180–187.
109. Freer PE. Mammographic breast density: impact on breast cancer risk
and implications for screening. Radiographics 2015;35(2):302–315.
110. Kerlikowske K, Zhu W, Hubbard RA, et al. Outcomes of screening
mammography by frequency, breast density, and postmenopausal
hormone therapy. JAMA Intern Med 2013;173(9):807–816.
111. Boyd NF, Martin LJ, Yaffe MJ, et al. Mammographic density and breast
cancer risk: current understanding and future prospects. Breast Cancer
Res 2011;13(6):223.
112. Checka CM, Chun JE, Schnabel FR, et al. The relationship of
mammographic density and age: implications for breast cancer
screening. AJR Am J Roentgenol 2012;198(3):W292–W295.
113. Yaghjyan L, Mahoney MC, Succop P, et al. Relationship between breast
cancer risk factors and mammographic breast density in the Fernald
Community Cohort. Br J Cancer 2012;106(5):996–1003.
114. Barlow WE, White E, Ballard-Barbash R, et al. Prospective breast
cancer risk prediction model for women undergoing screening
mammography. J Natl Cancer Inst 2006;98(17):1204–1214.
115. McCormack VA, dos Santos Silva I. Breast density and parenchymal
patterns as markers of breast cancer risk: a meta-analysis. Cancer
Epidemiol Biomarkers Prev 2006;15(6):1159–1169.
116. Boyd NF, Guo H, Martin LJ, et al. Mammographic density and the risk
and detection of breast cancer. N Engl J Med 2007;356(3):227–236.
117. D’Orsi CJ SE, Mendelson EB, Morris EA. Breast Imaging Reporting
And Data System: ACR BI-RADS—Breast Imaging Atlas. 5th ed.
Reston, VA: American College of Radiology; 2013.
118. Carney PA, Miglioretti DL, Yankaskas BC, et al. Individual and
combined effects of age, breast density, and hormone replacement
therapy use on the accuracy of screening mammography. Ann Intern
Med 2003;138(3):168–175.
119. Kerlikowske K, Hubbard RA, Miglioretti DL, et al. Comparative
effectiveness of digital versus film-screen mammography in community
practice in the United States: a cohort study. Ann Intern Med
2011;155(8):493–502.
120. Byrne C, Schairer C, Wolfe J, et al. Mammographic features and breast
cancer risk: effects with time, age, and menopause status. J Natl Cancer
Inst 1995;87(21):1622–1629.
121. Yaghjyan L, Colditz GA, Rosner B, et al. Mammographic breast density
and subsequent risk of breast cancer in postmenopausal women
according to the time since the mammogram. Cancer Epidemiol
Biomarkers Prev 2013;22(6):1110–1117.
122. Cuzick J, Warwick J, Pinney E, et al. Tamoxifen-induced reduction in
mammographic density and breast cancer risk reduction: a nested case-
control study. J Natl Cancer Inst 2011;103(9):744–752.
123. Hankinson SE, Schernhammer ES. Insulin-like growth factor and breast
cancer risk: evidence from observational studies. Breast Dis
2003;17:27–40.
124. Endogenous Hormones and Breast Cancer Collaborative Group, Key TJ,
Appleby PN, et al. Insulin-like growth factor 1 (IGF1), IGF binding
protein 3 (IGFBP3), and breast cancer risk: pooled individual data
analysis of 17 prospective studies. Lancet Oncol 2010;11(6):530–542.
125. Kaaks R, Johnson T, Tikk K, et al. Insulin-like growth factor I and risk
of breast cancer by age and hormone receptor status—A prospective
study within the EPIC cohort. Int J Cancer 2014;134(11):2683–2690.
126. Pasanisi P, Bruno E, Venturelli E, et al. Serum levels of IGF-I and
BRCA penetrance: a case control study in breast cancer families. Fam
Cancer 2011;10(3):521–528.
127. Yang TO, Reeves GK, Green J, et al. Birth weight and adult cancer
incidence: large prospective study and meta-analysis. Ann Oncol
2014;25(9):1836–1843.
128. Manders P, Pijpe A, Hooning MJ, et al. Body weight and risk of breast
cancer in BRCA1/2 mutation carriers. Breast Cancer Res Treat
2011;126(1):193–202.
129. Iwasaki M, Otani T, Inoue M, et al; Japan Public Health Center-Based
Prospective Study Group. Body size and risk for breast cancer in
relation to estrogen and progesterone receptor status in Japan. Ann
Epidemiol 2007;17(4):304–312.
130. Amadou A, Ferrari P, Muwonge R, et al. Overweight, obesity and risk
of premenopausal breast cancer according to ethnicity: a systematic
review and dose-response meta-analysis. Obes Rev 2013;14(8):665–678.
131. Baer HJ, Rich-Edwards JW, Colditz GA, et al. Adult height, age at
attained height, and incidence of breast cancer in premenopausal
women. Int J Cancer 2006;119(9):2231–2235.
132. Oberg S, Cnattingius S, Sandin S, et al. Birth weight-breast cancer
revisited: is the association confounded by familial factors? Cancer
Epidemiol Biomarkers Prev 2009;18(9):2447–2452.
133. Zhang B, Shu XO, Delahanty RJ, et al. Height and Breast Cancer Risk:
evidence From Prospective Studies and Mendelian Randomization. J
Natl Cancer Inst 2015;107(11):djv219.
134. Krishnan K, Bassett JK, MacInnis RJ, et al. Associations between
weight in early adulthood, change in weight, and breast cancer risk in
postmenopausal women. Cancer Epidemiol Biomarkers Prev
2013;22(8):1409–1416.
135. Lahmann PH, Hoffmann K, Allen N, et al. Body size and breast cancer
risk: findings from the European Prospective Investigation into Cancer
And Nutrition (EPIC). Int J Cancer 2004;111(5):762–771.
136. Opdahl S, Alsaker MD, Janszky I, et al. Joint effects of nulliparity and
other breast cancer risk factors. Br J Cancer 2011;105(5):731–736.
137. Wiren S, Haggstrom C, Ulmer H, et al. Pooled cohort study on height
and risk of cancer and cancer death. Cancer Causes Control
2014;25(2):151–159.
138. Collaborative Group on Hormonal Factors in Breast Cancer. Breast
cancer and hormonal contraceptives: collaborative reanalysis of
individual data on 53 297 women with breast cancer and 100 239
women without breast cancer from 54 epidemiological studies. Lancet
1996;347(9017):1713–1727.
139. Busund M, Bugge NS, Braaten T, et al. Progestin-only and combined
oral contraceptives and receptor-defined premenopausal breast cancer
risk: The Norwegian Women and Cancer Study. Int J Cancer
2018;142(11):2293–2302.
140. Beral V; Million Women Study Collaborators. Breast cancer and
hormone-replacement therapy in the Million Women Study. Lancet
2003;362(9382):419–427.
141. Schairer C, Lubin J, Troisi R, et al. Menopausal estrogen and estrogen-
progestin replacement therapy and breast cancer risk. JAMA
2000;283(4):485–491.
142. Chen WY. Postmenopausal hormone therapy and breast cancer risk:
current status and unanswered questions. Endocrinol Metab Clin North
Am 2011;40(3):509–518, viii.
143. Chlebowski RT, Hendrix SL, Langer RD, et al. Influence of estrogen
plus progestin on breast cancer and mammography in healthy
postmenopausal women: the Women’s Health Initiative Randomized
Trial. JAMA 2003;289(24):3243–3253.
144. Stefanick ML, Anderson GL, Margolis KL, et al. Effects of conjugated
equine estrogens on breast cancer and mammography screening in
postmenopausal women with hysterectomy. JAMA 2006;295(14):1647–
1657.
145. Chlebowski RT, Anderson GL, Gass M, et al. Estrogen plus progestin
and breast cancer incidence and mortality in postmenopausal women.
JAMA 2010;304(15):1684–1692.
146. Anderson GL, Chlebowski RT, Aragaki AK, et al. Conjugated equine
oestrogen and breast cancer incidence and mortality in postmenopausal
women with hysterectomy: extended follow-up of the Women’s Health
Initiative randomised placebo-controlled trial. Lancet Oncol
2012;13(5):476–486.
147. Collaborative Group on Hormonal Factors in Breast Cancer. Familial
breast cancer: collaborative reanalysis of individual data from 52
epidemiological studies including 58,209 women with breast cancer and
101,986 women without the disease. Lancet 2001;358(9291):1389–
1399.
148. Stratton MR, Rahman N. The emerging landscape of breast cancer
susceptibility. Nat Genet 2008;40(1):17–22.
149. Slavin TP, Maxwell KN, Lilyquist J, et al. The contribution of
pathogenic variants in breast cancer susceptibility genes to familial
breast cancer risk. NPJ Breast Cancer 2017;3:22.
150. Rebbeck TR, Mitra N, Wan F, et al. Association of type and location of
BRCA1 and BRCA2 mutations with risk of breast and ovarian cancer.
JAMA 2015;313(13):1347–1361.
151. King MC, Levy-Lahad E, Lahad A. Population-based screening for
BRCA1 and BRCA2: 2014 Lasker Award. JAMA 2014;312(11):1091–
1092.
152. Metcalfe K, Lynch HT, Ghadirian P, et al. Contralateral breast cancer in
BRCA1 and BRCA2 mutation carriers. J Clin Oncol 2004;22(12):2328–
2335.
153. Kuchenbaecker KB, Hopper JL, Barnes DR, et al. Risks of breast,
ovarian, and contralateral breast cancer for BRCA1 and BRCA2
mutation carriers. JAMA 2017;317(23):2402–2416.
154. Mahdavi M, Nassiri M, Kooshyar MM, et al. Hereditary breast cancer;
Genetic penetrance and current status with BRCA. J Cell Physiol
2019;234(5):5741–5750.
155. Malkin D. Germline p53 mutations and heritable cancer. Annu Rev
Genet 1994;28:443–465.
156. van Os NJ, Roeleveld N, Weemaes CM, et al. Health risks for ataxia-
telangiectasia mutated heterozygotes: a systematic review, meta-analysis
and evidence-based guideline. Clin Genet 2016;90(2):105–117.
157. Schmidt MK, Hogervorst F, van Hien R, et al. Age- and tumor subtype-
specific breast cancer risk estimates for CHEK2*1100delC carriers. J
Clin Oncol 2016;34(23):2750–2760.
158. Antoniou AC, Foulkes WD, Tischkowitz M. Breast-cancer risk in
families with mutations in PALB2. N Engl J Med 2014;371(17):1651–
1652.
159. Seal S, Thompson D, Renwick A, et al. Truncating mutations in the
Fanconi anemia J gene BRIP1 are low-penetrance breast cancer
susceptibility alleles. Nat Genet 2006;38(11):1239–1241.
160. Sharif S, Moran A, Huson SM, et al. Women with neurofibromatosis 1
are at a moderately increased risk of developing breast cancer and
should be considered for early screening. J Med Genet 2007;44(8):481–
484.
161. Uusitalo E, Rantanen M, Kallionpaa RA, et al. Distinctive cancer
associations in patients with neurofibromatosis type 1. J Clin Oncol
2016;34(17):1978–1986.
162. Couch FJ, Shimelis H, Hu C, et al. Associations between cancer
predisposition testing panel genes and breast cancer. JAMA Oncol
2017;3(9):1190–1196.
CHAPTER 2

Breast Cancer Screening and


Diagnosis, Including the Surgically
Altered Breast
TONI STORM | ALLEN GABRIEL
HISTORY
Breast cancer is common, affecting about 1 in 8 women (12.4%) with over
260,000 new cases per year in the United States (1). As of January 2019,
there were more than 3.1 million women either with a history of breast cancer
or being treated for breast cancer in the United States alone (2). Less than 1%
of breast cancers develop in men. Not including benign breast biopsies and
cosmetic breast surgery, there are over a half a million breast cancer–related
surgeries performed per year in the United States (3). In spite of all these
breast cancer surgeries, breast imaging recommendations remain
controversial with the United State Preventative Services Task Force
(USPSTF) recommendations differing, in varying degrees from most of our
other guiding bodies; American College of Radiology (ACR), American
Cancer Society (ACS), American Society of Breast Surgeons (ASBrS), and
Society of Surgical Oncology (SSO) (4).
In the United States, the 5-year survival rates for women with breast cancer
have improved from 75% in 1975–77 to 90% in 2003–09 (5). The risk of
distant or metastatic disease and death increases with both tumor size and
number of axillary lymph nodes involved (6–9). While mammography is not
a perfect test and may be particularly insensitive at detecting breast cancer
among selected groups of patients such as those with very dense breast,
extensive scarring from previous interventions (such as surgery and
radiation), or those with a subtype of malignancy which is often harder to
detect on imaging such as invasive lobular carcinoma, it remains effective at
finding smaller tumors, before they are palpable (10–13). When measuring
the benefit of an intervention as when measuring the harm, survival should
not be the only measure of efficacy. After tumor size and lymph node
involvement, survival is strongly influenced by tumor-related factors such as
hormone receptor, human epidermal growth factor receptor 2 (HER-2) status,
lymphovascular invasion (LVI), and grade (7–10). Screening mammography
is effective at finding many cancers early, before they are palpable, and
thereby reducing the number of women with cancers of advanced size and
stage. Finding cancers at an earlier stage allows for better outcomes, more
lives saved, and potential for both less extensive surgery and no or less
extensive chemotherapy.
IMAGING IN WOMEN 40 TO 70
In part, the controversy over when to initiate screening mammography arises
secondary to the fact that breast cancer is not only common, it is potentially
deadly, but not uniformly so. Breast cancer represents about 20% of all
cancers (men and women) and is the second most common cause of cancer
death among women over all (14). This number continues to improve in
women over 50, with breast cancer deaths having dropped by approximately
37% between 1989 and 2015 in this population (15) (Table 2-1, USPSTF
Grades). However, in women under 50, the death rate has remained steady
since 2007. Data has also shown that younger women are more likely to
develop more aggressive malignancies (HER-2+ and hormone receptor
negative) with higher risk of both distant and local recurrence (16–24).
We often think of breast cancer as a disease of the elderly, which is not
untrue (Figs. 2-1 and 2-2). However, this is a very limited picture of the true
impact and distribution of the disease. Breast cancer is most commonly
diagnosed in middle-aged women with a broad distribution extending to the
young adult and the very old. As stated earlier, the “lifetime” risk of
developing breast cancer is one in eight women, with 25.9% of all breast
cancers diagnosed between the ages of 55 and 64 with an average age of 62 at
diagnosis (Fig. 2-2). However, it is extremely important to note that there is
an almost equal distribution 10 years above and below this with, 20.4% of
women diagnosis between 45 and 54 years of age and 24.1% diagnosis
between 65 and 74 years of age. Context remains extremely important as seen
in Figure 2-3, with lifetime risk seen to be highest in women aged 80,
however, the age at which the largest number of women are diagnosed is 62
(Fig. 2-3). Further, survival improves with earlier stage at diagnosis; 5-year
survival for stage I breast cancer is 98.7% compared to 27% for metastatic
disease (25).

TABLE 2-1 The USPSTF Average Risk Breast Cancer Screening


Guidelines, 2015
Population Recommendation Grade (What’s
This?)
Women aged The USPSTF recommends biennial B
50–74 yrs screening mammography for
women aged 50–74 yrs.
Women aged The decision to start screening C
40–49 yrs mammography in women prior to
age 50 yrs should be an
individual one. Women who
place a higher value on the
potential benefit than the
potential harms may choose to
begin biennial screening between
the ages of 40 and 49 yrs.
• For women who are at average
risk for breast cancer, most of
the benefit of mammography
results from biennial screening
during ages 50–74 yrs. Of all
of the age groups, women aged
60–69 yrs are most likely to
avoid breast cancer death
through mammography
screening. While screening
mammography in women aged
40–49 yrs may reduce the risk
for breast cancer death, the
number of deaths averted is
smaller than that in older
women and the number of
false-positive results and
unnecessary biopsies is larger.
The balance of benefits and
harms is likely to improve as
women move from their early
to late 40s.
• In addition to false-positive
results and unnecessary
biopsies, all women
undergoing regular screening
mammography are at risk for
the diagnosis and treatment of
noninvasive and invasive
breast cancer that would
otherwise not have become a
threat to their health, or even
apparent, during their lifetime
(known as “overdiagnosis”).
Beginning mammography
screening at a younger age and
screening more frequently may
increase the risk for
overdiagnosis and subsequent
overtreatment.
• Women with a parent, sibling,
or child with breast cancer are
at higher risk for breast cancer
and thus may benefit more
than average-risk women from
beginning screening in their
40s.
• Go to the Clinical
Considerations section for
information on implementation
of the C recommendation.

Women aged 75 The USPSTF concludes that the I


yrs or older current evidence is insufficient to
assess the balance of benefits and
harms of screening
mammography in women aged
75 yrs or older.
All women The USPSTF concludes that the I
current evidence is insufficient to
assess the benefits and harms of
digital breast tomosynthesis
(DBT) as a primary screening
method for breast cancer.
Women with The USPSTF concludes that the I
dense breasts current evidence is insufficient to
assess the balance of benefits and
harms of adjunctive screening for
breast cancer using breast
ultrasonography, magnetic
resonance imaging, DBT, or
other methods in women
identified to have dense breasts
on an otherwise negative
screening mammogram.
These recommendations apply to asymptomatic women aged 40 yrs or older
who do not have pre-existing breast cancer or a previously diagnosed
high-risk breast lesion and who are not at high risk for breast cancer
because of a known underlying genetic mutation (such as a BRCA1 or
BRCA2 gene mutation or other familial breast cancer syndrome) or a
history of chest radiation at a young age.
Grade Definition Suggestions for
Practice
A The USPSTF recommends the Offer or provide
service. There is high certainty this service.
that the net benefit is substantial.
B The USPSTF recommends the Offer or provide
service. There is high certainty this service.
that the net benefit is moderate or
there is moderate certainty that
the net benefit is moderate to
substantial.
C The USPSTF recommends Offer or provide
selectively offering or providing this service for
this service to individual patients selected patients
based on professional judgment depending on
and patient preferences. There is individual
at least moderate certainty that circumstances.
the net benefit is small.
D The USPSTF recommends against Discourage the use
the service. There is moderate or of this service.
high certainty that the service has
no net benefit or that the harms
outweigh the benefits.
I The USPSTF concludes that the Read the clinical
Statement current evidence is insufficient to considerations
assess the balance of benefits and section of
harms of the service. Evidence is USPSTF
lacking, of poor quality, or Recommendation
conflicting, and the balance of Statement. If the
benefits and harms cannot be service is
determined. offered, patients
should
understand the
uncertainty about
the balance of
benefits and
harms.
Data from the USPSTF.
FIGURE 2-1 Declining death rate 37% between 1989 and 2015 for women over 50.
(Data from American Cancer Society SEERS Data, NIH 2016.)

We also know that the vast majority of breast cancers are sporadic at 85%
to 90% (25,26) thus, lacking a family history cannot be interpreted as
protective. Using lack of a family history to exclude women under 50 from
screening mammography leaves a large and vulnerable group of “average-
risk” women with a misimpression that they are somehow safe and will not
benefit from mammography. The United States Preventative Services Task
Force (USPSTF) is an independent panel of primary care physicians and
epidemiologists funded, staffed, and appointed by the U.S. Department of
Health and Human Services that make recommendations for clinical
preventative services. Their original recommendations, set forward in 2002,
used a meta-analysis of the eight large prospective mammography trials
designed to assess the effectiveness of mammography in reducing breast
cancer mortality but only included data from seven (27). All the trials had
limitations but the USPSTF excluded the Edinburgh study from the analysis,
secondary to imbalance between control and screened group. USPSTF
concluded: “mammography reduced breast cancer mortality among women
40 to 74 years of age with a greater benefit in women greater than 50” and at
that time continued to recommend mammograms annually starting at age 40.

FIGURE 2-2 Breast cancer: percentage of new cases per year, by age. (Data from
NIH [National Institutes of Health], SEERS [Surveillance Epidemiology and End
Results Program] 2019.)
FIGURE 2-3 Age-specific rates of breast cancer overlaid with percentile distribution
of breast cancers per year by age. (Data from NIH [National Institutes of Health],
SEERS [Surveillance Epidemiology and End Results Program] 2019.)

In 2009, the USPSTF updated their analysis to include data from the Age
trial from the United Kingdom that randomized women 39 to 41 to annual
screening mammography until age 48 (28). The purpose of their evaluation
was to “determine the effectiveness of mammography screening in
decreasing breast cancer mortality among average-risk women aged 40 to 49
years and 70 years or older, the effectiveness of clinical breast examination
and breast self-examination, and the harms of screening.” They published
their results in Annals of Internal Medicine November 2009. The study used
film and digital mammography and The Task Force again found a 15%
reduction in breast cancer mortality in favor of screening with an even greater
benefit for women over 60. They reported the false positive rate highest in
women aged 40 to 49 with the highest rate of additional imaging and
unnecessary biopsies in this age group. Secondary to their concerns for the
harm–benefit ratio, they changed their recommendations to consider starting
mammographic screening at age 50. Further they found no benefit for clinical
breast examination and self-breast examination was considered harmful.
In their conclusion they stated that “Our meta-analysis of mammography
screening trials indicates breast cancer mortality benefit for all age groups
from 39 to 69 years, with insufficient data for older women. False-positive
results are common in all age groups and lead to additional imaging and
biopsies. Women aged 40 to 49 years experience the highest rate of
additional imaging, whereas their biopsy rate is lower than that for older
women. Mammography screening at any age is a trade-off of a continuum of
benefits and harms. The ages at which this trade-off becomes acceptable to
individuals and society are not clearly resolved by the available evidence”
(29).
Of very significant import is that the USPSTF primary concern with
mammography was not its ability to detect cancers earlier than would be
found without imaging and thereby prevent breast cancer–related deaths, but
rather harm of imaging outweighing the benefit based on unnecessary
imaging and biopsies as well as costs. With this in mind, note that their
studies used plain films and digital mammography. We now have 3D breast
tomosynthesis, rapidly becoming the standard of care, which has shown a
reduction in false positives by 17.1% and increased rate of detection of breast
cancers by 33.9% over standard digital mammography (30).
If we combine (1) the improved diagnostics of tomosynthesis with fewer
false positives and better detection rate, (2) ≥15% decrease in mortality with
early diagnosis through mammography, (3) the fact that women under 50
account for approximately 24% of breast cancers diagnosed, (4) younger
women tend to have more aggressive disease which will progress rapidly and
cost more to treat, and (5) do not qualify for screening mammography by
USPSTF guidelines, we can make a very compelling argument to change the
recommendations on screening mammography to start at age 40.
THE ARGUMENT AGAINST IMAGING
This discussion requires the work of Welch et al. be addressed (31). In their
pivotal paper published in the New England Journal of Medicine, November
2012 they stated that while mammograms and early detection had
“marginally reduced the rate at which women present with advanced cancer”
it had “at best, only a small effect on the rate of death from breast cancer,”
resulting in pain and expense of unnecessary interventions.
Following the release of the 2014 SEER data, Welch et al. published in the
New England Journal of Medicine, October 2016 (32) their paper, which
argued that the precipitous drop in breast cancer–related deaths seen in the
2014 SEER data (15) was based solely on treatment rather than any benefit
form screening mammography or early detection. While it is very true, a
better understanding of biology and improved treatments are clearly a large
part of the overall survival picture, it is not the entire story and the data does
not support claims of “rampant overdiagnosis.” The Welch et al. 2016 paper
reiterated the SEER data finding of a 30% decrease in large tumors found in
American women following the advent of screening mammography. This
correlates directly with increase in detection of small invasive cancers and
improved survival. Otto et al. and Coldman et al. have shown that, in women
who regularly undergo screening mammography, the risk of dying from
breast cancer is cut nearly in half (33,34).
Plevritis et al. (35) nicely illustrated the changes seen in the
screening/treatment association with breast cancer mortality by molecular
subtype in U.S. women, in 2000 contrasted with 2012 in their article. These
authors looked at the six Cancer Intervention and Surveillance Modeling
Network (CISNET) models that simulated U.S. breast cancer mortality from
2000 to 2012 for women aged 30 to 79. In 2000 the overall estimated
reduction in breast cancer mortality rate was 37%, 44% (model range, 35% to
60%) from screening and 56% (model range, 40% to 65%) from treatment. In
2012, the estimated reduction in overall breast cancer mortality rate was 49%,
37% (model range, 26% to 51%) from screening and 63% (model range, 49%
to 74%) from treatment. Of the 63% associated with treatment; 31% (model
range, 22% to 37%) was attributed to chemotherapy, 27% (model range, 18%
to 36%) to hormone therapy, and 4% (model range, 1% to 6%) to
trastuzumab.
Baseline growth of breast cancer is also a critical factor in determining
overdiagnosis and an area of contention with Welch et al.’s interpretation of
the data. Puliti et al. published their results, based on actual patient data,
showing an over 1% per year increase in breast cancer diagnosis from 1940
to 1974, the start of the SEER program (36). If Welch et al. in their 2012
paper had used 1% breast cancer incidence growth rate, their findings would
have been vastly different, showing no evidence of overdiagnosis and a
marked decline in advanced cancers, which has led to the decline in breast
cancer deaths since screening began (37).
Sepideh et al. (37) looked at 173,797 women in the Netherlands diagnosed
with breast cancer between January 1999 and December 2012 to assess
survival differences based on changes in chemotherapy subdividing them into
two groups (1999 to 2005 and 2006 to 2012) to reflect changes in
chemotherapy over time, with the cutoff primarily chosen to reflect the
advent of trastuzumab (38). Their study included large populations of breast
cancer patients with, 80,228 (46%) diagnosed from 1999 to 2005 and 93,569
(54%) from 2006 to 2012, with a median age at diagnosis of 59.3 years and
60.0 years, respectively. They found that those women diagnosed between
2006 and 2012 had significantly smaller tumors, were more often lymph node
negative, and were more likely to have BCT and to receive systemic therapy
and radiation. Hormonal therapy increased by 10%, chemotherapy by 7%,
targeted therapy (mainly trastuzumab) by 7%, and a combination of
therapies, by 7%.
This translated into a 100% relative survival for ductal carcinoma in situ
(DCIS) after 15 years, in the 1999 to 2005 cohort and 101% after 8 years for
the 2006–12 cohort. Overall, the relative survival decreased with increasing
tumor and nodal status. They found a 17% increase in the diagnosis of breast
cancer between the two time periods, noting a very significant increase in the
ageing female population. During the study time frame the Dutch female
population grew by approximately 2.7% and the female population aged 60
to 69 years grew by approximately 23% (39). The median age at diagnosis
was approximately 59 years, with a peak associated with menopause (age 50
to 59 years). In the later cohort diagnosis included smaller tumors, more often
lymph node negative, and more often low grade compared to the earlier
cohort. Five-year relative survival rates improved over time to 100% in all
tumors 1 cm or smaller and to 98% for tumors between 1 cm and 2 cm and
improved increasingly with larger tumor size. The relative survival increased
especially in women aged over 75 years.
The authors concluded that there is a dual benefit to early detection
because as tumor size increases so does the likelihood of positive lymph
nodes (39). They found the influence of stage corrected for both tumor
biology and treatment with no difference in hazard rate for breast cancers
sized 1 cm or smaller. Lymph node–negative T1a and b tumors do not
receive chemotherapy in the Netherlands regardless of hormone status, that
is, ER negative. Women diagnosed between 2006 and 2012 had BCT and
axillary lymph node dissection less often, secondary to adoption of sentinel
lymph node biopsy (40). Surgery remains the corner stone of treatment and
BCT has an equivalent survival to mastectomy and has been shown to confer
improved survival in many patients which may be a reflection of axillary
radiation.
POLICY IMPLICATIONS FOR WOMEN 40 TO 70
Viewing the data in a new and more contextual manner may aid both policy
makers (USPSTF) and physicians, in clinical decision making, as well as
providing patients with less ambiguous recommendations regarding breast
cancer screening. While the USPSTF has softened on its stance it remains
committed to the recommendation of screening mammography to start at age
50 and then every other year. As the USPSTF guidelines determine insurance
coverage this has a critical impact on patients and policy. However, the data
supports the idea that while systemic therapies and prognosis have improved,
so too has breast imaging. We have shown: (1) that improved survival is
associated with smaller and node-negative tumors, (2) breast imaging has
also improved with fewer false-positive and improved cancer diagnostics, (3)
that the vast majority of breast cancers in women between 40 to 49 (and
indeed all women) are sporadic with (4) increased risk of more aggressive
disease in this age group requiring more extensive interventions, lost
productivity, and expense. Together, these make a strong argument for breast
cancer screening to start at age 40. Mammography remains an excellent,
although imperfect, screening tool for all women starting at age 40 and
continuing until age 70.
BREAST IMAGING AFTER 70
Recommendations on breast imaging after 70 were not put forth by the
USPSTF secondary to lack of data rather than secondary to evidence
suggesting lack of benefit. What we do know is that breast cancer in the
elderly, postmenopausal patient tends to be profile favorable and more likely
indolent and thus, this may be the subgroup to benefit most from every-other-
year imaging (41). Further, if a woman’s overall health is poor, such that her
life expectancy is less than 5 years, it is very reasonable to forgo all breast
imaging as death from breast cancer is not a significant concern. However, in
an otherwise healthy 70-year-old woman, actuary studies would suggest
another 16.5 years of life making every-other-year mammography very
reasonable and worthwhile intervention (38). Twenty-six percent of breast
cancer deaths are in women over the age of 75 and yet 50% of women over
age 80 are expected to live another 10 years. For this reason, every-other-year
screening mammograms should be performed in average-risk women over
the age of 70 in reasonably good health.
HIGH-RISK SCREENING
This could easily be a chapter unto itself but briefly, a woman qualifies for
high-risk screening when her lifetime risk of breast cancer exceeds 20% to
30%. High-risk screening is usually defined as staggered annual 3D
mammogram and MRI or whole breast ultrasound (US). There are several
factors that increase a woman’s risk for breast cancer. Genetic predisposition
is responsible for 10% to 15% of breast cancers and penetrance varies widely
by the both the gene and heterogeneity (42). This would include: the well-
recognized BRCA1 and 2 mutations (43), with lifetime risk of 50% to 85%
and 45%, respectively (38,44). Other less common mutations are TP53 and
CHEK2 (Li–Fraumeni syndrome), PTEN (Cowden and Bannayan–Riley–
Ruvalcaba syndromes), CDH1 (hereditary diffuse gastric cancer), STK11
(Peutz–Jeghers syndrome), PALB2 (interacts with BRCA2), and ATM
(ataxia-telangiectasia) genes.
There are also those women with very strong family histories of breast
cancer without a recognizable mutation, sometimes called gene X (45). Here
familiarity may be the key rather than genetics and a finding of two or more
first-degree relatives with breast cancer, especially those diagnosed at a
young age, remains significant. Exposure to mantle or chest radiation at a
young age also significantly increases the risk of breast cancer, starting
approximately 8 years post radiation therapy (42,46).
A personal history of breast cancer is a risk factor for breast cancer, but
clearly every woman with a history of breast cancer does not need high risk
screening. A meta-analysis of 10,801 women treated with lumpectomy/BCT
found a 10-year recurrence rate of 19.3% and a 15-year cancer death rate of
21.4% (47). Overall, radiation therapy reduced the 10-year risk of any (i.e.,
locoregional or distant) first recurrence from 35% to 19.3% (absolute
reduction 15.7%) and reduced the 15-year risk of breast cancer death from
25.2% to 21.4% (absolute reduction 3.8%); it reduced the absolute recurrence
risk at 10 years from 31.0% to 15.6% and absolute mortality rate from 20.5%
to 17.2%. In women with node-negative (pN0) disease, the absolute
recurrence reduction varied according to age, grade, ER status, tamoxifen
use, and extent of surgery, and these characteristics were used to predict large
(≥20%), intermediate (10% to 19%), or lower (<10%) absolute reductions in
the 10-year recurrence risk.
Based on a paper published 2018 in the Journal of the American College of
Radiology by Debra Monticciolo and Michael Hassett out of Dana-Farber
Cancer Institute and Brigham and Women’s Hospital, the take-home keys for
high-risk screening are (48):

1. For women with genetic-based increased risk (and their untested first-
degree relatives) or those with a calculated lifetime risk of 20% or more,
high-risk imaging should be performed annually beginning at age 30.
2. For women with histories of chest radiation therapy before the age of 30,
high-risk imaging should be performed annually beginning at age 25 or
8 years after radiation therapy, whichever is later.
3. For women with genetic-based increased risk (and their untested first-
degree relatives), histories of chest radiation (cumulative dose of ≥10 Gy
before age 30), or a calculated lifetime risk of 20% or more, breast MRI
should be performed annually beginning at age 25 to 30.
4. For women with personal histories of breast cancer and dense breast
tissue, or those diagnosed before age 45, high-risk imaging is
recommended.
5. For women with personal histories not included in the above, or with
atypical lobular hyperplasia (ADH), atypical lobular hyperplasia, or
lobular carcinoma in-situ (LCIS), high-risk imaging should be
considered, especially if other risk factors are present.
IMAGING THE SURGICALLY ALTERED BREAST
Discussion of imaging in the posttreatment breast needs to include changes
due to; surgery, radiation, and chemotherapy. BCS remains the mainstay of
breast cancer treatment, thus understanding the posttreatment breast is
imperative. Imaging the posttreatment breast is definitely more complicated
and concordance between imaging findings, expectations, and treatment
regimen, is imperative. Posttreatment imaging changes include skin
thickening/edema, parenchymal edema, postoperative fluid
collection/seroma, scar, fat necrosis, and dystrophic calcifications.
Dystrophic calcifications are more marked up to 6 months after therapy (49).
Benign calcifications are seen in approximately one-third of BCS patients
beginning 2 to 3 years after completion of therapy due to a combination of
surgical trauma and radiation. Morphologically these calcifications are large
(>5 mm) and irregular with no associated mass/density and occur at the site
of surgery (50). Fat necrosis is also a common posttreatment finding usually
appearing as rounded translucent masses or oil cysts.
Up to 65% of early recurrences occur at or within a few centimeters of the
original tumor site and usually within 6 to 7 years of treatment (51). Thus, on
follow-up imaging, it is essential to ensure that the lumpectomy site is visible
in two views (CC and MLO or additional views), for at least the first decade
after surgery (52). Further in the first 5 years post lumpectomy an irregular
and suspicious lesion may appear stable secondary to hormonal treatment.
Thus, stability does not indicate benign finding in a patient actively on
hormonal therapy. Morphology is the most important criterion, and it is
necessary to achieve a radiologic and pathologic concordance; better to
biopsy if morphologically suspicious.
Developing asymmetry at the lumpectomy site represents a recurrence in
27% of post–cancer treatment patients (53). Locoregional tumor recurrence is
seen in 2.3% of postoncoplastic or breast reconstruction patients. The most
common site of tumor recurrence is the contact line, at the junction of the flap
with the native tissue (54).
The overall rate of local recurrence after breast cancer surgery in profile-
favorable patients is 1% to 2% per year (55). Mammographic stability is
defined as no interval change on two successive mammographic studies (50)
and is generally seen around 2 to 3 years after the completion of radiation
therapy. Any retrograde change in imaging findings such as a new mass,
microcalcifications, architectural distortion, or an area of increased density at
the lumpectomy site post stability is suspicious for tumor recurrence.
What, then, is the optimum timing for the initial post-BCS/BCT
mammogram? The American Society of Clinical Oncology recommends the
first posttreatment mammogram 1 year after diagnosis but no earlier than 6
months after completion of radiation therapy. The National Comprehensive
Cancer Network recommends annual mammography. Hymas et al. (56) found
no benefit over the general population, in mammogram before 1-year post
BCT.

TABLE 2-2 American Cancer Society (ACS) 2015 Average Risk Breast
Cancer Screening Guidelines
Risk Age Recommendation
Average 40–44 Shared decision-making
process for women to elect
screening
Average 45–54 Annual screening
Average Over 55 Biennial screening
Elderly Continued screening as long
as life expectancy greater
than 10 yrs

ACS acknowledges definition of average risk is broad and excluded only:


• History of breast cancer
• Genetic mutation
• History of chest radiation therapy
Intermediate risk group that may require a different screening approach.
Data from the ACS.
In another study Hasan et al. (57) found patients undergoing mammogram
before 6 months from completion of BCT to include completion of adjuvant
radiation, were more likely to undergo additional workup in biopsies. Thus,
in normal-risk patients we do not advocate follow-up mammography prior to
1 year after completion of BCT. Earlier imaging in high-risk patients, that is,
those with extensive intraductal component is included in these
recommendations.
CONCLUSIONS AND CURRENT IMAGING GUIDELINES PER SOCIETY (TABLES
2-2 TO 2-4)
Due to the continued controversy on when screening should begin the ACS
and the USPSTF formed panels to revisit the question and their
recommendations. The latest update from the USPSTF 2015 (58) while
relaxing on their overall stance, continue to recommend biannual screening
mammography starting at age 50. Further, the ACS guidelines are somewhat
confusing recommending annual screening starting at age 40 as a “qualified
recommendation,” described as something “the majority of individuals in this
situation would want the suggested course of action, but many would not”
(59,60).

TABLE 2-3 The Society of Breast Imaging and the Breast Imaging
Commission of the American College of Radiologist (ACR) Average Risk
Breast Cancer Screening Guidelines
Risk Age Recommendation
High Chest radiation Age 25 or 8 yrs after Annual screening
before 30 radiation
High genetic-based 25–30 Annual mammogram and
increased risk and their consider MRI
untested first-degree
relatives, those with
>20% lifetime risk
High personal history of Start at diagnosis or Annual mammogram and
breast cancer 40 whichever if <50 consider MRI
comes first
High personal history of 40 Annual screening and
ADH, ALH consider MRI
especially if other risk
factors are present
Average 40–75 Annual screening
Average Elderly Annual screening until
life expectancy less
than 5–7 yrs
MRI should be considered, especially if other risk factors are present.
Without tomosynthesis, should be performed annually.
Atypical ductal hyperplasia, ADH; atypical lobular hyperplasia, ALH; lobular carcinoma in situ, LCIS.
Data from the ACR.

The main reason for recommending screening started at age 50 rather than
40 was in order to reduce the number of “false positive” defined as imaging
recalls and “unnecessary” or benign biopsies. However, they failed to define
what is acceptable in the context of lives lost, how many recalls avoided is
equivalent to one death. The National Cancer Institute’s CISNET, which was
used by both panels, showed that, if women in their 40s wait until age 50 to
start screening mammograms and then are screened every other year, as many
as 100,000 lives will be lost that could have been saved by annual screening
starting at age 40 (58). Waiting until age 45 to begin annual screening and
then shifting to biennial screening at age 55 would result in more than 38,000
women currently in their 40s unnecessarily dying from breast cancer (36).
Approximately 10% of women undergoing screening mammography will
require “something” more. Half will be told everything is good after
additional imaging (mammogram and/or ultrasound). Approximately 25%
(2.5% of those screened) are asked to return in 6 months for a short-interval
follow-up, and approximately 20% (2% of women screened) will be advised
to undergo minimally invasive, imaging-guided needle biopsy (55). Among
these women, 20% to 40% will be found to have cancer (61).
Much of this controversy is supported by the idea of “overdiagnosis,” the
finding and treating of malignancies that were never destined to cause death.
This is seen with some favorable, low-grade DCIS. However, invasive breast
cancer left alone, will grow into a palpable cancer, with lethal capability
(34,62). In Harvard’s two largest teaching hospitals over 70% of women
dying of breast cancer did not perform regular screening mammograms
including women in their 40s (63).

TABLE 2-4 American Society of Breast Surgeons (ASBrS) and Society of


Surgical Oncology (SSO) Breast Cancer Screening Guidelines
Risk Age Recommendation
Average 40–44 Consider screening based on a
discussion of risks and
benefits
Average 45–54 Annual screening
mammograms
Average 55 and older Annual or biennial screening
for women 55 and older
based on a shared decision
Average Older than 75 with life Biannual screening
expectancy greater mammogram
than 10 yrs
Asymptomatic 40 and older Consider use of annual
intermediate screening mammography for
risk women with greater than an
estimated 15% lifetime risk
for breast cancer
Asymptomatic 10 yrs younger than the Recommendations for
high risk first-degree relative, asymptomatic high-risk
or 10 yrs after chest women (20–25% or greater
wall radiation estimated lifetime risk)
therapy, or by age 40, Annual mammography and
whichever comes first MRI compliant with ACS
and NCCN guidelines
ACS, American Cancer Society; NCCN, National Comprehensive Cancer Network.
Data from the ASBrS and SSO.

The death rate from breast cancer remained unchanged from 1940 to 1980s
when screening mammography was first introduced. By the 1990s we began
to see the death rate drop and today 36% fewer women die each year from
breast cancer (64). Male breast cancer remains relatively stable, with higher
overall mortality secondary to more advanced stage at diagnosis, as tumors
are not identified until palpable and often symptomatic.
REFERENCES

1. Copeland G, Lake A, Firth R, et al. Cancer in North America: 2008–


2012. Volume One: Combined Cancer Incidence for the United States,
Canada and North America. Springfield, IL: North American
Association of Central Cancer Registries, Inc; June 2015.
2. De Angelis R, Tavilla A, Verdecchia A, et al. Breast cancer survivors in
the United States: Geographic variability and time trends, 2005–2015.
Cancer 2009;115:1954–1966.
3. Steiner CA, Karaca Z, Moore BJ, et al. Surgeries in hospital-based
ambulatory surgery and hospital inpatient settings, 2014: statistical brief
#223. 2017 May. In: Healthcare Cost and Utilization Project (HCUP)
Statistical Briefs. Rockville, MD: Agency for Healthcare Research and
Quality (US); Revised Feb 2018.
4. Smith TJ, Davidson NE, Schapira DV, et al. American Society of
Clinical Oncology 1998 update of recommended breast cancer
surveillance guidelines. J Clin Oncol 1999;17:1080–1082.
5. DeSantis CE, Lin CC, Mariotto AB, et al. Cancer treatment and
survivorship statistics, 2014. CA Cancer J Clin 2014;64:252–271.
6. Brekelmans CT, Tilanus-Linthorst MM, Seynaeve C, et al. Tumour
characteristics, survival and prognostic factors of hereditary breast
cancer from BRCA2-, BRCA1- and non-BRCA1/2 families as compared
to sporadic breast cancer cases. Eur J Cancer 2007;43:867–876.
7. Colzani E, Liljegren A, Johansson AL, et al. Prognosis of patients with
breast cancer: causes of death and effects of time since diagnosis, age,
and tumor characteristics. J Clin Oncol 2011;29:4014–4021.
8. De Boer M, van Dijck JA, Bult P, et al. Breast cancer prognosis and
occult lymph node metastases, isolated tumor cells, and
micrometastases. J Natl Cancer Inst 2010;102:410–425.
9. Tan LK, Giri D, Hummer AJ, et al. Occult axillary node metastases in
breast cancer are prognostically significant: results in 368 node-negative
patients with 20-year follow-up. J Clin Oncol 2008;26:1803–1809.
10. Buist DS, Porter PL, Lehman C, et al. Factors contributing to
mammography failure in women aged 40–49 years. J Natl Cancer Inst
2004;96:1432–1440.
11. Johnson K, Sarma D, Hwang ES. Lobular breast cancer series: imaging.
Breast Cancer Res 2015;17:94.
12. Chansakul T, Lai KC, Slanetz PJ. Pictorial essay. The postconservation
breast: part 1, imaging findings of tumor recurrence and other long-term
sequelae. Amer J Roen 2012;198:321–330.
13. Chansakul T, Lai KC, Slanetz PJ. Pictorial essay. The postconservation
breast: part 2, imaging findings of tumor recurrence and other long-term
sequelae. Amer J Roen 2012;198:331–343.
14. Jemal A, Ward EM, Johnson CJ, et al. Annual report to the nation on the
status of cancer, 1975–2014, featuring survival. J Natl Cancer Inst
2017;109(9).
15. Siegel RL, Miller KD, Jemal A. American Cancer Society SEERS Data,
NIH 2016. CA Cancer J Clin 2016;66(1):7–30.
16. El Saghir NS, Seoud M, Khalil MK, et al. Effects of young age at
presentation on survival in breast cancer. BMC Cancer 2006;6:194.
17. Anders CK, Johnson R, Litton J, et al. Breast cancer before age 40
years. Semin Oncol 2009;36(3):237–249.
18. Rocha-Brischiliari SC, Oliveira RR, Andrade L, et al. The rise in
mortality from breast cancer in young women: trend analysis in Brazil.
PLoS One 2017;12(1):e0168950.
19. Schmadeka R, Harmon BE, Singh M. Triple-negative breast carcinoma:
current and emerging concepts. Amer J Clin Path 2014;141(4):462–477.
20. Assi HA, Khoury KE, Dbouk H, et al. Epidemiology and prognosis of
breast cancer in young women. J Thor Dis 2013;5(Suppl 1):S2–S8.
21. Jonsson H, Bordás P, Wallin H, et al. Service screening with
mammography in Northern Sweden: effects on breast cancer mortality-
an update. J Med Screen 2007;14:87–93.
22. Hellquist BN, Duffy SW, Abdsaleh S, et al. Effectiveness of population-
based service screening with mammography for women ages 40 to 49
years: evaluation of the Swedish Mammography Screening in Young
Women (scry) cohort. Cancer 2011;117:714–722.
23. Paap E, Holland R, den Heeten GJ, et al. A remarkable reduction of
breast cancer deaths in screened versus unscreened women: a case-
referent study. Cancer Causes Control 2010;21:1569–1573.
24. Hofvind S, Ursin G, Tretli S, et al. Breast cancer mortality in
participants of the Norwegian Breast Cancer Screening Program. Cancer
2013;119:3106–3112.
25. Howlader N, Noone AM, Krapcho M, et al. SEER Cancer Statistics
Review, 1975–2012. American Cancer Society. Breast Cancer Facts &
Figures 2015–2016. Atlanta, GA: American Cancer Society, Inc; 2015,
based on November 2014 SEER data submission, posted to the SEER
web site, April 2015.
26. Thompson D, Easton D. The genetic epidemiology of breast cancer
genes. J Mammary Gland Biol Neoplasia 2004;9(3):221–236.
27. U.S. Preventive Services Task Force. Screening for breast cancer:
recommendations and rationale. Ann Intern Med 2002;137:344–346.
28. Moss SM, Wale C, Smith R, et al. Effect of mammographic screening
from age 40 years on breast cancer mortality in the UK Age Trial at 17
years’ follow-up: a randomised controlled trial. Lancet Oncol
2015;16:1123–1132.
29. Calonge N, Petitti DB, DeWitt TG, et al; US Preventive Services Task
Force. Screening for breast cancer: U.S. Preventive Services Task Force
recommendation statement. Ann Intern Med 2009;151:716–726.
30. Houssami N, Miglioretti DL. Digital breast tomosynthesis: a brave new
world of mammography screening. JAMA Oncol 2016;2(6):725–727.
31. Blyere A, Welch HG. Effects of three decades of screening
mammography on breast-cancer incidence. N Engl J Med
2012;365:1998–2005.
32. Welch HG, Prorok PC, O’Malley AJ, et al. Breast-cancer tumor size,
overdiagnosis, and mammography screening effectiveness. N Engl J
Med 2016;375:1438–1447.
33. Otto SJ, Fracheboud J, Verbeek AL, et al. Mammography screening and
risk of breast cancer death: a population-based case–control study.
Cancer Epidemiol Biomarkers Prev 2012;21:66–73.
34. Coldman AJ, Phillips N. Breast cancer survival and prognosis by
screening history. Br J Cancer 2014;110(3):556–559.
35. Plevritis SK, Munoz D, Kurian AW, et al. Association of screening and
treatment with breast cancer mortality by molecular subtype in US
Women, 2000–2012. JAMA 2018;319(2):154–164.
36. Puliti D, Duffy SW, Miccinesi G, et al; EURO-SCREEN Working
Group. Overdiagnosis in mammographic screening for breast cancer in
Europe: a literature review. J Med Screen 2012;19(suppl 1):42–56.
37. Sepideh S, Reini B, Sabine S, et al. Influence of tumour stage at breast
cancer detection on survival in modern times: population-based study in
173,797 patients. BMJ 2015;351:h4901.
38. Hopper JL. Genetics for population and public health. Int J Epidemiol
2017;46(1):8–11.
39. Ho VK, van der Heiden-van der Loo M, Rutgers EJ, et al.
Implementation of sentinel node biopsy in breast cancer patients in the
Netherlands. Eur J Cancer 2008;44:683–691.
40. Lash TL, Fox MP, Buist DS, et al. Mammography surveillance and
mortality in older breast cancer survivors. J Clin Oncol 2007;25:3001–
3006.
41. Olivieri A, Pitacco E. Life tables in actuarial models: from the
deterministic setting to a Bayesian approach. Adv Stat Anal
2012;96:127–153.
42. Veronesi U, Cascinelli N, Mariani L, et al. Twenty-year follow-up of a
randomized study comparing breast-conserving surgery with radical
mastectomy for early breast cancer. N Engl J Med 2002;347:1227–1232.
43. Weinstein SP, Localio AR, Conant EF, et al. Multimodality screening of
high-risk women: a prospective cohort study. J Clin Oncol
2009;27(36):6124–6128.
44. Moossdorff M, van Roozendaal LM, Strobbe LJ, et al. Maastricht
Delphi consensus on event definitions for classification of recurrence in
breast cancer research. J Natl Cancer Inst 2014;106(12):dju288.
45. Warner E, Messersmith H, Causer P, et al. Systematic review: using
magnetic resonance imaging to screen women at high risk for breast
cancer. Ann Intern Med 2008;148:671–679.
46. Vaittinen P, Hemminki K. Risk factors and age-incidence relationships
for contralateral breast cancer. Int J Cancer 2000;88:998–1002.
47. Punglia RS, Hassett MJ. Using lifetime risk estimates to recommend
magnetic resonance imaging screening for breast cancer survivors. J
Clin Oncol 2010;28(27):4108–4110.
48. Hendrick RE, Helvie MA. USPSTF Guidelines on screening
mammography recommendations: science ignored. Am J Roentgenol
2011;196(2):W112–W116.
49. Ramani SK, Rastogi A, Mahajan A, et al. Imaging of the treated breast
post breast conservation surgery/oncoplasty: pictorial review. World J
Radiol 2017;9(8):321–329.
50. Gutierrez R, Horst KC, Dirbas FM, et al. Breast imaging following
breast conservation therapy. In: Dirbas FM, Scott-Conner CEH, eds.
Breast Surgical Techniques and Interdisciplinary Management. New
York: Springer Science Business Media; 2011:975–995. [Google
Scholar].
51. Mendelson EB. Evaluation of the postoperative breast. Radiol Clin
North Am 1992;30:107–138.
52. Dershaw DD. Breast imaging and the conservative treatment of breast
cancer. Radiol Clin North Am 2002;40:501–516.
53. Leung JW, Sickles EA. Developing asymmetry identified on
mammography: correlation with imaging outcome and pathologic
findings. AJR Am J Roentgenol 2007;188:667–675.
54. Farras Roca JA, Dao TH, Lantieri L, et al. Ipsilateral breast cancer
recurrence after deep inferior epigastric perforator (DIEP) flap
reconstruction: incidence and radiological presentation. Diagn Interv
Imaging 2016;97:203–209.
55. Chansakul T, Lai KC, Slanetz PJ. The postconservation breast: part 2,
imaging findings of tumor recurrence and other long-term sequelae. AJR
Am J Roentgenol 2012;198:331–343.
56. Hymas RV, Gaffney DK, Parkinson BT, et al. Is short-interval
mammography necessary after breast conservation surgery and radiation
treatment in breast cancer patients? Int J Radiat Oncol Biol Phys
2012;83(2):519–524.
57. Hasan S, Abel S, Simpson-Camp L, et al. Short-term follow-up
mammography in breast conservation therapy likely leads to
unnecessary downstream workup: a longitudinal study. Int J Radiat
Oncol Biol Phys 2018;102(5):1489–1495.
58. Kopans DB. Breast cancer screening panels continue to confuse the facts
and inject their own biases. Curr Oncol 2015;22(5):e376–e379.
59. Rosenberg RD, Yankaskas BC, Abraham LA, et al. Performance
benchmarks for screening mammography. Radiology 2006;241(1):55–
66.
60. Oeffinger KC, Fontham ET, Etzioni R, et al. Breast cancer screening for
women at average risk. 2015 guideline update from the American
Cancer Society. JAMA 2015;314(15):1599–1614.
61. Tan KH, Simonella L, Wee HL, et al. Quantifying the natural history of
breast cancer. Br J Cancer 2013;109(8):2035–2043.
62. Webb ML, Cady B, Michaelson JS, et al. A failure analysis of invasive
breast cancer: most deaths from disease occur in women not regularly
screened. Cancer 2014;120(18):2839–2846.
63. DeSantis CE, Fedewa SA, Goding Sauer A, et al. Breast cancer
statistics, 2015: convergence of incidence rates between black and white
women. CA Cancer J Clin 2016;66(1):31–42.
64. U.S. Preventive Services Task Force. Draft Recommendation Statement.
Breast Cancer: Screening [Web page]. Rockville, MD: USPSTF
Program Office; 2015.
http://www.uspreventiveservicestaskforce.org/Page/Document/Recommendation
Statement Draft/breast-cancer-screening1. Accessed November 11,
2015.
CHAPTER 3

Molecular Pathology of the Breast


MOHIEDEAN GHOFRANI

Although histopathologic examination of breast tumors has been practiced


since the 19th century (1), the application of ancillary techniques such as
immunohistochemistry (IHC) and more recently molecular diagnostics
including gene expression profiling as adjuncts to surgical pathology have
greatly expanded our understanding of breast cancer (2). Conventional
microscopy methods to evaluate morphologic characteristics such as
histologic subtype, architectural differentiation, cytologic atypia, and mitotic
activity in routine hematoxylin and eosin (H&E)-stained glass slides had
already demonstrated the wide variety of histologic presentations of breast
cancer, suggesting that breast cancer is not one disease but rather a multitude
of diseases that happen to arise in the breast, each with a different prognosis
and response to therapy (3).
This concept was further reinforced with the advent of IHC in the latter
part of the 20th century, a diagnostic technique that highlights the expression
of specific antigens that are not readily detected by conventional staining
methods such as H&E. IHC not only provided prognostic information (for
example, that estrogen receptor [ER]-negative or human epidermal growth
factor receptor 2 [HER-2]–positive tumors have a poorer prognosis) but also
predictive information (e.g., that ER-positive or HER-2–positive tumors are
more likely to respond to tamoxifen or trastuzumab, respectively). The
College of American Pathologists (CAP) and American Society of Clinical
Oncology (ASCO) subsequently developed guidelines to standardize testing
and reporting of ER, progesterone receptor (PR) and HER-2, which are
updated regularly (4,5).
At the beginning of the 21st century, the tools of gene expression profiling
were applied to a variety of breast tumors leading to the theory that different
types of breast cancer can be prognostically categorized into certain
“intrinsic” molecular subtypes. Based on these and other discoveries, several
commercial tests have been developed to help elucidate the molecular
characteristics of each individual patient’s tumor, specifically its risk of
recurrence, mortality, and by extension, benefit from cytotoxic
chemotherapy, thereby paving the way to realize the promise of
“personalized medicine.”
MOLECULAR DIAGNOSTICS
From a certain viewpoint, techniques such as IHC, which highlight the
presence of specific protein molecules, may be considered “molecular”
diagnostic methods. By this logic, it may even be argued that the utility of
traditional H&E and other histochemical stains depends on distinctive
molecular features. However, for the purposes of this chapter, molecular
pathology will be defined as the study of disease through the examination of
nucleic acids, namely deoxyribonucleic acid (DNA) and ribonucleic acid
(RNA), in their various forms.
One of the tenets of molecular oncology is that cancer is the result of
nonlethal mutations in DNA that amplify the expression of oncogenes or
inactivate tumor suppressor genes, both of which lead to uninhibited cellular
proliferation. A variety of basic molecular techniques have been employed
over the past few decades for the study of cancer, first in the research
laboratory, and now incorporated in commercially available clinical tests.
These include various methods for nucleic acid extraction, separation (i.e.,
resolution), detection, characterization, amplification, and sequencing. Of the
variety of existing molecular techniques, this chapter will first briefly
describe two methods that are most commonly being utilized in breast cancer
molecular testing—the polymerase chain reaction (PCR) and gene expression
profiling—and then present an overview of the more common clinically
available molecular tests for breast cancer.
POLYMERASE CHAIN REACTION
During normal DNA replication, the hydrogen bonds that hold two strands of
DNA in the double helix together are split, exposing the two strands to serve
as templates for addition of new complementary nucleotides by the enzyme
DNA polymerase, ultimately resulting in the formation of two newly
replicated strands. Since each new double helix that is formed is composed of
one parent strand and one newly replicated strand, this replicative process is
semiconservative, which to a large extent maintains the sequence of
nucleotides in DNA through successive generations.
The PCR takes advantage of this natural process to replicate, that is,
amplify segments of nucleic acid in vitro (6). A typical PCR goes through
multiple cycles, whereby the amount of target DNA is doubled in each cycle.
In the first step of a typical cycle, target DNA is exposed to a temperature of
around 95°C, which leads to denaturation of the double helix, that is, the
hydrogen bonds between the two parent strands are broken (Fig. 3-1a). In
step 2, the temperature is reduced to 50° to 70°C, so two primers, which are
specific short sequences of DNA that determine the start point and end points
of the amplification process, form hydrogen bonds (“anneal”) with their
specific complementary sequence in the DNA template strands (Fig. 3-1b). In
the third step, temperatures are increased to 68° to 72°C, the optimal
temperature for the polymerase enzyme to extend a new DNA strand from the
primers (Fig. 3-1c). Then, the cycle is repeated. Given that the duration of
each step of the cycle—denaturation, annealing, and extension—is measured
in seconds, and that the amount of target doubles in each successive cycle,
automated PCR instruments (thermal cyclers) can now produce millions of
copies, or amplicons, of a specific target sequence within 1 or 2 hours (7).
FIGURE 3-1 The polymerase chain reaction (PCR) is an efficient molecular
technique to amplify (i.e., replicate) a specific DNA sequence in the genome. In each
PCR cycle DNA is first “denatured” (a), whereby the two strands of DNA are
separated through exposure to increased temperature. Then, the temperature is
lowered so two specific primers (purple and blue arrows) “anneal” (b) to their
complementary sequences in the two DNA templates (black). Finally, the enzyme
DNA polymerase (not pictured) facilitates the building or “extension” (c) of new
DNA strands (red) by attaching complementary nucleotides starting from the
primers and continuing in the 5’ to 3’ direction, leading to two double strands of
DNA that contain the sequence delimited by the two primers. Each time the cycle is
repeated, the DNA strands formed in the previous cycles, in turn, serve as templates
for the creation of new DNA strands.

Several variants of PCR have been developed. These include:

Multiplex PCR, in which more than one primer pair are added to the
reaction environment so that multiple target sequences are amplified
simultaneously;
Reverse transcriptase (RT-)PCR, where the initial target is RNA instead
of DNA, and the enzyme RT is used to essentially perform the mirror
opposite of normal transcription, that is, to form complementary DNA
(cDNA) off of an RNA template rather than messenger RNA (mRNA)
off of a DNA template;
Nested PCR, in which two pairs of primers are used in two successive
rounds of amplification—the second pair targeting sequences located
slightly inside the first primer pair to increase sensitivity and specificity
of the reaction; and
Real-time or quantitative PCR (which is confusingly also abbreviated as
RT-PCR, but more appropriately as qPCR or RT-qPCR) where the
amount of amplicon is monitored in real time using a fluorescent
marker, so that based on the cycle number in which fluorescence
exceeds a certain threshold, the starting amount of target in an unknown
specimen can be calculated—the assumption being that the more target
in the initial sample, the fewer cycles that would have been necessary
for the fluorescence to exceed the threshold (Fig. 3-2).

FIGURE 3-2 Real time quantitative PCR (RT-qPCR) is a type of PCR in which the
quantity of a specific nucleic acid sequence in a test sample can be estimated. At the end
of each PCR cycle, the amount of amplicon is measured, and based on the cycle number
in which that quantity exceeds a certain threshold, the initial quantity can be calculated,
since the higher the amount of targeted nucleic acid in the initial sample, the earlier the
measured amplicon will exceed the quantitative threshold. (From Königshoff M, Wilhelm
J, Bohle RM, et al. HER-2/neu gene copy number quantified by real-time PCR:
comparison of gene amplification, heterozygosity, and immunohistochemical status in
breast cancer tissue. Clin Chem 2003;49:219–229.)
GENE EXPRESSION PROFILING
Gene expression profiling is a method whereby the expression of thousands
of genes can be simultaneously measured in a patient’s tissue sample. This is
achieved using a DNA microarray or “chip,” a collection of microscopic
DNA spots attached to a solid surface typically no larger than the size of a
postage stamp (Fig. 3-3). Each of these DNA spots contains a very small
amount (on the order of 10−12 moles, a picomole) of a specific DNA
sequence or “probe.” DNA or RNA from a tissue sample is applied to this
DNA microarray under controlled conditions so that complementary
sequences in the sample hybridize (i.e., form hydrogen bonds) with their
respective probe in the microarray.
The amount of hybridization in each spot can be quantified and then
visualized in a heat map, in which, for example, overexpression of a certain
gene is shown as a red dot while underexpression is shown as a green dot.
Since the gene expression profile of a tumor sample will be different from
normal tissue, each tumor’s aggregate pattern of gene overexpression or
underexpression will form that tumor’s unique gene expression profile. By
extension, the gene expression profile of hundreds of different tumor and
normal tissue samples can be compared side by side in a two-dimensional
heat map, in which each column represents a sample and each row represents
a gene. Complex bioinformatic algorithms can identify a subset of genes that
are differentially expressed in tumors and sort the different tumor samples in
the heat map based on their similarity in expressing these informative genes
so that a hierarchical clustering emerges (Fig. 3-4). By correlating the shared
gene expression profile of these clusters of tumor samples with clinical
outcomes, it can be shown that each molecular subtype is typically associated
with a characteristic natural history, metastatic pattern, and sensitivity to
different treatments, demonstrating the causal relationship between genotype
and phenotype.
FIGURE 3-3 DNA microarrays or “gene chips” contain thousands of different DNA
sequences in minuscule spots attached to a solid surface. The expression levels of
thousands of genes can be simultaneously measured by applying DNA in a tissue sample
to the microarray.
INTRINSIC BREAST CANCER SUBTYPES
In 2000, Perou et al. published their seminal paper in Nature in which they
compared the expression of 8,102 genes in 65 breast tumor samples (8). By
hierarchical cluster analysis, they identified a small number of breast cancer
subtypes that were subsequently refined to four groups: luminal A, luminal B,
HER-2 enriched, and basal like.
On the molecular level, the luminal A subtype expresses keratins that
characterize the cells lining the inner lumen of normal breast ducts. Luminal
A tumors also coexpress ER. They are typically associated with low-grade
histology, most commonly low-grade invasive carcinoma of no special type
(ductal, not otherwise specified) as well as special types of low-grade
carcinoma such as tubular, cribriform, and mucinous carcinoma. These
tumors have an excellent prognosis and are responsive to hormone therapies
such as tamoxifen and aromatase inhibitors, so the administration of
cytotoxic chemotherapy will not provide any significant benefit to the patient.
Luminal B tumors also express luminal keratins but compared to their
luminal A counterparts exhibit diminished ER and especially PR expression,
typically overexpress genes associated with cellular proliferation, and may
overexpress the HER-2 oncogene. Histologically they are typically higher
grade, and the increased cellular proliferation manifests as higher mitotic
count by conventional H&E stain and increased Ki-67 (MIB1) index by IHC.
Compared to luminal A tumors, the luminal B subtype is generally less
sensitive to hormone therapy and are more likely to respond to
chemotherapy.
The HER-2–enriched subtype, as its name implies, is characterized by
increased expression of the HER-2 oncogene. These tumors are also by
definition negative for ER and PR expression. They usually exhibit high-
grade histology, including high proliferative rate. In terms of natural history,
these tumors are the most aggressive subtype with the highest mortality and
lowest survival. However, with the introduction and use of anti–HER-2
therapies such as trastuzumab, the outcome of patients who are found by
IHC, in situ hybridization (ISH), or other methods to be HER-2–positive has
significantly improved.
The basal-like subtype is characterized by expression of keratins produced
in the basal (myoepithelial) layer of normal breast ducts. Tumors that are
identified as basal like by gene expression profiling are typically associated
with high-grade histology reminiscent of medullary carcinoma, more frequent
metastases to brain and lung, association with breast cancer 1 (BRCA1) gene
mutations, and poor survival. They usually do not express ER, PR, or HER-2
(i.e., they are “triple negative”), which may also be more conveniently
demonstrated by IHC. Since few specific predictive markers have been
identified that would make patients with basal-like tumors eligible for
targeted therapy, they are often left with the option of cytotoxic
chemotherapy.
FIGURE 3-4 Gene expression profiling data can be visualized in a two-dimensional heat
map, where the expression levels of hundreds, even thousands, of genes in as many tissue
samples is graphically represented. In this example, each gene is represented by a row,
each sample is represented by a column, and the expression level of a gene in a sample is
color coded at the intersection of the respective row and column, with shades of red
denoting overexpression and shades of green representing underexpression. Samples with
similar gene expression profiles can then be sorted next to each other and their degree of
similarity can be shown by their hierarchical clustering in a tree diagram or
“dendrogram.” (From: Sørlie T, Perou CM, Tibshirani R, et al. Gene expression patterns
of breast carcinomas distinguish tumor subclasses with clinical implications. Proc Natl
Acad Sci U S A 2001;98(19):10869–10874.)

Although gene expression profiling has identified certain molecular


subtypes of breast cancer that are mostly characterized by their
underexpression or overexpression of ER, PR, HER-2, Ki-67, and luminal or
basal keratins (all of which can also be evaluated by IHC), it is essential that
this molecular data be interpreted in the context of routine H&E-based
histology. For example, not all triple-negative breast cancers that express
basal keratins (either by molecular techniques or IHC) are “basal like,” since
other less common tumors such as metaplastic carcinomas or adenoid cystic
carcinoma share a similar profile, yet often have a better prognosis (9). Also,
since molecular diagnostic methods depend on “grind and bind” techniques
where the tissue is homogenized and the measured mRNA levels represent
average gene expression across all cells in the tissue sample, they do not
account for tumor heterogeneity where different areas of the same tumor may
have different genomic profiles.
CLINICAL APPLICATIONS
As different laboratories adopted gene expression profiling techniques to the
study of breast cancer, a wide variety of genes were recognized to be of
potential prognostic and predictive value in testing clinical patient samples.
This has led to the development of several commercially available tests that
often measure mRNA levels in a patient tumor sample as a surrogate for the
expression of any number of genes, most commonly in the dozens. Each of
these multigene assays quantifies the expression of its included genes, and by
incorporating those values in a clinically validated formula that gives a
different weight to the expression level of each gene, a final score is
calculated that assigns the patient to a low-risk, high-risk, or in some cases
intermediate-risk prognostic category.
At the time of this writing, the current editions of the American Joint
Commission on Cancer (AJCC) Cancer Staging Manual (10) and the
National Comprehensive Cancer Network (NCCN) Clinical Practice
Guidelines in Oncology for Breast Cancer (11) provide guidance on the
clinical utility of the more common multigene assays in the staging and
treatment of breast cancer. These include the 21-gene (Oncotype DX), 70-
gene (MammaPrint), 50-gene (PAM-50), and 12-gene (EndoPredict) assays,
as well as the Breast Cancer Index (BCI), all of which have been validated in
ER-positive/HER-2–negative breast cancers. The published literature in this
field is constantly growing and as a result these recommendations are
currently in flux; the reader is referred to the newest editions of AJCC,
NCCN, and other evidence-based guidelines for the most up-to-date
recommendations.
ONCOTYPE DX
Oncotype DX is a multigene assay that utilizes RT-qPCR to measure the
expression of 21 genes in breast tumors (12). Sixteen of these genes are
cancer related, with a strong focus on the ER (four genes) and cellular
proliferation (five genes), while five genes serve as a reference for normal
gene expression. Gene expression levels are measured, and the results are
inserted into a formula that has been validated against clinical outcomes,
providing a numeric Recurrence Score.
The rationale for using tests such as the 21-gene assay is that patients that
are low risk by both clinicopathologic and gene expression criteria can be
assured that they will not derive any significant benefit from adding cytotoxic
chemotherapy to hormone therapy and can be spared the serious side effects
associated with additional treatment. On the other hand, in otherwise
clinicopathologically low-risk patients who are found to have a higher
Recurrence Score, additional chemotherapy should be considered given the
additional survival benefit it would provide (13).
According to NCCN Guidelines high-level (category 1) evidence from
studies such as the TAILORx (Trial Assigning Individualized Options for
Treatment [Rx]) study (14), Oncotype DX is the preferred multigene assay
that should be strongly considered for tumors with ductal, lobular, mixed, or
metaplastic histology measuring 0.5 to 5 cm that are hormone receptor
positive by IHC, HER-2 negative by IHC and/or ISH, and lymph node
negative. Also, lower level (category 2A) evidence suggests in patients with
up to three positive lymph nodes who are candidates for adjuvant
chemotherapy, a multigene assay such as Oncotype DX should be considered
to determine chemotherapy benefit, since patients who are identified as low
risk by multigene analysis may be safely treated with adjuvant hormone
therapy alone and spared the side effects of chemotherapy.
Based on level I evidence (multiple large, well-designed, and well-
conducted studies), the 8th edition of the AJCC Cancer Staging Manual
incorporates Oncotype DX Recurrence Score as a factor that may determine
Prognostic Stage Group: in tumors 5 cm or smaller that are ER positive,
HER-2 negative, lymph node negative, and without distant metastasis, a
Recurrence Score less than 11 would categorize the tumor as Stage IA, even
though the same tumor without this molecular information may be higher
stage in certain scenarios.
MammaPrint
MammaPrint was the first Food and Drug Administration (FDA)-approved
multigene assay for breast cancer (15). It is a multigene assay that utilizes
gene expression profiling to measure the expression of 70 genes associated
with breast cancer recurrence. The quantified expression levels of these 70
genes are inserted into a weighted formula that categorizes patients into a
good or poor prognosis category (16), the cutoff correlating with 90% of the
low-risk group having no metastatic disease within 10 years (17). Subsequent
clinical trials have confirmed the added value of information provided by the
70-gene signature in treatment decisions (18).
According to NCCN Guidelines category 1 Evidence derived from the
MINDACT (Microarray in Node-Negative and 1 to 3 Positive Lymph Node
Disease May Avoid Chemotherapy) trial (19), patients with up to three
positive lymph nodes or those who are otherwise at high clinical risk would
benefit from the 70-gene assay since a low-risk test result would indicate that
the benefit of adjuvant chemotherapy would be small. According to the
Eighth Edition of the AJCC Cancer Staging Manual, use of MammaPrint is
based on Level II Evidence (at least one large, well-designed, and well-
conducted study) and is not incorporated in prognostic staging. It must be
noted, however, that the AJCC Manual is not updated as frequently as NCCN
Guidelines and lags in incorporating published literature in its staging rules.
PAM50 (PROSIGNA)
PAM50 (Prosigna) is another gene expression profiling test that measures the
expression level of 50 genes resulting in a numerical score ranging from 0 to
100, which correlates with the risk of 10-year distant recurrence (20). It also
identifies a tumor’s molecular subtype (luminal A, luminal B, HER-2
enriched, or basal like).
Based on NCCN category 2A Evidence, tumors that are otherwise T1 or
T2 (i.e., up to 5 cm in size), ER positive, HER-2 negative, and lymph node
negative, may be treated as T1a-T1b tumors (i.e., up to 1 cm in size) if they
are categorized as low-risk by the 50-gene assay (21). Also, patients with up
to three positive lymph nodes but a low-risk PAM50 score have a less than
3.5% risk of 10-year distant recurrence with hormone therapy alone and
would not derive significant benefit from chemotherapy. At the time of this
writing, use of PAM50 is based on AJCC level II evidence and is not
incorporated in prognostic staging.
ENDOPREDICT
EndoPredict is another gene expression profiling assay that measures the
expression of 12 genes, 8 of which have been determined to be breast cancer-
related: 3 proliferation genes and 5 hormone receptor genes (22). It produces
a numeric score that, in conjunction with clinical features (tumor size and
lymph node status), predicts whether the tumor is at a low or high risk of
distant recurrence.
Like PAM50, NCCN Level 2A Evidence shows that a low risk
EndoPredict score of 5 or less places patients with T1 and T2 tumors in the
same prognostic category as T1a-T1b tumors (23). Also, patients with up to
three positive lymph nodes but a low-risk EndoPredict score had an only
5.6% risk of distant recurrence at 10 years, suggesting these patients would
likely not benefit from chemotherapy. However, since AJCC 8th edition
considers EndoPredict to be based on level II evidence, it is not included in
prognostic staging.
BREAST CANCER INDEX
The Breast Cancer Index (BCI) is a continuous risk model developed based
on prospective trial data of tamoxifen-treated patients that combines two
previously described biomarkers, the HOXB13:IL17BR ratio and molecular
grade index (a five-gene predictor). According to a predefined cutoff, it
categorizes patients into high- and low-risk based on their 10-year breast
cancer recurrence-free survival (24), thereby predicting the benefit of
extending endocrine therapy beyond 5 years in high-risk patients.
Similar to PAM50 and EndoPredict, NCCN Level 2A Evidence
categorizes patients with T1-T2 tumors that are in the BCI low-risk range in
the same prognostic category as those with T1a-T1b tumors. However, at the
time of this writing, NCCN considers data on the utility of BCI in lymph
node-positive patients to be limited, and AJCC 8th edition does not include
BCI in prognostic staging.
CONCLUSIONS
Although studies of molecular pathology of the breast have demonstrated that
each patient’s tumor has a unique molecular signature, some commonalities
can be identified to improve categorization, prognostication, and treatment
decisions. Researchers continue to search for specific therapeutic targets to
avoid the morbidity of cytotoxic chemotherapy in patients. Molecular
diagnostics can provide a wealth of genomic data from even the smallest of
tissue samples, but this data needs to be interpreted in the context of the
patient’s individual clinical and histologic findings, and potential issues such
as sample representativeness and tumor heterogeneity must be kept in mind.
The field of molecular diagnostics is rapidly advancing and promises to
deliver a much more detailed understanding of breast pathology, but as in any
growing field of science, its findings must be interpreted with caution.

REFERENCES

1. Gal AA. In search of the origins of modern surgical pathology. Adv Anat
Pathol 2001;8:1–13.
2. Sotiriou C, Wirapati P, Loi S, et al. Gene expression profiling in breast
cancer: understanding the molecular basis of histologic grade to improve
prognosis. J Natl Cancer Inst 2006;98:262–272.
3. Rakha EA, Reis-Filho JS, Baehner F, et al. Breast cancer prognostic
classification in the molecular era: the role of histological grade. Breast
Cancer Res 2010;12:207.
4. Hammond MEH, Hayes DF, Dowsett M, et al. American Society of
Clinical Oncology/College of American Pathologists guideline
recommendations for immunohistochemical testing of estrogen and
progesterone receptors in breast cancer. Arch Pathol Lab Med
2010;134:907–922.
5. Wolff AC, Hammond MEH, Allison KH, et al. Human epidermal
growth factor receptor 2 testing in breast cancer: American Society of
Clinical Oncology/College of American Pathologists clinical practice
guideline focused update. Arch Pathol Lab Med 2018;142:1364–1382.
6. Mullis KB, Faloona FA. Specific synthesis of DNA in vitro via a
polymerase-catalyzed chain reaction. Methods Enzymol 1987;155:335–
350.
7. Obeid PJ, Christopoulos TK, Crabtree HJ, et al. Microfabricated device
for DNA and RNA amplification by continuous-flow polymerase chain
reaction and reverse transcription-polymerase chain reaction with cycle
number selection. Anal Chem 2003;75:288–295.
8. Perou CM, Sørlie T, Eisen MB, et al. Molecular portraits of human
breast tumours. Nature 2000;406:747–752.
9. McCart Reed AE, Kalita-De Croft P, Kutasovic JR, et al. Recent
advances in breast cancer research impacting clinical diagnostic
practice. J Pathol 2019;247:552–562.
10. Hortobagyi GN, Connolly JL, D’Orsi CJ, et al. Breast. In: Amin MB,
Edge S, Greene F, et al., eds. AJCC Cancer Staging Manual. 8th ed.
Chicago, IL: Springer International Publishing, American Joint
Committee on Cancer; 2017.
11. National Comprehensive Cancer Network. Breast cancer. 2019.
(September 6, 2019). Available online at
https://www.nccn.org/professionals/physician_gls/pdf/breast.pdf
12. Paik S, Shak S, Tang G, et al. A multigene assay to predict recurrence of
tamoxifen-treated, node-negative breast cancer. N Engl J Med
2004;351:2817–2826.
13. Paik S, Tang G, Shak S, et al. Gene expression and benefit of
chemotherapy in women with node-negative, estrogen receptor-positive
breast cancer. J Clin Oncol 2006;24:3726–3734.
14. Sparano JA, Gray RJ, Makower DF, et al. Adjuvant chemotherapy
guided by a 21-gene expression assay in breast cancer. N Engl J Med
2018;379:111–121.
15. van de Vijver MJ, He YD, van’t Veer LJ, et al. A gene-expression
signature as a predictor of survival in breast cancer. N Engl J Med
2002;347:1999–2009.
16. van’t Veer LJ, Dai H, van de Vijver MJ, et al. Gene expression profiling
predicts clinical outcome of breast cancer. Nature 2002;415:530–536.
17. Buyse M, Loi S, van’t Veer L, et al. Validation and clinical utility of a
70-gene prognostic signature for women with node-negative breast
cancer. J Natl Cancer Inst 2006;98:1183–1192.
18. Drukker CA, Bueno-de-Mesquita JM, Retèl VP, et al. A prospective
evaluation of a breast cancer prognosis signature in the observational
RASTER study. Int J Cancer 2013;133:929–936.
19. Cardoso F, van’t Veer LJ, Bogaerts J, et al. 70-Gene signature as an aid
to treatment decisions in early-stage breast cancer. N Engl J Med
2016;375:717–729.
20. Wallden B, Storhoff J, Nielsen T, et al. Development and verification of
the PAM50-based Prosigna breast cancer gene signature assay. BMC
Med Genomics 2015;8:54.
21. Lænkholm AV, Jensen MB, Eriksen JO, et al. PAM50 risk of recurrence
score predicts 10-year distant recurrence in a comprehensive Danish
cohort of postmenopausal women allocated to 5 years of endocrine
therapy for hormone receptor-positive early breast cancer. J Clin Oncol
2018;36:735–740.
22. Filipits M, Rudas M, Jakesz R, et al. A new molecular predictor of
distant recurrence in ER-positive, HER2-negative breast cancer adds
independent information to conventional clinical risk factors. Clin
Cancer Res 2011;17:6012–6020.
23. Sestak I, Buus R, Cuzick J, et al. Comparison of the performance of 6
prognostic signatures for estrogen receptor-positive breast cancer: a
secondary analysis of a randomized clinical trial. JAMA Oncol
2018;4:545–553.
24. Jerevall PL, Ma XJ, Li H, et al. Prognostic utility of HOXB13:IL17BR
and molecular grade index in early-stage breast cancer patients from the
Stockholm trial. Br J Cancer 2011;104:1762–1769.
CHAPTER 4

Defining and Managing the High-Risk


Patient
NOEMI MAKKAI SIGALOVE
HISTORY
In light of the incidence, socioeconomic and personal impact of breast cancer,
being able to identify those who are at increased risk gives clinicians an
opportunity to intervene with risk-lowering strategies. Stratification of
individuals based on risk level allows for screening and prevention programs
based on personal risk and they also make such programs cost-effective (1).
The incidence of breast cancer in 2017 was 63,412 for in situ disease and
252,710 for invasive disease, leading to 40,610 deaths (2). Screening
programs applied indiscriminately to the general population are not adequate
for those at increased risk. We must individualize care and provide the most
effective strategy for dealing with both treatment and prevention of disease.
Today, high-risk individuals are identified by a multitude of sources,
including physicians, nonphysician providers, breast imaging centers, high-
risk programs, geneticists, community outreach programs, and web-based
self-assessment calculators. As physicians, we have an obligation to identify
and appropriately manage those patients who are at high risk for developing
breast cancer.
RISK STRATIFICATION
Risk stratification can be based on absolute, lifetime, or relative risk for
developing breast cancer. Absolute risk is the likelihood of being diagnosed
with cancer over a defined period of time. The American Society of Clinical
Oncology (ASCO) guidelines defines high risk to be an absolute 5-year risk
of 1.66% as calculated by the National Cancer Institute Breast cancer Risk
Assessment Tool (BCRAT) or equivalent measures (3,4).
Lifetime risk is the absolute risk of being diagnosed with cancer over the
course of a lifetime from birth to death. A woman in the United States has
about a 12% chance of being diagnosed with breast cancer in her lifetime (2).
In the United States, high lifetime risk for breast cancer is accepted to be a
risk greater than 20% as calculated by various risk assessment models.
Relative risk compares the absolute risk of diseases among people with a
particular risk factor to the risk among people without that risk factor. If the
relative risk is above 1, then risk is higher among those with the risk factor
than among those without the factor. Relative risk is useful for comparisons
but does not provide information about the absolute risk of the exposed group
(2). As shown in Table 4-1, known risk factors can be stratified into three
relative risk categories (2). The effects of screening or various intervention
measures can be studied based on their impact on relative risk.
The National Comprehensive Cancer Network (NCCN) uses a
combination of absolute, lifetime, and relative risk to categorize high-risk
groups. It identifies six specific groups that place individuals into the
increased risk category: (1) women with a prior history of breast cancer; (2)
women greater than 35 years of age with a 5-year risk of invasive breast
cancer greater than 1.7% (per Gail model); (3) women who have a lifetime
risk greater than 20% based on history of lobular carcinoma in situ (LCIS) or
atypical ductal hyperplasia (ADH)/atypical lobular hyperplasia (ALH); (4)
women who have a lifetime risk greater than 20% as defined by models that
are largely dependent on family history; (5) women between the ages of 10
and 30 years with prior thoracic radiation therapy (e.g., mantle irradiation);
and (6) women with a pedigree suggestive of or known genetic predisposition
(5). Women with a personal history of breast cancer will be omitted for the
purposes of this discussion. A guide to NCCN recommendations for each
remaining group for screening and risk reduction strategies is summarized in
Table 4-2 (5).
RISK ASSESSMENT MODELS
There are multiple risk assessment models available to calculate a woman’s
risk for developing breast cancer. The first step in risk assessment should be
to identify personal, familial, and genetic factors that may be associated with
a patient’s increased breast cancer risk. If these factors are absent, models
such as Gail/BCRAT (Breast Cancer Risk Assessment Tool, NCI) are
sufficient. For those individuals with personal, genetic, or familial factors, a
more extensive risk assessment needs to be undertaken (5). A recent review
of various risk assessment models by the United States Preventive Services
Task Force established that each risk assessment tool has advantages and
limitation and found insufficient evidence to recommend one over the other
(6). Models evaluated included the Ontario Family History Assessment Tool,
Manchester Scoring System, Referral Screening Tool, Pedigree Assessment
Tool, 7-Question Family History Screening Tool, International Breast Cancer
Intervention Study Instrument (Tyrer–Cuzick), and brief versions of
BRCAPRO. These familial risk assessment tools are primarily intended for
use by health care clinicians untrained in genetic cancer risk assessment in
order to guide referral to genetic counselors for more definitive evaluation.
These familial risk assessment models were found to have sensitivity
estimates between 77% and 100% and areas under the receiver operating
characteristic curve between 0.68 and 0.96 (7). Clinicians can safely
implement any of these risk assessment models into their practice.

TABLE 4-1 Factors That Increase the Relative Risk for Breast Cancer in
Women
Relative Risk Factor
>4.0 Age (65+ vs. <65 yrs, although risk increases across all ages
until age 80)
Biopsy-confirmed atypical hyperplasia
Certain inherited genetic mutations for breast cancer
(BRCA1/BRCA2)
Ductal carcinoma in situ
Lobular carcinoma in situ
Mammographically dense breasts (compared to least dense)
Personal history of early-onset (<40 yrs) breast cancer
Two or more first-degree relatives with breast cancer
diagnosed at an early age
2.1–4.0 Personal history of breast cancer (40+ yrs)
High endogenous estrogen or testosterone levels
(postmenopausal)
High-dose radiation to chest
One first-degree relative with breast cancer
1.1–2.0 Alcohol consumption
Ashkenazi Jewish heritage
Diethylstilbestrol exposure
Early menarche (<12 yrs)
Height (tall)
High socioeconomic status
Late age at first full-term pregnancy (>30 yrs)
Late menopause (>55)
Never breastfed a child
No full-term pregnancies
Obesity (postmenopausal)/adult weight gain
Personal history of endometrial or ovarian cancer
Proliferative breast disease without atypia (usual ductal
hyperplasia, fibroadenoma)
Recent and long-term use of menopausal hormone therapy
containing estrogen and progestin
Recent oral contraceptive use
GENETIC COUNSELING AND TESTING
Patients who are thought to have a high risk of genetic mutation based on
familial risk assessment models should be referred to genetic counseling.
Individuals will be identified for testing of specific deleterious mutations, and
discussion will ensue regarding benefits and harms of testing, interpretation
of results, and management options. Testing for mutations should be
performed if personal or family history suggests an inherited cancer
susceptibility.
Several societies have established criteria for referral to genetic counseling
and testing. These recommendations are summarized in Table 4-3 (8). The
outlier in genetic testing referral recommendation is the American Society of
Breast Surgeons. In its official statement, the society states that recent data
support that genetic testing should be offered to each patient with breast
cancer (newly diagnosed or with a personal history). If genetic testing is
performed, such testing should include BRCA1/BRCA2 and PALB2 with
other genes as appropriate for the clinical scenario and family history. For
patients with newly diagnosed breast cancer, identification of a mutation may
impact local treatment recommendations (surgery and potentially radiation)
and systemic therapy. Additionally, family members may subsequently be
offered testing and tailored risk-reduction strategies (9). The basis of this
recommendation was the observation that a significant number of pathogenic
mutation carriers remain undetected and undiagnosed. These are largely
women with “moderate-penetrance” mutations, but even women with
BRCA1/BRCA2 mutations may not be identified (10,11).
APPROACH TO MANAGING THE HIGH-RISK PATIENT
Management of the high-risk patient can be undertaken in many different
clinical settings. Primary care or surgical offices staffed by clinicians with
interest and knowledge for caring for high-risk patients is common. High-risk
clinics have been also been established for screening and management of the
high-risk population. These clinics tend to embrace a multidisciplinary
approach and often include services such as genetic counseling and testing,
nutrition, exercise, and weight control programs. Access is maintained to
oncologic and surgical specialties as needed. Regardless of the type of
clinical setting, the practical approach to managing the high-risk patient
includes the goals summarized in Table 4-4 as per NCCN recommendations
(12).

TABLE 4-2 NCCN Recommendations for Screening and Risk-Reduction


Strategies for High-Risk Patients

TABLE 4-3 Recommendations for Genetic Referral and Testing


Society Recommendation for Genetic
Counseling and Testing
American College of Medical Testing for a mutation when
Genetics individual has personal or family
cancer history suggestive of
inherited cancer susceptibility, the
test can be adequately interpreted
and the results will aid in
management
American Society of Clinical Testing for a mutation when
Oncology individual has personal or family
cancer history suggestive of
inherited cancer susceptibility, the
test can be adequately interpreted
and the results will aid in
management
American College of Obstetricians Perform a hereditary cancer risk
and Gynecologists assessment and subsequent referral
to a specialist in cancer genetics if
necessary
Society for Gynecologic Oncology Individuals with a likelihood of
inherited predisposition to cancer
based on personal or family
history should be offered genetic
counseling
American Society of Breast Surgeons Genetic testing be made available to
all patients with a personal history
of breast cancer
National Institute for Health and Health care professionals respond to
Care Excellence a patient who presents with
concerns but should not, in most
instances, actively seek to identify
persons with a family history of
breast cancer. In some
circumstances, including when a
patient has concerns about
relatives with breast cancer, a first-
and second-degree family history
be taken in primary care to assess
risk. Referral to secondary care is
recommended if risk factors are
identified in family history taking
United States Preventive Services Primary care clinicians assess women
Taskforce with a personal or family history
of breast, ovarian, tubal, or
peritoneal cancer or who have an
ancestry associated with
BRCA1/BRCA2 gene mutations
with an appropriate brief familial
risk assessment tool. Women with
a positive result on the risk
assessment tool should receive
genetic counseling, and if
indicated, genetic testing

TABLE 4-4 Components of Risk/Benefit Assessment and Counseling


Options Decision-Making Factors
Genetic Counseling • If a woman is at high risk secondary to a strong
family history or very early onset of breast or
ovarian cancer, genetic counseling should be
offered.
Healthy Lifestyle • Consider breast cancer risks associated with
combined estrogen/progesterone therapy greater
than or equal to 3–5-yr duration of use.
• Alcoholic drinks increase the risk for breast
cancer; limit alcohol consumption.
• Exercisea
• For premenopausal women, be vigorously
physically active.
• For postmenopausal women, be at least
moderately physically active. Be active daily,
taking part each week in at least 150 min of
moderate intensity, aerobic physical activity or
at least 75 min of vigorous, aerobic physical
activity (or a combination).
• Weight control
• For postmenopausal women, be a healthy
weight and avoid weight gain.
• Breastfeeding
Risk-Reducing • Discussion of relative and absolute risk reduction
Agents with tamoxifen, raloxifene, or aromatase
inhibitors.b
• Contraindications to tamoxifen or raloxifene:
history of deep venous thrombosis, pulmonary
embolus thromboembolic stroke, transient
ischemic attack, or known inherited clotting trait.
• Contraindications to tamoxifen, raloxifene, and
aromatase inhibitorsb: current pregnancy or
pregnancy potential without effective
nonhormonal method of contraception.
• Common and serious adverse effects of tamoxifen,
raloxifene, or aromatase inhibitorsb with emphasis
on age-dependent risks.
Risk-Reducing • Risk-reducing mastectomy should generally be
Surgery considered only in women with a genetic mutation
conferring a high risk for breast cancer,
compelling family history, or possibly with prior
thoracic RT at <30 yrs of age. While this approach
has been previously considered for LCIS, the
currently preferred approach is risk-reducing
therapy. The value of risk-reducing mastectomy in
women with deleterious mutations in other genes
associated with a two-fold or greater risk for
breast cancer (based on large epidemiologic
studies) in the absence of a compelling family
history of breast cancer is unknown.
Clinical Research • Option of participation in clinical research for
screening, risk assessment, or other risk-reducing
intervention.

aSee American Society Guidelines.


bExemestane and anastrozole are not currently FDA approved for breast cancer risk reduction. There
are currently no data comparing the benefits and risks of exemestane and anastrozole to those of
tamoxifen and raloxifene.
RT, radiation therapy; LCIS, lobular carcinoma in situ.

Genetic Testing
Once a patient has been established as high risk based on a strong family
history or very early onset of breast or ovarian cancer, genetic counseling
should be offered (12).
Healthy Lifestyle
As delineated in Table 4-1, multiple factors contribute to the increase of the
relative risk of breast cancer. Although factors such as age, height, family
history, or heritage cannot be controlled, a number of behavioral factors are
modifiable in the 1.1 to 2.0 relative risk category.
Regarding hormone replacement therapy (HRT), the NCCN panel
makes two recommendations: (1) when prescribing HRT, consider the risks
associated with combined estrogen/progesterone therapy for greater than or
equal to 3- to 5-year duration of use, and (2) hormone therapy (HT) is not
recommended for women taking tamoxifen, raloxifene, anastrozole, or
exemestane outside of a clinical trial (12). The conclusion of the panel was
based on 16 publications examining the effect of HRT on breast cancer risk.
Some of these included the larger Women’s Health Initiative studies (13,14),
the Black Women’s Health Study (15), the Million Women Study (16), and
the Nurses’ Health Study (17). Conclusions, weaknesses, and strengths of
each study were considered when making final recommendations.
Numerous studies have demonstrated that the intake of moderate amounts
of alcohol (1 to 2 drinks per day) is associated with an increased risk of
breast cancer (18,19). The mechanism thought to be responsible for this
increased risk is from the observation that alcohol increases levels of estrogen
and androgen (20). A population-based study examining postmenopausal
women showed an association between increased alcohol consumption and
development of ER-positive tumors (21). The NCCN Breast Cancer Risk
Reduction Panel recommends that alcohol consumption be limited to one
drink or less per day. One drink is defined as 1 oz of liquor, 6 oz of wine, or 8
oz of beer (12).
Increased levels of physical activity have been associated with a decreased
risk for breast cancer. Women who get regular physical activity have a 10%
to 20% lower risk of breast cancer compared to women who are inactive (22).
A population-based case control study with newly diagnosed invasive breast
cancer and control patients grouped according to race, showed that both black
and white women with annual lifetime exercise activity levels exceeding the
median activity level for active control subject were found to have 20% lower
risk for breast cancer when compared to inactive women (23). In a second
study, the greatest reduction was seen for women who reported
walking/hiking for 10 hours or more per week (24). The NCCN Breast
Cancer Risk Reduction Panel states that premenopausal women should be
vigorously physically active. Postmenopausal women should be at least
moderately physically active. Postmenopausal women should also be active
daily, taking part each week in at least 150 minutes of moderate-intensity,
aerobic physical activity or at least 75 minutes of vigorous, aerobic physical
activity (or a combination) (12).
Body mass index (BMI) is an independent risk factor for breast cancer,
especially in Caucasian women. Postmenopausal breast cancer risk is about
1.5 times higher in overweight women and about 2 times higher in obese
women than in lean women (25). Weight gain also increases the risk of
postmenopausal breast cancer. Each 5 kg gained during adulthood increases
risk of postmenopausal breast cancer by 11% (in women who did not use
HRT) (26). This same observation is not noted for premenopausal women, in
fact higher BMI seems to be protective against breast cancer in
premenopausal women (27). The NCCN Breast Cancer Risk Reduction Panel
recommends that postmenopausal women maintain a healthy weight and
avoid gaining weight (12).
Most studies suggest that breastfeeding for a year or more slightly reduces
a woman’s overall risk of breast cancer, with longer duration associated with
greater risk reduction (28). The protective effect seems stronger for triple-
negative than hormone-positive cancers (29). The NCCN Breast Cancer Risk
Reduction Panel recommends that women breastfeed.
Dense breast tissue as measured by mammography is increasingly
recognized as an important risk factor for breast cancer. For example, a report
of a large case-cohort study of women 35 years and older with no history of
breast cancer who underwent mammographic screening, first at baseline and
then at an average of 6 years later, suggested that longitudinal changes in
breast density are associated with changes of breast cancer risk (12,30).
Risk-Reducing Agents
Risk-reducing agents are recommended for women 35 and older with a Gail
Model 5-year breast cancer risk of 1.7 or greater or a history of LCIS (12).
ASCO guidelines recommend chemoprevention for women with a BCRAT
score of 1.66 or greater (3,4). The utility of risk-reduction agents for women
less than 35 years old is not known. Tamoxifen only is approved for
premenopausal women, whereas tamoxifen, raloxifene, anastrozole, and
exemestane may be used in postmenopausal women.
The NCCN Breast Cancer Risk Reduction Panel has made the following
recommendations regarding breast cancer risk reduction agents: (12)
Options for breast cancer risk reduction should be discussed in a shared
decision-making environment. The counseling should include a discussion
and consideration of: (1) the individual’s overall health status, including
menopausal status, medical history, and medication history (e.g.,
hysterectomy status, prior history of venous thromoboembolism [VTE],
current use of hormones or selective serotonin uptake inhibitors [SSRIs],
previous use of a selective estrogen receptor modulator [SERM]); (2)
absolute and relative breast cancer risk reduction achieved with the risk-
reduction intervention; (3) risks of risk-reduction therapy with an emphasis
on age-dependent risks; (4) the contraindications to therapy with tamoxifen
and raloxifene (e.g., history of VTE, history of thrombotic stroke, history of
transient ischemic attack, pregnancy, or pregnancy potential without an
effective nonhormonal method of contraception); and (5) the common and
serious side effects of tamoxifen and raloxifene.
Data regarding tamoxifen risk reduction are limited to pre- and
postmenopausal women 35 years of age or older with a Gail Model 5-year
breast cancer risk of 1.7 or greater or a history of LCIS.
Tamoxifen is prescribed at 20 mg per day for 5 years, and it has been
shown to reduce risk of breast cancer by 49%. Among women with a history
of atypical hyperplasia, this dose and duration of tamoxifen was associated
with an 86% reduction in breast cancer risk.
The efficacy of tamoxifen risk reduction in women who are carriers of
BRCA1/BRCA2 mutations or who have had prior thoracic radiation is less
well studied than in other risk groups. Limited retrospective data suggest
there may be a benefit.
For healthy high-risk premenopausal women, data regarding the
risk/benefit ratio for tamoxifen appear relatively favorable.
For high-risk postmenopausal women, data regarding the risk/benefit ratio
for tamoxifen are influenced by age, presence of uterus, or comorbid
conditions. There are insufficient data on ethnicity and race.
Germline mutations in PTEN occur in 85% of patients with Cowden
syndrome, an inherited condition associated with increased endometrial
carcinoma risk. Therefore, increased risk for endometrial cancer in women
with PTEN mutations should be discussed while considering tamoxifen.
Data regarding raloxifene risk reduction are limited to postmenopausal
women 35 years of age or older with a Gail Model 5-year breast cancer risk
of 1.7 or greater or a history of LCIS.
Raloxifene is prescribed at 60 mg per day and was found to be equivalent
to tamoxifen for breast cancer risk reduction in the initial comparison. While
raloxifene in long-term follow-up appears to be less efficacious in risk
reduction than tamoxifen, consideration of toxicity may still lead to the
choice of raloxifene over tamoxifen in women with an intact uterus.
There are no data regarding the use of raloxifene in women who are
carriers of BRCA1/BRCA2 mutations or who have had prior thoracic
radiation.
For high-risk postmenopausal women, data regarding the risk/benefit ratio
for raloxifene are influenced by age or comorbid conditions. There are
insufficient data on ethnicity and race.
Use of raloxifene for breast cancer risk reduction in premenopausal women
is inappropriate unless part of a clinical trial.
There are limited data regarding more than 5 years of tamoxifen or
raloxifene use in breast cancer prevention. Moreover, there may be safety
concerns related to use of tamoxifen for greater than 5 years. Based on the
recent update of the STAR trial data, continuing raloxifene beyond 5 years
may be an approach to maintain the risk-reducing activity of the agent.
When counseling postmenopausal women regarding the risk/benefit of
tamoxifen and raloxifene, refer to tables in Ref. 31.
Some SSRIs decrease the formation of endoxifen, the active metabolite of
tamoxifen. However, citalopram and venlafaxine appear to have minimal
impact on tamoxifen metabolism. The clinical impact of these observations is
not known.
Aromatase inhibitors are exemestane and anastrozole. Data regarding
exemestane are from a single large randomized study limited to
postmenopausal women 35 years of age or older with a Gail Model 5-year
breast cancer risk of 1.7 or greater or a history of LCIS.
Exemestane is given 25 mg per day and has been found to reduce the
relative incidence of invasive breast cancer by 65% from 0.55% to 0.19%
with a median follow-up of 3 years.
Data regarding anastrozole are from a single large randomized study
limited to postmenopausal women 40 to 70 years of age with the following
risk compared with the general population:

1. aged 40 to 44 years—four times higher


2. aged 45 to 60 years—more than or equal to two times higher
3. aged 60 to 70 years—more than or equal to 1.5 times higher.
Anastrozole is given 1 mg per day and was found to reduce the relative
incidence of breast cancer by 53% with a median follow-up of 5 years.

There are retrospective data that aromatase inhibitors can reduce the risk of
contralateral breast cancer in BRCA1/BRCA2 patients with ER-positive
breast cancer who take aromatase inhibitors as adjuvant therapy.
For high-risk postmenopausal women, data regarding the risk/benefit ratio
for aromatase inhibitor therapy are influenced by age and comorbid
conditions such as osteoporosis. There are insufficient data on ethnicity and
race.
Exemestane and anastrozole are not currently FDA approved for breast
cancer risk reduction. There are currently no data comparing the benefits and
risks of exemestane and anastrozole to those of tamoxifen or raloxifene.
Use of aromatase inhibitors for breast cancer risk reduction in
premenopausal women is inappropriate unless part of a clinical trial.
Monitoring of patients on chemoprevention is imperative. As patients are
deemed high risk, screening programs should include yearly bilateral
mammography with consideration for tomosynthesis, a clinical breast
examination every 6 to 12 months, and encouragement of breast awareness.
Supplemental screening with breast MRI may be indicated for certain women
at increased risk of breast cancer (5).
The incidence of both endometrial and uterine sarcoma is increased in
women taking tamoxifen when compared to placebo, however, the absolute
risk of developing endometrial cancer is low (32–34). Unlike tamoxifen, the
use of raloxifene has not been associated with increased incidence of
endometrial cancer (35,36). When considering chemoprevention with
tamoxifen, a baseline gynecologic examination should be performed. Patients
should be monitored for spotting and continue gynecologic assessment at
each visit (37,38).
Tamoxifen has been associated with an increased rate of cataract formation
(32,33,36). If a patient experiences visual changes while being treated with
tamoxifen, they should obtain an ophthalmologic evaluation. While data
regarding raloxifene is conflicting, cataract formation for raloxifene was
significantly lower than that associated with tamoxifen (36).
Changes in bone mineral density are concerning for women on aromatase
inhibitor therapy. A baseline bone mineral density scan is thus recommended
prior to starting therapy with exemestane or anastrozole. There is no need to
monitor bone mineral density in premenopausal women on tamoxifen (12),
and tamoxifen increases bone mineral density in postmenopausal women
(32,33). Raloxifene has been shown to increase bone mineral density and
reduce vertebral fractures in postmenopausal women as compared to placebo
(39). Weight-bearing exercise or use of a bisphosphonate (oral/IV) or
denosumab is acceptable to maintain or to improve BMD and reduce risk of
fractures in postmenopausal women (12).
Tamoxifen and raloxifene have been associated with an increased risk of
thromboembolic events such as deep venous thrombosis (DVT) and
pulmonary emboli (32,33,35,36). Women taking tamoxifen or raloxifene
should be educated regarding the symptoms associated with DVT and
pulmonary emboli. They should also be informed that prolonged
immobilization may increase risk of VTE, and they should be instructed to
contact their physicians immediately if they develop symptoms of DVT or
pulmonary emboli. Women with documented thromboembolic disease should
receive appropriate treatment for the thromboembolic condition and should
permanently discontinue tamoxifen or raloxifene therapy (12).
Hot flashes occur in approximately 81% of women treated with tamoxifen
and 69% of women treated with placebo (32). Raloxifene is also associated
with increased incidence of hot flashes as compared to placebo, but to a
lesser extent than tamoxifen (35,40). In women whose quality of life is
diminished by hot flashes, an intervention to eliminate or minimize hot
flashes should be undertaken. 900 mg of gabapentin (41), 35 mg of
venlafaxine with incremental increase to 75 mg if needed (42), 12.5 mg of
paroxetine (43,44), and clonidine in dose-dependent fashion (45) have been
shown to be helpful in reducing hot flashes. Estrogens and/or progestins have
the potential to interact with SERMs and are not recommended by the NCCN
Breast Cancer Risk Reduction Panel for the treatment of hot flashes for
women on a risk-reduction agent outside of a clinical trial (12).
Risk-Reducing Surgery
Risk-reducing mastectomy (RRM) can be considered in carriers of BRCA1,
BRCA2, PTEN, and TP53 genetic mutations. Consideration may also be
appropriate for patients with mutations in other genes when combined with a
significant family history of breast cancer (9,11,46,47), as well as for patients
who received early thoracic irradiation encompassing the chest/breast area
before age 30 (5,12).

TABLE 4-5 Survival Probability According to Breast/Ovarian Cancer Risk-


Reduction Strategy at Age 70a for 25-Year-Old BRCA1/BRCA2 Mutation
Carrier
Variable Survival Probability Survival Probability
(%) in BRCA1 (%) in BRCA2
Mutation Carriers Mutation Carriers
No intervention 53 (BCD = 41; OCD = 71 (BCD = 36; OCD =
36) 20)
RRSO Only at Age 40 68 (BCD = 45; OCD = 77 (BCD = 30; OCD =
12) 4)
RRSO Only at Age 50 61 (BCD = 51; OCD = 75 (BCD = 42; OCD =
20) 6)
RRM Only at Age 25 66 (BCD = 5; OCD = 79 (BCD = 4; OCD =
58) 30)
RRM Only at Age 40 64 (BCD = 13; OCD = 78 (BCD = 9; OCD =
53) 28)
Breast Screening Only 59 (BCD = 26; OCD = 75 (BCD = 21; OCD =
From Ages 25–69 46) 25)
RRSO at Age 40 and 79 (BCD = 6; OCD = 83 (BCD = 3; OCD = 6)
Breast RRM at Age 21)
25
RRSO at Age 40 and 74 (BCD = 30; OCD = 80 (BCD = 18; OCD =
Breast Screening 15) 5)
From Ages 25–69
RRSO and RRM at Age 77 (BCD = 18; OCD = 82 (BCD = 9; OCD = 6)
40, and Breast 18)
Screening From Ages
25–39
aSurvival probability for 70-year-old woman from general population = 84% (Probability of death as a
result of breast cancer [BCD] or ovarian cancer [OCD]).
RRSO, risk-reducing bilateral salpingo-oophorectomy; RRM, risk-reducing bilateral mastectomy;
Breast screening—annual mammography and MRI.
Data from Kurian AW, Sigal BM, Plevritis SK. Survival analysis of cancer risk reduction strategies for
BRCA1/BRCA2 mutation carriers. J Clin Oncol 2010;28:222–231.

Patients with BRCA1 or BRCA2 pathogenic variants should consider risk-


reducing bilateral salpingo-oophorectomy after child bearing or between the
ages of 35 and 40 to reduce ovarian and fallopian tube cancer risk. Women
with BRCA 1 should consider oophorectomy between ages 35 and 40, while
BRCA2 carriers should consider it between ages 40 and 45 (9,11,46,47).
Prophylactic oophorectomy in premenopausal women with BRCA2
pathogenic variants has also been shown to reduce the risk of breast cancer
by about 50%. There is also breast cancer risk reduction from RRSO in
BRCA1 patients but to a lesser degree (9,11,46,47).
The NCCN Breast Cancer Risk Reduction Panel recommends that women
at very high risk for breast cancer who are considering RRM address the
potential psychosocial effects of RRM. Such surgery has the potential to
negatively impact perceptions of body image, ease of forming new
relationships, and the quality of existing relationships. Moreover, the
procedure also eliminates the breast as a sexual organ. Multidisciplinary
consultations are recommended prior to surgery and should include a surgeon
familiar with the natural history and therapy of benign and malignant breast
disease (48) to enable the woman to become well informed regarding
treatment alternatives, the risks and benefits of surgery, nipple-sparing
mastectomy, and surgical breast reconstruction options. Immediate breast
reconstruction is an option for many women following RRM, and early
consultation with a reconstructive surgeon is recommended for those
considering either immediate or delayed breast reconstruction (49).
Psychological consultations may also be considered. Discussions regarding
the risk for ovarian cancer and the option of risk-reducing salpingo-
oophorectomy (RRSO) for breast and ovarian cancer risk reduction should
also be undertaken with women who are known carriers of a
BRCA1/BRCA2 mutation. Other topics that should be addressed with
respect to RRSO include the increased risk for osteoporosis and
cardiovascular disease associated with premature menopause, as well as the
potential effects of possible cognitive changes, accelerated bone loss, and
vasomotor symptoms on quality of life. Furthermore, the surgery itself may
have some associated complications.
It has been reported that short-term HT in women undergoing RRSO did
not negate the reduction in breast cancer risk associated with the surgery (50).
In addition, results of a case control study of BRCA1 mutation carriers
showed no association between use of HT and increased breast cancer risk in
postmenopausal BRCA1 mutation carriers (50). However, the consensus of
the NCCN Breast Cancer Risk Reduction Panel is that caution should be used
when considering HT use in mutation carriers following RRSO, given the
limitations inherent in nonrandomized studies (51,52). It is unlikely that a
prospective randomized study on the use of RRSO for breast cancer risk
reduction will be performed. Whether the resulting reduction in the risk for
breast cancer from this procedure is preferable to an RRM is likely to remain
a personal decision (53). Table 4-5 provides estimates based on a Monte
Carlo simulation model of the survival impact of breast and ovarian risk-
reduction strategies. These data can be used as a tool to facilitate shared
decision making regarding choice of a risk-reduction approach, particularly
with respect to issues related to risk-reduction surgery (see Table 4-5) (12).
CONCLUSION
Breast cancer risk assessment identifies healthy women without a personal
history of breast cancer who are at increased risk for developing the disease.
By obtaining a detailed history, the clinician can utilize the appropriate risk
assessment module to determine an individual’s risk for breast cancer. A
referral to genetic counseling and testing is made when indicated.
Risk stratification into groups allows for guidelines that provide
appropriate screening recommendations. Lifestyle modifications are made to
reduce relative risk associated with certain behavioral factors. When risk is
deemed high enough to warrant risk-reducing measures, harms are assessed
against benefits before proceeding with intervention. Appropriate counseling
is imperative for both chemoprevention and risk-reducing procedures, and the
clinician should strive to minimize complications and side effects related to
treatment.

REFERENCES

1. Cadiz F, Kuerer HM, Puga J, et al. Establishing a program for


individuals at high risk for breast cancer. J Cancer 2013;4(5):433–446.
2. American Cancer Society Breast cancer facts & figures 2017–2018.
American Cancer Society. Available at www.cancer.org.
3. Borgquist S, Hall P, Lipkus I, et al. Towards prevention of breast
cancer: what are the clinical challenges? Cancer Prev Res (Phila)
2018;11(5):255–264.
4. Visvanathan K, Hurley P, Bantug E, et al. Use of pharmacologic
interventions for breast cancer risk reduction: American Society of
Clinical Oncology clinical practice guideline. J Clin Oncol
2013;31:2942–2962.
5. National Comprehensive Cancer Network. Breast cancer screening and
diagnosis. Version 1.2019-May 17, 2019. NCCN Website.
6. US Preventive Services Task Force, Owens DK, Davidson KW, Krist
AH, et al. Risk assessment, genetic counseling, and genetic testing for
BRCA-related cancer: US Preventive Services Task Force
recommendation statement. JAMA 2019;322(7):652–665.
7. Nelson HD, Pappas M, Cantor A, et al. Risk Assessment, Genetic
Counseling and Genetic Testing for BRCA-Related Cancer: A
Systematic Review for the US Preventive Services Task force: Evidence
Synthesis NO. 182. Rockville MD: Agency for Healthcare Research and
Quality; 2019. AHRQ publication 19-05251-EF-1.
8. National Comprehensive Cancer Network (NCCN). Genetic/Familial
High Risk Assessment: Breast and Ovarian. NCCN website. 2012.
9. American Society of Breast Surgeons (ASBrS). Consensus Guideline on
Genetic Testing for Hereditary Breast Cancer. February 10, 2019.
ASBrS website.
10. National Research Genome Institute (NIH). Learning about the BRCAX
study. Available at www.nih.gov.
11. Domchek SM, Friebel TM, Singer CF, et al. Association of risk-
reducing surgery in BRCA1 or BRCA2 pathogenic variant carriers with
cancer risk and mortality. JAMA 2010;304:967–975.
12. National Comprehensive Cancer Network (NCCN). Breast Cancer Risk
Reduction Version 1.2019 – December 11, 2018. NCCN website.
13. Rossouw JE, Anderson GL, Prentice RL, et al. Risks and benefits of
estrogen plus progestin in healthy postmenopausal women: principal
results. From the Women’s Health Initiative randomized controlled trial.
JAMA 2002;288:321–333.
14. Anderson GL, Limacher M, Assaf AR, et al. Effects of conjugated
equine estrogen in postmenopausal women with hysterectomy: the
Women’s Health Initiative randomized control trial. JAMA
2004;291:1701–1712.
15. Rosenberg, L, Palmer JR, Wise LA, et al. A prospective study of female
hormone use and breast cancer among black women. Arch Intern Med
2006;166:760–765.
16. Beral V; Million Women Study Collaborators. Breast cancer and
hormone-replacement therapy in the Million Women Study. Lancet
2003;362:419–427.
17. Chen WY, Manson JE, Hankinson SE, et al. Unopposed estrogen
therapy and the risk of invasive breast cancer. Arch Intern Med
2006;166:1027–1032.
18. Chen WY, Rosner B, Hankinson SE, et al. Moderate alcohol
consumption during adult life, drinking patterns, and breast cancer risk.
JAMA 2011;306 1884–1890.
19. Liu Y, Nguyen N, Colditz GA. Links between alcohol consumption and
breast cancer: a look at the evidence. Womens Health (Lond)
2015;11:65–77.
20. Singletary KW, Gapstur SM. Alcohol and breast cancer: review of
epidemiologic and experimental evidence and potential mechanisms.
JAMA 2001;286:2143–2151.
21. Suzuki R, Ye W, Rylander-Rudqvist T, et al. Alcohol and
postmenopausal breast cancer risk defined by estrogen and progesterone
receptor status: a prospective cohort study. J Natl Cancer Inst
2005;97:1601–1608.
22. Pizot C, Boniol M, Mullie P, et al. Physical activity, hormone
replacement therapy and breast cancer risk: a meta-analysis of
prospective studies. Eur J Cancer 2016;52:138–154.
23. Bernstein L, Patel AV, Ursin G, et al. Lifetime recreational exercise
activity and breast cancer risk among black women and white women. J
Natl Cancer Inst 2005;97:1671–1679.
24. Howard RA, Leitzmann MF, Linet MS, et al. Physical activity and
breast cancer risk among pre-and postmenopausal women in the US
Radiologic Technologists cohort. Cancer Causes Control 2009;20:323–
333.
25. Mahoney MC, Bevers T, Linos E, et al. Opportunities and strategies for
breast cancer prevention though risk reduction. CA Cancer J Clin
2008;58:347–371.
26. Keum N, Greenwood DC, Lee DH, et al. Adult weight gain and
adiposity-related cancers: a dose-response meta-analysis of prospective
observational studies. J Natl Cancer Inst 2015;107.
27. Nelson HD, Zakher B, Cantor A, et al. Risk factors for breast cancer for
women aged 40–49 years: a systematic review and meta-analysis. Ann
Intern Med 2012;156:635–648.
28. Paupel-Badger JM, Araro KF, Balkam JJ, et al. Postpartum remodeling,
lactation, and breast cancer risk: summary of a National Cancer
Institute-sponsored workshop. J Natl Cancer Inst 2013;105;166–174.
29. Islami F, Liu Y, Jemal A, et al. Breastfeeding and breast cancer risk by
receptor status—a systematic review and meta-analysis. Ann Oncol
2015;26:2398–2407.
30. Vachon CM, Pankratz VS, Scott CG, et al. Longitudinal trends in
mammographic percent density and breast cancer risk. Cancer
Epidemiol Biomarkers Prev 2007;16(5):921–928.
31. Freedman AN, Yu B, Gail MH, et al. Benefit/risk assessment for breast
cancer chemoprevention with raloxifene or tamoxifen for women age 50
years or older. J Clin Oncol 2011;29(17):2327–2333.
32. Fisher B, Costantino JP, Wickerham DL, et al. Tamoxifen for the
prevention of breast cancer: report of the National Surgical Adjuvant
Breast and Bowel Project P-1 study. J Natl Cancer Inst 1998;90:1371–
1388.
33. Fisher B, Constantino JP, Wickerham DL, et al. Tamoxifen for the
prevention of breast cancer: current status of the National Surgical
Adjuvant Breast and Bowel Project P-1 study. J Natl Cancer Inst
2005;97:1652–1662.
34. Wickerham DL, Fisher B, Wolmark N, et al. Association of tamoxifen
and uterine sarcoma. J Clin Oncol 2002;20;2758–2760.
35. Cummings SR, Eckert S, Krueger KA, et al. The effect of raloxifene on
risk of breast cancer in postmenopausal women: results from the MORE
randomized trial. Multiple Outcomes of Raloxifene Evaluation. JAMA
1999;281:2189–2197.
36. Vogel VG, Costantino JP, Wickerham DL, et al. Update of the National
Surgical Adjuvant Breast and Bowel Project Study of Tamoxifen and
Raloxifene (STAR) P-2 Trial: preventing breast cancer. Cancer Prev
Res (Phila) 2010;3:696–706.
37. American College of Obstetricians and Gynecologists Committee on
Gynecologic Practice. ACOG committee opinion. No. 336: tamoxifen
and uterine cancer. Obstet Gynecol 2006;107:1475–1478.
38. Grady D, Ettinger B, Moscarelli E, et al. Safety and adverse effects
associated with raloxifene: multiple outcomes of raloxifene evaluation.
Obstet Gynecol 2004;104:837–844.
39. Ettinger B, Black DM, Mitlak BH, et al. Reduction of vertebral fracture
risk in postmenopausal women with osteoporosis treated with
raloxifene: results from a 3-year randomized clinical trial. Multiple
Outcomes of Raloxifene Evaluation (MORE) Investigators. JAMA
1999;282:637–645.
40. Land SR, Wickerham DL, Costantino JP, et al. Patient-reported
symptoms and quality of life during treatment with tamoxifen or
raloxifene for breast cancer prevention: the NSABP Study of Tamoxifen
and Raloxifene (STAR) P-2 trial. JAMA 2006;295:2742–2751.
41. Pandya KJ, Morrow GR, Roscoe JA, et al. Gabapentin for hot flashes in
420 women with breast cancer: a randomized double-blind placebo-
controlled trial. Lancet 2005;366:818–824.
42. Loprinzi CL, Kugler JW, Sloan JA, et al. Venlafaxine in management of
hot flashes in survivors of breast cancer: a randomized controlled trial.
Lancet 2000;356:2059–2063.
43. Stearns V, Beebe KL, Iyengar M, et al. Paroxetine controlled release in
the treatment of menopausal hot flashes: a randomized controlled trial.
JAMA 2003;289:2827–2834.
44. Stearns V, Slack R, Greep N, et al. Paroxetine is an effective treatment
for hot flashes: results from a prospective randomized clinical trial. J
Clin Oncol 2005;23:6919–6930.
45. Goldberg RM, Loprinzi CL, O’Fallon JR, et al. Transdermal clonidine
for ameliorating tamoxifen-induced hot flashes. J Clin Oncol
1994;12:155–158.
46. Kauff ND, Satagopan JM, Robson ME, et al. Risk-reducing salpingo-
oophorectomy in women with a BRCA1 or BRCA2 pathogenic variant.
N Engl J Med 2002;346:1609–1615.
47. Rebbeck TR, Lynch HT, Neuhausen SL, et al. Prophylactic
oophorectomy in carriers of BRCA1 or BRCA2 pathogenic variants. N
Engl J Med 2002;346:1616–1622.
48. Giuliano AE, Boolbol S, Degnim A, et al. Society of Surgical Oncology:
position statement on prophylactic mastectomy. Approved by the
Society of Surgical Oncology Executive Council, March 2007. Ann Surg
Oncol 2007;14:2425–2427.
49. Morrow M, Mehrara B. Prophylactic mastectomy and the timing of
breast reconstruction. Br J Surg 2009;96:1–2.
50. Rebbeck TR, Friebel T, Wagner T, et al. Effect of short-term hormone
replacement therapy on breast cancer risk reduction after bilateral
prophylactic oophorectomy in BRCA1 and BRCA2 mutation carriers:
the PROSE Study Group. J Clin Oncol 2005;23:7804–7810.
51. Chlebowski RT, Prentice RL. Menopausal hormone therapy in BRCA1
mutation carriers: uncertainty and caution. J Natl Cancer Inst
2008;100:1341–1343.
52. Garber JE, Hartman AR. Prophylactic oophorectomy and hormone
replacement therapy: protection at what price? J Clin Oncol
2004;22:978–980.
53. Grann VR, Jacobson JS, Thomason D, et al. Effect of prevention
strategies on survival and quality-adjusted survival of women with
BRCA1/2 mutations: an updated decision analysis. J Clin Oncol
2002;20:2520–2529.
CHAPTER 5

Heredity and Breast Cancer: Risk


Assessment, Genetic Testing, and
Management Options
MAGDOLNA SOLTI
RISK FACTORS FOR BREAST CANCER
It has been estimated that women in the United States have a 12% lifetime
risk of developing breast cancer. While overall cancer incidence rate
remained stable for women in the past few decades, there was a 0.3%
increase in the incidence of breast cancer since 2006 (1). This trend is seen in
the developed countries and could at least in part be a consequence of the
obesity epidemic, as well as declining parity.
Traditional risk factors such as gender, increasing age, family history of
breast cancer, and reproductive history (early menarche and late menopause,
fewer pregnancies, late childbearing, lack of breastfeeding) are considered as
pillars of risk assessment (2). The true risk however is much broader (Fig. 5-
1). This chapter will highlight new data that accumulated in the last decade in
cancer risk.
Approximately 5% to 10% of breast cancer cases are inheritable and are
driven by aberrant genes. Inherited breast cancer tends to occur at a younger
age than breast cancer in women without a genetic predisposition. Recent
advances in genotyping and next generation sequencing found that germline
mutations and somatic mutations interact with each other to drive
carcinogenesis. There is a dynamic interaction between the cancer genome
and the host immune system which determines the tumor growth rate and
metastatic potential.
FIGURE 5-1 Risk factors for breast cancer. (Data from Genetics of Breast and
Gynecologic Cancers (PDQ®). Health Professional Version. PDQ Cancer Genetics
Editorial Board. PDQ Cancer Information Summaries [Internet]. Bethesda, MD: National
Cancer Institute (US); 2002–2019.)

Lifestyle is considered an increasingly important contributing factor to


breast cancer etiology. Cohort studies link overweight and obesity, inactivity,
metabolic syndrome, and alcohol use to breast cancer. The impact of obesity
on breast cancer risk differs across menopausal status and disease subtypes.
Current evidence suggests that a high BMI associates with a reduced risk of
estrogen receptor (ER)–positive premenopausal breast cancer, but strongly
correlates with an increased risk after menopause (3). Breast cancers
occurring in obese premenopausal women tend to be ER-negative and triple-
negative subtypes (4). Even in women with normal BMI, high body fat levels
were associated with elevated risk of postmenopausal breast cancer (5).
Alcohol intake is a recognized risk factor in women for breast cancer. Each
unit of alcohol consumption (284 mL of 4% beer, 80 mL of 12% wine, or 25
mL of 40% spirit) daily is estimated to increase the risk by 2% to 12%. The
risk is thought to be related to acetaldehyde-induced DNA strand deletions,
chromosomal aberrations, and increased estrogen and prolactin receptor
activity (6).
How does composition of diet matter in breast cancer risk? Recent reviews
linked high fiber intake with a lower risk of breast cancer, with a 5%
reduction in every 10 g of fiber per day. Soluble fiber appears the most
protective by reducing the reabsorption of estrogens and androgens in the
bowel hence, their circulating level and effect on insulin sensitivity. Meat
consumption confer a slightly increased risk: 4% increase with each
additional 100 g of red meat per day and 3% increase with each additional 30
g of processed meat per day (7). Marine omega-3 fats are associated with
reduced breast cancer risk; each additional 0.7 g of marine omega-3
polyunsaturated fat per week reduces the risk by 5%. Many studies examined
the link between soy and breast cancer. Soy foods contain isoflavones with
weak estrogenic and antiestrogenic effect as well as antiproliferative effect on
cell cultures. Natural soy food intake (but not over-the-counter isoflavone
supplements) showed lowering breast cancer risk: intake of 5 g of soy protein
per day (170 mL of soymilk) was associated with a 4% reduction in risk.
Vitamin supplement use did not yield any beneficial effect (8).
Emerging data suggests that smoking during adolescence or early
adulthood increases later risk of breast cancer because of heightened
susceptibility to chemical carcinogens before full differentiation of the breast
(7). The effect of smoking appears to be mainly linked to ER-positive breast
cancers.
Breast density affects the risk of breast cancer. The ACR Breast Imaging
Reporting and Data System (BI-RADS) differentiates four categories of
breast composition: a) the breasts are almost entirely fatty; b) scattered
fibroglandular tissue; c) heterogeneously dense; d) extremely dense tissue.
Women with breast composition category d (extreme breast density) have a
four- to sixfold increased risk for breast cancer than those with BI-RADS
breast composition category a (fatty tissue) (9).
Reproductive factors have long been recognized in breast cancer
development. Studies of parity and breast cancer risk had variable results.
Some have reported a protective effect of younger age at first childbirth and
higher risk with first live birth at older ages. However, a recent pooled
analysis evaluating the cancer risk after childbirth reported increased risk
postpartum. Compared with women who had not given birth, parous women
had a 1.8-fold elevated breast cancer risk that peaked around 5 years after
childbirth and persisted for 20 years (10). The proposed underlying
mechanism is tumor-promoting microenvironment during pregnancy-induced
proliferation and the postpartum breast microenvironment (lactational
involution) facilitating cancer cell migration and metastases.
In the general population, oral contraceptive (OCP) use has been
associated with a slightly higher breast cancer risk that appears to decrease
after cessation of OCPs. A recent prospective cohort study using
contemporary hormonal contraception found a 1.2-fold increased relative risk
(RR) of breast cancer (1.09 with less than 1 year of OCP use to 1.38 with
more than 10 years of use). Progesterone-only intrauterine system posed
similar risk (RR = 1.21). The absolute increase in risk, however, was small:
13 per 100,000 person-years or 1 extra breast cancer for every 7,690 women
using hormonal contraception for 1 year (11). The addition of progestin
appears to increase the risk of breast cancer among postmenopausal women
who receive hormone therapy (12).
Breastfeeding has been associated with an estimated 12% to 25% lower
risk for premenopausal breast cancer overall and is thought to be particularly
beneficial in reducing risk for ER-negative breast cancer, which is relatively
more common at young ages than older ages. Although higher parity is
associated with an overall increase in risk for ER-negative breast cancer,
parous women who breastfeed have comparable risk to nulliparous women,
suggesting that breastfeeding may mitigate parity-related increases in risk for
ER-negative cancer (10).
Social factors, such as race/ethnicity, socioeconomic position (SEP),
access to care matter in assessing cancer risk. While all-cause mortality rates
had been steadily declined in the United States between 1999 and 2013, when
mortality rates were stratified by race and SEP, it became apparent that
midlife mortality was increased among one particular social group, non-
Hispanic Whites with low education. Recent findings suggest an increased
risk of breast cancer incidence among women born in states with Jim Crow
laws (postslavery laws in place in the United States from the 1870s to 1964
that limited Black advancements and freedoms). Poverty, insurance coverage,
and access to screening are modifiable risk factors that can influence cancer
risk (13).
Physical activity is emerging as a modifiable risk factor for breast cancer,
especially for premenopausal breast cancer. The World Cancer Research
Fund and American Cancer Society (ACS) cancer prevention guidelines
recommend maintaining a healthy weight, undertaking at least 150 minutes of
moderate-intensity exercise per week, limiting alcohol consumption, and
eating a plant-based diet. Recent expert reports estimate that successful
lifestyle changes could prevent 25% to 30% of cases of breast cancer (14). It
has been debated whether the reduction of the risk of breast cancer with
physical activity is attributable, in part, to its positive effect on weight and
body composition. Studies showed that the relationship between physical
activity and breast cancer is independent of BMI, ER status, weight gain, and
hormone replacement therapy (HRT) (15). A concerted effort of primary care
physicians, surgeons, and oncologists is needed to increase compliance with
the physical activity guidelines.
BREAST CANCER RISK ASSESSMENT
The paradigm has recently shifted from a uniform method of breast cancer
screening to an individualized approach that incorporates multiple risk factors
(16). Genetic cancer risk assessment is an interdisciplinary specialty practice
that uses genetic and genomic information to identify individuals with
inherited cancer risk and advise on high-risk screening, preventive care, and
targeted treatment.
Breast cancer risk assessment models are various mathematical models that
estimate a woman’s risk of breast cancer over defined time periods (Table 5-
1). The models are used to identify women who can benefit from
interventions, such as more intense screening with breast magnetic resonance
imaging (MRI) in addition to mammograms and chemoprevention. Most
models are not applicable to patients with a hereditary cancer syndrome. A
comprehensive breast cancer risk assessment includes calculation of risk via
multiple models, as they vary in their estimates and applicability to patients.
Additionally, clinical factors, such as history of mantle field radiation
between 10 and 30 years of age will automatically place a woman in a high-
risk category. The important features of each model are highlighted in Table
5-1.

TABLE 5-1 Commonly Used Breast Cancer Risk Assessment Models


The Gail model primarily focuses on nongenetic risk factors and includes
limited information on family history (17). The model combines the patient’s
reproductive history and limited family history, including age, age at
menarche, age at first live birth, number of first-degree female relatives with
breast cancer, number of previous breast biopsies, and results of those
biopsies. The Gail model was validated for white women as well as for those
of African American, Asian, and Pacific Islander descent. Limiting factors
that the Gail model is only applicable for women aged 35 or older, excludes
personal history of breast cancer or ductal carcinoma in situ (DCIS) and only
accounts for first-degree relatives with breast cancer independent of the age
of onset. It is not recognized by the ACS as a model to identify candidates for
breast MRI screening or as an adjunct to mammography and it is used for
identifying candidates for chemoprevention when the 5-year risk is 1.67% or
greater.
The Claus model gathers input on family history of female breast cancer as
well as ovarian cancer. The model assumes that breast cancer risk is
transmitted as an autosomal-dominant trait, and its risk estimates are based
on the patients’ relation to their affected relatives (18). This model includes
age and a comprehensive family history with paternal relatives as well but
excludes high-risk breast cancer genes and does not account for male
relatives with breast cancer and hormonal and reproductive risk factors. The
data are presented in a series of tables.
The Tyrer–Cuzick model integrates a wide variety of personal risk factors
as well as an extensive family history of breast and ovarian cancer (19). This
model incorporates age, height, weight, Jewish inheritance, age at menarche,
menopausal status, age at first live birth, hormone replacement use, history of
high-risk breast lesions (including atypia and lobular carcinoma in situ
[LCIS]), as well as extended paternal and maternal family history of both
breasts, male breast and ovarian cancer, including ages of onset. It also
incorporates positive and negative BRCA1/2 genetic test results.
The BRCAPRO model calculates lifetime breast cancer risk as well as the
probability of a BRCA1/2 mutation. It requires input of a full family history,
including breast cancer under age 50 and ovarian cancer (20). The
BRCAPRO model will underestimate risk in BRCA-negative, breast cancer–
only families because it does not account for genes other than BRCA1/2 that
can contribute to cancer risk.
In addition to the Claus model and Tyrer–Cuzick model, the BRCAPRO
and Breast and Ovarian Analysis of Disease Incidence and Carrier Estimation
Algorithm (BOADICEA) models are also endorsed by the ACS for
identifying candidates for breast MRI screening as an adjunct to
mammography.
The BOADICEA model accounts for BRCA1/2 mutations as well as a
polygenic factor that aims to address the idea that multiple genes exist and
that each have small effects on breast cancer risk but act multiplicatively
when factored together. BOADICEA does not incorporate information about
nonhereditary risk factors and will likely underestimate risk in these women
(21).
Future directions include models that incorporate additional risk factors to
improve discriminatory power. A recently developed deep learning model
that uses full-field mammograms yielded substantially improved risk
discrimination compared with the Tyrer–Cuzick (version 8) model (22).
CONSIDERATIONS WHEN CONDUCTING GENETIC TESTING
Genetic testing for hereditary susceptibility to cancer increasingly informs
oncology care, allowing tailored treatment and preventive care. Genomic
cancer risk assessment serves as a tool to identify patients and families who
are at elevated risk for cancer. Several organizations published clinical
practice guidelines describing indications for genetic testing, including the
American Society of Breast Surgeons (ASBrS) (23), the National
Comprehensive Cancer Network (NCCN) (24), and the U.S. Preventive
Services Task Force (USPSTF) (25). Table 5-2 summarizes the commonly
used criteria.
Genetic counseling serves to guide the patient through a genetic testing
process. The counselor (1) assesses personal and familial risk for a cancer
syndrome and identifies candidates for testing; (2) provides education about a
cancer syndrome and mode of inheritance; (3) explains the benefits, harms,
and limitations of genetic testing; (4) helps with interpretation of the test
results; and (5) identifies potential strategies for risk reduction. The genetic
counselor also helps to guide the patient through the emotional aspects of
genetic testing, assists the patient to make an informed decision to proceed
with testing or halt/defer the workup and treatment processes.
The possible outcomes of genetic testing is a true positive, a true negative
(i.e., an individual in a family with a known mutation tests negative for that
mutation), uninformative (i.e., a negative test in a family where a mutation
has yet to be identified), or a variant of unknown significance (VUS). By
definition, a VUS is a detected genetic change without a good description of
any correlating clinical risk.
The passing of the Genetic Information Nondiscrimination Act of 2008 by
Congress provides protection against health insurance discrimination based
on genetic information, but not against life or disability insurance
discrimination. The availability of testing options has changed since the 2013
U.S. Supreme Court ruling that determined human genes are not patentable
(Association for Molecular Pathology et al. v. Myriad Genetics). Since the
ruling, the number of testing options has significantly increased, with more
than 80 multigene panels that include BRCA1 and BRCA2. The nature of
genetic counseling has grown increasingly complex with the identification of
non-BRCA mutations associated with breast cancer syndromes. While
guidelines for some non-BRCA hereditary syndromes have been established
(i.e., Li–Fraumeni syndrome [LFS], Cowden syndrome), it has been
suggested that genetic counseling and preventive strategies be carefully
recommended to patients with less common mutations in the absence of
strong consensus or official guidelines.

TABLE 5-2 Indications for Genetic Testing in Patients With and Without a
Personal History of Breast Cancer (BC)
Indications for Patients Indications for Patients WITH a
WITHOUT a Personal History of Personal History of BC
BC
First- or second-degree relative with BC diagnosis at 50 years or younger
BC, onset at 50 yrs or younger
Two or more relatives on the same Triple-negative BC at 60 years or
side of the family with BC, younger
pancreatic cancer, or prostate
cancer (Gleason score ≥7) at any
age
Family or personal history of ovarian Two or more primary BCs
cancer, fallopian tube cancer, or
primary peritoneal cancer
Two or more primary BCs (includes One or more close relatives with BC
asynchronous, synchronous, diagnosed 50 years or younger;
bilateral, or multicentric) in one ovarian cancer; male BC;
relative pancreatic cancer, or metastatic
prostate cancer
Male BC Two relatives on same side of family
with BC
Ashkenazi Jewish heritage and Personal history of ovarian cancer,
family history of BC at any age male BC, pancreatic cancer,
metastatic or high grade (Gleason
score ≥7) prostate cancer
Known deleterious BRCA1 or Ashkenazi Jewish heritage
BRCA2 germline mutation in Family member with a known
family mutation

Several interventions showed to reduce the incidence of BRCA-related


cancer and mortality. These include intensive screening (earlier and more
frequent mammography or breast MRI), risk-reducing medications
(aromatase inhibitors, tamoxifen, or raloxifene), and risk-reducing surgery
(mastectomy or salpingo-oophorectomy).There are rare potential adverse
effects however, that include harms associated with breast imaging, risk-
reducing medications, and risk-reducing surgery and ethical, legal, and social
implications. Therefore, genetic counseling and testing should be offered by
appropriately trained health care providers to minimize harm from inaccurate
risk assessment, inappropriate testing, or misinterpretation of test results (26).
Recent studies suggest that up to 50% of women with germline
predisposing mutations do not qualify for testing based on current testing
criteria. In addition, family history–based criteria have limited applicability in
patients who are adopted, have limited family structure, or are not aware of
the cancer history in the family. In response to these limitations, the ASBrS
(23) recently updated their guidelines to suggest that all patients with breast
cancer should receive genetic testing, regardless of age at onset of disease or
the extent of family history. Although the logistical challenges of testing all
patients with breast cancer, including insurance coverage, are not clear at this
time, it is evident that testing criteria will continue to be modified to include a
greater proportion of possible mutation carriers. Although population-based
testing for hereditary breast cancer risk is not yet ready for clinical practice, it
may become a reality in the future, as studies evaluating population-based
mutation screening provide information on the feasibility of population
testing, improved yield, and cost effectiveness. Until that happens, clinicians
should understand that genetic risk evaluation is not a one-time event but an
ongoing assessment, because guidelines for testing are frequently updated
and the personal and family history of patients may change (27).
GENES ASSOCIATED WITH BREAST CANCER SUSCEPTIBILITY

High-Penetrance Genes
Understanding the genetic base for cancer is an important goal of clinical
science. Roughly 5% to 10% of all breast cancers are linked to genetic
abnormalities. In the 1990s, family-based genetic linkage studies identified
two major breast and ovarian cancer genes, BRCA1 and BRCA2 that
accounted for 25% of familial cancer clusters. In the past decade, several
more breast cancer susceptibility genes were identified from large case
control association studies. Next generation sequencing identified new cancer
susceptibility genes, such as CDH1, PTEN, STK11, and TP53 that were
associated with increased risk for breast cancer. Genetic variants for breast
cancer can be broadly categorized into high-, moderate-, and low-penetrance
alleles. The high-penetrance alleles typically confer lifetime risks of breast
cancer of >50%, sufficient to warrant intervention to reduce risk. Multigene
panel testing allowed rapid assessment of these high-penetrant genes (Table
5-3).

TABLE 5-3 High-Risk Genes for Breast Cancer


Penetrance Relative Risk Other Associated Cancers
of Breast
Cancer
BRCA1 AD 5.9–11.4 Ovarian, pancreas, male
breast, prostate
BRCA2 AD 3.3–11.7 Ovarian, male breast cancer,
pancreas, prostate,
melanoma
PTEN AD 2.0–5.8 Hamartoma, endometrial,
thyroid, renal, colorectal
TP53 AD 4.3–9.3 Sarcoma, CNS tumors,
leukemia, adrenocortical
carcinoma
STK11 AD 2.0–6.0 Peutz–Jeghers syndrome
CDH1 AD 5.9–7.3 Hereditary diffuse gastric
cancer
AD: autosomal dominant.

BRCA1 is a multifunctional protein that plays multiple roles in checkpoint


activation, DNA repair, and gene transcription in response to DNA damage
(28). BRCA1 is located on chromosome 17q and is inherited in an autosomal
dominant pattern. Approximately 1 in 400 individuals in the general
population carries a pathogenic BRCA1 mutation, but the frequency is
increased to 1 in 50 in Ashkenazi Jews. Overall risk of breast cancer in
BRCA1 mutation carriers is estimated to be about 2.5% per year. The
cumulative breast cancer risk to age 80 is 67% and cumulative ovarian cancer
risk is 45%. The mean age at diagnosis is 44 years and there is an increased
risk of contralateral breast cancer. Most BRCA1-related breast cancers are
triple negative and basal-like. Men with BRCA1 mutation are at risk for
breast cancer (lifetime risk 1%) and prostate cancer. BRCA1 mutations also
confer increased risk for melanoma and pancreas cancer, but the risk is not
high enough to warrant systematic screening. (29).
BRCA2 is a large nuclear DNA repair protein that plays an integral role in
the homologous recombination repair of DNA double-strand breaks. BRCA2
is located on chromosome 13q and has autosomal dominant inheritance. The
cumulative breast cancer risk for age 80 is 61% to 77% and cumulative
ovarian cancer risk is 18%. The mean age at diagnosis is 47 years, but age of
onset varies by family. BRCA2-related breast cancers tend to be estrogen and
progesterone receptor positive. The lifetime risk of breast cancer for men
with BRCA2 mutation is 8%. Epidemiologic studies observed excess risks of
pancreatic (RR 4.1), high-grade prostate cancers (RR 6.3), and melanoma
(risk not well quantified) (30).
Phosphate and Tensin homolog (PTEN) gene on chromosome 10q23 is one
of the most important tumor suppressor genes that is associated with risk of
breast cancer. PTEN protein helps regulate the cycle of cell division and cell
growth. PTEN hamartoma tumor syndrome (PHTS) encompasses a clinical
spectrum of heritable disorders including Cowden syndrome (CS),
Bannayan–Riley–Ruvalcaba syndrome, and Proteus and Proteus-like
syndrome that are associated with germline mutations in the PTEN tumor
suppressor gene. Breast cancer risk is estimated at 67% to 85% for women
with germline PTEN mutations. CS is a multisystem disorder characterized
by increased risk of endometrial (28%), thyroid (35%), renal (33%),
colorectal cancers and a 29% risk of a second breast cancer as well as a
combination of mucocutaneous findings such as trichilemmomas, oral
papillomas, and acral keratoses. An association between germline PTEN
mutations and autism has been well documented in the literature with several
groups identifying a 10% to 20% prevalence of germline PTEN pathogenic
variants in patients with macrocephaly and autism spectrum disorders. An
increasing number of benign findings such as GI polyposis, lipomas,
Lhermitte–Duclos disease, and arteriovenous malformations have been found
to be associated with CS as well (24,31).
TP53 gene is located on chromosome 17 and encodes tumor protein 53,
which is a tumor suppressor protein and plays a critical role in DNA repair in
response to cellular stresses. TP53 is a strong transcription factor that
activates numerous genes involved in cell cycle control, DNA repair, and
apoptosis when damaged DNA is present. Germline pathogenic mutations
cause LFS and Li–Fraumeni–like syndrome, predisposition for bone and soft
tissue sarcomas, CNS tumors, leukemias, early-onset breast cancers, and
adrenocortical carcinomas. Clinical hallmarks of LFS have included cancers
at young ages, with half of LFS tumors occurring by age 30 years, and
frequent multiple primary tumors in survivors. It is suggested that these
early-onset breast cancers show an increased rate of HER-2/neu positivity
(32). Cancer penetrance has been estimated to be nearly 100% in women and
73% in men by age 60 years (33).
STK11 is a serine–threonine kinase gene on chromosome 19p that is a
tumor suppressor and can cause Peutz–Jeghers syndrome. Peutz–Jeghers
syndrome is an autosomal-dominantly inherited rare cancer syndrome
characterized by mucocutaneous pigmentation and hamartomatous polyps in
the small bowel. In addition to an elevated risk of gastrointestinal cancers it
has also been linked to breast cancer, pancreatic cancer, sex cord stromal
ovarian tumors, and lung and testicular cancers. Lifetime risk of breast cancer
is 45% and of gastrointestinal cancers is 57%. Cord cell tumors of the ovaries
can be associated (lifetime risk around 20%) and increased risk of cervical
cancer is also described (lifetime risk around 10%) (34).
CDH1 gene is located on chromosome 16q and encodes for the E-cadherin
protein. E-cadherin on epithelial tissues is responsible for cell adhesion, and
functions as cell invasion suppressor. CDH1 mutation leads to hereditary
diffuse gastric cancer and an increased risk of lobular breast cancer, with a
lifetime risk of 39% (35). The cumulative risk of diffuse gastric cancer is
around 70% for men and 56% for women by age 80 (36).
Moderate-Penetrance Genes
The increasing availability of multigene panels allowed testing not only for
well-defined high-risk genes, but a growing numbers of low/moderate risk
genes, for which the penetrance and spectrum of cancer risk are less well
characterized. Moderate-risk genes are defined as genes that, when altered by
a pathogenic variant, confer a two- to fivefold RR of cancer, corresponding to
a lifetime risk of ≥20%. Prospective data and consensus management
guidelines for moderate-risk genes are limited. Table 5-4 summarizes the
common moderate- and low-penetrance genes.
Ataxia telangiectasia mutated (ATM) gene is located on chromosome 11q
and encodes a serine threonine kinase that is activated in response to DNA
double-strand breaks. ATM participates in DNA repair by phosphorylating
proteins involved in cell cycle checkpoint control and apoptosis. Pathogenic
biallelic variants in ATM result in ataxia-telangiectasia, a disease
characterized by progressive cerebellar degeneration, oculocutaneous
telangiectasia, immune deficiency, radiosensitivity, and increased risk of
cancer. Heterozygous carriers do not display features of ataxia-telangiectasia
but do share an increased predisposition to cancer. The RR of breast cancer in
heterozygous carriers is 2.8 and is mostly associated with ER-positive breast
cancer. Retrospective reviews were unable to quantify colon, prostate, or
pancreas cancer risk (37).

TABLE 5-4 Moderate- and Low-Risk Genes for Breast Cancer


Penetrance Relative Risk of Other Associated
Breast Cancer Cancers
ATM AD, AR 1.7–3.8 Colon, prostate,
pancreas,
ataxia-
telangiectasia
CHEK2 AD 1.58–4.8 Colon, prostate
PALB2 AD 1.4–7.5 Fanconi anemia,
pancreas
BARD1 — 1.9–2.3 Ovarian,
neuroblastoma
BRIP1 AD Conflicting Ovarian
RAD51 C — Conflicting Ovarian
RAD51D — Conflicting Ovarian
MSH2, MLH1, — Conflicting GI, endometrial,
MSH6, PMS2, ovarian
EPCAM
NF1 — Conflicting Neurofibromatosis
NBN — 1.4–6.6 Nijmegen
breakage
syndrome
AD: autosomal dominant; AR: autosomal recessive.

Checkpoint serine-threonine kinase 2 (CHEK2) is located on chromosome


22 and encodes a serine threonine kinase involved in DNA damage response.
CHEK2 is phosphorylated in response to double-strand DNA breaks,
alkylation, or replicative stress and activates p53 to mediate cell cycle arrest
and apoptosis. Previous studies have demonstrated that mutations in CHEK2
gene increase breast cancer risk, particularly among women with a family
history of breast cancer. Truncating and pathogenic missense variants in
CHEK2 confer a RR of 3.0 and 1.58, respectively, mostly ER-positive breast
cancers. While possible association with colon and prostate cancers was
reported, the exact risk is unknown (37). CHEK2 1100delC and I157T
mutations are the most common genetic mutations associated with breast
cancer. The risk of CHEK2 1100delC gene mutation is higher in women with
a family history of the disease and it is estimated that women with one copy
of this mutation have at least twice the risk of breast cancer.
PALB2 gene, also known by the localizer of the BRCA2 gene, is related to
the production of a functional protein that interacts with BRCA2 to repair
damaged DNA. Fanconi anemia type N is a disease caused by the inheritance
of two abnormal PALB2 genes and it is characterized by extremely low
levels of red and white blood cells, and platelets. Mutations in the PALB2
gene predispose to breast and pancreatic cancers. It is important to recognize
that several factors, such as family history or race/ethnicity, can modify
cumulative lifetime absolute risk estimates. Absolute breast risk for PALB2
female mutation carriers by age 70 has been estimated at 33% for those with
no family history of breast cancer but 58% for those with two or more first-
degree relatives with breast cancer (27), therefore some authors consider
PALB2 as a high-risk gene.
The BRCA1-associated RING domain protein-1 (BARD1) was initially
reported as a BRCA1-interacting protein in 1996. The interaction between
BARD1 and BRCA1 promotes tumor suppressor functions by acting in
double-strand break repair and apoptosis initiation. Recent case control
studies from European-Caucasian cohorts established the role of BARD1
associated with a moderately increased risk of breast cancer (odds ratio [OR]
= 1.9 to 2.3), especially with bilateral and triple-negative breast cancer
(TNBC). Exome sequencing suggested that BARD1 also has a role in ovarian
cancer (OR = 4.2) (38).
Low-Penetrance Genes
Beyond high- and moderate-risk genes, common single nucleotide
polymorphisms (SNPs) associated with a slightly increased risk (usually
between 1.05-fold and 1.50-fold) for breast cancer have been identified
through genome-wide association studies. Individually, these alleles confer
smaller increases in risk (i.e., 10% to 20% lifetime risk), but their combined
effect, when summarized as a polygenic risk score (PRS), can be substantial
(39). By using a new 313 SNP PRS, women in the top 1% of distribution has
a fourfold larger predicted risk of breast cancer and the lifetime risk in the top
centile of PRSs was 32.6% (40). Incorporating the PRS into risk prediction
models can improve screening and risk prevention strategies in the future.
PRSs may also be useful in further stratifying the risk of breast cancer among
women with pathogenic mutations in breast cancer-predisposition genes.
Studies evaluating the clinical utility, long-term clinical implications,
benefits, and risks of PRS testing are ongoing to better understand the role of
PRSs in clinical practice. In the future whole-exome sequencing combined
with single nucleotide polymorphism genotyping or whole-genome will aid
in identifying new putative genes in familial breast cancer and to estimate
personalized breast cancer risk (27).
CLINICAL MANAGEMENT OF BRCA PATHOGENIC VARIANTS

Screening and Prevention


Clinical breast examination for healthy women with a high breast cancer risk
has a low sensitivity but a high specificity. Thus, even if it is not considered
as a screening tool, it is still recommended in most guidelines starting at age
25 (Table 5-5). In women with BRCA1/2 mutation who did not choose a
bilateral prophylactic mastectomy, in addition to a biannual clinical breast
examination, biannual radiologic screening is recommended (35).

TABLE 5-5 NCCN Guidelines for Breast Cancer Screening

Most guidelines recommend the combined use of MRI and mammography.


Multiple international screening studies have demonstrated the superior
sensitivity of breast MRI to mammograms or ultrasound (US) or the
combined use of both methods, and interval cancer are significantly less
frequent in case of a screening combining MRI, mammography, and clinical
examination. Evidence-based guidelines provide recommendations for
initiation of breast surveillance with MRI alone at age 25, with the addition
of mammograms at age 30, with alternating imaging every 6 months (Table
5-5). Sensitivity of MRI is higher than that of mammography (89% vs. 22%)
in BRCA-positive women. Breast cancer screening with MRI seems to be
associated with a significant gain in mortality in women aged 26 to 60. On
the other side, side effects of MRI have to be taken into account: anxiety,
more biopsies (due to false-positive results). Repeated administration of
gadolinium-based contrast agents causes gadolinium deposition in deep
nuclei of the brain. The long-term clinical significance of the retained
gadolinium is unknown (41).
There is no effective ovarian surveillance currently, though active research
is ongoing. The risk of contralateral breast cancer is estimated to be around
25% to 40% in BRCA1/2 carriers.
Risk-Reducing Strategies: Surgeries and Chemoprevention
The breast cancer is often bilateral and multicentric in BRCA mutation
carriers. BRCA1/2 carriers with breast cancer may opt for total mastectomy
of the affected breast to reduce the risk of a second ipsilateral breast cancer
and contralateral prophylactic mastectomy to reduce the risk of contralateral
disease. For BRCA1/2 mutation carriers, bilateral prophylactic mastectomy is
associated with a 97% risk reduction of contralateral breast cancer. Recent
studies showed that prophylactic mastectomy confer an overall survival (OS)
benefit as well. In a prospective case control study (42) 105 female BRCA1/2
carriers and 105 matched controls who did not undergo prophylactic
mastectomy were analyzed. The 10-year OS was 89% in women electing for
prophylactic mastectomy compared to 71% in the nonmastectomy group;
p < 0.001. The survival advantage remained after matching for
oophorectomy, gene, grade, and stage (hazard ratio [HR] = 0.37), and
prophylactic mastectomy appeared to act independently of risk-reducing
salpingo-oophorectomy (RRSO). The rates of bilateral mastectomies have
been rising as reconstructive options have improved, with the more frequent
use of nipple-sparing and autologous tissue procedures, as well as novel
approaches to implant reconstruction.
The lifetime ovarian cancer risk is 40% to 60% in BRCA1 and 15% to
20% in BRCA2 carriers, with population risk in the range of 1.3%. RRSO
has been shown to reduce the risk of ovarian cancer by more than 90% and to
reduce breast cancer risk by 50% to 70% with the greatest benefit observed if
the surgery is performed before the age of 50. RRSO was also associated
with a significant risk reduction of ovarian–fallopian tube cancer as well (HR
= 0.21) (43). Moreover, RRSO has been shown to reduce both ovarian and
breast cancer mortality in carriers. NCCN guidelines recommend risk-
reducing bilateral salpingo-oophorectomies after completion of childbearing
at about age 35 to 40 for BRCA1 mutation carriers. Because ovarian cancer
onset in patients with BRCA2 mutations is an average 8 to 10 years later than
in patients with BRCA1 mutations, it is reasonable to delay RRSO until age
45 to 50 in patients with BRCA2 mutations.
The oral selective ER modulator, tamoxifen, taken daily for 5 years,
substantially reduces breast cancer risk for women who are at increased risk
owing to their family cancer history, reproductive risk factors, or personal
history of atypical hyperplasia or LCIS. The only data for tamoxifen in
primary prevention of breast cancer in mutation carriers come from a
subgroup analysis of the NSABP-P1 breast cancer prevention trial. That trial
randomized 13,388 women at increased risk of breast cancer to receive either
tamoxifen 20 mg daily or placebo for 5 years. The risk ratio for breast cancer
with tamoxifen was 1.67 (95% CI 0.32 to 10.7) for BRCA1 mutation carriers
and 0.38 (95% CI: 0.06 to 1.56) for BRCA2 mutation carriers. However, few
mutation carriers were enrolled: only 8 BRCA1 and 11 BRCA2 mutation
carriers were identified among 288 study participants who developed breast
cancer, so the confidence intervals were quite wide. Nevertheless, this study
raised the possibility that tamoxifen could modulate breast cancer risk, at
least for BRCA2 mutation carriers (44). In a secondary prevention setting,
adjuvant tamoxifen use after a first breast cancer was associated with a
reduced risk of contralateral breast cancer with HR of 0.38 for BRCA1
mutation carriers and 0.33 for BRCA2 mutation carriers. Data from the
randomized primary prevention studies suggested that the benefit of
tamoxifen was confined to the prevention of ER-positive breast cancer.
Paradoxically, however, observational studies suggest that tamoxifen can
reduce hormone receptor–negative tumors in BRCA1 mutation carriers,
consistent with the prevention properties afforded by RRSO. There are no
completed prospective studies evaluating the preventive role of aromatase
inhibitors in women with BRCA mutations; however there is an ongoing
French study evaluating letrozole versus placebo in postmenopausal women
with BRCA mutations (45).
OCPs have been shown to reduce or delay ovarian cancer risk in both
BRCA1 and BRCA2 carriers. Because OCP have been shown to modestly
increase the risk of breast cancer in the general population, there is a similar
theoretical concern regarding BRCA carriers. A meta-analysis from 2013
demonstrated a trend toward increased risk of breast cancer under
contraceptive use in both BRCA1 (OR = 1.19; 95% CI 0.92 to 1.55) and
BRCA2 carriers (OR = 1.21; 95% CI 0.93 to 1.58) and to a higher extent than
reported for the general population (OR = 1.08). However, this did not reach
statistical significance (46).
Hormone replacement therapy (HRT) has been shown to be safe after
RRSO, even in women who retain their breasts. In a prospective study of
1,299 BRCA1/2 mutation carriers with limited follow-up, HRT following
RRSO was not associated with an increased risk of breast cancer. While this
is the largest study of its kind, it is important to recall that the data are not
randomized. Also, the type of HRT (combination hormones vs. estrogen
only) did not appear to matter, but the numbers are too small to evaluate this
specific question. In conclusion, these data are reassuring in suggesting that
HRT is probably not contraindicated in women with a BRCA1 mutation (47).
Screening of Male BRCA Carriers
In men, BRCA mutation carriers are at increased risk of breast, prostate,
gastric, pancreatic, melanoma, and colorectal cancers.
Male breast cancer is rare in the general population with a lifetime risk of
0.1%, although the risk is significantly increased to 7% to 8% with BRCA2
mutation and 1% with a BRCA1 mutation (48). BRCA2 mutations have been
shown to confer a significantly higher risk of breast cancer in men than
BRCA1 mutations (76% and 16%, respectively). Two prior studies have
reported worse prognosis in male breast cancer patients with a deleterious
BRCA1/2 mutation compared to those without a mutation (49,50). However,
both studies were limited by their small sample size. In a recent retrospective
review of 102 male BRCA mutation carriers, the majority of BRCA-
associated male breast cancers were high grade, hormone receptor positive,
and associated with lymph node metastases (48).
In case control and family-based studies BRCA1 and BRCA2 mutations
confer an up to 4.5-fold and 8.3-fold increased risk of prostate cancer,
respectively. BRCA2 mutations are associated with an increased risk of high-
grade disease, progression to metastatic castration–resistant disease, and 5-
year cancer-specific survival rates of 50% to 60%. The RR of pancreas
cancer increase was between 2.26 and 5.9 compared to the general population
(51).
NCCN guidelines recommend breast self-examination training and
education starting at age 35, and a clinical breast examination, every 12
months. At 45 years of age BRCA2 carriers should begin prostate cancer
screening with prostate specific antigen (PSA) test and BRCA1 carriers are
advised to consider it. Prostatic biopsy is recommended at PSA > 3.0 ng/mL
in this population. There is only limited data for mammography in men,
which is only recommended for breast mass, bloody nipple discharge, or
asymmetric gynecomastia (24). Finasteride and dutasteride inhibit 5-alpha
reductase and block downstream production of dihydrotestosterone from
testosterone. Two independent trials, the Prostate Cancer Prevention Trial
(PCPT) and the Reduction by Dutasteride of Prostate Cancer Events
(REDUCE), found reductions of prostate cancer incidence of 25% (18.4% vs.
24.4%; P < 0.001) and 23% reduction (19.9% vs. 25.1%; P < 0.001) for
finasteride and dutasteride, respectively (52). Unfortunately, in the PCPT, the
proportion of high-grade tumors (Gleason ≥ 7) was 27% higher in the
finasteride arm, and in the REDUCE trial, there was clearly a trend toward
increased risk in Gleason ≥ 8 tumors (29 [0.9%] vs. 19 [0.6%]; P = 0.15).
Despite the level-1 evidence that 5-alpha reductase inhibitors prevent prostate
cancer, the risk of high-grade disease and reported long-term side-effects
(e.g., erectile dysfunction) have led to diminished use of 5-alpha reductase
inhibitors for chemoprevention (53).
There is no consensus on pancreas cancer screening. BRCA2 carrier men
with family history of pancreas cancer are recommended a baseline
endoscopic US or MRI/magnetic resonance cholangiopancreatography
(MRCP) per International Cancer of the Pancreas Screening (CAPS)
Consortium guidelines (54). Currently, available guidelines for the care of
BRCA1/BRCA2 mutation carriers recommend informing the mutation carrier
of a possible increased risk for colorectal cancer and encouraging the
individual to follow screening guidelines for the general population.
Reproductive Considerations
Persons with a BRCA mutation have a 50% prospect of passing on the
susceptibility for hereditary breast and ovarian cancer (HBOC) to their
offspring. Preimplantation genetic diagnosis (PGD) and prenatal diagnosis
(PND) are available methods for couples who choose to prevent BRCA gene
inheritance. With PND, noninvasive fetal sex determination is performed at 9
weeks of pregnancy and, in case of a female, this is followed by chorionic
villus sampling with the intention to terminate the pregnancy if the fetus is
affected. Many families oppose this route for moral or ethical concern. With
PGD, in vitro fertilized (IVF) embryos are genetically diagnosed before
implantation and only unaffected embryos are transferred to the uterus. For
PGD, IVF/intracytoplasmic sperm injection (ICSI) treatment is necessary
regardless of the couple’s fertility (55).
The aim of PGD is to provide an alternative reproductive option for
couples at risk of giving birth to offspring with inheritable serious diseases so
as to avoid the physical and psychological trauma related to abortions when
an affected pregnancy is diagnosed after spontaneous pregnancy. There are
some ethical concerns regarding the use of PGD in these adult-onset diseases
or conditions with incomplete penetrance, because there is a possibility,
although very slim, that the individuals carrying the mutations may not
develop the genetic conditions. The techniques used in PGD are evolving
quickly, and emergence of new techniques with strict laboratory protocols
will hopefully reduce the cost and minimize the chance of misdiagnosis.
However, proper genetic counseling is needed before PGD (56).
Treatment Strategies in BRCA1/ 2-Related Cancers
At present, adjuvant systemic therapy decisions in breast cancer treated with
curative local therapy are not affected by the results of germline genetic
testing. Treatment options for BRCA1-related TNBCs include surgery,
radiotherapy, and chemotherapy. Radiation therapy appears to be safe and
effective in reducing ipsilateral tumor recurrences in mutation carriers with
breast cancer. BRCA-associated breast cancers found to be associated with a
higher median Oncotype DX recurrence score in hormone receptor–positive,
node-negative disease compared to non-BRCA carrier breast cancer controls
(57). In a neoadjuvant trial of 355 patients BRCA1/2 mutation status lead to
better responses to neoadjuvant chemotherapy in breast cancer. However,
pathologic complete response was the main predictor of disease-free survival
and OS, independently of BRCA1/2 mutation status (58).
For metastatic breast cancer the understanding of the role of BRCA1/2 in
DNA repair assisted in the development of therapies that target the associated
deficiencies. Germline BRCA1/2 mutations lead to impaired homologous
repair of chromosomal double-strand breaks, with at least a fivefold reduction
in DNA double-strand break repair. This leads to chromosomal instability
and unique treatment opportunities with DNA-damaging agents to induce
double-strand breaks in DNA such as cisplatin or carboplatin and poly (ADP-
ribose) polymerase (PARP) inhibitors (32).
Platins are alkylating agents that exert their effect by binding to DNA and
inducing multiple single-strand breaks, which result in apoptosis and cell
death. The synergy of two different mechanisms that potentially induce DNA
damage (platins causing single-strand breaks and BRCA mutations
inefficiently repairing double-strand breaks) is known as synthetic lethality,
which is the rationale for a potential benefit of platins in BRCA-mutated
patients. In a phase II study including 20 BRCA1-mutated metastatic breast
cancer patients, treatment with six cycles of cisplatin was associated with an
overall response rate (ORR) of 80%, with 9 out of 20 patients (45%)
experiencing a complete clinical response and 7 out of 20 patients (35%)
experiencing a partial response (PR) (59). Similarly, in the TNT trial, a subset
of metastatic TNBCs with BRCA1/2 mutations had a significantly better ORR
with carboplatin compared with docetaxel (60).
PARP inhibitors (PARPis) give rise to accumulation of double-stranded
DNA breaks by binding to PARP1, which repairs DNA single-strand breaks.
Thus, double-strand breaks cannot be repaired and give rise to genomic
instability and eventually tumor cell death. In BRCA1/2 carriers with HER2-
negative advanced breast cancer who failed previous chemotherapy,
treatment with olaparib or talazoparib was associated with improved
progression-free survival (PFS), fewer side effects, and better quality of life
compared with single-agent chemotherapy (61,62). Olaparib, niraparib, and
rucaparib are also approved by the FDA for advanced ovarian cancer.
Clinical trials with PARPi monotherapy or combination therapy are ongoing
in the adjuvant and neoadjuvant setting in breast, ovarian, and prostate
cancers (45).
Prognosis
BRCA-related breast cancer is characterized by a more aggressive phenotype
than sporadic breast cancer, with BRCA1-related breast cancers defined by
the high expression of basal layer genes, and 80% TNBCs. Histologic
characterization of germline BRCA1 mutant tumors has been well defined,
featuring a high histologic grade, atypical medullary features, high
proliferation indices, invasive borders, and lymphocytic infiltrates. BRCA2
mutation carriers present tumors with a higher risk of contralateral breast
cancer and ER positivity in most cases.
A meta-analysis by Zhong et al. in 2015 suggested inferior OS, but not
worse PFS in BRCA1 mutation carriers with breast and ovarian cancer as
compared with noncarrier patients (63). Notably, however, this OS difference
was not seen in BRCA2 mutation patients and there was significant
heterogeneity between these small studies cited. This result contrasts with a
2011 study showing similar overall prognosis of TNBC in BRCA carriers and
noncarriers within the first 5 years following initial diagnosis (43,64).
Two recent studies demonstrated different results with respect to the role
of BRCA mutations on breast cancer prognosis. The first meta-analysis,
which utilized a database containing the mutation status of 105,220 breast
cancer patients with 3.4% BRCA carriers, BRCA1 mutation carriers displayed
a worse OS (HR = 1.3) and breast cancer–specific survival (HR = 1.45) than
sporadic/BRCA-negative breast cancer cases (65). The same study also
suggested that BRCA2 mutation carriers have worse disease-specific survival
than sporadic/BRCA-negative breast cancer cases (HR = 1.29), although with
a similar OS. In the same year, Templeton et al. (66) evaluated a total of 16
studies comprising data from 10,180 patients concluding that BRCA
mutations were not associated with worse OS. Taken together, the results
suggest that BRCA mutation may be inadequate as an independent outcome
predictor.
CLINICAL MANAGEMENT OF OTHER (NON-BRCA–RELATED)
HEREDITARY BREAST SYNDROMES
Table 5-5 summarizes the current screening guidelines recommended by
NCCN. NCCN guidelines for breast cancer screening in LFS recommend
clinical breast examination and breast screening with annual MRI ±
mammogram until age 75 and consideration of risk-reducing mastectomy
(24). In the absence of major contraindications, total mastectomy could be
preferred over breast-conserving surgery in order to avoid the need of
adjuvant radiation, as radiation may predispose to secondary malignancies in
patients with LFS. Axillary staging and management should follow standard
guidelines. Due to the high risk for breast cancer in patients with LFS,
discussion of risks and benefits of prophylactic mastectomy needs to be
addressed in all cases. While no specific systemic treatment
recommendations are standard of care in patients with cancer with LFS with
germline TP53 mutations beyond minimizing radiation exposure, somatic
mutations in the TP53 gene have been linked with decreased response to both
radiotherapy as well as DNA-damaging cytotoxic agents, which are
considered to induce p53-dependent apoptosis (67). The multimodal Toronto
protocol recommends surveillance for adrenocortical carcinoma (abdominal
US and blood/urine biomarkers), breast cancer (annual mammogram and
MRI, breast self-examination, clinical breast examination), brain tumor
(annual brain MRI), soft-tissue and bone sarcoma (annual rapid whole-body
MRI, abdominal US), leukemia/lymphoma (complete blood count,
erythrocyte sedimentation rate, lactate dehydrogenase), colorectal cancer
(colonoscopy every 2 years), and melanoma (annual dermatologic
examination) along with a general assessment (physical examination every 3
to 4 months) (68).
For CS expert opinion currently recommends annual comprehensive
physical examination with special attention paid to skin, thyroid (all ages),
and breast (adult women) as well as annual formal dermatologic examination,
starting at 18 years. Due to very high risk of breast cancer, women with
PTEN mutations should have access to the same high-risk screening and
surgical options as are offered to women with HBOC. NCCN guidelines
recommend starting breast cancer surveillance using a combination of clinical
breast examinations every 6 months along with imaging, alternating between
mammography and MRI starting at the age of 30 to 35. A prophylactic
mastectomy can be discussed from the age of 25 to 30 years (69). Few
specific treatment options exist for breast cancer patients with CS, but by
virtue of the role of PTEN in the PI3 kinase (PI3K) signal transduction
cascade, inhibitors targeting the PI3K/AKT/mTOR pathway are attractive
candidates in this patient subset (32).
In Peutz–Jeghers syndrome clinical breast cancer screening should start by
age 25, with annual MRI starting at age 25 to 30 years, with mammography
being substituted after the age of 50. For ovarian and cervical cancer
screening an annual pelvic examination and pap smear is recommended from
18 to 20 years old. A baseline colonoscopy, small bowel screening using
video capsule endoscopy and upper GI endoscopy is indicated at age 8 years.
In those in whom significant polyps are detected these should be repeated
every 3 years. In those in whom there are no significant polyps at baseline
endoscopy, routine surveillance is repeated at age 18, or sooner should
symptoms arise, and then every 2 to 3 years (70). NCCN guidelines
recommend MRCP and endoscopic US every 1 to 2 years for pancreas cancer
screening starting at age 30 to 35 (24).
For CDH1 mutation clinical breast cancer screening should start by age 25.
Imaging modalities and scheduling are still under study, but NCCN
guidelines recommend annual screening with mammogram and MRI starting
at age 30 (24). However, prophylactic mastectomy is not routinely
recommended due to the scarce information about genetic penetrance, and
breast surveillance is preferred. A prophylactic gastrectomy should be
discussed and annual endoscopic surveillance is recommended for patients
who delay gastrectomy (71).
The inclusion of moderate-penetrance cancer susceptibility genes in
multigene panel testing posed challenges regarding the optimal management
of individuals found to have pathogenic variants in these genes. A recently
published counseling framework has provided evidence-based guidance for
moderate-penetrance breast and ovarian cancer genes (72). The calculated
average lifetime risks for women with pathogenic mutations in PALB2, ATM,
NBN, and CHEK2 (excluding certain missense mutations, such as p.I157T)
approach or exceed 30%. NCCN recommends beginning annual
mammography at an age 10 years younger than the earliest age at which a
family member was diagnosed with the disease (but not before the age of 30
years). Women carrying pathogenic mutations in these genes can be
considered for MRI surveillance in the United States (72).
There is no evidence showing that bilateral mastectomy in patients who are
found to carry a pathogenic mutation in moderate-risk breast cancer genes
has any effect on the outcome of the patient. The effects of radiation therapy
in patients with breast cancer who carry a pathogenic mutation in moderate-
risk breast cancer genes have not been studied adequately. Breast
conservation therapy, followed by radiation therapy, if possible, is the
preferred approach for local treatment of breast cancer in these patients.
Based on animal studies, there have been some concerns expressed regarding
excess toxicity of radiation in ATM mutation carriers, but this has not been
definitively confirmed clinically (27).
PSYCHOSOCIAL ISSUES IN INHERITED BREAST AND OVARIAN CANCER
SYNDROMES
Even though it is well recognized that many individuals will benefit from
genetic counselling and testing for hereditary cancer in general, there have
also been reports that it may induce a number of psychosocial problems. In a
review on individuals requesting genetic counselling and testing for
hereditary cancer syndromes, six dominant problem areas were identified: (1)
coping with cancer risk; (2) practical problems (such as obtaining life
insurance/loans and employment when found to be a mutation carrier); (3)
family-related problems (e.g., communication problems with family
members, feeling responsible for family members); (4) children-related
problems (e.g., concerns for children having increased risk, fear of leaving
young children); (5) living with cancer (e.g., fear of developing cancer, pain
about the loss of family members); and (6) emotions (e.g., anxiety, anger,
feelings of loss, but also relief and reassurance) (73). A psychological support
should be offered to all women having a genetic assessment (35).

REFERENCES

1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2019. CA Cancer J


Clin 2019;69:7–34.
2. Genetics of Breast and Gynecologic Cancers (PDQ®). Health
Professional Version. PDQ Cancer Genetics Editorial Board. PDQ
Cancer Information Summaries [Internet]. Bethesda (MD): National
Cancer Institute (US); 2002–2019.
3. Kerr J, Anderson C, Lippman SM. Physical activity, sedentary
behaviour, diet, and cancer: an update and emerging new evidence.
Lancet Oncol 2017;18(8):e457–e471.
4. Yang XR, Chang-Claude J, Goode EL, et al. Associations of breast
cancer risk factors with tumor subtypes: a pooled analysis from the
Breast Cancer Association Consortium studies. J Natl Cancer Inst
2011;103(3):250–263.
5. Iyengar NM, Arthur R, Manson JE, et al. Association of body fat and
risk of breast cancer in postmenopausal women with normal body mass
index: a secondary analysis of a randomized clinical trial and
observational study. JAMA Oncol 2019;5(2):155–163.
6. Scoccianti C, Lauby-Secretan B, Bello PY, et al. Female breast cancer
and alcohol consumption: a review of the literature. Am J Prev Med
2014;46(3 Suppl 1):S16–S25.
7. Harvie M, Howell A, Evans DG. Can diet and lifestyle prevent breast
cancer: what is the evidence? Am Soc Clin Oncol Educ Book 2015:e66–
e73.
8. Solti M, Webb T. Nutrition and exercise in cancer survivors. J
Community Oncology 2012;9:266–268.
9. American Cancer Society. Breast Cancer Facts & Figures 2015–2016.
Atlanta: American Cancer Society, Inc; 2012.
10. Nichols HB, Schoemaker MJ, Cai J, et al. Breast cancer risk after recent
childbirth: a pooled analysis of 15 prospective studies. Ann Intern Med
2019;170(1):22–30.
11. Morch LS, Skovlund CW, Hannaford PC, et al. Contemporary hormonal
contraception and the risk of breast cancer. N Engl J Med
2017;377(23):2228–2239.
12. Chlebowski RT, Kuller LH, Prentice RL, et al. Breast cancer after use of
estrogen plus progestin in postmenopausal women. N Engl J Med
2009;360:573–587.
13. Dean LT, Gehlert S, Neuhouser ML, et al. Social factors matter in
cancer risk and survivorship. Cancer Causes Control 2018;29(7):611–
618.
14. Makarem N, Lin Y, Bandera EV, et al. Concordance with World Cancer
Res Fund/American Institute for Cancer Res (WCRF/AICR) guidelines
for cancer prevention and obesity-related cancer risk in the Framingham
Offspring cohort (1991-2008). Cancer Causes Control 2015;26:277–
286.
15. Bellocco R, Marrone G, Ye W, et al. A prospective cohort study of the
combined effects of physical activity and anthropometric measures on
the risk of post-menopausal breast cancer. Eur J Epidemiol
2016;31:395–404.
16. Barke LD, Freivogel ME. Breast cancer risk assessment models and
high-risk screening. Radiol Clin North Am 2017;55(3):457–474.
17. Amir E, Evans DG, Shenton A, et al. Evaluation of breast cancer risk
assessment packages in the family history evaluation and screening
programme. J Med Genet 2003;40:807–814.
18. Claus EB, Risch N, Thompson WD. Autosomal dominant inheritance of
early onset breast cancer: implications for risk prediction. Cancer
1994;73:643–651.
19. Tyrer J, Duffy SW, Cuzick J. A breast cancer prediction model
incorporating familial and personal risk factors. Stat Med 2004;23:1111–
1130.
20. Berry DA, Iverson ES, Gudbjartsson DF, et al. BRCAPRO validation,
sensitivity of genetic testing of BRCA1/BRCA2, and prevalence of
other breast cancer susceptibility genes. J Clin Oncol 2002;20:2701–
2712.
21. Antoniou AC, Pharoah PP, Smith P, et al. The BOADICEA model of
genetic susceptibility to breast and ovarian cancer. Br J Cancer
2004;91:1580–1590.
22. Yala A, Lehman C, Schuster T, et al. A deep learning mammography-
based model for improved breast cancer risk prediction. Radiology
2019;292(1):60–66.
23. The American Society of Breast Surgeons Consensus guideline:
https://www.breastsurgeons.org/docs/statements/Consensus-Guideline-
on-Genetic-Testing-for-Hereditary-Breast-Cancer.pdf
24. National Comprehensive Cancer Network. NCCN clinical practice
guidelines in oncology: genetic/familial high-risk assessment: breast and
ovarian, version 3. 2019.
https://www.nccn.org/professionals/physician_gls/pdf/genetics_screening.pdf
Published January 18, 2019. Accessed July 9, 2019.
25. U.S. Preventive Services Task Force. BRCA-related cancer: risk
assessment, genetic counseling, and genetic testing: recommendation
summary.
http://www.uspreventiveservicestaskforce.org/Page/Document/UpdateSummaryFinal
related-cancer-risk-assessment-genetic-counseling-and-genetic-testing?
ds=1&s=. Published December 2013. May 26, 2019.
26. Valencia OM, Samuel SE, Viscusi RK, et al. The role of genetic testing
in patients with breast cancer: a review. JAMA Surg 2017;152(6):589–
594.
27. Yadav S, Couch FJ. Germline genetic testing for breast cancer risk: the
past, present, and future. Am Soc Clin Oncol Educ Book 2019;39:61–74.
28. Huen MS, Sy SM, Chen J. BRCA1 and its toolbox for the maintenance
of genome integrity. Nat Rev Mol Cell Biol 2010;11(2):138–148.
29. Bland KI, Copeland EM, Klimberg VS, et al. The Breast:
Comprehensive Management of Benign and Malignant Diseases.
Elsevier; 2017. https://doi.org/10.1016/C2014-0-01946-6
30. Kuchenbaecker KB, Hopper JL, Barnes DR, et al. Risks of breast,
ovarian and contralateral breast cancer for BRCA1 and BRCA2
mutation carriers. J Am Med Assoc 2017;317:2402–2416.
31. Ngeow J, Sesock K, Eng C. Breast cancer risk and clinical implications
for germline PTEN mutation carriers. Breast Cancer Res Treat
2017;165(1):1–8.
32. Parkes A, Arun BK, Litton JK. Systemic treatment strategies for patients
with hereditary breast cancer syndromes. Oncologist 2017;22(6):655–
666.
33. Rana H, Gelman R, LaDuca H, et al. Differences in TP53 mutation
carrier phenotypes emerge from panel-based testing. J Natl Cancer Inst
2018;110(8):863–870.
34. Hearle N, Schumacher V, Menko FH, et al. Frequency and spectrum of
cancers in the Peutz–Jeghers Syndrome. Clin Cancer Res
2006;12:3209–3215.
35. Rousset-Jablonski C, Gompel A. Screening for familial cancer risk:
focus on breast cancer. Maturitas 2017;105:69–77.
36. Hansford S, Kaurah P, Li-Chang H, et al. Hereditary diffuse gastric
cancer syndrome: CDH1 mutations and beyond. JAMA Oncol
2015;1(1):23–32.
37. West AH, Blazer KR, Stoll J, et al. Clinical interpretation of pathogenic
ATM and CHEK2 variants on multigene panel tests: navigating
moderate risk. Fam Cancer 2018;17(4):495–505.
38. Couch FJ, Shimelis H, Hu C, et al. Associations between cancer
predisposition testing panel genes and breast cancer. JAMA Oncol
2017;3(9):1190–1196.
39. Michailidou K, Lindström S, Dennis J, et al; NBCS Collaborators,
ABCTB Investigators, ConFab/AOCS Investigators. Association
analysis identifies 65 new breast cancer risk loci. Nature 2017;551:92–
94.
40. Mavaddat N, Michailidou K, Dennis J, et al. Polygenic risk scores for
prediction of breast cancer and breast cancer subtypes. Am J Hum Genet
2019;104:21–34.
41. Gulani V, Calamante F, Shellock FG, et al. Gadolinium deposition in the
brain: summary of evidence and recommendations. Lancet Neurol
2017;16(7):564–570.
42. Evans DG, Ingham SL, Baildam A, et al. Contralateral mastectomy
improves survival in women with BRCA1/2-associated breast cancer.
Breast Cancer Res Treat 2013;140(1):135–142.
43. Bayraktar S, Arun B. BRCA mutation genetic testing implications in the
United States. Breast 2017;31:224–232.
44. Phillips KA, Lindeman GJ. Breast cancer prevention for BRCA1 and
BRCA2 mutation carriers: is there a role for tamoxifen? Future Oncol
2014;10(4):499–502.
45. https://clinicaltrials.gov/. Accessed July 7, 2019.
46. Tschernichovsky R, Goodman A. Risk-reducing strategies for ovarian
cancer in BRCA mutation carriers: a balancing act. Oncologist
2017;22(4):450–459.
47. Domchek SM, Neuhausen SL, PROSE Consortium, et al. Is hormone
replacement therapy (HRT) following risk-reducing salpingo-
oophorectomy (RRSO) in BRCA1 (B1)- and BRCA2 (B2)-mutation
carriers associated with an increased risk of breast cancer? [abstract].
JCO. 2011;29:Abstract 1501.
48. Ibrahim M, Yadav S, Ogunleye F, et al. Male BRCA mutation carriers:
clinical characteristics and cancer spectrum. BMC Cancer
2018;18(1):179.
49. Gargiulo P, Pensabene M, Milano M, et al. Long-term survival and
BRCA status in male breast cancer: a retrospective single-center
analysis. BMC Cancer 2016;16:375.
50. Ottini L, Silvestri V, Rizzolo P, et al. Clinical and pathologic
characteristics of BRCA-positive and BRCA-negative male breast
cancer patients: results from a collaborative multicenter study in Italy.
Breast Cancer Res Treat 2012;134:411–418.
51. Mohamad HB, Apffelstaedt JP. Counseling for male BRCA mutation
carriers—a review. Breast 2008;17(5):441–450.
52. Andriole GL, Bostwick DG, Brawley OW, et al. Effect of dutasteride on
the risk of prostate cancer. N Engl J Med 2010;362(13):1192–1202.
53. Leao RRN, Price AJ, James Hamilton R. Germline BRCA mutation in
male carriers-ripe for precision oncology? Prostate Cancer Prostatic
Dis 2018;21(1):48–56.
54. Canto MI, Harinck F, Hruban RH, et al. International Cancer of the
Pancreas Screening (CAPS) Consortium summit on the management of
patients with increased risk for familial pancreatic cancer. Gut
2013;62(3):339–347.
55. Derks-Smeets IAP, Gietel-Habets JJ, Tibben A, et al. Decision-making
on preimplantation genetic diagnosis and prenatal diagnosis: a challenge
for couples with hereditary breast and ovarian cancer. Hum Reprod
2014;29(5):1103–1112.
56. Lee VCY, Chow JFC, Yeung WSB, et al. Preimplantation genetic
diagnosis for monogenic diseases. Best Pract Res Clin Obstet Gynaecol
2017;44:68–75.
57. Shah PD, Patil S, Dickler MN, et al. Twenty-one-gene recurrence score
assay in BRCA-associated versus sporadic breast cancers: Differences
based on germline mutation status. Cancer 2016;122:1178–1184.
58. Wunderle M, Gass P, Häberle L, et al. BRCA mutations and their
influence on pathological complete response and prognosis in a clinical
cohort of neoadjuvantly treated breast cancer patients. Breast Cancer
2018;171(1):85–89.
59. Byrski T, Dent R, Blecharz P, et al. Results of a phase II open-label,
non-randomized trial of cisplatin chemotherapy in patients with
BRCA1-positive metastatic breast cancer. Breast Cancer Res
2012;14:R110.
60. Tutt A, Tovey H, Cheang MCU, et al. Carboplatin in BRCA1/2-mutated
and triple-negative breast cancer BRCAness subgroups: the TnT trial.
Nat Med 2018;24:628–637.
61. Robson M, Im SA, Senkus E, et al. Olaparib for metastatic breast cancer
in patients with a germline BRCA mutation. N Engl J Med
2017;377:523–533.
62. Litton JK, Rugo HS, Ettl J, et al. Talazoparib in patients with advanced
breast cancer and a germline BRCA mutation. N Engl J Med
2018;379:753–763.
63. Zhong Q, Peng HL, Zhao X, et al. Effects of BRCA1- and BRCA2-
related mutations on ovarian and breast cancer survival: a meta-analysis.
Clin Cancer Res 2015;21:211–220.
64. Bayraktar S, Gutierrez-Barrera AM, Liu D, et al. Outcome of triple-
negative breast cancer in patients with or without deleterious BRCA
mutations. Breast Cancer Res Treat 2011;130:145–153.
65. Baretta Z, Mocellin S, Goldin E, et al. Effect of BRCA germline
mutations on breast cancer prognosis: a systematic review and meta-
analysis. Medicine (Baltimore) 2016;95(40):e4975.
66. Templeton AJ, Gonzalez LD, Vera-Badillo FE, et al. Interaction
between hormonal receptor status, age and survival in patients with
BRCA1/2 germline mutations: a systematic review and meta-regression.
PLoS One 2016;11(5):e0154789.
67. Kappel S, Janschek E, Wolf B, et al. TP53 germline mutation may affect
response to anticancer treatments: analysis of an intensively treated Li-
Fraumeni family. Breast Cancer Res Treat 2015;151(3):671–678.
68. Villani A, Shore A, Wasserman JD, et al. Biochemical and imaging
surveillance in germline TP53 mutation carriers with Li-Fraumeni
syndrome: 11 year follow-up of a prospective observational study.
Lancet Oncol 2016;17(9):1295–1305.
69. Mester J, Eng C. Cowden syndrome: recognizing and managing a not-
so-rare hereditary cancer syndrome. J Surg Oncol 2015;111(1):125–130.
70. Beggs AD, Latchford AR, Vasen HF, et al. Peutz-Jeghers syndrome: a
systematic review and recommendations for management. Gut
2010;59:975–986.
71. Van der Post RS, Vogelaar IP, Carneiro F, et al. Hereditary diffuse
gastric cancer: updated clinical guidelines with an emphasis on germline
CDH1 mutation carriers. J Med Genet 2015;52(6):361–374.
72. Tung N, Domchek SM, Stadler Z, et al. Counselling framework for
moderate-penetrance cancer-susceptibility mutations. Nat Rev Clin
Oncol 2016;13:581–588.
73. Eijzenga W, Hahn DE, Aaronson NK, et al. Specific psychosocial issues
of individuals undergoing genetic counseling for cancer—a literature
review. J Genet Couns 2014;23:133–146.
CHAPTER 6

Patient Selection for Breast-


Conservation Therapy
MICHELE L. B. LEY | JEFFREY A. SUGANDI

Breast-conservation therapy (BCT) has been accepted as an appropriate


treatment modality for many patients with early-stage breast cancer. The term
BCT encompasses breast-conserving surgery or lumpectomy followed by
radiation therapy to treat any microscopic residual tumor. Prior to the advent
of BCT, all breast cancer patients underwent mastectomy as a part of their
treatment. With BCT, patients are able to preserve their breast without
sacrificing oncologic outcomes. The goals of BCT are to provide minimal
loss of breast tissue while achieving survival equivalency of mastectomy, and
minimizing risks of breast cancer recurrence. The National Comprehensive
Cancer Network continues to recognize BCT as being supported by the
highest level of evidence (category 1) in terms of its equivalency to
mastectomy for treatment of early breast cancer in majority of women with
respect to overall survival (1).
From 1973 to 1980, recruitment of patients at the Milan Cancer Institute
was designed to compare radical mastectomy to breast-conserving surgery
“quadrantectomy.” The goal of the surgical technique was to remove the
primary carcinoma and a generous amount of surrounding tissue, including
skin and muscular fascia. Preliminary data published between 1977 and 1981
showed that survival rates were equal (2). Of the 701 women who entered the
trial, 177 died of breast cancer—86 in the radical mastectomy group and 91
in the group that received breast-conserving therapy. Local recurrences were
higher in the group that received breast conservation. The highest rate of
recurrence was in women 45 years of age or younger. The 20-year follow-up
study by Veronesi showed that the long-term survival of women with early
breast cancer who were treated with breast-conserving surgery and
postoperative radiotherapy to the breast was identical to women who
underwent radical mastectomy (41.7% vs. 41.2%) (2).
Similarly, in 1971, the National Surgical Adjuvant Breast and Bowel
Project (NSABP) initiated the B-04 study, a randomized clinical trial to
resolve controversy over the surgical management of breast cancer. The 25-
year follow-up showed there was no survival difference between the Halsted
mastectomy and less extensive surgery—partial mastectomy (3).
The NSABP B-06 trial was then designed to evaluate breast-conserving
surgery in women with stage 1 and 2 tumors that were less than 4 cm in size.
Patients were randomized to lumpectomy alone, lumpectomy with radiation,
or total mastectomy. In a 20-year follow-up study, no survival differences
were noted among the three groups. The local recurrence rate in patients who
underwent lumpectomy without radiation was 39.2% versus 14.3% in the
group that received radiation (4). Therefore, in terms of survival, data has
shown that breast-conserving surgery has a similar long-term outcomes
compared to mastectomy. Table 6-1 summarizes the results of randomized
prospective trials comparing mastectomy to BCT for invasive breast cancer.
Local recurrence is an important aspect of BCT due to its implications of
risks of disease return, risks of increased mortality, as well as morbidity
associated with retreatment. In the early trials, higher local recurrence rate for
BCT was reported to be in the range of approximately 5% to 20%. With the
advancement of current systemic therapy, local recurrences have been
evaluated to be approximately 2% at 10 years (9).
PATIENT SELECTION FOR BCT
With the evidence of similar survival benefit, BCT has become an acceptable,
attractive alternative to mastectomy for many patients with invasive breast
cancer (Table 6-2).
However, not every patient is an appropriate candidate for BCT. In fact,
careful patient selection with a multidisciplinary approach is essential to the
success of BCT.
Patients diagnosed with invasive breast cancer should undergo thorough
evaluation, including the different components as described below, in order
to determine eligibility for this approach (15).
HISTORY AND PHYSICAL
A complete history and physical examination can provide remarkable amount
of information required to determine eligibility. Important elements that
should be elucidated in history includes the presence and characteristics of
nipple discharge, palpable mass, symptoms suggestive of metastasis, date of
last menstrual period, possibility of pregnancy, family history of breast
cancer or ovarian cancer, history of prior radiation treatment, and history of
prior cosmetic breast surgery.

TABLE 6-1 Comparison of Prospective Randomized Trials Mastectomy


Versus BCT for Invasive Breast Cancer

During physical examination, it is important to note the presence of scars,


implants, palpable mass, tumor size and location, skin or nipple retraction,
skin involvement, ratio of tumor size to breast size, axillary and
supraclavicular adenopathy, presence of multiple tumors, and evidence of
inflammatory breast cancer such as peau d’orange and lymphedema of
ipsilateral limb. It is important to note that nipple involvement, small area of
skin involvement, and regional nodal disease are not considered absolute
contraindications to breast-conserving surgery.
RADIOLOGIC EVALUATION
Typical preoperative imaging workup should include a combination of
diagnostic mammogram with appropriate magnifications, and ultrasound if
indicated. The surgeon should review the imaging studies in order to
determine the extent of patient’s disease, the presence or absence of
multicentricity, and other factors that may influence treatment decisions such
as lymph node appearance and the presence or absence and location
(submuscular or subglandular) of implants. Bilateral breast imaging is
important to evaluate the status of contralateral breast. If microcalcifications
are present, their extent, location, and distribution should be noted. Ipsilateral
disease multifocality and/or multicentricity may influence the eligibility of
breast-conserving surgery as described below.
The routine use of magnetic resonance imaging (MRI) in patients with
newly diagnosed breast cancer remains controversial. Although MRI may be
useful as an adjunct for investigation of multifocal or multicentric disease,
some patients may not benefit from the routine use of breast MRI. Fancellu et
al. found that MRI in BCT candidate patients may increase the rate of
mastectomy and did not significantly reduce reoperation rate for positive
margins (16). MRI may be indicated in patients with dense breast tissue and
who have evidence of multicentricity on mammography or on physical
examination.

TABLE 6-2 Comparison of Prospective Randomized Trials of BCS With or


Without RT for Invasive Breast Cancer
PATIENT PREFERENCES REGARDING BREAST CONSERVATION VERSUS
MASTECTOMY
Patient’s choice is often influenced by the experience of friends or relatives,
their perception of what is a better treatment, access to radiation therapy
facilities, as well as their body image and fear of local recurrence. Each
patient and her surgeon must thoroughly discuss risk and benefits comparing
mastectomy versus BCT. Topics of discussion must include expectations
regarding treatment course, cosmetic outcome, long-term survival, the risks
and possibility of recurrence, and the effect on patient’s psychological and
perceived quality of life.
Often patients report that their physicians did not present both BCT and
mastectomy options to them (17). Morrow et al. reported a significant
correlation between the approach of mastectomy and poor prognostic factors
such as nodal status and tumor grade, suggesting that some surgeons may
view breast conservation as less aggressive (18). This rationale is not
necessarily sound; if a patient has a poor prognosis, they are generally more
likely to recur systemically rather than locally. Surgeon practice volume also
has been correlated with the use of breast conservation, suggesting that
experience and therapeutic bias may influence the surgical options offered
(19). Continuing physician education and encouraging the use of high-
volume centers should continue to decrease this problem.
CONTRAINDICATIONS FOR BCT
The rationale of contraindications for BCT is largely related to inability to
obtain margin control or noncandidacy for adjuvant radiotherapy. There are
absolute contraindications for BCT and relative contraindications for BCT.
Tables 6-3 and 6-4 summarize the absolute and relative contraindications of
BCT.
Absolute contraindications for BCT include a diagnosis of inflammatory
breast cancer, multiple ipsilateral tumors unable to be included in single
specimen, mammographic appearance of diffuse suspicious or malignant-
appearing microcalcifications, history of prior radiation therapy which
included a portion of the diseased breast, pregnant patient who will require
radiation treatment during pregnancy, and persistent positive resection
margins despite multiple reexcision attempts.
Inflammatory breast cancer is a rare and aggressive form of breast cancer
that is characterized by diffuse erythema and edema of the breast. This
disease has an aggressive local and systemic course that requires
multimodality treatment with neoadjuvant chemotherapy followed by surgery
and radiation as the current standard of care. An aggressive surgical approach
with mastectomy and axillary dissection, followed by radiation therapy has
been shown to improve survival and local control in this subset of patients
(20,21). In contrast, limited data showed that breast-conservation surgery in
inflammatory breast cancer failed to achieve satisfactory local control
resulting in higher rate of local recurrences (22).

TABLE 6-3 Absolute Contraindications for Breast-Conserving Therapy


• Inflammatory breast cancer
• Multicentric or multifocal disease unable to be included in single
specimen
• Previous history of radiation to affected breast
• Pregnancy
• Persistent positive margins despite multiple reexcisions

TABLE 6-4 Relative Contraindications for Breast-Conserving Therapy


• Connective tissue disease
• A large tumor in small breast size
• Severe obesity with body habitus precluding radiation therapy

Multiple ipsilateral tumors are described as multifocal (more than one


tumor within a single quadrant) or multicentric (multiple tumors involving
different quadrants). Earlier studies from patients with multiple tumors who
underwent breast-conserving surgery revealed local recurrence rate of 15% to
40%, thus resulting in this feature to be considered as a contraindication for
BCT (23–25). However, later studies showed that breast-conserving surgery
in multiple tumors could achieve improved margins and outcomes. Therefore
the general consensus deemed that BCT might be attempted as long as the
tumors can be excised with negative margins within a single lumpectomy
specimen, without compromising cosmetic outcome of residual breast tissue
(26).
Currently, the Alliance Z11102 trial (ClinicalTrials.gov identifier:
NCT01556243), a phase II trial by the Alliance for Clinical Trials in
Oncology, is evaluating the feasibility of BCT in women with two or three
sites of malignancy in ipsilateral breast. Initial report showed that 134 out of
184 patients (67%) successfully achieved margin-negative excision in a
single operation with 7.1% patients requiring conversion to mastectomy due
to positive margins (27). With advancement of surgical techniques, more data
are required to determine the feasibility of BCT in patients with multifocal or
multicentric tumors.
Pregnancy is considered a contraindication for BCT in the event that
radiation is anticipated during gestation. This is due to the contraindication to
the use of radiotherapy in pregnancy. The associated risks to the fetus consist
of pregnancy loss, malformation, developmental anomalies, and carcinogenic
effects (28).
In certain scenarios, BCT can still be considered in patients diagnosed with
breast cancer during second or third trimester of pregnancy, only when
radiation therapy can be delayed until after delivery. Breast-conserving
surgery itself has been shown to be safe and feasible during pregnancy, when
combined with other treatment modalities, with no increased adverse impacts
on local recurrence or complications (29,30).
Relative contraindications to BCT include prior radiation therapy to the
chest wall or breast, connective tissue disorder involving the skin, large
tumor relative to breast size, and severely obese body habitus prohibitive to
radiation therapy. Severely morbid obese patients may not be able to
participate in radiation therapy due to logistical problems related to
transportation, as well as logistical issues of ensuring consistent dosage of
radiation to excessive breast size. Although oncoplastic surgical technique is
discussed elsewhere in this book (Chapters 33 and 34), reduction mastopexy
is one of oncoplastic strategies that can be utilized for patients with large
breasts. Breast reduction may help because it improves positioning of the
breast for radiotherapy (31).
Patients with connective tissue disease involving the skin are at elevated
risks for complications with BCT. Scleroderma patients have proven elevated
risk of radiation therapy complications (32). Several published reports
showed that patients with connective tissue diseases (especially scleroderma,
systemic lupus erythematosus), had poor tolerance to radiation therapy
component of BCT (33,34).
Although tumor size does not constitute a contraindication to BCT, a large
tumor size in a small breast is a relative contraindication due to poor cosmetic
outcome caused by extensive breast tissue removal in order to achieve
adequate resection. Furthermore, tumor size greater than 5 cm does not
preclude patients from BCT. Neoadjuvant treatment with hormonal therapy
or chemotherapy has been shown to reduce tumor size significantly, therefore
improving patient eligibility for BCT (35–37). Boughey et al. showed that
patients with triple-negative breast cancer and HER-2–positive breast cancer
receiving neoadjuvant chemotherapy had higher rate of breast-conserving
surgery than those with hormone receptor positive, HER-2–negative tumor
(38).
PATHOLOGIC FEATURES OF BREAST CANCER
The most common type of breast cancer is invasive ductal carcinoma (IDC),
accounting for more than 70% of all cases, followed by invasive lobular
carcinoma (ILC), with a frequency of approximately 10%. A number of
pathologic features may help provide disease prognostication. These features
include histology type and grade, presence or absence of tumor necrosis,
vascular or lymphatic infiltrate, inflammatory infiltrate, hormone receptor
status and HER-2 status, and presence of ductal carcinoma in situ (DCIS) in
association with invasive breast carcinoma (38–43).
According to current guidelines recommended by Society of Surgical
Oncology (SSO), American Society for Radiation Oncology (ASTRO), and
American Society of Clinical Oncology (ASCO), excision with at least 2-mm
clear margins is adequate in DCIS patients treated with lumpectomy followed
by radiation therapy. This was based on meta-analysis of 20 studies and
7,883 patients with DCIS who underwent lumpectomy followed by
radiotherapy. Patients with margins of at least 2 mm were associated with
significantly reduced risk of ipsilateral breast tumor recurrence compared to
patients with margins <2 mm (12% vs. 24%, respectively). There was no
evidence that wider margins greater than 2 mm resulted in reduction of
recurrence (44).
In situations where invasive breast cancer is present with DCIS,
SSO/ASTRO/ASCO guidelines recommend “no ink on tumor” as adequate
margin for patients treated with lumpectomy followed by whole breast
radiation (45). This is based on meta-analysis of 33 studies including more
than 28,000 patients where positive margins (defined by ink on invasive
tumor) are associated with twofold increase in the risks of ipsilateral breast
tumor recurrence compared with negative margins. However, there was no
evidence that more widely clear margins were associated with decreased the
rate of recurrence (46).
POST BCT SURVEILLANCE
According to ASCO guidelines, patients who underwent BCT should obtain
posttreatment mammogram within 6 months after radiation therapy followed
by every 6 to 12 months for surveillance of abnormalities. In addition, all
patients should be counseled for breast self-examination, regular pelvic
examination, and genetic counseling as indicated for high-risk women (47).
CONCLUSION
BCT consists of breast-conserving surgery and radiation therapy. Its goal is
to provide survival equivalency of mastectomy while achieving preservation
of the breast. Radiotherapy is employed to decrease the rate of recurrence.
Patient selection is of paramount importance to ensure the success of BCT.
Patient and physician should proceed with BCT after a shared decision-
making process. To arrive at the optimal option for the treatment, the
physician should assess patient’s needs and expectations, perform thorough
history and examination, review imaging, and provide all the necessary
information to allow patients to make an informed decision.

REFERENCES

1. Gradishar WJ, Anderson BO, Balassanian R, et al. Invasive breast


cancer version 1.2016, NCCN clinical practice guidelines in oncology. J
Natl Compr Canc Netw 2016;14:324–354.
2. Veronesi U, Cascinelli N, Mariani L, et al. Twenty-year follow-up of a
randomized study comparing breast-conserving surgery with radical
mastectomy for early breast cancer. N Engl J Med 2002;347(16):1227–
1232.
3. Fisher B, Jeong JH, Anderson S, et al. Twenty-five-year follow-up of a
randomized trial comparing radical mastectomy, total mastectomy, and
total mastectomy followed by irradiation. N Eng J Med 2002;347:567–
575.
4. Fisher B, Anderson S, Bryant J, et al. Twenty-year follow-up of a
randomized trial comparing total mastectomy, lumpectomy, and
lumpectomy plus irradiation for the treatment of invasive breast cancer.
N Engl J Med 2002;347(16):1233–1241.
5. Arriagada R, Le MG, Rochard F, et al. Conservative treatment versus
mastectomy in early breast cancer: patterns of failure with 15 years of
follow-up data. Institut Gustave Roussy Breast Cancer Group. J Clin
Oncol 1996;14:1558–1564.
6. Jacobson JA, Danfort DN, Cowan KH, et al. Ten-year results of a
comparison of conservation with mastectomy in the treatment of stage I
and II breast cancer. N Engl J Med 1995;332:907–911.
7. Van Dongen JA, Voogd AC, Fentiman IS, et al. Long-term results of a
randomized trial comparing breast-conserving therapy with mastectomy:
European Organization for Research and Treatment of Cancer 108901
trial. J Natl Cancer Inst 2000;92:1143–1150.
8. Blichert-Toft M, Nielsen M, During M, et al. Long-term results of breast
conserving surgery vs. Mastectomy for early stage invasive breast
cancer: 20-year follow-up of the Danish randomized DBCG-82TM
protocol. Acta Oncol 2008;47:672–681.
9. Poortmans P, Arenas M, Livi L. Over-irradiation. Breast 2017;31:295–
302.
10. Veronesi U, Marubini E, Mariani L, et al. Radiotherapy after breast-
conserving surgery in small breast carcinoma: long-term results of a
randomized trial. Ann Oncol 2001;12:997–1003.
11. Clark RM, Whelan T, Levine M, et al. Randomized clinical trial of
breast irradiation following lumpectomy and axillary dissection for
node-negative breast cancer: an update. Ontario Clinical Oncology
Group. J Natl Cancer Inst 1996;88:1659–1664.
12. Liljegren G, Holmberg L, Bergh J, et al. 10-year results after sector
resection with or without postoperative radiotherapy for stage I breast
cancer: a randomized trial. J Clin Oncol 1999;17:2326–2333.
13. Holli K, Hietanen P, Saaristo R, et al. Radiotherapy after a segmental
resection of breast cancer with favorable prognostic features: 12-year
follow-up results of a randomized trial. J Clin Oncol 2009;27:927–932.
14. Fisher B, Bryant J, Dignam JJ, et al. Tamoxifen, radiation therapy, or
both for prevention of ipsilateral breast tumor recurrence after
lumpectomy in women with invasive breast cancers of one centimeter or
less. J Clin Oncol 2002;20:4141–4149.
15. Morrrow M, Strom EA, Bassett LW, et al. Standard for breast
conservation therapy in the management of invasive breast carcinoma.
CA Cancer J Clin 2002;52(5):277–300.
16. Fancellu A, Soro D, Castiglia P, et al. Usefulness of magnetic resonance
in patients with invasive cancer eligible for breast conservation: a
comparative study. Clin Breast Cancer 2014;14(2):114–121.
17. Morrow M, White J, Moughan J, et al. Factors predicting the use of
breast-conserving therapy in stage I and II breast carcinoma. J Clin
Oncol 2001;19(8):2254–2262.
18. Morrow M. Rational local therapy for breast cancer. N Engl J Med
2002;347(16):1270–1271.
19. McKee MD, Cropp MD, Hyland A, et al. Provider case volume and
outcome in the evaluation and treatment of patients with mammogram-
detected breast carcinoma. Cancer 2002;95(4):704–712.
20. Perez CA, Fields JN, Fracasso PM, et al. Management of locally
advanced carcinoma or the breast. II. Inflammatory carcinoma. Cancer
1994;74(1):466–476.
21. Panades M, Olivotto IA, Speers CH, et al. Evolving treatment strategies
for inflammatory breast cancer: a population–based survival analysis. J
Clin Oncol 2005;23(9):1941–1950.
22. Brun B, Otmezguine Y, Feuilhade F, et al. Treatment of inflammatory
breast cancer with combination chemotherapy and mastectomy versus
breast conservation. Cancer 1988;61(6):1096–1103.
23. Wilson LD, Beinfield M, McKhann CF, et al. Conservative surgery and
radiation in the treatment of synchronous ipsilateral breast cancers.
Cancer 1993;72:137–142.
24. Leopold KA, Recht A, Schnitt SJ, et al. Results of conservative surgery
and radiation therapy for multiple synchronous cancers of one breast. Int
J Radiat Oncol Biol Phys 1989;16:11–16.
25. Kurtz JM, Jacquemier J, Amalric R, et al. Breast-conserving therapy for
macroscopically multiple cancers. Ann Surg 1990;212:38–44.
26. Newman LA. Decision making in the surgical management of invasive
breast cancer-part 2: expanded applications for breast conserving
surgery. Oncology (Williston Park) 2017;31(5):415–420.
27. Rosenkranz KM, Balman K, McCall L, et al. The feasibility of breast-
conserving surgery for multiple ipsilateral breast cancer: an initial report
from ACOSOG Z11102 (Alliance) trial. Ann Surg Oncol
2018;25(10):2858–2866.
28. Kal HB, Struikmans H. Radiotherapy during pregnancy: fact and fiction.
Lancel Oncol 2005;6(5):328–333.
29. Kuerer HM, Gwyn K, Ames FC, et al. Conservative surgery and
chemotherapy for breast carcinoma during pregnancy. Surgery
2002;131(1):108–110.
30. Annane K, Bellocq JP, Brettes JP, et al. Infiltrative breast cancer during
pregnancy and conservative surgery. Fetal Diagn Ther 2005;20(5):442–
444.
31. Masetti R, Di Leone A, Franceschini G, et al. Oncoplastic techniques in
the conservative surgical treatment of breast cancer: an overview. Breast
J 2006;12(5 Suppl 2):S174–S180.
32. Chen AM, Obedian E, Hafty BG. Breast-conserving therapy in the
setting of collagen vascular disease. Cancer 2001;7(6):480–491.
33. Fleck R, McNeese MD, Ellerbrock NA, et al. Consequences of breast
irradiation in patients with pre-existing collagen vascular disease. Int J
Radiat Oncol Biol Phys 1989;17:829–833.
34. Robertson JH, Clarke DH, Pevzner MM, et al. Breast conservation
therapy: severe breast fibrosis after radiation therapy in patients with
collagen vascular disease. Cancer 1991;68:502–508.
35. Man VC, Cheung PS. Neoadjuvant chemotherapy increases rates of
breast-conserving surgery in early operable breast cancer. Hong Kong
Med J 2017;23(3):251–257.
36. Francheschini G, Di Leone A, Natale M, et al. Conservative surgery
after neoadjuvant chemotherapy in patients with operable breast cancer.
Ann Ital Chir 2018;89:290.
37. Boughey JC, McCall LM, Ballman KV, et al. Tumor biology correlates
with rates of breast-conserving surgery and pathologic complete
response after neoadjuvant chemotherapy for breast cancer: findings
from the ACOSOG Z1071 (Alliance) Prospective Multicenter Clinical
Trial. Ann Surg 2014;260(4):608–614; discussion 614–616.
38. Harvey JM, Clark GM, Osborne CK, et al. Estrogen receptor status by
immunohistochemistry is superior to the ligand-binding assay for
predicting response to adjuvant endocrine therapy in breast cancer. J
Clin Oncol 1999;17(5):1474–1481.
39. Tandon AK, Clark GM, Chamness GC, et al. Her-2/neu oncogene
protein and prognosis in breast cancer. J Clin Oncol 1989;7(8):1120–
1128.
40. Pertschuk LP, Kim DS, Nayer K, et al. Immunocytochemical estrogen
and progestin receptor assays in breast cancer with monoclonal
antibodies. Histopathologic, demographic, and biochemical correlations
and relationship to endocrine response and survival. Cancer
1990;66(8):1663–1670.
41. Elston CW, Ellis IO. Pathological prognostic factors in breast cancer. I.
The value of histological grade in breast cancer: experience from a large
study with long term follow up. Histopathology 1991;19(5):403–410.
42. Silverstein MJ, Lagios MD, Craig PH, et al. A prognostic index for
ductal carcinoma in situ of the breast. Cancer 1996;77:2267–2274.
43. Vargas C, Kestin L, Go N, et al. Factors associated with local recurrence
and cause-specific survival in patients with ductal carcinoma in situ of
the breast treated with breast-conserving therapy or mastectomy. Int J
Radiat Oncol Biol Phys 2005;63(5):1514–1521.
44. Morrow M, Van Zee KJ, Solin LJ, et al. Society of surgical oncology-
American Society for Radiation-Oncology-American Society of Clinical
Oncology Consensus Guideline on margins for breast-conserving
surgery with whole-breast irradiation in ductal carcinoma in situ. J Clin
Oncol 2016;34:4040–4046.
45. Moran MS, Schnitt SJ, Giuliano AE, et al. Society of Surgical
Oncology-American Society for Radiation Oncology consensus
guideline on margins for breast-conserving surgery with whole-breast
irradiation in stages I and II invasive breast cancer. J Clin Oncol
2014;32(14):1507–1515.
46. Houssami N, Macaskill P, Marinovich ML, et al. The association of
surgical margins and local recurrence in women with early-stage
invasive breast cancer treated with breast-conserving therapy: a meta
analysis. Ann Surg Oncol 2014;21(3):717–730.
47. Khatcheressian JL, Hurley P, Bantug E. Breast cancer follow-up and
management after primary treatment: American Society of Clinical
Oncology clinical practice guideline update. J Clin Oncol
2013;31(7):961–965.
CHAPTER 7

Axillary Nodal Recurrence


KRISTIN LIMBACH | JENNIFER R. GARREAU

Axillary nodal recurrence is a comparatively rare event after the treatment of


a primary breast cancer with axillary staging and targeted therapy to the
axilla, but it carries significant implications for the patient’s prognosis. Of
note, nodal recurrence in the supraclavicular and/or cervical regions is
considered distant nodal recurrence.
RATES OF AXILLARY NODAL RECURRENCE
Rates of axillary nodal recurrence vary between methods of surgical
management and whether radiotherapy is used. Early trials in the era of
mastectomy and axillary lymph node dissection as treatment for all breast
cancer patients, such as the National Surgical Adjuvant Breast and Bowel
Project (NSABP) B-04 trial, showed rates of regional recurrence that ranged
from 4% to 6% for women with negative nodes at their primary operation and
8% to 11% for women with positive nodes at their primary operation after 25
years of follow-up (1). Improvements in systemic and radiation therapy
appear to have lowered these rates, as was observed in 2000 by Katz et al.
who noted an isolated axillary nodal recurrence rate of 1.2% after adjuvant
systemic therapy (median follow-up 116 months) (2). It is also difficult to
extrapolate these rates to the modern era, as all the women in these studies
underwent axillary dissection, regardless of nodal status.
Similarly, prior to the wide acceptance of sentinel lymph node biopsy,
early reports of regional recurrence after breast-conserving therapy showed
rates of axillary recurrence of 1% to 3%, with the majority of these occurring
in previously unirradiated areas (3–5). The retrospective study by Fodor et al.
in 1999, in which 894 patients with early-stage breast cancer (49.2% node
positive) were observed for axillary recurrence after axillary dissection with
either mastectomy or breast-conserving therapy, found that those without
irradiation had a 1.2% axillary recurrence rate and those with had a 1.6% rate
of axillary nodal recurrence after median follow-up of 120 months (5).
The findings of the NSABP-32 trial, that sentinel lymph node biopsy
minimized side effects of surgical axillary staging without compromising
regional control or survival (6), ushered in the current era of sentinel lymph
node biopsy. However, the wide acceptance of sentinel lymph node biopsy
brought new concerns regarding axillary recurrence rates, particularly fears
that rates would significantly increase without routine performance of
complete axillary lymph node dissection. This has not been the case. A
number of studies have examined this question, of which one of the larger
retrospective studies is that by Naik et al. in 2004. The investigators of this
study included 2,340 patients who were prospectively entered into an
institutional database and had undergone sentinel lymph node biopsy with
negative sentinel lymph nodes between 1996 and 2003. Median follow-up
was 31 months. Of these patients, 81.1% had breast-conserving therapy and
18.9% underwent mastectomy. The total axillary nodal recurrence rate was
0.12%, with 0.04% as a first event, 0.04% occurring coincident with breast
recurrence, and 0.04% occurring coincident with distant recurrence (7).
Longer follow-up, though, has shown that long-term rates may be higher. The
Swedish Multicentre Cohort Study of over 2,000 patients found slightly
higher rates of axillary nodal recurrence for those with early-stage breast
cancer and negative sentinel lymph node biopsy (8), and the 10-year follow-
up study ultimately determined a total axillary recurrence rate of 1.6% as a
first, isolated event and an additional 1.0% rate of coincident axillary and
breast recurrence (9).
The landmark American College of Surgeons Oncology Group
(ACOSOG) Z0011 trial, which included women with T1 or T2 primary
tumors and clinically negative nodes undergoing breast-conserving therapy
with at least one positive sentinel lymph node on frozen section, initially
reported a regional recurrence rate of 0.9% at median follow-up of 6.3 years
(10). Long-term follow-up of this study ultimately found a rate of ipsilateral
axillary recurrence of 1.5% at 10 years with no significant difference between
the sentinel lymph node biopsy and axillary lymph node dissection arms (11).
Similar results were also noted in the International Breast Cancer Study
Group’s multicenter, randomized, controlled, noninferiority trial examining
sentinel lymph node biopsy alone versus axillary lymph node dissection in
women undergoing either breast-conserving therapy or mastectomy. Patients
who underwent sentinel lymph node biopsy alone and were noted to have
micrometastases within the sentinel lymph node(s) had a 2% axillary failure
rate (median follow-up of 9.7 years). When only patients who underwent
breast-conserving therapy were included, failure rate was <1%. Those who
underwent mastectomy had a 2% axillary failure rate when micrometastases
were present (12).
RISK FACTORS FOR AXILLARY RECURRENCE
A number of risk factors have been identified that increase the risk of axillary
nodal recurrence. Among studies that examine women who underwent
axillary lymph node dissection regardless of nodal status, node positivity has
emerged as one of the predominant risk factors (in Fodor et al., 0.5% axillary
recurrence for node negative vs. 2.8% for node positive, p = 0.0014) (4,5).
Age younger than 50 years, estrogen receptor–negative biology, and larger
tumor size were also associated with increased risk (4). However, a greater
tumor burden in the axilla appears to be a risk regardless of the type of
axillary surgical staging, as Houvenaeghel et al. in 2016 found that larger
metastases in sentinel lymph nodes were also associated with an increased
rate of axillary recurrence (13). This was confirmed by the work of Aalders et
al. in 2016, in which 52,626 breast cancer cases from the Netherlands Cancer
Registry were evaluated by the investigators. Those staged as N2–3 at
primary surgery had a significantly increased risk of axillary recurrence
within 5 years (14).
Among studies that included patients who underwent sentinel lymph node
biopsy, such as ACOSOG Z0011 and the Swedish Multicentre Cohort Study,
negative hormone receptor status was noted as a common risk factor (10-year
isolated axillary recurrence-free survival rate in the Swedish Multicentre
Cohort Study was 96.7% in hormone receptor–negative tumors compared
with 99.1% in luminal A biology tumors, p = 0.004) (8). Additional factors
noted in these studies included high histologic grade, multifocal tumors, and
larger tumor size (9,11).
TIME TO AXILLARY NODAL RECURRENCE
Historically, the accepted time to axillary recurrence was that reported by the
NSABP B-04 trial, which after 25 years of follow-up determined that the
majority of axillary nodal recurrences after axillary lymph node dissection
occur within the first 5 years. This study showed that 73% to 87% of axillary
recurrences occurred during this time for node-negative women and 91% to
94% for node-positive women (1). Katz et al. also reported the median time
to axillary recurrence for women who had undergone axillary lymph node
dissection, and in this study the investigators found a median time to
recurrence of 40 months for all patients combined, including node-negative
patients (2).
Time to axillary nodal recurrence appears to be similar after sentinel lymph
node biopsy. For a negative sentinel lymph node biopsy, 10-year follow-up of
the Swedish Multicentre Cohort Study found a median time to isolated
axillary recurrence of 46 months (range 4 to 157 months). Those with a high
histologic grade had a faster time to recurrence than those with a low- or
intermediate-grade primary tumor (median 29 vs. 50.5 vs. 88 months,
respectively, p = 0.032) (9). Time to recurrence is also similar after a positive
sentinel lymph node biopsy with subsequent whole breast irradiation, as
ACOSOG Z0011 reported a median time to regional recurrence of 4.0 years,
with only one patient having a regional recurrence after 76 months (11).
DIAGNOSIS
The National Comprehensive Cancer Network (NCCN) guidelines for
surveillance after treatment of a primary breast cancer recommend a history
and physical examination one to four times per year as clinically appropriate
for the first 5 years, then annually thereafter (15). The majority of axillary
nodal recurrence presents during this 5-year time frame (1), and physical
examination or mammography findings that are concerning for recurrence
should be seriously investigated.
The NCCN guidelines recommend that those with findings concerning for
recurrent disease should undergo a history and physical, laboratory testing
including a complete blood count and complete metabolic panel that contains
liver function tests and an alkaline phosphatase, a chest CT with contrast,
either an abdominal and pelvic CT with contrast or an MRI with contrast, a
bone scan or sodium fluoride PET/CT, an fluorodeoxyglucose-positron
emission tomography/computerized tomography FDG PET/CT) (optional),
and a biopsy of the first recurrent site with hormone receptor and HER-2
status testing (15). For concerns of axillary nodal recurrence, it is the authors’
practice to proceed with a dedicated axillary ultrasound with an image-guided
biopsy unless the area of palpable concern is fairly large and easily identified,
in which case a core needle biopsy without imaging can be performed. If the
patient endorses central nervous system symptoms, a brain MRI should also
be obtained, and if the patient complains of back pain or symptoms of spinal
cord compression a spine MRI with contrast should be performed (15).
TREATMENT AND PROGNOSIS
Once a diagnosis of axillary nodal recurrence has been confirmed by biopsy
and concurrent distal recurrence has been ruled out, the NCCN guidelines
recommend surgical resection to clear margins if possible and radiation if
possible, followed by consideration of systemic therapy. If clear margins
cannot be obtained, one may consider systemic therapy until best response is
reached, at which point resection should proceed if possible. Radiation may
not be an option due to the patient’s radiotherapy history (15).
These recommendations are based largely on studies examining patients
who underwent salvage surgical and radiotherapy after regional recurrence.
Two of these are the European Organization for Research and Treatment of
Cancer (EORTC) 10801 trial and the Dutch Breast Cancer Group (DBCG)
trial 82TM, which both accrued just over 900 patients over 6 years and
compared breast-conserving therapy with axillary lymph node dissection
versus mastectomy with axillary lymph node dissection. One hundred and
thirty-three patients from these two trials developed isolated locoregional
recurrence without concurrent distant recurrence, and the majority underwent
salvage therapy with curative intent, which constituted either radiotherapy
with or without excision for patients who had previously undergone
mastectomy and excision with or without radiotherapy for those who had
previously undergone breast-conserving therapy. A portion of patients (39%
of the mastectomy patients and 27% of breast-conserving therapy patients)
were also given additional adjuvant systemic therapy. The 5-year survival
rates in these studies were 58% and 59% for the mastectomy and breast-
conserving therapy patients, respectively (16). Konkin et al. also investigated
patient prognosis after axillary recurrence. The investigators found an
improved 5-year overall survival rate with a combination of surgery and
radiation (63% vs. 38.3%, p < 0.001), and they noted an improvement with
the addition of systemic therapy (p = 0.02) (17). This was confirmed by the
Chemotherapy as Adjuvant for LOcally Recurrent breast cancer (CALOR)
trial, which accrued 162 patients with resected isolated locoregional
recurrence between 2003 and 2010 and randomized them to adjuvant
systemic therapy versus no further systemic therapy. The 5-year disease-free
survival rate was 69% for those with adjuvant chemotherapy (vs. 57%, p =
0.046) and the 5-year overall survival rate was 88% (vs. 76%, p = 0.02), with
chemotherapy noted to be more effective in hormone receptor–negative
cancers (18). Final analysis after 10 years of follow-up confirmed that benefit
was predominantly in hormone receptor–negative locoregional recurrence
and did not support the use of adjuvant chemotherapy for estrogen receptor–
positive cancers (19).
SUMMARY
Axillary nodal recurrence is an uncommon event after primary breast cancer
treatment that includes surgical axillary staging, typically occurring in 1% to
3% of cases. Patients with a higher axillary tumor burden as well as those
with age younger than 50, larger and/or multifocal tumor, high histologic
grade, and/or hormone receptor–negative biology may be at higher risk of
axillary recurrence. Recurrences should be treated with surgical resection and
radiation therapy if possible, and consideration should be given to adjuvant
systemic therapy, especially in hormone receptor–negative cancers. Although
axillary nodal recurrence is associated with a poorer prognosis, patients
treated per these recommendations may have 5-year overall survival rates up
to 90%.

REFERENCES

1. Fisher B, Jeong JH, Anderson S, et al. Twenty-five-year follow-up of a


randomized trial comparing radical mastectomy, total mastectomy, and
total mastectomy followed by irradiation. N Engl J Med
2002;347(8):567–575.
2. Katz A, Strom EA, Buchholz TA, et al. Locoregional recurrence patterns
after mastectomy and doxorubicin-based chemotherapy: implications for
postoperative irradiation. J Clin Oncol 2000;18(15):2817–2827.
3. Wapnir IL, Anderson SJ, Mamounas EP, et al. Prognosis after ipsilateral
breast tumor recurrence and locoregional recurrences in five National
Surgical Adjuvant Breast and Bowel Project node-positive adjuvant
breast cancer trials. J Clin Oncol 2006;24(13):2028–2037.
4. Harris EE, Hwang WT, Seyednejad F, et al. Prognosis after regional
lymph node recurrence in patients with stage I-II breast carcinoma
treated with breast conservation therapy. Cancer 2003;98(10):2144–
2151.
5. Fodor J, Toth J, Major T, et al. Incidence and time of occurrence of
regional recurrence in stage I-II breast cancer: value of adjuvant
irradiation. Int J Radiat Oncol Biol Phys 1999;44(2):281–287.
6. Mamounas EP. NSABP breast cancer clinical trials: recent results and
future directions. Clin Med Res 2003;1(4):309–326.
7. Naik AM, Fey J, Gemignani M, et al. The risk of axillary relapse after
sentinel lymph node biopsy for breast cancer is comparable with that of
axillary lymph node dissection: a follow-up study of 4008 procedures.
Ann Surg 2004;240(3):462–468; discussion 468–471.
8. Bergkvist L, de Boniface J, Jonsson PE, et al. Axillary recurrence rate
after negative sentinel node biopsy in breast cancer: three-year follow-
up of the Swedish Multicenter Cohort Study. Ann Surg
2008;247(1):150–156.
9. de Boniface J, Frisell J, Bergkvist L, et al; Swedish Breast Cancer Group
and the Swedish Society of Breast Surgery. Ten-year report on axillary
recurrence after negative sentinel node biopsy for breast cancer from the
Swedish Multicentre Cohort Study. Br J Surg 2017;104(3):238–247.
10. Giuliano AE, McCall L, Beitsch P, et al. Locoregional recurrence after
sentinel lymph node dissection with or without axillary dissection in
patients with sentinel lymph node metastases: the American College of
Surgeons Oncology Group Z0011 randomized trial. Ann Surg
2010;252(3):426–432; discussion 432–433.
11. Giuliano AE, Ballman K, McCall L, et al. Locoregional recurrence after
sentinel lymph node dissection with or without axillary dissection in
patients with sentinel lymph node metastases: long-term follow-up from
the American College of Surgeons Oncology Group (Alliance)
ACOSOG Z0011 randomized trial. Ann Surg 2016;264(3):413–420.
12. Galimberti V, Cole BF, Viale G, et al. Axillary dissection versus no
axillary dissection in patients with breast cancer and sentinel-node
micrometastases (IBCSG 23-01): 10-year follow-up of a randomised,
controlled phase 3 trial. Lancet Oncol 2018;19(10):1385–1393.
13. Houvenaeghel G, Classe JM, Garbay JR, et al. Survival impact and
predictive factors of axillary recurrence after sentinel biopsy. Eur J
Cancer 2016;58:73–82.
14. Aalders KC, van Bommel AC, van Dalen T, et al. Contemporary risks of
local and regional recurrence and contralateral breast cancer in patients
treated for primary breast cancer. Eur J Cancer 2016;63:118–126.
15. National Comprehensive Cancer Network. 2019. Clinical Practice
Guidlines in Oncology. Breast Cancer (Version 1.2019).
https://www.nccn.org. Accessed April 2019.
16. van Tienhoven G, Voogd AC, Peterse JL, et al. Prognosis after treatment
for loco-regional recurrence after mastectomy or breast conserving
therapy in two randomised trials (EORTC 10801 and DBCG-82TM).
EORTC Breast Cancer Cooperative Group and the Danish Breast
Cancer Cooperative Group. Eur J Cancer 1999;35(1):32–38.
17. Konkin DE, Tyldesley S, Kennecke H, et al. Management and outcomes
of isolated axillary node recurrence in breast cancer. Arch Surg
2006;141(9):867–872; discussion 872–874.
18. Aebi S, Gelber S, Anderson SJ, et al. Chemotherapy for isolated
locoregional recurrence of breast cancer (CALOR): a randomised trial.
Lancet Oncol 2014;15(2):156–163.
19. Wapnir IL, Price KN, Anderson SJ, et al. Efficacy of chemotherapy for
ER-negative and ER-positive isolated locoregional recurrence of breast
cancer: final analysis of the CALOR trial. J Clin Oncol
2018;36(11):1073–1079.
CHAPTER 8

Role of Nonsurgical Management of


Breast Cancer: Endocrine Therapy
and Tumor Ablation
DENNIS R. HOLMES

The optimal surgical approach to the management of localized early-stage


breast cancer is breast-conserving surgery combined with adjuvant
radiotherapy and systemic therapy, or both. This approach has been
supported by multiple randomized controlled trials that have demonstrated
comparable breast cancer–specific and overall survival among women treated
with breast-conserving therapy compared to mastectomy. However, by
comparison, breast-conserving therapy is associated with less cosmetic
impairment, enhanced surgical recovery, more rapid return to daily activities,
improved sexual function, and an overall improvement in quality of life.
Despite the large body of data supporting primary surgical management of
early-stage breast cancer, the increasing appreciation of shared decision
making between patients and physicians provides the ethical and legal
context for considering nonoperative strategies to manage breast cancer for
individual women who for personal and health reasons are seeking an
alternative to traditional surgery. Furthermore, in the absence of data showing
inferior breast cancer–specific and overall survival outcomes with
nonoperative management, it is reasonable for surgeons and patients to
include nonoperative strategies when discussing the benefits, risks, and
alternatives of traditional surgery.
The opportunity for nonoperative management of breast cancer has been
facilitated by the widespread use of screening mammography, which has
contributed to the more frequent diagnosis of small, node-negative breast
cancers, creating an opportunity for less-invasive and noninvasive
management options. Furthermore, the trend favoring targeted local therapy
reflects several important clinical observations: control of local disease can
be achieved by a variety of strategies targeted at the tumor site; tumor
biology is more important than tumor anatomy for estimating prognosis and
predicting response to systemic therapy; control of systemic disease, not
extent of local treatment, is the chief determinant of overall survival; and
surgical removal of lymph nodes is of diminishing significance.
Nonsurgical management of breast cancer can be categorized based on its
intent (curative vs. palliative) or by the modality by which it is provided
(systemic therapy, radiotherapy, or percutaneous ablation). This chapter will
review the most common nonoperative alternatives to breast-conserving
surgery and the evidence supporting each approach. Apart from its potential
role in the management of poor surgical candidates, a more important factor
contributing to growing interest in nonsurgical management of breast cancer
is the increasing population of elderly breast cancer patients, most of whom
are more likely to die from intercurrent disease rather than breast cancer.
PRIMARY ENDOCRINE THERAPY
In contrast with neoadjuvant endocrine therapy to facilitate tumor
downstaging prior to surgery, primary endocrine therapy has been the focus
of numerous studies since this approach was first introduced by Preece et al.
in 1983 as an alternative to surgery in frail and elderly women (1). The
rationale for primary endocrine therapy is that estrogen receptor–positive
disease is the predominant type of breast cancer among elderly patients and
that these patients are most likely to die from nonbreast cancer causes. Thus,
endocrine therapy could provide a means to preserve quality of life while also
limiting symptomatic local and systemic disease progression.
Seven randomized controlled trials have compared tamoxifen alone to
primary surgery (mastectomy or wide local excision) with or without
tamoxifen therapy in women aged 70 and older. Though unrepresentative of
younger women or those with hormone receptor-negative disease, a meta-
analysis of the randomized controlled trials revealed a key finding that should
guide the informed consent discussion when considering primary endocrine
therapy: with up to 28 years of follow-up, there was no difference in the
breast cancer–specific or overall survival between women treated with
tamoxifen alone and those treated with surgery with or without tamoxifen (2).
Furthermore, a single randomized controlled trial found no quality-of-life
differences between the two groups (3). However, despite the lack of a
survival advantage to primary surgical resection, all randomized controlled
trials demonstrated lower disease-free survival with primary endocrine
therapy which led to local disease progression and recommendations for
surgical intervention in a majority of patients.
Although randomized controlled trials showed no survival advantage of
tamoxifen alone over surgery, interpretation of the meta-analysis is limited by
the fact that all trials were initiated in an era before routine testing of tumor
receptors. However, based on the distribution of tumor receptor by age,
approximately 10% of study subjects would have had hormone receptor–
negative disease and would not have benefitted from endocrine therapy (4).
The modern use of genomic assays greatly increases the odds of identifying
the subset of tumors that is likely to be keenly sensitive to primary endocrine
therapy regardless of age, tumor size, or nodal status. Furthermore, none of
the trials utilized third-generation aromatase inhibitors, a more effective
alternative to tamoxifen and the current standard of care for postmenopausal
women with hormone receptor–positive breast cancer.
Optimal breast cancer therapy employs both surgery and endocrine
therapy, not one or the other. However, for the patient opposed to surgery due
to personal values or health state, the available data support the compliant use
of endocrine therapy for hormone-sensitive breast cancer. The decision to
proceed with primary endocrine therapy should consider the fact that a large
proportion of patients treated with primary endocrine therapy ultimately
require surgical intervention for management of disease progression, which
could potentially be associated with greater surgical morbidity and greater
quality-of-life impairment than would have been encountered had the tumor
been resected when less extensive and when the patient was relatively more
fit.
IN SITU ABLATION
In situ ablation performed under image guidance is a minimally invasive
nonsurgical approach to cancer therapy. Using different types of thermal
energy to destroy tumor cells, the main aim of in situ ablation is the
destruction of the primary lesion as well as an adjacent margin of
surrounding normal breast tissue, treating essentially the same volume of
breast tissue that would be removed with lumpectomy.
There are several potential advantages to in situ ablation as an alternative
to surgery. In situ ablation has the potential to eliminate the morbidity of
primary surgery (e.g., symptomatic seroma, hematoma, infection). Most in
situ ablation procedures can be performed in the office setting under local
anesthesia or conscious sedation, eliminating common side effects of general
anesthesia (e.g., nausea, vomiting) and avoiding exacerbation of preexisting
comorbidities. In situ ablation also greatly reduces the quality-of-life impact
of surgery by enhancing surgical recovery and expediting return to usual
activities. Depending on the technique, in situ ablation may be performed
percutaneously via a scar of a few millimeters length or transcutaneously,
avoiding a scar altogether. Since no breast tissue is removed, in situ ablation
preserves breast volume and symmetry while eliminating the need for
preemptive or corrective surgical procedures to maintain or restore breast
volume, contour, and symmetry. As a result, in situ ablation has the ability to
minimize or completely eliminate the adverse cosmetic effects of tumor
resection.
There are currently no randomized controlled trials comparing the efficacy
or safety of in situ ablation to conventional surgery. However, numerous
relatively small publications have reported the feasibility of various types of
in situ ablation, nearly all involving ablation followed by surgical resection.
Though individual trial results vary widely, a systematic review and meta-
analysis of 45 studies involving 1,156 patients demonstrated that image-
guided in situ ablation achieved a high level of technical success (96% [93%
to 98%]), a moderate rate of complete tumor ablation (75% [49% to 90%],
and a low rate of major complications (6% [4% to 8%], e.g., skin necrosis
and pneumothorax) and minor complications (8% [5% to 13%], e.g., grade 1
and 2) (Table 8-1) (5). These findings were assessed to be independent of
tumor size although most studies involved tumors under 3 cm. While the
moderate rate of complete tumor ablation falls well below the threshold that
would be accepted for a breast cancer therapy, the widely variant outcomes
summarized in the meta-analysis capture the historical learning curves of
each of the in situ ablation approaches most of which have since undergone
significant technical and/or procedural modification to improve technical
success, efficacy, safety, and patient selection.
Patient Selection
The ideal patient for in situ ablation has yet to be fully established since little
long-term outcome data exist for patients treated with in situ ablation without
surgical resection. Based on the results of postablation excision trials,
multiple tumor characteristics have been correlated with successful ablation:
unifocality, invasive ductal carcinoma histology, size ≤1.5 cm; well-
demarcated borders by mammogram, ultrasound, and/or MRI; and a low
percentage of ductal carcinoma in situ. On the other hand, larger or multifocal
tumors, invasive lobular histology, poorly visualized lesions, or tumors with
an extensive intraductal component have been correlated with a high rate of
incomplete ablation. At present, there is no indication that the ablation
technique should be influenced by these patient selection criteria.
Complications and procedural discomfort can also be minimized by
selecting patients with tumors >1 cm from the nearest skin or chest wall.
However, depending on the ablation approach, the risk of thermal skin injury
can be reduced with the use of coolant spray and ice packs to lower skin
temperature, warm packs to raise skin temperature, or injection of saline or
5% glucose solution adjacent to the skin or chest wall.

TABLE 8-1 Summary of Data From a Systemic Review of 45 Publications


In Situ Ablation Techniques
Cryoablation
Cryoablation (cryosurgery, cryotherapy, or targeted cryoablation therapy) is
the use of ultrafreezing temperatures to induce cytodestruction of diseased
tissues. Modern cryoablation units are liquid nitrogen-based systems that
utilize a disposable needle–like handheld probe and a control console. The
internal design of the cryoprobe consists of three concentric tubes: an inner
tube through which high-pressure liquid nitrogen flows from the console
toward the distal end of the cryoprobe tip, a middle tube that conducts
gaseous nitrogen from the distal end of the cryoprobe back to the console,
and a vacuum-insulated outer tube that prevents inadvertent freezing of
tissues along the length of the cryoprobe (6). A valve at the end of the inner
tube causes high-pressure liquid nitrogen to vaporize before leaving the
cryoprobe through the middle tube. This liquid-to-gaseous phase transition
causes the temperature of the gas to drop (the Joule–Thompson effect), which
extracts heat from the tissue surrounding an uninsulated segment of the
cryoprobe. Continuous flow of liquid nitrogen lowers the central probe
temperature to −160° to −190°C. An alternative method of cryoablation
employs liquid argon, which similar to liquid nitrogen, cause a marked
reduction in central probe temperature (-180° to -190°C) during the phase
change from liquefied argon to argon gas. For both liquid nitrogen and liquid
argon based systems, cryoprobe thawing in accomplished with the use of a
built-in electrical heating element.
Cryoablation induces cytodestruction through five key mechanisms: cell
membrane damage caused by fluid shifts of water between intracellular and
extracellular spaces (osmotic injury); nuclear, mitochondrial, and intracellular
cytoskeleton damage caused by intracellular ice crystal formation
(mechanical injury); thrombosis, reperfusion injury, and direct mechanical
damage of tumor vasculature (vascular injury); programmed cell death at the
border of the ablation zone induced by sublethal temperatures (typically −10°
to 6°C) (apoptotic injury); and immune response to tumor-specific antigens
exposed by osmotic and mechanical damage (immunogenic injury) (6,7). A
relatively long thaw phase and rapid rate of freeze are the major factors
contributing to ice crystal formation and osmotic injury and hence to the
magnitude of cytodestruction. Unlike the hyperthermic ablation techniques
where protein denaturation is the primary means of protein damage,
cryoablation generally maintains the secondary and tertiary structure of tumor
proteins which enhances their ability to induce an immune response. The
clinical significance of a breast cancer–specific antigen-mediated immune
response, which might have both local and systemic benefits, is currently the
focus of the expanding field of cancer cryoimmunology (8–10).
Breast cryoablation is typically performed under ultrasound guidance, but
MRI compatible systems also exist. After making a small (3-mm)
dermotomy, the cryoprobe is inserted under image guidance through the
center of the tumor to position the uninsulated segment of the cryoprobe
through the central axis of the tumor. Real-time monitoring of ice ball
formation permits intermittent injection of saline between the overlying skin
and expanding ice ball to prevent thermal skin damage; the underlying chest
wall is more resistant to thermal damage. Skin injury can also be reduced by
the use of a heating pad or warmed water bottle applied to the skin surface.
Cryoablation is almost exclusively performed in the office setting under local
anesthesia facilitated by the fact that the tissue chilling has a direct analgesic
effect on the breast. A single cryoablation procedure consists of two freeze
cycles separated by a 10-minute thaw cycle. Total treatment time is typically
less than 30 minutes.
Radiofrequency Ablation
Radiofrequency ablation (RFA) utilizes a high-frequency (100- to 500-KHz)
current to induce agitation or frictional heating of water molecules,
generating heat to induce hyperthermia of surrounding tissues. RFA is
administered using an insulated, internally cooled, needle electrode equipped
with 4 to 11 retractable arrays which may be expanded to a maximum
diameter of 7 cm when fully deployed, depending on the length of the arrays
and the electrode design (11,12). The radiofrequency electrode is inserted
through a small dermotomy and passed under image guidance through the
central axis of the tumor. Electrode placement is performed under ultrasound
or stereotactic guidance as available RFA equipment is not MRI compatible.
Once positioned, the arrays are then deployed until the tips of the arrays
reach the edges of the tumor. The electrode is attached to a monopolar
radiofrequency generator supplied with internal circuitry to monitor
impedance, and grounding pads are applied to each thigh to complete the
current circuit. As treatment is initiated, alternating currents flow into the
tumor from the uninsulated tip of the electrode to cause friction between
water molecules as they try to follow the direction of the alternating current.
Power is gradually increased in increments until tissue impedance rises
rapidly, indicating that coagulative necrosis has occurred (11).
Thermocouples integrated into the tips of each array permit real-time,
continuous monitoring of tissue temperature. Tumor cell death begins when
tissue reaches 60°C, though temperatures as high at 100°C are commonly
achieved. In addition to coagulative necrosis, hyperthermia causes tissue
dehydration, cell membranes thermal injury, cytoskeleton and nuclear protein
destruction, and DNA replication disruption (13). Macroscopically, this
produces a central area of charring along the electrode tract surrounded by a
rim of coagulative necrosis and an outer ring of hemorrhagic, hyperemia
tissue.
RFA is commonly performed under general anesthesia but may also be
performed under conscious sedation and/or local anesthesia following
injection of a generous amount of local anesthetic around the tumor and
along the chest wall. Treatment may be completed in one or more <15-minute
sessions depending on tumor size, tumor vascularity, and breast tissue
composition, among other factors. One ablation session is typically sufficient
for a tumor 2 cm or less.

High-Intensity Focused Ultrasound


High-intensity focused ultrasound (HIFU) focuses multiple, sublethal,
converging pressure waves transdermally at a small volume target, producing
frictional heat at the focal point while sparing other tissues in the beam path.
As no skin incision is required, HIFU is a transcutaneous in situ ablation
technique that is truly noninvasive. HIFU systems utilize two transducers,
one higher-frequency (1- to 20-MHz) diagnostic transducer for visualizing
and targeting the lesion and a second lower-frequency (0.8- to 3.5-MHz)
therapeutic transducer for delivering high-frequency pressure waves to the
target volume (14,15). HIFU may be performed under ultrasound or MRI
guidance, either of which permits real-time assessment of treatment efficacy.
Ultrasound-guided systems are less costly and more mobile but have less
anatomic resolution compared to MRI-guided systems. Ultrasound-guided
systems are equipped with skin thermocouples that cool the skin adjacent to
the transducer. Ultrasound-guided systems also allow real-time visualization
of the ablation volume which appears at a hyperechoic area of coagulative
necrosis as the energy level reaches a therapeutic temperature (15). Treatment
is continued as a series of overlapping sonication pulses, each less than 1 cm
in maximal diameter, under direct visualization until the entire target volume
is treated. Cytodestruction is accomplished through nonlinear wave
propagation and cavitation which causes coagulative necrosis and
denaturation of proteins at tissue temperatures exceed 60°C (16,17).
MRI-guided HIFU system consists of the MRI unit, the HIFU workstation
and console which controls all components of the ultrasound system, and a
modified MRI table containing a water bath equipped with a concave-shaped,
multielement phased array transducer mounted on a mechanical arm. A
personal computer supplied with the HIFU workstation enables control of
both the MRI unit and HIFU console, monitoring of the power output, and
termination of the power output if preset safety thresholds are breached
(15,18). The water bath is filled with cooled, degassed water to eliminate air
between the transducer and skin surface and to prevent thermal skin injuries.
Compared to ultrasound-guided HIFU, MRI-guided HIFU has the
advantage of improved anatomic resolution and sensitivity for detection of
invasive cancer, as well as the ability to perform an MRI immediately after
the procedure to assess residual tissue perfusion in the ablation zone.
Notwithstanding the fact that temperature mapping may be reduced in fatty
breast tissues, MRI systems can enable temperature mapping of the target
volume to enhance the accuracy of treatment planning and assessment of
treatment efficacy.
With MRI-guided HIFU, successive pulses of cigar-shaped (1- to 3-mm
diameter × 8- to 15-mm axial length) sonication pulses are delivered in a grid
guided by tumor anatomy and a temperature map to ensure treatment of the
entire target volume (18). Treatment time is determined by tumor volume.
Unlike ultrasound-guided HIFU which is performed in the supine position,
MRI-guided HIFU is performed in the prone position which necessitates
immobilization of the breast to minimize movement caused by breathing.
General anesthesia or conscious sedation also reduces patient movement due
to positional discomfort and pain. Each sonication pulse lasts less than 2
minutes followed by a brief cooling period (30 to 60 seconds) to minimize
overheating of tissues outside the target zone. Typical treatment time is 2
hours for a tumor 3 cm or less.
LASER Thermotherapy
Laser technology ablation employs a micrometer diameter flexible quartz
optic fiber to transmit a predetermined quantity of laser energy to the center
of a tumor. The laser fiber is inserted percutaneously through a 16- to 18-
gauge steel trocar, positioning the rounded tip of the laser just beyond the end
of the trocar when fully deployed (19). The laser fiber is a Nd:YAG
continuous pulse-wave laser that emits infrared light with spherical symmetry
with energy output up to 100 W (20). An infusion of saline through the trocar
at 0.5 to 2.0 mL/hr keeps the tip of the catheter from exceeding 100°C, avoids
carbonization of the laser tip, and improves transmission of laser energy to
the edges of the tumor. Continuous monitoring of the peripheral tumor
temperature is accomplished with the use of a copper multisensory thermal
probe inserted parallel to and 1 cm away from the optic fiber, with the tip of
the thermal probe extending 1 cm beyond the end of the laser. During laser
ablation, laser energy transmission is continued until core temperature is
maintained between 80° and 100°C and peripheral temperature is maintained
at 60°C. Temperature feedback control is provided by a personal computer
and automatic thermotherapy system connected to the thermal probe (21).
The resulting ablation zone consists of a central core of carbonized, necrotic
tissue surrounded by a zone of coagulative necrosis and an outer rim of
inflammation and hyperemia. Laser ablation may be performed under local
anesthesia using stereotactic, MRI, or ultrasound guidance. Typical treatment
time is 30 minutes for a tumor 3 cm or less.
Microwave Ablation
Microwave ablation or microwave coagulation utilizes a microwave
generator, a flexible coaxial cable, and an internally cooled antenna
containing a 2-mm irradiating port located 1 cm from the tip of the antenna
(22). Through a small dermotomy, the antenna is inserted under imaging
guidance through the central axis of the tumor, then connected to the
microwave generator via the coaxial cable. After attachment of the antenna
shaft to a circulating cooling water source, the microwave is activated to
produce an elliptical zone of ablation reaching temperatures of 60° to 90°C.
Microwave ablation may be evaluated real time under ultrasound guidance,
which displays transient loss of tumor hypogenicity as ablation occurs.
Average treatment time is less than 10 minutes for tumors 3 cm or less.
Microwave ablation has potential advantages over other types of in situ
ablation due to its ability to ablate larger volumes of tissue with greater
rapidity.
CONCLUSION

Limitations
There are several practical limitations to the in situ ablation of breast cancer.
Foremost is the lack of long-term outcome data for women treated with in
situ ablation without subsequent surgical resection. However, the most
promising experience reported to date is a single center study of luminal A
invasive ductal carcinoma measuring ≤1.5 cm treated with cryoablation,
whole breast radiotherapy, sentinel node biopsy, and endocrine therapy,
demonstrating a 0.98% (3/304) local recurrence rate at 6-year median follow-
up. While clearly a low-risk group, each of these patients would likely have
been managed with lumpectomy or mastectomy if not for the opportunity to
undergo cryoablation.
Although available evidence indicates a high potential to induce tumor
kills, in situ ablation does not permit confirmation of the adequacy of surgical
margins. Consequently, optimal target volume should include the primary
lesion as well as a 5- to 10-mm margin of surrounding tissue. Ultimately, the
ability to target a tumor for successful ablation depends on how well the
anatomic extent of disease is displayed by available imaging. Thus, it’s a
matter of patient selection.
Both surgery and in situ ablation produce a palpable mass at the tumor site
where previously there might have been none. Following surgery or in situ
ablation, the palpable lump might take months or years to resolve. However,
unlike surgery where there is histologic confirmation of tumor removal,
patients treated with in situ ablation must be advised to expect a persistent
mass at the ablation site which may take one or more years to become
impalpable depending on initial ablation volume, tumor location, and breast
density. A planned follow-up core needle biopsy of the ablation site weeks or
months post ablation should reduce patient and physician anxiety about the
significance of a persistent mass.
Follow-up surveillance imaging might also be a source of anxiety for
physicians who are unfamiliar within the mammographic, sonographic, or
MRI appearance of a breast that has been treated with in situ ablation. This
challenge will gradually be overcome as in situ ablation grows in popularity
and as future publications expand the knowledge base regarding temporal
postablation imaging characteristics. However, based on the available
evidence, contrast-enhanced MRI exhibits the best balance of sensitivity and
specificity for postablation imaging, revealing in successful ablation cases a
nonenhancing ablation zone surrounded by a thin rim of peripheral
enhancement (11,23).
Finally, an essential consideration when evaluating in situ ablation as an
alternative to surgery is that in situ ablation does not obviate the need or
potential benefit of adjuvant radiotherapy or adjuvant systemic therapy, both
of which contribute significantly to reducing the risk of local, regional, and
systemic recurrence.

REFERENCES

1. Preece P, Wood R, Mackie C, et al. Tamoxifen as initial sole treatment


of localized breast-cancer in elderly women—a pilot study. Br Med J
1982;284(6319):869–870.
2. Morgan JL, Reed MW, Wyld L. Primary endocrine therapy as a
treatment for older women with operable breast cancer—a comparison
of randomized controlled trial and cohort study findings. Eur J Surg
Oncol 2014;40:676–684.
3. Bates T, Riley DL, Houghton J, et al. Breast cancer in elderly women: a
cancer research campaign trial comparing treatment with tamoxifen and
optimal surgery with tamoxifen alone. Br J Surg 1991;78:591–594.
4. Shacher SS, Jolly TA, Jones E, et al. Management of triple-negative
breast cancer in older patients: how is it different? Oncology
2018;32(2):58–63.
5. Mauri G, Sconfienza LM, Pescatori LC, et al. Technical success,
technique efficacy and complications of minimally-invasive imaging-
guided percutaneous ablation procedures of breast cancer: a systematic
review and meta-analysis. Eur Radiol 2017;27:3199–3210.
6. Rubinsky B. Cryosurgery. Ann Rev Biomed Eng 2000;02:157–187.
7. Sidana A. Cancer immunotherapy using tumor cryoablation.
Immunotherapy 2014;6(1):85–93.
8. McArthur HL, Diab A, Page D, et al. A pilot study of preoperative
single-dose ipilimumab and/or cryoablation in women with early-stage
breast cancer with comprehensive immune profiling. Clin Cancer Res
2016:22(23):5729–5737.
9. Liang S, Niu L, Xu K, et al. Tumor cryoablation in combination with
natural killer cells therapy and Herceptin in patients with HER2-
overexpressing recurrent breast cancer. Mol Immunol 2017;92:45–53.
10. Kudo-Saito C, Fuwa T, Kawakami Y. Targeting ALCAM in the cryo-
treated tumour microenvironment successfully induces systemic anti-
tumor immunity. Eur J Cancer 2016;62:54–61.
11. Ohtani S, Kochi M, Ito M, et al. Radiofrequency ablation of early breast
cancer followed by delayed surgical resection—a promising alternative
to breast-conserving surgery. Breast 2011;20:431–436.
12. Burak WE, Agnese DM, Povoski SP, et al. Radiofrequency ablation of
invasive breast carcinoma followed by delayed surgical excision.
Cancer 2003;98:1369–1376.
13. Nagashima T, Sakakibara M, Sangai T, et al. Surrounding rim formation
and reduction in size after radiofrequency ablation for primary breast
cancer. Jpn J Radiol 2009;27:197–204.
14. Merckel LG, Bartels LW, Kohler MO, et al. MR-guided high-intensity
focused ultrasound ablation of breast cancer with a dedicated breast
platform. Cardiovasc Intervent Radiol 2013;36:292–301.
15. Peek MCL, Wu F. High-intensity focused ultrasound in the treatment of
breast tumors. Ecancermedicalscience 2018;12:794.
16. Haar T, Coussios C. High intensity focused ultrasound: physical
principle and devices. Int J Hyperthermia 2007;23(2):89–104.
17. Zderic V, Keshavarzi A, Andrew MA. Attenuation of porcine tissues in
vivo after high-intensity ultrasound treatment. Ultrasound Med Biol
2004;30(1):61–66.
18. Gianfelice D, Khiat A, Boulanger Y, et al. Feasibility of magnetic
resonance imaging-guided focused ultrasound surgery as an adjunct to
tamoxifen therapy in high-risk surgical patients with breast carcinoma. J
Vasc Interv Radiol 2003;14:1275–1282.
19. Dowlatshahi K, Fan M, Gould VE, et al. Stereotactically guided laser
therapy of occult breast tumors. Arch Surg 2000;135:1345–1352.
20. Van Esser S, Stapper G, van Diest P. Ultrasound-guided laser-induced
thermal therapy for small palpable invasive breast carcinomas: a
feasibility study. Ann Surg Oncol 2009;16:2259–2263.
21. Haraldsdottir KH, Ivarsson K, Gotberg S, et al. Interstitial laser
thermotherapy (ILT) of breast cancer. Eur J Surg Oncol
2008;34(7):739–745.
22. Zhou W, Zha X, Liu X, et al. US-guided percutaneous microwave
coagulation of small breast cancers: a clinical study. Radiology
2012;263(2):364–373.
23. Furusawa H, Namba K, Thomsen S, et al. Magnetic resonance-guided
focused ultrasound surgery of breast cancer: reliability and
effectiveness. J Am Coll Surg 2006;203:54–63.
CHAPTER 9

Oncoplastic Approach to Maximizing


the Lumpectomy-Level I
PAMELA LI | JILL R. DIETZ

The role of breast conservation, partial mastectomy with adjuvant radiation,


in the surgical management of breast cancer has shown equivalent disease-
free and overall survival to that of mastectomy with improved aesthetic
outcomes, quality of life, and patient satisfaction (1). There are however
limitations to breast conservation. For breast conservation to be successful,
adequate negative surgical margins need to be achieved with a cosmetically
acceptable result. In some instances, the extent of tissue that needs to be
excised might compromise the resulting breast cosmesis. In this
circumstance, a patient would be offered mastectomy.
Many patients still desire breast conservation, even when a large volume
resection of tissue is required. Additionally, given the importance of patient
appearance and satisfaction after treatment, there has been a drive to improve
cosmetic outcomes after breast cancer surgery and treatment. With this came
the development of oncoplastic breast surgery.
GOALS AND BENEFITS OF ONCOPLASTIC BREAST SURGERY
The primary goal of oncoplastic breast surgery is to optimize oncologic and
cosmetic outcomes of breast conservation. Oncoplastic breast surgery allows
for large cancer resections with reshaping of the breast performed during the
same operation. Because of this, oncoplastic surgery facilitates partial
mastectomy, especially in the setting of more extensive resections in patients
who previously would be offered mastectomy. Oncoplastic surgery has been
shown to reduce mastectomy and reexcision rates with improved cosmetic
results and increased patient satisfaction (2). Because the cancer resection
and reconstruction are performed during the same surgery, it avoids a
subsequent surgery to repair a cosmetic deformity. Partial mastectomy also
requires less recovery time and decreased surgical morbidity when compared
to mastectomy.
LEVEL I VERSUS LEVEL II ONCOPLASTIC TECHNIQUES
There are a wide variety of techniques and procedures used in oncoplastic
breast surgery. These can be more broadly divided into two categories: level I
versus level II procedures (3). They are categorized based on the volume of
tissue excised and the degree of complexity necessary to reshape the breast
mound. Level I procedures involve resection of less than 20% of the breast
volume; these are the focus of this chapter. Level I techniques include
glandular flaps that can be advanced or rotated to fill the lumpectomy cavity.
Level II procedures are more complex. These include resection of more than
20% of the breast volume and the reconstruction of the breast usually
involves mammoplasty techniques. Level II procedures often also involve
excision of skin and are sometimes performed in conjunction with a plastic
surgeon. Glandular density should also be considered in choosing the optimal
oncoplastic techniques. When the breast tissue is fattier in composition, level
II techniques will often provide a superior cosmetic result. When level large
tumor resections are performed without level II techniques, the cosmetic
result can be compromised (Fig. 9-1).
PERFORMING LEVEL I ONCOPLASTIC SURGERY

Preoperative Evaluation
All patients undergoing a breast cancer surgery should be considered a
candidate for oncoplastic surgery. The assessment begins at the initial
surgical consultation. Pertinent patient history includes complicating medical
conditions, prior radiation, and smoking history. Physical examination should
assess breast size, breast shape, degree of breast ptosis, and skin quality. Prior
incisions should also be noted. Patient discussion should include their
aesthetic desires and goals with regard to breast size and shape.

FIGURE 9-1 Aesthetically placed incision but resection volume greater than 20%. Level
II procedure would improve cosmetic outcome.

Multidisciplinary evaluation of preoperative imaging between the surgeon


and the radiologist helps to determine the location of the resection, the
volume of tissue to be excised, and the overall glandular density of the breast.
These factors help to determine the type of oncoplastic surgery to perform.
Nonpalpable lesions are often excised with image-guided localization
techniques such as wire localization, various types of seed localization, or
ultrasound-guided excision. For those practices using wire localization,
optimal localization approach can be discussed preoperatively.
Patient photographs are also a valuable aspect of preoperative planning and
documentation. Photographs require informed consent. Photography consent
can be included in a standard consent to treat or as a separate consent when
photographs are taken.
Operative Markings for Surgical Planning
Performing preoperative marking is necessary in performing successful
oncoplastic breast surgery (4). Markings should be performed with the patient
standing in the normal anatomical position. Initial fixed anatomic landmarks
to be marked include the sternal notch, the midline, the clavicles, and the
inframammary crease. The nipple meridian is a line that starts at a point on
the clavicle approximately 6 cm from the sternal notch and extends to the
center of the nipple. This line divides the breast in half. The final nipple
position should be along the nipple meridian. Pitanguy point is identified by
placing your fingers behind the breast at the inframammary ridge and
marking the point on the skin. The nipple should ideally be placed at this
point so if there is significant ptosis, then an oncoplastic level II procedure
might yield a better cosmetic result. See Figure 9-2.
Intraoperative Surgical Steps for Performing General Level I
Procedures
Though there are many different level I procedures, the general components
of performing these procedures are similar. Clough et al. describes six steps
to performing all level I oncoplastic surgery procedures (3).

Step 1: Optimizing Incision Location


Oncoplastic surgery does not emphasize minimizing the incision length. It
does prioritize incision location. The choice of incision/technique can be
guided based on tumor location. The location of the incision needs to allow
for good operative exposure, wide excision of the cancer, and extensive
mobilization of the neighboring tissue to allow for reshaping of the breast.
Upper pole tumors can be approached with crescent, batwing, or hemi-
batwing incisions. Many lower pole lesions can be accessed through an
inframammary incision. An axillary incision can be used for lesions in the
upper outer quadrant. Circumareolar or donut mastopexy incisions can be
used to access multiple areas of the breast (see Fig. 9-3). All of these
approaches will be discussed in more detail in this chapter.
FIGURE 9-2 Sternal notch, xiphoid process, inframammary ridge, breast meridian are
marked with the patient standing. Pitanguy point is marked by identifying the
inframammary ridge projected through the breast.
FIGURE 9-3 A: Schematic well-placed incision. B: Fibroadenoma in upper outer
quadrant. C: Closed circumareolar incision with hidden scar.

Step 2: Undermining of Skin


Skin undermining is a key component to performing level I oncoplastic
surgery. The skin should be undermined in the mastectomy plane beyond the
lesion to be excised. This will aid in both exposure for lesion excision and for
the reapproximation of glandular breast tissue (see Fig. 9-4). Consideration
of breast density and other risk factors such as current/recent tobacco use or
diabetes are necessary to reduce the risk of fat necrosis with extensive
undermining. Fatty density breast tissue carries a higher risk of fat necrosis
limiting options with level I techniques. Fat necrosis can lead to infection and
wound complications with subsequent cosmetic deformity.
FIGURE 9-4 Undermining the skin in the mastectomy plane for exposure and
mobilization of the glandular tissue during level I oncoplastic procedure.

Step 3: Undermining of the Nipple Areolar Complex


Unfortunately, with the resection of a large area of tissue, there is a
subsequent deviation of the nipple areolar complex toward the area of
excision. Undermining the nipple areolar complex (NAC) allows for nipple
repositioning. Undermining of the NAC should be performed with a 5- to 10-
mm thickness of residual attached glandular tissue at the terminal ducts to
retain the glandular blood supply. Superficial undermining of the NAC can
result in nipple necrosis. Understanding the blood supply to the NAC is
crucial (5). The NAC depends on the dermal vasculature and the blood
supply from the underlying parenchyma. If the glandular blood supply to the
nipple is disrupted, the NAC is dependent on the lateral or medial dermal
vasculature. Undermining the NAC can also result in decreased sensation.

Step 4: Resection of Cancer


Complete excision of the targeted lesion is not to be compromised in
oncoplastic breast surgery. It is optimally excised as a single contiguous
piece of tissue for the most accurate margin assessment. The specimen should
be oriented by the surgeon. Specimen orientation can be performed with
marking sutures, clips, a variety of commercially available metallic markers,
or intraoperative inking. Specimen x-ray should be performed to confirm its
removal with an adequate margin on imaging. Cavity shave margins have
been shown to decrease reexcision rates (6). Clips are placed to mark the
lumpectomy cavity for radiation therapy planning.

Step 5: Closure of Defect


In the early practice of lumpectomy, the resection defect was left open and a
seroma was allowed to fill the cavity. Unfortunately, seroma formation does
not result in ideal long-term cosmetic results. Seroma resorption will
eventually occur resulting in fibrosis and an obvious defect at the excision
cavity. Thus, tissue mobilization around the excision cavity and
reapproximation of the defect is necessary. Mobilization of tissue beyond the
lesion can be performed prior to lesion excision optimizing visualization.
Dense glandular breast tissue can then be sutured together to close the cavity.
Care must be taken to ensure the closure is performed without tension.
Interrupted 2-0 Vicryl sutures can be placed from deep to superficial. Dyed
suture can be helpful to easily identify the sutures if reexcision is needed.
Additional superficial mobilization is necessary if dimpling is noted in the
skin (see Fig. 9-5).

Step 6: Deepithelialization and NAC Repositioning


NAC position is an important component of cosmesis after breast
conservation. As previously mentioned, the NAC will tend to deviate toward
the direction of the area of excision. To correct the malposition of the NAC, a
crescent-shaped area opposite the side of excision can be deepithelialized.
Deepithelialization should be performed sharply taking care not to disrupt the
vascular supply of the NAC within the dermis. Adequate counter tension
facilitates deepithelialization in the appropriate plane. In order to prevent
widening of the areolar border, closure should be performed with an
interlocking permanent suture, such as a Gore-Tex, to secure the areolar
dermis to the outer crescent of tissue. Interrupted deep dermal sutures can
then be placed to inset the NAC to the outer skin followed by a running
subcuticular stitch (7).

FIGURE 9-5 Closing the glandular tissue to prevent seroma.


LEVEL I ONCOPLASTIC INCISIONS/TECHNIQUES
Different incisions and procedures can be used based on tumor location and
the extent of excision required. Though the location and type of incision may
differ, all techniques will include the general steps of level I oncoplastic
surgery discussed previously.
Basic Incisions
Oncoplastic surgery can be performed with basic incisions in aesthetically
pleasing locations such as circumareolar, in the axilla, or in the
inframammary fold. These incisions leave the skin envelope intact and thus
should not be used in the setting of skin involvement or superficial lesions.
Circumareolar Incision
A circumareolar incision can be used for a lesion in any quadrant of the
breast. Considering the blood supply of the NAC, the length of the incision
should encompass one-third or less of the total circumference of the NAC.
Flap mobilization, lesion resection, and glandular rearrangement need be
performed through this incision. Thus, in a patient would a smaller areola,
another technique may need to be considered (see Fig. 9-6).
Inframammary Incision
An inframammary incision can be used to excision lower pole lesions or
lesions in the posterior breast. The incision is made in the skin of the
inframammary fold. The length of the incision depends on the size of the
lesion and mobilization required to excise the lesion. Glandular
reapproximation is facilitated by mobilization of the breast off of the chest
wall (see Fig. 9-7).
FIGURE 9-6 Circumareolar incision used for excision gynecomastia.

Incisions That Include Resection of Skin


Crescent Mastopexy
This technique allows for the excision of centrally located tumors that are
superior to the NAC (8). Ideally these lesions would be located from the
10:00 position to the 1:00 position in either breast. The skin incisions consist
of two curvilinear incisions (Fig. 9-8). One incision is along the superior
areolar edge and a second incision is slightly superior to the first incision.
The incisions meet at the corners so that the resection includes a crescent of
skin. If you want to preserve some volume, you can deepithelialize the skin
and fold it under.
FIGURE 9-7 Inframammary excision used for a large benign upper outer quadrant mass.
FIGURE 9-8 A: Crescent mastopexy incision with skin deepithelialized. B: Access
through the incision to multiple quadrants. C: One week postop.

Batwing Resection
The batwing incision (Fig. 9-9) is similar to a crescent incision, but because
the incision extends medially and laterally, it allows for greater exposure,
resection of larger lesions, and also allows for resection of lesions that are
slightly medial and lateral to the NAC (9). This incision also allows for the
resection of skin and the correction of ptosis.
FIGURE 9-9 Scott-Conner & Dawson batwing incision (A) and closure (B). The skin
within the darkened area in A will be excised. C: Intraoperative markings of batwing
procedure. D: Closure of batwing. E: One week postop.

Hemi-Batwing Resection
This incision is similar to the batwing technique, though only one wing,
usually the lateral wing, is excised. Using only the medial wing would result
in a scar in the upper inner breast (8). The hemi-batwing incision can be used
for an upper outer quadrant lesion that requires excision of overlying skin
(see Fig. 9-10).
Incision With Skin Deepithelialization
Donut Mastopexy
The donut mastopexy is also referred to as a Benelli resection or a round
block mastopexy (10,11). This is a more complex level I technique. The
donut mastopexy incision allows for increased access to all quadrants of the
breast when compared to a standard circumareolar incision. It also
accommodates the resection of skin if necessary. Because the basis of this
procedure involves concentric incisions around the areola (Fig. 9-3), the
incisions can result in change in nipple position, which can advantageously
be used to improve ptosis. In planning the incision, the outer aspect of the
NAC should be marked and then a concentric circle around this. The initial
incision should be made through the epidermis only so that the skin between
the two circles can be deepithelialized. The full-thickness incision should be
made at the outer edge of the donut in the direction of the lesion. When
closing the incision, using permanent suture, a purse-string or interlocking
stitch can be used to begin periareolar closure. This can be completed with
interrupted deep dermal sutures and a running subcuticular stitch (Fig. 9-11).
FIGURE 9-10 Hemi-batwing markings to incorporate two lesions.
FIGURE 9-11 Donut Mastopexy. A: Deepithelialize. B: Raise flap and resect tumor.
C: Close glandular defect and recreate the breast mound. D: Close the skin around
the areola. E: One week postop bilateral donut mastopexy.
POSTOPERATIVE COMPLICATIONS OF LEVEL I ONCOPLASTIC SURGERY
There are complications specific to oncoplastic techniques that surgeons need
to be aware of. Complications involving the NAC have been discussed.
Because these techniques involve the undermining of skin and mobilization
of breast tissue off of the pectoralis muscle, glandular necrosis can occur. The
risk of glandular necrosis is increased in the setting of fatty breast tissue.
Glandular necrosis can result in subsequent infection and wound
complications delaying treatment and resulting in cosmetic deformity.
CONCLUSION
The goal of oncoplastic breast surgery is to perform an oncologic surgical
resection with negative margins while optimizing the cosmetic result. Level I
oncoplastic techniques can be used when less than 20% of the breast volume
will be excised. Examples of level I oncoplastic techniques include the donut
mastopexy. The steps to performing level I oncoplastics build on basic
surgical skills that can be easily incorporated into clinical practice.

REFERENCES

1. Fisher B, Anderson S, Bryant J, et al. Twenty-year follow-up of a


randomized trial comparing total mastectomy, lumpectomy, and
lumpectomy plus irradiation for the treatment of invasive breast cancer.
N Engl J Med 2002;347:1233–1241.
2. Chatterjee A, Gass J, Patel K, et al. A consensus definition and
classification system of oncoplastic surgery developed by the American
Society of Breast Surgeons. Ann Surg Oncol 2019;26(11):3436–3444.
3. Clough KB, Kaufman GJ, Nos C, et al. Improving breast cancer surgery:
a classification and quadrant per quadrant atlas for oncoplastic surgery.
Ann Surg Oncol 2010;17:1375–1391.
4. El-Tamer MB. Principles and Techniques in Oncoplastic Breast Cancer
Surgery. Singapore: World Scientific; 2013.
5. Van Deventer PV. The blood supply to the nipple-areola complex of the
human mammary gland. Aesthet Plast Surg 2004;28(6):393–398.
6. Dupont E, Tsangaris T, Garcia-Cantu C, et al. Resection of cavity shave
margins in stage 0-III breast cancer patients undergoing breast
conserving surgery: a prospective multicenter randomized controlled
trial. Ann Surg 2019. doi: 10.1097/SLA.0000000000003449. [Epub
ahead of print]
7. Hammond DC, Khuthaila DK, Kim J. The interlocking Gore-Tex suture
for control of areolar diameter and shape. Plast Reconstr Surg
2007;119(3):804–809.
8. Nahabedian MY. Oncoplastic Surgery of the Breast. China: Elsevier;
2009.
9. Anderson BO, Masetti R, Silverstein MJ. Oncoplastic approaches to
partial mastectomy: an overview of volume-displacement techniques.
Lancet Oncol 2005;6(3):145–157.
10. Benelli L. A new periareolar mammaplasty: the “round block”
technique. Aesthetic Plast Surg 1990;14:93–100.
11. Bramhall RJ, Lee J, Concepcion M, et al. Central round block repair of
large breast resection defects: oncologic and aesthetic outcomes. Gland
Surg 2017;6(6):689–697.
CHAPTER 10

Oncoplastic Approach to Maximizing


the Lumpectomy-Level II
BARRY S. ROSEN | ANNE PELED-WARREN | TONI STORM

Oncoplastic breast surgery involves applying plastic surgical principles to


cancer operations to provide the best aesthetic outcome without
compromising cancer treatment. The term “oncoplastic surgery” was first
coined and popularized in the 1990s, with early papers describing a variety of
different techniques to optimize reconstruction of lumpectomy defects (1–5).
The central tenet of oncoplastic breast surgery is to “design the operation to
fit the patient,” incorporating the patient’s desires and goals, their unique
breast shape and size, and size and location of their breast cancer to find the
perfect balance. Oncoplastic surgery is the ultimate example of personalized
medicine, combining these variables so that “one size fits one.”
The challenge of breast-conserving surgery is to remove the tumor in its
entirety without creating a deformity that would otherwise defeat the purpose
of breast conservation (6–8). Oncoplastic breast surgery allows for the best of
both worlds, optimizing both tumor excision and aesthetic outcome.
Oncoplastics is more of a philosophy than a technique, applicable to all
patients undergoing breast cancer surgery. In the past, the goal was just to
mitigate the deformity inherent with breast cancer surgery; now this has
evolved to where we may offer to patients the option of possibly looking
better after oncoplastic surgery than they did prior to their cancer diagnosis.
A critical component of patient education is to explain that this is not about
vanity, but rather recovery: living beyond a cancer diagnosis mandates
removal of daily reminders of the trauma.
The defects created by tumor excision may be repaired by either displacing
adjacent breast tissue to fill the space or replacing the tissue with an
autologous flap. In the now-classic article published by Clough et al. in 2010
(9), oncoplastic surgery was divided into level I and level II techniques,
based upon the amount of breast tissue removed and the need to perform a
contralateral symmetrizing procedure. Most breast cancers can be managed
by level I techniques, which entails hiding the scar and obliterating the defect
after tumor excision. If cancer excision requires removal of 20% to 50% of
the breast volume or if the patient desires a breast lift and/or reduction, level
II techniques are ideal and are the focus of this chapter. Figure 10-1 presents
an algorithm for considering oncoplastic options incorporating both clinical
factors and patient preference.
LITERATURE REVIEW

Benefits of Oncoplastic Surgery


Given the excellent oncologic outcomes seen following lumpectomy and
modern radiotherapy and systemic therapy protocols, with recent studies
showing 5-year local recurrence rates of less than 5% (10), some surgeons
may feel that lumpectomy alone is sufficient for many women with early-
stage breast cancer, without adding the potential additional complexity of an
oncoplastic procedure. Additionally, a lack of specialized training and
concern about compromise in oncologic safety may be barriers to offering
oncoplastic procedures (11,12). However, oncoplastic surgery has been
demonstrated to improve outcomes and offers many benefits in addition to
the expected improvements in aesthetic outcome and patient satisfaction.

Margins
Multiple studies have shown superior margin control during breast
conservation when concurrent oncoplastic surgery is performed (13–16).
Presumably, these improved rates stem from the ability of the oncoplastic
surgeon to resect a larger volume of tissue when reconstruction of the defect
will be included as part of the procedure. Additionally, many women
undergoing oncoplastic reduction mammoplasty have symptomatic breast
hypertrophy at baseline and would benefit from a significant reduction in
breast volume, so a much larger volume of noncancerous breast tissue can be
removed as part of the tumor specimen. This improvement in margin control
is seen in a meta-analysis by Losken et al. comparing outcomes from nearly
5,500 lumpectomy cases to 3,100 oncoplastic reduction mammoplasty cases
(17). Overall tumor size was larger in the oncoplastic group (mean 2.5 cm
compared to 1.2 cm), yet the positive margin rate was significantly lower in
the oncoplastic group (12.4% vs. 20.6%, p < 0.0001). Another large single-
institution study from MD Anderson Cancer Center including nearly 4,800
patients undergoing breast conservation echoed these findings, with a
statistically significant reduction in positive margin rate when oncoplastic
surgery was performed compared to lumpectomy alone (18).
FIGURE 10-1 Algorithm for oncoplastic surgery options.

Aesthetics/Patient-Reported Outcomes
Poor scarring and soft tissue defects left by lumpectomy alone can
significantly impact the aesthetic outcome for women undergoing breast-
conservation therapy (19–21). With oncoplastic procedures, particularly level
II procedures, aesthetic outcome is significantly improved compared to
lumpectomy alone, and may actually be improved from the patient’s
preoperative baseline, with associated improvement in quality-of-life
parameters (22–24). Additionally, for women who are candidates for either
oncoplastic surgery or mastectomy and reconstruction, oncoplastic
procedures have been shown to have significantly higher rates of patient-
reported satisfaction with breast appearance and psychosexual outcomes
(25,26).
Safety
Although oncoplastic surgery has many documented benefits, there are still
some concerns regarding the long-term oncologic safety and the potential for
increased surgical complications and possible associated treatment delay.
While extended long-term data is still being gathered, shorter-term oncologic
outcomes and immediate surgical outcomes are very favorable and
comparable to lumpectomy alone.
First, looking at oncologic control, oncoplastic procedures have not been
shown to negatively impact local–regional recurrence rates. A matched
cohort study of nearly 1,400 patients with median follow-up of 7.2 years (27)
showed equivalent 10-year local recurrence rates following oncoplastic
procedures compared to lumpectomy alone. Other studies of patients
undergoing oncoplastic surgery documenting longer-term follow-up
demonstrate local regional recurrence rates similar to those historically seen
with lumpectomy alone (28,29).
While margin positivity is lower following oncoplastic breast surgery, the
consequence of a positive margin is higher, with meta-analyses showing
mastectomy rates of 6.5% compared to 3.8% following traditional
lumpectomy (17). Factors that may contribute to positive margins include
variables intrinsic to the cancer such as high-grade cancers, lobular cancers,
extensive ductal carcinoma in situ (DCIS), and HER-2/neu-amplified tumors
(30–32).
A consensus conference was held in 2015 sponsored by the American
Society of Breast Surgeons addressing factors that may reduce positive
margin rates following breast conservation, summarized as the CALLER
Toolbox (33). Updated recommendations and other prospective studies have
discussed a number of extrinsic factors that may reduce positive margin rates
including use of neoadjuvant chemotherapy, preoperative imaging beyond 2D
mammography, surgeon use of ultrasound, intraoperative margin analysis,
oncoplastic surgery, and routine cavity side-wall shaves (34–36). However,
even if margins are positive after oncoplastic surgery, with proper tumor-bed
marking, reexcision lumpectomy +/− repeat mammoplasty can be safely
performed with low subsequent local recurrence rates (37).
Oncoplastic surgery has also been shown to be safe from a complications’
standpoint. Large meta-analyses comparing oncoplastic surgery to
lumpectomy alone have shown equivalent rates of overall complications, in
the range of 15% to 20% (17). Systematic review of oncoplastic surgery
procedures shows the most common immediate surgical complications,
including wound dehiscence, infection, and fat necrosis, occur in less than
5% of cases (14). Additionally, oncoplastic procedures have not been shown
to lead to delays in adjuvant treatment (38). A recent population-based cohort
study of over 1,700 patients demonstrated no time difference from surgery to
chemotherapy whether the patient underwent lumpectomy, mastectomy, or
oncoplastic breast surgery (39).
PATIENT EVALUATION
The key to successful oncoplastic outcomes is devising a well-thought-out
plan at the time of evaluation. This requires a directed history, physician
examination, and review of imaging.
History
A thorough history necessitates identifying potential contraindications to
oncoplastic surgery such as a history of connective tissue diseases or prior
radiation, as well as relative contraindications including comorbidities and
nicotine use. However, the most critical part of the history is to pivot from an
oncologic to an aesthetic focus and ask patients what they think of their
breast size and shape. This simple question puts all patients on level footing
and helps to remove any subjective bias that a surgeon might have about what
best fits that patient.
Physical Examination
Oncoplastic surgical planning necessitates examining patients when supine
and upright and using this examination to point out to patients natural
asymmetries. Important measurements include breast size, degree of ptosis,
and tumor location and extent. This requires photographic documentation
before and after surgery, ideally using a consistent background and standard
five views to include anterior, left and right lateral, and left and right oblique.
The photos should extend from the neck to the upper abdomen, ideally
removing any identifiable jewelry.
Imaging
The most critical aspect of imaging is to help map out the location and extent
of the tumor relative to the normal breast. However, useful information can
be obtained by identifying the anterior mammary fascia and measuring the
thickness of the subcutaneous tissue. This can usually be obtained by
reviewing standard two-view mammography; if an MRI was performed, this
information may be more precise, including a topographic map of the blood
supply to the breast. Office-based ultrasound is particularly beneficial for
identifying the tumor relative to the location of the nipple areolar complex
(NAC), measuring the distance to the skin, and the size of the
cancer. Ultimately, becoming adept at ultrasound teaches the surgeon to think
three dimensionally, with the information translated from office to operating
room.
IDEAL CANDIDATES FOR LEVEL II ONCOPLASTIC SURGERY
In order to be considered for level II oncoplastic surgery, a patient should be
moderate or large breasted and have some degree of ptosis. Ideal candidates
for level II oncoplastic surgery include:
Patients With Multifocal Tumors
With multifocal tumors, larger excisions may be needed in order to
completely resect all tumor foci. If complete tumor excision necessitates
removal of over 20% of the breast volume, combining the excision with an
oncoplastic mastopexy and contralateral reduction mammoplasty for
symmetry or bilateral reduction mammoplasty (depending on the patient’s
goals) may obviate the need for a mastectomy (40).
Patients Who Desire Breast Reduction/Mastopexy
Many patients may consider being able to have a concurrent mastopexy or
reduction mammaplasty at the time of their lumpectomy as a “silver lining”
to their cancer diagnosis. Oftentimes women express that they would likely
never have electively undergone breast surgery, but being offered the
opportunity to have these procedures as part of their cancer surgery gives
them something positive to focus on in the midst of their cancer diagnosis.
Furthermore, the effects of radiation therapy are more pronounced with large-
breasted and ptotic patients, so these oncoplastic procedures can have a
functional benefit in both the short and long term as well.
Patients With Large Tumors
While neoadjuvant chemotherapy can often be applied in such circumstances
to downstage tumors and increase breast-conserving surgery rates, some
tumors are chemoresistant such as large areas of DCIS or luminal A breast
cancers. Even after neoadjuvant chemotherapy, some tumors may shrink in a
manner where the overall tumor volume decreases but its footprint and/or
extent of microcalcifications may not and a large resection is still required
(41). Level II oncoplastic procedures are ideal for these patients to optimize
margin control and avoid the higher rates of complications that could occur in
women who alternatively undergo mastectomy and implant reconstruction
and require radiation therapy based on tumor characteristics (42).
Patients Who Desire Nipple-Sparing Mastectomy
Nipple-sparing mastectomy has been shown to be a safe, cosmetically
superior option when mastectomy is either desired or necessary (43).
However, the technical challenges of nipple-sparing mastectomy and
associated surgical complications are most pronounced in large-breasted,
ptotic patients (44). Initial bilateral oncoplastic reduction mammaplasty can
be a very effective segue to eventual nipple-sparing mastectomy by reducing
the skin envelope/breast size and placing the NAC in its ideal location (45).
This is particularly useful for patients who are uncertain whether they would
like breast conservation or mastectomy or have not completed the testing
necessary to make an informed decision.
TIMING OF OPERATIVE INTERVENTION
Different timing options for performing oncoplastic surgery have been
proposed, including immediate (at the time of lumpectomy), delayed
immediate (after the lumpectomy but before adjuvant radiation therapy), and
delayed (after lumpectomy and adjuvant radiation therapy). Studies have
shown immediate oncoplastic reconstruction to have lower complication rates
compared to the other approaches (46,47), as well as increased patient
satisfaction (48). In addition to these benefits, as well as the convenience and
safety of having only one surgical procedure, we have also found in our
practices that women often choose not to return for oncoplastic surgery once
they’ve completed their adjuvant treatment—having been through all of the
trauma and disruption of their initial treatment, the thought of an additional
medical intervention is often very undesirable and ends up feeling more
“elective,” which often deters women from delayed oncoplastic
reconstruction.
TECHNIQUE
For women with anticipated breast volume resection representing less than
20% of their total breast volume, level I oncoplastic techniques with local
tissue rearrangement can be very effective. However, for women requiring
larger resections or those desiring a reduction or mastopexy, level II
techniques should be used for optimal outcome. Level II oncoplastic
approaches include both volume displacement techniques (reconstructing the
tumor defect with breast tissue alone) and volume replacement techniques
(using either local or distant flaps or implants for reconstruction). With
careful surgical planning using appropriate localization strategies to minimize
the extent of noncancerous breast tissue resection, most patients can have
successful partial breast reconstruction with volume displacement techniques,
which eliminates the need for a separate donor site and associated potential
morbidity or prolonged recovery.
Volume Displacement Approaches
The two main options for level II volume displacement procedures are
circumvertical reduction/mastopexy and Wise-pattern reduction/mastopexy.
Decision about which option to use is primarily based on the degree of
preoperative ptosis and the amount of breast volume and excess breast skin
that will need to be resected to optimize breast appearance and achieve the
patient’s breast size goals.
Circumvertical approaches are also known as “short-scar” or “lollipop”
techniques as the final scar is limited to a periareolar scar with an inferior
vertical component without the inframammary fold extension seen with
Wise-pattern approaches. The blood supply for the NAC can be adjusted
based on the tumor location, though superior or superior-medial pedicles are
most commonly used to optimize both sensation and vascularity. These
pedicles are optimal for many tumor locations and can be very versatile in
oncoplastic reconstruction (49). Ideal candidates for this approach are women
with mild-to-moderate ptosis and small-to-moderate–sized breasts, as it is
difficult to resect a sufficient amount of skin or breast volume in women with
greater degrees or ptosis or larger resection volumes of breast tissue required
or desired. It is also a good approach for women with pseudoptosis, as the
vertically oriented skin resection in the lower pole of the breast narrows the
breast width and helps correct the heavy appearance of the breast seen with
pseudoptosis (Fig. 10-2).
Wise-pattern approaches entail more extensive incisions than
circumvertical ones, leaving so-called “inverted T” or “anchor” scars. Similar
to circumvertical approaches, any type of NAC pedicle can be used with this
incision pattern, although many surgeons are taught during training to use an
inferior pedicle as it is thought to be easier to learn and more reliable (50).
For larger-breasted women desiring a large reduction or women with
significant ptosis, the Wise-pattern approach can allow for more skin and
parenchymal resection than a circumvertical approach and is often necessary
in these cases to achieve a good cosmetic outcome.
In the oncoplastic setting, Wise-pattern approaches are used in similar
scenarios regarding women with very large breasts or significant ptosis, but
can also be very helpful when greater access to the breast parenchyma would
be helpful during resection of larger tumors (30,51). The axilla can also be
accessed fairly easily with Wise-pattern reductions, thus avoiding the need
for an additional external incision in the axilla (Fig. 10-3).
FIGURE 10-2 A, B: 51-year-old woman with 1.5-cm left breast invasive ductal
carcinoma. C: The patient underwent left wire–localized lumpectomy and axillary
sentinel lymph node biopsy with bilateral circumvertical mastopexy and
autoaugmentation with inferior pole tissue. D, E: Two-year postoperative
appearance following adjuvant radiation therapy.
FIGURE 10-3 A, B: 54-year-old woman with bilateral clinically stage I invasive
lobular carcinomas. C: Magnetic resonance imaging (MRI) demonstrating tumors in
the central upper breast (right breast) and upper outer quadrant (left breast). D:
The patient underwent bilateral wire–localized lumpectomy and axillary sentinel
lymph node biopsy and bilateral Wise-pattern reduction mammoplasty with an
inferior pedicle. E, F: Nine-month postoperative appearance following bilateral
adjuvant radiation therapy.
FIGURE 10-4 A, B: A 52-year-old patient with invasive ductal carcinoma (2.9 cm) of
the left breast. C, D: The patient underwent a left superior-lateral quadrantectomy
and sentinel lymph node biopsy, immediately followed by left lateral thoracodorsal
flap. In this patient, no contralateral breast procedure was performed; a total of 245
g was removed from the left breast. E, F: Two-month postoperative appearance
during the radiotherapy. G, H: Three-year postoperative appearance after the
radiotherapy with a very good outcome.

Volume Replacement Approaches


As mentioned above, most women can have successful reconstruction with
volume displacement approaches, even with larger tumors or multifocal
disease (41). When greater than 50% of the breast volume will be resected,
consideration should be given for total mastectomy (and reconstruction if
desired), as this approach may lead to better long-term aesthetic results. For
women who are strongly committed to breast conservation, volume
replacement techniques can allow for preservation of the remaining breast
tissue while adding volume to fill the defect left after the resection. There are
a variety of different local flaps that can be used in this setting, including
perforator flaps or partial muscle flaps from the lateral chest and back (Fig.
10-4) (52–54). In cases where the vascular supply to these flaps has been
compromised as a result of axillary surgery, in delayed reconstruction with
significant radiation injury to the soft tissue of local/regional flaps, or
challenging tumor locations, free flap reconstruction can be used as an
alternative with good outcomes (55,56).
MANAGEMENT OF CENTRAL TUMORS
A challenging scenario is performing breast conservation for tumors that
involve the NAC, which requires resection of the nipple in continuity with
the tumor. Additionally, patients who either desire or require a breast
reduction whose tumor lies centrally within the breast may require excision
of the NAC due to disruption of its blood supply. Traditional teaching
incorporated excising a transversely oriented ellipse of skin around the NAC
to allow for a simple primary closure. However, this flattens the breast and
creates a deformity in the breast shape that cannot be easily corrected (57).
Oncoplastic options in small-to-moderate–breasted patients include
transposing an island of normal skin inferior to the NAC and incorporating
the excision with an inferior j-extension (the Grisotti technique), a
circumareolar purse-string type closure, or even local pedicled flaps (58,59).
Larger-breasted patients are best served by modifying a Wise-pattern
reduction with an inferior pedicle to include excision of the NAC and
performing a contralateral symmetrizing procedure (60).
Conclusion
Level II oncoplastic techniques can be successfully utilized in a number of
different clinical scenarios, ranging from large tumor resections to patient
preference for smaller or more lifted breasts to a staged approach to optimize
nipple-sparing mastectomy outcomes. The safety profile is comparable to
standard lumpectomy, with additional benefits seen in quality-of-life
outcomes and margin control. These approaches are an essential part of any
oncoplastic surgeon’s toolbox to ensure optimal and tailored options for
breast cancer patients.

REFERENCES

1. Clough KB, Nos C, Salmon RJ, et al. Conservative treatment of breast


cancers by mammaplasty and irradiation: a new approach to lower
quadrant tumors. Plast Reconstr Surg 1995;96:363–370.
2. Raja MA, Straker VF, Rainsbury RM. Extending the role of breast-
conserving surgery by immediate volume replacement. Br J Surg
1997;84:101–105.
3. Rainsbury RM, Paramanathan N. Recent progress with breast-
conserving volume replacement using latissimus dorsi miniflaps in UK
patients. Breast Cancer 1998;5:139–147.
4. Clough KB, Kroll SS, Audretsch W. An approach to the repair of partial
mastectomy defects. Plast Reconstr Surg 1999;104:409–420.
5. Nos C, Fitoussi A, Bourgeois D, et al. Conservative treatment of lower
pole breast cancers by bilateral mammoplasty and radiotherapy. Eur J
Surg Oncol 1998;24:508–514.
6. Kaiviani A, Sodagari N, Shiekhbahaei S, et al. From radical mastectomy
to breast-conserving therapy and oncoplastic breast surgery: a narrative
review comparing oncological result, cosmetic outcome, quality of life,
and health economy. ISRN Oncol 2013;2013:742462.
7. Cochrane RA, Valasiadou P, Wilson AR, et al. Cosmesis and
satisfaction after breast-conserving surgery correlates with the
percentage of breast volume excised. Br J Surg 2003;90:1505–1509.
8. Munshi A, Kakkar S, Bhutani R, et al. Factors influencing cosmetic
outcome in breast conservation. Clin Oncol (R Coll Radiol)
2009;21:285–293.
9. Clough KB, Kaufman GJ, Nos C, et al. Improving breast cancer surgery:
a classification and quadrant per quadrant atlas for oncoplastic surgery.
Ann Surg Oncol 2010;17:1375–1391.
10. Neuman H. Local recurrence rates after breast conserving therapy in
patients receiving modern era therapy. Presented at The American
Society of Breast Surgeons Annual Meeting; May 2–5, 2018; Orlando,
FL.
11. Chatterjee A, Gass J, Burke MB, et al. Results from the American
Society of Breast Surgeons Oncoplastic Surgery Committee 2017
survey: current practice and future directions. Ann Surg Oncol
2018;25:2790–2794.
12. Challoner T, Skillman J, Wallis K, et al. Oncoplastic techniques:
attitudes and changing practice amongst breast and plastic surgeons in
Great Britain. Breast 2017;34:58–64.
13. Losken A, Pinell-White X, Hart AM, et al. The oncoplastic reduction
approach to breast conservation therapy: benefits for margin control.
Aesthet Surg J 2014;34:1185–1191.
14. Piper ML, Esserman LJ, Sbitany H, et al. Outcomes following
oncoplastic reduction mammoplasty: a systematic review. Ann Plast
Surg 2016;76 Suppl 3:S222–S226.
15. Down SK, Jha PK, Burger A, et al. Oncological advantages of
oncoplastic breast-conserving surgery in treatment of early breast
cancer. Breast J 2013;19:56–63.
16. Yang JD, Lee JW, Kim WW, et al. Oncoplastic surgical techniques for
personalized breast conserving surgery in breast cancer patient with
small to moderate sized breast. J Breast Cancer 2011;14:253–261.
17. Losken A, Dugal C, Styblo T, et al. A meta-analysis comparing breast
conservation therapy alone to the oncoplastic technique. Ann Plast Surg
2014;72:145–149.
18. Carter SA, Lyons GR, Kuerer HM, et al. Operative and oncologic
outcomes in 9861 patients with operable breast cancer: single-institution
analysis of breast conservation with oncoplastic reconstruction. Ann
Surg Oncol 2016;23:3190–3198.
19. Gass J, Mitchell S, Hanna M. How do breast cancer surgery scars impact
survivorship? Findings from a nationwide survey in the United States.
BMC Cancer 2019;19:342.
20. Vrouwe SQ, Somogyi RB, Snell L, et al. Patient-reported outcomes
following breast conservation therapy and barriers to referral for partial
breast reconstruction. Plast Reconstr Surg 2018;14:1–9.
21. Negenborn VL, Volders JH, Krekel NMA, et al. Breast-conserving
therapy for breast cancer: cosmetic results and options for delayed
reconstruction. J Plast Reconstr Aesthet Surg 2017;70:1336–1344.
22. Losken A, Hart AM, Broecker JS, et al. Oncoplastic breast reduction
technique and outcomes: an evolution over 20 years. Plast Reconstr
Surg 2017;139:824e–833e.
23. Shekhawat L, Busheri L, Dixit S, et al. Patient-reported outcomes
following breast reconstruction surgery and therapeutic mammoplasty:
prospective evaluation 1 year post-surgery with BREAST-Q
questionnaire. Indian J Surg Oncol 2015;6:356–362.
24. Kelemen P, Pukancsik D, Ujhelyi M, et al. Comparison of
clinicopathologic, cosmetic and quality of life outcomes in 700
oncoplastic and conventional breast-conserving surgery cases: a single-
centre retrospective study. Eur J Surg Oncol 2019;45:118–124.
25. Chand ND, Browne V, Paramanathan N, et al. Patient-reported
outcomes are better after oncoplastic breast conservation than after
mastectomy and autologous reconstruction. Plast Reconstr Surg Global
Open 2017;5:e1419.
26. Hart AM, Pinell-White X, Egro FM, et al. The psychosexual impact of
partial and total breast reconstruction: a prospective one-year
longitudinal study. Ann Plast Surg 2015;75:281–286.
27. De Lorenzi F, Hubner G, Rotmensz N, et al. Oncological results of
oncoplastic breast-conserving surgery: long term follow-up of a large
series at a single institution: a matched-cohort analysis. Eur J Surg
Oncol 2016;42:71–77.
28. Clough KB, van la Parra RFD, Thygesen HH, et al. Long-term results
after oncoplastic surgery for breast cancer: a 10-year follow-up. Ann
Surg 2018;268:165–171.
29. Vieira RA, Carrara GF, Scapulatempo NC, et al. The role of oncoplastic
breast conserving treatment for locally advanced breast tumors. A
matching case-control study. Ann Med Surg (Lond) 2016;10:61–68.
30. Losken A, Styblo TM, Carlson GW, et al. Management algorithm and
outcome evaluation of partial mastectomy defects treated using
reduction or mastopexy techniques. Ann Plast Surg 2007;59:235–242.
31. Miller AR, Brandao G, Prihoda TJ, et al. Positive margins following
surgical resection of breast carcinoma: analysis of pathologic correlates.
Am J Surg 2004;187:647–650.
32. Song J, Styblo TM, Carlson G, et al. The use of oncoplastic reduction
techniques to reconstruct partial mastectomy defects in women with
ductal carcinoma in situ. Breast J 2010;16:141–146.
33. Landercasper J, Attai D, Atisha D, et al. Toolbox to reduce lumpectomy
reoperations and improve cosmetic outcome in breast cancer patients:
the American Society of Breast Surgeons Consensus Conference. Ann
Surg Oncol 2015;22:3174–3183.
34. Landercasper J, Borgert AJ, Fayanju OM, et al. Factors associated with
reoperation in breast-conserving surgery for cancer: a prospective study
of American Society of Breast Surgeon members. Ann Surg Oncol
2019;26:3321–3336.
35. Dupont E, Tsangaris T, Garcia-Cantu C, et al. Resection of cavity shave
margins in stage 0-III breast cancer patients undergoing breast
conserving surgery: a prospective multicenter randomized controlled
trial [Epub ahead of print]. Ann Surg 2019. doi:
10.1097/SLA.0000000000003449
36. McEvoy MP, Landercasper J, Naik HR, et al. Update of the American
Society of Breast Surgeons Toolbox to address the lumpectomy
reoperation epidemic. Gland Surg 2018;7:536–553.
37. Clough KB, Gouveia PF, Benyahi D, et al. Positive margins after
oncoplastic surgery for breast cancer. Ann Surg Oncol 2015;22:4247–
4253.
38. Tong WM, Baumann DP, Villa MT, et al. Obese women experience
fewer complications after oncoplastic breast repair following partial
mastectomy than after immediate total breast reconstruction. Plast
Reconstr Surg 2016;137:777–791.
39. Klit A, Tvedskov TF, Kroman N, et al. Oncoplastic breast surgery does
not delay the onset of adjuvant chemotherapy: a population-based study.
Acta Oncol 2017;56:719–723.
40. Silverstein MJ, Savalia N, Khan S, et al. Extreme oncoplasty: breast
conservation for patients who need mastectomy. Breast J 2015;21:52–
59.
41. Chang EI, Peled AW, Foster RD, et al. Evaluating the feasibility of
extended partial mastectomy and immediate reduction mammoplasty
reconstruction as an alternative to mastectomy. Ann Surg
2012;255:1151–1157.
42. Peled AW, Sbitany H, Foster RD, et al. Oncoplastic mammoplasty as a
strategy for reducing reconstructive complications associated with
postmastectomy radiation therapy. Breast J 2014;20:302–307.
43. Mitchell SD, Willey SC, Beitsch P, et al. Evidence based outcomes of
the American Society of Breast Surgeons Nipple Sparing Mastectomy
Registry. Gland Surg 2018;7:247–257.
44. Frey JD, Saliban AA, Karp NS, et al. The impact of mastectomy weight
on reconstructive trends and outcomes in nipple-sparing mastectomy:
progressively greater complications with larger breast size. Plast
Reconstr Surg 2018;14:795e–804e.
45. Saliban AA, Frey JD, Karp NS, et al. Does staged breast reduction prior
to nipple-sparing mastectomy decrease complications? A matched
cohort study between staged and non-staged techniques. Plast Reconstr
Surg 2019;144(5):1023–1032.
46. Egro FM, Pinell-White X, Hart AM, et al. The use of reduction
mammaplasty with breast conservation therapy: an analysis of timing
and outcomes. Plast Reconstr Surg 2015;135:963e–971e.
47. Roughton MC, Shenaq D, Jaskowiak N, et al. Optimizing delivery of
breast conservation therapy: a multidisciplinary approach to oncoplastic
surgery. Ann Plast Surg 2012;69:250–255.
48. Patel KM, Hannan CM, Gatti ME, et al. A head-to-head comparison of
quality of life and aesthetic outcomes following immediate, staged-
immediate, and delayed oncoplastic reduction mammaplasty. Plast
Reconstr Surg 2011;127:2167–2175.
49. Barnea Y, Inbal A, Barsuk D, et al. Oncoplastic reduction using the
vertical scar superior-medial pedicle pattern technique for immediate
partial breast reconstruction. Can J Surg 2014;57:E134–E140.
50. Rohrich RJ, Gosman AA, Brown SA, et al. Current preferences for
breast reduction techniques: a survey of board-certified plastic surgeons.
Plast Reconstr Surg 2004;114:1724–1733; discussion 1734–1736.
51. Di Micco R, O’Connell RL, Barry PA, et al. Bilateral mammoplasty for
cancer: surgical, oncological, and patient-reported outcomes. Eur J Surg
Oncol 2017;43(1):68–75.
52. Kim JB, Eom JR, Lee JW, et al. Utility of two surgical techniques using
a lateral intercostal artery perforator flap after breast-conserving surgery:
a single-center retrospective study. Plast Reconstr Surg 2019;143:477e–
487e.
53. Munhoz AM, Montag E, Arruda E, et al. The role of the lateral
thoracodorsal fasciocutaneous flap in immediate conservative breast
surgery reconstruction. Plast Reconstr Surg 2006;117:1699–1710.
54. Hamdi M. Oncoplastic and reconstructive surgery of the breast. Breast
2013;22 Suppl 2:S100–S105.
55. Smith ML, Molina BJ, Dayan E, et al. Defining the role of free flaps in
partial breast reconstruction. J Reconstr Microsurg 2018;34:185–192.
56. Spiegel AJ, Eldor L. Partial breast reconstruction with mini superficial
inferior epigastric artery and mini deep inferior epigastric perforator
flaps. Ann Plast Surg 2010;65:147–154.
57. Fitzal F, Mittlboeck M, Trischler H, et al. Breast-conserving therapy for
centrally located breast cancer. Ann Surg 2008;247:470–476.
58. Huemer GM, Schrenk P, Moser F, et al. Oncoplastic techniques allow
breast-conserving treatment in centrally located breast cancers. Plast
Reconstr Surg 2007;120:390–398.
59. Carstensen L, Bigaard J. Management of central breast tumours with
immediate reconstruction of the nipple-areola complex; a suggested
guide. Breast 2015;24:38–45.
60. Park HC, Kim HY, Kim MC, et al. Partial breast reconstruction using
various oncoplastic techniques for centrally located breast cancer. Arch
Plast Surg 2014;41:520–528.
CHAPTER 11

Breast Conservation Failure: When to


Do a Completion Mastectomy
ANITA MAMTANI | HIRAM S. CODY III

Among all present-day patients presenting with breast cancer, breast


conservation therapy (BCT) is suitable for 70% to 80%, is attempted in most
of those eligible, and succeeds in about 90% of these cases (1). Ten-year rates
of ipsilateral breast recurrence (IBTR) in contemporary randomized
controlled trials (RCTs) which have included systemic therapy are low, 6%
for node-negative and 9% for node-positive disease (Table 11-1) and trending
lower (2–4). The “textbook” treatment for IBTR—both historically and by
current NCCN guidelines (5)—has been mastectomy for all, but with
advances in breast imaging, radiotherapy (RT), and systemic therapy this
may no longer be the case. Since the topics of case selection for BCT, margin
assessment, axillary management, local recurrence, oncoplasty, RT and
reconstruction are covered in detail elsewhere (see Chapters 6, 7, 9, 10, 12,
20, 26, 33, 34, Sections 1–3), we will focus specifically on treatment
strategies for failed BCT.
DECLINING RATE OF EVENTS
The first generation of RCTs comparing mastectomy with BCT demonstrated
equivalent long-term survivals but higher rates of locoregional recurrence
(LRR) for BCT (6,7). In more contemporary RCTs—including systemic
adjuvant therapy—local control for BCT and mastectomy are equivalent (4),
as are the rates of survival following IBTR (8). Further, a meta-analysis
comprising 53 RCTs of adjuvant chemo- and hormonal therapy (1990 to
2011) demonstrates that the number of LRRs as a proportion of all breast
cancer events is declining as well, from 30% to 15%, independent of the
receipt of RT or type of surgery (9). Therefore, BCT makes sense as initial
treatment whenever possible.

TABLE 11-1 Rates of IBTR and Post-IBTR Survival in NSABP


Randomized Trials of BCT Including Systemic Therapy
Trial 10-Year IBTR 5-Year Survival
(%) After IBTR (%)
NSABP Trials of Node-Negative 6 76
Patients
B-13, 14, 19, 20, 23 (2)
NSABP Trials of Node-Positive 9 60
Patients
B-15, 16, 18, 22, 25 (3)
IMMEDIATE INDICATIONS FOR MASTECTOMY
Some patients who appear suitable for BCT will have unexpectedly extensive
disease—not apparent on preoperative imaging—on final pathology.
Although one (or more) reexcisions can achieve negative margins in a most
cases, persistently positive margins or deteriorating cosmesis are a clear
indication for mastectomy. Some patients will have received neoadjuvant
therapy in an effort to downstage a tumor otherwise unsuitable for BCT, and
require mastectomy based on an inadequate response to treatment. Some
patients will have predisposition on the basis of prior RT for lymphoma, a
strong family history, or a deleterious gene mutation, and elect mastectomy to
minimize the risk of second breast events. Finally, a few patients who are
otherwise suitable for BCT in every way will elect mastectomy for reasons of
their own.
DIAGNOSIS AND WORKUP OF IBTR
Following successful BCT, routine follow-up typically comprises physical
examination, annual mammography, and—for patients with heterogeneously
dense breasts—screening ultrasound. In this setting, most IBTR will be small
lesions detected by imaging and diagnosed by image-guided core biopsy.
MRI makes sense whenever the extent of the lesion is unclear on
conventional imaging, and for patients with larger lesions a metastatic
workup is indicated to exclude distant metastases, which are present in as
many as half of patients with invasive IBTR. Patients with large or
inflammatory IBTR may be candidates for downstaging by neoadjuvant
therapy prior to surgery. Finally, as for patients who present initially with
stage IV disease, most patients with coincident IBTR and distant metastases
respond sufficiently well to systemic therapy that only a small minority will
ever need surgery (10).
TREATMENT OF IBTR

The Ipsilateral Breast: Mastectomy


Historically, the only option for the treatment of failed BCT—in the absence
of distant metastases—was mastectomy, and this makes sense whenever
dictated by the extent of the breast recurrence or by a significant cosmetic
defect from the earlier BCT procedure. In this setting there is a range of
options for breast reconstruction and plastic surgical consultation should be
considered for all patients with IBTR. Mastectomy without reconstruction is
absolutely reasonable for any patient who is opposed to reconstruction, who
is uncertain whether to proceed (delayed reconstruction is almost always
feasible), or who has medical contraindications. On the other hand,
reconstruction makes sense for any patient who is certain, and in this setting
an immediate reconstruction is suitable for most. Tissue expanders (TEs)
have the advantage of simplicity and a satisfactory result in about two-thirds
of carefully selected patients, but with a history of prior RT, TEs are
associated with higher complication rates, including skin flap necrosis,
infection, implant loss, limited expansion, and capsular contracture,
compared to other methods (11,12). Latissimus flap reconstruction has the
morbidity of a more extensive procedure, including that of the donor site, and
requires an implant to restore volume, but is associated with fewer early
wound complications and a lower rate of capsular contracture (13). Free flaps
—most commonly from the abdomen (“deep inferior epigastric perforator
[DIEP]”)—require the greatest expertise, the most extensive surgery, and
entail the morbidity of a large abdominal donor site, but appear to offer the
best long-term patient-reported outcomes, especially for patients with a
history of prior RT (14–16).

TABLE 11-2 Studies of Second Breast Conservation for Locally Recurrent


Breast Cancer
The Ipsilateral Breast: Reconservation
Mastectomy need not be routine for all patients with IBTR, especially in an
era when many are small image-detected lesions, and a growing literature
addresses the topic of reconservation (Table 11-2). In the most recent of these
from the European Institute of Oncology (1997 to 2004), 314 of 12,337
patients (1997 to 2004) developed IBTR as a first event, and 161 (51%) had
reconservation rather than mastectomy. For reconservation the 5-year risk of
a second IBTR was 29% overall: 15% for IBTR ≤2 cm with >48-month
disease-free interval (DFI), 31% for IBTR ≤2 cm with DFI <48 months, and
71% for IBTR >2 cm (17). In considering reconservation surgery, patients
with IBTR must understand that the risks of recurrence are generally higher
than the risk of the first IBTR (Table 11-2), and that reconservation therefore
makes the most sense for IBTR which are in situ or small invasive lesions
and occur as late events, indicating indolent biology. Of note, most late IBTR
will be estrogen receptor (ER) positive, consistent with the long natural
history of ER-positive breast cancers, in which there are as many events in
years 5 to 10 and 10 to 15 as there are in years 0 to 5 (18).
For patients with IBTR electing reconservation surgery, whole breast RT is
indicated for any who did not initially receive it. For those who were
previously irradiated, whole breast RT cannot be repeated but—depending on
the location of the IBTR and the use of a “boost” to the initial tumor site—
partial breast RT may be an option (23–26), and consultation with a radiation
oncologist makes sense.
The Axilla
Management of the axilla in patients with IBTR comprises several scenarios.
If the patient has had a prior sentinel lymph node biopsy (SLNB) or axillary
lymph node dissection (ALND) and presents with IBTR coincident with
axillary recurrence, then—whether treated by mastectomy or reconservation
—a completion ALND is appropriate. For patients who had a prior SLNB or
ALND and present with IBTR and a clinically negative axilla, ALND has
been the historic norm, but reoperative SLNB is quite feasible. A total of 26
studies collectively demonstrated that reoperative SLNB succeeds more often
following SLNB than ALND, 81% versus 52%, but it remains unclear
whether the information gained is useful (27). We were the first to report
reoperative SLNB and were early advocates (28), but among our own
surgeons treating IBTR there appear to be no differences in (a) treatment
rendered or (b) subsequent local/regional/distant events among patients who
did versus did not have axillary restaging (29). Regardless of node status,
patients with invasive IBTR are at sufficient risk of distant relapse that
systemic therapy is always indicated (Table 11-1).
The Contralateral Breast
Many patients with IBTR request a contralateral prophylactic mastectomy
(CPM), and—except for those with genetic predisposition—need to
understand (a) the low risk of developing a contralateral breast cancer (3% to
5% per decade) (30), (b) the absence of a survival benefit from CPM (31),
and (c) the increased short- and long-term morbidity associated with CPM.
Options for the contralateral breast include no surgery, mastopexy,
augmentation, reduction, or CPM, and in a small minority of patients CPM
may be the only way to achieve symmetry. Management of the contralateral
breast is best decided in joint consultation between the oncologic surgeon, the
reconstructive surgeon, and the patient.
PROGNOSIS FOLLOWING IBTR
As above, patients with IBTR are at increased risk of other local events or of
distant relapse so consultation with a radiation oncologist to address the
possibility of additional RT and a medical oncologist to address systemic
therapy is reasonable. The spectrum of prognosis of patients with IBTR is a
function of the initial tumor stage, the DFI, and the extent/subtype of the
IBTR (32). At one extreme, mastectomy, ALND, and chemotherapy would
make the most sense for patients with IBTR whose initial cancers were high
risk and ER negative, with a short DFI, and an ER-negative invasive
recurrence in both breast and axilla. At the other extreme, reconservation and
hormonal therapy would be appropriate for patients with a low-risk ER-
positive primary cancer, a long DFI, and a small invasive or pure in situ
IBTR. In managing IBTR, one size does not fit all.
FOLLOW UP POST IBTR
For patients with IBTR treated with reconservation surgery, annual breast
imaging by mammography (+/− ultrasound) should continue. There is no
evidence to support imaging more often than annually, and except for
patients with genetic predisposition there is no evidence to support screening
MRI. For patients with IBTR treated by mastectomy (with or without breast
reconstruction) physical examination is sufficient to detect local recurrence
and in the absence of physical findings there is no role for local imaging of
any kind. For patients who presented with isolated IBTR and remain
asymptomatic following treatment, there is no evidence to support continued
screening for distant disease, but a metastatic workup (bone scan/CT or
PET/CT) makes sense for any patient with symptoms which are new,
persistent, and suspicious.
CONCLUSIONS
IBTR following BCT is infrequent and—if not associated with distant
metastases—is potentially curable. The breast can be managed by
mastectomy or reconservation, dependent on the initial tumor characteristics,
the DFI, and the extent of the IBTR. The axilla can be managed by ALND for
patients with coincident axillary metastasis and by reoperative SLNB for
those with clinically negative nodes. For patients treated by reconservation,
reirradiation may be feasible. For patients treated by mastectomy, there is a
wide range of options for reconstruction and for management of the
contralateral breast. Systemic adjuvant therapy must be considered for all
patients with invasive IBTR. The management of IBTR requires close
collaboration between the radiologist, oncologic surgeon, plastic surgeon,
radiation oncologist, and medical oncologist.

REFERENCES

1. Morrow M, Jagsi R, Alderman AK, et al. Surgeon recommendations and


receipt of mastectomy for treatment of breast cancer. JAMA
2009;302(14):1551–1556.
2. Anderson SJ, Wapnir I, Dignam JJ, et al. Prognosis after ipsilateral
breast tumor recurrence and locoregional recurrences in patients treated
by breast-conserving therapy in five National Surgical Adjuvant Breast
and Bowel Project protocols of node-negative breast cancer. J Clin
Oncol 2009;27(15):2466–2473.
3. Wapnir IL, Anderson SJ, Mamounas EP, et al. Prognosis after ipsilateral
breast tumor recurrence and locoregional recurrences in five national
surgical adjuvant breast and bowel project node-positive adjuvant breast
cancer trials. J Clin Oncol 2006;24(13):2028–2037.
4. Clarke M, Collins R, Darby S, et al. Effects of radiotherapy and of
differences in the extent of surgery for early breast cancer on local
recurrence and 15-year survival: an overview of the randomised trials.
Lancet 2005;366(9503):2087–2106.
5. National Comprehensive Cancer Network Clinical Practice Guidelines
in Oncology: Breast Cancer (Version 3.2018).
https://www.nccn.org/professionals/physician_gls/pdf/breast.pdf.
Accessed February 6, 2019.
6. Veronesi U, Cascinelli N, Mariani L, et al. Twenty-year follow-up of a
randomized study comparing breast-conserving surgery with radical
mastectomy for early breast cancer. N Engl J Med 2002;347(16):1227–
1232.
7. van Dongen JA, Voogd AC, Fentiman IS, et al. Long-term results of a
randomized trial comparing breast-conserving therapy with mastectomy:
European Organization for Research and Treatment of Cancer 10801
trial. J Natl Cancer Inst 2000;92(14):1143–1150.
8. van Tienhoven G, Voogd AC, Peterse JL, et al. Prognosis after treatment
for loco-regional recurrence after mastectomy or breast conserving
therapy in two randomised trials (EORTC 10801 and DBCG-82TM).
EORTC Breast Cancer Cooperative Group and the Danish Breast
Cancer Cooperative Group. Eur J Cancer 1999;35(1):32–38.
9. Bouganim N, Tsvetkova E, Clemons M, et al. Evolution of sites of
recurrence after early breast cancer over the last 20 years: implications
for patient care and future research. Breast Cancer Res Treat
2013;139(2):603–606.
10. Neuman HB, Morrogh M, Gonen M, et al. Stage IV breast cancer in the
era of targeted therapy: does surgery of the primary tumor matter?
Cancer 2010;116(5):1226–1233.
11. Peled AW, Sears M, Wang F, et al. Complications after total skin-
sparing mastectomy and expander-implant reconstruction: effects of
radiation therapy on the stages of reconstruction. Ann Plast Surg
2018;80(1):10–13.
12. Cordeiro PG, Snell L, Heerdt A, et al. Immediate tissue
expander/implast breast reconstruction after salvage mastectomy for
cancer recurrence following lumpectomy/irradiation. Plast Reconstr
Surg 2012;129(2):341–350.
13. DeLong MR, Tandon VJ, Rudkin GH, et al. Latissimus dorsi flap breast
reconstruction—a nationwide inpatient sample review. Ann Plast Surg
2017;78(5 Suppl 4):S185–S188.
14. Levine SM, Patel N, Disa JJ. Outcomes of delayed abdominal-based
autologous reconstruction versus latissimus dorsi flap plus implant
reconstruction in previously irradiated patients. Ann Plast Surg
2012;69(4):380–382.
15. Erdmann-Sager J, Wilkins EG, Pusic AL, et al. Complications and
patient-reported outcomes after abdominally based breast reconstruction:
results of the mastectomy reconstruction outcomes consortium study.
Plast Reconstr Surg 2018;141(2):271–281.
16. Macadam SA, Zhong T, Weichman K, et al. Quality of life and patient-
reported outcomes in breast cancer survivors: a multicenter comparison
of four abdominally based autologous reconstruction methods. Plast
Reconstr Surg 2016;137(3):758–771.
17. Gentilini O, Botteri E, Veronesi P, et al. Repeating conservative surgery
after ipsilateral breast tumor reappearance: criteria for selecting the best
candidates. Ann Surg Oncol 2012;19(12):3771–3776.
18. Early Breast Cancer Trialists’ Collaborative Group (EBCTCG). Effects
of chemotherapy and hormonal therapy for early breast cancer on
recurrence and 15-year survival: an overview of the randomised trials.
Lancet 2005;365(9472):1687–1717.
19. Salvadori B, Marubini E, Miceli R, et al. Reoperation for locally
recurrent breast cancer in patients previously treated with conservative
surgery. Br J Surg 1999;86(1):84–87.
20. Voogd AC, van Oost FJ, Rutgers EJ, et al. Long-term prognosis of
patients with local recurrence after conservative surgery and
radiotherapy for early breast cancer. Eur J Cancer 2005;41(17):2637–
2644.
21. Ishitobi M, Komoike Y, Nakahara S, et al. Repeat lumpectomy for
ipsilateral breast tumor recurrence after breast-conserving treatment.
Oncology 2011;81(5-6):381–386.
22. Komoike Y, Motomura K, Inaji H, et al. Repeat lumpectomy for patients
with ipsilateral breast tumor recurrence after breast-conserving surgery.
Preliminary results. Oncology 2003;64(1):1–6.
23. Deutsch M. Repeat high-dose external beam irradiation for in-breast
tumor recurrence after previous lumpectomy and whole breast
irradiation. Int J Radiat Oncol Biol Phys 2002;53(3):687–691.
24. Resch A, Fellner C, Mock U, et al. Locally recurrent breast cancer: pulse
dose rate brachytherapy for repeat irradiation following lumpectomy—a
second chance to preserve the breast. Radiology 2002;225(3):713–718.
25. Kauer-Dorner D, Potter R, Resch A, et al. Partial breast irradiation for
locally recurrent breast cancer within a second breast conserving
treatment: alternative to mastectomy? Results from a prospective trial.
Radiother Oncol 2012;102(1):96–101.
26. Trombetta M, Hall M, Julian TB. Long-term followup of breast
preservation by re-excision and balloon brachytherapy after ipsilateral
breast tumor recurrence. Brachytherapy 2014;13(5):488–492.
27. Maaskant-Braat AJ, Voogd AC, Roumen RM, et al. Repeat sentinel
node biopsy in patients with locally recurrent breast cancer: a systematic
review and meta-analysis of the literature. Breast Cancer Res Treat
2013;138(1):13–20.
28. Port ER, Fey J, Gemignani ML, et al. Reoperative sentinel lymph node
biopsy: a new option for patients with primary or locally recurrent breast
carcinoma. J Am Coll Surg 2002;195(2):167–172.
29. Ugras S, Matsen C, Eaton A, et al. Reoperative sentinel lymph node
biopsy is feasible for locally recurrent breast cancer, but is it
worthwhile? Ann Surg Oncol 2016;23(3):744–748.
30. Nichols HB, Berrington de Gonzalez A, Lacey JV Jr, et al. Declining
incidence of contralateral breast cancer in the United States from 1975
to 2006. J Clin Oncol 2011;29(12):1564–1569.
31. Wong SM, Freedman RA, Sagara Y, et al. Growing use of contralateral
prophylactic mastectomy despite no improvement in long-term survival
for invasive breast cancer. Ann Surg 2017;265(3):581–589.
32. Witteveen A, Kwast AB, Sonke GS, et al. Survival after locoregional
recurrence or second primary breast cancer: impact of the disease-free
interval. PloS One 2015;10(4):e0120832.
CHAPTER 12

Radiation Therapy Following Breast-


Conserving Surgery
JENNIFER L. PRETZ | LAURA E. G. WARREN

In 2019, an estimated 270,000 women were diagnosed with breast cancer,


making the disease the most common nonskin malignancy in women.
Radiation therapy (RT) is an integral component of breast cancer care for
many women (1). Fifty years ago, RT was only used after mastectomy in
patients with high-risk disease. However, as surgical techniques evolved from
radical mastectomy to less invasive and less morbid procedures, RT became
an important adjuvant treatment after lumpectomy as a means to reduce the
risk of local recurrence (LR) in the setting of a less aggressive surgical
resection.
Over the last several decades, several prospective clinical trials have been
conducted to demonstrate the equivalence of less extensive surgical
techniques to radical mastectomy. The National Surgical Adjuvant Breast and
Bowel Project (NSABP) B-04 trial (2), initiated in 1971, led to a paradigm
shift away from radical mastectomy to modified radical mastectomy (MRM).
Contemporaneously, investigators at the Milan Cancer Institute compared
MRM with breast-conserving surgery (BCS) and adjuvant RT and
demonstrated equivalent long-term survival rates (3). Additional studies
confirmed the equivalence of breast conserving therapy with MRM (4–8).
Given the potential physical and psychosocial morbidity of mastectomy, BCS
followed by radiotherapy became the standard of care for the treatment of
early-stage breast cancer in the late 1980s.
RT planning and delivery techniques were relatively rudimentary at the
time of these early trials. Over the subsequent decades, breast RT evolved
and improved. The adoption of computed tomography (CT) into radiation
planning allowed for three-dimensional (3D) dose calculation. It also allowed
for direct visualization of a patient’s unique anatomy. By directly visualizing
the tumor bed and/or area at risk, dose delivery could be optimized to avoid
neighboring normal tissues and maximize delivery to the target. CT imaging
could also confirm patient positioning and reduce uncertainty in patient setup.
This same period saw similar improvements in surgical techniques,
imaging, and pathologic evaluation. Multidisciplinary improvements in care
led to decreased risks of locoregional recurrence; the risk of LR is now
thought to be approximately 0.5% per year (9–11). Many studies have also
now confirmed the relationship between breast cancer subtype and LR, with
estrogen receptor (ER)-positive or progesterone receptor (PR)-positive,
human epidermal growth factor receptor (HER-2)–negative patients and
ER+/PR+/HER-2+ patients demonstrating low rates of LR compared to
patients with triple-negative (ER−/PR−/HER-2−) or ER−/PR−/HER-2+
subtypes (12–14). For some patients, such excellent local control outcomes
have compelled attempts to reduce the total volume of breast tissue treated
(by using partial breast irradiation) or to consider omission of RT in select
populations. For women undergoing BCS with involvement of their axillary
lymph nodes, recent trials have attempted to better understand the role of RT
directed at the regional draining nodal basins given the potential toxicities
associated with larger radiation fields. This chapter will address the evolving
role of adjuvant RT after BCS including current practices and future
directions.
INVASIVE DISEASE
Radical mastectomy, introduced by Halsted and Meyer, was the standard of
care for the surgical management of breast cancer for most of the 20th
century. In 1971, the NSABP initiated the B-04 clinical trial to determine if
radical mastectomy was equivalent to other locoregional treatment
approaches; treatment approaches were stratified based on clinical lymph
node involvement. Although the study was not powered to detect small
differences between arms, no statistically significant advantages in either
disease-free or overall survival (OS) were seen with more aggressive surgery
after 20 years of follow-up (2).
After radical surgery was not shown to improve outcomes, several groups
began to investigate breast-conserving therapy with lumpectomy or
quadrantectomy followed by whole breast RT. Several prospective,
randomized trials were initiated to determine whether a breast conserving
approach would be equivalent to mastectomy. The largest U.S. breast-
conservation trial, NSABP B-06, randomized women to mastectomy,
lumpectomy alone, or lumpectomy followed by radiotherapy. After greater
than 20 years of follow-up, no significant differences in either local control or
survival were observed between patients treated with mastectomy and those
treated with lumpectomy and radiotherapy (5). The results of six modern
trials are shown in Table 12-1. With long-term follow-up available, these
trials consistently demonstrate no adverse effect on survival with breast-
conservation therapy versus mastectomy (3–8).

TABLE 12-1 Prospective Randomized Trials of Mastectomy Versus


Breast-Conserving Treatment for Invasive Breast Cancer
After the results of these trials became available, the National Institutes of
Health held a consensus development conference on the treatment of early-
stage breast cancer. The panel concluded that BCS followed by radiotherapy
was preferable to mastectomy because it provides equivalent outcome while
preserving the breast and reducing physical and psychological morbidity
(15).
The trials cited above demonstrated that BCS and adjuvant RT could
afford patients with breast cancer the opportunity to preserve their breast and
receive equivalent cancer-directed therapy to mastectomy. However, the
relative contribution of RT to these comparable outcomes was an active
question of research. Therefore, several randomized trials were undertaken to
see if BCS alone would result in similar outcomes to BCS and adjuvant RT
(5,16–20). In NSABP B-06 described above, patients treated with
lumpectomy alone compared to lumpectomy followed by RT showed a
significantly increased incidence of LR at 20 years. Specifically, the addition
of radiotherapy decreased the risk of LR after BCS from 39.2% to 14.3% (5).
The long-term results of these trials are summarized in Table 12-2. These
trials consistently demonstrated that adjuvant RT decreased the relative risk
of LR by approximately 55% to 80%; however, they failed to show a survival
benefit with the addition of adjuvant RT to BCS.

TABLE 12-2 Prospective Randomized Trials of Breast-Conserving Surgery


With or Without Radiotherapy for Invasive Breast Cancer

However, in 2005, the Early Breast Cancer Trialists’ Collaborative Group


(EBCTCG) published the results of a meta-analysis of 42,000 women in 78
randomized treatment comparisons. These patients included 7,300 women
treated in 10 trials with BCS, with or without radiotherapy. In this first
publication, radiotherapy reduced the risk of LR from 26% to 7% at 5 years.
Notably, the addition of radiotherapy decreased the 15-year breast cancer
mortality risk from 35.9% to 30.5%, with an overall mortality reduction of
5.3% (21). In 2011, the EBCTCG published an updated analysis, now
including 10,801 women (with both pathologically involved and uninvolved
axillary lymph nodes) and again demonstrated a significant reduction in the
10-year risk of any (i.e., locoregional or distant) first recurrence from 35.0%
to 19.3% and a reduction in the 15-year risk of breast cancer deaths from
25.2% to 21.4% (absolute reduction 3.8%, confidence interval 0.8% to 5.8%)
(22). These benefits were consistent across subgroups of women. While
individual trials could not confirm a survival benefit to adjuvant RT despite a
significant benefit in LR, the EBCTCG analysis provided evidence that
adjuvant RT after BCS reduced the risk of dying from breast cancer.
DUCTAL CARCINOMA IN SITU
As with invasive disease, ductal carcinoma in situ (DCIS) was initially
managed with mastectomy, but breast conservation was subsequently offered
as an alternative option given equivalent outcomes when compared to
mastectomy. Investigators again questioned the relative benefit of RT after
BCS, resulting in four large, prospective trials randomizing patients with
DCIS to adjuvant RT or no RT after BCS. These trials consistently showed
significant reductions in LR with radiotherapy and are summarized in Table
12-3. In the NSABP B-17 trial, 818 patients were randomized to BCS versus
BCS plus RT. At a median follow-up of 17.3 years, adjuvant RT reduced the
risk of an ipsilateral breast event from 35% to 19.7% (23). The European
Organization for Research and Treatment of Cancer (EORTC) 10853 trial
similarly randomized 1,010 patients to BCS with or without adjuvant RT
(24). RT reduced the risk of local failure at 10 years from 26.4% to 15.0%
(24). A United Kingdom, Australia, and New Zealand (UK/ANZ) group
conducted a trial designed with a 2 × 2 factorial approach to assess the effects
of both radiotherapy and tamoxifen after lumpectomy. Long-term results of
this trial were published at a median follow-up of 12.7 years and showed that
in 1,701 women, RT reduced the incidence of ipsilateral invasive disease and
DCIS from 19.4% to 7.1% in 10 years (25). In a Swedish trial, 1,046 patients
were randomized to resection with or without radiotherapy. At a mean
follow-up of 8 years, the absolute risk reduction from RT on ipsilateral breast
events was 16% at 10 years (26). A meta-analysis of these four randomized
trials reported that the addition of radiotherapy reduces the risk of LR by
approximately 60% (27). Although no trial was sufficiently powered to
demonstrate a significant improvement in OS, the trials that reported event-
free or disease-free survival (DFS) consistently showed a significant benefit
from radiotherapy (24,26).

TABLE 12-3 Prospective Randomized Trials of Lumpectomy With or


Without Radiotherapy for Ductal Carcinoma in Situ
OMISSION OF RADIATION THERAPY IN SELECT POPULATIONS
As demonstrated in the multiple randomized trials reviewed above, adjuvant
breast RT decreases the risk of a LR and may in some cases improve OS.
Indeed, postoperative whole breast RT remains the standard of care for most
patients treated by BCS.
In some select cases, however, the risk of a LR is quite low, and studies
have suggested that there may be a subgroup of patients in whom adjuvant
radiation may provide only modest benefit (20,28–31). This subgroup
generally includes older women with early-stage, hormone-positive invasive
breast cancer. This raises the question of whether radiation can be reasonably
omitted without compromising clinical outcomes.
This question was investigated in a randomized fashion by the Cancer and
Leukemia Group B (CALGB), who ran the CALGB 9343 trial that compared
adjuvant tamoxifen alone versus adjuvant tamoxifen and RT in elderly
women with favorable disease (32). In this study, 636 women aged 70 or
older who had clinical T1N0 and ER+ breast cancer treated with lumpectomy
were randomized to receive tamoxifen alone for 5 years, or tamoxifen in
combination with whole breast RT. With a median follow-up of 12.6 years
the 10-year freedom from local regional recurrence was 98% in the tamoxifen
and RT arm versus 90% in the tamoxifen-alone arm. Of the patients who had
recurrences, there was no difference in time to mastectomy or time to distant
metastases (DM). Further, there was no difference in 10-year breast cancer–
specific survival or OS between the arms (10-year OS was 67% in the
tamoxifen and RT arm vs. 66% in the tamoxifen-alone arm).
Another randomized trial aimed to address the omission of radiation in a
favorable population was reported in the United Kingdom. The PRIME II
study was a multicenter trial that randomized 1,326 women aged 65 or older
with hormone-positive, low-risk, invasive breast cancer who were receiving
adjuvant endocrine therapy, to whole breast radiation versus no radiation
(33). Low risk was defined by the study investigators as tumors that were less
than or equal to 3 cm in size with excision to at least 1-mm margins, and
pathologic axillary node negative. Patients could have a grade 3 tumor or
lymphovascular invasion but not both. After a median follow-up of 5 years,
ipsilateral breast recurrence rates were 1.3% in the RT group and 4.1% in the
no-RT group (p = 0.0002). There was no difference in regional recurrence,
DM, or breast cancer–specific survival. The 5-year OS was also the same
(93.9% in both groups). Taken together, these two large randomized studies
are consistent in showing that while RT does lower ipsilateral breast tumor
recurrence, recurrence rates in these select populations are overall quite low.
Furthermore, the absolute difference in LR between the RT and no-RT arms
does not translate into differences in other important endpoints, including OS.
Current ongoing studies are looking to further characterize and identify
patients with invasive breast cancer where radiation may be reasonably
omitted. The LUMINA trial being run by the Ontario Clinical Oncology
Group is a prospective cohort study evaluating LR risk following BCS and
endocrine therapy (and no radiation) in a population of women felt to be at
very low risk of ipsilateral breast tumor recurrence based on patient and
pathologic characteristics (ClinicalTrials.gov Identifier: NCT01791829).
They define this group of women as being 55 years or older with a single
focus of invasive disease measuring 2 cm or less and excised to at least a 1-
mm margin; ER and PR positive, HER-2 negative; grade 1 to 2; without
lymphovascular invasion and pathologically node negative. Subjects are
being followed for 10 years and will be assessed for disease recurrence, new
primary cancers, and survival.
Additional ongoing studies are now also considering tumor gene
expression profiling, in addition to traditional pathologic characteristics, as a
means by which to select patients who may avoid RT. The IDEA study
(Individualized Decisions for Endocrine Therapy Alone) out of the
University of Michigan is prospectively collecting rates of locoregional
recurrence in selected patients who receive endocrine therapy but do not
receive RT after lumpectomy (ClinicalTrials.gov Identifier: NCT02400190).
Patients in this study must be aged 50 to 69, postmenopausal, have ER+, PR+
and HER-2–negative breast cancer, and have an Oncotype DX breast
recurrence score less than or equal to 18. Also ongoing is the PRECISION
trial (Profiling Early Breast Cancer for Radiotherapy Omission), a phase II
study led by the Dana-Farber Cancer Institute (ClinicalTrials.gov Identifier:
NCT02653755). PRECISION is enrolling women between the ages of 50 and
75 with ER+ or PR+ and HER-2–negative, T1N0 breast cancer. In this trial,
all enrolled patients have their tumor sample analyzed via a transcriptional
profile of 50 genes (the Prosigna Breast Cancer Prognostic Gene Signature
Assay, formerly called the PAM50 test) for risk stratification purposes.
Eligible patients have ER+ or PR+/HER-2− tumors and Prosigna results
deemed low risk by study investigators. If the patient is eligible and willing
to participate on trial, they omit adjuvant RT and proceed with adjuvant
hormonal therapy alone. If the Prosigna results deem the patient not low risk,
the patient is ineligible for omission of radiation, and they are recommended
to proceed with radiation and endocrine therapy as per the standard of care.
All enrolled patients, regardless of receipt of RT, are being followed for
tumor recurrence and survival endpoints.
The above omission studies investigate omission of adjuvant radiation in
the setting of invasive disease. Patients with DCIS who have BCS in the
modern era also generally have low recurrence rates and many have favorable
features, which makes tailoring adjuvant therapy of interest in this population
as well. In 1996, investigators from the University of Southern California
introduced the Van Nuys Prognostic Index. This was a retrospective analysis
of 333 patients with DCIS treated with BCS (195 by excision only and 138
by excision followed by radiotherapy). Pathologic evaluation of surgical
specimens was particularly rigorous, with tissue sectioned in 2- to 3-mm
intervals and processed in sequence. Multivariate analysis showed tumor size,
margin width, and pathologic classification to be predictors of recurrence.
This report concluded that patients with low-grade tumors ≤15 mm without
necrosis that were resected with at least a 10-mm surgical margin could be
treated with excision alone (34). Since its introduction, however, several
authors have attempted to independently validate the Van Nuys Prognostic
Index and these series have not shown the index to be a reliable predictor of
LR (35,36).
Investigators at the Dana-Farber Cancer Institute attempted to
prospectively determine whether radiotherapy can be reasonably omitted in
patients with small (<2.5 cm), low- or intermediate-grade DCIS tumors
resected with at least 10-mm surgical margins. Use of tamoxifen was not
permitted in this study. In 2002, their study was closed to accrual after an
interim analysis found that recurrence rates were unexpectedly high. With a
median follow-up of 11 years and 143 patients available for analysis, the 10-
year rate of ipsilateral LR was 15.6%. Of the LRs, 32% were invasive (37).
The authors concluded that there was still a substantial ongoing risk of LR
even in this population of patients with favorable DCIS.
The Radiation Therapy Oncology Group (RTOG) designed a randomized
trial for omission of radiation for patients diagnosed with DCIS undergoing
BCS. RTOG 9804 randomized 636 patients with mammographically
detected, low or intermediate grade DCIS measuring less than 2.5 cm and
excised with margins of at least 3 mm to adjuvant radiation or observation
(38). Tamoxifen use was optional and reported in 62% of enrolled patients.
This study closed early due to slow accrual. With a median follow-up of 7.17
years, the 7-year local failure rate was 0.9% in the radiation arm and 6.7% in
the observation arm (p < 0.001). There was no difference in DFS or OS
between the arms. Long-term results have been presented in abstract form to
date. At a median follow-up of 12.4 years, the 12-year cumulative incidence
of LR was 2.8% for patients receiving adjuvant RT and 11.4% with
observation (p = 0.0001). Again there were no significant differences
observed with regard to OS, DFS, or mastectomy use (39). Investigators are
now trying to better understand the risk of recurrence for a given individual
patient with DCIS and therefore the absolute benefit of adjuvant RT. Tests
such as Oncotype DX Breast DCIS (Genomic Health) and DCISionRT
(Prelude Dx) have been developed specifically for this purpose and are
integrating into clinical use.
Omission of radiation offers the opportunity to spare patients the physical
and emotional burden of radiation-associated side effects and saves treatment
time and cost. Ultimately however, the decision must be made on a patient-
by-patient basis and in consultation with a radiation oncologist. Universally it
has been shown that even in very low–risk breast cancer populations, in
invasive and DCIS tumors alike, radiation decreases the chance of a LR.
Patients should be counseled that without radiation, the rate of an ipsilateral
breast recurrence may be higher over time. The omission trials to date are
also heterogeneous in the use of adjuvant endocrine therapy, and in the
definition of a low-risk patient, in particular, as it pertains to tumor grade,
tumor size, lymphovascular invasion, and margin status. Thus, the choice to
omit adjuvant RT should not only take into consideration disease-specific
characteristics, but other important patient characteristics including
comorbidities, willingness to take endocrine therapy, interest in ongoing
clinical trials, and their personal values and preferences.
FIGURE 12-1 A patient immobilization device (A) and patient setup (B).
RADIATION TARGET VOLUME, DOSE, AND FRACTIONATION
The target for standard postoperative radiotherapy is the entire ipsilateral
breast. In general, the breast is treated with megavoltage photons generated
by a linear accelerator using opposed tangential fields that encompass the
entirety of the breast, chest wall, and low axilla. If the regional lymph node
chains are at risk for harboring microscopic disease, additional or modified
fields are used to encompass the full axilla, supraclavicular lymph nodes,
and/or internal mammary lymph nodes at the discretion of the treating
radiation oncologist. The treatment planning process begins with a planning
session, where the patient is set up on a treatment couch in a position that
allows access to the intended target. Typically, the patient is positioned in the
supine position with the ipsilateral arm abducted such that RT beams do not
enter or exit through the arm, and immobilization devices are utilized to limit
patient motion. An alternative approach is to position the patient prone with
her arms abducted on a specialized board with an opening for the target
breast only. When the patient lies on the board, the breast being treated falls
through the opening and away from the body. The goal is to identify, for each
patient, a position that facilitates treatment of the breast that is also
reproducible on a day-to-day basis. A typical patient setup is shown in
Figure 12-1. A CT scan is obtained of the patient in the treatment position.
This CT data set is then imported into the radiation treatment planning
system such that a 3D model of the patient’s body in the treatment position is
created. This process allows the radiation oncologist to precisely identify the
target breast tissue and also nearby nontarget tissue (including the lungs,
heart, and contralateral breast). Radiation beam angles and beam energies are
customized to each patient’s anatomy so that an optimized radiation plan is
created. This process is known as three-dimensional conformal radiotherapy
(3D-CRT).
The early trials that evaluated whole breast radiation after lumpectomy
typically employed radiation dose of 50 Gy given in 25 daily fractions (2 Gy
per fraction) over a period of 5 weeks (3,20). This protracted schedule of
radiation (referred to as “conventional fractionation” [CF]), while proven
effective, is time consuming for patients, and resource intensive for the
treating radiation oncology department. Many women (up to 20% in some
estimates) who undergo BCS may not receive the recommended course of
adjuvant radiation because of these factors (40,41). Additionally, studies
suggested that a higher dose per day given over a fewer number of total days
(referred to as “hypofractionation” [HF]) may be as effective in controlling
tumor recurrence without added toxicity (42–45).
Two large-scale randomized trials have directly compared outcomes
between CF and HF. The Canadian study randomized women with invasive
breast cancer measuring less than 5 cm who had undergone BCS and had
pathologic negative axillary nodes to 50 Gy of radiation given in 25 fractions
versus 42.5 Gy given in 16 fractions (46). Radiation was delivered to the
whole breast, without treatment of additional nodal regions. There were 1,234
patients enrolled, and with a median follow-up of 12 years, there was no
difference in breast recurrence, OS, acute radiation toxicity, or cosmetic
results. The 10-year LR rates were 6.7% (CF) versus 6.2% (HF). Grade 3
toxicity was reported 70.5% (CF) versus 66.8% (HF). Approximately 70% of
women in both arms reported their overall cosmetic outcome to be good or
excellent.
The START trials from the United Kingdom also provided evidence that
HF is an acceptable and perhaps even more effective radiation schedule for
the appropriately chosen breast cancer patient (47). These multicenter
randomized trials included women with invasive early-stage and node-
negative breast cancer that was completely excised. Approximately 90% of
patients enrolled on these trials underwent BCS. The START-A trial enrolled
2,236 patients and compared 50 Gy in 25 fractions to 41.6 Gy or 39 Gy in 13
fractions (all courses delivered over a period of 5 weeks). The START-B trial
enrolled 2,215 patients and compared 50 Gy in 25 fractions (given over 5
weeks) with 40 Gy in 15 fractions (given over 3 weeks). In START-A, the
10-year local regional recurrence was not statistically different between the
arms: 7.4% (50-Gy arm) versus 6.3% (41.6-Gy arm) versus 8.8% (39-Gy
arm). In START-B, the 10-year local regional recurrence was also
comparable between arms: 5.5% (50-Gy arm) versus 4.3% (40-Gy arm). The
START-B trial also interestingly showed improvement in DM and all-cause
mortality with HF versus CF (DM 7.5% vs. 10.5%, respectively, p = 0.014
and OS 7.9% vs. 10.9%, respectively, p = 0.042). Furthermore, in START-B,
breast shrinkage, telangiectasias, and breast edema were all significantly less
in the HF group.
The results of these studies confirm that a HF RT schedule is at least as
good as the historic CF schedule, when it comes to multiple important
endpoints including local regional control and radiation-associated toxicity.
HF RT has thus become common practice in patients who are similar to those
enrolled on these studies, generally when treatment of the whole breast alone
is indicated. Limited data is available regarding hypofractionation when
regional nodal radiation is indicated, though studies are ongoing.
In addition to treatment of the whole breast, it is typical to add a “boost,”
or additional radiation dose beyond that delivered to the whole breast, to the
lumpectomy cavity. Data for this approach was initially reported by
investigators from Lyon, France, who randomized 1,024 women with early
breast cancer (tumors ≤3 cm) resected with negative margins to 50 Gy of
postoperative whole breast radiotherapy with or without an additional 10-Gy
boost (48). The boost dose was delivered to the tumor bed using an “en face”
electron field. At 5 years, the risk of LR was reduced from 4.5% to 3.6% (p =
0.044) with the addition of the boost. No deleterious cosmetic outcomes with
the addition of the boost were reported. The EORTC also randomized 5,318
patients with T1–2 N0–1 breast cancer resected with negative margins to 50
Gy of whole breast radiotherapy with or without a 16-Gy electron boost.
After a median follow-up of 10.8 years, the risk of LR was reduced from
10.2% to 6.2% (p < 0.0001). Severe fibrosis, however, was reported in 4.4%
of patients in the boost group, compared to 1.6% in the control arm (p <
0.0001) (49).
After the results of these trials became available, the addition of a boost
became standard for most patients after lumpectomy. In the United States, the
most common treatment schedule when using CF is the delivery of 50 Gy to
the entire breast followed by a 10-Gy boost to the tumor bed, given over 30
daily treatments (5 days/wk or 6 weeks). When HF is utilized, it is also
common to add boost dose, although the use of boost has not been
specifically studied in the setting of hypofractionation. The Canadian
hypofractionation trial did not allow for a boost, and the START-B trial had a
boost delivered in only 43% of patients. In 2018, the American Society of
Radiation Oncology (ASTRO) published their evidence-based guidelines for
whole breast RT (50). Their preferred dose-fractionation scheme for whole
breast HF RT was 4,000 cGy in 15 fractions or 4,250 cGy in 16 fractions. A
1,000 cGy boost in either 4 to 5 fractions for selected patients was
recommended. For either CF or HF, they recommended omission of the
tumor bed boost in patients older than 70 with hormone receptor–positive
cancer and low- or intermediate-grade tumors resected with widely negative
margins (> or equal to 2 mm) but described the evidence as “moderate” when
making these recommendations.
While whole breast RT remains the standard of care across patient
subgroups, there is evidence that in selected patients targeted treatment of
only the portion of the breast where the tumor was removed may be as
effective as whole breast RT in regard to oncologic outcomes, and may also
reduce treatment time and toxicity. This technique of RT delivery to a limited
area of the breast is referred to as accelerated partial breast irradiation
(APBI).
The rationale behind whole breast RT originates in older pathologic studies
suggesting that microscopic disease may be present several centimeters from
the primary lesion (51,52). In the modern era, lumpectomy is usually
performed after image-guided wire or radioseed localization of the tumor.
Likely better tumor imaging and surgical localization informs more modern
studies that suggest that microscopic disease extends only 1 to 2 cm beyond
the lumpectomy cavity (53,54). In addition, studies of failure patterns after
BCS indicate that the vast majority of recurrences occur in close proximity to
the original tumor and that the incidence of new primary lesions does not
appear to be reduced by whole breast radiotherapy (55–57). Thus, treatment
of only the area surrounding the lumpectomy cavity may be appropriate for
conservatively selected patients.
The benefits of APBI include the reduction of treatment time from 4 to 6
weeks to as few as 1 to 5 days. However, in order to facilitate more rapid
treatment delivery, a larger dose per fraction is utilized and therefore
localization of the therapy requires precision and a very conformal treatment
plan. Additional benefits include decreased cost and inconvenience to
patients with decreased treatment time, potentially improved utilization of
BCS as patients who could not previously undergo adjuvant RT may now be
able to, potential reduction in acute and chronic toxicity, and improved
quality of life for patients. There are many available techniques for delivering
APBI including interstitial brachytherapy, intracavity therapy, and external
beam RT. APBI was originally investigated using multicatheter interstitial
brachytherapy. Brachytherapy refers to a delivery method in which the source
of radiation is placed within the target tissue. The multicatheter technique
involves the placement of afterloading catheters into the breast and around
the lumpectomy cavity. Catheters are placed by the radiation oncologist
under either ultrasound or CT guidance. A thorough understanding of
brachytherapy physics is essential for proper catheter positioning. As with
external beam therapy, multicatheter implant treatments are planned using 3D
software. Treatments are delivered using a high-dose–rate afterloaded 192Ir
source. Technically complex, multicatheter implants offer a high degree of
dosimetric flexibility and can be used to treat targets of any shape or location,
regardless of breast size. An example of a multicatheter implant and
treatment plan can be seen in Figure 12-2.
Multicatheter brachytherapy is the APBI technique associated with the
longest follow-up and outcome data. Mature results from several single-
institution series demonstrate low risk of ipsilateral breast cancer recurrence
and good cosmetic results in appropriately selected patients. A pooled
multicenter analysis including 1,131 patients treated 1992 to 2013 with
adjuvant APBI delivered with interstitial multicatheter brachytherapy showed
a 10-year risk of an ipsilateral tumor recurrence of 7.6%. Other 10-year
outcomes included the risk of regional failure, 2.3%, DM, 3.8%, and cause-
specific survival, 96.3%. Physician-reported cosmesis was excellent/good in
84% of patients with greater than 5 years of follow-up (58). More recently,
results from the phase III multicenter Groupe Européen de Curiethérapie of
European Society for Radiotherapy and Oncology (GEC-ESTRO)
randomizing patients to APBI using multicatheter brachytherapy or whole
breast RT were published (59). At a median 5-year follow-up, among the
1,184 patients with low-risk invasive and in situ breast cancer, the incidence
of LR was 1.55% with APBI and 0.92% with whole breast RT (p = 0.42).
There was a trend toward increased risk of grade 2 to 3 late side effects to the
skin with whole breast RT (5.7% vs. 3.2% respectively, p = 0.08). The
authors concluded that APBI was not inferior to adjuvant whole breast RT
with respect to local control. The challenges of interstitial brachytherapy are
that it is an invasive procedure requiring clinical expertise, formal training,
and either a hospital stay or multiple visits with the catheters in place.
Intracavitary therapy was developed to try to improve upon some of the
disadvantages of interstitial implants. It can be delivered with an applicator,
such as the MammoSite (Hologic, Inc., Bedford, MA) or SAVI (Merit
Medical Systems, Inc., South Jordan, UT) devices, or in the operating room
utilizing intraoperative RT (IORT). Many clinical experiences using the
MammoSite have been published with good results in terms of oncologic and
cosmetic outcomes. The American Society of Breast Surgeons (ASBrS)
registry trial represents the largest published series to date. A total of 1,449
patients with early-stage breast cancer (87% invasive disease, 13% DCIS)
were treated. At a median follow-up of 63.1 months, the 5-year actuarial rate
of ipsilateral breast tumor recurrence was 3.8% (3.7% for invasive breast
cancer and 4.1% for DCIS). The percentage of patients with excellent/good
cosmetic results at 60 months was 91.3% (60).
FIGURE 12-2 A multicatheter implant (A) and treatment plan (B).

IORT is an APBI technique that delivers adjuvant RT in a single fraction at


the time of lumpectomy. Advantages to this intracavitary technique include
being able to precisely visualize the surgical cavity, and potentially decrease
dose to neighboring skin and subcutaneous tissue as these can be retracted
during treatment. However, given the delivery of dose at the time of surgery,
final pathology including margin status is typically not available. Two major
randomized IORT trials have been completed. The first, TARGIT-A,
randomized 3,451 patients to IORT delivered with orthovoltage photons
versus whole breast RT. At a median follow-up of 2 years 5 months, the 5-
year risk of LR was 3.3% for TARGIT versus 1.3% for whole breast RT (61).
The authors concluded that TARGIT in appropriately selected patients was
noninferior. The ELIOT trial compared single fraction IORT delivered with
intraoperative electrons to whole breast RT (62). The investigators found that
after a median follow-up of 5.8 years, the risk of in-breast tumor recurrence
(IBTR) was 4.4% for the 651 patients receiving IORT and 0.4% for the 654
patients receiving whole breast RT. Fewer skin side effects were noted in the
IORT arm. While the rate of IBTR was within the prespecified margin of
equivalence, the authors noted that it was notably greater than for those
patients receiving whole breast RT.
A major limitation to brachytherapy and intraoperative APBI techniques is
that they require special equipment and specialty personnel training in order
to safely and effectively deliver radiation dose. A standard linear accelerator
can also deliver dose to a partial breast volume, and external beam ABPI
techniques are much more generalizable, as most existing radiation centers
could implement external beam ABPI without additional resources. External
beam APBI techniques are also becoming increasingly feasible given modern
imaging and surgical techniques. Surgeons are routinely leaving radio-opaque
clips in the tumor bed, and with CT-based imaging utilized during planning,
radiation oncologists are better able to identify the surgical bed. The dose
typically delivered for patients receiving external beam APBI is 3,500 to
3,850 cGy in 10 fractions, either once a day for 2 weeks or twice a day for 1
week.
Patients receiving external beam APBI are treated in the supine or prone
position, and multiple beams are typically employed to maximize
conformality. An example of a 3D-CRT APBI plan is seen in Figure 12-3. A
variety of techniques have been described, including using multiple
noncoplanar photon beams in the supine position as pioneered by Dr. Frank
Vicini; treating patients in the prone position with multiple photon beams as
developed by Dr. Sylvia Formenti; and mixed photons and electrons as
developed at Massachusetts General Hospital. Published results using these
techniques have shown comparable oncologic outcomes and toxicities to
whole breast RT (63–65). NSABP B-39/RTOG 0413 is a randomized phase
III study of CF whole breast RT versus APBI for women with stage 0, I, or II
breast cancer. Preliminary results presented at the San Antonio Breast Cancer
Symposium (SABCS) in 2018 showed a 10-year rate of IBTR of 4.8% in the
APBI arm and 4.1% in the whole breast RT arm (66). Although this did not
meet the prespecified criteria for equivalence, the absolute difference was
<1%. Grade 3 to 5 toxicities were more common for APBI than whole breast
RT. Similarly, the RAPID trial randomized women with invasive tumors 3
cm or smaller or DCIS with negative lymph nodes and surgical margins to
APBI versus whole breast RT. Data were presented in abstract form at
SABCS 2018; median follow-up was 8.6 years, and the 8-year cumulative
rates of IBTR were noninferior for the APBI arm (3.0% and 2.8% for the
APBI and whole breast RT patients, respectively) (67). While acute radiation
toxicity was less in patients receiving APBI, late radiation toxicity was
greater in patients receiving APBI. Adverse cosmesis was similarly higher for
patients treated with APBI at 5 years (32% vs. 16%).

FIGURE 12-3 A rendering (A) and treatment plan (B) for accelerated partial breast
irradiation with three-dimensional conformal radiotherapy.

Another recent study evaluating a partial breast approach using external


beam radiation is the United Kingdom IMPORT LOW trial (68). This was a
multicenter randomized trial that enrolled women over the age of 50 who had
BCS for invasive ductal carcinoma. The disease had to be unifocal, 3 cm or
less, and excised to at least 2 mm. Zero to three pathologically involved
nodes were allowed. This was a three-arm study that compared 40 Gy in 15
fractions to the whole breast (control arm) versus 36 Gy in 15 fractions to the
whole breast with integrated partial breast including tumor bed to 40 Gy in 15
fractions (reduced-dose group) versus 40 Gy in 15 fractions to the partial
breast including tumor bed only (partial breast group). With a median follow-
up of 72.2 months, local relapse was 1.1%, 0.2%, and 0.5% respectively, and
not statistically different between arms. Patient-related outcomes were
generally better in the partial breast group, with a statistically better breast
appearance at 5 years. The IMPORT LOW study is unique in that it is only
randomized trial to date that uses the same-dose fractionation regimen and
technique in the whole breast and partial breast groups.

TABLE 12-4 American Society for Radiology Oncology Patient Selection


Guidelines for Treatment With Accelerated Partial Breast Irradiation
Suitable Cautionary Unsuitable
• Age ≥50 yrs old • Age 40–49 yrs old if • Age <40 yrs
• T1 or Tis tumor all other suitable • Positive margins
• if Tis must be criteria met • DCIS >3 cm
screen detected, • Age ≥50 yrs old with BRCA1/2 mutation
low to intermediate one of the pathologic present
grade, size ≤2.5 features below Size >3 cm
cm, margins ≥3 without any
Axillary nodes
mm unsuitable factors
positive
• Invasive ductal • Size 2.1–3.0 cm
EIC >3 cm
carcinoma/other • T2
Extensive LVSI
favorable histology • Close margins (<2
Use of neoadjuvant
• Surgical margins mm)
therapy
negative by at least 2 • Limited/focal LVSI
mm for T1 • ER−
Pathologically node • Invasive lobular
negative histology
• No lymphovascular • Pure DCIS ≤3 cm
space invasion but criteria for
(LVSI) suitable not
Estrogen receptor entirely met
(ER) positive • EIC ≤3 cm
No EIC
DCIS, ductal carcinoma in situ; EIC, extensive intraductal component; Tis, carcinoma in-situ.

The appropriate application of APBI begins with careful patient selection.


Patients with a significant risk of microscopic disease remote from the
lumpectomy cavity are not optimal candidates for APBI. ASTRO has
published consensus guidelines for patient selection, most recently updated in
2017 (69,70). In general, patients aged ≥50 years with T1 or favorable risk
Tis as defined by the RTOG 9804, and who are lymph node negative, are
appropriate for treatment with APBI outside the setting of a clinical trial. The
ASTRO guidelines are summarized in Table 12-4.
REGIONAL NODAL RADIATION THERAPY
Local management of the regional lymph nodes is a complex topic requiring
multidisciplinary collaboration between radiologists, radiation oncologists,
and breast surgeons. Historically, axillary lymph node dissection (ALND)
was performed as a therapeutic and prognostic tool; it also provided
important pathologic information that guided adjuvant systemic therapy and
RT. However, additional information such as tumor biology and response to
neoadjuvant therapy have proven valuable when predicting clinical outcomes
and how much be taken into consideration when making clinical
recommendations.
For patients with clinically negative axillary lymph nodes, sentinel lymph
node biopsy is a less morbid means by which to stage the axilla and there
does not appear to be an oncologic detriment to this approach when
compared to ALND as seen in several clinical trials (71,72). Subsequent to
these trials, the question of whether SLNB alone is adequate axillary surgical
management in node-positive patients was evaluated. The landmark
American College of Surgeons Oncology Group (ACOSOG) Z0011 trial
addressed whether SLNB alone resulted in diminished survival in women
with early-stage breast cancer (73,74). Eligible patients were clinically stage
T1 or T2, node negative, but had one or two positive sentinel nodes at
surgery. Patients with matted lymph nodes and/or gross extranodal disease
were excluded. Patients undergoing BCS and adjuvant RT were randomized
to receive sentinel lymph node biopsy with or without completion ALND.
The borders of the tangential RT fields were unspecified, but the protocol did
prohibit a specific RT field directed at the lymph nodes. At a median follow-
up of 6.3 years, regional recurrence rates were 0.9% in the sentinel lymph
node biopsy arm alone compared to 0.5% in the ALND group. There were no
differences in DFS or OS. Surgeons were quick to adopt these findings and
studies examining surgical practices subsequent to this publication
demonstrated increasing omission of ALND in patients with positive sentinel
nodes undergoing whole breast irradiation (75,76). A recent evaluation of the
RT fields from a subset of trial patients complicates the interpretation of these
results (77). Information regarding RT administration was available for 605
(71%) patients. More detailed RT records, including fields used, were
available for 228 (27%) patients. A retrospective analysis of the extent of RT
coverage among the larger cohort of 605 patients demonstrated that, although
89% of patients received whole breast RT, 15% of patients also had
documented treatment to the supraclavicular region. Review of the records
from the 228 patients with detailed records available demonstrated that
18.9% received directed nodal RT using three or more fields. Given the
variability in RT fields, it is problematic to draw conclusions about the
necessity of either high tangents or directed nodal irradiation with the use of a
third field. However, it is likely for some proportion of the SLNB-alone
group that axillary RT contributed to the low regional recurrence rates.
The EORTC After Mapping of the Axilla: Radiotherapy Or Surgery?
(AMAROS) (10981/22023) trial also addressed the omission of completion
ALND in women with early-stage breast cancer (78). Patients with clinical
T1 to T2, N0 breast cancer with a positive sentinel lymph node biopsy were
randomized to receive ALND or nodal RT. In contrast to the Z0011 study,
however, all patients undergoing nodal radiation received treatment to both
the full axilla and the supraclavicular nodes. The 5-year axillary recurrence
rate was low in both arms: 0.43% in the ALND group and 1.19% in the
axillary RT group. DFS and OS rates were comparable. Lymphedema rates
and treatment were significantly higher in the ALND group (28% vs. 13.6%).
Although Z0011 and AMAROS demonstrated that in select groups of
node-positive early-stage breast cancer patients, ALND may not be required,
the studies did not address the relative contribution of regional nodal RT to
these outcomes. Two recent trials have attempted to address the value of
adjuvant nodal RT in the era of modern systemic therapy, and surgical and
RT techniques for patients undergoing BCS. NCIC- CTG MA.20 randomized
high-risk node-negative or node-positive breast cancer patients who
underwent BCS to whole breast RT or whole breast RT and regional lymph
node RT, which included the internal mammary nodes in the first three
intercostal spaces, the supraclavicular, and high axillary lymph nodes (79).
High-risk patients were defined as having a 5-cm or larger breast primary or a
2-cm or larger primary with fewer than 10 lymph nodes removed and one of
the following higher-risk features: ER-, grade 3 disease, or lymphovascular
invasion. At 10 years, there was no significant difference in OS but there was
improved DFS in patients receiving nodal irradiation, 82.0% compared to
77.0% (p = 0.01). Patients receiving regional nodal irradiation did
demonstrate higher rates of acute pneumonitis and lymphedema. Ten-year
results from the phase 3 EORTC 22922/10925 trial were surprisingly similar
(80). Eligible patients had pathologically positive axillary lymph nodes or
were node negative with central or medial tumors. Patients were randomized
to whole breast RT with or without internal mammary and medial
supraclavicular-directed radiation fields. At a median follow-up of 10.9 years,
this trial showed a trend toward improved OS (82.3% vs. 80.7%, P = 0.06)
and significantly improved DFS (72.1% vs. 69.1%, respectively; P = 0.04).
These trials do not distinguish between whether the benefit of nodal RT was
the result of supraclavicular or internal mammary RT.
In contrast, a trial from France attempted to measure the impact of internal
mammary node RT on OS and DFS in patients with breast cancer with
pathologically involved lymph nodes or central/medial tumors with or
without lymph node involvement. Although underpowered, the study did not
show an OS benefit with the use of internal mammary irradiation (81). There
was suggestion of a possible but not significant benefit in OS in a subgroup
analysis of pathologically node-negative patients with medial/central tumors.
Taken together, these data seem to suggest that untreated local regional
disease is detrimental to long-term survival, particularly in women for whom
their competing risk of distant disease is relatively small. The decision to
specifically target the regional lymph nodes with RT, and what lymph node
basins to target, is guided by patient and tumor specifics and ultimately at the
discretion of the treating radiation oncologist.
CONCLUSION
Adjuvant RT after BCS was originally adopted after studies showed
comparable local control and OS when compared to MRM. In recent years,
studies have demonstrated comparable oncologic results and improved
quality of life and decreased inconvenience for patients with shorter treatment
courses, so called hypofractionated RT. For women with lymph node–
positive breast cancer, radiation targeted at the regional lymph nodes in
addition to whole breast RT appears to not only offer a locoregional control
benefit but also a benefit in terms of DFS. Other studies have introduced the
concept of partial breast RT for selected, low-risk patients in whom the whole
breast may not need to be treated given that the risk of LR is highest at or
near the original tumor location. RT after BCS has been demonstrated across
patient subgroups to offer a local control benefit; however, after discussion
with their radiation oncologist, some patients with early-stage invasive or in
situ breast cancer may choose to omit adjuvant RT given the low absolute
benefit of treatment. Overall, RT after BCS remains standard of care for
patients with breast cancer as a means by which to reduce the risk of LR. It is
likely that the radiation target and treatment technique will continue to evolve
in coming years.

REFERENCES

1. American Cancer Society. Cancer Facts and Figures 2019. Atlanta:


American Cancer Society; 2019.
2. Fisher B, Jeong JH, Anderson S, et al. Twenty-five-year follow-up of a
randomized trial comparing radical mastectomy, total mastectomy, and
total mastectomy followed by irradiation. N Engl J Med 2002;347:567–
575.
3. Veronesi U, Cascinelli N, Mariani L, et al. Twenty-year follow-up of a
randomized study comparing breast-conserving surgery with radical
mastectomy for early breast cancer. N Engl J Med 2002;347:1227–1232.
4. Arriagada R, Lê MG, Rochard F, et al. Conservative treatment versus
mastectomy in early breast cancer: patterns of failure with 15 years of
follow-up data. Institut Gustave-Roussy Breast Cancer Group. J Clin
Oncol 1996;14:1558–1564.
5. Fisher B, Anderson S, Bryant J, et al. Twenty-year follow-up of a
randomized trial comparing total mastectomy, lumpectomy, and
lumpectomy plus irradiation for the treatment of invasive breast cancer.
N Engl J Med 2002;347:1233–1241.
6. Jacobson JA, Danforth DN, Cowan KH, et al. Ten-year results of a
comparison of conservation with mastectomy in the treatment of stage I
and II breast cancer. N Engl J Med 1995;332:907–911.
7. van Dongen JA, Voogd AC, Fentiman IS, et al. Long-term results of a
randomized trial comparing breast-conserving therapy with mastectomy:
European Organization for Research and Treatment of Cancer 10801
trial. J Natl Cancer Inst 2000;92:1143–1150.
8. Blichert-Toft M, Nielsen M, Düring M, et al. Long-term results of breast
conserving surgery vs. mastectomy for early stage invasive breast
cancer: 20-year follow-up of the Danish randomized DBCG-82TM
protocol. Acta Oncol 2008;47:672–681.
9. Buchholz TA, Tucker SL, Erwin J, et al. Impact of systemic treatment
on local control for patients with lymph node-negative breast cancer
treated with breast-conservation therapy. J Clin Oncol 2001;19:2240–
2246.
10. Cabioglu N, Hunt KK, Buchholz TA, et al. Improving local control with
breast-conserving therapy: a 27-year single-institution experience.
Cancer 2005;104:20–29.
11. Fisher B, Jeong JH, Dignam J, et al. Findings from recent National
Surgical Adjuvant Breast and Bowel Project adjuvant studies in stage I
breast cancer. J Natl Cancer Inst Monogr 2001;(30):62–66.
12. Arvold ND, Taghian AG, Niemierko A, et al. Age, breast cancer
subtype approximation, and local recurrence after breast-conserving
therapy. J Clin Oncol 2011;29:3885–3891.
13. Lowery AJ, Kell MR, Glynn RW, et al. Locoregional recurrence after
breast cancer surgery: a systematic review by receptor phenotype.
Breast Cancer Res Treat 2012;133:831–841.
14. Metzger-Filho O, Sun Z, Viale G, et al. Patterns of recurrence and
outcome according to breast cancer subtypes in lymph node-negative
disease: results from international breast cancer study group trials VIII
and IX. J Clin Oncol 2013;31:3083–3090.
15. NIH. Consensus statement: treatment of early-stage breast cancer.
National Institutes of Health Consensus Development Panel. J Natl
Cancer Inst Monogr 1992;1–5.
16. Veronesi U, Marubini E, Mariani L, et al. Radiotherapy after breast-
conserving surgery in small breast carcinoma: long-term results of a
randomized trial. Ann Oncol 2001;12:997–1003.
17. Clark RM, Whelan T, Levine M, et al. Randomized clinical trial of
breast irradiation following lumpectomy and axillary dissection for
node-negative breast cancer: an update. Ontario Clinical Oncology
Group. J Natl Cancer Inst 1996;88:1659–1664.
18. Liljegren G, Holmberg L, Bergh J, et al. 10-year results after sector
resection with or without postoperative radiotherapy for stage I breast
cancer: a randomized trial. J Clin Oncol 1999;17:2326–2333.
19. Holli K, Hietanen P, Saaristo R, et al. Radiotherapy after segmental
resection of breast cancer with favorable prognostic features: 12-year
follow-up results of a randomized trial. J Clin Oncol 2009;27:927–932.
20. Fisher B, Bryant J, Dignam JJ, et al. Tamoxifen, radiation therapy, or
both for prevention of ipsilateral breast tumor recurrence after
lumpectomy in women with invasive breast cancers of one centimeter or
less. J Clin Oncol 2002;20:4141–4149.
21. Clarke M, Collins R, Darby S, et al. Effects of radiotherapy and of
differences in the extent of surgery for early breast cancer on local
recurrence and 15-year survival: an overview of the randomised trials.
Lancet 2005;366:2087–2106.
22. Early Breast Cancer Trialists’ Collaborative Group (EBCTCG), Darby
S, McGale P, Correa C, et al. Effect of radiotherapy after breast-
conserving surgery on 10-year recurrence and 15-year breast cancer
death: meta-analysis of individual patient data for 10,801 women in 17
randomised trials. Lancet 2011;378:1707–1716.
23. Wapnir IL, Dignam JJ, Fisher B, et al. Long-term outcomes of invasive
ipsilateral breast tumor recurrences after lumpectomy in NSABP B-17
and B-24 randomized clinical trials for DCIS. J Natl Cancer Inst
2011;103:478–488.
24. Bijker N, Meijnen P, Peterse JL, et al. Breast-conserving treatment with
or without radiotherapy in ductal carcinoma-in-situ: Ten-year results of
European Organisation for Research and Treatment of Cancer
randomized phase III trial 10853—A study by the EORTC breast cancer
cooperative group and EORTC radiotherapy group. J Clin Oncol
2006;24:3381–3387.
25. Cuzick J, Sestak I, Pinder SE, et al. Effect of tamoxifen and
radiotherapy in women with locally excised ductal carcinoma in situ:
long-term results from the UK/ANZ DCIS trial. Lancet Oncol
2011;12:21–29.
26. Holmberg L, Garmo H, Granstrand B, et al. Absolute risk reductions for
local recurrence after postoperative radiotherapy after sector resection
for ductal carcinoma in situ of the breast. J Clin Oncol 2008;26:1247–
1252.
27. Viani GA, Stefano EJ, Afonso SL, et al. Breast-conserving surgery with
or without radiotherapy in women with ductal carcinoma in situ: a meta-
analysis of randomized trials. Radiat Oncol 2007;2:28.
28. Fyles AW, McCready DR, Manchul LA, et al. Tamoxifen with or
without breast irradiation in women 50 years of age or older with early
breast cancer. N Engl J Med 2004;351:963–970.
29. Pötter R, Gnant M, Kwasny W, et al. Lumpectomy plus tamoxifen or
anastrozole with or without whole breast irradiation in women with
favorable early breast cancer. Int J Radiat Oncol Biol Phys
2007;68:334–340.
30. Blamey RW, Bates T, Chetty U, et al. Radiotherapy or tamoxifen after
conserving surgery for breast cancers of excellent prognosis: British
Association of Surgical Oncology (BASO) II trial. Eur J Cancer
2013;49:2294–2302.
31. Winzer KJ, Sauerbrei W, Braun M, et al. Radiation therapy and
tamoxifen after breast-conserving surgery: updated results of a 2 × 2
randomised clinical trial in patients with low risk of recurrence. Eur J
Cancer 2010;46:95–101.
32. Solin LJ, Gray R, Baehner FL, et al. A multigene expression assay to
predict local recurrence risk for ductal carcinoma in situ of the breast. J
Natl Cancer Inst 2013;105:701–710.
33. Kunkler IH, Williams LJ, Jack WJL, et al. Breast-conserving surgery
with or without irradiation in women aged 65 years or older with early
breast cancer (PRIME II): a randomised controlled trial. Lancet Oncol
2015;16:266–273.
34. Silverstein MJ, Lagios MD, Craig PH, et al. A prognostic index for
ductal carcinoma in situ of the breast. Cancer 1996;77:2267–2274.
35. De Mascarel I, Bonichon F, Macgrogan G, et al. Application of the Van
Nuys prognostic index in a retrospective series of 367 ductal carcinomas
in situ of the breast examinated by serial macroscopic sectioning:
practical considerations. Breast Cancer Res Treat 2000;61:151–159.
36. Boland GP, Chan KC, Knox WF, et al. Value of the Van Nuys
Prognostic Index in prediction of recurrence of ductal carcinoma in situ
after breast-conserving surgery. Br J Surg 2003;90:426–432.
37. Wong JS, Chen YH, Gadd MA, et al. Eight-year update of a prospective
study of wide excision alone for small low- or intermediate-grade ductal
carcinoma in situ (DCIS). Breast Cancer Res Treat 2014;143:343–350.
38. McCormick B, Winter K, Hudis C, et al. RTOG 9804: a prospective
randomized trial for good-risk ductal carcinoma in situ comparing
radiotherapy with observation. J Clin Oncol 2015;33:709–715.
39. McCormick B. Randomized trial evaluating radiation following surgical
excision for “good risk” DCIS: 12-year report from NRG/RTOG 9804.
Int J Radiat Oncol 2018;102:1603.
40. Lazovich D, Solomon CC, Thomas DB, et al. Breast conservation
therapy in the United States following the 1990 National Institutes of
Health Consensus Development Conference on the treatment of patients
with early stage invasive breast carcinoma. Cancer 1999;86:628–637.
41. Morrow M, White J, Moughan J, et al. Factors predicting the use of
breast-conserving therapy in stage I and II breast carcinoma. J Clin
Oncol 2001;19:2254–2262.
42. Fowler JF. The linear-quadratic formula and progress in fractionated
radiotherapy. Br J Radiol 1989;62:679–694.
43. Ash DV, Benson EA, Sainsbury JR, et al. Seven-year follow-up on 334
patients treated by breast conserving surgery and short course radical
postoperative radiotherapy: a report of the Yorkshire breast cancer
group. Clin Oncol (R Coll Radiol) 1995;7:93–96.
44. Olivotto IA, Weir LM, Kim-Sing C, et al. Late cosmetic results of short
fractionation for breast conservation. Radiother Oncol 1996;41:7–13.
45. Shelley W, Brundage M, Hayter C, et al. A shorter fractionation
schedule for postlumpectomy breast cancer patients. Int J Radiat Oncol
Biol Phys 2000;47:1219–1228.
46. Whelan TJ, Pignol JP, Levine MN, et al. Long-term results of
hypofractionated radiation therapy for breast cancer. N Engl J Med
2010;362:513–520.
47. Haviland JS, Owen JR, Dewar JA, et al. The UK Standardisation of
Breast Radiotherapy (START) trials of radiotherapy hypofractionation
for treatment of early breast cancer: 10-year follow-up results of two
randomised controlled trials. Lancet Oncol 2013;14(11):1086–1094.
48. Romestaing P, Lehingue Y, Carrie C, et al. Role of a 10-Gy boost in the
conservative treatment of early breast cancer: results of a randomized
clinical trial in Lyon, France. J Clin Oncol 1997;15:963–968.
49. Bartelink H, Horiot JC, Poortmans PM, et al. Impact of a higher
radiation dose on local control and survival in breast-conserving therapy
of early breast cancer: 10-year results of the randomized boost versus no
boost EORTC 22881-10882 trial. J Clin Oncol 2007;25:3259–3265.
50. Smith BD, Bellon JR, Blitzblau R, et al. Radiation therapy for the whole
breast: executive summary of an American Society for Radiation
Oncology (ASTRO) evidence-based guideline. Pract Radiat Oncol
2018;8(3):145–152.
51. Holland R, Veling SHJ, Mravunac M, et al. Histologic multifocality of
tis, T1–2 breast carcinomas implications for clinical trials of breast-
conserving surgery. Cancer 1985;56:979–990.
52. Faverly DRG, Hendriks JHCL, Holland R. Breast carcinomas of limited
extent: frequency, radiologic-pathologic characteristics, and surgical
margin requirements. Cancer 2001;91:647–659.
53. Haffty BG, Carter D, Flynn SD, et al. Local recurrence versus new
primary: clinical analysis of 82 breast relapses and potential applications
for genetic fingerprinting. Int J Radiat Oncol Biol Phys 1993;27:575–
583.
54. Vicini FA, Kestin LL, Goldstein NS. Defining the clinical target volume
for patients with early-stage breast cancer treated with lumpectomy and
accelerated partial breast irradiation: a pathologic analysis. Int J Radiat
Oncol Biol Phys 2004;60:722–730.
55. Smith TE, Lee D, Turner BC, et al. True recurrence vs. new primary
ipsilateral breast tumor relapse: an analysis of clinical and pathologic
differences and their implications in natural history, prognoses, and
therapeutic management. Int J Radiat Oncol Biol Phys 2000;48:1281–
1289.
56. Huang E, Buchholz TA, Meric F, et al. Classifying local disease
recurrences after breast conservation therapy based on location and
histology: new primary tumors have more favorable outcomes than true
local disease recurrences. Cancer 2002;95:2059–2067.
57. Fowble B, Solin LJ, Schultz DJ, et al. Breast recurrence following
conservative surgery and radiation: patterns of failure, prognosis, and
pathologic findings from mastectomy specimens with implications for
treatment. Int J Radiat Oncol Biol Phys 1990;19:833–842.
58. Kamrava M, Kuske RR, Anderson B, et al. Outcomes of breast cancer
patients treated with accelerated partial breast irradiation via
multicatheter interstitial brachytherapy: the Pooled Registry of
Multicatheter Interstitial Sites (PROMIS) experience. Ann Surg Oncol
2015;22 Suppl 3:S404–S411.
59. Strnad V, Ott OJ, Hildebrandt G, et al. 5-year results of accelerated
partial breast irradiation using sole interstitial multicatheter
brachytherapy versus whole-breast irradiation with boost after breast-
conserving surgery for low-risk invasive and in-situ carcinoma of the
female breast: a randomised, phase 3, non-inferiority trial. Lancet
2016;387:229–238.
60. Shah C, Badiyan S, Ben Wilkinson J, et al. Treatment efficacy with
accelerated partial breast irradiation (APBI): final analysis of the
American Society of Breast Surgeons MammoSite(®) breast
brachytherapy registry trial. Ann Surg Oncol 2013;20:3279–3285.
61. Vaidya JS, Wenz F, Bulsara M, et al. Risk-adapted targeted
intraoperative radiotherapy versus whole-breast radiotherapy for breast
cancer: 5-year results for local control and overall survival from the
TARGIT-A randomised trial. Lancet 2014;383(9917):603–613.
62. Veronesi U, Orecchia R, Maisonneuve P, et al. Intraoperative
radiotherapy versus external radiotherapy for early breast cancer
(ELIOT): a randomised controlled equivalence trial. Lancet Oncol
2013;14(13):1269–1277.
63. Formenti SC, Hsu H, Fenton-Kerimian M, et al. Prone accelerated
partial breast irradiation after breast-conserving surgery: five-year
results of 100 patients. Int J Radiat Oncol Biol Phys 2012;84:606–611.
64. Vicini F, Winter K, Wong J, et al. Initial efficacy results of RTOG 0319:
three-dimensional conformal radiation therapy (3D-CRT) confined to
the region of the lumpectomy cavity for stage I/ II breast carcinoma. Int
J Radiat Oncol Biol Phys 2010;77:1120–1127.
65. Pashtan IM, Recht A, Ancukiewicz M, et al. External beam accelerated
partial-breast irradiation using 32 Gy in 8 twice-daily fractions: 5-year
results of a prospective study. Int J Radiat Oncol Biol Phys
2012;84:e271–e277.
66. Vicini F, Cecchini R, White J, et al. Abstract GS4-04: Primary results of
NSABP B-39/RTOG 0413 (NRG Oncology): a randomized phase III
study of conventional whole breast irradiation (WBI) versus partial
breast irradiation (PBI) for women with stage 0, I, or II breast cancer.
American Association for Cancer Research (AACR), pp GS4-04-GS4-
04.
67. Whelan T, Julian J, Levine M, et al. Abstract GS4-03: RAPID: A
randomized trial of accelerated partial breast irradiation using 3-
dimensional conformal radiotherapy (3D-CRT). American Association
for Cancer Research (AACR), pp GS4-03-GS4-03.
68. Coles CE, Griffin CL, Kirby AM, et al. Partial-breast radiotherapy after
breast conservation surgery for patients with early breast cancer (UK
IMPORT LOW trial): 5-year results from a multicentre, randomised,
controlled, phase 3, non-inferiority trial. Lancet 2017;390:1048–1060.
69. Smith BD, Arthur DW, Buchholz TA, et al. Accelerated partial breast
irradiation consensus statement from the American Society for
Radiation Oncology (ASTRO). Int J Radiat Oncol Biol Phys
2009;74:987–1001.
70. Correa C, Harris EE, Leonardi MC, et al. Accelerated partial breast
irradiation: executive summary for the update of an ASTRO evidence-
based consensus statement. Pract Radiat Oncol 2017;7(2):73–79.
71. Veronesi U, Paganelli G, Viale G, et al. Sentinel-lymph-node biopsy as
a staging procedure in breast cancer: update of a randomised controlled
study. Lancet Oncol 2006;7:983–990.
72. Krag DN, Anderson SJ, Julian TB, et al. Technical outcomes of sentinel-
lymph-node resection and conventional axillary-lymph-node dissection
in patients with clinically node-negative breast cancer: results from the
NSABP B-32 randomised phase III trial. Lancet Oncol 2007;8:881–888.
73. Giuliano AE, McCall L, Beitsch P, et al. Locoregional recurrence after
sentinel lymph node dissection with or without axillary dissection in
patients with sentinel lymph node metastases: the American College of
Surgeons Oncology Group Z0011 randomized trial. Ann Surg
2010;252:426–432; discussion 432–433.
74. Giuliano AE, Hunt KK, Ballman K V, et al. Axillary dissection vs no
axillary dissection in women with invasive breast cancer and sentinel
node metastasis: a randomized clinical trial. JAMA 2011;305:569–575.
75. Caudle AS, Hunt KK, Tucker SL, et al. American College of Surgeons
Oncology Group (ACOSOG) Z0011: impact on surgeon practice
patterns. Ann Surg Oncol 2012;19:3144–3151.
76. Gainer SM, Hunt KK, Beitsch P, et al. Changing behavior in clinical
practice in response to the ACOSOG Z0011 trial: a survey of the
American Society of Breast Surgeons. Ann Surg Oncol 2012;19:3152–
3158.
77. Jagsi R, Chadha M, Moni J, et al. Radiation field design in the
ACOSOG Z0011 (Alliance) trial. J Clin Oncol 2014;32:3600–3606.
78. Donker M, van Tienhoven G, Straver ME, et al. Radiotherapy or surgery
of the axilla after a positive sentinel node in breast cancer (EORTC
10981–22023 AMAROS): a randomised, multicentre, open-label, phase
3 non-inferiority trial. Lancet Oncol 2014;15:1303–1310.
79. Whelan TJ, Olivotto IA, Parulekar WR, et al. Regional nodal irradiation
in early-stage breast cancer. N Engl J Med 2015;373:307–316.
80. Poortmans PM, Collette S, Kirkove C, et al. Internal mammary and
medial supraclavicular irradiation in breast cancer. N Engl J Med
2015;373:317–327.
81. Hennequin C, Bossard N, Servagi-Vernat S, et al. Ten-year survival
results of a randomized trial of irradiation of internal mammary nodes
after mastectomy. Int J Radiat Oncol Biol Phys 2013;86:860–866.
CHAPTER 13

The Surgical Management of Locally


Advanced and Stage IV Breast Cancer
SUSIE X. SUN | SARAH M. DESNYDER
LOCALLY ADVANCED BREAST CANCER

Epidemiology
The definition of locally advanced breast cancer remains heterogeneous and
includes tumors that encompass a large portion of the breast, involve the skin
and/or chest wall, or have the presence of bulky metastatic disease to regional
lymph node. Approximately 12% of breast cancers are found to be locally
advanced at the time of diagnosis (1). Survival and recurrence rates vary
depending on stage at the time of diagnosis. However, patients with locally
advanced breast disease have higher rates of locoregional recurrence, distant
metastasis, and lower survival when compared with patients with early breast
cancers. The American Cancer Society found that the 5-year survival is 99%
for patients with localized disease, 85% for those with regional disease, and
27% for those with distant disease (2).
Diagnosis
Physical examination is of the utmost importance in the diagnosis of locally
advanced breast cancer. A complete breast examination should be performed
including inspection and palpation of the breasts and regional nodal basins.
The breast examination should be performed with the patient in the upright
and supine positions with arm-raising maneuvers. It is important to compare
the breasts and note any asymmetry. Special attention is needed to assess for
skin changes (dimpling, peau d’orange, redness, and erosions), nipple
changes (retraction, flaking, and irritation), and nipple discharge (Fig. 13-1).
Palpation of all draining regional lymph node basins should be performed. If
a palpable mass is present, a history should be obtained from the patient to
determine the length of time the mass has been present and if there have been
any changes in the size of the mass, as rapidly growing masses may lead to
changes in care.
Imaging of the breast and regional lymph nodes should be obtained
including mammogram and ultrasound (US) (Fig. 13-2). Core needle biopsy
should be performed to acquire tissue from the primary tumor. The biopsy
specimen also needs to be evaluated for hormone receptor (HR) status and
HER-2 overexpression. For purposes of future treatment planning, a clip
needs to be placed within the tumor. If abnormal-appearing lymph nodes are
found on imaging, biopsy should be performed via fine-needle aspiration. If a
dominant axillary node is biopsied a clip should be placed to identify this
node at surgery.
Complete staging workup should be performed to evaluate for distant
metastatic disease. This consists of a complete blood count, comprehensive
metabolic panel including liver function tests and alkaline phosphatase, CT
scan of the chest and abdomen, and bone scan. If there is clinical suspicion
for brain metastasis, an MRI of the head may be obtained. Per National
Comprehensive Cancer Network (NCCN) guidelines, PET scan remains
optional and its use is at the discretion of the provider (3). Patients with
breast cancer, especially those with locally advanced disease, need to be
evaluated by a multidisciplinary team including a breast surgeon, a medical
oncologist, a radiation oncologist, a radiologist, and a plastic surgeon. A
multidisciplinary team approach is critical for treatment planning, especially
for patients with locally advanced breast cancer.

FIGURE 13-1 Patient with locally advanced breast cancer.


FIGURE 13-2 Bulky axillary lymph nodes seen on mammogram.

Systemic Treatment
Neoadjuvant systemic therapy has become a key component in the treatment
of locally advanced breast cancer. While studies have shown that there is no
significant difference in survival between patients who received neoadjuvant
and adjuvant treatment, there are several advantages to neoadjuvant systemic
therapy (4). For example, a previously inoperable breast cancer may become
operable after neoadjuvant treatment. In randomized controlled trials, more
patients who received neoadjuvant systemic therapy became candidates for
breast-conserving therapy compared to those who received adjuvant
treatment (5). Lastly, neoadjuvant systemic therapy provides information
about the biology of the cancer by allowing assessment of an in vivo response
to treatment. Pathologic response to treatment has been shown to be
associated with an improvement in disease-free and overall survival (6). The
specific regimen for systemic therapy varies depending on tumor receptor
status. In general, regimens containing both an anthracycline and a taxane are
recommended for HER-2–negative disease. For HER-2–positive disease,
protocols with HER-2 targeted therapy (trastuzumab, pertuzumab) in
combination with an anthracycline have been shown to be associated with
improved rates of clinical and pathologic response (7,8).
Surgical Treatment
Although surgical management of locally advanced breast cancer has
historically consisted of modified radical mastectomy, breast-conserving
surgery is being performed more frequently for patients with a favorable
response to neoadjuvant systemic therapy. For patients who received
neoadjuvant treatment and were candidates for breast-conserving surgery,
there was no difference in overall or disease-free survival for those who
underwent mastectomy compared to those who received breast-conserving
therapy (9). Eligibility for breast-conserving surgery includes tumor size that
would not result in unacceptable cosmesis following excision, unifocal
disease, minimal skin involvement, patient desire for breast conservation, and
no contraindications to radiation therapy. If involvement of the nipple areolar
complex is present, a central segmentectomy with removal of the nipple
areolar complex can be performed. When performing mastectomy or partial
mastectomy, it is important to resect all grossly abnormal–appearing skin. If
there is involvement of the underlying pectoralis muscle or the chest wall,
resection of the muscle or full-thickness chest wall resection may be
indicated. In these cases, multidisciplinary care with a thoracic surgeon and a
plastic surgeon is important.
For clinically node-negative patients, sentinel lymph node biopsy (SLNB)
has been showed to be safe and effective for axillary staging. Studies,
including the NSABP B-32, have shown that SLNB has low false-negative
rates with no difference in overall and disease-free survival when compared
with axillary lymph node dissection (ALND) (10,11). Of note, clinically
node-negative patients who receive neoadjuvant systemic therapy followed
by breast-conserving therapy were not evaluated as part of the American
College of Surgeons Oncology Group (ACOSOG) Z011 trial and thus this
patient cohort should undergo completion ALND if they are found to have
positive nodes at the time of SLNB (3,12).
Patients with clinically involved axillary lymph nodes have historically
undergone ALND. For patients with locally advanced breast cancer, 20% to
40% will achieve a complete clinical response (7,13,14). For these patients,
the possibility for omission of ALND has been evaluated (7,15). If bulky
lymph node disease remains after systemic therapy or if the patient initially
presents with high-volume tumor burden within the axillary lymph nodes (>4
abnormal-appearing lymph nodes on preoperative imaging) then ALND is
indicated. In select patients with low-volume lymph node disease, especially
for those with clinical complete response after neoadjuvant systemic therapy,
consideration may be given to omission of ALND. These patients may also
qualify for enrollment in the Alliance A011202 trial which is randomizing
patients with clinical N1 disease at time of diagnosis and residual nodal
disease after neoadjuvant systemic therapy to completion ALND with nodal
irradiation or no further axillary surgery with axillary and nodal irradiation.
Optimal management of the axilla after neoadjuvant therapy remains highly
debated and is discussed in more detail in Chapter 27.
STAGE IV BREAST CANCER
In the United States, approximately 5% of patients are found to have stage IV
breast cancer at the time of initial diagnosis (2). However, the incidence of
stage IV disease is higher for African American patients at approximately
10%. This has been attributed to differences in socioeconomic status and
overestimation in the rate of screening mammography use in African
American patients (16). Five-year survival for patients with distant metastasis
is 25%. However, this is also lower at 15% for African American patients
(16).
Traditionally, the treatment for stage IV breast cancer has consisted mainly
of systemic therapy with surgical resection reserved for palliation. For
patients with stage IV disease who have a fungating mass, ulceration of the
skin, bleeding, or pain, palliative surgery is clearly indicated (Fig. 13-3).
More recently, studies have evaluated the role of surgery for stage IV breast
cancer outside of palliation. While surgical resection has not been formally
included in the NCCN guidelines for the treatment of stage IV breast cancer,
the group recently added a statement acknowledging that surgery for
metastatic breast cancer is the subject of ongoing investigation and that the
performance of breast surgery is reasonable in select patients with a favorable
response to initial systemic therapy (3).
FIGURE 13-3 Patient with stage IV disease and a bleeding breast mass.

Aggressive local therapy has been shown to improve survival in the setting
of metastatic cancer in nonbreast disease sites including renal cell cancer,
colorectal cancer, gastric cancer, and ovarian cancer (17–20). With
multimodality systemic treatment, survival for patients with stage IV breast
cancer has improved within the past 10 to 20 years, thus eliciting increased
interest in evaluating the benefit of surgery for this patient cohort. The
underlying principle for the potential benefit of surgical resection at a
biologic level has been studied. Hypotheses include decreasing the risk of
metastasis by removing the cancer stem cells within the primary tumor,
limiting tumor-related immunosuppression by decreasing tumor burden, and
disrupting the molecular signaling pathways between the primary tumor and
the metastatic sites (21–23).
Several retrospective studies have shown a survival advantage associated
with resection of the primary tumor. Khan et al. used the National Cancer
Database to evaluate 16,203 patients from 1990 to 1993 (24). They found that
the 3-year survival for patients who underwent no surgery was 17.3%
compared to 27.7% in those who underwent segmental mastectomy, and
31.8% for those who underwent mastectomy. Independent covariates
associated with survival included metastatic burden, the presence of visceral
metastasis, and the use of systemic therapy. For patients who underwent
resection, superior 3- and 5-year survival was seen in women who had
negative margins compared to those with involvement of the margins (24). A
study from The University of Texas MD Anderson Cancer Center also
showed improved survival for patients who underwent resection of their
primary tumor (25). Additionally, they found that patients in the surgical
group were more likely to have only one site of distant metastasis, be
younger, have lower nodal tumor burden, have HER-2–positive disease, and
to be treated with systemic therapy. A recent meta-analysis that included 30
retrospective studies showed improved survival following primary tumor
resection with a hazard ratio of 0.65, p < 0.001 (26). Sensitivity analysis
showed that surgery was beneficial in patients with one site of metastatic
disease, bone metastasis only, and negative surgical margins. Within these
retrospective studies, patients who underwent surgery have been shown to be
younger, have fewer comorbidities, and have less tumor burden compared
with patients who did not undergo surgery. Studies have attempted to account
for the aforementioned selection bias by performing propensity score–
matched analyses, after which the survival advantage associated with surgical
resection was no longer present (27,28). Improved survival has also been
shown in patients who underwent surgery only if they had a favorable
response to systemic therapy (28,29). The role of axillary surgery has also
been explored. Two retrospective studies have shown improved survival in
patients who underwent ALND at the time of resection of their primary tumor
compared to those who underwent SLNB alone or no axillary surgery
(29,30).
Because patient selection may be a strong bias leading to the observed
survival benefit associated with resection of the primary tumor for patients
with stage IV breast cancer, randomized controlled trials are currently in
progress. The Translational Breast Cancer Research Consortium (TBCRC)
013 is a multicenter prospective registry study evaluating the role of surgical
excision of the primary tumor along with response to systemic therapy,
incidence of disease progression, and molecular characteristics of the tumor
(31). A total of 127 patients from 14 sites were categorized into two cohorts,
stage IV with an intact primary tumor (cohort A, n = 112) or metastasis
within 3 months of primary surgery (cohort B, n = 15). All patients received
first-line neoadjuvant systemic therapy. Initial results presented at the San
Antonio Breast Cancer Symposium in 2013 showed superior survival in
cohort B compared with cohort A (100% vs. 84%, p = 0.03). When patients
in both cohort A and cohort B were considered together, resection of the
primary tumor was associated with improved 2-year overall survival (96% vs.
74%, p = 0.002). No survival difference was seen in cohort A patients with
response (partial, complete response, or stable disease) to systemic therapy
who then underwent elective surgery when compared to those who did not
(94% vs. 92%, p = 0.5). Updated results for this trial were presented at the
2016 American Society of Clinical Oncology (ASCO) annual meeting (32).
Patients with intact primaries were classified by response to systemic therapy
and the 3-year overall survival was better for responders compared to
nonresponders (78% vs. 24%, p < 0.001). Again, among patients who
responded to systemic therapy, no difference in 3-year survival was seen
between those who underwent resection of their primary tumor and those
who did not (77% vs. 76%, p = 0.85). Patients who had surgery were more
likely to have larger tumors, single-organ metastasis, and receive first-line
chemotherapy.
Two prospective randomized controlled trials have been published
evaluating the role of surgical resection of the primary tumor in the setting of
stage IV breast cancer. The MF07-01 is a multicenter trial conducted in
Turkey comparing initial locoregional surgery followed by systemic
treatment with systemic therapy alone (33). While there was no survival
difference seen between the two groups at 3 years (60% vs. 51%, p = 0.10),
overall survival was higher for the locoregional surgery group at 5 years
(41.6% vs. 24.4%, p = 0.005). This study enrolled 274 patients with 138 in
the surgery arm and 136 in the systemic treatment–only arm. Most of the
patients who had initial locoregional surgery underwent mastectomy with
ALND followed by systemic therapy. The systemic therapy regimen and
rates of use were similar between the two groups. Subgroup analysis of
patients who underwent locoregional surgery showed that improved survival
was associated with HR positivity, HER-2–negative disease, age less than 55,
and solitary bone metastasis. Additional analysis of the solitary bone
metastasis group showed improved overall 5-year survival in the locoregional
surgery group (51.7% vs. 29.3%, p = 0.04). Also of note, locoregional disease
progression or relapse, defined as clinical or radiologic progression of the
primary tumor, ulceration, bleeding, or new locoregional lesions, was 1% in
the locoregional surgery group compared to 11% in the systemic therapy–
alone group (p = 0.001). When patients with multiple pulmonary or liver
metastases were evaluated, 3-year survival was significantly lower in the
surgery group (31% vs. 67%, p = 0.05). While this study shows improved
survival associated with surgical resection of the primary tumor, there are
several limitations that warrant consideration. First, it is important to
highlight that the patient cohort in the MF07-01 differs from that of the
TBCRC 013 as it reflects patients who underwent upfront surgery and thus
included those who would have been considered nonresponders in the
TBCRC 013. With recent improvements in systemic therapy, especially with
targeted therapies, it is difficult to justify not giving patients neoadjuvant
systemic treatment in the setting of metastatic breast cancer, thus limiting the
applicability of these study results. Additionally, patient and tumor
characteristics such as receptor status were not taken into account during
randomization leading to a higher proportion of patients with HR-positive
disease in the surgery arm (85.5% vs. 71.8%, p = 0.01) and a higher rate of
triple-negative disease in the systemic treatment–only arm (17.4% vs. 7.3%,
p = 0.01). This indicates that patients in the surgery arm likely had more
indolent disease which contributed to the observed survival advantage. In
summary, the MF07-01 study suggests that patients who may derive benefit
from resection of the primary tumor are younger with HR-positive, HER-2–
negative disease. Those with triple-negative disease and/or large metastatic
burden, such as liver or pulmonary metastases, are less likely to benefit from
removal of the primary tumor.
A prospective trial by Badwe et al. from Tata Memorial Center in India
randomized patients to surgical resection of the primary tumor after treatment
with systemic therapy and systemic therapy alone (34). For patients who
presented with resectable primary tumors, neoadjuvant endocrine therapy was
initiated (n = 25). Patients initially found to be unresectable were started on
systemic therapy (n = 691). Only patients with response to therapy were
eligible for randomization. A total of 350 eligible patients were subsequently
randomized to neoadjuvant systemic treatment (endocrine therapy or
chemotherapy) with or without locoregional treatment (surgery with or
without radiation). Randomization was stratified based on patient and tumor
characteristics including site of metastasis, number of metastasis, HR status,
and HER-2 status. They found no difference in 2-year survival between the
locoregional treatment group and systemic treatment–only group (41.9% vs.
43%). Subgroup analysis also showed no differences in survival between the
two groups based on menopause status, metastatic site, number of metastases,
HR status, and HER-2 status. It is important to note that only 2% of patients
with HER-2–positive disease in the surgery arm and no patients in the
systemic therapy–alone arm received HER-2–targeted therapy which is
considered the standard of care in most centers. This may contribute to the
lower survival observed in this study compared to reported data from more
developed countries.
There are currently two additional ongoing randomized trials designed to
gain clarity into the controversy of locoregional surgery in stage IV breast
cancer. The Japan Clinical Oncology Group (JCOG) 1017 trial seeks to
evaluate the overall survival, local recurrence rate, and local control rate of
patients who have a favorable response after 3 months of systemic therapy
who then undergo resection of their primary tumor compared to those who
continue on systemic therapy without surgical resection. The Eastern
Cooperative Oncology Group (ECOG) E-2108 trial has randomized patients
with no evidence of disease progression after 16 to 32 weeks of optimal
systemic therapy to locoregional treatment or continued systemic therapy.
This study differs from the JCOG 1017 trial in that delivery of radiotherapy
and management of the axillary lymph nodes parallels current guidelines for
nonmetastatic breast cancer.
At this time there are no definitive recommendations as to which patients
with stage IV breast cancer should be offered surgical resection of their
primary tumor. For the majority of patients with asymptomatic primary
tumors (resection not needed for palliation), optimal systemic therapy based
on tumor biology continues to be the mainstay of treatment. Pending results
from additional randomized trials, surgical resection as a means to improve
survival in patients with stage IV breast cancer is not currently the standard
of care and should not be offered on a routine basis.
INFLAMMATORY BREAST CANCER

Epidemiology
Inflammatory breast cancer (IBC) is a rare form of breast cancer that
accounts for 1% to 3% of all breast malignancies (35,36). The incidence of
IBC increases sharply with age plateauing at 65 years of age. The mean age
of diagnosis for IBC has been shown to be slightly younger at 58 years of age
compared to 68 years of age for those with non-IBC locally advanced breast
cancer (36). Studies have also shown that the incidence of IBC is
disproportionally higher in African American women, who are more likely to
be diagnosed at an earlier age (37). Analysis of the California Cancer
Registry by Zell et al. showed that IBC tumors were less likely to be estrogen
receptor (ER)/progesterone receptor (PR) positive when compared to non-
IBC locally advanced cancers (56%/45% vs. 67%/54%) (38). Patients with
IBC are also more likely to be HER-2 positive when compared with non-IBC
locally advanced patients (40% vs. 35%).
Despite its relative rarity, 7% of all breast cancer related deaths in the
United States are due to IBC (36). In addition, survival is lower when
compared with equivalently staged non-IBC breast cancers (39). Hance et al.
showed that the median survival for patients with non-IBC locally advanced
cancer was 6.4 years compared with 2.9 years for IBC patients (36). Five-
year and 10-year survival rates for patients with IBC are also poor at 55%
and 37.3%, respectively, if patients receive optimal multimodality treatment
consisting of neoadjuvant systemic therapy, surgery, and radiation. Breast
cancer–specific survival for patients with IBC has improved since the 1990s.
However this improvement was seen to a lesser extent in African American
women. This improvement in breast cancer–specific survival for patients with
IBC may be attributed to the recent improvements in neoadjuvant systemic
therapy and the increased utilization of multimodality therapy (40). When
survival was stratified by HR status, triple negative subtypes have been
shown to be associated with worse prognosis. However, Masuda et al.
showed that, unlike non-IBC tumors, no survival differences were seen
between HR-positive/HER-2– positive, HR-positive/HER-2–negative, and
HR-negative/HER-2–positive subtypes (41). When survival was compared
between patients with stage IV inflammatory and noninflammatory cancer,
IBC was associated with lower survival rates (42).
Diagnosis
Physical examination is of the upmost importance in the diagnosis of IBC.
The American Joint Committee on Cancer (AJCC) staging manual states that
IBC is primarily a clinical diagnosis and physical examination is of the
upmost importance (43). Rather than presenting with a palpable breast mass,
most patients with IBC present with breast symptoms including pain, redness,
and skin changes (37). The differential diagnosis includes mastitis, trauma,
non-IBC breast cancer, primary breast lymphoma, and other malignancies.
Physical examination may reveal skin thickening, peau d’orange, erythema,
engorgement of the affected breast, and nipple changes (Fig. 13-4). An
underlying mass may or may not be palpable. Because upward of 80% of
patients with IBC have metastatic disease to the axillary lymph nodes at the
time of presentation, it is important to perform a thorough examination of the
regional draining lymph node basins (44–46).
Recognition of IBC can be quite challenging. Thus, a set of criteria has
been defined to aid in the diagnosis of IBC. These include rapid onset of
breast skin changes (erythema, edema, peau d’orange, warmth), nipple
changes (retraction, flattening, crusting), history of mastitis that does not
resolve with antibiotics, history of symptoms lasting less than 6 months,
examination revealing erythema involving at least one-third of the breast, and
pathologic confirmation of underlying malignancy (47). Because patients
often initially seek care from nononcologic providers, lack of response to a
trial of antibiotic therapy or progression of erythema despite antibiotic
treatment should heighten the suspicion for IBC. At initial evaluation and
throughout the patients’ treatment course, medical photography should be
used to document the scope of disease, especially the degree of skin
involvement and its response to treatment. This will serve to assist in future
treatment planning including the extent of surgical resection and the plan for
adjuvant radiation.
All patients with breast cancer, including IBC, should undergo radiologic
evaluation including mammogram and US of the breast and regional lymph
node basins. In a study from MD Anderson Cancer Center evaluating
imaging in patients with IBC, parenchymal abnormalities (mass, architectural
distortion, asymmetry, or calcifications) were seen on mammogram in 80%
of patients and skin thickening was seen in 83%. On US, parenchymal
abnormalities and skin thickening were found in 95% of patients. MRI
identified parenchymal findings in 100% of patients and skin thickening in
96%. Sensitivity in detecting breast lesions was highest for MRI at 100%. US
and positron emission tomography (PET) also had high sensitivity for
detecting breast lesions at 95% and 96%, respectively. US had the highest
sensitivity and specificity for the detection of axillary metastasis at 100%. If
suspicious lymph nodes are seen on US, biopsy should be performed via fine-
needle aspiration. The extent of lymph node involvement should also be
documented as a measure of tumor burden. These results suggest that
mammography may not be the most useful imaging tool in patients with IBC,
but rather multimodality imaging should be used (48). While MRI was very
effective in identifying parenchymal lesions, it has several limitations
including high cost, extended length of examination, and discomfort
associated with prolonged confinement/positioning. Routine use of MRI in
IBC is not currently recommended. However, use of MRI should be
considered in patients in whom breast lesions are not detected using
mammography and US.
FIGURE 13-4 Patient with breast skin changes due to inflammatory breast cancer.

Because approximately 30% of patients with IBC have distant metastatic


disease at the time of presentation, identifying the extent of disease is
important for future treatment planning (47). Current NCCN guidelines
recommend bone scan and CT scan of the chest, abdomen, and pelvis for
staging in patients with IBC. While routine use of fluoro-2-deoxy-D-glucose
positron emission tomography (FDG-PET) is not currently recommended, its
use may be indicated if suspicious or equivocal findings are seen on standard
staging studies (3).
IBC is currently categorized as stage T4d by the most recent AJCC TNM
classification (43). Thus, patients with nonmetastatic disease are designated
as stage IIIB and those with metastatic disease are stage IV. If a patient was
initially diagnosed with IBC (cT4d) before neoadjuvant therapy, the cancer
will still be categorized as T4b after treatment even if there is clinical
complete response with resolution of the inflammatory component. It is
important to highlight that although IBC has been shown to have lower stage
for stage survival when compared with noninflammatory locally advanced
breast cancers, the AJCC TNM staging system does not currently
differentiate between these two groups (42,49–51).
Pathologic identification of the underlying malignancy is key in the
diagnosis of IBC. This should be obtained by image-guided core needle
biopsy of the area of breast parenchymal abnormality. Fine-needle aspiration
or core needle biopsy of abnormal-appearing regional lymph nodes should
also be performed. In addition to identifying the malignancy, the biopsy
specimens should also be evaluated for tumor receptor status. The classic
skin changes associated with IBC are secondary to lymphedema from tumor
emboli into the dermal lymphatic system. Even though dermal lymphatic
invasion is considered to be the hallmark of IBC, its presence on skin punch
biopsy is not necessary for the diagnosis of IBC. This is because dermal
lymphatic invasion may not be present in the small areas that are biopsied via
skin punch. However, in patients meeting clinical criteria for IBC, skin punch
biopsy is still recommended to confirm the diagnosis, especially if
malignancy is unable to be identified within the breast parenchyma. Two 8-
mm punch biopsies should be performed in the most pronounced area of skin
abnormality (47).
Neoadjuvant Systemic Treatment
A multidisciplinary approach is essential in the treatment of IBC. The team
will determine a multimodality treatment plan for the patient that includes
neoadjuvant systemic therapy, surgery, and radiation. A study using the
National Cancer Database showed that the underuse of trimodality treatment
negatively impacts survival in patients with IBC (40). Because most patients
with IBC present with locally advanced disease with extensive skin
involvement and likely regional lymph node metastasis, upfront surgery is
not recommended as there is a high probability of leaving behind residual
disease. Therefore, current recommendations are to initiate neoadjuvant
systemic therapy after the clinical diagnosis of IBC is made (3). Data is
lacking from large randomized controlled trials assessing the optimal
chemotherapeutic regimens for patients with IBC. However, there have been
many retrospective or small prospective trials. An analysis from MD
Anderson evaluating 178 patients with IBC treated with anthracycline-based
neoadjuvant chemotherapy showed that overall survival for patients at 5
years was 40%, 10 years was 33%, and 15 years was 29% (52). Patients with
partial or complete response to preoperative therapy were shown to have
improved survival compared to those with less than partial response. Baldini
et al. pooled data from two prospective trials of 68 patients who received
CAF (cyclophosphamide, Adriamycin, 5-FU) or CEF (cyclophosphamide,
epirubicin, 5-FU), followed by surgery and radiation (53). They found that
the overall survival for their patient cohort was 44% at 5 years and 32% at 10
years. Later studies found that, similar to non-IBC cases, the incorporation of
taxanes led to improved outcomes in IBC. A study by Cristofanilli et al.
showed that the addition of paclitaxel increased rates of response for patients
who were not initially responsive to anthracycline-based therapy (54). The
incorporation of paclitaxel has also been shown to improve survival in
patients with ER-negative IBC (55). The NCCN currently recommends
neoadjuvant therapy with anthracycline plus taxane-based regimens for HER-
2–negative IBC (3).
For patients with HER-2–positive disease, the use of trastuzumab is the
current standard of care (3). Numerous studies have shown that targeted
HER-2 therapy is associated with increased rates of pathologic complete
response (pCR) and survival. The NOAH randomized controlled trial
evaluated patients with HER-2–positive locally advanced breast cancer (IBC
and non-IBC) (8,56). The authors found that the addition of trastuzumab to
chemotherapy led to improvements in 5-year overall survival (74% vs. 44%)
and event-free survival (64% vs. 24%) when compared to chemotherapy
alone in the inflammatory cohort. Patients treated with trastuzumab also had
higher rates of pCR, which was independently predictive of improved overall
and disease-free survival (8,56). The NeoSphere study evaluated the addition
of pertuzumab to trastuzumab and chemotherapy in the neoadjuvant setting
(14). Although the study was underpowered to show statistical significance,
there was a trend toward improved disease-free and progression-free survival
in patients treated with pertuzumab and trastuzumab plus docetaxel (14).
It is important to highlight that in the previously discussed studies,
response to treatment was one of the best predictors of survival. A study by
Masuda et al. specifically evaluated treatment response in IBC patients based
on receptor status (41). This study demonstrated that after treatment with
first-line neoadjuvant systemic therapy guided by biomarker studies, the
overall pCR rate for patients with IBC was 15.2%. The highest rate of pCR
was seen in HER-2-positive/HR-negative tumors at 30.5% and pCR was
lowest for HR-positive/HER-2-negative tumors at 7.4%. These rates are
lower when compared with non-IBC malignancies. This suggests differences
in tumor biology between inflammatory and non-IBCs (41).
Surgery
The current surgical standard for the treatment of IBC after neoadjuvant
therapy is total mastectomy with ALND (modified radical mastectomy) (3).
While some studies have evaluated with use of breast-conserving surgery and
SLNB in the setting of IBC, these practices are not currently advised (57,58).
The recommendation against breast-conserving therapy is multifaceted. First,
because IBC often does not present with a distinct unifocal mass within the
breast parenchyma, localization for breast conservation may be difficult if not
impossible. Second, while the NSABP B-18 trial showed that the use of
neoadjuvant chemotherapy led to higher rates of breast-conserving therapy
due to downsizing of the primary tumor, patients with IBC were not included
in their patient cohort (59). Finally, despite clinical evidence of tumor
response, residual disease may still be present in grossly normal-appearing
skin. Thus, skin-sparing mastectomy and partial mastectomy may leave
behind residual disease which serves as a nidus for future recurrence and
local failure. Medical photographs taken at time of diagnosis, prior to
treatment, may aid in deciding the extent of skin resection (Fig. 13-5). SLNB
has been shown to be unreliable in the setting of IBC (60–62). A study by
DeSnyder et al. showed that sentinel lymph nodes were successfully
identified in only 25% of IBC patients in their study group (60). Two other
studies showed that the SLNB was associated with high false-negative rates
therefore making the procedure unreliable in patients with IBC (61,62).
FIGURE 13-5 Medical photography used to document extent of disease in a patient
with inflammatory breast cancer.

Patients with IBC may need to be referred to a plastic surgeon prior to


surgery to discuss chest wall coverage. However, immediate reconstruction is
not recommended for patients with IBC because they will receive adjuvant
radiation. Reconstructed breasts have been shown to limit the delivery of
radiation, especially to the internal mammary chain, and are associated with
increased long-term toxicity (63).
Adjuvant Treatment
Radiation is recommended in all patients with IBC following modified
radical mastectomy. In addition to the chest wall with its overlying skin, the
radiation fields need to encompass all regional nodal basins including the
axillary, infraclavicular, supraclavicular, and internal mammary nodal basins
(3,47).
In patients with ER-positive disease, adjuvant treatment with tamoxifen or
aromatase inhibitors, depending on menopause status, is recommended for at
least 5 years (3,47). For those with HER-2–positive disease, continuation of
HER-2–targeted therapy for 1 year is recommended. This can be given
concurrently with radiation and/or antiestrogen therapy if indicated (3).
Stage IV Inflammatory Breast Cancer
Outcomes for patients with metastatic IBC are poor. When treated with
chemotherapy alone, the 5-year survival is less than 10%. However resection
of the primary tumor has been shown to decrease the risk of death by 51%
(50,64,65). In a recent study of the National Cancer Database by Weiss et al.,
overall survival was found to be higher for patients with stage IV IBC who
underwent resection of their primary tumor compared with those who did not
have surgery (36 months vs. 20 months, p < 0.0001). The ability to obtain
negative margins was also associated with improved survival (66). A study
from MD Anderson of 172 patients with stage IV IBC showed 29% 5-year
overall survival and 17% 5-year progression-free survival. The higher
survival observed in this study compared to previous studies is likely due to
advances in targeted therapy (HER-2–targeted regimens) and more
aggressive radiotherapy. When compared to patients who did not have
surgery, overall (47% vs. 10%, p < 0.0001) and distant progression-free
survival (30% vs. 3%, p < 0.0001) were higher for those who underwent
surgical resection of their primary tumor. Multimodality treatment with
surgery and radiation was also associated with improved survival (67). A
study by Takiar et al. found that patients with stage IV IBC treated with
neoadjuvant chemotherapy, modified radical mastectomy, followed by
aggressive radiation to the chest wall, regional lymph node basins, and M1
disease sites had a 5-year locoregional control rate of 86% and 5-year overall
survival of 54% (68). This shows that even though stage IV IBC has lower
survival compared to non-IBC stage IV disease, likely due to severity of local
disease, resistance to systemic therapy, and high rates of local failure,
aggressive local therapy should be considered in select patients.

REFERENCES
1. Iqbal J, Ginsburg O, Rochon PA, et al. Differences in breast cancer
stage at diagnosis and cancer-specific survival by race and ethnicity in
the United States. JAMA 2015;313(2):165–173.
2. American Cancer Society. Breast Cancer Facts & Figures 2017–2018.
Atlanta, MD: American Cancer Society, Inc; 2017.
3. National Comprehensive Cancer Network. NCCN Clinical Practice
Guidelines in Oncology: Breast Cancer (Version 3.2018).
https://www.nccn.org/professionals/physician_gls/pdf/breast.pdf.
Accessed January 22, 2019.
4. Rastogi P, Anderson SJ, Bear HD, et al. Preoperative chemotherapy:
updates of National Surgical Adjuvant Breast and Bowel Project
Protocols B-18 and B-27. J Clin Oncol 2008;26(5):778–785.
5. Fisher B, Bryant J, Wolmark N, et al. Effect of preoperative
chemotherapy on the outcome of women with operable breast cancer. J
Clin Oncol 1998;16(8):2672–2685.
6. Kuerer HM, Newman LA, Smith TL, et al. Clinical course of breast
cancer patients with complete pathologic primary tumor and axillary
lymph node response to doxorubicin-based neoadjuvant chemotherapy.
J Clin Oncol 1999;17(2):460–469.
7. Buzdar AU, Valero V, Ibrahim NK, et al. Neoadjuvant therapy with
paclitaxel followed by 5-fluorouracil, epirubicin, and cyclophosphamide
chemotherapy and concurrent trastuzumab in human epidermal growth
factor receptor 2-positive operable breast cancer: an update of the initial
randomized study population and data of additional patients treated with
the same regimen. Clin Cancer Res 2007;13(1):228–233.
8. Gianni L, Eiermann W, Semiglazov V, et al. Neoadjuvant chemotherapy
with trastuzumab followed by adjuvant trastuzumab versus neoadjuvant
chemotherapy alone, in patients with HER2-positive locally advanced
breast cancer (the NOAH trial): a randomised controlled superiority trial
with a parallel HER2-negative cohort. Lancet 2010;375(9712):377–384.
9. Mieog JS, van der Hage JA, van de Velde CJ. Preoperative
chemotherapy for women with operable breast cancer. Cochrane
Database Syst Rev 2007;(2):CD005002.
10. Krag DN, Anderson SJ, Julian TB, et al. Sentinel-lymph-node resection
compared with conventional axillary-lymph-node dissection in clinically
node-negative patients with breast cancer: overall survival findings from
the NSABP B-32 randomised phase 3 trial. Lancet Oncol
2010;11(10):927–933.
11. Veronesi U, Paganelli G, Viale G, et al. A randomized comparison of
sentinel-node biopsy with routine axillary dissection in breast cancer. N
Engl J Med 2003;349(6):546–553.
12. Giuliano AE, Ballman KV, McCall L, et al. Effect of axillary dissection
vs no axillary dissection on 10-year overall survival among women with
invasive breast cancer and sentinel node metastasis: the ACOSOG
Z0011 (Alliance) randomized clinical trial. JAMA 2017;318(10):918–
926.
13. Buzdar AU, Ibrahim NK, Francis D, et al. Significantly higher
pathologic complete remission rate after neoadjuvant therapy with
trastuzumab, paclitaxel, and epirubicin chemotherapy: results of a
randomized trial in human epidermal growth factor receptor 2-positive
operable breast cancer. J Clin Oncol 2005;23(16):3676–3685.
14. Gianni L, Pienkowski T, Im YH, et al. 5-year analysis of neoadjuvant
pertuzumab and trastuzumab in patients with locally advanced,
inflammatory, or early-stage HER2-positive breast cancer (NeoSphere):
a multicentre, open-label, phase 2 randomised trial. Lancet Oncol
2016;17(6):791–800.
15. Caudle AS, Gonzalez-Angulo AM, Hunt KK, et al. Predictors of tumor
progression during neoadjuvant chemotherapy in breast cancer. J Clin
Oncol 2010;28(11):1821–1828.
16. Siegel R, Ward E, Brawley O, et al. Cancer statistics, 2011: the impact
of eliminating socioeconomic and racial disparities on premature cancer
deaths. CA Cancer J Clin 2011;61(4):212–236.
17. Goldberg RM, Fleming TR, Tangen CM, et al. Surgery for recurrent
colon cancer: strategies for identifying resectable recurrence and success
rates after resection. Eastern Cooperative Oncology Group, the North
Central Cancer Treatment Group, and the Southwest Oncology Group.
Ann Intern Med 1998;129(1):27–35.
18. Flanigan RC, Salmon SE, Blumenstein BA, et al. Nephrectomy followed
by interferon alfa-2b compared with interferon alfa-2b alone for
metastatic renal-cell cancer. N Engl J Med 2001;345(23):1655–1659.
19. Lin SZ, Tong HF, You T, et al. Palliative gastrectomy and
chemotherapy for stage IV gastric cancer. J Cancer Res Clin Oncol
2008;134(2):187–192.
20. Rafii A, Deval B, Geay JF, et al. Treatment of FIGO stage IV ovarian
carcinoma: results of primary surgery or interval surgery after
neoadjuvant chemotherapy: a retrospective study. Int J Gynecol Cancer
2007;17(4):777–783.
21. Danna EA, Sinha P, Gilbert M, et al. Surgical removal of primary tumor
reverses tumor-induced immunosuppression despite the presence of
metastatic disease. Cancer Res 2004;64(6):2205–2211.
22. Norton L, Massague J. Is cancer a disease of self-seeding? Nat Med
2006;12(8):875–878.
23. Chambers AF, Groom AC, MacDonald IC. Dissemination and growth of
cancer cells in metastatic sites. Nat Rev Cancer 2002;2(8):563–572.
24. Khan SA, Stewart AK, Morrow M. Does aggressive local therapy
improve survival in metastatic breast cancer? Surgery 2002;132(4):620–
626; discussion 626–627.
25. Babiera GV, Rao R, Feng L, et al. Effect of primary tumor extirpation in
breast cancer patients who present with stage IV disease and an intact
primary tumor. Ann Surg Oncol 2006;13(6):776–782.
26. Xiao W, Zou Y, Zheng S, et al. Primary tumor resection in stage IV
breast cancer: a systematic review and meta-analysis. Eur J Surg Oncol
2018;44(10):1504–1512.
27. Dominici L, Najita J, Hughes M, et al. Surgery of the primary tumor
does not improve survival in stage IV breast cancer. Breast Cancer Res
Treat 2011;129(2):459–465.
28. Cady B, Nathan NR, Michaelson JS, et al. Matched pair analyses of
stage IV breast cancer with or without resection of primary breast site.
Ann Surg Oncol 2008;15(12):3384–3395.
29. Rao R, Feng L, Kuerer HM, et al. Timing of surgical intervention for the
intact primary in stage IV breast cancer patients. Ann Surg Oncol
2008;15(6):1696–1702.
30. Wu SG, Li FY, Chen Y, et al. Therapeutic role of axillary lymph node
dissection in patients with stage IV breast cancer: a population-based
analysis. J Cancer Res Clin Oncol 2017;143(3):467–474.
31. King TA, Lyman JP, Gonen M, et al. TBCRC 013: a prospective
analysis of the role of surgery in stage IV breast cancer. Cancer Res
2013;73.
32. King TA, Lyman J, Gonen M, et al. A prospective analysis of surgery
and survival in stage IV breast cancer (TBCRC 013). J Clin Oncol
2016;34(15).
33. Soran A, Ozmen V, Ozbas S, et al. Randomized trial comparing
resection of primary tumor with no surgery in stage IV breast cancer at
presentation: protocol MF07-01. Ann Surg Oncol 2018;25(11):3141–
3149.
34. Badwe R, Hawaldar R, Nair N, et al. Locoregional treatment versus no
treatment of the primary tumour in metastatic breast cancer: an open-
label randomised controlled trial. Lancet Oncol 2015;16(13):1380–1388.
35. Goldner B, Behrendt CE, Schoellhammer HF, et al. Incidence of
inflammatory breast cancer in women, 1992–2009, United States. Ann
Surg Oncol 2014;21(4):1267–1270.
36. Hance KW, Anderson WF, Devesa SS, et al. Trends in inflammatory
breast carcinoma incidence and survival: the surveillance, epidemiology,
and end results program at the National Cancer Institute. J Natl Cancer
Inst 2005;97(13):966–975.
37. Denu RA, Hampton JM, Currey A, et al. Racial and Socioeconomic
disparities are more pronounced in inflammatory breast cancer than
other breast cancers. J Cancer Epidemiol 2017;2017:7574946.
38. Zell JA, Tsang WY, Taylor TH, et al. Prognostic impact of human
epidermal growth factor-like receptor 2 and hormone receptor status in
inflammatory breast cancer (IBC): analysis of 2,014 IBC patient cases
from the California Cancer Registry. Breast Cancer Res 2009;11(1):R9.
39. Fouad TM, Barrera AMG, Reuben JM, et al. Inflammatory breast
cancer: a proposed conceptual shift in the UICC-AJCC TNM staging
system. Lancet Oncol 2017;18(4):e228–e232.
40. Rueth NM, Lin HY, Bedrosian I, et al. Underuse of trimodality
treatment affects survival for patients with inflammatory breast cancer:
an analysis of treatment and survival trends from the National Cancer
Database. J Clin Oncol 2014;32(19):2018–2024.
41. Masuda H, Brewer TM, Liu DD, et al. Long-term treatment efficacy in
primary inflammatory breast cancer by hormonal receptor- and HER2-
defined subtypes. Ann Oncol 2014;25(2):384–391.
42. Fouad TM, Kogawa T, Liu DD, et al. Overall survival differences
between patients with inflammatory and noninflammatory breast cancer
presenting with distant metastasis at diagnosis. Breast Cancer Res Treat
2015;152(2):407–416.
43. Giuliano AE, Edge SB, Hortobagyi GN. Eighth edition of the AJCC
cancer staging manual: breast cancer. Ann Surg Oncol 2018;25(7):1783–
1785.
44. Ionta MT, Atzori F, Massidda B. Inflammatory breast cancer in Italy:
epidemiological and clinical aspects. Cancer 2010;116(11 Suppl):2736–
2740.
45. Wecsler JS, Tereffe W, Pedersen RC, et al. Lymph node status in
inflammatory breast cancer. Breast Cancer Res Treat 2015;151(1):113–
120.
46. Walshe JM, Swain SM. Clinical aspects of inflammatory breast cancer.
Breast Dis 2005;22:35–44.
47. Dawood S, Merajver SD, Viens P, et al. International expert panel on
inflammatory breast cancer: consensus statement for standardized
diagnosis and treatment. Ann Oncol 2011;22(3):515–523.
48. Yang WT, Le-Petross HT, Macapinlac H, et al. Inflammatory breast
cancer: PET/CT, MRI, mammography, and sonography findings. Breast
Cancer Res Treat 2008;109(3):417–426.
49. Schlichting JA, Soliman AS, Schairer C, et al. Inflammatory and non-
inflammatory breast cancer survival by socioeconomic position in the
surveillance, epidemiology, and end results database, 1990–2008. Breast
Cancer Res Treat 2012;134(3):1257–1268.
50. Dawood S, Ueno NT, Valero V, et al. Identifying factors that impact
survival among women with inflammatory breast cancer. Ann Oncol
2012;23(4):870–875.
51. Dawood S, Ueno NT, Valero V, et al. Differences in survival among
women with stage III inflammatory and noninflammatory locally
advanced breast cancer appear early: a large population-based study.
Cancer 2011;117(9):1819–1826.
52. Ueno NT, Buzdar AU, Singletary SE, et al. Combined-modality
treatment of inflammatory breast carcinoma: twenty years of experience
at M. D. Anderson Cancer Center. Cancer Chemother Pharmacol
1997;40(4):321–329.
53. Baldini E, Gardin G, Evagelista G, et al. Long-term results of combined-
modality therapy for inflammatory breast carcinoma. Clin Breast
Cancer 2004;5(5):358–363.
54. Cristofanilli M, Buzdar AU, Sneige N, et al. Paclitaxel in the
multimodality treatment for inflammatory breast carcinoma. Cancer
2001;92(7):1775–1782.
55. Cristofanilli M, Gonzalez-Angulo AM, Buzdar AU, et al. Paclitaxel
improves the prognosis in estrogen receptor negative inflammatory
breast cancer: the M. D. Anderson Cancer Center experience. Clin
Breast Cancer 2004;4(6):415–419.
56. Gianni L, Eiermann W, Semiglazov V, et al. Neoadjuvant and adjuvant
trastuzumab in patients with HER2-positive locally advanced breast
cancer (NOAH): follow-up of a randomised controlled superiority trial
with a parallel HER2-negative cohort. Lancet Oncol 2014;15(6):640–
647.
57. Brzezinska M, Williams LJ, Thomas J, et al. Outcomes of patients with
inflammatory breast cancer treated by breast-conserving surgery. Breast
Cancer Res Treat 2016;160(3):387–391.
58. Bonev V, Evangelista M, Chen JH, et al. Long-term follow-up of breast-
conserving therapy in patients with inflammatory breast cancer treated
with neoadjuvant chemotherapy. Am Surg 2014;80(10):940–943.
59. Fisher ER, Wang J, Bryant J, et al. Pathobiology of preoperative
chemotherapy: findings from the National Surgical Adjuvant Breast and
Bowel (NSABP) protocol B-18. Cancer 2002;95(4):681–695.
60. DeSnyder SM, Mittendorf EA, Le-Petross C, et al. Prospective
feasibility trial of sentinel lymph node biopsy in the setting of
inflammatory breast cancer. Clin Breast Cancer 2018;18(1):e73–e77.
61. Hidar S, Bibi M, Gharbi O, et al. Sentinel lymph node biopsy after
neoadjuvant chemotherapy in inflammatory breast cancer. Int J Surg
2009;7(3):272–275.
62. Stearns V, Ewing CA, Slack R, et al. Sentinel lymphadenectomy after
neoadjuvant chemotherapy for breast cancer may reliably represent the
axilla except for inflammatory breast cancer. Ann Surg Oncol
2002;9(3):235–242.
63. Sinnott CJ, Persing SM, Pronovost M, et al. Impact of postmastectomy
radiation therapy in prepectoral versus subpectoral implant-based breast
reconstruction. Ann Surg Oncol 2018;25(10):2899–2908.
64. Elias EG, Vachon DA, Didolkar MS, et al. Long-term results of a
combined modality approach in treating inflammatory carcinoma of the
breast. Am J Surg 1991;162(3):231–235.
65. Sutherland S, Ashley S, Walsh G, et al. Inflammatory breast cancer—
The Royal Marsden Hospital experience: a review of 155 patients
treated from 1990 to 2007. Cancer 2010;116(11 Suppl):2815–2820.
66. Weiss A, Menen RS, Lin HY, et al. Factors associated with improved
outcomes for metastatic inflammatory breast cancer patients. Breast
Cancer Res Treat 2018;169(3):615–623.
67. Akay CL, Ueno NT, Chisholm GB, et al. Primary tumor resection as a
component of multimodality treatment may improve local control and
survival in patients with stage IV inflammatory breast cancer. Cancer
2014;120(9):1319–1328.
68. Takiar V, Akay CL, Stauder MC, et al. Predictors of durable no
evidence of disease status in de novo metastatic inflammatory breast
cancer patients treated with neoadjuvant chemotherapy and post-
mastectomy radiation. Springerplus 2014;3:166.
CHAPTER 14

Neoadjuvant and Adjuvant Systemic


Therapy
MAGDOLNA SOLTI

Most patients with newly diagnosed breast cancer present with an early,
potentially curable stage. Despite tremendous advances in diagnosis and
treatment, some patients still develop metastatic disease and the risk of
recurrence (ROR) persists decades after initial occurrence (1). The aim of
systemic therapy, defined as the administration of cytotoxic chemotherapy,
biologic therapy, and/or endocrine manipulation, is to eradicate clinically
inapparent micrometastatic disease. Randomized clinical trials and the
overviews published by the Early Breast Cancer Trialists’ Collaborative
Group (EBCTCG) (2) have shown that adjuvant therapy for early-stage
breast cancer is effective in reducing the rate of recurrence and mortality
from this disease. The more recent neoadjuvant approach—that is, systemic
treatment administered before breast cancer surgery—helps with
downstaging and provides similar reduction in mortality (3).
In this chapter, we review the current approach to systemic treatment, with
a focus on the factors involved in patient selection, the available treatment
modalities, and recommendations for the management of specific subgroups
of patients.
PROGNOSTIC FACTORS IN EARLY BREAST CANCER

Overview
Determining the appropriate adjuvant systemic therapy regimen for an
individual patient requires an estimate of her underlying risk of disease
recurrence and a determination of the therapy to which she is most likely to
respond. The former is based primarily on tumor-related prognostic factors
that reflect tumor biology irrespective of the treatment administered. This
contrasts with predictive factors, which are indicative of responsiveness to
specific therapies and are discussed later in association with general treatment
recommendations. It is important to note, however, that individual factors
may be prognostic, predictive, or both (6).
Prognostic markers are patient- or tumor-related factors that allow for a
determination of clinical outcome in the absence of systemic therapy. The use
of prognostic factors provides the clinician with a means to estimate the
benefits of adjuvant therapy and thus forms the basis for systemic treatment
recommendations. Prognostic factors tend to reflect the underlying biology of
the tumor, such as its ability to proliferate, invade, and induce angiogenesis.
Tumor size, hormone receptor status, human epidermal growth factor
receptor (HER)-2/neu (i.e., c-erbB2) status, histopathologic features,
including tumor type and grade, and the number of involved lymph nodes are
all markers that have documented prognostic value. Other indicators, such as
proliferative rate, the presence of circulating tumor cells (CTCs), have been
evolving in different studies. Gene expression profiles generated by high-
throughput, DNA or RNA-based methodologies simultaneously measure the
expression of thousands of genes and have led to the identification of
biology-based prognostic profiles, several of which have been validated and
are in clinical use.
Pathologic Factors
Tumor Stage
The Tumor, Node, Metastasis (TNM) staging system for breast cancer is an
internationally accepted system used to determine the disease stage. The 5-
year relative survival rates are 95%, 85%, 70%, 52%, 48%, and 18% for
women presenting with anatomic stage I, IIA, IIB, IIIA, IIIB, and IV disease,
respectively (4). A SEER study with more than 13,000 node-negative patients
demonstrated a significant correlation between tumor size and patient
outcomes (5). The 5-year breast cancer survival rates ranged from 91% for T
<2 cm, to 80% for T 2 to 5 cm, and 63% for T >5 cm.
Axillary lymph node status is recognized as a strong predictor of breast
cancer recurrence. A Surveillance Epidemiology and End Results (SEER)
analysis of 24,740 breast cancer cases demonstrated a clear association
between the number of involved lymph nodes and survival (5). Five-year
overall survival (OS) was 92% for women with node-negative disease, 81%
for those with one to three positive axillary lymph nodes, and 57% for those
with four or more involved nodes. Moreover, residual axillary nodal
micrometastases after neoadjuvant chemotherapy (NACT) predicted for
poorer disease-free survival (DFS) and OS compared to node-negative
patients (7).

Histopathologic Features
Certain histopathologic subtypes, including pure tubular, papillary, mucinous,
and medullary carcinomas, are associated with a particularly good prognosis
(8). By contrast, micropapillary and metaplastic carcinomas confer a worse
prognosis (9).
In addition, histologic grade has been shown to provide prognostic
information. The currently used Nottingham grading system characterizes the
degree of tumor differentiation based on morphologic features such as degree
of tubule or gland formation, nuclear pleomorphism, and mitotic activity
(10). Even in the molecular era the tumor histologic grade serves as an
independent prognostic factor (11,12).
The Ki67 index is defined as the percentage of tumor cells showing
positivity for a nuclear antigen expressed in the G1, S, G2, and M phases of
the cell cycle (13). Ki-67 is a protein used as a marker for cellular
proliferation and has been shown to be an independent prognostic parameter
in breast cancer. It is most commonly assessed via immunohistochemistry
(14). According to St. Gallen guidelines, high Ki-67 is one of the features
that indicate increased ROR in estrogen receptor (ER)-positive HER-2–
negative breast cancer, indirectly supporting the value of adding
chemotherapy to endocrine therapy in these patients (15). Ki-67 proliferative
index (Ki-67) has become a predictive and prognostic factor in breast cancer
(16).

Hormone Receptor and HER-2 Expression


Women with ER-positive tumors have a small but statistically significant
survival advantage of 9% to 10% in comparison to those with ER-negative
tumors. In the National Surgical Adjuvant Breast and Bowel Project
(NSABP) B-06 study, ER positivity was associated with a 5-year DFS of
74% and a 5-year OS of 92% (17), compared with 66% and 82%,
respectively, for patients with ER-negative tumors. Progesterone receptor
(PR) has a prognostic value independent of ER. A large population-based
cohort study of 1,074 patients with early breast cancer showed that absence
of PR expression was strongly associated with worse breast cancer–specific
survival (BCSS) (HR 3.24, 95% confidence interval [CI] 2.42 to 4.34) (18).
HER-2 positivity accounts for about 15% to 20% of breast cancers and is
defined as evidence of HER-2 protein overexpression measured by
immunohistochemistry status (IHC3+) or by fluorescence in situ
hybridization (FISH) measurement of a HER-2 gene copy number of six or
more or a HER-2/CEP17 ratio of 2.0 or greater (19). HER-2 has been
established as an important prognostic factor in early-stage breast cancer in
large patient populations and has been associated with shorter overall and
DFS (20,21). In breast cancer, HER-2 and the HRs remain the only predictive
factors for the selection of targeted therapies (22,23).
Genomic Profiles/Intrinsic Molecular Subtypes
While clinicopathologic parameters aid in decision on adjuvant treatment for
breast cancer, substantial tumor heterogeneity occur. Gene expression
profiling is a molecular tool that more precisely defines the intrinsic
characteristics of each individual tumor.
In 2000, Perou (24) and Sørlie (25) demonstrated that ER-positive and ER-
negative breast cancers are completely distinct diseases on a molecular level.
In addition, hierarchical cluster analyses of genes that vary more between
tumors than between repeated samples of the same tumor, the so-called
intrinsic genes, revealed at least four molecular subtypes of breast cancer,
namely, luminal, HER-2 enriched, basal like, and normal breast like (24).
Luminal A tumors, which probably make up about 40% of all breast
cancers, usually have high expression of ER-related genes (ER alpha, GATA-
binding protein 3, X-box binding protein 1), low expression of the HER-2
cluster of genes, and low expression of proliferation-related genes (26,27).
Luminal A tumors are the most common subtype and in general, carry the
best prognosis of all breast cancer subtypes (28). The less common (about
20%) luminal B tumors have relatively lower (although still present)
expression of ER-related genes, variable expression of the HER-2 cluster,
and higher expression of the proliferation cluster. Luminal B tumors carry a
worse prognosis than luminal A tumors (29).
The HER-2–enriched subtype makes up about 10% to 15% of breast
cancers and is characterized by high expression of the HER-2 and
proliferation gene clusters (ERBB2 amplicon at 17q22.24, including ERBB2
and GRB7) and low expression of the luminal and basal clusters. For this
reason, these tumors are most often negative for ER and PR, and positive for
HER-2. However, the HER-2–enriched subtype is not synonymous with
clinically HER-2–positive breast cancer. While half of clinically HER-2–
positive breast cancers are HER-2 enriched, the other half can include any
molecular subtype but is mostly made up of HER-2–positive luminal
subtypes (30).
The ER-negative genomic profile includes multiple subtypes, such as basal
like, claudin low, and interferon rich, among others. Most of these fall under
the category of triple-negative breast cancers (TNBCs) because they are also
PR negative and HER-2 negative.
Multiple independent datasets have shown the prognostic effect of intrinsic
subtyping of breast cancer with luminal A cases to be at low risk of early
recurrence. Apart from its prognostic implication, the intrinsic molecular
subclassification seems to predict responsiveness to chemotherapy. Studies
evaluating the association between molecular subtype and pathologic
complete response (pCR) rate to preoperative (neoadjuvant) chemotherapy
have reported the highest rate of pCR in basal-like (30% to 45%) and HER-
2–enriched (33% to 55%) subtypes, while pCR rates for luminal B (1% to
15%) and luminal A disease (0% to 7%) were substantially lower (31).

TABLE 14-1 Validated Multi-Gene Panels in Early-Stage Breast Cancer


Gene Expression Profiling for Early-Stage Breast Cancer
Standard clinicopathologic features have suboptimal prognostic and
predictive utilities in predicting chemotherapy benefit (32). Multigene
expression profiles have significantly increased our ability to estimate distant
recurrence in ER-positive HER-2–negative breast cancer (33). In recent
years, several novel gene expression prognostic tests have been developed.
The commonly used multigene profiles are listed in Table 14-1.
The 21-gene Recurrence Score (RS) (Oncotype DX; Genomic Health, Inc.,
Redwood City, CA) uses a real-time reverse transcriptase-polymerase chain
reaction–based method and requires formalin-fixed, paraffin-embedded
tumor tissue. The assay includes genes related to cellular proliferation, ER
signaling, the HER-2/neu pathway, and tumor invasive potential in addition
to five reference genes that serve as an internal control to generate scores of 0
to 100, where higher scores indicate a higher probability of distant recurrence
at 10 years in patients treated with adjuvant tamoxifen therapy alone (34).
The RS result represents an individualized estimate of risk of distant
recurrence and/or breast cancer–specific mortality (prognosis) and predicts
the likelihood of adjuvant chemotherapy benefit (35). The Oncotype DX
assay achieved level IB evidence and has been incorporated into current
National Comprehensive Cancer Network and American Society of Clinical
Oncology guidelines, to aid in treatment decisions for patients with HR-
positive, node-negative, early-stage breast cancer (36). Results of the
TAILORx study suggest little-to-no benefit of adjuvant chemotherapy for
patients with HR+, HER-2–negative, node-negative breast cancer and RS ≤25
(35,37). Endocrine treatment alone was noninferior to chemoendocrine
treatment in women ≤ 50 years of age with RS of 11 to 15 and in women >
50 years of age with RS of 11 to 25. When adjusted for age, chemotherapy
benefit was supported in women ≤ 50 years of age with RS of 16 to 25. An
ongoing study, Treatment for Positive Node, Endocrine Responsive Breast
Cancer (RxPONDER; SWOG S1007), should provide further insight into the
RS cutoff at which a chemotherapy benefit can be detected in patients with
N+ breast cancer (38).
The 70-gene profile (MammoPrint; Agendia, Huntingdon Beach, CA),
originally designed for unfixed tissue, has recently been adapted to formalin-
fixed tissue. The 70-gene MammaPrint assay stratifies patients into low or
high risk for distant metastases at 5 years. Large-scale retrospective
validation of this profile was performed on frozen breast tumor specimens
collected from 326 node-negative patients through a collaborative effort of
the TRANSBIG consortium (39). The Microarray in Node-Negative Disease
May Avoid Chemotherapy (MINDACT) trial reported that women with a
high–clinical risk and low-risk MammaPrint result had a risk of distant
metastases only 1.5% higher at 5 years without chemotherapy, suggesting
that these patients can safely forgo chemotherapy (40).
In 2009, Parker et al. (41) developed an efficient 50-gene classifier, called
Prediction Analysis of Microarray (PAM50) that reanalyzed the previous
subgroups defining the four major intrinsic subtypes currently known:
luminal A, luminal B, HER-2 enriched, and basal like. The PAM50 gene
signature has been developed into a clinical test, the Prosigna gene signature
assay (Prosigna; NanoString Technologies, Inc., Seattle, WA) validated to
estimate the prognosis for postmenopausal patients with ER-positive early-
stage breast cancer. Along with the identification of subtypes, PAM50 has
been shown to be an independent predictor of survival in breast cancer (42).
PAM50 generates a numerical score ROR that along with clinical features
estimates the risk of relapse at 10 years in postmenopausal women with stage
I/II node-negative or stage II node-positive (one to three positive lymph
nodes) and HR-positive breast cancer (43).
The Breast Cancer Index (BCI; Biotheranostics, Inc., San Diego, CA)
combines two biomarkers (HOXB13:IL17BR ratio and molecular grade
index) to derive the BCI score. The BCI score has been validated to provide
prognostic information in the NCIC MA.14 study (44). The BCI linear (BCI-
L) model was also found to be strongly prognostic of both early and late
recurrences, and its strength may be the ability to identify patients at risk of
late recurrence as candidates for extended endocrine therapy (45). For node-
positive patients treated in the aTTom trial BCI predicted benefit of
extending tamoxifen therapy from 5 to 10 years (46).
EndoPredict (Myriad Genetics, Salt Lake City, UT) is a 12-gene RT-
polymerase chain reaction–based assay. The EP classifies tumors into high-
and low-risk categories and can also be combined with tumor size and nodal
status to derive the EPclin. EPclin can potentially reduce the use of adjuvant
chemotherapy by identifying patients with a good prognosis that would have
been classified as intermediate or high risk based on clinicopathologic criteria
and spares the use of chemotherapy in this group (47). The EPclin has been
shown to be able to accurately prognosticate recurrence risk up to 10 years in
LN0 and LN+ patients (48). There is no prospective data relating to
chemotherapy benefit for EndoPredict or EPclin.
Circulating Tumor Cells
CTCs represent the liquid component of solid tumors and indicate the
presence of residual disease. CellSearch (Menarini Silicon Biosystems, Inc;
Bologna, Italy) is the only FDA-cleared assay for CTC analysis that uses a
positive selection method with antibody-coated magnetic beads for detection
and enumeration of EpCAM-positive CTCs. Ten percent to 30% of patients
with localized breast cancer have detectable CTCs (≥1 CTC per 7.5 mL
blood) at the time of diagnosis, before or after neoadjuvant or adjuvant
chemotherapy, which is prognostic for higher recurrence and breast cancer
mortality rates (49,50). In the phase III SUCCESS-A trial at 2 years, a
positive CTC assay was associated with a 3.9-fold higher risk of death and a
2.3-fold higher ROR in multivariate models that included clinicopathologic
features and CTC status at baseline; sensitivity analysis showed this effect
only in HER-2–negative disease (49). CTCs were reported in 5% of patients
with localized HR-positive breast cancer 5 years after diagnosis and were
associated with higher ROR (51). In a meta-analysis that included individual
patient data from 21 studies, CTCs were detected in 25.2% of patients before
NACT, and a higher CTC number had a detrimental impact on OS (P <.001),
distant DFS (P <.001), and locoregional relapse–free interval (P <.001) but
not on pCR (52). CTCs have not been predictive of benefit from any specific
systemic therapy or change in therapy. A recent study from a large national
database cohort and the SUCCESS trial demonstrated that CTC status was a
predictive factor of the benefit of radiotherapy in early-stage breast cancer
(53).
Summary
The use of advanced diagnostics in breast cancer has increased our
understanding of disease biology and is currently applied to clinical practice.
Evaluation of standard biomarkers (ER, PR, and HER-2) in primary breast
cancer can be supplemented by molecular profiling with significant
information on disease subtyping, which constitutes prognostic and predictive
data that can help in treatment planning.
NEOADJUVANT THERAPY

Overview
Neoadjuvant therapy originally was developed as a way of reducing tumor
size, to facilitate surgical resection and increase breast-conserving surgery
(BCS) rates. More recently, neoadjuvant treatment has also been used for
operable early breast tumors to eliminate axillary node metastases and avoid
axillary node dissection (54).
Neoadjuvant systemic therapy is at least as effective as in an adjuvant
setting but has several additional benefits. It allows for in vivo determination
of tumor chemosensitivity. pCR after NACT has been identified as an
independent prognostic factor defined by ypT0/Tis (55). Lastly, the
neoadjuvant setting is a powerful model for the development of new drugs by
using pCR as a surrogate outcome for event-free and overall survival and
enables seeking prognostic and predictive biomarkers (56).
Selection criteria for neoadjuvant therapy include axillary node
involvement, tumor size >2 cm, triple-negative or HER-2–positive subset,
high proliferative index, unresectable tumors, and inflammatory carcinoma
(57). The best management approach involves a multidisciplinary tumor
board discussion at the time of diagnosis. The current standard treatment for
triple-negative, and HER-2–positive and HR-positive subtypes is reviewed.
Neoadjuvant Chemotherapy in TNBC
The main aim of systemic treatment in addition to local treatment is to
eradicate distant micrometastases to increase OS. The selection of patients for
neoadjuvant therapy is based on tumor characteristics, stage of breast cancer,
and patient performance status and comorbidities. Although TNBC is
generally associated with the poorest prognosis among breast cancer types,
the rate of pCR to NACT in TNBC is relatively high. Up to 45% of triple-
negative tumors show a pCR after NACT. Achieving pCR is associated with
longer PFS and OS (58). In contrast, triple-negative tumors with residual
disease have a high probability of recurrence (59).
The chemotherapy regimens employed in the neoadjuvant setting are the
same as those used in the adjuvant setting. Standard anthracycline–taxane
(A/T)-based NACT combinations yield pCR rates between 25% and 40%. A
meta-analysis of the EBCTCG in 44,000 patients showed that the addition of
a taxane to a fixed anthracycline-based regimen improves BCSS, with a
hazard ratio (HR) of 0.86 (standard error [SE] 0.04, p = 0.0005) (60).
Taxanes are equally effective if administered concurrently or sequentially
with anthracyclines, although concurrent regimens such as
docetaxel/doxorubicin/cyclophosphamide (TAC) show increased toxicity and
require prophylactic administration of granulocyte colony–stimulating factor
(Sparano-3) (61). Within the sequential regimens, weekly paclitaxel improves
DFS and OS compared with 3-weekly paclitaxel. Three-weekly docetaxel
also improves DFS compared with 3-weekly paclitaxel, but not OS (Sparano-
3).
More frequent administration of cytotoxic therapy (dose dense) is a more
effective way of minimizing residual tumor burden than dose escalation. In a
meta-analysis of 10 randomized controlled trials (RCTs), dose-dense–
administered chemotherapy improved OS by 16% (HR 0.84, 95% CI 0.72 to
0.98, p = 0.03) and DFS by 17% (HR 0.83, 95% CI 0.73 to 0.94, p = 0.005)
(62). In the few trials that were designed to analyze the pure effect of dose-
dense compared with standard-dose chemotherapy, the benefit on both OS
and DFS was largest for HR-negative tumors (62,63). A recent pooled
analysis of two Italian trials showed a larger benefit of the dose-dense
regimen for premenopausal women (64).
The addition of carboplatin to standard anthracycline–taxane-containing
NACT in unselected TNBCs improved pCR rates from 37% to 53% in the
GeparSixto trial (65), and from 31% to 58% in the BrighTNess trial (66),
albeit with higher toxicity. Longer follow-up is needed to detect change in
event-free survival or OS. However, despite an early signal in the metastatic
disease setting that platinum agents may preferentially benefit TNBC patients
with BRCA mutations, this observation has not been replicated in the early-
stage setting (66,67).
Patients unfit for anthracyclines (e.g., due to cardiac dysfunction) or
having node-negative early-stage triple-negative cancers may benefit from
four cycles of docetaxel/cyclophosphamide (TC) every 3 weeks. This
regimen improved OS compared with four cycles of
Adriamycin/cyclophosphamide (AC) after a median follow-up of 7 years (HR
0.69, 95% CI 0.50 to 0.97, p = 0.032) (68). An anthracycline-free docetaxel
and carboplatin combination × 6 cycles yielded a 55% pCR rate with 3-year
OS of 87% (69).

TABLE 14-2 Currently Used HER-2 Targeted Agents

Adding the programmed death-1 (PD-1) inhibitor pembrolizumab to


NACT may improve outcomes in early-stage TNBC. In KEYNOTE-522,
researchers assigned 1,174 patients with newly diagnosed, early-stage TNBC
in a 2:1 ratio to receive neoadjuvant pembrolizumab plus chemotherapy or a
placebo plus chemotherapy. In an analysis of the first 602 patients, performed
after a median follow-up of 15.5 months, 64.8% of those in the
pembrolizumab arm experienced a pCR compared with 51.2% of those in the
chemotherapy-only group—a statistically significant difference that was seen
regardless of nodal stage, tumor size, patient age, chemotherapy regimen, or
PD-L1 expression (70).
Poly ADP-ribose polymerase (PARP) inhibitors have been evaluated in
this scenario, targeting the potential homologous recombination deficiency in
TNBC. The PARTNER study (NCT03150576) will test olaparib in addition
to platinum-based NACT for TNBC and/or BRCA-mutant patients.
Neoadjuvant HER-2 Targeted Therapy
Approximately 15% to 20% of breast cancers are HER-2 positive. Without
HER-2–directed treatment, HER-2–positive breast cancer is characterized by
an aggressive course of disease and a poor prognosis. Anti–HER-2 treatment
has changed the natural biology of this disease. Several studies have
demonstrated a high pCR rate (up to 60%) with neoadjuvant therapy that
includes anti–HER-2 regimen. The response rates are higher in ER-negative
than in ER-positive cases. Targeted agents currently in use are summarized in
Table 14-2.
Trastuzumab
Trastuzumab, the first approved HER-2–targeted agent, is a humanized
monoclonal antibody directed against the extracellular domain (subdomain
IV) of HER-2. Trastuzumab exerts antitumor activity by interfering with
HER-2 signalling and via immune mechanisms such as antibody-dependent
cellular cytotoxicity and complement-dependent cytotoxicity (71).
Trastuzumab as a single agent has modest antitumor activity (72). The
introduction of trastuzumab in combination with chemotherapy substantially
improved the outcome of patients with metastatic HER-2–positive breast
cancer (73).
The NOAH trial was the first phase III neoadjuvant study powered for
event-free survival that compared chemotherapy with chemotherapy plus
neoadjuvant and adjuvant trastuzumab (74). In the NOAH trial, addition of
trastuzumab to the treatment regimen of women with locally advanced breast
cancer increased pCR from 19% to 38% and event-free survival from 56% to
71% (HR 0.59) with a borderline (not statistically significant) improvement
in OS. Updated results after a median follow-up of 5.4 years confirmed a
sustained long-term event-free survival benefit of trastuzumab-containing
neoadjuvant therapy. Among patients who achieved a pCR, event-free
survival (HR 0.29, 95% CI 0.11 to 0.78) and OS (HR 0.27, CI 0.09 to 0.83)
were significantly superior with the addition of trastuzumab, whereas
trastuzumab did not confer additional benefit in patients with residual disease
(75). The interaction between trastuzumab, pCR, and long-term outcomes
was statistically significant.
A single-institution trial from MD Anderson Cancer Center investigated
the effect of adding trastuzumab to NACT. The trial was stopped early by the
data monitoring committee after the initial 34 patients due to superiority of
trastuzumab plus chemotherapy (66.7% of patients achieved a pCR with
trastuzumab vs. 25% without trastuzumab) (76).
The TECHNO trial demonstrated 39% pCR rate after NACT plus
trastuzumab, which predicted favorable DFS (88% in patients with pCR
compared to 73% in patients without pCR, P = .01) and OS (96% at 3 years
in patients with pCR compared to 86% in patients without pCR, P = .025)
(77).
Several trastuzumab biosimilars are in development. The use of
trastuzumab biosimilars could expand treatment options while mitigating cost
barriers to increase access to HER-2 targeted therapy.

Pertuzumab
The NeoSphere trial tested the potential benefit of dual targeting of HER-2 by
coadministration of trastuzumab and pertuzumab (78). In NeoSphere,
pertuzumab was selected as a companion treatment of trastuzumab in a
comparison of four different preoperative regimens for 12 weeks: (1) a
control regimen of docetaxel plus trastuzumab, (2) the same control regimen
plus pertuzumab, (3) pertuzumab and trastuzumab without chemotherapy,
and (4) docetaxel plus pertuzumab. A significantly higher proportion of
patients achieved a pCR with pertuzumab and trastuzumab plus docetaxel
than with trastuzumab plus docetaxel (p = 0.014). The three-drug
combination had little additional toxicity.
The TRYPHAENA trial also tested the efficacy of dual blockade of HER-2
with pertuzumab, by combining pertuzumab with different anthracycline-
containing and nonanthracycline chemotherapy regimens (79). The results
confirmed that a high proportion of patients had a pCR with pertuzumab and
trastuzumab in combination with any of the chemotherapy regimens, with a
similarly low incidence of symptomatic left ventricular systolic dysfunction
for the anthracycline combinations. In NeoSphere and TRYPHAENA,
evidence suggested that an immune signature and tumor-infiltrating
lymphocytes are linked to the pCR.
The HannaH trial investigated the safety and efficacy of subcutaneous
trastuzumab in women with HER-2–positive early breast cancer by
comparing intravenous (IV) and subcutaneous formulations of neoadjuvant
trastuzumab, with the coprimary end points of noninferiority for
pharmacokinetics and antitumor activity. Noninferiority was shown for both
end points, which introduced the possibility of using a new modality of
trastuzumab administration (80).
In the last decade, the number and quality of HER-2–directed therapies has
profoundly changed the course of HER-2–positive breast cancer (81).
Neoadjuvant Endocrine Therapy
Endocrine therapy is the mainstay of treatment for ER-positive (ER+) breast
cancer. At approximately 75% of all breast cancers, ER-positive constitutes
the most common subtype of the disease. Although medical therapy for
localized breast cancer is primarily used in the adjuvant setting, it can also be
effectively used in the neoadjuvant (preoperative) setting.
The rationale for neoadjuvant therapy in HR+ breast cancer is similar to
other clinical subtypes of breast cancer: (1) the ability to downstage breast
cancers in postmenopausal women with ER-positive tumors, thus making
breast-conserving therapy possible; (2) to understand prognosis based on
progression-free survival (PFS) or OS; and (3) for biomarker evaluation and
targeted therapy development. pCR to a given therapy is often used as a
surrogate of long-term survival and cure from breast cancer.
Neoadjuvant endocrine therapy (NET) historically has been reserved to
treat elderly patients with ER-positive breast cancer, who were not
considered good candidates for systemic chemotherapy or surgery (82). More
recently, the ability to identify early endocrine responsiveness and the
development of highly effective aromatase inhibitors (AIs) has resulted in a
broader use of NET. NET, however, has been less frequently incorporated
into practice due to the slow tumor response requiring prolonged therapy as
well as the less defined prognostic information that is obtained after treatment
(84). A systemic review and meta-analysis of 20 randomized clinical trials
with a total sample size of 3,490 women, NET, even as monotherapy, was
associated with response rates like those of neoadjuvant combination
chemotherapy but with lower toxicity (83). NET can also be used in selected
premenopausal women and is often combined with ovarian suppression (85).
Complete pathologic responses are infrequent with NET; however, residual
disease does not imply poor prognosis. AIs are more effective than tamoxifen
in downstaging ER-positive tumors. From the available data in studies of
postmenopausal women, 4 months to 6 months of an AI seems optimal with
modest persistent benefits thereafter. NET has been shown to cause a
significant reduction in Ki67, with the degrees of suppression related to the
level of ER expression. Ki67 levels after NET have been shown to be
prognostic. The IMPACT trial demonstrated that high Ki67 expression levels
after 2 weeks of NET was associated with a poorer recurrence-free survival
(RFS) (86). The 21-gene RS has also been shown to have predictive value.
Ueno et al. evaluated pretreatment and posttreatment tumor tissue from
patients with estrogen-positive tumors treated with neoadjuvant exemestane.
The clinical response rate was 59% in patients with a low RS compared with
20% in patients with a high RS (87). The TransNEOS study validated the 21-
gene test as a predictor of clinical response to neoadjuvant hormonal therapy.
Among patients with large tumors (≥ 2 cm), 54% of those with RS <18
achieved complete response or partial response (CR or PR) with neoadjuvant
letrozole, and 79% were BCS recipients, including many who were BCS
noncandidates before neoadjuvant treatment. In contrast, patients with RS ≥
31 had a higher rate of PD with neoadjuvant letrozole. Multivariate analyses
showed that the RS result significantly predicted clinical response to
neoadjuvant hormonal therapy, even after adjustment for clinical covariates
(age, tumor size, and tumor grade). RS group was significantly associated
with rate of BCS after neoadjuvant treatment (RS < 18 vs. RS ≥ 31, p =
0.010) (88).
Multiple additional studies are presently underway to better define the
impact of NET on early-stage breast cancer. The New Primary Endocrine-
therapy Origination Study (NEOS), a multicenter phase III randomized trial,
will assess the need for adjuvant chemotherapy in postmenopausal women
with stage T1c-T2N0M0, HR-positive tumors who responded to neoadjuvant
letrozole (89). The Alternate Approaches for Clinical Stage II or III Estrogen
Receptor–Positive Breast Cancer Neoadjuvant Treatment (ALTERNATE) in
Postmenopausal Women: A Phase III Study, is an ongoing trial that seeks to
define the rate of endocrine-resistant disease, RFS, and rates of pCR in this
population after treatment with fulvestrant, anastrozole, or the combination of
the two agents (90). The ability to identify good and poor responses to NET
early in treatment provides a strategy to triage poor responders into clinical
trials of targeted agents to address endocrine resistance. Multiple trials are
ongoing that combine molecularly targeted agents with endocrine therapy in
the neoadjuvant setting. NeoPalAna is enrolling the endocrine-resistant
population based on high Ki67 on endocrine therapy to receive the
combination of the cyclin dependent kinase (CDK)4/6 inhibitor palbociclib
and anastrozole to overcome endocrine resistance.
TREATMENT OF RESIDUAL DISEASE POST NEOADJUVANT THERAPY
Absence of pCR to NACT correlates with poor long-term survival in patients
with TNBC. Until recently there was no standard treatment after failure to
respond to neoadjuvant therapy. Residual disease after neoadjuvant therapy
poses a great opportunity for drug development exploring new treatments in
the adjuvant/post neoadjuvant setting. The goal is to treat subclinical
micrometastases, identify new biomarkers, explore resistance pathways, and
test targeted therapies.
Treating Residual Disease in TNBC
The Capecitabine for Residual Cancer as Adjuvant Therapy (CREATE-X)
trial was conceived with the aim of improving the prognosis of patients who
did not achieve a pCR after NAT. This multicenter, open-label, randomized,
phase III trial enrolled patients with stage I to IIIB HER-2–negative early
breast cancer who had residual invasive disease and/or tumor-positive lymph
nodes after standard NAT containing anthracycline, taxane, or both. After
surgery, the capecitabine group received oral capecitabine (1,250 mg/m2,
twice per day, on days 1 to 14) every 3 weeks for 6 to 8 cycles. The trial was
terminated early after 887 patients for meeting its primary end point: at the
final analysis, the 5-year DFS improved from 67.6% to 74.1% (HR 0.70, 95%
CI 0.53 to 0.92, p = .01) and OS improved from 83.6% to 89.2% (HR 0.59,
95% CI 0.39 to 0.90, p = .01). The most prominent HR was seen in the
subgroup of 286 patients (32.2%) with TNBC (DFS: HR 0.58, 95% CI 0.39
to 0.87; OS: HR 0.52, 95% CI 0.30 to 0.90) (91).
Two randomized phase III trials are currently investigating the role of
immune checkpoint inhibitors in this setting: the A-Brave trial
(NCT02926196), with the anti–PD-L1 avelumab tested as adjuvant or post-
NAT treatment for high-risk TNBC patients, and the SWOG S1418 trial
(NCT02954874), in which TNBC patients with residual disease (RD) after
NAT are randomized to adjuvant pembrolizumab or observation.
No evidence is available on the efficacy of post-NAT platinum-based
chemotherapy for TNBC, but the ongoing ECOG-ACRIN EA1131 study
(NCT02445391) will examine this issue further, with patients who did not
achieve pCR randomized to adjuvant carboplatin, cisplatin, or observation.
Based on the results of the CREATE-X trial, the observation arm was
replaced by adjuvant capecitabine as comparator.
Additionally, PARP inhibitors have been evaluated in this scenario,
targeting the potential homologous recombination deficiency in TNBC. The
ongoing phase III OlympiA trial (NCT02032823) will evaluate the role of
olaparib as adjuvant or post-NAT treatment for high-risk HER-2–negative
BRCA-mutant patients.
Treating Residual Disease in HER-2–Positive Breast Cancer
In the ExteNET trial, patients with stage II to IIIc HER-2–positive early
breast cancer or residual disease after neoadjuvant therapy (25% of the whole
trial population) received adjuvant neratinib for 1 year after completion of
standard therapy, with a significant benefit in terms of 5-year DFS rate
(90.2% vs. 87.7%, HR 0.73, 95% CI 0.57 to 0.92, p = .008), particularly for
those with HR-positive breast cancer (91.2% vs. 86.8, HR 0.60, 95% CI 0.43
to 0.83)(92). Of note, OS data are not yet mature and 39.9% of patients
treated with neratinib experienced grade 3 to 4 diarrhea, hence efficacy–
toxicity trade-offs and loperamide prophylaxis are both recommended when
considering its use.
The KATHERINE trial compared ado-trastuzumab emtansine (T-DM1) to
trastuzumab in patients with early-stage HER-2–overexpressing breast cancer
with residual invasive disease in the breast or axilla after neoadjuvant
therapy. Ado-trastuzumab emtansine is a HER-2–directed antibody–drug
conjugate of trastuzumab and maytansine, a microtubule inhibitor (93). The
result of a planned interim analysis of 1,486 randomly assigned patients
revealed that 88.3% of patients in the T-DM1 arm were free of invasive
disease at 3 years compared to 77% in the trastuzumab control group (HR for
invasive disease or death 0.50, 95% CI 0.39 to 0.64, P < 0.001) (94). Based
on the KATHERINE study results T-DM1 is now FDA approved for the
adjuvant treatment of patients with HER-2–positive early breast cancer who
have residual invasive disease after neoadjuvant taxane and trastuzumab-
based treatment.
Treating Residual Disease in HR-Positive Breast Cancer
HR-positive breast cancer (BC) shows a poor response to NACT. New
treatment targets like the Cyclin D1-CDK4/CDK6 complex are promising
adjuvant/post neoadjuvant therapeutic strategies. Upcoming studies will also
explore the post-NAT treatment of HR-positive breast cancer, uncovering the
role of CDK 4/6 inhibitors in this setting. Two phase III, placebo-controlled
trials, the PENELOPE-B (NCT01864746) and the CLEE011G2301
(NCT03078751), are currently randomizing HR-positive/HER-2–negative
patients with RD after NAT to receive adjuvant palbociclib or ribociclib,
respectively, in addition to standard adjuvant endocrine therapy (95).
ADJUVANT THERAPY
Systemic therapy is an integral part of the multidisciplinary curative
treatment of primary breast cancer and results in significant reductions in
ROR and death. Randomized clinical trials have demonstrated that adjuvant
therapy reduces the risk of recurrent breast cancer and improves the survival
of patients with both lymph node–negative and lymph node–positive disease.
The results of the EBCTCG overview (96) indicate that the percentage
reduction in the ROR and mortality is identical for both node-negative and
node-positive patients. The identification of the patients most likely to benefit
from therapy and the use of optimal adjuvant regimens is therefore key to
maximizing the benefits of systemic treatment.
Adjuvant Chemotherapy
Historically, trials of adjuvant chemotherapy have been ongoing since the
mid-1970s, and the long-term effectiveness of this therapy has been
established. Initial chemotherapy trials were conducted in node-positive
patients, demonstrating that chemotherapy administration is associated with
significant reductions in the rates of recurrence and death. The Milan trial
randomized women with node-positive breast cancer to receive no adjuvant
systemic therapy or to receive the combination of cyclophosphamide,
methotrexate, and 5-fluorouracil (CMF) over 12 months. At 20 years’ follow-
up, the RFS rate was 36% for those receiving CMF and 27% in the control
patients, with an OS rate of 34% in those treated with chemotherapy and 24%
in patients who had mastectomy alone (97). Similarly, significant
improvements in DFS with the use of adjuvant chemotherapy have been
demonstrated in node-negative women. Results from three NSABP
sequentially conducted randomized trials of postoperative chemotherapy in
women with ER-negative tumors and negative axillary lymph nodes have
demonstrated that a combination of methotrexate and 5-fluorouracil (MF) is
more effective than surgery alone, that cyclophosphamide with MF (CMF) is
more effective than MF, and that CMF and AC are equally beneficial. An
updated report of the NSABP B-13, B-19, and B-26 trials with 8 to 16 years
of follow-up showed that the outcomes in CMF- or AC-treated women with
ER-negative tumors and negative axillary lymph nodes were similar in all age
groups, with a 58% reduction in recurrence and a 40% reduction in mortality
as a result of the chemotherapy (98).
The 2011 EBCTCG polychemotherapy overview provides a
comprehensive overview of the benefits of adjuvant chemotherapy (99).
Comparison of the older CMF and anthracycline-based regimens versus no
chemotherapy confirms a significant reduction not only in breast cancer
mortality, but also in overall mortality. These two types of regimen resulted
in a 20% to 25% proportional reduction in breast cancer mortality rate, which
in the population studied produced absolute reductions in breast cancer
mortality of 6.2% and 6.5%, respectively, at 10 years. These old studies in
which controls received no adjuvant chemotherapy underpin the rationale for
use of systemic chemotherapy after surgery to improve OS.
Although the overall efficacy of adjuvant chemotherapy is firmly
established, the optimal regimen for women with early-stage breast cancer
continues to be refined for various subsets of patients. Trials of more modern
chemotherapy regimens evaluated the role of taxanes given in combination or
sequentially with anthracycline-based regimens in patients with node-positive
breast cancer. Initial studies compared addition of four cycles paclitaxel after
four cycles of standard 3-weekly AC showed a significant 15% to 20%
further improvement in breast cancer mortality (corresponding to a 2.8%
absolute gain at 8 years) with the addition of paclitaxel but not from the
escalating dose of doxorubicin (100,101). Another study demonstrating that
concurrent administration of docetaxel with doxorubicin and
cyclophosphamide was more effective than fluorouracil, doxorubicin, and
cyclophosphamide led to regulatory approval of docetaxel for node-positive
breast cancer (102).
Furthermore, additional benefit is achieved with increased dose density, as
demonstrated by Cancer and Leukemia Group B (CALGB) protocol 9741;
administration of AC and paclitaxel at the same doses in 2-weekly treatment
cycles with granulocyte growth factor support (as opposed to the standard 3-
weekly cycles) led to incremental but statistically significant improvements
in DFS (7% absolute improvement; HR 0.74, p = 0.01) and OS (2% absolute
benefit; HR 0.69, p = 0.01) with 3 years’ median follow-up (103).
Other randomized clinical trials confirm the DFS and OS benefits at 5
years with sequential or concurrent anthracycline and taxane-based
chemotherapy in patients with operable, node-positive invasive breast cancer
(Table 14-3). Of note, most of these studies included node-positive patients.
In a recent meta-analysis of three phase III trials, significant differences in
favor of sequential regimen were seen in DFS (event-based risk ratios [RR]
0.90, 95% CI 0.84 to 0.98, P = 0.01) and in OS (RR 0.88, 95% CI 0.79 to
0.98, P = 0.02) (107). The HORG trial comparing sequential versus
concurrent administration of an anthracycline and a taxane in a population of
high-risk node-negative breast cancer patients suggests a nonsignificant
difference in DFS favoring the use of sequential anthracyclines and taxanes
over the concurrent regimen (92.6% vs. 88.2%; HR 1.591, 95% CI 0.990 to
2.556, P = 0.055). This difference appeared to be primarily driven by the HR-
negative cohort for DFS (92.2% vs. 83.6%; HR 2.214, 95% CI 1.068 to
4.593, P = 0.033) and for OS (HR 3.369, 95% CI 0.94 to 12.081, P = 0.062).
The trial adds further to the foundation of evidence that supports the
recommendation of a sequential, appropriately dose-intensified
anthracycline–taxane-based regimen in early-stage breast cancer (Table 14-
3).
Given the efficacy of taxane-based chemotherapy regimens and the rare
but potentially serious risk of anthracycline-associated cardiotoxicity, there is
interest in eliminating anthracycline use in the adjuvant treatment of selected
patient populations. In the US Oncology Protocol 9735, patients with stages I
to III operable breast cancer were randomized to AC versus docetaxel and
cyclophosphamide (TC). At a median follow-up of 7 years DFS was 81%
with TC versus 75% AC, P = .033, HR, 0.74. OS also favored the
nonanthracycline regimen (87% TC vs. 82% AC, P = .032, HR 0.69) (68).
In the modern era, patients with triple-negative and HER-2–positive breast
cancers receive chemotherapy in the neoadjuvant setting. For HR-positive
breast cancers selection of patients who benefit from adjuvant
chemotherapies are guided by clinical data and genomic risk. A 21-gene
assay (Oncotype DX) predicts benefit from adjuvant chemotherapy in
patients with HR-positive, lymph node–negative early breast cancer. The
TAILORx study indicated a chemotherapy benefit among patients with a RS
of 26 or higher and among those with a score of ≥21 if they were ≤50 years
of age (35,37). By integrating the 21-gene assay with clinical-risk
stratification from TAILORx trial, Sparano et al. found that patients with
breast cancer and RS of 11 to 25 who were at low clinical risk had a low
probability of distant recurrence. This low ROR was independent of whether
the women had received chemotherapy and increased only slightly across the
genomic risk groups (Sparano-3) (109). This finding is consistent with the
results of the MINDACT study, which suggested that women with small,
low-grade, well-defined breast tumors combined with a low-risk 70-gene
MammaPrint profile have only a 1.4% ROR within 5 years (40). The 21-gene
assay and 70-gene profile provide clinically useful prognostic and predictive
information that is complementary to clinicopathologic features, has clinical
utility in determining whether to recommend chemotherapy for patients at
low clinical risk who may be undertreated with endocrine therapy alone, or to
not recommend chemotherapy for patients at high clinical risk who are
unlikely to benefit from it.
It is unlikely that further dramatic gains will be made in future by slight
modifications of cytotoxic chemotherapeutic regimens or schedules. Ongoing
clinical trials will focus on the use of genomic assays to enrich patient
populations enrolled into adjuvant systemic trials, and the addition of targeted
agents (either in combination or in sequence) to standard-of-care therapy to
further improve clinical outcomes in early-stage breast cancer.*

TABLE 14-3 Taxane-Containing Chemotherapy Regimens for High-Risk,


Early-Stage Breast Cancer
Chemotherapy-Related Side Effects
The most common side effects associated with chemotherapy include
alopecia; gastrointestinal disturbance manifest as nausea, vomiting, oral
mucositis, or diarrhea; myelosuppression; fatigue; myalgias and arthralgias;
and peripheral neuropathy (particularly with the taxanes). These toxicities are
typically manageable in the outpatient setting, and the frequency and severity
of nausea and vomiting have been significantly reduced with the widespread
administration of steroids, serotonin receptor, and neurokinin-1 receptor
antagonists.
Long-term side effects include amenorrhea with secondary infertility and
premature menopause, the potential for myelodysplasia or acute leukemia
(particularly with the alkylating agents), and cardiac toxicity (particularly
with anthracyclines). The risk of amenorrhea varies, depending on the
patient’s age and the agents used. In a meta-analysis of 75 studies, the
chemotherapy-induced amenorrhea rate was 26% for women age <35, 39%
for age 35 to 40, and 77% for >40 years old (110). The risk of chemotherapy-
related amenorrhea directly correlates with cyclophosphamide dose, because
alkylating agents are particularly gonadotoxic (111). Referral to a fertility
clinic is considered standard of care for all premenopausal patients scheduled
to undergo chemotherapy. Embryo and oocyte cryopreservation are the best-
established methods but require a few weeks delay in cancer treatment. In
addition, luteinizing hormone–releasing hormone (LHRH) analogs, used
concurrent with chemotherapy, have been put forth as alternative strategies
for maintaining ovarian function and fertility preservation during adjuvant
chemotherapy in younger patients (112).
In terms of the leukemogenic effects of chemotherapy, the risk of
myelodysplastic syndrome (MDS) or leukemia secondary to
cyclophosphamide or anthracyclines used in standard breast cancer regimens
has been estimated to be very low (113). In four Alliance studies in older
women treated with adjuvant anthracyclines the risk of MDS and acute
myeloid leukemia (AML) varied from 0.2% to 1%, increasing with age (114).
In addition, some studies suggest that this secondary risk is higher in those
undergoing chemotherapy and radiation therapy (115,116).

TABLE 14-4 Trastuzumab-Containing Chemotherapy Regimens for HER2-


Positive, Node-Positive, or High-Risk Node-Negative, Early-Stage Breast
Cancer
Finally, the incidence of clinically significant congestive heart failure
following adjuvant therapy with doxorubicin has been reported to be <1%
when the total dose of doxorubicin is 240 to 300 mg per m2 (117), and there
are conflicting data on whether adjuvant radiation therapy to the left breast
further increases the risk of developing congestive heart failure (118).
Emerging data in heart failure suggest that signs of cardiac dysfunction can
be seen early, before the development of symptoms and early intervention
with cardioprotective medications results in better long-term cardiac function
(119). Therefore, NCCN Survivorship guidelines call for early detection with
echocardiogram within 1 year of anthracycline exposure and early initiation
of heart failure therapy to maintain better long-term cardiac function (120).
Adjuvant HER-2 Targeted Therapy
HER-2-overexpressing invasive breast cancers are associated with poor DFS
and OS as well as advanced stage, HR negativity, and a higher risk of
visceral and bone marrow micrometastases. Its higher expression in
malignant versus normal tissue and its expression in both primary and
metastatic tumors make it an attractive target for directed therapy. Over the
past decade, the management of HER-2–positive breast cancer has evolved
dramatically.

Trastuzumab
Trastuzumab is a humanized murine monoclonal antibody directed against
the extracellular domain of the HER-2/neu transmembrane receptor and
exhibits a synergistic effect with the taxanes, platinum-based agents, and
several other chemotherapeutics. Table 14-4 summarizes the results of four
large randomized clinical trials in patients with operable HER-2/neu-positive,
node-positive, and/or high-risk node-negative early-stage breast cancer. The
results of these trials provide strong evidence of significant DFS and OS
benefits with the incorporation of trastuzumab into adjuvant chemotherapy
regimens (120–123).
The NSABP B-31 trial included only those patients with node-positive
breast cancer, whereas the North Central Cancer Treatment Group N9831
trial included patients with either node-positive or node-negative breast
cancer (defined as a HR-positive tumor >2 cm in maximum dimension or a
HR-negative tumor >1 cm in maximum dimension). Both clinical trials
evaluated 1 year of trastuzumab in the setting of a defined anthracycline and
taxane–based adjuvant chemotherapy regimen, such that they were analyzed
jointly (121,122). The addition of trastuzumab to paclitaxel after doxorubicin
and cyclophosphamide in early-stage HER-2–positive breast cancer resulted
in a substantial and durable improvement in survival.
The optimal duration of trastuzumab has been studied in the HERA and
PHARE trials. The HERA trial included operable patients with either node-
positive or node-negative early breast cancer who received adjuvant
chemotherapy and randomly assigned patients to one of three groups: a
control group, 1 year of trastuzumab, or 2 years of trastuzumab (123,124).
HERA showed no improvement in DFS with the longer duration (HR 1.02,
95% CI 0.89 to 1.17); increased rates of cardiac toxicity were observed in the
2-year arm compared with the 1-year arm (7.3% vs. 4.4%). The PHARE trial
conducted in France tested a shorter duration of adjuvant trastuzumab
randomizing patients to 12 months versus 6 months of trastuzumab (125).
This study did not reach its primary end point as noninferiority of the 6
months was not demonstrated. Hence, adjuvant trastuzumab standard
duration should remain 12 months.
The Breast Cancer International Research Group 006 trial included both
node-positive and high-risk node-negative patients and evaluated trastuzumab
in combination with an anthracycline and taxane-based chemotherapy
regimen versus with a non–anthracycline-containing regimen (docetaxel and
carboplatin). Survival in both trastuzumab-containing arms was superior to
that of the control group (23). The nonanthracycline TCH showed a more
favorable cardiac safety profile.
A subcutaneous formulation of trastuzumab has been assessed in one phase
III neoadjuvant randomized trial, the HannaH trial (80). SC trastuzumab was
noninferior to the standard IV formulation of trastuzumab with respect to
trough drug concentrations and pCR in patients with HER-2–positive early
breast cancer. Other clinical outcomes, including event-free survival and OS
rates, were generally similar between the formulation groups.

Different HER-2 Targeted Agents and Combinations in the Adjuvant


Setting
Lapatinib is a dual tyrosine kinase inhibitor of both HER-2/neu and HER-1
(also known as the epidermal growth factor receptor). In the phase III
ALTTO trial patients were randomly assigned to 1 year of adjuvant therapy
with trastuzumab (T), lapatinib (L), their sequence (T → L), or their
combination (L+T). With a median follow-up of 4.5 years lapatinib did not
significantly improve DFS compared with trastuzumab alone and added
toxicity (126).
The APHINITY trial looked at adding a second HER-2–directed agent,
pertuzumab, to trastuzumab postoperatively in women with HER-2–positive
disease (127). More than 4,800 women were randomized to receive 18 weeks
of standard-of-care chemotherapy with trastuzumab plus placebo or
trastuzumab plus pertuzumab for 1 year. At 3 years, 94.1% of patients in the
trastuzumab plus pertuzumab arm were disease free compared with 93.2% in
the trastuzumab plus placebo arm (HR for an invasive event, 0.81, 95% CI
0.66 to 1.00, P = .045). In a subset analysis of patients with node-positive
disease, the 3-year DFS rate was 92% in the pertuzumab arm compared with
90.2% in the placebo arm (HR for invasive event, 0.77, 95% CI 0.62 to 0.96,
P = .02). These results indicate a modest benefit for a dual HER-2–targeted
approach in the adjuvant setting, particularly in patients with higher-risk
disease (e.g., node-positive or HR-negative disease).
When one considers gastrointestinal, cardiac toxicities as well as financial
implications, contrasted with the modest benefit, the role of dual HER-2
targeting in the adjuvant setting remains controversial.
Principles of Adjuvant Endocrine Therapy
Overview
Estrogen manipulation is the oldest form of proven treatment for breast
cancer, dating back to Beatson’s observations of breast cancer regression
following oophorectomy in 1896 (128). Such manipulation was initially
achieved by surgical oophorectomy, adrenalectomy, hypophysectomy, or
ovarian ablation by irradiation. Pharmaceutical advances have since led to the
documentation of therapeutic benefit with estrogens, progestins, androgens,
selective ER modulators, pure antiestrogens, AIs, and LHRH analogs in the
treatment of HR-positive, invasive breast cancer. All these agents have been
studied in the metastatic setting, and those with a favorable benefit–risk ratio
have been evaluated in the adjuvant therapy of early-stage disease as well.

Tamoxifen
Selective ER modulators regulate the transcription of target genes by binding
the ER alpha protein or by interacting with the receptor’s coregulatory
proteins. These agents have tissue-specific ER antagonist and agonist
properties that account for the associated benefits and toxicities. Tamoxifen is
a nonsteroidal, selective ER modulator, and it has been studied the most
extensively of all the available endocrine agents.
EBCTCG updated their comprehensive overview of randomized clinical
trials investigating the use of adjuvant tamoxifen in early-stage breast cancer
in 2011 (22). A meta-analysis of 20 trials with 15-year follow-up
demonstrated that 5 years of therapy with tamoxifen decreased the annual
ROR by 47% in the first 4 years and 32% during years 5 to 9. Breast cancer
mortality was reduced by about a third throughout the first 15 years in
patients with ER-positive breast cancer. Of note, most of the benefit on
mortality occurred in later years. The same degree of benefit was observed
regardless of age, and proportional reductions in recurrence and mortality
were similar irrespective of axillary lymph node status. In addition, no clear
benefit was observed in women with ER-negative breast cancer. One of the
pivotal trials included in the EBCTCG overview is a randomized, double-
blind, clinical trial of tamoxifen versus placebo in node-negative women with
ER-positive tumors measuring <5 cm (NSABP B-14). At 15 years of follow-
up, tamoxifen was associated with significant benefits in both RFS (HR 0.58
p < 0.0001) and OS (HR 0.80, p = 0.0008) irrespective of age or menopausal
status (129). Notably, a statistically significant reduction in the risk of
developing a contralateral breast cancer was also observed.
The high number of recurrences occurring after 5 years suggested that
extended endocrine therapy could further improve outcome, which led to the
start of several randomized clinical trials investigating the effects of extended
use of endocrine therapy. The Adjuvant Tamoxifen Longer Versus Shorter
(ATLAS) trial randomized 12,894 women to continue tamoxifen to 10 years
or stop at 5 years. Continued use of tamoxifen for 10 years resulted in a 25%
reduction in the relative ROR and a 29% reduction in breast cancer mortality
after 10 years (130). The findings from the Adjuvant Tamoxifen to Offer
More (aTTom) trial of 6,953 patients also revealed a DFS advantage for 10
years of tamoxifen over 5 years with HR = 0.84 (95% CI 0.73 to 0.95) during
years 7 to 9 and HR = 0.75 (0.66 to 0.86) beyond year 10 (131). Breast
cancer–specific mortality was reduced in the experimental arm after 10 years
(HR = 0.77 [0.64 to 0.92]). The ATLAS and aTTom trials provided a new
treatment paradigm of extended therapy that is particularly attractive for
those patients who remain premenopausal on completion of 5 years of
adjuvant endocrine therapy.
In terms of the timing of endocrine therapy relative to chemotherapy, this
issue was addressed in a prospective, randomized trial that demonstrated an
estimated 16% DFS advantage with sequential versus concurrent
chemotherapy and tamoxifen administration, but it did not reach significance
(HR 0.84, 0.70 to 1.01, p = 0.061) (132).
The most commonly reported side effects associated with tamoxifen are
vasomotor instability, increased vaginal discharge, symptoms of atrophic
vaginitis, menstrual irregularities, mild nausea, and fluid retention. Other
potential toxicities include liver function abnormalities with the potential for
hepatic steatosis, a 1% to 2% incidence of thromboembolic phenomena (i.e.,
deep venous thrombosis, pulmonary embolism, and cerebrovascular events),
rare but typically reversible ocular effects (i.e., decreased visual acuity,
macular edema, and retinal and corneal opacities), and a twofold to threefold
increase in the risk of endometrial cancer. Most uterine cancers that develop
in relation to the administration of tamoxifen are early-stage
adenocarcinomas with histologic and clinical features that are like those
expected in the general population. A meta-analysis of four randomized
clinical trials found that the cumulative risk of endometrial malignancy
increased twofold from 1.5% to 3.2% with extended therapy compared with
the standard 5 years of tamoxifen (133). No clear benefit has been shown
however for routine endometrial surveillance in asymptomatic patients on
tamoxifen therapy.

Aromatase Inhibitors
The aromatase enzyme catalyzes the final step in estrogen biosynthesis,
allowing for the peripheral conversion of androgens to estrone and estradiol.
Peripheral estrogen production is clinically significant only in the
postmenopausal setting, but it represents a valuable therapeutic target
considering that most women with estrogen-sensitive breast cancer are older
than age 50 years. A number of AIs have been developed that fall into two
broad categories: (a) the nonsteroidal, imidazole-based agents that reversibly
bind the cytochrome P450 moiety of aromatase, such that their continued
presence is required for the inhibition of estrogen biosynthesis (e.g.,
anastrozole and letrozole), and (b) the steroidal, androgen-like agents that
irreversibly bind the catalytic site of aromatase, such that enzymatic activity
is lost until more enzyme can be produced (e.g., exemestane). These agents
effectively decrease postmenopausal circulating estrogen levels by >95%
(134).
Studies in tamoxifen-resistant metastatic breast cancer show that these
agents have a favorable therapeutic index, subsequently leading to several
large, randomized clinical trials of an AI in lieu of or in sequence with
tamoxifen as adjuvant therapy for postmenopausal women with HR-positive
(or unknown) operable breast cancer. The schema for these trials have
explored several possible strategies: (a) 5 years of upfront therapy with an AI
instead of tamoxifen (135,136), (b) 5 years of sequential therapy with 2 to 3
years of tamoxifen followed by an AI (136–139), and (c) 10 years of
extended therapy (140–144). The sequential therapy trials varied somewhat
in design, as randomization occurred at the initiation of all endocrine therapy
in some trials but after the completion of 2 to 3 years of tamoxifen in others.
The significance of this difference in timing relates to interpretation of the
results, as survival calculations relate to the date of randomization as opposed
to the date of diagnosis. In aggregate, these trials included >45,000
postmenopausal women with demonstration of a statistically significant DFS
benefit with incorporation of an AI, as summarized in Table 14-5, with
evidence of a small but statistically significant OS benefit seen in some trials
(138,141) but not others.
Longer follow-up and additional studies are required to determine the best
endocrine therapy approach for postmenopausal women with HR-positive
breast cancer. In some cases, the choice of endocrine therapy may be guided
by a consideration of the toxicity profiles of tamoxifen versus the AIs. That
is, the AIs are associated with a lower risk of endometrial cancer, venous
thromboembolic disease, ischemic cerebrovascular events, vasomotor
instability, and vaginal bleeding but a higher risk of bone mineral density loss
and fracture, arthralgias and myalgias, and gynecologic side effects
(146–148).
Several molecular risk scores aid in decision making concerning adjuvant
chemotherapy. Recently validated predictive biomarker use was reported to
aid in patient selection for extended endocrine therapy. The TransATAC trial
showed promising results in predicting which women had a low risk of
developing distant recurrences 5 to 10 years after breast cancer diagnosis,
thereby identifying the women in whom extended therapy is not justified
(48,149). BCI was validated in the Trans-aTTom study as a predictor of
benefit from prolonged endocrine therapy (46). In the future a combination of
clinicopathologic and molecular factors integrated with multigene expression
profiles will determine the optimal selection of patients for extended therapy
(150).

TABLE 14-5 Aromatase Inhibitors in Early-Stage Breast Cancer


Furthermore, several studies are now combining endocrine therapy with a
targeted drug, such as mTOR inhibition or CDK 4/6 inhibition. The SWOG
S1207 trial (NCT01674140) adds 1 year of everolimus to standard endocrine
therapy. CDK 4/6 inhibitors are tested in the EarLEE (NCT03078751 with
ribociclib), MonarchE (NCT03155997 with abemaciclib), and PALLAS trials
(NCT02513394 with palbociclib). Given the added toxicity, most studies
have chosen to select only high-risk patients based on tumor size, nodal
status, and/or histologic grade.

Ovarian Ablation and Ovarian Functional Suppression


Ovarian ablation is irreversibly achieved either through surgery or radiation,
and ovarian functional suppression (OFS) can be reversibly achieved with the
administration of LHRH agonists (goserelin, triptorelin, leuprolide) that
downregulate gonadotropin-releasing HRs in the pituitary gland. Although
ovarian ablation or suppression (OAS) has been widely used in
premenopausal women with breast cancer, its effect is controversial in
previous studies (151,152). The EBCTCG meta-analysis (2) included an
evaluation of about 8,000 women <50 years of age with ER-positive or ER-
unknown breast cancer who were randomized to ovarian treatment (i.e.,
ablation or OFS) versus not. With 15-year follow-up, ovarian treatment
resulted in a 4.3% (p = 0.0001) and 3.2% (p = 0.004) reduction in the ROR
and mortality, respectively. However, these benefits appear to be significant
only in the absence of other systemic therapies. One of the large-scale trials
to report on the efficacy of ovarian treatment is the Austrian Breast and
Colorectal Cancer Study Group trial 12 (153). This four-arm study
randomized premenopausal women with HR-positive early-stage breast
cancer to receive adjuvant goserelin and tamoxifen versus goserelin and
anastrozole, with or without zoledronic acid. No significant difference in
benefits of DFS or OS was observed between tamoxifen and anastrozole.
Recently, the results of two large randomized trials (SOFT/TEXT) were
published that addressed the role of ovarian ablation in the management of
premenopausal HR-positive breast cancer. These studies randomly assigned
premenopausal women with HR-positive early breast cancer to exemestane
plus ovarian suppression or tamoxifen plus ovarian suppression for a period
of 5 years. In a combined analysis DFS at 5 years was 91.1% in the
exemestane-ovarian suppression group and 87.3% in the tamoxifen-ovarian
suppression group (HR 0.72; 95% CI, 0.60 to 0.85; P < 0.001) (154). Ovarian
suppression over tamoxifen alone only provided DFS benefit in high-risk
women who needed adjuvant chemotherapy and who remained
premenopausal (155). There was a 10% to 15% absolute improvement in 8-
year freedom from distant recurrence with exemestane plus OFS versus
tamoxifen plus OFS or tamoxifen alone in women with high recurrence risk,
defined by clinicopathologic characteristics, but no benefit for those at low
recurrence risk (156).
The HOBOE study (157) showed that in premenopausal patients with early
breast cancer undergoing ovarian function suppression with triptorelin,
zoledronic acid with letrozole significantly improved DFS compared to
tamoxifen. There was no additive benefit of zoledronic acid to letrozole and
the combination increased toxicity while worsening compliance.
BONE-MODIFYING THERAPY
Standard adjuvant therapies for breast cancer such as chemotherapy or AI and
LHRH agonist hormone therapy are associated with significant survival gains
but also induce bone loss by aggravating the estrogen deprivation (158).
Bisphosphonates can delay the onset and reduce the risk of skeletal-related
events in patients with bone-metastatic breast cancer and can prevent and
treat cancer treatment–induced bone loss (159). Emerging data has
accumulated about the anticancer potential of adjuvant bisphosphonates for
early breast cancer.
A meta-analysis of 18,766 women published by EBCTCG with median
follow-up of 5.6 years found that the reductions in recurrence, distant
recurrence, and breast cancer mortality were of only borderline significance,
but the reduction in bone recurrence was more definite (0.83, 0.73 to 0.94; 2p
= 0.004). Among premenopausal women, treatment had no apparent effect on
any outcome, but among 11,767 postmenopausal women it produced highly
significant reductions in recurrence (RR 0.86, 95% CI 0.78 to 0.94, 2p =
0.002), and breast cancer mortality (RR 0.82, 95% CI 0.73 to 0.93, 2p =
0.002) (160).
In the Austrian Breast and Colorectal Cancer Study Group trial 12 (153)
the addition of twice yearly zoledronic acid to adjuvant endocrine therapy
with goserelin significantly improved DFS at 94 months with HR = 0.77
(0.60 to 0.99), but the OS benefit was not significant. Similarly, the AZURE
trial (161) found DFS benefit only in the postmenopausal subset HR = 0.82
(0.67 to 1.00), and the benefit persisted in both trials at 8 to 10 years of
follow-up. Potential mechanism of zoledronic acid activity involves targeting
dormant tumor cells in the bone marrow and the bone microenvironment
(Coleman-3). The updates ASCO guidelines recommend zoledronic acid
every 6 months or clodronate as adjuvant therapy for postmenopausal
patients with breast cancer (160). Risk factors for osteonecrosis of the jaw
and renal impairment should be assessed.
CONCLUSION
Randomized clinical trials and the overview analysis provide strong evidence
that neoadjuvant and adjuvant therapy results in modest but clear benefits in
pCR, DFS, and OS in premenopausal and postmenopausal women with early-
stage breast cancer. Given the high incidence of breast cancer and the known
high rate of failure in women treated with locoregional therapy alone, it is
clear that the improvement in outcome associated with adjuvant therapy
results in thousands of lives saved per year in the United States. Many
questions remain regarding the criteria for selecting the patients most likely
to benefit from treatment and the optimal therapeutic regimens. Areas of
current investigation include the role of new prognostic and predictive
factors, novel chemotherapeutic agents, new-generation HER-2–directed
therapies, immunotherapies, and the bisphosphonates. Increased participation
in clinical trials is needed to help answer these questions and to improve the
treatment of breast cancer.

REFERENCES

1. Cheng L, Swartz MD, Zhao H, et al. Hazard of recurrence among


women after primary breast cancer treatment—a 10-year follow-up
using data from SEER-Medicare. Cancer Epidemiol Biomarkers Prev
2012;21:800–809.
2. Early Breast Cancer Trialists’ Collaborative Group (EBCTCG). Effects
of chemotherapy and hormonal therapy for early breast cancer on
recurrence and 15-year survival: an overview of the randomised trials.
Lancet 2005;365(9472):1687–1717.
3. Early Breast Cancer Trialists’ Collaborative Group (EBCTCG). Long-
term outcomes for neoadjuvant versus adjuvant chemotherapy in early
breast cancer: meta-analysis of individual patient data from ten
randomised trials. Lancet Oncol 2018;19(1):27–39.
4. Newman LA. Epidemiology of locally advanced breast cancer. Semin
Radiat Oncol 2009;19(4):195–203.
5. Carter CL, Allen C, Henson DE. Relation of tumor size, lymph node
status, and survival in 24,740 breast cancer cases. Cancer
1989;63(1):181–187.
6. Moffat FL. Clinical and pathologic prognostic and predictive factors. In:
Harris JR, Lippman ME, Morrow M, et al., eds. Diseases of the Breast.
Philadelphia, PA: Lippincott Williams & Wilkins; 2014:439–451.
7. Wong SM, Almana N, Choi J, et al. Prognostic significance of residual
axillary nodal micrometastases and isolated tumor cells after
neoadjuvant chemotherapy for breast cancer. Ann Surg Oncol
2019;26(11):3502–3509.
8. Li CI, Moe RE, Daling JR. Risk of mortality by histologic type of breast
cancer among women aged 50 to 79 years. Arch Intern Med
2003;163:2149–2153.
9. Terando AM, Agnese DM, Holmes DR. Treatment and prognosis of rare
breast cancers. Ann Surg Oncol 2015;22(10):3225–3229.
10. Elston CW, Ellis IO. Pathological prognostic factors in breast cancer. I.
The value of histological grade in breast cancer: experience from a large
study with long-term follow-up. Histopathology 1991;19(5):403–410.
11. Ehinger A, Malmström P, Bendahl PO. Histological grade provides
significant prognostic information in addition to breast cancer subtypes
defined according to St Gallen 2013. Acta Oncol 2017;56(1):68–74.
12. Rakha EA, Reis-Filho JS, Baehner F, et al. Breast cancer prognostic
classification in the molecular era: the role of histological grade. Breast
Cancer Res 2010;12(4):207.
13. Beresford MJ, Wilson GD, Makris A. Measuring proliferation in breast
cancer: practicalities and applications. Breast Cancer Res 2006;8:216.
14. Inwald EC, Klinkhammer-Schalke M, Hofstädter F, et al. Ki-67 is a
prognostic parameter in breast cancer patients: results of a large
population-based cohort of a cancer registry. Breast Cancer Res Treat
2013;139(2):539–552.
15. Focke CM, van Diest PJ, Decker T. St Gallen 2015 subtyping of luminal
breast cancers: impact of different Ki-67-based proliferation assessment
methods. Breast Cancer Res Treat 2016;159:257–263.
16. Penault-Llorca F, Radosevic-Robin N. Biomarkers of residual disease
after neoadjuvant therapy for breast cancer. Nat Rev Clin Oncol
2016;13:487–503.
17. Fisher B, Redmond C, Fisher ER, et al. Relative worth of estrogen or
progesterone receptor and pathologic characteristics of differentiation as
indicators of prognosis in node negative breast cancer patients: findings
from National Surgical Adjuvant Breast and Bowel Project Protocol B-
06. J Clin Oncol 1988;6(7):1076–1087.
18. Purdie CA, Quinlan P, Jordan LB, et al. Progesterone receptor
expression is an independent prognostic variable in early breast cancer:
a population-based study. Br J Cancer 2014;110(3):565–572.
19. Wolf AC, Hammond ME, Hicks DG, et al. Recommendations for
human epidermal growth factor receptor 2 testing in breast cancer:
American Society of Clinical Oncology/College of American
Pathologists clinical practice guideline update. J Clin Oncol
2013;31:3997–4013.
20. Press MF, Bernstein L, Thomas PA, et al. HER-2/neu gene
amplification characterized by fluorescence in situ hybridization: poor
prognosis in node-negative breast carcinomas. J Clin Oncol
1997;15(8):2894–2904.
21. Ross JS, Slodkowska EA, Symmans WF, et al. The HER-2 receptor and
breast cancer: ten years of targeted anti-HER-2 therapy and personalized
medicine. Oncologist 2009;14(4):320–368.
22. Early Breast Cancer Trialists’ Collaborative Group (EBCTCG), Davies
C, Godwin J, et al. Relevance of breast cancer hormone receptors and
other factors to the efficacy of adjuvant tamoxifen: patient-level meta-
analysis of randomised trials. Lancet 2011;378(9793):771–784.
23. Slamon D, Eiermann W, Robert N, et al. Adjuvant trastuzumab in
HER2-positive breast cancer. N Engl J Med 2011;365(14):1273–1283.
24. Perou CM, Sørlie T, Eisen MB, et al. Molecular portraits of human
breast tumours. Nature 2000;406:747–752.
25. Sørlie T, Perou CM, Tibshirani R, et al. Gene expression patterns of
breast carcinomas distinguish tumor subclasses with clinical
implications. Proc Natl Acad Sci USA 2001;98:10869–10874.
26. Fan C, Oh DS, Wessels L, et al. Concordance among gene-expression-
based predictors for breast cancer. N Engl J Med 2006;355(6):560–569.
27. Toss A, Cristofanilli M. Molecular characterization and targeted
therapeutic approaches in breast cancer. Breast Cancer Res 2015;17:60.
28. Loi S, Haibe-Kains B, Desmedt C, et al. Definition of clinically distinct
molecular subtypes in estrogen receptor-positive breast carcinomas
through genomic grade. J Clin Oncol 2007;25(10):1239–1246.
29. Voduc KD, Cheang MC, Tyldesley S, et al. Breast cancer subtypes and
the risk of local and regional relapse. J Clin Oncol 2010;28(10):1684–
1691.
30. Harbeck N, Gnant M. Breast cancer. Lancet 2017;389(10074):1134–
1150.
31. Ribnikar D, Cardoso F. Tailoring chemotherapy in early-stage breast
cancer: based on tumor biology or tumor burden? Am Soc Clin Oncol
Educ Book 2016;35:e31–e38.
32. Albain KS, Paik S, van’t Veer L. Prediction of adjuvant chemotherapy
benefit in endocrine responsive, early breast cancer using multigene
assays. Breast 2009;18:S141–S145.
33. Liu R, Wang X, Chen G, et al. The prognostic role of a gene signature
from tumorigenic breast-cancer cells. N Engl J Med 2007;356(3):217–
226.
34. Paik S, Shak S, Tang G, et al. A multigene assay to predict recurrence of
tamoxifen-treated, node-negative breast cancer. N Engl J Med
2004;351(27):2817–2826.
35. Sparano JA, Gray RJ, Makower DF, et al. Adjuvant chemotherapy
guided by a 21-gene expression assay in breast cancer. N Engl J Med
2018;379(2):111–121.
36. Albain KS, Barlow WE, Shak S, et al. Prognostic and predictive value
of the 21-gene recurrence score assay in postmenopausal women with
node-positive, oestrogen-receptor-positive breast cancer on
chemotherapy: a retrospective analysis of a randomised trial. Lancet
Oncol 2010;11:55–65.
37. Sparano JA, Gray RJ, Makower DF, et al. Prospective validation of a
21-gene expression assay in breast cancer. N Engl J Med
2015;373(21):2005–2014.
38. ClinicalTrials.Gov. Tamoxifen citrate, letrozole, anastrozole, or
exemestane with or without chemotherapy in treating patients with
invasive RxPONDER breast cancer. 2011. https://clinicaltrials-
gov.offcampus.lib.washington.edu/ct2/show/NCT01272037
39. Buyse M, Loi S, van’t Veer L, et al. Validation and clinical utility of a
70-gene prognostic signature for women with node-negative breast
cancer. J Natl Cancer Inst 2006;98(17):1183–1192.
40. Cardoso F, van’t Veer LJ, Bogaerts J, et al. 70-gene signature as an aid
to treatment decisions in early-stage breast cancer. N Engl J Med
2016;375(8):717–729.
41. Parker JS, Mullins M, Cheang MC, et al. Supervised risk predictor of
breast cancer based on intrinsic subtypes. J Clin Oncol 2009;27:1160–
1167.
42. Chia SK, Bramwell VH, Tu D, et al. A 50-gene intrinsic subtype
classifier for prognosis and prediction of benefit from adjuvant
tamoxifen. Clin Cancer Res 2012;18:4465–4472.
43. Filipits M, Nielsen TO, Rudas M, et al. The PAM50 risk-of-recurrence
score predicts risk for late distant recurrence after endocrine therapy in
postmenopausal women with endocrine-responsive early breast cancer.
Clin Cancer Res 2014;20:1298–1305.
44. Sgroi DC, Chapman JA, Badovinac-Crnjevic T, et al. Assessment of the
prognostic and predictive utility of the Breast Cancer Index (BCI): an
NCIC CTG MA.14 study. Breast Cancer Res 2016;18(1):1–7.
45. Sgroi DC, Sestak I, Cuzick J, et al. Prediction of late distant recurrence
in patients with oestrogen-receptor-positive breast cancer: a prospective
comparison of the breast-cancer index (BCI) assay, 21-gene recurrence
score, and IHC4 in the TransATAC study population. Lancet Oncol
2013;14(11):1067–1076.
46. Bartlett JMS, Sgroi DC, Treuner K, et al. Breast cancer index and
prediction of benefit from extended endocrine therapy in breast cancer
patients treated in the Adjuvant Tamoxifen – To Offer More? (aTTom)
Trial. Ann Oncol 2019;30(11):1776–1783.
47. Dubsky P, Filipits M, Jakesz R, et al; Austrian Breast and Colorectal
Cancer Study Group (ABCSG). EndoPredict improves the prognostic
classification derived from common clinical guidelines in ER-positive,
HER2-negative early breast cancer. Ann Oncol 2013;24(3):640–647.
48. Buus R, Sestak I, Kronenwett R, et al. Comparison of EndoPredict and
EPClin with Oncotype DX Recurrence Score for prediction of risk of
distant recurrence after endocrine therapy. J Natl Cancer Inst
2016;108(11).
49. Rack B, Schindlbeck C, Jückstock J, et al; SUCCESS Study Group.
Circulating tumor cells predict survival in early average-to-high risk
breast cancer patients. J Natl Cancer Inst 2014;106(5):dju066
50. Lucci A, Hall CS, Lodhi AK, et al. Circulating tumour cells in non-
metastatic breast cancer: a prospective study. Lancet Oncol
2012;13(7):688–695.
51. Sparano J, O’Neill A, Alpaugh K, et al. Association of circulating tumor
cells with late recurrence of estrogen receptor-positive breast cancer: a
secondary analysis of a randomized clinical trial. JAMA Oncol
2018;4(12):1700–1706.
52. Bidard FC, Michiels S, Riethdorf S, et al. Circulating tumor cells in
breast cancer patients treated by neoadjuvant chemotherapy: a meta-
analysis. J Natl Cancer Inst 2018;110(6):560–567.
53. Goodman CR, Seagle BL, Friedl TW, et al. Association of circulating
tumor cell status with benefit of radiotherapy and survival in early-stage
breast cancer. JAMA Oncol 2018;4(8):e180163.
54. Moo TA, Sanford R, Dang C, et al. Overview of breast cancer therapy.
PET Clin 2018;13(3):339–354.
55. Cortazar P, Zhang L, Untch M, et al. Pathological complete response
and long-term clinical benefit in breast cancer: the CTNeoBC pooled
analysis. Lancet 2014;384(9938):164–172.
56. Steenbruggen TG, van Ramshorst MS, Kok M, et al. Neoadjuvant
therapy for breast cancer: established concepts and emerging strategies.
Drugs 2017;77(12):1313–1336.
57. Kaufmann M, von Minkwitz G, Mamounas EP, et al. Recommendations
from an international consensus conference on the current status and
future of neoadjuvant systemic therapy in primary breast cancer. Ann
Surg Oncol 2012;19;1508–1516.
58. Berruti A, Amoroso V, Gallo F, et al. Pathologic complete response as a
potential surrogate for the clinical outcome in patients with breast cancer
after neoadjuvant therapy: a meta-regression of 29 randomized
prospective studies. J Clin Oncol 2014;32:3883–3891.
59. Liedtke C, Mazouni C, Hess KR, et al. Response to neoadjuvant therapy
and long-term survival in patients with triple-negative breast cancer. J
Clin Oncol 2008;26:1275–1281.
60. Early Breast Cancer Trialists’ Collaborative Group (EBCTCG), Peto R,
Davies C, et al. Comparisons between different polychemotherapy
regimens for early breast cancer: meta-analyses of long-term outcome
among 100,000 women in 123 randomised trials. Lancet 2012;379:432–
444.
61. Sparano JA, Zhao F, Martino S, et al. Long-term follow-up of the E1199
phase III trial evaluating the role of taxane and schedule in operable
breast cancer. J Clin Oncol 2015;33:2353–2360.
62. Bonilla L, Ben-Aharon I, Vidal L, et al. Dose-dense chemotherapy in
nonmetastatic breast cancer: a systematic review and meta-analysis of
randomized controlled trials. J Natl Cancer Inst 2010;102:1845–1854.
63. Budd GT, Barlow WE, Moore HCF, et al. SWOG S0221: a phase III
trial comparing chemotherapy schedules in high-risk early-stage breast
cancer. J Clin Oncol 2015;33:58–64.
64. Lambertini M, Ceppi M, Cognetti F, et al. Dose-dense adjuvant
chemotherapy in premenopausal breast cancer patients: a pooled
analysis of the MIG1 and GIM2 phase III studies. Eur J Cancer
2017;71:34–42.
65. von Minckwitz G, Schneeweiss A, Loibl S, et al. Neoadjuvant
carboplatin in patients with triple-negative and HER2-positive early
breast cancer (GeparSixto; GBG 66): a randomised phase 2 trial. Lancet
Oncol 2014;15(7):747–756.
66. Loibl S, O’Shaughnessy J, Untch M, et al. Addition of the PARP
inhibitor veliparib plus carboplatin or carboplatin alone to standard
neoadjuvant chemotherapy in triple-negative breast cancer
(BrighTNess): a randomised, phase 3 trial. Lancet Oncol
2018;19(4):497–509.
67. Hahnen E, Lederer B, Hauke J, et al. Germline mutation status,
pathological complete response, and disease-free survival in triple-
negative breast cancer: secondary analysis of the Geparsixto randomized
clinical trial. JAMA Oncol 2017;3:1378–1385.
68. Jones S, Holmes FA, O’Shaughnessy J, et al. Docetaxel with
cyclophosphamide is associated with an overall survival benefit
compared with doxorubicin and cyclophosphamide: 7-year follow-up of
US Oncology Research Trial 9735. J Clin Oncol 2009;27:1177–1183.
69. Sharma P, Lopez-Tarruella S, Garcia-Saenz JA, et al. Pathological
response and survival in triple-negative breast cancer following
neoadjuvant carboplatin plus docetaxel. Clin Cancer Res
2018;24(23):5820–5829.
70. Schmid P, Cortes J, Dent R, et al. KEYNOTE-522: phase III study of
pembrolizumab (pembro) + chemotherapy (chemo) vs placebo (pbo) +
chemo as neoadjuvant treatment, followed by pembro vs pbo as adjuvant
treatment for early triple-negative breast cancer (TNBC). Ann Oncol
2019;30(Supplement_5):mdz394.003.
71. Bianchini G, Gianni L. The immune system and response to HER2-
targeted treatment in breast cancer. Lancet Oncol 2014;15:e58–e68.
72. Vogel CL, Cobleigh MA, Tripathy D, et al. Efficacy and safety of
trastuzumab as a single agent in first-line treatment of HER2-
overexpressing metastatic breast cancer. J Clin Oncol 2002;20:719–726.
73. Baselga J, Carbonell X, Castañeda-Soto NJ, et al. Phase II study of
efficacy, safety, and pharmacokinetics of trastuzumab monotherapy
administered on a 3-weekly schedule. J Clin Oncol 2005;23:2162–2171.
74. Gianni L, Eiermann W, Semiglazov V, et al. Neoadjuvant chemotherapy
with trastuzumab followed by adjuvant trastuzumab versus neoadjuvant
chemotherapy alone, in patients with HER2-positive locally advanced
breast cancer (the NOAH trial): a randomised controlled superiority trial
with a parallel HER2-negative cohort. Lancet 2010;375:377–384.
75. Gianni L, Eiermann W, Semiglazov V, et al. Neoadjuvant and adjuvant
trastuzumab in patients with HER2-positive locally advanced breast
cancer (NOAH): follow-up of a randomised controlled superiority trial
with a parallel HER2-negative cohort. Lancet Oncol 2014;15:640–647.
76. Buzdar AU, Ibrahim NK, Francis D, et al. Significantly higher
pathologic complete remission rate after neoadjuvant therapy with
trastuzumab, paclitaxel, and epirubicin chemotherapy: results of a
randomized trial in human epidermal growth factor receptor 2-positive
operable breast cancer. J Clin Oncol 2005;23:3676–3685.
77. Untch M, Fasching PA, Konecny G, et al. Pathologic complete response
after neoadjuvant chemotherapy plus trastuzumab predicts favorable
survival in human epidermal growth factor receptor 2–overexpressing
breast cancer: results from the TECHNO trial of the AGO and GBG
study groups. J Clin Oncol 2011;29:3351–3357.
78. Gianni L, Pienkowski T, Im YH, et al. Efficacy and safety of
neoadjuvant pertuzumab and trastuzumab in women with locally
advanced, inflammatory, or early HER2-positive breast cancer
(NeoSphere): a randomised multicentre, open-label, phase 2 trial. Lancet
Oncol 2012;13:25–32.
79. Schneeweiss A, Chia S, Hickish T, et al. Pertuzumab plus trastuzumab
in combination with standard neoadjuvant anthracycline-containing and
anthracycline-free chemotherapy regimens in patients with HER2-
positive early breast cancer: a randomized phase II cardiac safety study
(TRYPHAENA). Ann Oncol 2013;24:2278–2284.
80. Ismael G, Hegg R, Muehlbauer S, et al. Subcutaneous versus
intravenous administration of (neo)adjuvant trastuzumab in patients with
HER2-positive, clinical stage I-III breast cancer (HannaH study): a
phase 3, open-label, multicentre, randomised trial. Lancet Oncol
2012;13:869–878.
81. Loibl S, Gianni L. Her-2 positive breast cancer. Lancet 2017;389:2415–
2429.
82. Leal F, Liutti VT, Antunes dos Santos VC, et al. Neoadjuvant endocrine
therapy for resectable breast cancer: a systematic review and meta-
analysis. Breast 2015;24(4):406–412.
83. Spring LM, Gupta A, Reynolds K. Neoadjuvant endocrine therapy for
estrogen receptor–positive breast cancer: a systematic review and meta-
analysis. JAMA Oncol 2016;2(11):1477–1486.
84. Chiba A, Hoskin TL, Heins CN, et al. Trends in neoadjuvant endocrine
therapy use and impact on rates of breast conservation in hormone
receptor-positive breast cancer: a national cancer data base study. Ann
Surg Oncol 2017;24:418–424.
85. Grossman J, Ma C, Aft R. Neoadjuvant endocrine therapy: who benefits
most? Surg Oncol Clin N Am 2018;27(1):121–140.
86. Dowsett M, Nielsen TO, A’Hern R, et al. Assessment of Ki67 in breast
cancer: recommendations from the International Ki67 in Breast Cancer
working group. J Natl Cancer Inst 2011;103:1656–1664.
87. Ueno T, Masuda N, Yamanaka T, et al. Evaluating the 21-gene assay
Recurrence Score® as a predictor of clinical response to 24 weeks of
neoadjuvant exemestane in estrogen receptor-positive breast cancer. Int
J Clin Oncol 2014;19:607–613.
88. Iwata H, Masuda N, Yamamoto Y, et al. Validation of the 21-gene test
as a predictor of clinical response to neoadjuvant hormonal therapy for
ER+, HER2-negative breast cancer: the TransNEOS study. Breast
Cancer Res Treat 2019;173(1):123–133.
89. Iwata H. Neoadjuvant endocrine therapy for postmenopausal patients
with hormone receptor-positive early breast cancer: a new concept.
Breast Cancer 2011;18:92–97.
90. Suman VJ, Ellis MJ, Ma CX. The ALTERNATE trial: assessing a
biomarker driven strategy for the treatment of post-menopausal women
with ER+/Her2- invasive breast cancer. J Clin Oncol 2015;4(3):34.
91. Masuda N, Lee SJ, Ohtani S, et al. Adjuvant capecitabine for breast
cancer after preoperative chemotherapy. N Engl J Med
2017;376(22):2147–2159.
92. Chan A, Delaloge S, Holmes FA, et al. Neratinib after trastuzumab-
based adjuvant therapy in patients with HER2-positive breast cancer
(ExteNET): a multicentre, randomised, double-blind, placebo-
controlled, phase 3 trial. Lancet Oncol 2016;17:367–377.
93. Lewis Phillips GD, Li G, Dugger DL, et al. Targeting HER2positive
breast cancer with trastuzumab-DM1, an antibody-cytotoxic drug
conjugate. Cancer Res 2008;68:9280–9290.
94. von Minckwitz G, Huang CS, Mano MS, et al. Trastuzumab emtansine
for residual invasive HER2-positive breast cancer. N Engl J Med
2019;380:617–628.
95. Pelizzari G, Gerratana L, Basile D, et al. Post-neoadjuvant strategies in
breast cancer: from risk assessment to treatment escalation. Cancer
Treat Rev 2019;72:7–14.
96. Darby S, Davies C, Gale P. The Early Breast Cancer Trialists’
Collaborative Group: a brief history of results to date. In: Davison AC,
Dodge Y, Wermuth N, eds. Oxford: Celebrating statistics, Oxford
University Press; 2005.
97. Bonadonna G, Valagussa P, Moliterni A, et al. Adjuvant
cyclophosphamide, methotrexate, and fluorouracil in node-positive
breast cancer: the results of 20 years of follow-up. N Engl J Med
1995;332(14):901–906.
98. Fisher B, Jeong JH, Anderson S, et al. Treatment of axillary lymph
node-negative, estrogen receptor-negative breast cancer: updated
findings from National Surgical Adjuvant Breast and Bowel Project
clinical trials. J Natl Cancer Inst 2004;96(24):1823–1831.
99. Early Breast Cancer Trialists’ Collaborative Group (EBCTCG), Peto R,
Davies C, et al. Comparisons between different polychemotherapy
regimens for early breast cancer: meta-analyses of long-term outcome
among 100,000 women in 123 randomised trials. Lancet
2012;379(9814):432–444.
100. Henderson IC, Berry DA, Demetri GD, et al. Improved outcomes from
adding sequential paclitaxel but not from escalating doxorubicin dose in
an adjuvant chemotherapy regimen for patients with node-positive
primary breast cancer. J Clin Oncol 2003;21(6):976–983.
101. Mamounas EP, Bryant J, Lembersky B, et al. Paclitaxel after
doxorubicin plus cyclophosphamide as adjuvant chemotherapy for node-
positive breast cancer: results from NSABP B-28. J Clin Oncol
2005;23(16):3686–3696.
102. Martin M, Pienkowski T, Mackey J, et al. Adjuvant docetaxel for node-
positive breast cancer. N Engl J Med 2005;352(22):2302–2313.
103. Citron ML, Berry DA, Cirrincione C, et al. Randomized trial of dose-
dense versus conventionally scheduled and sequential versus concurrent
combination chemotherapy as postoperative adjuvant treatment of node-
positive primary breast cancer: first report of Intergroup Trial
C9741/Cancer and Leukemia Group B Trial 9741. J Clin Oncol
2003;21(8):1431–1439.
104. Eiermann W, Pienkowski T, Crown J, et al. Phase III study of
doxorubicin/cyclophosphamide with concomitant versus sequential
docetaxel as adjuvant treatment in patients with human epidermal
growth factor receptor 2–normal, node-positive breast cancer: BCIRG-
005 trial. J Clin Oncol 2011;29:3877–3884.
105. Francis P, Crown J, Di Leo A, et al. Adjuvant chemotherapy with
sequential or concurrent anthracycline and docetaxel: breast
International Group 02–98 randomized trial. J Natl Cancer Inst
2008;100:121–133.
106. Swain SM, Jeong JH, Geyer CE, et al. Longer therapy, iatrogenic
amenorrhea, and survival in early breast cancer. N Engl J Med
2010;362:2053–2065.
107. Shao N, Wang S, Yao C, et al. Sequential versus concurrent
anthracyclines and taxanes as adjuvant chemotherapy of early breast
cancer: a meta-analysis of phase III randomized control trials. Breast
2012;21(3):389–393.
108. Mavroudis D, Saloustros E, Boukovinas I, et al. Sequential vs
concurrent epirubicin and docetaxel as adjuvant chemotherapy for high-
risk, node-negative, early breast cancer: an interim analysis of a
randomised phase III study from the Hellenic Oncology Research
Group. Br J Cancer 2017;117(2):164–170.
109. Sparano JA, Gray RJ, Ravdin PM, et al. Clinical and genomic risk to
guide the use of adjuvant therapy for breast cancer. N Engl J Med
2019;380:2395–2405.
110. Zavos A, Valachis A. Risk of chemotherapy-induced amenorrhea in
patients with breast cancer: a systematic review and meta-analysis. Acta
Oncol 2016;55(6):664–670.
111. Waks A, Partridge AH. Fertility preservation in patients with breast
cancer: necessity, methods, and safety. J Natl Compr Canc Netw
2016;14(3):355–363.
112. Lambertini M, Ceppi M, Poggio F, et al. Ovarian suppression using
luteinizing hormone-releasing hormone agonists during chemotherapy to
preserve ovarian function and fertility of breast cancer patients: a meta-
analysis of randomized studies. Ann Oncol 2015;26:2408–2419.
113. Patt DA, Duan Z, Fang S, et al. Acute myeloid leukemia after adjuvant
breast cancer therapy in older women: understanding risk. J Clin Oncol
2007;25:3871–3876.
114. Freedman RA, Seisler DK, Foster JC, et al. Risk of acute myeloid
leukemia and myelodysplastic syndrome among older women receiving
anthracycline-based adjuvant chemotherapy for breast cancer on Modern
Cooperative Group Trials (Alliance A151511). Breast Cancer Res Treat
2017;161(2):363–373.
115. Jabagi MJ, Goncalves A, Vey N, et al. Risk of hematologic malignant
neoplasms after postoperative treatment of breast cancer. Cancers
(Basel) 2019;11(10):E1463.
116. Murthi GS, Abedin S. Myeloid malignancies after treatment for solid
tumours. Best Pract Res Clin Haematol 2019;32(1):40–46.
117. Swain SM, Whaley FS, Ewer MS. Congestive heart failure in patients
treated with doxorubicin: a retrospective analysis of three trials. Cancer
2003;97:2869–2879.
118. Shah A, Gradishar WJ. Adjuvant anthracyclines in breast cancer: what is
their role? Oncologist 2018;23:1153–1161.
119. Thakur A, Witteles RM. Cancer therapy-induced left ventricular
dysfunction: interventions and prognosis. J Card Fail. 2014;20:155–
158.
120. Denlinger CS, Sanft T, Baker KS, et al. Survivorship, version 2.2018,
NCCN clinical practice guidelines in oncology. J Natl Compr Canc
Netw 2018;16(10):1216–1247.
121. Romond EH, Perez EA, Bryant J, et al. Trastuzumab plus adjuvant
chemotherapy for operable HER2-positive breast cancer. N Engl J Med
2005;353(16):1673–1684.
122. Perez EA, Romond EH, Suman VJ, et al. Trastuzumab plus adjuvant
chemotherapy for human epidermal growth factor receptor 2-positive
breast cancer: planned joint analysis of overall survival from NSABP B-
31 and NCCTG N9831. J Clin Oncol 2014;32(33):3744–3752.
123. Piccart-Gebhart MJ, Procter M, Leyland-Jones B, et al. Trastuzumab
after adjuvant chemotherapy in HER2-positive breast cancer. N Engl J
Med 2005;353(16):1659–1672.
124. Cameron D, Piccart-Gebhart MJ, Gelber RD, et al. 11 years’ follow-up
of trastuzumab after adjuvant chemotherapy in HER2-positive early
breast cancer: final analysis of the HERceptin Adjuvant (HERA) trial.
Lancet 2017;389:1195–1205.
125. Pivot X, Romieu G, Debled M, et al. 6 months versus 12 months of
adjuvant trastuzumab in early breast cancer (PHARE): final analysis of a
multicentre, open-label, phase 3 randomised trial. Lancet
2019;393(10191):2591–2598.
126. Piccart-Gebhart M, Holmes E, Baselga J, et al. Adjuvant lapatinib and
trastuzumab for early human epidermal growth factor receptor 2-positive
breast cancer: results from the randomized phase III adjuvant lapatinib
and/or trastuzumab treatment optimization Trial. J Clin Oncol
2016;34:1034–1042.
127. von Minckwitz G, Procter M, de Azambuja E, et al. Adjuvant
pertuzumab and trastuzumab in early HER2-positive breast cancer. N
Engl J Med 2017;377:122–131.
128. Beatson GT. On the treatment of inoperable cases of carcinoma of the
mamma: suggestions for a new method of treatment with illustrative
cases. Lancet 1896; 2:104–107.
129. Fisher B, Jeong JH, Bryant J, et al. Treatment of lymph-node-negative,
oestrogen-receptor-positive breast cancer: long-term findings from
National Surgical Adjuvant Breast and Bowel Project randomised
clinical trials. Lancet 2004;364(9437):858–868.
130. Davies C, Pan H, Godwin J, et al. Long-term effects of continuing
adjuvant tamoxifen to 10 years versus stopping at 5 years after diagnosis
of oestrogen receptor-positive breast cancer: ATLAS, a randomised trial.
Lancet 2013;381(9869):805–816.
131. Gray RG, Rea DW, Handley K, et al. aTTOM: long-term effects of
continuing adjuvant tamoxifen to 10 years versus stopping at 5 years in
6953 women with early breast cancer. J Clin Oncol 2013;31(18
Suppl):5.
132. Albain KS, Barlow WE, Ravdin PM, et al. Adjuvant chemotherapy and
timing of tamoxifen in postmenopausal patients with endocrine-
responsive, node-positive breast cancer: a phase 3, open-label,
randomised controlled trial. Lancet 2009;374(9707):2055–2063.
133. Fleming CA, Heneghan HM, O’Brien D, et al. Meta-analysis of the
cumulative risk of endometrial malignancy and systematic review of
endometrial surveillance in extended tamoxifen therapy. Br J Surg
2018;105(9):1098–1106.
134. Miller WR. Aromatase inhibitors: mechanism of action and role in the
treatment of breast cancer. Semin Oncol 2003;30(4 Suppl 14):3–11.
135. Cuzick J, Sestak I, Baum M, et al. Effect of anastrozole and tamoxifen
as adjuvant treatment for early-stage breast cancer: 10-year analysis of
the ATAC trial. Lancet Oncol 2010;11(12):1135–1141.
136. Ruhstaller T, Giobbie-Hurder A, Colleoni M, et al. Adjuvant letrozole
and tamoxifen alone or sequentially for postmenopausal women with
hormone receptor-positive breast cancer: long-term follow-up of the
BIG 1-98 trial. J Clin Oncol. 2019;37:105–114.
137. Coombes RC, Kilburn LS, Snowdon CF, et al. Survival and safety of
exemestane versus tamoxifen after 2–3 years’ tamoxifen treatment
(Intergroup Exemestane Study): a randomised controlled trial. Lancet
2007;369(9561):559–570.
138. Jakesz R, Jonat W, Gnant M, et al. Switching of postmenopausal women
with endocrine-responsive early breast cancer to anastrozole after 2
years’ adjuvant tamoxifen: combined results of ABCSG trial 8 and
ARNO 95 trial. Lancet 2005;366(9484):455–462.
139. Regan MM, Neven P, Giobbie-Hurder A, et al. Assessment of letrozole
and tamoxifen alone and in sequence for postmenopausal women with
steroid hormone receptor-positive breast cancer: The BIG 1–98
randomised clinical trial at 8.1 years median follow-up. Lancet Oncol
2011;12:1101–1108.
140. Derks MGM, Blok EJ, Seynaeve C, et al. Adjuvant tamoxifen and
exemestane in women with postmenopausal early breast cancer
(TEAM): 10-year follow-up of a multicentre, open-label, randomised,
phase 3 trial. Lancet Oncol 2017;18(9):1211–1220.
141. Jin H, Tu D, Zhao N, et al. Longer-term outcomes of letrozole versus
placebo after 5 years of tamoxifen in the NCIC CTG MA.17 trial:
analyses adjusting for treatment crossover. J Clin Oncol 2012;30:718–
721.
142. Tjan-Heijnen VCG, van Hellemond IEG, Peer PGM, et al. Extended
adjuvant aromatase inhibition after sequential endocrine therapy
(DATA): a randomised, phase 3 trial. Lancet Oncol 2017;18(11):1502–
1511.
143. Blok EJ, Kroep JR, Meershoek-Klein Kranenbarg E, et al. Optimal
duration of extended adjuvant endocrine therapy for early breast cancer;
results of the IDEAL trial (BOOG 2006-05). J Natl Cancer Inst
2018;110(1).
144. Mamounas EP, Bandos H, Lembersky BC, et al. Use of letrozole after
aromatase inhibitor-based therapy in postmenopausal breast cancer
(NRG Oncology/NSAPB B-42): a randomised, double-blind, placebo-
controlled, phase 3 trial. Lancet Oncol 2019;20(1):88–99.
145. Goss PE, Ingle JN, Pritchard KI, et al. Extending aromatase-inhibitor
adjuvant therapy to 10 years. N Engl J Med 2016;375(3):209–219.
146. Arimidex, Tamoxifen, Alone or in Combination Trialists’ Group,
Buzdar A, Howell A, et al. Comprehensive side-effect profile of
anastrozole and tamoxifen as adjuvant treatment for early-stage breast
cancer: long-term safety analysis of the ATAC trial. Lancet Oncol
2006;7(8):633–643.
147. Coleman RE, Banks LM, Girgis SI, et al. Skeletal effects of exemestane
on bone-mineral density, bone biomarkers, and fracture incidence in
postmenopausal women with early breast cancer participating in the
Intergroup Exemestane Study (IES): a randomised controlled study.
Lancet Oncol 2007;8(2):119–127.
148. Mouridsen H, Keshaviah A, Coates AS, et al. Cardiovascular adverse
events during adjuvant endocrine therapy for early breast cancer using
letrozole or tamoxifen: safety analysis of BIG 1–98 trial. J Clin Oncol
2007;25(36):5715–5722.
149. Sestak I, Cuzick J, Dowsett M, et al. Prediction of late distant recurrence
after 5 years of endocrine treatment: a combined analysis of patients
from the Austrian breast and colorectal cancer study group 8 and
Arimidex, tamoxifen alone or in combination randomized trials using
the PAM50 risk of recurrence score. J Clin Oncol 2015;33(8):916–922.
150. Dowsett M, Sestak I, Regean MM, et al. Integration of clinical variables
for the prediction of late distant recurrence in patients with estrogen
receptor–positive breast cancer treated with 5 years of endocrine
therapy: CTS5. J Clin Oncol 2018;36(19):1941–1948.
151. LHRH-agonists in Early Breast Cancer Overview group, Cuzick J,
Ambroisine L, et al. Use of luteinising-hormone-releasing hormone
agonists as adjuvant treatment in premenopausal patients with hormone-
receptor-positive breast cancer: a meta-analysis of individual patient
data from randomised adjuvant trials. Lancet 2007;369:1711–1723.
152. Yan S, Li K, Jiao X, et al. Tamoxifen with ovarian function suppression
versus tamoxifen alone as an adjuvant treatment for premenopausal
breast cancer: a meta-analysis of published randomized controlled trials.
Onco Targets Ther 2015;8:1433–1441.
153. Gnant M, Mlineritsch B, Stoeger H, et al. Zoledronic acid combined
with adjuvant endocrine therapy of tamoxifen versus anastrozole plus
ovarian function suppression in premenopausal early breast cancer: final
analysis of the Austrian Breast and Colorectal Cancer Study Group Trial
12. Ann Oncol 2015;26(2):313–320.
154. Pagani O, Regan MM, Walley BA, et al. Adjuvant exemestane with
ovarian suppression in premenopausal breast cancer. N Engl J Med
2014;371(2):107–118.
155. Francis PA, Regan MM, Fleming GF, et al. Adjuvant ovarian
suppression in premenopausal breast cancer. N Engl J Med
2015;372:436–446.
156. Pagani O, Francis PA, Fleming GF, et al. Absolute improvements in
freedom from distant recurrence to tailor adjuvant endocrine therapies
for premenopausal women: results from TEXT and SOFT. J Clin Oncol
2019:JCO1801967.
157. Perrone F, De Laurentiis M, De Placido S, et al. Adjuvant zoledronic
acid and letrozole plus ovarian function suppression in premenopausal
breast cancer: HOBOE phase 3 randomised trial. Eur J Cancer
2019;118:178–186.
158. Shapiro CL, Halabi S, Hars V, et al. Zoledronic acid preserves bone
mineral density in premenopausal women who develop ovarian failure
due to adjuvant chemotherapy: final results from CALGB trial 79809.
Eur J Cancer 2011;47:683–689.
159. Brufsky AM, Harker WG, Beck JT, et al. Final 5-year results of Z-
FAST trial: adjuvant zoledronic acid maintains bone mass in
postmenopausal breast cancer patients receiving letrozole. Cancer
2012;118:1192–1201.
160. Early Breast Cancer Trialists’ Collaborative Group (EBCTCG).
Adjuvant bisphosphonate treatment in early breast cancer: meta-analyses
of individual patient data from randomised trials. Lancet
2015;386:1353–1361.
161. Coleman R, Gnant M, Morgan G, et al. Effects of bone-targeted agents
on cancer progression and mortality. J Natl Cancer Inst 2012;104:1059–
1067.
162. Dhesy-Thind S, Fletcher GG, Blanchette PS, et al. Use of adjuvant
bisphosphonates and other bone-modifying agents in breast cancer: a
cancer care Ontario and American Society of Clinical Oncology Clinical
Practice Guideline. J Clin Oncol 2017;35(18):2062–2081.
CHAPTER 15

Breast Cancer Diagnosis, Prognosis,


and Treatment in Augmented Women
NEAL HANDEL
HISTORY
Over the years concerns have been raised about the possible effects of
silicone implants on the incidence, detection, treatment, and prognosis of
breast cancer. Breast augmentation is a commonly performed elective
procedure, making these concerns legitimate. Recent statistics published by
the American Society of Plastic Surgery (ASPS) indicate breast augmentation
is the most popular cosmetic surgical procedure in the United States. Nearly
314,000 primary breast augmentations were performed in 2018, up 4% from
2017 (1).

TABLE 15-1 Incidence of Breast Cancer in Augmented Patients

Carcinoma of the breast is also common (2). The American Cancer Society
estimates that women in the United States have nearly a 1 in 7 (13.4%)
lifetime risk of developing breast cancer (3). In 2019, an estimated 268,600
women in the United States will be diagnosed with invasive breast cancer,
and 62,930 women will be diagnosed with in situ breast cancer.
It is estimated that 42,260 deaths from breast cancer will occur this year
(4). Extrapolating from these statistics, more than 42,000 augmented women
will be diagnosed annually with breast cancer. It is therefore important to
understand the potential effects of implants on the incidence, detection,
treatment, and prognosis of breast cancer.
IMPLANTS AND CANCER RISK
There have long been questions about a possible association between
implants and the risk of developing carcinoma of the breast or other benign or
malignant breast tumors. The origin of these concerns was based on the
observation that when solid foreign bodies made of various different
substances were implanted in rodents, they frequently elicited the
development of sarcomas (5,6). This phenomenon, known as the
Oppenheimer effect, has never been observed in humans (7–9). Numerous
epidemiologic studies have investigated the incidence of breast cancer in
augmented patients compared to nonaugmented cohorts. These studies
unequivocally demonstrate that breast implants are not associated with an
increased risk of developing carcinomas or other types of benign or
malignant breast tumors (10–12). In fact, recently published studies (13–16)
have documented a lower-than-expected incidence of breast cancer in
augmented patients (Table 15-1). The observation that augmented women
appear to be at a somewhat lower risk of developing breast cancer has led to
speculation about possible mechanisms whereby breast implants might
inhibit tumorigenesis. Among the hypotheses that have been suggested are
that implants cause a heightened immune response, leading to earlier
detection and destruction of precancerous cells; that the compression effect of
the implant on surrounding breast tissue results in an alteration of cell growth
rate; and that the implant acts as insulation, lowering the ambient temperature
of the breast, with subsequent reduction of local tissue metabolic rates (13).
While it clearly has been established that augmented women are not at
increased risk for developing breast cancer, due to the frequency of this
disease, many augmented women eventually will be diagnosed with breast
cancer. This has resulted in persistent and valid concerns about the possible
effects of implants on cancer detection (22,23). Conceivably, implants could
alter physical examination of the breast, reduce the sensitivity of various
imaging modalities, or even interfere with adequate biopsy of suspicious
lesions.
PHYSICAL EXAMINATION OF THE AUGMENTED BREAST
Breasts implants, whether submammary, submuscular, or in a dual plane
pocket, always reside beneath the parenchyma. For that reason, the presence
of the prosthesis alone should not compromise palpation of a lesion.
However, there are numerous ways implants may alter physical examination
of the breast. Sometimes breast augmentation (particularly when combined
with mastopexy) causes parenchymal scarring or areas of fat necrosis. This
may result in thickened regions or even discrete lumps palpable on physical
examination. If such findings are clinically suspicious, further diagnostic
testing is indicated.
A significant number of augmented patients develop capsular contracture.
Ordinarily contracture does not interfere with palpation of breast tissue, but
occasionally the capsule tears, allowing part of the implant to herniate into
adjacent parenchyma; this may result in a palpable (or even visible) mass
within the breast (Fig. 15-1). Typically, such a palpable bulge or “knuckle”
of the implant is not confusing to plastic surgeons. However, primary care
physicians, gynecologists, and nurse practitioners may not be familiar with
these findings; when such an abnormal mass is identified, it needs to be
differentiated from a pathologic lesion. Calcification of the capsule
sometimes occurs, and rigid calcium deposits may be palpated immediately
adjacent to the implant. These benign calcifications must be distinguished on
both physical examination and mammography from malignant
microcalcifications (Fig. 15-2A,B).
FIGURE 15-1 Augmented patient with a herniated silicone gel breast implant
presenting as a palpable and visible breast mass.
FIGURE 15-2 A: Dense calcification of scar tissue capsule surrounding silicone gel
implant. B: Digital mammogram showing diffuse “egg shell” calcifications within the
capsule surrounding the implant.

FIGURE 15-3 Multiple siliconomas in breast parenchyma and adjacent soft tissues
in a patient with a ruptured silicone gel implant.

One of the recognized complications of silicone gel implants is leakage of


filler material, from either gel bleed or frank rupture of the elastomeric shell.
When silicone gel leaks from the implant, it may elicit an inflammatory
foreign body reaction, leading to fibrosis and sometimes formation of
siliconomas. These abnormalities may be palpable adjacent to the implant or
in other areas of the breast or chest wall (Fig. 15-3), depending upon where
the silicone migrates. Siliconomas typically present as firm, discrete lumps
and must be differentiated from other pathologic masses. If a silicone implant
ruptures and there is spread of silicone into the breast parenchyma or adjacent
structures (extracapsular rupture), it is readily apparent on mammograms
(Fig. 15-4). When the silicone gel leaking from the implant remains
intracapsular, it may be difficult or impossible to detect on physical
examination (silent rupture). This is especially true with newer-generation,
more highly cohesive gel-filled implants. Intracapsular rupture can
sometimes be diagnosed on mammography (Fig. 15-5) and can reliably be
imaged by magnetic resonance imaging (MRI).
Saline implants are inflated with a fill tube inserted via a self-sealing valve
on the anterior or posterior surface of the implant. In some patients,
particularly those with a thin layer of breast tissue, the valve may be palpable.
Generally it will be felt in the central portion of the breast, beneath the nipple
areolar complex. Even in cases in which the valve is on the posterior surface,
the device can flip over and the valve may be felt. Surgeons sometimes
unwittingly perform biopsies only to discover that the palpable mass is a
filler valve.
When performing surgical or needle biopsy of a suspected abnormality,
caution must be exercised to avoid damaging the implant. In the case of fine-
needle aspiration or core needle biopsy, the implant can usually be
manipulated away from the area where the sharp tip is introduced. However,
if the lesion is immediately adjacent to the implant, it may be preferable to
perform open biopsy to avoid damaging the prosthesis (Fig. 15-6). Core
needle biopsy can be problematic because multiple needle insertions may be
required to obtain adequate tissue samples, increasing the risk of puncturing
the prosthesis. Vacuum-assisted biopsy (Mammotome, MIBB) facilitates
biopsy in women with implants (Fig. 15-7) (24,25). With this technique,
stereotactic mammography or real-time ultrasonography is used to guide the
needle tip adjacent to the suspicious area. The vacuum-assisted biopsy needle
can be accurately positioned near the lesion to avoid damaging the implant.
Unlike core needle biopsy, the vacuum-assisted biopsy probe is inserted just
once into the breast through a single small skin incision. Multiple tissue
samples may be taken by rotating the needle aperture and using vacuum
assistance. The precision and directional capabilities of vacuum-assisted
biopsy make this the preferred technique for percutaneous biopsy in
augmented women.
FIGURE 15-4 Mammogram of a patient with extracapsular rupture of a silicone gel
implant, showing extravasation of free silicone into the ducts and breast
parenchyma.
FIGURE 15-5 Digital mammogram of a patient with intracapsular rupture of a
silicone gel implant; the arrow indicates abnormal contour where silicone has
escaped from the implant but remains confined within the capsule.
FIGURE 15-6 Mammogram of augmented patient with a breast cancer in close
proximity to breast implant.

When open biopsy is performed, steps can be taken to minimize the risk of
damaging the implant. Dissection is best performed with a blunt-tipped
electrocautery. If the surface of the implant is encountered, care should be
taken to avoid damaging the shell with any pointed or sharp instrument. If the
surgical biopsy also includes a portion of the capsule, it is unnecessary to
repair the capsule; a new layer of scar tissue will regenerate over the implant
surface.
RADIOLOGIC IMAGING OF THE AUGMENTED BREAST

Mammography
Routine mammographic screening of asymptomatic women facilitates early
diagnosis of breast cancer. Over the years concerns have been raised about
the accuracy of mammography in augmented patients (26,27). There are
several ways implants may affect mammograms. The surgery can cause
parenchymal scarring, resulting in architectural distortions, densities, or
calcifications that appear on mammography. Implants (particularly when
present over a prolonged period of time) compress breast tissue, increasing
radiodensity, reducing contrast, and potentially interfering with identification
of subtle lesions (28). The best-quality mammograms are obtained when the
breast is maximally compressed so the x-ray beam penetrates the thinnest
possible layer of tissue. With less compression, the volume of visualized
tissue per unit area increases, causing more superimposition and potentially
reducing mammographic sensitivity. Because implants are less compliant
than breast tissue, they make it difficult to achieve the desired compression.
During mammography the average nonaugmented breast can be compressed
to a thickness of 4.5 cm, while the average augmented breast can be
compressed only to a thickness of 7 cm (29).
The most important factor, affecting mammography in the augmented
breast is the radiopaque shadow cast by the implant. Early reports estimated
that only 25% of the breast is visualized after augmentation (30). Gumucio et
al. (31) demonstrated that both saline and silicone implants can totally
obscure early lesions such as microcalcifications. Hayes et al. (32) reported
that 22% to 83% (38% on average) of the breast tissue could be obscured by
the implant.
The extent to which an implant shadow interferes with mammography
depends upon its size (33) and radiodensity (34). The density of the shadow
is determined primarily by the physical and radiologic characteristics of the
filler material. Both silicone and saline create a dense, radiopaque shadow
that completely blocks visualization of adjacent breast tissue. Over the years
several prostheses (e.g., Misti Gold implant, Trilucent implant) containing
alternative filler materials have been introduced. However, none of these
fillers proved entirely satisfactory and at the present time only saline- and
silicone gel–filled implants are commercially available.
Prior studies have investigated how breast implants affect the amount of
tissue visualized on mammograms (27,34). Preoperative and postoperative
mammography was performed in a consecutive series of breast augmentation
patients, and the amount of tissue visualized on each film was measured.
Changes in area visualized were correlated with various parameters,
including the degree of capsular contracture, implant position (submammary
vs. submuscular), type of mammography (compression vs. displacement),
preoperative breast size, implant size, and implant type.
FIGURE 15-7 Diagram of vacuum-assisted (Mammotome, MIBB) biopsy in an
augmented patient. A: The biopsy needle tip is guided adjacent to the suspicious
area. B: The vacuum draws the tissue into the biopsy needle aperture. C: A rotating
cutter is advanced to harvest tissue. D: The specimen has been transected. E: The
vacuum withdraws and transports the specimen. F: A marker can be placed at the
biopsy site to facilitate later radiologic follow-up.

Our study revealed that in most patients there is a decrease in measurable


breast tissue on postaugmentation films. The most important factor is
capsular contracture: Little or no contracture (Baker 1 or 2) resulted in a 30%
reduction in the area visualized, while moderate or severe contracture (Baker
3 or 4) resulted in a 50% reduction (Fig. 15-8). In patients who had serial
mammography in the face of worsening contracture, there was progressive
reduction in the amount of tissue visualized (Fig. 15-9). Implant position
(submammary vs. submuscular) also proved important; on average, patients
with submammary implants had a 37% reduction in area visualized, while
patients with submuscular implants had only a 17% reduction.
In order to facilitate mammography in augmented women, Eklund et al.
(35) developed the displacement or “push-back” technique (Fig. 15-10A,B),
by which the implant is displaced posteriorly to allow a greater proportion of
breast tissue to be captured on the mammogram. Using standard compression
mammography, Eklund et al. determined that up to 97% of the breast tissue
could be obscured by the implant, greatly increasing the likelihood of missing
a significant lesion. The displacement technique led to an improvement in
99% of cases. Part of this improvement is likely attributable to the fact that
implant displacement results in a compression advantage of up to 5 cm,
leading to improved image quality and greater sensitivity. Subsequent studies
confirmed the results of Eklund et al. in obtaining better visualization of
breast tissue using implant displacement (36,37). Our study (38) also
confirmed that slightly more tissue is visualized with displacement (average
reduction of 25%) than with standard compression mammography (average
decrease of 30%); however, with either technique there is a substantial
reduction in area visualized compared to preaugmentation mammograms
(Fig. 15-11).
FIGURE 15-8 Effect of contracture on area visualized post augmentation. Little or
no contracture (Baker 1 or 2) results in about 30% reduction in the area visualized,
while moderate or severe contracture (Baker 3 or 4) results in about 50% reduction.

While no one refutes that the shadow cast by an implant interferes with
visualization of breast tissue, there has been debate about whether this
translates into diminished mammographic sensitivity. It has been established
that mammography in nonaugmented women is highly sensitive. In
nonaugmented women with palpable tumors, the mammogram is positive in
>90% and the false-negative rate is <10%. There are several published
reports suggesting that the false-negative rate in augmented patients is
considerably higher (37,39,40). We recently reviewed the mammograms of
all patients with palpable tumors treated over a 23-year period (41).
Mammograms among 1,741 nonaugmented women failed to visualize the
tumor in 153 (false-negative rate of 8.8%). The mammograms of 87
augmented patients failed to reveal the lesion in 36 cases (false-negative rate
of 41.4%). This difference is highly significant (p < 0.0001) (Table 15-2) and
suggests that implants dramatically reduce the sensitivity of mammography.

FIGURE 15-9 Effect of worsening contracture. Left: Compression mammography in


a patient before augmentation mammaplasty. Middle: Postaugmentation
mammogram, at which time the patient had a Baker 1 capsule. Right: A subsequent
mammogram, by which time the patient had developed Baker 4 capsular
contracture.

FIGURE 15-10 A: Diagram of compression mammography. B: Diagram of


displacement (Eklund technique) mammography.
FIGURE 15-11 Compression versus displacement mammography. Left:
Mammogram of a patient before augmentation. Middle: Postaugmentation
compression mammogram. Right: Postaugmentation displacement mammogram.
Slightly more tissue is visualized with displacement than with compression, but with
either technique there is a substantial reduction in area visualized compared to the
preaugmentation study.

Digital Mammography
Digital mammography is a technique by which an electronic image of the
breast is captured and stored on a computer, allowing the recorded data to be
magnified, enhanced, or otherwise manipulated to increase sensitivity. A
recently published clinical trial comparing digital to film mammography
demonstrated no difference in the accuracy of detecting breast cancer (42).
No studies have been published specifically comparing digital and film
mammography in augmented women. Some radiologists have observed that
in patients with saline implants, the tissue beneath the implant shadow
appears to be better visualized with digital mammography; this is particularly
true if a manual technique is used instead of automated settings (Fig. 15-
12A,B). However, it is likely that the same adverse effects breast implants
have on conventional mammography will also apply to digital
mammography.
Magnetic Resonance Imaging
MRI has proven useful in diagnosing breast implant ruptures and leakage
(43,44). MRI can also be used as an adjunct to film screen mammography for
detecting parenchymal abnormalities in augmented women. MRI is not
impaired by the presence of radiopaque implants, can be used to examine
breast tissue compressed by the implant, and reliably images adjacent
structures, such as the muscles and chest wall. Furthermore, scarring can be
differentiated from malignancy because malignant lesions demonstrate an
early and strong enhancement of the contrast medium (45–47). However,
MRI requires administration of intravenous contrast, is much costlier than
conventional mammography, and has limitations in sensitivity and
specificity.

TABLE 15-2 Sensitivity of Mammography in Women With Palpable


Cancers
FIGURE 15-12 A: Digital mammography of a patient with a saline-filled implant
using automated settings; the implant appears as a dense, radiopaque shadow,
effectively blocking visualization of all breast tissue within its path. B: Repeat digital
mammogram of the same patient using a manual technique; structures previously
hidden by the implant can now be visualized.

The International Consensus Conference recently issued a report on state-


of-the-art diagnosis and treatment of breast cancer. This panel concluded that
MRI might be helpful in pretreatment evaluation of newly diagnosed breast
cancer in augmented women and for patients in whom mammography is
inconclusive, such as women with injected silicone (48). However,
conventional mammography remains the best tool for screening and
diagnosing breast cancer and MRI is not recommended as a cancer screening
tool in augmented patients. There is increasing data to support MRI screening
for younger patients at high risk of breast cancer (e.g., BRCA1 or BRCA2
mutation, strong family or personal history of breast cancer). However, these
high-risk patients probably should be discouraged from undergoing elective
breast augmentation because implants might interfere with the earliest
possible detection of cancer and may diminish the usefulness of breast-
conservation therapy (BCT) (49).
Ultrasound
Breast ultrasound can be useful for detecting implant rupture or leakage
(50,51) and has the advantage of being less expensive than MRI (52).
However, ultrasound is not as sensitive or specific for detecting parenchymal
abnormalities as mammography or MRI (53). Currently, ultrasound is most
useful for characterizing masses, detecting unsuspected invasive disease in
lesions presenting as microcalcifications, and measuring tumor size of mass
lesions. There currently is no recognized role for ultrasound as a screening
tool in augmented women.
EFFECTS OF IMPLANTS ON DISEASE STAGE AND PROGNOSIS
While there is a good deal of evidence that breast implants decrease the
sensitivity of mammography, there are conflicting reports regarding the stage
of disease at the time of diagnosis in augmented women. Several years ago
we reported that among our breast cancer population, augmented women
were diagnosed at a comparatively advanced stage (23,28). Others have
reported similar observations. In a multicenter study, Brinton et al. (17) found
that augmented cancer patients had a lower incidence of in situ and local
disease and a higher rate of axillary nodal metastases and distant spread than
nonaugmented patients. Similarly, Karanas et al. (54) reported a low rate of
early lesions (stages 0 and 1) and a relatively high rate of advanced disease
(stages 3 and 4) in augmented cancer patients. On the other hand, some
published reports suggest that the stage of disease at diagnosis is equivalent
in augmented and nonaugmented women (55–58). Carlson et al. (59)
demonstrated in their 1993 study that the pathologic staging found in
augmented and nonaugmented cancer patients was similar. Deapen et al. (60)
came to the same conclusion. Leibman and Kruse (36,37) found that 28% of
breast cancers detected in augmented patients were asymptomatic at the time
of diagnosis, implying that even in augmented patients, breast cancer can be
detected while still in its occult stages.

TABLE 15-3 Palpability at Time of Diagnosis

To further examine this question, we recently reviewed our experience


with 4,082 consecutive breast cancer patients treated between 1981 and 2004
at the Breast Center in Van Nuys, California, and the Kenneth Norris
Comprehensive Cancer Center in Los Angeles, California (41). For the
purpose of comparing augmented and nonaugmented patients, only women
with infiltrating ductal, infiltrating lobular, ductal carcinoma in situ (DCIS),
and lobular carcinoma in situ were included (unusual tumors such as
angiosarcomas and lymphomas were excluded). This yielded a total of 3,922
nonaugmented patients and 129 augmented patients in the final analysis.
All patients were entered into a prospective database, which included,
among other information, tumor palpability, size of the primary (measured at
the time of surgical excision), nuclear grade, the presence or absence of
lymphovascular invasion, and axillary lymph node status. Breast cancer
recurrence and mortality rates were carefully tracked. Mammograms were
reviewed (when available) to compare the sensitivity of mammography in
augmented and nonaugmented patients with palpable lesions. The findings in
the two groups were compared. Statistical significance was determined using
appropriate methodology: Comparison of average tumor size was done with
t-tests on independent groups; comparison of survival until recurrence and
survival until death was done using log rank tests from Kaplan–Meier
survival analysis; analyses of counts and percentages were done with chi-
square tests.

TABLE 15-4 Stage of Disease at Time of Diagnosis

TABLE 15-5 Mean Tumor Sizea


Number of Patients Mean Tumor Size
(mm)
Nonaugmented 2,235 23.8
Augmented 86 23.2
Total 2,321 23.7
aPatientswith infiltrating ductal cancer only.
p = 0.8066 (nonsignificant).

Among nonaugmented women, mean age at time of diagnosis was 53.5


years (range 22 to 95 years); in augmented patients, mean age was 46.8 years
(range 29 to 71 years). In the augmented group, for cases in which data were
available (N = 104), implants were present a mean of 10.5 years (range 0.5 to
37 years). In cases in which information regarding the degree of capsular
contracture was available (N = 106) 30% were Baker grade 1, 40% were
grade 2, 22% were grade 3, and 8% were grade 4.
Augmented patients presented with a significantly lower percentage of
occult (nonpalpable) tumors (25% compared to 46%) (p < 0.0001) (Table 15-
3), a slightly lower incidence of early in situ lesions (27% compared to 33%),
and a greater incidence of positive axillary lymph nodes (46% compared to
35%). Overall, however, there was no significant difference in stage of
disease between augmented and nonaugmented patients (Table 15-4).
For purposes of comparing tumor size we considered only patients with
infiltrating ductal lesions (infiltrating ductal tumors are the type most
commonly encountered and measurement of which is most reliable). Among
the 3,922 nonaugmented patients, there were 2,235 infiltrating ductal cancers,
with an average tumor size of 23.8 mm. Among 120 augmented patients, 86
had infiltrating ductal lesions, with an average size of 23.2 mm (no
significant difference) (Table 15-5). Breast cancer recurrence rates (Table 15-
6) and breast cancer–specific survival rates (Table 15-7) were the same for
augmented and nonaugmented cancer patients. Kaplan–Meier analyses
confirm that there was no significant difference in breast cancer recurrence
(Fig. 15-13) or survival (Fig. 15-14) between the two groups over time.

TABLE 15-6 Cancer Recurrence Rate


TABLE 15-7 Breast Cancer Mortality Rate

Our data revealed that augmented cancer patients were less likely to
present with occult lesions and had a significantly higher rate of false-
negative mammograms; however, tumor size was virtually identical in
augmented and nonaugmented women. One possible explanation is that
implants may facilitate palpation of tumors. Others have suggested that the
augmented breast is easier to examine (9); there are several reasons why this
is plausible. Palpation of a breast lesion is dependent upon feeling the
abnormality and distinguishing it from surrounding normal breast tissue. This
is more difficult in women with large breasts and deep tumors because the
lesion simply is not as accessible to the touch. Breast implants compress
breast parenchyma and, over time, cause tissue atrophy. It is not uncommon
to observe that the parenchymal envelope in augmented patients (particularly
when implants have been present for many years) has been reduced to a thin
layer, often just 1 to 2 cm in thickness. In our population implants had been
present an average of more than 10 years prior to diagnosis, ample time for
the prosthesis to cause tissue compression, thinning, and atrophy. This may
explain why lesions of virtually the same size were more frequently palpable
in augmented patients (Fig. 15-15).
FIGURE 15-13 Breast cancer recurrence. Kaplan–Meier plot of cumulative cancer
recurrence in augmented and nonaugmented patients (no significant difference).

A recently published study by Sosin et al. (61) looked at whether


augmentation mammaplasty might affect breast cancer detection, stage, and
treatment. This case control study was based on augmented patients
undergoing breast cancer treatment from 2000 to 2013. Forty-eight cases and
302 controls were analyzed. Palpable lesions were detected at a smaller size
in augmentation patients (1.6 cm vs. 2.3 cm; p < 0.001). Fewer lesions in
augmented patients were detected by screening mammography (77.8% of
cases vs. 90.7% of controls; p = 0.010). The authors concluded “Palpable
detection of breast cancer is more likely at a smaller size in augmented
patients, yet it is less likely on screening mammography than in controls.
Augmentation breast cancer patients have a comparable disease stage…”
These findings closely resemble the conclusions of prior published data on
this topic.
TREATMENT OF BREAST CANCER IN AUGMENTED PATIENTS
The two currently accepted modalities for treatment of breast cancer are
mastectomy and BCT. There is little reason to believe that implants interfere
with mastectomy. The prosthesis and scar tissue capsule are removed with
the mastectomy specimen, and reconstruction may be performed as either an
immediate or delayed procedure. In fact, the presence of a breast implant may
actually facilitate healing because the mastectomy flaps have been delayed as
a result of undermining performed at the time of augmentation.
BCT consists of lumpectomy, axillary lymph node dissection, whole breast
irradiation, and, in selected cases, a boost to the tumor bed (62). BCT has
proven effective in the majority of women with breast cancer and yields
survival rates equivalent to mastectomy for women with stage 1 (T1 N0),
stage 2A (T0 N1, T1 N1, T2 N0), and stage 2B (T2 N1, T3 N0) breast cancer
(63–69). The cosmetic results of BCT have been reported as good to
excellent in the majority of cases (70–73). Because of the excellent survival
rates and good cosmetic results, BCT is now often considered the treatment
of choice in patients with stage 1 or stage 2 disease (74,75).

FIGURE 15-14 Breast cancer mortality. Kaplan–Meier plot of breast cancer–specific


survival in augmented and nonaugmented patients (no significant difference).

Several studies have investigated radiation physics in the presence of


implants (76–78). Neither silicone gel–filled nor saline-filled implants
attenuate x-rays, and it is widely held by physicists and radiation oncologists
that x-ray therapy can be effectively delivered in the presence of an implant;
BCT is believed to be equally curative in augmented and nonaugmented
patients (79,80). It is further established that electron beams, due to their
finite penetration and rapid falloff, cause minimal damage to adjacent normal
structures (such as the lungs and heart). Studies of radiation dose distribution
reveal no significant difference in the amount of radiation delivered to
adjacent structures in the presence of implants (78).
The other major concerns regarding the use of BCT in augmented women
are cosmetic results and radiation-related complications. Some investigators
report that good results are routinely obtained following irradiation of the
augmented breast (81–83). Others suggest a high rate of capsular contracture
and poor cosmesis (84). Several years ago we reviewed our experience with a
consecutive series of augmented breast cancer patients who underwent BCT
(85). Between 1981 and 1994 we treated 66 augmented women with primary
breast cancer; 27 had modified radical mastectomy, 3 (with DCIS) had
lumpectomy only, and 3 had other forms of treatment. The remaining 33
patients underwent BCT.
FIGURE 15-15 Palpation of a lesion may be facilitated by the long-term presence of
an implant, which causes atrophy, thinning, and compression of breast parenchyma.

Of the patients who received BCT, 4 were explanted prior to radiation, and
in 3 others complete details regarding treatment were unavailable. The
remaining 26 patients comprised the study population. These patients ranged
in age at time of augmentation from 22 to 55 years (mean age 37 years) and
ranged in age at time of cancer diagnosis from 31 to 67 years (mean age 45
years). The interval from augmentation to cancer diagnosis was 0.5 to 20
years (mean 7.5 years). The firmness of each breast (according to the Baker
classification) was rated at the time of cancer diagnosis and at intervals
following completion of radiation therapy. Data were also collected regarding
the rates and reasons for secondary implant surgery after BCT.
Average Baker grade at time of diagnosis was 1.19 on the cancer side and
1.15 on the opposite side. At the latest follow-up visit after radiation therapy,
average Baker grade was 3.08 on the treated side and 1.73 on the opposite
side (see Fig. 15-14). Altogether, 17 (65%) of the augmented women treated
with BCT had a significant increase in contracture on the treated side
(significant increase was defined as a change from either Baker grade 1 or 2
to Baker grade 3 or 4). Among the 17 women with radiation-induced
contracture, average Baker grade on the treated side went from 1.06 at the
time of diagnosis to 3.71 following completion of radiation. There was also
an increase in firmness on the opposite side, which rose from an average
Baker grade of 1.06 to 1.94 (Table 15-8). The interval from completion of
radiation to onset of capsular contracture averaged 22.4 weeks. Figure 15-16
shows an example of radiation-induced capsular contracture in an augmented
patient treated with BCT.

TABLE 15-8 Change in Baker Grade Following Breast-Conservation


Therapy (BCT)
Before Treatment After BCT
Cancer Side 1.19 3.08
Opposite Side 1.15 1.73
Twenty-eight augmented cancer patients.

FIGURE 15-16 Left: Augmented patient diagnosed with cancer of the right breast
(location of the tumor is indicated by the circular mark adjacent to the nipple
areolar complex). Right: Following breast cancer therapy, the patient developed
radiation-induced capsular contracture (Baker 4).

Eight patients with radiation-induced contracture required revision surgery.


Five had explantation, capsulectomy, and replacement with new implants,
and two had unilateral explantation and autologous (transverse rectus
abdominis myocutaneous flap) reconstruction. One patient had bilateral
explantation and capsulectomy without replacement. Based on this
experience, it appears the majority of augmented patients treated with BCT
will have unsatisfactory cosmetic results, and many will require secondary
corrective procedures.
CONCLUSION
Due to the prevalence of breast cancer in the population it is inevitable that
many augmented women will develop carcinoma of the breast. There remain
concerns about the effect of implants on breast cancer detection, prognosis,
and treatment. Multiple studies document that implants obscure
mammograms, and there are data to suggest that the sensitivity of
mammography is reduced in augmented women. Because of the possible
adverse effects of implants on visualization of breast tissue, screening
mammography may not be ideal in augmented patients, and it may be
preferable to perform diagnostic mammography. When evaluating these
patients, physical and mammographic findings should be correlated. Any
palpable abnormalities should be studied with ultrasound. In appropriate
cases, MRI should be considered as an adjunct.
Careful review of a large series of breast cancer patients treated over a 23-
year period revealed that augmented women presented significantly more
often with palpable tumors and had a much higher rate of false-negative
mammography. Despite this, tumor size, stage of disease, recurrence rates,
and breast cancer–specific survival were virtually identical in augmented and
nonaugmented patients. These findings suggest that tumors of equal size may
be more easily palpated in augmented patients, and this beneficial effect may
compensate for the impairment of mammography.
When it comes to the treatment of breast cancer in augmented patients,
there is little reason to believe that implants interfere with mastectomy or
breast reconstruction. On the other hand, there is ample evidence that BCT
may be compromised in augmented women. These patients experience a high
rate of radiation-induced contracture, frequently require reoperation, and are
prone to postoperative complications because of the adverse effect of
radiation on wound healing. In addition to compromised cosmesis and a high
rate of reoperation, there are other potential concerns for augmented women
considering BCT. Because an implant (particularly in the presence of
capsular contracture) may impair mammographic follow-up, the earliest
possible detection of a local recurrence could be delayed. In addition, these
patients are at increased risk of developing a second primary cancer in the
opposite breast, and, hypothetically, the contralateral implant might interfere
with early detection of a new cancer. Based on these considerations, BCT
may be an undesirable option in augmented cancer patients, unless the
implants are removed prior to treatment.
ACKNOWLEDGMENTS
The author wishes to acknowledge the contributions of his colleagues who
were instrumental in the design and execution of several of the studies
referenced in this manuscript. These include Melvin J. Silverstein, Parvis
Gamagami, Bernard Lewinsky, James Waisman, and J. Arthur Jensen.

REFERENCES

1. 2018 Plastic Surgery Statistics Report. ASPS National Clearinghouse of


Plastic Surgery Procedural Statistics. American Society of Plastic
Surgeons. 2019
2. The American Cancer Society. Breast Cancer Facts & Figures 2003–
2004. Atlanta, GA: The American Cancer Society; 2003.
3. Leis HP. Epidemiology in breast cancer. In: Strombeck JO, Rosato FE,
eds. Surgery of the Breast—Diagnosis and Treatment of Breast
Diseases. Stuttgart, Germany: Georg Thieme Verlag; 1986.
4. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2019. CA: A Cancer
Journal for Clinicians. 2019;69(1):7–34.
5. Turner FC. Sarcomas at sites of subcutaneously implanted Bakelite
disks in rats. J Natl Cancer Inst 1941;2:81–86.
6. Oppenheimer BS, Oppenheimer ET, Stout AP. Sarcomas induced in rats
by implanting cellophane. Proc Soc Exp Biol Med 1948;67:33–38.
7. Hoopes JE, Edgerton MT, Shelley W. Organic synthetics for
augmentation mammoplasty: their relation to breast cancer. Plast
Reconstr Surg 1967;39(3):263–270.
8. Brand KG, Johnson KH, Buon LC. Foreign body tumorigenesis. CRC
Crit Rev Toxicol 1976;4(4):353–394.
9. Morgan RW, Elcock M. Artificial implants and soft tissue sarcomas. J
Clin Epidemiol 1995;48(4):545–549.
10. Deapen DM, Pike MC, Casagrande JT, et al. The relationship between
breast cancer and augmentation mammaplasty: an epidemiologic study.
Plast Reconstr Surg 1986;77(3):361–368.
11. Brinton LA, Malone KE, Coates RJ, et al. Breast enlargement and
reduction: results from a breast cancer case–control study. Plast
Reconstr Surg 1996;97(2):269–275.
12. McLaughlin JK, Nyren O, Blot WJ, et al. Cancer risk among women
with cosmetic breast implants: a population-based cohort study in
Sweden. J Natl Cancer Inst 1998;90(2):156–158.
13. Deapen DM, Bernstein L, Brody GS. Are breast implants
anticarcinogenic? A 14-year follow-up of the Los Angeles study. Plast
Reconstr Surg 1997;99(5):1346–1353.
14. Hoshaw SJ, Klein PJ, Clark BD, et al. Breast implants and cancer:
causation, delayed detection, and survival. Plast Reconstr Surg
2001;107(6):1393–1407.
15. Dreyfuss DA, Singh S, Dowlatshahi K. Silicone implants as an
anticarcinogen. Surg Forum 1987;38:587–592.
16. Su CW, Dreyfuss DA, Krizek A, et al. Silicone implants and the
inhibition of cancer. Plast Reconstr Surg 1995;96(3):513–518;
discussion 519–520.
17. Brinton LA, Lubin JH, Burich MC, et al. Breast cancer following
augmentation mammaplasty. Cancer Causes Control 2000;11(9):819–
827.
18. Pukkala E, Boice JD Jr, Hovi SL, et al. Incidence of breast and other
cancers among Finnish women with cosmetic breast implants, 1970–
1999. J Long Term Eff Med Implants 2002;12(4):271–279.
19. Brisson J, Holowaty EJ, Villeneuve PJ, et al. Cancer incidence in a
cohort of Ontario and Quebec women having bilateral breast
augmentation. Int J Cancer 2006;118(11):2854–2862.
20. Deapen DM, Hirsch EM, Brody GS. Cancer risk among Los Angeles
women with cosmetic breast implants. Plast Reconstr Surg
2007;119(7):1987–1992.
21. Lipworth L, Tarone RE, Friis S, et al. Cancer among Scandinavian
women with cosmetic breast implants: a pooled long-term follow-up
study. Int J Cancer 2009;124(2):490–493.
22. Jakub JW, Ebert MD, Cantor A, et al. Breast cancer in patients with
prior augmentation: presentation, stage, and lymphatic mapping. Plast
Reconstr Surg 2004;114(7):1737–1742.
23. Silverstein MJ, Handel N, Gamagami P. The effect of silicone gel–filled
implants on mammography. Cancer 1991;68(5 suppl):1159–1163.
24. Trevathan-Ramirez D. Innovations in breast disease diagnosis. Radiol
Technol 1998;70(2):197–203.
25. Cangiarella J, Waisman J, Symmans WF, et al. Mammotome core
biopsy for mammary microcalcification: analysis of 160 biopsies from
142 women with surgical and radiologic follow-up. Cancer
2001;91(1):173–177.
26. Rintala AE, Svinhufvud UM. Effect of augmentation mammaplasty on
mammography and thermography. Plast Reconstr Surg 1974;54(4):390–
396.
27. Handel N, Silverstein MJ, Gamagami P, et al. Factors affecting
mammographic visualization of the breast after augmentation
mammaplasty. JAMA 1992;268(14):1913–1917.
28. Silverstein MJ, Handel N, Gamagami P, et al. Breast cancer in women
after augmentation mammoplasty. Arch Surg 1988;123(6):681–685.
29. Monsees BS, Destouet JM. Mammography in aesthetic and
reconstructive breast surgery. Perspect Plast Surg 1991;5:103–107.
30. Wolfe JN. On mammography in the presence of breast implants [Letter].
Plast Reconstr Surg 1978;62(2):286–288.
31. Gumucio CA, Pin P, Young VL, et al. The effect of breast implants on
the radiographic detection of microcalcification and soft-tissue masses.
Plast Reconstr Surg 1989;84(5):772–778; discussion 779–782.
32. Hayes H Jr, Vandergrift J, Diner WC. Mammography and breast
implants. Plast Reconstr Surg 1988;82(1):1–8.
33. Beisang AA, Geise RA, Ersek RA. Radiolucent prosthetic gel. Plast
Reconstr Surg 1991;87(5):885–892.
34. Handel N, Silverstein MJ, Gamagami P. The effect of silicone implants
on mammography and breast cancer detection. Perspect Plast Surg
1993;7:1–14.
35. Eklund GW, Busby RC, Miller SH, et al. Improved imaging of the
augmented breast. Am J Roentgenol 1988;151(3):469–473.
36. Leibman AJ, Kruse BD. Breast cancer: mammographic and sonographic
findings after augmentation mammoplasty. Radiology 1990;174(1):195–
198.
37. Leibman AJ, Kruse BD. Imaging of breast cancer after augmentation
mammoplasty. Ann Plast Surg 1993;30(2):111–115.
38. Silverstein MJ, Handel N, Gamagami P, et al. Mammographic
measurements before and after augmentation mammaplasty. Plast
Reconstr Surg 1990;86(6):1126–1130.
39. Silverstein MJ, Handel N, Gamagami P, et al. Breast cancer diagnosis
and prognosis in women following augmentation with silicone gel–filled
prostheses. Eur J Cancer 1992;28(2–3):635–640.
40. Fajardo LL, Harvey JA, McAleese KA, et al. Breast cancer diagnosis in
women with subglandular silicone gel filled augmentation implants.
Radiology 1995;194(3):859–862.
41. Handel N, Silverstein MJ. Breast cancer diagnosis and prognosis in
augmented women. Plast Reconstr Surg 2006;118(3):587–593;
discussion 594–596.
42. Pisano ED, Gatsonis C, Hendrick E, et al. Diagnostic performance of
digital versus film mammography for breast cancer screening—the
results of the American College of Radiology Imaging Network
(ACRIN) Digital Mammographic Imaging Screening Trial (DMIST). N
Engl J Med 2005;353(17):1773–1783.
43. Ahn CY, Shaw WW, Narayanan K, et al. Definitive diagnosis of breast
implant rupture using magnetic resonance imaging. Plast Reconstr Surg
1993;92(4):681–691.
44. Holmich LR, Fryzek JP, Kjoller K, et al. The diagnosis of silicone
breast-implant rupture: clinical findings compared with findings at
magnetic resonance imaging. Ann Plast Surg 2005;54(6):583–589.
45. Everson LI, Parantainen H, Detlie T, et al. Diagnosis of breast implant
rupture: imaging findings and relative efficacies of imaging techniques.
AJR Am J Roentgenol 1994;163(1):57–60.
46. Westerhof JP, Fischer U, Moritz JD, et al. MR imaging of
mammographically detected clustered microcalcifications: is there any
value? Radiology 1998;207(3):675–681.
47. Hickman PF, Moore NR, Shepstone BJ. The indeterminate breast mass:
assessment using contrast enhanced magnetic resonance imaging. Br J
Radiol 1994;67(793):14–20.
48. Silverstein MJ, Lagios MD, Recht A, et al. Image-detected breast
cancer: state of the art diagnosis and treatment. J Am Coll Surg
2005;201(4):586–597.
49. Handel N, Lewinsky B, Silverstein M, et al. Conservation therapy for
breast cancer following augmentation mammaplasty. Plast Reconstr
Surg 1991;87(5):873–878.
50. Azavedo E, Bone B. Imaging breasts with silicone implants. Eur Radiol
1999;9(2):349–355.
51. Shestak KC, Ganott MA, Harris KM, et al. Breast masses in the
augmentation mammaplasty patient: the role of ultrasound. Plast
Reconstr Surg 1993;92(2):209–216.
52. Peters W, Pugash R. Ultrasound analysis of 150 patients with silicone
gel breast implants. Ann Plast Surg 1993;31(1):7–9.
53. Piccoli CW. Imaging of the patient with silicone gel breast implants.
Magn Reson Imaging Clin N Am 2001;9(2):393–408, vii–viii.
54. Karanas YL, Leong DS, Da Lio A, et al. Surgical treatment of breast
cancer in previously augmented patients. Plast Reconstr Surg
2003;111(3):1078–1083; discussion 1084–1086.
55. Clark CP 3rd, Peters GN, O’Brien KM. Cancer in the augmented breast:
diagnosis and prognosis. Cancer 1993;72(7):2170–2174.
56. Friis S, McLaughlin JK, Mellemkjaer L, et al. Breast implants and
cancer risk in Denmark. Int J Cancer 1997;71(6):956–958.
57. Birdsell DC, Jenkins H, Berkel H. Breast cancer diagnosis and survival
in women with and without breast implants. Plast Reconstr Surg
1993;92(5):795–800.
58. Cahan AC, Ashikari R, Pressman P, et al. Breast cancer after breast
augmentation with silicone implants. Ann Surg Oncol 1995;2(2):121–
125.
59. Carlson GW, Curley SA, Martin JE, et al. The detection of breast cancer
after augmentation mammaplasty. Plast Reconstr Surg 1993;91(5):837–
840.
60. Deapen D, Hamilton A, Bernstein L, et al. Breast cancer stage at
diagnosis and survival among patients with prior breast implants. Plast
Reconstr Surg 2000;105(2):535–540.
61. Sosin M, Devulapalli C, Fehring C, et al. Breast cancer following
augmentation mammaplasty: a case-control study. Plast Reconstr Surg
2018;141(4):833–840.
62. Recht A, Harris JR. Selection of patients with early-stage breast cancer
for conservative surgery and radiation. Oncology 1990;4(2):23–30;
discussion 31–32.
63. Veronesi U, Saccozzi R, Del Vecchio M, et al. Comparing radical
mastectomy with quadrentectomy, axillary dissection, and radiotherapy
in patients with small cancers of the breast. N Engl J Med
1981;305(1):6–11.
64. Harris JR, Hellman S. Primary radiation therapy for early breast cancer.
Cancer 1983;51(12 suppl):2547–2552.
65. Montague ED, Ames FC, Schell SR, et al. Conservative surgery and
irradiation as an alternative to mastectomy in the treatment of clinically
favorable breast cancer. Cancer 1984;54(11 suppl):2668–2672.
66. Fisher B, Bauer M, Margolese R, et al. Five-year results of a
randomized clinical trial comparing total mastectomy and segmental
mastectomy with or without radiation in the treatment of breast cancer.
N Engl J Med 1985;312(11):665–673.
67. Calle R, Vilcoq JR, Zafrani B, et al. Local control and survival of breast
cancer treated by limited surgery followed by irradiation. Int J Radiat
Oncol Biol Phys 1986;12(6):873–878.
68. Fisher B, Redmond C, Poisson R, et al. Eight-year results of a
randomized clinical trial comparing total mastectomy and lumpectomy
with or without radiation in the treatment of breast cancer. N Engl J Med
1989;320(13):822–828.
69. Rose MA, Olivotto I, Cady B, et al. Conservative surgery and radiation
therapy for early breast cancer. Long-term cosmetic results. Arch Surg
1989;124(2):153–157.
70. Harris JR, Levene MB, Svensson G, et al. Analysis of cosmetic results
following primary radiation therapy for stage I and stage II carcinoma of
the breast. Int J Radiat Oncol Biol Phys 1979;5(2):257–261.
71. Clarke D, Martinez A, Cox RS. Analysis of cosmetic results and
complications in patients with stage I and state II breast cancer treated
by biopsy and irradiation. Int J Radiat Oncol Biol Phys
1983;9(12):1807–1813.
72. Rose MA, Olivotto I, Cady B, et al. Conservative surgery and radiation
therapy for early breast cancer: long term cosmetic results. Arch Surg
1989;124(2):153–157.
73. Berrino P, Campora E, Leone S, et al. Correction of type II breast
deformities following conservative cancer surgery. Plast Reconstr Surg
1992;90(5):846–853.
74. NIH Consensus Conference. Treatment of early stage breast cancer.
JAMA 1991;265(3):391–395.
75. Schain WS, Fetting JH. Modified radical mastectomy versus breast
conservation: psychosocial considerations. Semin Oncol
1992;19(3):239–243.
76. Ryu J, Yahalom J, Shank B, et al. Radiation therapy after breast
augmentation or reconstruction in early or recurrent breast cancer.
Cancer 1990;66(5):844–847.
77. McGinley PH, Powell WR, Bostwick J. Dosimetry of a silicone breast
prosthesis. Radiology 1980;135(1):223–224.
78. Krishnan L, Krishnan EC. Electron beam irradiation after reconstruction
with silicone gel implant in breast cancer. Am J Clin Oncol
1986;9(3):223–226.
79. Kuske RK, Schuster R, Klein E, et al. Radiotherapy and breast
reconstruction: clinical results and dosimetry. Int J Radiat Oncol Biol
Phys 1991;21(2):339–346.
80. Shedbalkar AR, Devata A, Padanilam T. A study of effects of radiation
on silicone prosthesis. Plast Reconstr Surg 1980;65(6):805–810.
81. Stabile RJ, Santoro E, Dispaltro F, et al. Reconstructive breast surgery
following mastectomy and adjunctive radiation therapy. Cancer
1980;45(11):2738–2743.
82. Der Hagopian RP, Zaworski RE, Sugarbaker EV, et al. Management of
locally recurrent breast cancer adjacent to prosthetic implants. Am J
Surg 1981;141(5):590–592.
83. Jacobson GM, Sause WT, Thompson JW, et al. Breast irradiation
following silicone gel implants. Int J Radiat Oncol Biol Phys
1986;12(5):835–838.
84. Halpern J, McNeese MD, Kroll SS, et al. Irradiation of prosthetically
augmented breasts: a retrospective study on toxicity and cosmetic
results. Int J Radiat Oncol Biol Phys 1990;18(1):189–191.
85. Handel N, Lewinsky B, Jensen JA, et al. Breast conservation therapy
after augmentation mammaplasty: is it appropriate? Plast Reconstr Surg
1996;98(7):1216–1224.
CHAPTER 16

Guidelines and Patient Selection


Criteria for Nipple and Skin-Sparing
Mastectomy
COSTANZA COCILOVO | MAURICE Y. NAHABEDIAN
HISTORY
Over the past few years, nipple-sparing mastectomy (NSM) has been
increasing performed and requested by more and more patients. At present,
most major breast centers are performing NSM with favorable outcomes in
the vast majority of patients. Initial questions regarding safety and efficacy
have been answered; however, the present focus is centered around the
evolving guidelines for NSM based on tumor characteristics as well as breast
volume and dimensions.
The Halsted radical mastectomy was first performed in 1894. In the 1960s,
Patey described the modified radical mastectomy (MSM) that achieved
comparable local recurrence risk. In 1991 as plastic surgeons began
performing immediate breast reconstruction, skin-sparing mastectomy (SSM)
became the standard. SSM had the same recurrence risk as MSM (1). Early
clinical trials performed in the 1990s demonstrated that the nipple areolar
complex (NAC) was involved in 5% to 12% of cases, a relatively low
number (2). However, at the time, the technique did not achieve wide
acceptance because of the concerns regarding oncologic safety. It was 2002
before Veronese published his 20-year data demonstrating that breast
conservation with NAC preservation was oncologically equivalent to
mastectomy (3).
INDICATIONS
As NSM has increased in incidence and popularity, a variety of studies have
clarified the indications and risks associated with NSM. Morimoto reported a
direct relationship between nipple involvement, tumor diameter, and distance
to the tumor. Forty-one percent of T2 tumors and 78% of tumors greater than
5 cm had nipple involvement (4). Luttges found that tumors within 1 to 2 cm
of the nipple had a 36% incidence of nipple involvement versus 13% if the
distance is between 2 and 3 cm (5). Nipple involvement was 19.4% when
tumor was less than 4 cm away and 3.7% when it was greater than 4 cm (6).
In 2006, Sacchini et al. reported that NSM may be considered for tumors less
than 2.5 cm, greater than 4 cm from the nipple with negative axilla, and no
lymphovascular invasion or extracapsular extension (7).
In the setting of NSM, the terminal duct units are left behind in the NAC
and are not associated with breast size or obesity. Interestingly, the highest
recurrence rates are found in younger-age women and lactating women but
the retroareolar region was still not a common area for recurrence. Studies
have demonstrated that the lateral quadrant and axillary tail are more
common areas of recurrence compared to the NAC (8). In 2012 Murthy and
Chamberlain summarized 10 series of NSM ranging in number from 42 to
579 mastectomies which showed a nipple recurrence risk of 0% to 1.6% (9).
CONTRAINDICATIONS
Absolute contraindications to NSM include evidence of NAC involvement,
locally advanced breast cancer with skin involvement, and inflammatory
breast cancer and bloody nipple discharge (10). Things to consider but are no
longer exclusion criteria when determining if a patient is a candidate for
NSM include tumor size, tumor-to-nipple distance, positive nodes, prior chest
wall radiation, smoking, diabetes, and obesity. All of these are no longer
considered an absolute exclusion criterion. Other potential contraindications
include significant ptosis and potentially stretch marks on the skin. Coopey et
al. reported feeling comfortable with a majority of women undergoing
mastectomy because of the low local recurrence risk of 2.6% with 2-year
follow-up and no recurrence in the nipple. They report that any tumor size
and any distance to the nipple are safe as long as the margin is clear (10).
Schneider et al. reported a favorable experience with a subset of 19 patients
with large ptotic breasts (11).
PREOPERATIVE PLANNING
The physical examination is a critical component in determining candidacy
for NSM. Optimal preoperative planning is based on the tumor location and
size as well as breast volume, degree of ptosis, and likelihood of maintaining
viability of the NAC. In general, ideal candidates for NSM include women
with mild-to-moderate breast volume in which the bra cup size ranges from A
to C. In women with mammary hypertrophy or grade 3 ptosis, NSM may be
fraught with complications such as delayed healing, partial necrosis or total
necrosis. In these patients, a premastectomy procedure such as a reduction
mammaplasty or mastopexy can be considered as initially described by Spear
(12). In this scenario, a partial mastectomy and oncoplastic reduction
mammaplasty is performed followed 1 to 3 months by the NSM.
When considering NSM, it is important to assess prior breast surgery,
location of scars, and prior history of radiation therapy. In general, prior
breast operations do not preclude NSM, unless the incisions are extensive and
have violated the perfusion to the NAC. Prior radiation therapy and a history
of smoking will potentially compromise the circulation to the NAC following
the mastectomy and may increase the likelihood of necrosis.
OPERATIVE TECHNIQUE

Patient Selection
The operative technique of NSM will vary from surgeon to surgeon;
however, there are technical details that will be common to all. The choice of
incision will be based on surgeon and patient preference but also upon tumor
location. In general, the majority of NSMs are preformed through an
inframammary incision but can also be performed through a vertical incision
extending from the inferior areolar edge to the inframammary fold (IMF), a
lateral incision from the lateral areolar edge to the anterior axillary line, as
well as a supra-areolar incision either at or slightly above the areolar edge.
Figures 16-1 to 16-3 illustrate a woman following NSM through an
inframammary incision.
Tumors that are located laterally or superolaterally are typically
approached through a lateral incision. Another advantage of this incision is in
the unfortunate event that the NAC has to be removed due to positive
margins. In this case, the lateral incision is extended around the NAC in an
elliptical fashion. In the event of a positive NAC margin following the IMF
approach for the NSM, excision of the NAC is usually performed vertically,
thus creating an inverted T incision. Figures 16-4 to 16-6 illustrate a woman
following NSM and postoperative radiation.
FIGURE 16-1 Preoperative photograph of a woman with right breast cancer
scheduled for unilateral nipple-sparing mastectomy through an inframammary
incision.
FIGURE 16-2 Intraoperative photograph demonstrating the inframammary
approach with a prepectoral prosthetic device.
FIGURE 16-3 Postoperative photograph following excellent volume and contour
symmetry with nipple viability.
FIGURE 16-4 Preoperative photograph of a woman with right breast cancer
scheduled for bilateral nipple-sparing mastectomy via an inframammary approach.
She is scheduled to have bilateral prepectoral prosthetic reconstruction and
postoperative radiation therapy.

The decision making for NSM is more complex in the setting of mammary
hypertrophy or severe breast ptosis. In these patients in whom the risk of
nipple areolar necrosis is high, alternative strategies can be considered and
discussed preoperatively. They include performing a mastopexy or
oncoplastic reduction mammaplasty prior to NSM, preserving the NAC on a
de-epithelized inferior dermal mastectomy skin flap, and free nipple graft.
The preoperative discussion points will be elaborated upon.
FIGURE 16-5 Postoperative image 1 month following right radiation therapy.
FIGURE 16-6 Postoperative image 1 year following right radiation therapy.

NSM and Oncoplastic Reduction Mammaplasty


In patients with mammary hypertrophy who would under normal
circumstances be good candidates for reduction mammaplasty who desire
mastectomy and preservation of the NAC, an oncoplastic approach can be
considered in cancer patients and a reduction mammaplasty or mastopexy can
be considered in gene-positive patients. In cancer patients, a partial
mastectomy is performed followed by internal tissue rearrangement to create
a natural breast shape and contour. In gene-positive patients, a mastopexy or
standard reduction mammaplasty is performed. It is advised to minimize
disruption to the periareolar subdermal plexus to maintain perfusion of the
NAC. Spear has demonstrated success using this approach with a 96%
success rate based on viability of the NAC following NSM (12). It is
important to explain to patients that this is a staged approach to mastectomy
with the NSM being performed 1 to 3 months following the oncoplastic
reduction in cancer patients and the standard reduction mammaplasty in
BRCA(+) patients.

NSM and De-Epithelized Inferior Dermal Mastectomy Flap


In patients with moderate mammary hypertrophy who prefer NSM, the
preservation of the NAC on a de-epithelized inferior dermal flap is possible.
This requires that the mastectomy be performed using an inverted T
mastectomy approach. Patients must be counseled preoperatively regarding
the risks and benefits. The vascularity must be assessed intraoperatively using
perfusion imaging and requires good inflow and outflow of blood. If the
vascularity is not sufficient, the distal inferior dermal flap is excised
including the NAC. Figures 16-7 to 16-11 illustrate a woman following
NSM on a de-epithelized inferior dermal flap.
FIGURE 16-7 Preoperative photograph of a patient with mammary hypertrophy
and left breast cancer who is interested in nipple-sparing mastectomy.
OUTCOMES
In a recent systematic review of NSM, De La Cruz et al. reviewed 851
articles of which 20 studies with 5,594 patients met selection criteria. They
found five studies with a 9.6% risk difference between NSM and modified
radical or SSM. Eight studies found a 0.4% difference between NSM and
MRM/SSM. All were in favor of NSM in terms of overall survival, disease-
free survival, and local recurrence. The authors found high rates of overall
and disease-free survival and low rates of recurrence following NSM.
Although the women in the nipple-sparing group were younger, there did not
appear to be difference in treatments (13).

FIGURE 16-8 Preoperative markings of the inverted T pattern. The nipple areolar
complex will be preserved on an inferior pedicle.
FIGURE 16-9 Intraoperative photograph following the mastectomy with
preservation of the nipple areolar complex on a de-epithelized inferior dermal
pedicle.
FIGURE 16-10 Intraoperative fluorescent angiography demonstrating good arterial
inflow and venous outflow to the nipple areolar complex.
FIGURE 16-11 Postoperative photograph following bilateral nipple-sparing
mastectomy and prosthetic reconstruction.

Interestingly studies using the Breast Q and BIS have not demonstrated a
difference in patient satisfaction or body image following NSM. Both patient
satisfaction tools reported decreased sensitivity (14). A 12-year Italian
retrospective study of 1,647 patients was performed that excluded patients
over 65 years of age, BMI greater than 30 kg/m2, and positive intraoperative
frozen section from under the nipple. The mean age of all patients was 46 and
the mean BMI was 27 kg/m2. Comorbidities included tobacco use in 19.7%,
diabetes mellitus in 7.8%, and hypertension in 27.8%. Periareolar incision
was the most commonly used. The study demonstrated a recurrence risk of
1.3%. The authors found that inframammary incisions enabled the best
contouring. Breast ptosis is a contraindication (15).
Similarly, recent reports from the Mayo Clinic have reported that the
incidence of patients requesting and having NSM has increased. Their criteria
include cancers 2 cm or smaller located more than 2 cm from the nipple.
Contraindications include inflammatory breast cancer and extension of cancer
to the nipple. Relative contraindications involve patients with high body mass
index, large and or ptotic breasts, prior radiation, or prior breast surgery such
as reduction or augmentation; although they have become less stringent on
this latter criterion. They do not routinely perform MRI on every patient. In
their experience they found that placement of the incision away from the
areola lowered nipple necrosis rates (16). Figures 16-12 and 16-13 illustrate
a woman following NSM and deep inferior epigastric perforator (DIEP) flap
reconstruction.

FIGURE 16-12 Preoperative photograph of a BRCA-positive patient scheduled for


bilateral nipple-sparing mastectomy through a lateral areolar approach.
FIGURE 16-13 Postoperative photograph following bilateral nipple-sparing
mastectomy and DIEP flap reconstruction.

A more recent series from Washington University reviewed their


experience from 2008 to 2014. Seventy-three NSMs were performed for
cancer and 124 were performed prophylactically. A total of 34 (17.2%)
complications occurred and included infection, hematoma, and nipple
necrosis, with 9 patients requiring removal of the NAC and 13 requiring
removal of the tissue expander or implant. Active tobacco use was associated
with a 36.0% (9/25) complication rate, compared with 14.5% (25/172) in
patients who denied tobacco use (<0.05). During follow-up, one recurrence
was noted, located on the chest wall. There were no recurrences in the NAC
group. The study conclusions were that NSM may safely be performed
without compromising oncologic outcomes or increasing complication rates
(17).
Endara and Chen reviewed 48 studies yielding 6,615 nipple-sparing
mastectomies for analysis. The overall pooled complication rate was 22%, the
nipple necrosis rate was 7%, the locoregional recurrence rate was 1.8%, and
the distant metastasis rate was 2.2% (18). These are comparable rates to skin
sparing (19). Ischemia is a more common complication than nipple
recurrence. Nahabedian et al. found that the hyperbaric chamber could help
with postoperative nipple ischemia and produced twice the healing rate but
was not statistically significant (20). Wengler et al. showed that immediate
reconstruction after neoadjuvant chemotherapy is safe. Thirty-day
complication rate was low at 13.2% and associated with increased BMI and
smoking history (20). The highest complications rates were in patients that
had additional chemotherapy after surgery. This had a NAC necrosis rate of
42.9% (21).
Colwell and Christensen looked at going direct-to-implant with NSM (23).
In their series they placed the implant under the muscle and held it in place
with acellular dermal matrix. The complication rate in direct-to-implant
reconstruction was similar to two-stage reconstruction with an infection rate
of 3% and explantation rate of 1.5%. Other series reported higher skin flap
necrosis with direct to implant. The revision rate at 20.3% was also
comparable to two-stage technique when you include fat grafting,
malposition, capsular contraction, and change in size (22). Figures 16-14 to
16-16 illustrate a patient having preoperative reduction mammaplasty
followed by NSM demonstrating mild desquamation of the NAC.
FIGURE 16-14 Preoperative photograph of a woman with right breast cancer who
had an initial partial mastectomy and oncoplastic reduction who is interested in
nipple-sparing mastectomy.
FIGURE 16-15 Early postoperative photograph following bilateral nipple-sparing
mastectomy and prosthetic reconstruction demonstrating superficial desquamation
of the right nipple areolar complex.
FIGURE 16-16 Late postoperative photograph demonstrating viability of the nipple
areolar complex bilaterally.

NSM and radiation therapy has been closely evaluated. Reish et al.
reported a nipple retention rate of 90% in previously radiated patients
(23,24). Spear et al. reviewed 18 patients that had NSM following breast
conservation (72%) or before postmastectomy radiation (28%) (25). A high-
riding NAC was noted in 55.6% of patients. Capsular contracture occurred
more often in patients who had postmastectomy radiation compared to patient
that had prior breast conservation (40% vs. 7.8%). The most common
revisions included correction of malposition (27.8%), capsular contracture
(16.7%), and high-riding nipple (22.4%). The authors concluded that NSM
should be approached with caution in the setting of radiation therapy. Sbitany
et al. reviewed 63 breasts with a prior history of radiation therapy before
NSM (26). The authors demonstrated that any radiation resulted in an
increase rate of infection (21.6%) and an increased rate of device loss
(18.75%). A higher incidence of wound breakdown was also noted in the
radiated patients (p = 0.012).
CONCLUSIONS
The criteria for nipple sparing have evolved such that nipple involvement and
inflammatory breast cancer are the only absolute contraindications. Our
practice includes obtaining an MRI on patients less than 70 years to assist
with clarification as to whether or not the tumor extends toward the nipple.
Intraoperatively, a soft tissue button from under the nipple is sent to
pathology for permanent analysis rather than frozen section analysis. If a
nipple margin is found to be positive on final pathology, the NAC is usually
excised at a second stage that correlates with the exchange of the tissue
expander to implant or independently if the reconstruction was performed
using autologous tissue or a direct-to-implant approach. Fluorescence
imaging technology is frequently used to assist with real-time visualization of
perfusion. In women with ptotic breasts who desire NSM an oncoplastic
reduction can be performed with removal of the tumor at the first stage,
followed 1 to 3 months later with a NSM. Another possibility is to use a
nipple-delay technique in which the lower two-thirds of the breast is
undermined 2 to 4 weeks prior to the NSM.

REFERENCES

1. Agha R, Wellstead G, Sagoo H, et al. Nipple sparing versus skin sparing


mastectomy: a systemic review protocol. BMJ Open 2016;6:e010151.
2. Hinton CP, Doyle PJ, Blamey RW, et al. Subcutaneous mastectomy for
primary operable breast cancer. Br J Surg 1984;71:469–472.
3. Veronesi U, Cascinelli N, Mariani L, et al. Twenty year follow up of a
randomized study comparing breast conserving surgery with radical
mastectomy for early breast cancer. N Engl J Med 2002;347:1227–1232.
4. Morimoto T, Komaki K, Inui K, et al. Involvement of nipple and areola
in early breast cancer. Cancer 1985;55:2459–2463.
5. Luttges J, Kalbfleisch, Prinz P. Nipple involvement and multicentricity
in breast cancer. A study on whole organ sections. J Cancer Res Clin
Oncol 1987;113:481–487.
6. Vlajcic Z, Zic R, Stanec S, et al. Nipple areola complex preservation:
predictive factors of neoplastic nipple areola complex invasion. Ann
Plast Surg 2005;55:240–244.
7. Sacchini V, Pinotti JA, Barros AC, et al. Nipple sparing mastectomy for
breast cancer and risk reduction oncologic or technical problem? J Am
Coll Surg 2006;203:704–714.
8. Van Verschuer VMT, van Deurzen CHM, Westenend PJ, et al.
Prophylactic nipple-sparing mastectomy leaves more terminal duct
lobular units in situ as compared with skin sparing mastectomy. Am J
Surg Pathol 2014;38(5):706–712.
9. Murthy V, Chamberlain RS. Defining a place for nipple sparing
mastectomy in modern breast care: an evidence-based review. Breast J
2013;19(6):571–581.
10. Coopey SB, Tang R, Lei L, et al. Increasing eligibility for nipple sparing
mastectomy. Ann Surg Oncol 2013;20:3218–3222.
11. Schneider LF, Chen CM, Stolier AJ, et al. Nipple sparing mastectomy
and immediate free flap reconstruction in the large ptotic breast. Ann
Plast Surg 2012;69:425–428.
12. Spear SL, Rottman SJ, Seiboth LA, et al. Breast reconstruction using a
staged nipple-sparing mastectomy following mastopexy or reduction.
Plast Reconstr Surg 2012;129(3):572–581.
13. Spear SL, Rottman SJ, Seiboth LA, et al. Breast reconstruction using a
staged nipple-sparing mastectomy following mastopexy or reduction.
Plast Reconstr Surg 2012;129:572.
14. De La Cruz L, Moody A, Tappy EE, et al. Overall survival, disease-free
survival, local recurrence and nipple areolar recurrence in the setting if
nipple sparing mastectomy: a metaanalysis and systemic review. Ann
Surg Oncol 2015;22(10):3241–3249.
15. Van Verschuer VTM, Mureau MAM, Gopie JP, et al. Patient
satisfaction and nipple areola sensitivity after bilateral prophylactic
mastectomy and immediate implant breast reconstruction in high breast
cancer risk population. Ann Plast Surg 2016;77(2):145–152.
16. De Vita R, Zoccali G, Buccheri EM, et al. Outcome evaluation after
2023 nipple sparing mastectomies: our experience. Plast Reconstr Surg
2017;139(2);335e–347e.
17. Krajewski AC, Boughey JC, Degnim AC, et al. Expanded indications
and improved outcomes for nipple-sparing mastectomy over time. Ann
Surg Oncol 2015;22:3317–3323.
18. Endara M, Chen D, Verma K, et al. Breast reconstruction following
nipple-sparing mastectomy: a systematic review of the literature with
pooled analysis. Plast Reconstr Surg 2013;132(5):1043–1054.
19. Dull B, Conant L, Myckatyn T, et al. Nipple-sparing mastectomies:
clinical outcomes from a single academic institution. Mol Clin Oncol
2017;6(5):737–742.
20. Shuck J, O’Kelly N, Endara M, et al. A critical look at the effect of
hyperbaric oxygen on the ischemic nipple following nipple sparing
mastectomy and implant based reconstruction: a case series. Gland Surg
2017;6(6):659–665.
21. Wengler CA, Valente SA, Al-Hilli Z, et al. Determinants of short and
long term outcomes in patients undergoing immediate breast
reconstruction following neoadjuvant chemotherapy. J Surg Oncol
2017;116;797–802.
22. Frey JD, Choi M, Karp NS. The effect of neoadjuvant chemotherapy
compared to adjuvant chemotherapy in healing after nipple sparing
mastectomy. Plast Reconstr Surg 2017;139:10e–19e.
23. Colwell AS, Christensen JM. Nipple sparing mastectomy and direct to
implant breast reconstruction. Plast Reconstr Surg 2017;140:44S–50S.
24. Reish RG, Lin A, Phillips NA, et al. Breast reconstruction outcomes
after nipple sparing mastectomy and radiation therapy. Plast Reconstr
Surg 2015;135:959–966.
25. Spear SL, Shuck J, Hannan L, et al. Evaluating long-term outcomes
following nipple-sparing mastectomy and reconstruction in the
irradiated breast. Plast Reconstr Surg 2014;133(5):605–614.
26. Sbitany H, Wang F, Peled AW, et al. Immediate implant-based breast
reconstruction following total skin-sparing mastectomy: defining the
risk of preoperative and postoperative radiation therapy for surgical
outcomes. Plast Reconstr Surg 2014;134:396–404.
CHAPTER 17

Invasive Carcinoma: Radiation


Therapy After Mastectomy
LAURA E. G. WARREN
HISTORY
Of the 270,000 women diagnosed with breast cancer in 2019 (1), many of
them underwent mastectomy due to patient or tumor characteristics or patient
preference. Unlike for women who undergo breast-conserving surgery, where
adjuvant radiation therapy (RT) is standard of care as a means by which to
reduce locoregional recurrence (LRR), the recommendation for
postmastectomy RT (PMRT) is based on patient characteristics and
pathologic findings at the time of mastectomy. At the time of mastectomy for
invasive breast cancer, patients also undergo axillary lymph node evaluation,
either by sentinel lymph node biopsy (SLNB) or axillary lymph node
dissection (ALND). The approach to axillary lymph node sampling and
number of involved axillary lymph nodes have implications on the decision
to recommend PMRT and the radiation fields to treat. For women who have
undergone breast reconstruction, the recommendation for PMRT has
implications in terms of short- and long-term side effects, specifically the risk
of reconstruction complications and patient satisfaction with cosmetic results.
This chapter will focus on the efficacy of PMRT, patient and tumor
characteristics guiding the recommendation for PMRT, radiation techniques,
and potential side effects, with specific attention paid to patients who have
undergone reconstruction.
ORIGINAL TRIALS SUPPORTING USE OF POSTMASTECTOMY RADIATION
THERAPY
Multiple older randomized trials compared mastectomy alone to mastectomy
with adjuvant RT. PMRT consistently reduced the risk of LRR but in early
trials there was no demonstrated benefit with regard to overall survival. An
early meta-analysis, first published in 1987 and updated in 1994, examined
7,941 patients treated across 10 trials and showed a 7% decrement in overall
survival when comparing patients who did and did not receive PMRT;
however this difference was nonsignificant (2,3). It appeared that patients
who received PMRT had an excess of cardiac mortality compared to patients
not receiving PMRT. Interestingly, the meta-analysis showed that for patients
receiving RT on trials with a later start date did significantly better than those
patients on older trials, likely reflecting improvements in more modern
radiation planning and delivery and resultant decrease in cardiac toxicity.
Given these findings, there was significant concern about the relative value
of PMRT, particularly in the context of data showing that systemic therapy
not only reduced the risk of distant recurrence but also significantly
decreased local recurrence (4). As a result, multiple studies examined
whether or not there was a benefit of adjuvant RT for patients receiving
chemotherapy. Two notable trials were conducted by the Danish Breast
Cancer Cooperative Group. In the 82b trial, a total of 1,708 high-risk
premenopausal women with breast cancer who had undergone mastectomy
randomly were assigned to receive cyclophosphamide, methotrexate, and
fluorouracil chemotherapy with or without PMRT to the chest wall and
regional lymph nodes (5). Patients were defined as high risk in this trial if
they had pathologically involved lymph nodes, primary tumors greater than 5
cm in size, or invasion of the skin or pectoralis fascia. Patients receiving
PMRT had a significantly lower risk of locoregional recurrence, either in
isolation or with synchronous distant disease, than those who did not receive
radiotherapy. Similarly, PMRT resulted in improved disease-free survival
and overall survival at 10 years. Protocol 82c was a complementary trial
examining outcomes in high-risk postmenopausal patients with breast cancer
(6). Patients were deemed high risk by the same criteria as those in 82b and
were randomized to either adjuvant tamoxifen alone or adjuvant tamoxifen
and PMRT. RT again was found to significantly decrease the risk of
locoregional recurrence and improve disease-free survival and overall
survival. A similar trial examining the role for PMRT in premenopausal
patients with lymph node–positive breast cancer was conducted in British
Columbia around the same time (7). At a median follow-up of 249 months,
the addition of RT to chemotherapy was associated with significant
improvement in all endpoints examined including decreased 20-year risk of
isolated LRR (26% to 10%), improved breast cancer–specific survival (28%
to 53% at 20 years), and improved overall survival (37% to 47% at 20 years).
When the investigators stratified patients by number of involved lymph
nodes, patients with one to three positive lymph nodes and those with four or
more positive lymph nodes benefited from adjuvant RT; there was an overall
survival benefit also demonstrated for both subgroups.
Together these trials demonstrated that there was a role for PMRT in
selected patients deemed high risk by study investigators although by slightly
different criteria. They also demonstrated a relationship between a reduction
in local recurrence and improved overall outcomes, likely because of
persistent or recurrent locoregional disease acting as a source of distant
metastases, which subsequently impacted survival. However, there have been
several criticisms of these trials. One criticism is regarding the adequacy of
systemic therapy; some feel that the chemotherapy given to patients in these
trials was not as efficacious as moderate chemotherapy and that patients
received too short a tamoxifen treatment course. Another criticism is
regarding the adequacy of surgical treatment in the Danish studies given that
only a mean of seven lymph nodes were recovered during ALND.
Additionally, the LRR rate was felt to be higher than anticipated in the
patients who did not receive PMRT. A subsequent analysis intended to
address this criticism retrospectively analyzed outcomes for patients with
eight or more lymph nodes removed (8). For the 1,152 patients who met this
criterion, the overall 15-year survival rate was improved with adjuvant
PMRT from 29% to 39% (p = 0.015). A stratified subgroup analysis of
patients with one to three and those with four or more positive lymph nodes
was performed and showed that LRR was significantly decreased and overall
survival was improved with PMRT for both subgroups.
Based on these trials and others, in 2000 the National Institutes of Health
published a consensus statement regarding adjuvant therapy for breast cancer
(9). In regard to PMRT, they expressed a need to balance the potential
benefits in terms of locoregional control and overall survival with the
potential side effects of treatment, particularly the previously documented
excess of non—breast cancer deaths. Although they acknowledged that these
deaths were likely related to outdated radiation techniques contributing to
high doses received by the heart and great vessels, they felt PMRT should
only be recommended for women with high-risk disease, which they defined
as having four or more positive lymph nodes or an advanced primary tumor.
They felt the role for PMRT in women with one to three positive lymph
nodes remained uncertain. PMRT for patients with one to three positive
lymph nodes was the subject of a randomized trial run by the Southwest
Oncology Group (SWOG), trial s9927. Patients with pathologically staged
T1–2, N1 tumors with one to three positive axillary lymph nodes who had
undergone modified radical mastectomy and axillary dissection with a
minimum of 10 lymph nodes recovered were randomized to PMRT or no
PMRT. The targeted accrual for the trial was 2,500 patients; unfortunately, it
closed after fewer than 100 patients enrolled and no conclusions could be
drawn.
In 2005 the Early Breast Cancer Trialists’ Collaborative Group (EBCTCG)
published a meta-analysis examining outcomes for women with early-stage
breast cancer enrolled on randomized trials in the 1960s–1980s (10). For
8,500 women with lymph node–positive breast cancer treated with
mastectomy and axillary clearance, PMRT improved local recurrence at 5
years from 23% to 6% (absolute reduction of 17%) and 15-year breast cancer
mortality from 60.1% to 54.7% (absolute reduction 5.4%, p = 0.0002). This
proportional reduction in local recurrence was seen across multiple subgroups
analyzed. An overall mortality benefit was also demonstrated with a 4.4%
absolute improvement at 15 years, with radiotherapy decreasing the risk from
64.2% to 59.8%. In contrast, for women with lymph node–negative disease,
the 5-year local recurrence risk was only 6% in the absence of radiotherapy.
PMRT reduced this risk to 2% (absolute benefit 4%) and there was no
significant reduction seen in 15-year breast cancer mortality.
This meta-analysis was updated in 2014 at a median follow-up of 10 years
(11). It showed that for women with lymph node–negative disease there was
no significant improvement in LRR, any first recurrence, or breast cancer
mortality. In comparison, for women with one to three positive lymph nodes,
PMRT improved 10-year isolated locoregional recurrence (20.3% to 3.8%; p
< 0.00001) and 20-year breast cancer mortality (50.2% to 42.3%; p = 0.01).
PMRT showed similar benefits for women with four more positive lymph
nodes (10-year isolated locoregional recurrence: 32.1% to 13.0%; p <
0.00001; 20-year breast cancer mortality: 80.0% to 70.7%; p = 0.04).
Although these data were significant and inform modern practice, the LRR
rates in this analysis were higher than more recently published trials and
likely the absolute benefit of PMRT is smaller in the modern era. The results
of several more modern trials examining locoregional failure rates in the
absence of PMRT are presented in Table 17-1.
Some radiation oncologists feel that not all patients with one to three
positive lymph nodes benefit from PMRT. In particular, the absolute number
of lymph nodes involved seems to be predictive of local recurrence. A
number of studies examined the impact of having only one positive lymph
node versus two or three positive lymph nodes and found that the risk of LRR
is significantly higher for those with two or three positive lymph nodes
(16,17). Therefore, in addition to the number of lymph nodes involved with
metastatic carcinoma, other risk factors are considered when deciding
whether or not to offer PMRT for patients with one to three positive lymph
nodes. Additional factors that predict for LRR include age, tumor size, grade,
presence of lymphovascular invasion (LVI), margin status, tumor subtype,
and response to neoadjuvant therapy. Younger patients (14,18–20), those
with larger tumors (21), higher-grade tumors (19,22,23), and with evidence
of LVI (14,20,23) are at higher risk of LRR. Tumor subtype is another
predictive variable for LRR. Retrospective evaluation of estrogen receptor
(ER), progesterone receptor (PR), and human epidermal growth factor
receptor 2 (HER-2) status of patients on the Danish Breast Cancer
Cooperative Group Trials 82b and 82c showed that on multivariable analysis,
patients with ER−/PR−/HER-2− tumors and those with ER-/PR-/HER-2+
tumors were most likely to have a LRR (24). Interestingly, in this analysis,
there was only a survival benefit with PMRT for patients with ER+, PR+, or
HER-2− tumors; a survival benefit was not seen among ER−, PR−, or
HER2+ patients.

TABLE 17-1 Locoregional Recurrence After Mastectomy in Patients With


pT1–2 Breast Cancer and 1–3 Positive Lymph Nodes (pN1) Treated With
Systemic Therapy
Trial Dates of Accrual Follow-Up (Mo) Locoregional
Recurrence Rate
(%)
CALGB 9344 1994–1997 67 8
(12)
EIO Milan (13) 1997–2001 120 10
MDACC (14) 2000–2007 84 7
Tianjin Medical 2001–2005 86 11
University (15)
CALGB, Cancer and leukemia group B; EIO, European Institute of Oncology; MDACC, MD Anderson
Cancer Center.

In an effort to again evaluate the benefit of PMRT in patients with one to


three positive lymph nodes, a United Kingdom Medical Research Council
trial, the Selective Use of Postoperative Radiotherapy aftEr Mastectomy
(SUPREMO), was initiated. It enrolled patients undergoing mastectomy with
pT1-2N1 disease, pT3N0 disease, or pT2N0 disease with grade III histology
and/or LVI. All patients had to have undergone axillary node clearance
(minimum 10 lymph nodes removed if lymph node positive; minimum of 4
nodes removed if lymph node negative). Patients were randomized to receive
PMRT or no PMRT. The study has completed accrual. Quality-of-life (QOL)
results at 2 years have been published (25). Patients receiving PMRT had
significantly more local symptoms but the difference between groups was
small. There were no other differences in other 2-year QOL scores. Results
regarding the primary outcome of the trial, overall survival, have not yet been
published.
Other attempts have been made to try to identify those patients at highest
risk of LRR and therefore perhaps most likely to benefit from PMRT. The
21-gene recurrence score (RS), as provided by the Oncotype DX assay
developed by Genomic Health, Inc., has been widely adopted to try to help
understand a patient’s individual benefit from chemotherapy. For patients
with ER+ cancers, the question is whether the RS can also predict
locoregional outcomes. Two retrospective analyses, one of patients enrolled
on National Surgical Adjuvant Breast and Bowel Project (NSABP) B-28 (26)
and the other of patients on NSABP B-14 and B-20 (27) have examined the
role of the RS in potentially helping to guide local therapy recommendations.
Patients enrolled on NSABP B-28 had resected, node-positive breast cancer
and the trial compared two different chemotherapy regimens. Patients who
underwent mastectomy did not receive RT. In an analysis of 1,065 patients
with lymph node–positive disease, the RS significantly predicted LRR, with a
10-year cumulative incidence of LRR of 3.3%, 7.2%, 12.2% for patients with
low (<18), intermediate (18 to 30), and high (≥31) RSs, respectively (p <
0.001) (28). On multivariable analysis, RS remained an independent predictor
of LRR as did tumor size and pathologic nodal status for four or more versus
one to three positive lymph nodes.
Patients on NSABP B-14 had lymph node–negative disease and were
randomized to tamoxifen versus placebo. Patients on NSABP B-20 had
lymph node–negative breast cancer and were randomized to tamoxifen-alone
or tamoxifen plus chemotherapy. Patients from these two trials were grouped
together and the predictive value of the RS on LRR was examined (27). For
patients treated with tamoxifen, the RS was predictive, with LRR rates at 10
years of 4%, 7.2%, and 15.8% for those with low, intermediate and high RS,
respectively. Similar findings were seen in patients treated with placebo and
those treated with chemotherapy plus tamoxifen. Taken together, these data
suggest that the RS may be beneficial in helping to determine who might
benefit from PMRT.
To further understand the prognostic impact of the RS on locoregional
outcomes, a prospective, randomized trial run by the Canadian Clinical Trials
Group (CCTC) TailorRT (MA.39) (clinicaltrials.gov Identifier:
NCT03488693) is currently enrolling patients with a RS of less than 18, a
pathologic T1 or T2 tumor, and pN1 nodal involvement. Eligible patients can
have one to three positive axillary lymph nodes (macrometastases) if treated
with ALND, one to two positive axillary lymph nodes if treated with breast-
conserving surgery and SLNB alone, and one positive lymph node if treated
with mastectomy and SLNB alone. Patients undergoing lumpectomy are
randomized to whole breast RT with or without regional lymph node RT.
Patients undergoing mastectomy are randomized to PMRT or no PMRT. The
primary outcome is breast cancer recurrence-free survival. The study is
currently anticipated to be completed in 2027.
For patients with a higher lymph node burden, the definition of which is
variable but most often defined as having four or more positive lymph nodes,
PMRT is routinely recommended given the high risk of LRR seen in this
patient population. For patients with one to three positive lymph nodes, a
variety of risk factors are considered as described above when considering
whether or not to offer PMRT. In 2016, the American Society of Clinical
Oncology (ASCO), American Society for Radiation Oncology (ASTRO), and
Society of Surgical Oncology (SSO) published a focused guideline update on
Postmastectomy Radiation (29). They stated that “the available evidence
shows that PMRT reduces the risk of locoregional failure, any recurrence,
and breast cancer mortality for patients with T1–2 breast cancer and one to
three positive lymph nodes. However, some subsets of these patients are
likely to have such a low risk of locoregional failure that the absolute benefit
of PMRT is outweighed by its potential toxicities. Thus, the decision to
recommend PMRT or not requires a great deal of clinical judgement.”
POSTMASTECTOMY RADIATION THERAPY IN SELECT NODE-NEGATIVE
POPULATIONS
As described above, in the EBCTCG meta-analysis there was no significant
improvement in LRR, any first recurrence, or breast cancer mortality with the
use of PMRT in patients without pathologic axillary lymph node
involvement. However, several investigators have wondered if patients with
risk factors for LRR, even in the absence of axillary lymph node metastases,
would benefit from PMRT. One such study retrospectively examined nearly
9,000 lymph node–negative patients enrolled in five NSABP studies (30).
The analysis specifically examined patients with tumors 5 cm or larger. At a
median follow-up of 15.1 years, 28 out of 313 patients had experienced
locoregional failure. Cumulative incidence for isolated LRR was 7.0% for
patients with 5-cm tumors and 7.2% for patients with tumors larger than 5
cm. The investigators concluded that as locoregional failure was low for these
patients, PMRT should not be routinely recommended for patients with
tumors 5 cm or larger.
In contrast, two studies performed at Massachusetts General Hospital
similarly tried to address the risk of LRR in high-risk lymph node–negative
patients. In a retrospective analysis of nearly 900 patients who were
diagnosed between 1980 and 2000 who did not receive adjuvant PMRT, they
identified four significant and independent risk factors for LRR: size greater
than 2 cm, margin less than 2 mm, premenopausal status, and LVI (31). Ten-
year LRR was 1.2%, 10%, 17.9%, and 40.6% for those with zero, one, two or
three risk factors, respectively. The investigators concluded that patients with
multiple risks factors despite negative axillary lymph nodes therefore would
benefit from PMRT given the high LRR rates seen in this population. A
subsequent analysis specifically examined patients with no axillary lymph
node involvement but tumors 5 cm or larger (32). At a median follow-up of
85 months, the risk of locoregional failure was only 7.6% (96% confidence
interval [CI], 3% to 16%); however, for those patients with evidence of LVI,
the 5-year actuarial local failure rate was 21% (CI = 5% to 45%) compared to
those without LVI (4%, 1% to 11%). The presence of LVI was also
associated with overall survival and disease-free survival. The authors
suggested, therefore, that for those patients with pT3N0 breast cancer the
presence of LVI may help identify a population of lymph node–negative
patients most likely to benefit from PMRT.
POSTMASTECTOMY RADIATION THERAPY IN PATIENTS RECEIVING
NEOADJUVANT CHEMOTHERAPY
Increasingly patients with lymph node–positive breast cancer are receiving
neoadjuvant chemotherapy and therefore the question arises of how best to
incorporate the response to chemotherapy into the decision regarding whether
to recommend PMRT. A combined analysis of patients treated on NSABP B-
18 and B-27 examined predictors of LRR after neoadjuvant chemotherapy
(33). A total of 2,961 patients had complete data available for analysis.
Predictors of LRR on multivariable analysis included age at randomization,
clinical tumor size before neoadjuvant chemotherapy (greater than 5 cm vs. 5
cm or less), clinical nodal status before neoadjuvant chemotherapy, and
pathologic nodal status/pathologic breast tumor response. For patients who
remained persistently lymph node positive (ypN+) after neoadjuvant
chemotherapy versus those who were lymph node negative (ypN0) and had a
pathologic complete response (pCR) in the breast, the hazard ratio for LRR
was 2.71 (95% CI, 1.79 to 4.09; P < 0.001). The investigators stratified
patients by both initial tumor size (less than or equal to 5 cm) and surgery
received. For patients undergoing mastectomy with tumors less than or equal
to 5 cm, the 10-year cumulative incidence of LRR was 6.5% for those with
ypN0 disease and a pCR in the breast in comparison to those who were ypN+
where the risk was 17%. For those with tumors greater than 5 cm, the
locoregional risks were 6.2% versus 22.4%, respectively. Drawing definitive
conclusions from these results is limited by small numbers of patients in
these subgroups but suggests that those with persistently positive lymph
nodes after chemotherapy may benefit most from PMRT.
Another analysis from the University of Texas M.D. Anderson Cancer
Center (MDACC) examined the outcome of 150 patients with breast cancer
treated with neoadjuvant chemotherapy and mastectomy without PMRT. The
median follow-up of surviving patients was 4.1 years. The 5- and 10-year
actuarial rates of locoregional recurrence (LRR) were both 27%. Eighteen
patients had a pCR; for those patients the LRR rate was 19% (34). Clinical
Stage IIB or greater disease, pathologic involvement of four or more lymph
nodes, and no use of Tamoxifen independently predicted for LRR. The
investigators concluded that achievement of pCR does not preclude the need
for PMRT depending on the pretreatment characteristics of the breast. A
subsequent analysis from MDACC of patients receiving neoadjuvant
chemotherapy found that patients with clinically advanced Stage III or IV
disease who achieved a pCR still had a high rate of LRR, which was
significantly reduced with PMRT (10-year rates: 33% to 3%; p = 0.006) (35).
Taken together, these studies suggest that for patients with clinical stage III
disease PMRT after neoadjuvant chemotherapy is indicated, regardless of
response to chemotherapy. Patients with residual pathologic lymph node
involvement after neoadjuvant chemotherapy also appear to benefit from
PMRT. For patients with clinical stage II breast cancer who achieve a pCR,
the risk of LRR is likely relatively low and these patients may not require
PMRT.
To further help clarify the role for PMRT in patients receiving neoadjuvant
chemotherapy, NSABP B-51 is a randomized phase III trial examining the
role for PMRT and regional nodal RT in patients who have positive axillary
lymph nodes before neoadjuvant chemotherapy who convert to
pathologically negative axillary lymph nodes after neoadjuvant chemotherapy
(clinicaltrials.gov Identifier: NCT01872975). For patients enrolled on this
trial who undergo mastectomy, they are randomized to PMRT or no PMRT.
The study is estimated to be completed in August 2028.
RADIATION TARGET VOLUME, DOSE, AND FRACTIONATION
The target of PMRT is always inclusive of the chest wall, as this is the most
frequent site of LRR. For patients with lymph node–positive disease, the
regional lymph nodes, including the axillary and supraclavicular lymph node
basins, are treated. The decision of how much of the draining axillary lymph
node region to cover in the RT fields is often based on the extent of axillary
lymph node sampling. For patients undergoing SLNB, the full axillary basin
is included based on the randomized European Organization for Research and
Treatment of Cancer (EORTC) 10981–22023 (AMAROS) trial (36). In this
trial, patients with a clinical pT1–2 primary and a positive sentinel lymph
node were randomized to axillary RT or ALND. Axillary RT fields included
axillary levels I to III and the medial supraclavicular lymph nodes. Rates of
axillary recurrence at 5 years were low in both randomization arms. The
incidence of lymphedema, as calculated as an arm circumference increase of
greater than 10%, was significantly lower for patients undergoing RT than
ALND (5% vs. 13% at 5 years; p < 0.0001). A similar French trial of women
with breast cancer smaller than 3 cm in size who were clinically node
negative compared axillary dissection versus axillary radiotherapy and found
slightly improved axillary control with ALND (1% vs. 3%; p = .04) but
similar overall survival (37). For patients who undergo ALND, the decision
as to whether or not to include the dissected axilla in the RT fields is often
dependent on the pathologic findings at the time of surgery, including the
number of lymph nodes involved, presence of extranodal extension or tumor
deposits in the axillary fat, and concern for residual gross nodal disease. As
discussed below, the decision to include the dissected axilla in the radiation
fields has to take into account the potential increased risk of lymphedema by
doing so.
Whether or not to include the internal mammary lymph nodes (IMNs) is
controversial. The initial trials demonstrating a benefit to PMRT, including
the Danish 82b and 82c trials and contemporaneous British Columbia trial,
included the IMNs in their treatment fields. Both the NCIC-CTG MA.20 and
EORC 22922 trials that demonstrated a significant disease-free survival
benefit to regional nodal RT in a randomized fashion included the IMNs in
their treatment fields (38,39). The Danish Breast Cancer Cooperative Group
decided to irradiate the IMNs only in patients with right-sided breast cancer
given concerns of radiation-related cardiac toxicity if the IMNs were treated
in patients with left-sided breast cancer (40). In this population-based cohort
study, IMN RT significantly increased the 8-year overall survival rate (75.9%
with IMN RT vs. 72.2% without IMN RT; p = .005). In contrast, a trial from
France attempted to measure the impact of internal mammary node RT on
overall survival and disease-free survival in patients with breast cancer with
pathologically involved lymph nodes or central/medial tumors with or
without lymph node involvement. Although underpowered, the study did not
show an overall survival benefit with the use of internal mammary irradiation
(41). The ASCO/ASTRO/SSO PMRT guidelines recommended that
treatment be administered to both the IMNs and supraclavicular–axillary
apical nodes in addition to the chest wall or reconstructed breast for those
patients with positive axillary lymph nodes.
A variety of techniques are used to deliver postmastectomy radiotherapy.
All require precise immobilization and methods to ensure daily
reproducibility. In general, the chest wall or reconstructed breast is treated
with megavoltage photons generated by a linear accelerator using opposed
tangential fields that encompass the entirety of the chest wall and low axilla.
The supraclavicular area and high axilla is treated with an anterior–posterior
photon field. The angle of this field is angled 5 to 15 degrees to the
contralateral side to avoid divergence through the spinal cord. The target
regional lymph node basins are contoured by the treating radiation oncologist
and the lateral border of the supraclavicular field is adjusted to adequately
cover the target volumes. If coverage is inadequate with an anterior–posterior
field alone, a posterior–anterior field may be added. The chest wall is treated
with 6 MV photons, with higher energies added for large separations. The
photon energy required for the supraclavicular field is based on the depth of
the target lymph nodes. Bolus generally is applied to the native skin on the
chest wall (but not the supraclavicular field or separate IMN field, if used) for
at least part of the course of treatment in order to ensure adequate dose at the
skin surface. However, the more extensive the use of bolus, the higher is the
surface dose, and there is some suggestion that the use of bolus has a negative
impact on reconstruction cosmesis (42).
FIGURE 17-1 Technique for postmastectomy radiation therapy using a single-
isocenter photon technique. The patient received 5,000 cGy to the chest wall and
4,800 cGy to the regional lymph nodes, including the internal mammary lymph
nodes. Panel A: Axial view of the supraclavicular field angled to avoid the spinal
cord and esophagus, if possible. Panel B: Chest wall tangential beams inclusive of the
first three intercostal spaces to cover IMNs as visualized on the skin surface. Panel
C: Coronal view of the matched supraclavicular and chest wall fields, with
distribution of radiation dose depicted by isodose lines.

Treatment of the IMN can be accomplished with several approaches. Often


the medial border of the tangents is extended across midline to encompass
intercostal spaces one through three or four in a so-called “partially wide
tangent” technique. An example of PMRT fields, including IMN coverage
with partially wide tangents, is seen in Figure 17-1. An alternative approach
is to match a small electron field to the photon tangents, but this is more
complicated dosimetrically and there are some concerns about increased
cardiac dose with this approach.
Treatment of the chest wall and regional lymph nodes is typically 1.8 to
2.0 Gy per day, 5 days a week, to a dose of 45 to 50.4 Gy. However, there is
increasing interest in hypofractionated RT for patients receiving PMRT as it
has been widely adopted in patients undergoing breast-conserving surgery.
One phase II prospective study delivered PMRT at a dose of 36.63 Gy in 11
fractions to the chest wall and regional lymph nodes with an optional
mastectomy scar boost (43). At a median follow-up of 32 months, 24% of
patients experienced grade 2 skin toxicities and the total all-cause group 3
and 4 reconstruction complication rate attributable to RT was 32%. A trial in
China randomized patients to receive chest wall and regional nodal RT to 50
Gy in 25 fractions over 5 weeks or 43.5 Gy in 15 fractions over 3 weeks (44).
There were no significant differences in 5-year LRR or acute and late
toxicities except that fewer patients in the hypofractionated radiotherapy
group had grade 3 acute skin toxicity. Two currently enrolling randomized
trials are studying hypofractionated versus conventionally fractionated RT in
patients who have undergone mastectomy and reconstruction
(clinicaltrials.gov Identifiers: NCT03422003; NCT03414970). Patient-
reported outcomes, physician-reported toxicities including reconstruction
complications, and oncologic outcomes are being analyzed.
SIDE EFFECTS OF POSTMASTECTOMY RADIATION THERAPY
The potential benefits of PMRT are weighed against the potential both short-
and long-term toxicities. Nearly all patients receiving PMRT develop acute
radiation dermatitis, which can range from mild erythema to desquamation to
very rarely tissue necrosis. Moist desquamation has been shown to increase
the likelihood of treatment breaks or early termination of treatment, which
can increase the risk of local recurrence (45). A randomized trial of twice-
daily mometasone in patients receiving PMRT found that mometasone
significantly decreased the risk of moist desquamation (66.7% to 43.8%, p =
0.012) (46). However, there was no difference in patient-reported skin
outcomes between treatment groups. Late skin toxicities include radiation-
induced fibrosis, hyperpigmentation, and telangiectasias. Another common
acute toxicity of breast RT is fatigue, which can persist for up to 3 months or
longer after RT (47–49).
The contribution of RT to the incidence of lymphedema is variable across
studies; several studies have suggested no increase in lymphedema with chest
wall radiation alone (50,51). However, results from studies that have
examined the effect of regional lymph node RT on the risk of lymphedema,
with the use of either supraclavicular or supraclavicular and full axillary RT,
are mixed. Several studies showed no significantly increased risk when
compared to breast RT alone (52,53). However, other studies did demonstrate
an increased risk of lymphedema with regional lymph node RT (50,54,55).
Reports have also varied regarding the effect of certain technical
considerations, such as the location of the lateral border of the supraclavicular
field, on the risk of lymphedema (53,56).
The recommendation for PMRT can impact breast reconstruction
outcomes in multiple ways, including the timing of reconstruction, type of
reconstruction performed, timing of PMRT, and risk of complications. Breast
reconstruction has been shown to improve the physical, psychological, and
emotional well-being for women undergoing mastectomy (57,58).
Reconstruction can either be performed at the time of mastectomy
(“immediate”) or at a later time in a separate surgery (“delayed”). There
appears to be a psychological benefit of immediate versus delayed
reconstruction (59). Immediate reconstruction also affords the plastic surgeon
the opportunity to use more native breast skin, which may improve the
ultimate cosmetic outcome. The current National Comprehensive Cancer
Network guidelines suggest that for patients undergoing immediate
reconstruction, two approaches are reasonable (60). For those undergoing
implant reconstruction, a staged approach with immediate tissue expander
placement followed by implant placement is preferred. For those for whom
autologous reconstruction is planned, reconstruction can be initiated at the
time of mastectomy with an immediate tissue expander placement and
subsequent autologous tissue reconstruction after PMRT. Most women
requiring PMRT undergo implant-based reconstruction although the optimal
type of reconstruction is controversial. A recent study analyzing the patterns
of mastectomy in the United States suggests a shift away from autologous
tissue to implant-based reconstruction, perhaps driven by patients requiring
PMRT (61). However, several studies have suggested lower rates of surgical
complications and increased satisfaction for patients receiving PMRT who
undergo autologous versus implant-based reconstruction (62–64) and
autologous reconstruction, even in women requiring PMRT, should be
considered. The timing of PMRT for those undergoing immediate
reconstruction is controversial. Two systematic reviews suggest similar
complication and reconstruction failure rates for those completing
reconstruction prior to PMRT (65,66). The rates of severe capsular
contracture, however, may be lower for those receiving PMRT with tissue
expanders in place compared to permanent implants. For those undergoing
two-stage reconstruction with PMRT to the expander, a delayed approach to
permanent implant placement of at least 4 to 6 months after RT has been
recommended in an effort to minimize infection and decrease likelihood of
implant failure (67,68).
For women felt to be at particularly high risk of LRR, delayed
reconstruction may be preferred to try to minimize postoperative
complications resulting in a delay of PMRT initiation. Additionally, delayed
reconstruction may be preferred for high-risk women given studies
suggesting that reconstruction may result in less optimal radiation plans and
decreased coverage of the clinical targets (69,70). If delayed reconstruction is
recommended, implant-based reconstruction is usually not possible or
advisable given the long-term side effects of RT, specifically chest wall and
skin tightness secondary to radiation-induced fibrosis. Therefore, most often
autologous tissue reconstruction is performed in patients undergoing delayed
reconstruction after PMRT.
PMRT has been shown to increase the risk of a variety of complications
for patients undergoing implant-based reconstruction or autologous tissue
reconstruction, including the risk of capsular contracture and reconstruction
failure (71–74). Other reported complications with PMRT include an
increased risk of infection (75,76). PMRT has also been shown to
compromise the cosmetic outcome (77). Several patient characteristics,
including higher BMI and actively smoking at the time of PMRT, further
increase the risk of reconstruction complications (78,79).
Further complicating the relationship between reconstruction and PMRT is
the potential impact of the reconstruction on the PMRT fields. Several studies
have suggested that reconstruction results in suboptimal target coverage and
suboptimal avoidance of organs at risk, specifically the heart and lungs (70).
In particular, prepectoral implants, which are increasingly being utilized by
plastic surgeons (80), increase the complexity of radiation planning even
further. The radiation target after mastectomy is considered to be the space
between the skin and anterior surface of the pectoralis muscle. Adequate
coverage at the posterior (deep) edge of the implant is sometimes challenging
to achieve. For those patients undergoing subpectoral implants, the posterior
edge of the implant is far away from the target volume. For patients
undergoing prepectoral implants, the posterior edge of the implant is in the
radiation target volume with resultant concerns about undercoverage of the
at-risk area (81).
PMRT can significantly impact the risks of reconstruction. Women have
reported less satisfaction and worse health-related quality of life with
reconstruction in the setting of PMRT when compared to women who do not
require PMRT (82). Most studies addressing the optimal approach are
retrospective with heterogenous populations and there is significant
variability across institutions in terms of the optimal approach to patient
undergoing reconstruction and PMRT. Prospective and randomized studies
would offer higher-quality evidence by which to guide practice and advise
patients for whom PMRT is recommended and who are considering
reconstruction.
CONCLUSION
PMRT has consistently been found to reduce LRR by approximately two-
thirds and in older studies was shown to offer a survival benefit of
approximately 10% at 10 years. However, in the more modern era, while the
relative benefit of PMRT remains similar, the absolute magnitude of benefit
in terms of LRR is smaller due to improvements in surgical and systemic
treatments. There are groups of patients in whom the risk of LRR remains
high enough that PMRT is recommended as a means by which to reduce LRR
and improve overall survival. In patients with an intermediate risk of LRR,
identifying which patients may benefit from PMRT involves careful
consideration of recognized clinicopathologic factors balanced with the
potential side effects of PMRT. Whenever possible, enrollment onto clinical
trials should be considered.

REFERENCES

1. American Cancer Society. Cancer Facts and Figures 2019. Atlanta,


MD: American Cancer Society; 2019.
2. Cuzick J, Stewart H, Rutqvist L, et al. Cause-specific mortality in long-
term survivors of breast cancer who participated in trials of
radiotherapy. J Clin Oncol 1994;12(3):447–453.
3. Cuzick J, Stewart H, Peto R, et al. Overview of randomized trials
comparing radical mastectomy without radiotherapy against simple
mastectomy with radiotherapy in breast cancer. Cancer Treat Rep
1987;71(1):7–14.
4. Early Breast Cancer Trialists’ Collaborative Group (EBCTCG). Effects
of chemotherapy and hormonal therapy for early breast cancer on
recurrence and 15-year survival: an overview of the randomised trials.
Lancet 2005;365(9472):1687–1717.
5. Overgaard M, Hansen PS, Overgaard J, et al. Postoperative radiotherapy
in high-risk premenopausal women with breast cancer who receive
adjuvant chemotherapy. Danish Breast Cancer Cooperative Group 82b
Trial. N Engl J Med 1997;337(14):949–955.
6. Overgaard M, Jensen MB, Overgaard J, et al. Postoperative radiotherapy
in high-risk postmenopausal breast-cancer patients given adjuvant
tamoxifen: Danish Breast Cancer Cooperative Group DBCG 82c
randomised trial. Lancet 1999;353(9165):1641–1648.
7. Ragaz J, Olivotto IA, Spinelli JJ, et al. Locoregional radiation therapy in
patients with high-risk breast cancer receiving adjuvant chemotherapy:
20-year results of the British Columbia randomized trial. J Natl Cancer
Inst 2005;97(2):116–126.
8. Overgaard M, Nielsen HM, Overgaard J. Is the benefit of
postmastectomy irradiation limited to patients with four or more positive
nodes, as recommended in international consensus reports ? A subgroup
analysis of the DBCG 82 b & c randomized trials. Radiother Oncol
2007;82:247–253.
9. National Institutes of Health Consensus Development Panel. National
Institutes of Health Consensus Development Conference Statement:
adjuvant therapy for breast cancer, November 1–3, 2000. J Natl Cancer
Inst Monogr 2001;2001(30):5–15.
10. Clarke M, Collins R, Darby S, et al; Early Breast Cancer Trialists’
Collaborative Group (EBCTCG). Effects of radiotherapy and of
differences in the extent of surgery for early breast cancer on local
recurrence and 15-year survival: an overview of the randomised trials.
Lancet 2005;366(9503):2087–2106.
11. EBCTCG (Early Breast Cancer Trialists’ Collaborative Group). Effect
of radiotherapy after mastectomy and axillary surgery on 10-year
recurrence and 20-year breast cancer mortality: meta-analysis of
individual patient data for 8135 women in 22 randomised trials. Lancet
2014;383(9935):2127–2135.
12. Sartor CI, Peterson BL, Woolf S, et al. Effect of addition of adjuvant
paclitaxel on radiotherapy delivery and locoregional control of node-
positive breast cancer: Cancer and Leukemia Group B 9344. J Clin
Oncol 2005;23(1):30–40.
13. Botteri E, Gentilini O, Rotmensz N, et al. Mastectomy without
radiotherapy: outcome analysis after 10 years of follow-up in a single
institution. Breast Cancer Res Treat 2012;134(3):1221–1228.
14. McBride A, Allen P, Woodward W, et al. Locoregional recurrence risk
for patients with T1,2 breast cancer with 1–3 positive lymph nodes
treated with mastectomy and systemic treatment. Int J Radiat Oncol Biol
Phys 2014;89(2):392–398.
15. Lu C, Xu H, Chen X, et al. Irradiation after surgery for breast cancer
patients with primary tumours and one to three positive axillary lymph
nodes: yes or no? Curr Oncol 2013;20(6):e585–e592.
16. He ZY, Wu SG, Zhou J, et al. Postmastectomy radiotherapy improves
disease-free survival of high risk of locoregional recurrence breast
cancer patients with T1-2 and 1 to 3 positive nodes. PLoS One
2015;10(3):e0119105.
17. Truong PT, Berthelet E, Lee J, et al. The prognostic significance of the
percentage of positive/dissected axillary lymph nodes in breast cancer
recurrence and survival in patients with one to three positive axillary
lymph nodes. Cancer 2005;103(10):2006–2014.
18. Recht A, Gray R, Davidson NE, et al. Locoregional failure 10 years
after mastectomy and adjuvant chemotherapy with or without tamoxifen
without irradiation: Experience of the Eastern Cooperative Oncology
Group. J Clin Oncol 1999;17(6):1689–1700.
19. Truong PT, Olivotto IA, Kader HA, et al. Selecting breast cancer
patients with T1-T2 tumors and one to three positive axillary nodes at
high postmastectomy locoregional recurrence risk for adjuvant
radiotherapy. Int J Radiat Oncol Biol Phys 2005;61(5):1337–1347.
20. Moo TA, McMillan R, Lee M, et al. Selection criteria for
postmastectomy radiotherapy in T1-T2 tumors with 1 to 3 positive
lymph nodes. Ann Surg Oncol 2013;20(10):3169–3174.
21. Fodor J, Polgár C, Major T, et al. Locoregional failure 15 years after
mastectomy in women with one to three positive axillary nodes with or
without irradiation: the significance of tumor size. Strahlenther Onkol
2003;179(3):197–202.
22. Tendulkar RD, Rehman S, Shukla ME, et al. Impact of postmastectomy
radiation on locoregional recurrence in breast cancer patients with 1–3
positive lymph nodes treated with modern systemic therapy. Int J Radiat
Oncol Biol Phys 2012;83(5):e577–e581.
23. Yu JI, Park W, Huh SJ, et al. Determining which patients require
irradiation of the supraclavicular nodal area after surgery for N1 breast
cancer. Int J Radiat Oncol Biol Phys 2010;78(4):1135–1141.
24. Kyndi M, Sørensen FB, Knudsen H, et al. Estrogen receptor,
progesterone receptor, HER-2, and response to postmastectomy
radiotherapy in high-risk breast cancer: the Danish Breast Cancer
Cooperative Group. J Clin Oncol 2008;26(9):1419–1426.
25. Velikova G, Williams LJ, Willis S, et al. Quality of life after
postmastectomy radiotherapy in patients with intermediate-risk breast
cancer (SUPREMO): 2-year follow-up results of a randomised
controlled trial. Lancet Oncol 2018;19(11):1516–1529.
26. Mamounas EP, Liu Q, Paik S, et al. 21-Gene Recurrence Score and
locoregional recurrence in node-positive/ER-positive breast cancer
treated with chemo-endocrine therapy. JNCI J Natl Cancer Inst
2017;109(4).
27. Mamounas EP, Tang G, Fisher B, et al. Association between the 21-
gene recurrence score assay and risk of locoregional recurrence in node-
negative, estrogen receptor-positive breast cancer: results from NSABP
B-14 and NSABP B-20. J Clin Oncol 2010;28(10):1677–1683.
28. Mamounas EP, Liu Q, Paik S, et al. 21-gene recurrence score and
locoregional recurrence in node-positive/ER-positive breast cancer
treated with chemo-endocrine therapy. J Natl Cancer Inst
2017;109(4):4–11.
29. Recht A, Comen EA, Fine RE, et al. Postmastectomy radiotherapy: an
American Society of clinical oncology, American Society for Radiation
Oncology, and Society of Surgical Oncology focused guideline update. J
Clin Oncol 2016;34(36):4431–4442.
30. Taghian AG, Jeong JH, Mamounas EP, et al. Low locoregional
recurrence rate among node-negative breast cancer patients with tumors
5 cm or larger treated by mastectomy, with or without adjuvant systemic
therapy and without radiotherapy: results from five National Surgical
Adjuvant Breast and Bowel Project randomized clinical trials. J Clin
Oncol 2006;24(24):3927–3932.
31. Jagsi R, Raad RA, Goldberg S, et al. Locoregional recurrence rates and
prognostic factors for failure in node-negative patients treated with
mastectomy: implications for postmastectomy radiation. Int J Radiat
Oncol Biol Phys 2005;62(4):1035–1039.
32. Floyd SR, Buchholz TA, Haffty BG, et al. Low local recurrence rate
without postmastectomy radiation in node-negative breast cancer
patients with tumors 5 cm and larger. Int J Radiat Oncol Biol Phys
2006;66(2):358–364.
33. Mamounas EP, Anderson SJ, Dignam JJ, et al. Predictors of
locoregional recurrence after neoadjuvant chemotherapy: results from
combined analysis of National Surgical Adjuvant Breast and Bowel
Project B-18 and B-27. J Clin Oncol 2012;30(32):3960–3966.
34. Buchholz TA, Tucker SL, Masullo L, et al. Predictors of local-regional
recurrence after neoadjuvant chemotherapy and mastectomy without
radiation. J Clin Oncol 2002;20(1):17–23.
35. Huang EH, Tucker SL, Strom EA, et al. Postmastectomy radiation
improves local-regional control and survival for selected patients with
locally advanced breast cancer treated with neoadjuvant chemotherapy
and mastectomy. J Clin Oncol 2004;22(23):4639–4647.
36. Donker M, van Tienhoven G, Straver ME, et al. Radiotherapy or surgery
of the axilla after a positive sentinel node in breast cancer (EORTC
10981–22023 AMAROS): a randomised, multicentre, open-label, phase
3 non-inferiority trial. Lancet Oncol 2014;15(12):1303–1310.
37. Louis-Sylvestre C, Clough K, Asselain B, et al. Axillary treatment in
conservative management of operable breast cancer: dissection or
radiotherapy? Results of a randomized study with 15 years of follow-up.
J Clin Oncol 2004;22(1):97–101.
38. Whelan TJ, Olivotto IA, Parulekar WR, et al. Regional nodal irradiation
in early-stage breast cancer. N Engl J Med 2015;373(4):307–316.
39. Poortmans PM, Collette S, Kirkove C, et al. Internal mammary and
medial supraclavicular irradiation in breast cancer. N Engl J Med
2015;373(4):317–327.
40. Thorsen LBJ, Offersen BV, Danø H, et al. DBCG-IMN: a population-
based cohort study on the effect of internal mammary node irradiation in
early node-positive breast cancer. J Clin Oncol 2016;34(4):314–320.
41. Hennequin C, Bossard N, Servagi-Vernat S, et al. Ten-year survival
results of a randomized trial of irradiation of internal mammary nodes
after mastectomy. Int J Radiat Oncol Biol Phys 2013;86(5):860–866.
42. Huang EY, Chen HC, Sun LM, et al. Multivariate analyses of
locoregional recurrences and skin complications after postmastectomy
radiotherapy using electrons or photons. Int J Radiat Oncol Biol Phys
2006;65(5):1389–1396.
43. Khan AJ, Poppe MM, Goyal S, et al. Hypofractionated postmastectomy
radiation therapy is safe and effective: first results from a prospective
phase II trial. J Clin Oncol 2017;35(18):2037–2043.
44. Wang S, Fang H, Song Y, et al. Hypofractionated versus conventional
fractionated postmastectomy radiotherapy for patients with high-risk
breast cancer: a randomised, non-inferiority, open-label, phase 3 trial.
Lancet Oncol 2019;20(3):352–360.
45. Tieu MT, Graham P, Browne L, et al. The effect of adjuvant
postmastectomy radiotherapy bolus technique on local recurrence. Int J
Radiat Oncol Biol Phys 2011;81(3):e165–e171.
46. Ho AY, Olm-Shipman M, Zhang Z, et al. A randomized trial of
mometasone furoate 0.1% to reduce high grade acute radiation
dermatitis in breast cancer patients receiving postmastectomy radiation.
Int J Radiat Oncol Biol Phys 2018;101(2):325–333.
47. Wratten C, Kilmurray J, Nash S, et al. Fatigue during breast
radiotherapy and its relationship to biological factors. Int J Radiat Oncol
Biol Phys 2004;59(1):160–167.
48. Manir KS, Bhadra K, Kumar G, et al. Fatigue in breast cancer patients
on adjuvant treatment: course and prevalence. Indian J Palliat Care
2012;18(2):109–116.
49. Knobf MT, Sun Y. A longitudinal study of symptoms and self-care
activities in women treated with primary radiotherapy for breast cancer.
Cancer Nurs 2005;28(3):210–218.
50. Warren LEG, Miller CL, Horick N, et al. The impact of radiation
therapy on the risk of lymphedema after treatment for breast cancer: a
prospective cohort study. Int J Radiat Oncol Biol Phys 2014;88(3):565–
571.
51. Liljegren G, Holmberg L. Arm morbidity after sector resection and
axillary dissection with or without postoperative radiotherapy in breast
cancer stage I. Results from a randomised trial. Uppsala-Orebro Breast
Cancer Study Group. Eur J Cancer 1997;33(2):193–199.
52. Shah C, Wilkinson JB, Baschnagel A, et al. Factors associated with the
development of breast cancer-related lymphedema after whole-breast
irradiation. Int J Radiat Oncol Biol Phys 2012;83(4):1095–1100.
53. Graham P, Jagavkar R, Browne L, et al. Supraclavicular radiotherapy
must be limited laterally by the coracoid to avoid significant adjuvant
breast nodal radiotherapy lymphoedema risk. Australas Radiol
2006;50(6):578–582.
54. Coen JJ, Taghian AG, Kachnic LA, et al. Risk of lymphedema after
regional nodal irradiation with breast conservation therapy. Int J Radiat
Oncol Biol Phys 2003;55(5):1209–1215.
55. Hayes SB, Freedman GM, Li T, et al. Does axillary boost increase
lymphedema compared with supraclavicular radiation alone after breast
conservation? Int J Radiat Oncol Biol Phys 2008;72(5):1449–1455.
56. Chandra RA, Miller CL, Skolny MN, et al. Radiation therapy risk
factors for development of lymphedema in patients treated with regional
lymph node irradiation for breast cancer. Int J Radiat Oncol
2015;91(4):760–764.
57. Rowland JH, Desmond KA, Meyerowitz BE, et al. Role of breast
reconstructive surgery in physical and emotional outcomes among breast
cancer survivors. J Natl Cancer Inst 2000;92(17):1422–1429.
58. Dean C, Chetty U, Forrest AP. Effects of immediate breast
reconstruction on psychosocial morbidity after mastectomy. Lancet
1983;1(8322):459–462.
59. Al-Ghazal SK, Sully L, Fallowfield L, et al. The psychological impact
of immediate rather than delayed breast reconstruction. Eur J Surg
Oncol 2000;26(1):17–19.
60. National Comprehensive Cancer Network. NCCN Clinical Practice
Guidelines in Oncology: Breast Cancer.
https://www.nccn.org/professionals/physician_gls/pdf/breast.pdf.
Published 2019. Accessed December 2, 2019.
61. Cemal Y, Albornoz CR, Disa JJ, et al. A paradigm shift in U.S. breast
reconstruction: Part 2. The influence of changing mastectomy patterns
on reconstructive rate and method. Plast Reconstr Surg
2013;131(3):320e–326e.
62. Jagsi R, Momoh AO, Qi J, et al. Impact of radiotherapy on
complications and patient-reported outcomes after breast reconstruction.
J Natl Cancer Inst 2017;110(2):1–9.
63. Barry M, Kell MR. Radiotherapy and breast reconstruction: a meta-
analysis. Breast Cancer Res Treat 2011;127(1):15–22.
64. Pusic AL, Matros E, Fine N, et al. Patient-reported outcomes 1 year
after immediate breast reconstruction: results of the mastectomy
reconstruction outcomes consortium study. J Clin Oncol
2017;35(22):2499–2506.
65. Momoh AO, Ahmed R, Kelley BP, et al. A systematic review of
complications of implant-based breast reconstruction with
prereconstruction and postreconstruction radiotherapy. Ann Surg Oncol
2014;21(1):118–124.
66. Lee KT, Mun GH. Optimal sequencing of postmastectomy radiotherapy
and two stages of prosthetic reconstruction: a meta-analysis. Ann Surg
Oncol 2017;24(5):1262–1268.
67. Lentz R, Ng R, Higgins SA, et al. Radiation therapy and expander-
implant breast reconstruction: an analysis of timing and comparison of
complications. Ann Plast Surg 2013;71(3):269–273.
68. Peled AW, Foster RD, Esserman LJ, et al. Increasing the time to
expander-implant exchange after postmastectomy radiation therapy
reduces expander-implant failure. Plast Reconstr Surg 2012;130(3):503–
509.
69. Bjöhle J, Onjukka E, Rintelä N, et al. Post-mastectomy radiation therapy
with or without implant-based reconstruction is safe in terms of clinical
target volume coverage and survival—A matched cohort study.
Radiother Oncol 2019;131:229–236.
70. Motwani SB, Strom EA, Schechter NR, et al. The impact of immediate
breast reconstruction on the technical delivery of postmastectomy
radiotherapy. Int J Radiat Oncol Biol Phys 2006;66(1):76–82.
71. Tallet AV, Salem N, Moutardier V, et al. Radiotherapy and immediate
two-stage breast reconstruction with a tissue expander and implant:
complications and esthetic results. Int J Radiat Oncol Biol Phys
2003;57(1):136–142.
72. Ascherman JA, Hanasono MM, Newman MI, et al. Implant
reconstruction in breast cancer patients treated with radiation therapy.
Plast Reconstr Surg 2006;117(2):359–365.
73. Ho AL, Bovill ES, Macadam SA, et al. Postmastectomy radiation
therapy after immediate two-stage tissue expander/implant breast
reconstruction: a University of British Columbia perspective. Plast
Reconstr Surg 2014;134(1):1e–10e.
74. Fowble B, Park C, Wang F, et al. Rates of reconstruction failure in
patients undergoing immediate reconstruction with tissue expanders
and/or implants and postmastectomy radiation therapy. Int J Radiat
Oncol Biol Phys 2015;92(3):634–641.
75. Nahabedian MY, Tsangaris T, Momen B, et al. Infectious complications
following breast reconstruction with expanders and implants. Plast
Reconstr Surg 2003;112(2):467–476.
76. El-Sabawi B, Carey JN, Hagopian TM, et al. Radiation and breast
reconstruction: algorithmic approach and evidence-based outcomes. J
Surg Oncol 2016;113(8):906–912.
77. Shah C, Kundu N, Arthur D, et al. Radiation therapy following
postmastectomy reconstruction: a systematic review. Ann Surg Oncol
2013;20:1313–1322.
78. Pignol JP, Vu TTT, Mitera G, et al. Prospective evaluation of severe
skin toxicity and pain during postmastectomy radiation therapy. Int J
Radiat Oncol Biol Phys 2015;91(1):157–164.
79. Wright JL, Takita C, Reis IM, et al. Racial variations in radiation-
induced skin toxicity severity: data from a prospective cohort receiving
postmastectomy radiation. Int J Radiat Oncol Biol Phys
2014;90(2):335–343.
80. Kaplan J, Wagner RD, Braun TL, et al. Prepectoral breast
reconstruction. Semin Plast Surg 2019;33(04):236–239.
81. Mitchell MP, Wagner J, Butterworth J. Subcutaneous implant-based
breast reconstruction, a modern challenge in postmastectomy radiation
planning. Pract Radiat Oncol 2018;8(3):153–156.
82. Albornoz CR, Matros E, McCarthy CM, et al. Implant breast
reconstruction and radiation: a multicenter analysis of long-term health-
related quality of life and satisfaction. Ann Surg Oncol
2014;21(7):2159–2164.
CHAPTER 18

Optimizing Mastectomy Flaps Based


on Breast Anatomy
NOLAN S. KARP | JORDAN D. FREY | ARA A. SALIBIAN
HISTORY
The first reported radical mastectomy was performed in New York City in
1882 by Dr. William Halsted (1). Since the first description of this aggressive
and morbid procedure, techniques for the surgical management of breast
cancer have evolved to becoming less invasive while maintaining oncologic
safety. This progression led to the development of the modified radical
mastectomy, skin-sparing mastectomy, and finally the total skin-sparing, or
nipple-sparing mastectomy (1). Each of these techniques, while different in
terms of sacrificing or sparing certain structures, holds one aspect in constant:
the separation of the breast gland from the more superficial breast skin and
subcutaneous tissue. However, the precision required to perform this
anatomic dissection, as well as its importance in maintaining mastectomy flap
tissue perfusion, is often overlooked (1).
Maintaining mastectomy flap perfusion during mastectomy dissection may
represent the most important factor in ensuring a successful ensuing
immediate breast reconstruction. From superficial to deep, the breast is
composed of skin, superficial subcutaneous fat, and a thin layer of superficial
breast fascia (analogous to Camper fascia throughout the body) with an
underlying deeper layer of adipose tissue (2,3). The underlying breast gland
is separated from these superficial layers by a deeper fascial layer, also
termed the breast capsule (2,3). This breast capsule is alternatively referred to
as the superficial breast fascia. However, to avoid confusion with the thinner,
more superficial layer of fascia between the two layers of subcutaneous
breast fat, it is referred to herein as the breast capsule (Fig. 18-1).
After mastectomy, the remaining breast skin flaps are dependent on the
subdermal plexus as well as perforators in the subcutaneous plane for
perfusion (Fig. 18-2) (4–6). Anatomic dissection at the level of the breast
capsule maximizes oncologic resection of the breast gland while also
minimizing trauma to the skin flaps, thereby optimizing perfusion.
Mastectomy dissection in a plane deep to the breast capsule thus risks
incomplete oncologic resection. Meanwhile, overaggressive suprafascial
dissection compromises blood flow to the mastectomy flap, risking ischemia
changes with no oncologic advantage, as taking tissue above the breast gland
offers no survival benefit (7).
INDICATIONS/CONTRAINDICATIONS
The goal in reconstructive breast surgery is to provide the postmastectomy
patient with a durable and aesthetic breast, whether that is utilizing implants
or autologous tissue. However, even the most elegant reconstruction is
condemned to fail if the overlying skin flaps are poorly perfused. Maintaining
the viability of the native breast skin envelope through precise, anatomic
mastectomy dissection is therefore critical in obtaining ideal reconstructive
and aesthetic outcomes. While anatomic mastectomy dissection may be the
most important factor in achieving a successful immediate breast
reconstruction, it similarly may be the most difficult to assess clinically and
scientifically investigate (8).
Given the oncologic and reconstructive significance of precise mastectomy
flap creation, care should be taken in all patients to perform this dissection as
anatomically as possible at the level of the breast capsule. This dissection is
independent of the mastectomy procedure, whether being a total, skin-
sparing, or nipple-sparing mastectomy. No matter how much skin will be
taken, all remaining breast skin flaps should be created equally in the fascial
plane. Similarly, there are no contraindications to this dissection. The goal of
a mastectomy, again regardless of mastectomy procedure, is to remove the
glandular breast tissue. This tissue lies below the level of the breast capsule;
therefore, only tissue below this deep fascia should be removed in a patient-
specific and anatomic manner, leaving the superficial subcutaneous tissue
and skin intact. As will be discussed, various preoperative and intraoperative
considerations can facilitate this dissection to ensure optimal outcomes.
PREOPERATIVE PLANNING
Execution of an anatomic mastectomy flap dissection with optimal perfusion
begins with preoperative assessment and planning. Various patient- and
disease-specific risk factors for ischemic complications must be considered,
including smoking, obesity, radiation, chemotherapy, as well as particular
mastectomy incisions and mastectomy weight (9,10). These factors can
contribute to the occurrence of ischemic complications even in the face of a
perfectly dissected mastectomy flap. This underscores the importance of
identifying such factors as much as possible preoperatively in an effort to
make evidence-based decisions along with the patient as well as set realistic
expectations regarding postmastectomy breast reconstruction. Protective
measures should be preferentially pursued in patients at higher risk of
ischemic complications. This may include offering non–nipple-sparing
techniques, submuscular rather than prepectoral techniques, or even delayed
reconstruction.

FIGURE 18-1 Ultrasonography of breast demonstrating the layers of the breast


from superficial to deep: skin (short red arrow), superficial subcutaneous fat,
superficial breast fascia (analogous to Camper fascia; blue arrow), deep
subcutaneous fat, breast capsule (long red arrow), and breast gland. An anatomic
dissection will occur at the level of the breast capsule to maximize oncologic resection
while maintaining optimal perfusion to the mastectomy skin flaps based on the
subdermal plexus and subcutaneous perforators.
Selection of mastectomy incisions, particularly in nipple-sparing
mastectomy, is another critical component of preoperative planning. As
discussed, perfusion of the breast skin envelope after mastectomy is reliant
on the subdermal plexus and subcutaneous perforators. All of this blood
supply, after mastectomy, originates from the periphery of the breast. Placing
a surgical incision on the breast further alters this perfusion. As the distance
from the circumferential periphery of the breast to the edge of the
mastectomy incision increases, marginal perfusion at the incision decreases.
Further, surgical access to the breast differs depending on where an incision
is placed. This can have significant impact on the technical facility of
performing an anatomic flap dissection. The decision of what incision to
utilize should be made in concert with the breast and plastic surgeon and may
be based on tumor location, tumor size, prior scars, reconstructive modality,
and/or patient preference.
In total and skin-sparing mastectomy, elliptical or circular incisions
surrounding the nipple areola complex are generally chosen. These should be
designed as central as possible such that it is equidistant from the periphery
of the breast in all directions, maximizing perfusion in all breast quadrants. In
larger breasts, designing a larger circle or ellipse can increase the amount of
skin excised, effectively shortening the distance from skin edge to breast
periphery. These incisions generally allow for excellent surgical access to
both identify the breast capsule and dissect in this plane circumferentially in
all directions.
The most common incision options in nipple-sparing mastectomy include
inframammary fold, lateral radial, vertical radial, Wise pattern, and
periareolar incisions (11). Inframammary fold incisions are placed along the
bottom of the breast, maximizing the distance from the superior breast
periphery to the incisional margin at the inframammary fold. Perfusion can
thus be tenuous in this area, notably in patients with large breasts. These
incisions can also make dissection more tedious, especially in the superior
quadrant due to limited access and requires greater experience for precise
dissection in the correct, anatomic plane. Lateral and vertical radial incisions
split the lateral or inferior quadrants of the breast in half. Perfusion in all
directions is thus maximized while surgical access is superior to
inframammary incisions for mastectomy dissection. Wise pattern incisions
allow for skin reduction and excellent surgical access but maximize incisions
on the breast and risk perfusion issues. Lastly, periareolar incisions disrupt
perfusion to the nipple-areola complex and are not used in our practice (11).

FIGURE 18-2 Intraoperative view of a subcutaneous perforator supplying the


subdermal plexus after mastectomy performed in the anatomic plane of the breast
capsule.
Once oncologic and reconstructive plans have been established, the
predicted thickness of the breast skin and subcutaneous tissue should be
assessed. The perfusion of the skin flaps will largely be dependent on these
layers given their dependence on the subdermal plexus and subcutaneous
perforators after mastectomy. The thickness of this layer will inherently be
variable among patients. Specifically, we have identified breast morphology
and body-mass index as significant determinants of ideal mastectomy flap
thickness (12). Patients with higher body mass index and larger mastectomy
weights, as proxies for breast size, were found to have thicker mastectomy
flaps with a more robust layer of subcutaneous fat (12). This highlights the
need for an individualized approach to mastectomy flap dissection. The
breast capsule layer is not at a constant depth across a patient population and
therefore, mastectomy flap dissection is not “one size fits all.”
While predicted mastectomy flap thickness can be qualitatively assessed
clinically in the preoperative setting based on breast morphology and patient
examination, quantitative measurement can be difficult. The increased
availability of preoperative breast imaging provides a unique opportunity to
review and quantify each patient’s unique breast anatomy. Digital
mammography can be utilized for this purpose; however, ultrasonography
and magnetic resonance imaging (MRI) are more commonly utilized in our
practice (8,12,13).
We believe in an oncoplastic approach to immediate postmastectomy
breast reconstruction, relying on cooperative coordination being the ablative
and reconstructive teams (14,15). At our institution, a majority of patients
will have undergone preoperative MRI for oncologic planning. Therefore,
each patient’s preoperative breast MRI can be reviewed by the breast and
plastic surgeon. The distance from the breast skin to the breast capsule may
be measured at multiple points in both the axial and sagittal planes (Fig. 18-
3). This provides a quantitative estimation of predicted mastectomy flap
thicknesses based on each patient’s anatomy. Prior to infiltration of any dilute
lidocaine with epinephrine solution in the operating room, hand-held
ultrasonography may be utilized to confirm these estimated thicknesses using
a second imaging modality in roughly the same locations as those measured
on MRI (Fig. 18-4). We have found that this aids in the identification of the
breast capsule intraoperatively, facilitating an anatomic mastectomy flap
dissection in the optimal plane.
FIGURE 18-3 Preoperative breast MRI demonstrating measurement of predicted
mastectomy flaps measured from skin to the breast capsule layer at multiple
locations in the axial plane. Note that the skin and subcutaneous layer is thicker as
one progresses from anterior to posterior on the breast (A–F). Note the superficial
breast fascia (red arrow) dividing the subcutaneous fat above the breast capsule into
a superficial and a deep layer.
FIGURE 18-4 Intraoperative, postmastectomy breast ultrasonography of patient
from Figure 18-3 confirming predicted mastectomy flaps measured on MRI. Again
noted is the superficial breast fascia splitting the subcutaneous fat above the breast
capsule into a superficial and a deep layer that is observed in the MRI as well.
OPERATIVE TECHNIQUE
The most important method of ensuring optimally perfused breast skin flaps
for immediate breast reconstruction is a precise and anatomic mastectomy
dissection at the level of the breast capsule. Anatomic mastectomy flap
dissection requires an individualized approach. We infiltrate a dilute
lidocaine and epinephrine containing solution prior to incision to help control
hemostasis and assist in hydrodissection. Once the mastectomy incision is
made, dissection should proceed directly posterior until the breast capsule is
encountered. This is recognizable as a firm, white fascia separating the
superficial, yellow subcutaneous fat from the deeper, paler glandular breast
tissue (Fig. 18-5). Preoperative measurements on MRI and/or ultrasound can
help guide the identification of this structure by estimating its depth from the
skin. Once encountered, this fascia should be followed to the superior,
inferior, medial, and lateral limits of the mastectomy dissection. This is an
avascular plane and minimal operative bleeding should be expected. Any
subcutaneous perforators encountered should be carefully preserved,
specifically those arising from the second, third, and fourth intercostal
interspaces which represent significant contributors to skin flap perfusion.
Given the avascular nature of this plane, we prefer sharp dissection, only
using electrocautery as needed for hemostasis, to minimize trauma to the
overlying subcutaneous tissue and skin.
The variable and patient-specific nature of the breast gland, and thus the
investing breast capsule, has been recognized pathologically and
radiographically (8,16,17). Based on preoperative and postoperative MRI, we
have previously identified that mastectomy flap thickness increases as one
progresses from anterior to posterior on the breast (8). Absolute mastectomy
flap thickness will not be uniform throughout a patient’s entire breast. Thus,
the surgeon must be cautious to follow the breast capsule precisely rather
than maintaining an unchanging flap thickness throughout the dissection, as
this will either unnecessarily thin the flap in some areas or leave breast tissue
behind in others, compromising the reconstructive or oncologic outcome,
respectively. Specifically, Cooper ligaments carry breast tissue more
superficially toward the dermis and these areas should thus be taken more
superficially for a complete oncologic resection (13).
FIGURE 18-5 During the mastectomy, dissection should proceed directly posterior
until the breast capsule is encountered. As visualized below, this layer is recognizable
as a firm, white fascia separating the yellow subcutaneous fat superficially from the
deeper, paler glandular breast tissue.

It is important for the surgeon to continually assess the quality of the


mastectomy flaps as they are being dissected. This will help to ensure that the
correct plane is being followed throughout the course of this dissection. The
significant impact of mastectomy flap quality and perfusion based on
anatomic intraoperative dissection to ensure optimal outcomes cannot be
overstated. We have identified an absolute mastectomy flap thickness of 8
mm as a threshold value. Ischemic complications were found to be
significantly higher in flaps with a thickness less than 8 mm compared to
thicknesses greater than this value (8). However, as previously noted, an
anatomically dissected mastectomy flap is not uniform in thickness as the
depth of the breast capsule varies among patients and even within a patient
depending on breast location.
With this in mind, we found that nipple-sparing mastectomies with
ischemic complications had a postoperative flap thickness, as measured on
MRI, that was only approximately 50% as thick as the corresponding average
flap thickness measured on preoperative MRI. This ratio of overall
postoperative to preoperative MRI mastectomy flap thickness was
significantly lower compared to reconstructions without ischemic
complications. Thus, patients with postoperative flap thicknesses that more
closely approximated their predicted thicknesses based on preoperative MRI
had decreased ischemic complications (8). This signifies that anatomic
dissection improved mastectomy flap tissue perfusion, which in turn
decreased risk of flap ischemia. While each patient’s unique breast anatomy
will vary, this demonstrates the importance of dissecting the breast at the
level of the breast capsule during the mastectomy, regardless of absolute
mastectomy flap thickness.
INTRAOPERATIVE CARE
As discussed, mastectomy flaps must be assessed clinically in a continual
fashion during dissection to ensure that an anatomic plane is established and
then followed. Even if the majority of the mastectomy flap is precisely
dissected in the correct plane, one small area of impaired perfusion due to
flap thinning can lead to reconstructive demise. Conversely, if one area of the
flap is left overly thick, breast tissue can be left behind, risking locoregional
recurrence. Clinical assessment is critical in this regard. If it is recognized
during dissection that the breast capsule plane has been left, care should be
taken to reestablish the correct plane. Any overly thick areas can be trimmed
to the correct level using the reestablished plane as a guide. Overly thinned
areas are more difficult to treat and the subcutaneous tissue cannot be
replaced. However, this information can be utilized to guide and alter the
intraoperative plan as necessary to minimize risk of ischemic complications.
After the mastectomy dissection is complete, the reconstructive surgeon
must assess the perfusion of the remaining skin flaps in determining the
reconstructive plan that will be followed in a manner to optimize outcomes
and minimize risk of complications, including reconstructive failure. This
assessment should be made clinically with or without the assistance of
adjunctive technology.
In our experience, clinical assessment is a reliable and cost-effective
manner of evaluating tissue perfusion. Once the mastectomy is performed,
the flaps are assessed for the presence of skin edge bleeding, which indicates
good perfusion, as well as exposed dermis on the underside of the flaps,
bruising of the external skin, or electrocautery burns which obviously would
lead to concern for suboptimal perfusion (18). Adjunctive tools for assessing
mastectomy flap skin perfusion include indocyanine green angiography and
tissue oximetry, both of which report the relative perfusion of areas of the
mastectomy flap and can help in determining global or localized mastectomy
flap ischemia (19,20). However, there are no absolute guidelines as to what
device values indicate irreversible flap ischemia, confounding intraoperative
decision-making (20). Further, use of epinephrine-containing solutions at the
beginning of a case precludes the use of these technologies due to persistent
drug-induced vasoconstriction of the vessels perfusing the skin flaps. In our
practice, injection of these dilute solutions optimizes operative conditions for
anatomic mastectomy dissection with benefits that outweigh the disadvantage
of impeding tissue angiography or oximetry. We therefore rely on clinical
assessment in dictating intraoperative decision-making with regard to tissue
perfusion.
If the mastectomy flaps are assessed to be compromised after mastectomy,
various intraoperative maneuvers can be employed to minimize risk and
maximize chances of a successful reconstruction. Any decision should be
made with an aim to decrease tension on the mastectomy flaps to minimize
further perfusion impairment. If a direct-to-implant reconstruction is planned,
conversion to a tissue expander–based reconstruction should be considered.
Similarly, the amount of intraoperative tissue expander fill should be minimal
or none to lessen tension placed on overlying skin flaps. A planned
prepectoral implant–based reconstruction may be converted to a submuscular
reconstruction. This will provide a vascularized tissue layer between the
device and the compromised skin flaps. In autologous-based reconstructions,
a larger skin paddle can be left to fit within the mastectomy incision. This
will offload tension on the skin flaps and minimize tension on the
mastectomy flaps. In cases of severe skin flap compromise, all of the
autologous skin paddle may be left “banked” below the mastectomy flaps. In
a second stage, mastectomy flaps can be widely debrided as necessary and
the underlying banked flap skin can be inset. The most extreme course of
action when mastectomy flap compromise is encountered is to delay
reconstruction. In this case, the mastectomy flaps are simply closed and
delayed reconstruction is performed after at least 2 weeks.
POSTOPERATIVE CARE
Postoperatively, any areas of potential or actual ischemia must be diagnosed
and treated expeditiously to avoid damage and risk to the reconstruction.
Nitroglycerin ointment has been demonstrated to be a cost-effective treatment
in minimizing mastectomy flap necrosis when employed pre-emptively (21).
Once apparent, areas of necrosis must be diagnosed as partial or full
thickness. Partial-thickness injuries may be managed conservatively with
local wound care until they are completely healed. We firmly believe in the
importance of early intervention in cases of full-thickness mastectomy flap
necrosis, which permits proactive, rather than reactive, management. Early
debridement and/or excision of areas of full-thickness necrosis along with
wound closure, if possible, minimizes propagation of the issue and provides
the patient the best chance for a successfully salvaged reconstruction.
It is important to recognize the difference in urgency of treating these
ischemic lesions based on the type of reconstruction that a patient has
undergone. Implant-based reconstructions are obviously more susceptible to
reconstructive failure in the face of mastectomy flap ischemia, especially
when the ischemic area is over any tissue scaffold or an uncovered prosthetic
device. In these cases, early intervention with excision and primary closure of
small areas of necrosis with or without implant exchange may salvage a
reconstruction. Alternatively, larger areas should be managed with expedient
excisional debridement, implant removal, and closure as able followed by
delayed reconstruction, preferentially using autologous tissue. Conversely,
areas of necrosis in autologous reconstruction represent a lesser threat to the
overall reconstruction although they can still impart significant morbidity to
the aesthetics of the resultant breast. We still favor early debridement and
excision of full-thickness areas of necrosis in these cases with primary
closure versus wound care as necessary.

CASES

As discussed, the absolute thicknesses of mastectomy skin flaps after


mastectomy dissection will be variable among individuals and even
within each individual’s breast depending on the location within the
breast. This fact underscores the utility of and need for anatomic
mastectomy dissection at the level of the breast capsule to perform a
complete oncologic resection while maximizing skin flap perfusion and
chances for reconstructive success. This technique requires early
identification of the breast capsule and meticulous following of its course
during dissection to the anatomic limits of the mastectomy. Inherently,
due to the variable nature of this deep structure of the breast capsule, this
dissection must be individualized to each patient’s anatomy with variable
absolute flap thicknesses in each unique case.

CASE 1

The variable nature of the breast capsule and resultant mastectomy flap
thicknesses is evident in examining patients’ pre- and postoperative
breast MRIs. Preoperatively, representative measurements can be made at
the midbreast level in the sagittal plane from the skin to the level of the
breast capsule on the superior and inferior prospective mastectomy flaps.
Both patient 1 and patient 2 presented herein underwent immediate
implant-based breast reconstruction after nipple-sparing mastectomy. In
patient 1, these measurements are 14.2 and 8.5 mm, respectively. In this
patient, the postoperative MRI after implant-based reconstruction reveals
midbreast superior and inferior flap thicknesses of 3.9 and 3.4 mm,
respectively, only. This patient had a thinner breast skin and
subcutaneous tissue layer with postoperative/preoperative flap thickness
ratios of 27.5% and 40.0%, respectively. This suggests that the
mastectomy flaps were created thinner than those that would result from
an anatomic mastectomy dissection in the same patient (Fig. 18-6).
FIGURE 18-6 A: Preoperative breast MRI in patient 1 who has an overall
thinner breast skin and subcutaneous tissue layer. Predicted superior and
inferior mastectomy flap thicknesses are measured at 14.2 and 8.5 mm at the
midbreast level in the sagittal plane from the skin to the level of the breast
capsule prior to nipple-sparing mastectomy and immediate implant-based
breast reconstruction. B: Postoperative MRI of the same patient reveals
actual midbreast superior and inferior mastectomy flap thicknesses of 3.9
and 3.4 mm only for postoperative/preoperative flap thickness ratios of
27.5% and 40.0%, respectively. This suggests that an anatomic mastectomy
plane at the level of the breast capsule was not followed.

CASE 2

Alternatively, patient 2 had ideal superior and inferior mastectomy flap


thicknesses in the midbreast plane of 18.6 and 18.4 mm, respectively, on
preoperative MRI. This patient would be expected to have ideal
mastectomy flaps that are thicker overall after anatomic mastectomy
dissection than those expected in patient 1. Postoperatively, this patient
has superior and inferior mastectomy flap thicknesses of 14.2 and 12.9
mm, respectively. Post-/preoperative flap thickness ratios are therefore
100.0% and 70.1%, respectively. An anatomic dissection preserving
greater vascularity to the skin flaps was therefore accomplished in this
case (Fig. 18-7).

FIGURE 18-7 A: Preoperative MRI of patient 2 with ideal superior and


inferior mastectomy flap thicknesses in the midbreast plane measured at 18.6
and 18.4 mm, respectively, on preoperative MRI. Ideal mastectomy flaps in
this patient are thicker overall than those expected in patient 1. B:
Postoperatively, this patient has superior and inferior mastectomy flap
thicknesses of 14.2 and 12.9 mm on MRI with pre-/postoperative flap
thickness ratios of 76.3% and 70.1%, respectively. A more anatomic
mastectomy dissection was thus followed in this patient.
GENERIC RISKS
As with any mastectomy procedure, an anatomic mastectomy dissection
carries inherent risk of mastectomy flap compromise with impaired perfusion.
Depending on the severity of this compromise, mastectomy flap necrosis,
whether partial or full thickness, may result. Impaired mastectomy flap
perfusion also leaves the tissue more susceptible to infection, which can be
more severe in these cases. In either the face of mastectomy flap necrosis or
infection, overall reconstructive success is severely threatened and surgical
intervention, dictated by the type of reconstruction and clinical circumstance
as discussed above, will often be necessary for salvage. However, an
anatomic dissection can minimize the risk of these potentially devastating
outcomes. We have previously demonstrated that nipple-sparing
mastectomies with ischemic complications were found to have a
postoperative mastectomy flap thickness that was only approximately 50% as
thick as the corresponding average preoperative anatomic breast flap
thickness. This ratio of overall postoperative to preoperative flap thickness
was significantly lower compared to the group without ischemic
complications. This highlights the importance of performing an anatomic
mastectomy dissection at the level of the breast capsule while maintaining
maximal perfusion to the overlying skin flaps in order to minimize risk of
complications.
OUTCOMES
In assessing outcomes with anatomic mastectomy dissection at the level of
the breast capsule to optimizing mastectomy flaps, it is imperative to consider
both oncologic as well as reconstructive results.
Using nipple-sparing mastectomy as a representation of the most recent
advances in mastectomy technique, meta-analyses have identified rates of
locoregional recurrence in therapeutic, prophylactic, and well as mixed NSM
populations ranging from 0.0% to 25.7% with a wide variability in follow-up
times (22). We have recently identified a per breast rate of local recurrence
of 1.6% with a per breast rate of regional recurrence of 0.6% in 496 nipple-
sparing mastectomies undertaken for therapeutic indications (22). These rates
compare favorably with locoregional recurrence rates with total and skin-
sparing techniques. Importantly, in univariate analysis, tumor to nipple
distance ≤1 cm was the only significant risk factor for recurrence (OR =
13.5833, p = 0.0385) while no factors were significant in regression analysis
in our analysis (22). Moreover, we have also found that mastectomy flap
thicknesses after therapeutic (8.86 mm) and prophylactic (8.54 mm) nipple-
sparing mastectomies were similar (p = 0.5822). This underscores the
concept that mastectomy dissection should and may occur safely in the same
anatomic plane of the breast capsule regardless of mastectomy indication and
across patient populations.
With regard to reconstructive outcomes, it is most important to consider
ischemic complications when assessing outcomes using an anatomic
dissection technique. In a recent review, we demonstrate overall rates of
ischemic complications in greater than 1,000 nipple-sparing mastectomies
including partial and complete nipple necrosis along with major and minor
mastectomy flap necrosis with rates ranging from approximately 2.7% to
9.9% (23). Within these favorable results, the impact of mastectomy flap
quality and perfusion based on intraoperative anatomic dissection in
immediate breast reconstruction cannot be overstated. In our study examining
the impact of mastectomy flap thickness on outcomes using MRI, we have
identified an absolute mastectomy flap thickness of 8 mm as a threshold
value. Mastectomies with an average, overall thickness below this value had
a significantly higher rate of ischemic complications compared to those with
a thickness greater than 8 mm (8). However, as previously noted, an
anatomically dissected mastectomy flap is not uniform in thickness among
individuals and even within the same patient.
In this same study, we found that nipple-sparing mastectomies with
ischemic complications had a postoperative flap thickness, as measured on
MRI, that was only approximately 50% as thick as the corresponding average
flap thickness measured on preoperative MRI. This ratio of overall
postoperative to preoperative MRI mastectomy flap thickness was
significantly lower compared to the group without ischemic complications, in
whom this ratio was near 75%. Thus, when a patient’s postoperative flap
thickness more closely approximates the thickness predicted on that same
patient’s preoperative MRI, ischemic complications were decreased (8).
Anatomic dissection at the breast capsule level thus improved mastectomy
flap tissue perfusion, which in turn decreased risk of ischemic complications.
While each patient’s unique breast anatomy will vary, dissecting the breast at
the level of the breast capsule during the mastectomy, regardless of absolute
thickness, will optimize flaps and maximize reconstructive success (Fig. 18-
8).

FIGURE 18-8 Average overall postoperative to preoperative NSM flap thickness


ratio stratified by ischemic complications in patients undergoing immediate breast
reconstruction.
CONCLUSION
Mastectomy flap tissue perfusion represents perhaps the most important
factor in the surgeon’s ability to provide a patient with an aesthetic immediate
breast reconstruction. This perfusion is dependent on an optimized, anatomic,
and patient-specific dissection at the level of the breast capsule that
maximizes oncologic resection and minimizes trauma to the overlying skin
flaps. Preoperative patient assessment along with careful consideration of
preoperative as well as intraoperative imaging can help facilitate this
dissection. Intraoperative, continuous care must be taken to assess that the
breast capsule has been identified and that this plane is followed
circumferentially in performing the mastectomy. Postoperatively, areas of
impaired perfusion should be managed expeditiously to minimize their effect
and maximize chances of salvaging a successful immediate reconstruction.
Plastic and oncologic surgeons must be active and collaborative in achieving
their mutual oncologic and reconstructive goals in optimizing surgical care
for patients undergoing mastectomy.

REFERENCES

1. Jones C, Lancaster R. Evolution of operative technique for mastectomy.


Surg Clin North Am 2018;98(4):835–844.
2. Robertson SA, Rusby JE, Cutress RI. Determinants of optimal
mastectomy skin flap thickness. Br J Surg 2014;101:899–911.
3. Rehnke RD, Groening RM, Van Buskirk ER, et al. Anatomy of the
superficial fascia system of the breast: a comprehensive theory of breast
fascial anatomy. Plast Reconstr Surg 2018;142(5):1135–1144.
4. Kuhl C. The current status of breast MR imaging. Part I. Choice of
technique, image interpretation, diagnostic accuracy, and transfer to
clinical practice. Radiology 2007;244:356–378.
5. Kuhl CK. Current status of breast MR imaging. Part 2. Clinical
applications. Radiology 2007;244:672–691.
6. Ponzone R, Maggiorotto F, Carabalona S, et al. MRI and intraoperative
pathology to predict nipple-areola complex (NAC) involvement in
patients undergoing NAC-sparing mastectomy. Eur J Cancer
2015;51:1882–1889.
7. Storm-Dickerson T, Sigalove N. Prepectoral breast reconstruction: the
breast surgeon’s perspective. Plast Reconstr Surg 2017;140(6S
Prepectoral Breast Reconstruction):43S–48S.
8. Frey JD, Salibian AA, Choi M, et al. Mastectomy flap thickness and
complications in nipple-sparing mastectomy: objective evaluation using
magnetic resonance imaging. Plast Reconstr Surg Glob Open
2017;5:e1439.
9. Colwell AS, Tessler O, Lin AM, et al. Breast reconstruction following
nipple-sparing mastectomy: predictors of complications, reconstruction
outcomes, and 5-year trends. Plast Reconstr Surg 2014;133:496–506.
10. Frey JD, Choi M, Salibian AA, et al. Comparison of outcomes with
tissue expander, immediate implant, and autologous breast
reconstruction in greater than 1000 nipple-sparing mastectomies. Plast
Reconstr Surg 2017;139:1300–1310.
11. Frey JD, Salibian AA, Levine JP, et al. Incision choices in nipple-
sparing mastectomy: a comparative analysis of outcomes and evolution
of a clinical algorithm. Plast Reconstr Surg 2018;142(6):826e–835e.
12. Frey JD, Salibian AA, Choi M, et al. Moving towards optimizing
outcomes in nipple-sparing mastectomy: ideal mastectomy flap
thickness is not one size fits all. Plast Reconstr Surg Glob Open
2019;7(1):e2103.
13. Rancati A, Angrigiani C, Hammond D, et al. Preoperative digital
mammography imaging in conservative mastectomy and immediate
reconstruction. Gland Surg 2016;5(1):9–14.
14. Salibian AH, Harness JK, Mowlds DS. Nipple-sparing mastectomy in
the large, ptotic breast. In: Harness J, Willey S, eds. Operative
Approaches to Nipple-Sparing Mastectomy. Switzerland, Cham:
Springer; 2017.
15. Salibian AH, Harness JK, Mowlds DS. Subcutaneous reconstruction
without acellular dermal matrix. In: Harness J, Willey S, eds. Operative
Approaches to Nipple-Sparing Mastectomy. Switzerland, Cham:
Springer; 2017.
16. Beer GM, Varga Z, Budi S, et al. Incidence of the superficial fascia and
its relevance in skin-sparing mastectomy. Cancer 2002;94:1619–1625.
17. Larson DL, Basir Z, Bruce T. Is oncologic safety compatible with a
predictably viable mastectomy skin flap? Plast Reconstr Surg
2011;127:27–33.
18. Sbitany H, Piper M, Lentz R. Prepectoral breast reconstruction: a safe
alternative to submuscular prosthetic reconstruction following nipple-
sparing mastectomy. Plast Reconstr Surg 2017;140:432–443.
19. Lin SJ, Nguyen MD, Chen C, et al. Tissue oximetry monitoring in
microsurgical breast reconstruction decreases flap loss and improves
rate of flap salvage. Plast Reconstr Surg 2011;127:1080–1085.
20. Chattha A, Bucknor A, Chen AD, et al. Indocyanine green angiography
use in breast reconstruction: a national analysis of outcomes and cost in
110,320 patients. Plast Reconstr Surg 2018;141:825–832.
21. Turin SY, Li DD, Vaca EE, et al. Nitroglycerin ointment for reducing
the rate of mastectomy flap necrosis in immediate implant-based breast
reconstruction. Plast Reconstr Surg 2018;142:264e–270e.
22. Frey JD, Salibian AA, Lee J, et al. Oncologic trends, outcomes, and risk
factors for locoregional recurrence: an analysis of tumor-to-nipple
distance and critical factors in therapeutic nipple-sparing mastectomy.
Plast Reconstr Surg 2019;143(6):1575–1585.
23. Frey JD, Salibian AA, Karp NS, et al. Comparing therapeutic versus
prophylactic nipple-sparing mastectomy: does indication inform
oncologic and reconstructive outcomes? Plast Reconstr Surg
2018;142(2):306–315.
CHAPTER 19

Male Breast Cancer: Surgery of the


Breast
JOHN VINCENT KILUK | BLAISE P. MOONEY | HATEM SOLIMAN | ROBERTO DIAZ
HISTORY
Male breast cancer is a rare form of cancer that comprises approximately 1%
of all cases of breast malignancies. Males carry a 0.1% lifetime risk of
developing breast cancer that is significantly less than the 12% risk of
women. In 2019, there will be an estimated 2,670 new cases of male breast
cancer in the United States compared to 268,600 cases of the female variant
(1). As a result of the rarity of this cancer, studying male breast cancer has
been challenging, as prospective trials would be difficult to accrue. Current
recommendations toward management have mostly been based on
retrospective male data and the assumption that outcomes of treatments
would be similar as female breast cancer, for which data are more robust.
RISK FACTORS
Even though most patients present without any risk factors, several potential
features have been identified to increase the risk of male breast cancer. Risk
assessment should always start with genetic testing. Male patients often carry
a family history of malignancies with 15% to 20% of patients reporting a
family member with either breast or ovarian cancer (2). Many genes have
been associated with male breast cancer including BRCA1, CHEK2, P53,
PTEN, PALB2 but the most common association is with BRCA2 mutations.
BRCA2 carriers demonstrate a 5% to 10% lifetime risk of developing cancer
that is interestingly less than the average woman’s lifetime risk of breast
cancer (3). Despite a lack in data supporting prophylactic mastectomy in
genetic carriers, results in genetic testing are critical for assessing other
family members risk of cancer (daughters, sisters, etc.) and may affect
screening of other cancers (BRCA2 carriers are increased risk of prostate and
skin cancers).
Hormonal factors that lead to increased estrogen to testosterone levels
appear to be influential in patients developing male breast cancer (4).
Klinefelter syndrome, which is characterized with the XXY karyotype, has
been reported in to up to 7.5% of patients with male breast cancer (5). These
patients have low testosterone levels and high gonadotropin concentrations.
Other factors that increase estrogen and/or lower testosterone (prostate cancer
treatment, hormonal therapies, testicular/liver damage) have been associated
with male breast cancer as well.
Additional risk factors are similar to females with breast cancer. Male
patients with a history of radiation treatments for Hodgkin disease may be
prone to developing a future cancer within the treatment field years after the
completion of treatment. Age is a risk factor of breast cancer with the peak
risk of developing breast cancer to be approximately 75 years of age (2).
Environmental exposures while working with chemicals, synthetics, or
electromagnetic fields have also demonstrated increased risks of male breast
cancer (4).
In discussing risk of male breast cancer, it is important to mention
gynecomastia. To date, there has been no association between gynecomastia
and male breast cancer.
CLINICAL PRESENTATION
The most common presentation for male breast cancer is a painless,
subareolar breast mass. Nipple discharge, skin involvement, axillary
lymphadenopathy are additional features that may be present on examination.
Nonpalpable breast cancers are rare as males do not undergo routine,
screening mammography.
Compared to females, males may present at more advanced stages of
disease. Multiple factors may play a role in this later presentation ranging
from less routine screening to a possible lack of awareness of male breast
cancer by both patients and providers. Figure 19-1 demonstrates a locally
advanced male breast cancer at presentation. A SEER review by Leon-Ferre
compared stage at presentation between male and female breast cancer
demonstrated more advanced stages in male patients (6). Stage 2 (43% vs.
28%), stage 3 (8% vs. 5%), and stage 4 (3% vs. 2%) disease were all more
common in male patients with breast cancer.
FIGURE 19-1 Patient presenting with a locally advanced male breast cancer.
RADIOLOGY
Radiologic workup of the male breast for a palpable mass or clinical finding
begins with a diagnostic mammogram (7). A bilateral mammogram is
extremely useful. Even if symptoms are unilateral, having the opposite side
as a comparison is helpful in making diagnosis and deciding if Ultra Sound
(US) is appropriate. The finding is often gynecomastia, which can be bilateral
or unilateral. Gynecomastia, proliferation of ducts and stroma, is the most
common abnormality in the male breast. There are three main imaging
patterns of gynecomastia (nodular, dendritic and diffuse glandular). It is
classically described as flame shaped and should have indistinct borders,
existing in harmony with surrounding tissue. The most important thing to
remember about gynecomastia is that it must be subareolar. From an imaging
perspective, differentiating a malignancy from gynecomastia in the
subareolar region relies upon evaluation of the borders (Fig. 19-2).
Malignancies often have convex borders, however when the borders are
spiculated, this can cause some confusion and mimic gynecomastia. Even
though male breast cancers most commonly occur in the subareolar location,
they can be located anywhere. Any mass in the male breast that is not
subareolar is not gynecomastia, and will require additional action (8).
FIGURE 19-2 Image on Left is a Right MLO digital mammogram of subareolar
invasive ductal carcinoma. Note visible inferior and superior convex margins. Image
on Right is a Right MLO digital mammogram of benign gynecomastia with classic
“flame-shaped” margins.

If the appearance is classic “flame shaped” on mammogram and there is


NO evidence of a mass, then US should be avoided as this will usually lead
to an unnecessary biopsy. US is indicated if the mammogram demonstrates a
visible mass or the palpable breast mass is located away from the nipple (Fig.
19-3). Figure 19-4 demonstrates a left subareolar mass with convex borders
and coarse calcifications on mammography. Calcifications seen on
mammography deserve workup in the male breast. Magnification views
should be performed to determine extent and plan safe core biopsy. US of the
area of calcifications is recommended, as this might facilitate a safer US-
guided biopsy. A negative US should not dissuade one from sampling
calcifications in the male breast as calcifications are frequently associated
with ductal carcinoma in situ (DCIS). MRI of the breast offers little
advantage other than assisting in ruling out chest-wall involvement.
FIGURE 19-3 US images of the mass found on mammogram demonstrating a
heterogeneous hypoechoic hypervascular oval mass with fairly circumscribed
borders. US-guided biopsy revealed invasive ductal carcinoma.

In the male breast, the majority of malignancies are subareolar and


metastasis to the axilla is common. It has been reported that 50% of men have
axillary nodal metastasis at initial presentation (9). US of the ipsilateral axilla
should be included. It is important to note the morphology of the nodes
matters more than the overall size. Displacement of the fatty hilum, increased
cortical thickness >3 mm or irregular contour of the cortex are suspicious
findings and warrant tissue sampling (Fig. 19-5). If US-guided axillary
lymph node biopsy reveals metastatic disease, then additional staging
examinations similar to what female breast cancer patients undergo are
indicated. Computed tomography (CT) of the thorax and abdomen and
Tc99m-HDP whole-body bone scan are recommended.
FIGURE 19-4 LEFT MLO and CC digital mammogram demonstrate a spiculated
mass with calcifications in the retroareolar location. Note that no LEFT axillary
nodes are seen on the LEFT MLO mammogram.
PATHOLOGY
The most common histology encountered in male breast cancer is invasive
ductal cancer. Isolated ductal carcinoma in situ (DCIS) is very uncommon as
this usually presents with calcifications on mammography and males do not
receive screening mammography. Other histologic subtypes (lobular,
papillary, metaplastic, mucinous, or tubular) are rare.
The vast majority of male breast cancers are estrogen receptor (ER)
positive. The most comprehensive pathologic review of male breast cancer
was performed by the EORTC 10085/TBCRC/BIG/NABCG International
Male Breast Cancer Program (10). In this study, close to 1,500 male breast
cancer cases were centrally reviewed by pathology. Using immunochemistry,
41.9% of cases were classified as Luminal A and 49.2% of cases were
Luminal B, HER2 negative. ER-negative tumors were exceeding rare as
Basal subtypes and Nonluminal HER2 subtypes comprised 1% and 0.1% of
cases, respectively. Clinically, we have become suspicious of any male
presenting with an ER- male breast cancer. Upon further workup, many of
these “male breast cancers” turn up having a nonbreast primary, most
commonly a skin malignancy.

FIGURE 19-5 High-frequency US of LEFT axilla demonstrates a lymph node with


abnormal thickened cortex >3 mm and a scalloped appearance (arrows). US-guided
biopsy of node revealed metastatic adenocarcinoma.

HER2 is usually negative in male breast cancer but up to 8% may be


HER2 positive. These tumors are important to identify, as HER2 results
would strongly influence decisions on chemotherapy and trastuzumab
(Herceptin).
SURGICAL MANAGEMENT
Surgical management of male breast cancer is similar to female breast cancer
in that both mastectomy and lumpectomy are options for patients. As most
male breast cancers are in a subareolar location and may be closely associated
with the nipple, most males elect to pursue mastectomy. Not only does this
option remove the nipple ensuring clear margins, it may spare the patient the
need for radiation that would absolutely be required in a lumpectomy. For
tumors not directly associated with the nipple, lumpectomy is a potential
alternative to mastectomy (11,12).
Axillary staging with sentinel node biopsy is well established (11,13). The
technique for this procedure is identical to female patients. At this time, the
standard for a positive axillary node is still an axillary dissection. While
multiple studies have looked at the role of avoiding an axillary dissection
despite having a positive sentinel node, none of these studies have included
males. Discussions with patients regarding need for dissection following a
positive sentinel node need to emphasize an overall lack of long-term data
regarding recurrence risk. On the other hand, clinicians need to balance the
benefit of axillary dissection with potential complications of lymphedema
that could seriously impact the patient’s quality of life.
Although patients usually do not have reconstruction, options are available
to patients who wish to improve the cosmetic appearance of their mastectomy
incision. Simple options for male patients include nipple reconstruction and
fat grafting to the mastectomy site to increase volume (14). 3D Tattooing
offers an additional simple option to improve the appearance to the surgical
site. More complex reconstructive options of using a small implant or flap
have been described but are rarely performed (15,16).
MEDICAL ONCOLOGY MANAGEMENT
In a normal adult male, circulating levels of estradiol range between 10 and
40 pg/mL which is significantly less than the normal range in a
premenopausal female (15 to 350 pg/mL). Certain disease states such as
Klinefelter syndrome, exogenous estrogen intake in transsexual males, and
cirrhosis lead to increases in circulating estrogen which can increase the risk
of male breast cancer (17). However, the majority of male breast cancer cases
will not arise in the setting of very high estrogen states. Understanding
appropriate use of endocrine therapy in male breast cancer is important as
>90% of male breast tumors are estrogen/progesterone receptor positive (18).
A large National Cancer Database study revealed males were less likely to
receive endocrine therapy compared to females, possibly due to less
experience in treating these cases (19). Testosterone produced by the
testicular Leydig cells is converted by aromatase into estradiol, while adrenal
androstenedione is converted by aromatase to estrone (17). The standard
endocrine treatment for male breast cancer is tamoxifen 20 mg/day for 5 to
10 years unless there is a significant contraindication. There is no prospective
comparative adjuvant data between tamoxifen and aromatase inhibitors, but a
German registry study of 257 males (207 treated with tamoxifen and 50
treated with aromatase inhibitors) demonstrated an improved survival with
tamoxifen (20). There are concerns that use of an aromatase inhibitor without
gonadal suppression is inadequate to completely suppress estradiol
production by testicular Leydig cells. So if an aromatase inhibitor is used it is
recommended to combine it with gonadal suppression. Interestingly,
estrogens do play a role in regulating male libido, spermatogenesis, and
erectile function. Perturbations in estrogen function during treatment can lead
to side effects such as decreased libido (particularly in lower testosterone
states), altered mood, hot flashes, fatigue, and weight gain (21). In the
metastatic setting there is limited data regarding the use of aromatase
inhibitors (combined with gonadal suppression) and the selective estrogen
receptor downregulator fulvestrant (22,23). However, they do appear to be
effective in males and can be used alongside other targeted therapies used in
females such as cyclin-dependent kinase 4/6 inhibitors and the mammalian
target of rapamycin inhibitor everolimus.
The use of adjuvant chemotherapy in male breast cancer is also
extrapolated from the current guidelines for female breast cancer.
Historically, clinicopathologic factors such as tumor size, nodal involvement,
and grade were used to determine adjuvant chemotherapy use (24). Recent
data on the use of genomic assays such as the 21 gene recurrence score (RS)
in males indicate a similar distribution of scores to female breast cancer with
low rates of chemotherapy prescription in low-risk cases (25). Males tended
to have higher expression levels of estrogen and progesterone receptors, and
the rarity of lobular cancer in males may also affect the biology of tested
cases as compared to female cohorts. The 5-year breast cancer–specific
survival rates for men with RS <18 was 99% and RS ≥31 was 81% in an
NCDB study of 3,806 men demonstrating the prognostic capability of the 21
gene RS in early-stage male breast cancer (26). No males were enrolled in the
TAILORx trial so no prospective data using the newer risk cutoffs are
available, but it is likely that the decision-making process around
chemotherapy prescription will be extrapolated from the female data (27).
Limited data on the use of adjuvant cyclophosphamide/methotrexate/5-
fluorouracil and 5-fluorouracil/doxorubicin/cyclophosphamide chemotherapy
did demonstrate improved survival rates over untreated historical controls in
small cohorts (28,29). For HER2 tumors typical taxane or anthracycline-
taxane regimens are offered when indicated. Cases that are HER2
overexpressing receive similar targeted therapies containing trastuzumab and
pertuzumab as warranted based on limited efficacy data in male breast cancer
cases.
RADIATION ONCOLOGY MANAGEMENT
Current recommendations for the treatment of male breast cancer patients
with radiation therapy follow the similar algorithms employed to treat female
breast cancer patients, including the use of postlumpectomy radiation therapy
and adjuvant postmastectomy radiation therapy (PMRT) in high-risk male
breast cancer patients (2,12,30–34). Stage for stage, the pattern of local
recurrence in male breast cancer is similar to female breast cancer (32), and
radiotherapy should be considered in cases with axillary nodal involvement,
muscle invasion, and retroareolar location (2).
An analysis of 1,337 men with invasive ductal carcinoma who underwent
primary surgical resection from 1983 to 2002 using the surveillance,
epidemiology, and end results (SEER) database found that radiotherapy was
associated with improved overall survival (OS) for stage I and a trend for
improved survival for stage II. The factors that predicted for worse OS on
multivariate analysis were no postoperative radiotherapy and advancing age,
stage, and grade. Postoperative radiotherapy predicted for improved OS but
not cause-specific survival in multivariate analysis when controlled for stage,
grade, and age (35).
In a SEER database analysis of 5,425 men with breast cancer from 1983 to
2009, 86.8% underwent mastectomy and 13.2% underwent lumpectomy. The
authors found no differences in breast cancer–specific survival by the type of
surgery (36). However, the authors did not stratify the partial mastectomy
patients by receipt of radiotherapy (12,36).
In a National Cancer Database Analysis (NCDB) of 8,445 stage I-II men
from 2004 to 2014, patients who underwent partial mastectomy with
radiation therapy had greater 10-year overall survival (73.8%) compared to
partial mastectomy alone (56.3%) and total mastectomy with (56.3%) and
without (58.0%) radiation therapy. These findings remained significant after
controlling for clinicopathologic and demographic group differences in
multivariable models. Based on these surprising findings, the authors
advocate greater consideration and adoption of breast conservation therapy
for men with breast cancer because their data show a survival benefit with
radiotherapy in male breast cancer patients after partial mastectomy (12).
The majority of studies describing PMRT in male breast cancer are small
retrospective analyses (2). In a retrospective series of 81 men with IDC,
PMRT had a significant improvement in local recurrence (24% vs. 4%), but
no benefit in overall survival (37). In a SEER database analysis of 1,933 men
with localized or regional nonmetastatic breast cancer from 1998 to 2013,
PMRT was associated with improved 5-year overall survival in men with
node-positive breast cancer (83% vs. 54%, p < 0.001). In men with one to
three positive nodes, PMRT was associated with improved 5-year OS (79%
vs. 72%, p = 0.05), with an absolute risk reduction of 7%. In men with four or
more positive nodes, PMRT was associated with improved 5-year OS (73%
vs. 53%, p < 0.001), with an absolute risk reduction of 20%. In 883 patients
with pN0 disease, PMRT was not associated with a significant effect on 5-
year OS (86% vs. 82%, p = 0.334). On multivariate analysis of their
unmatched cohort, use of PMRT and ER-positive disease were independent
predictors for improved OS. Patients who would benefit from PMRT are the
ones with known high-risk factors for locoregional recurrence: increasing
number of positive lymph nodes, high grade, and larger size (30).
Radiotherapy improves oncologic outcomes in men with breast cancer who
undergo partial mastectomy (12) and total mastectomy with pN+ disease
(30). However, there are studies showing lower rates of compliance with
radiotherapy among men with breast cancer when compared to women
(31,33). For instance, Cardoso et al. report that PMRT was not given to
30.7% of men with pN+ disease and postlumpectomy radiation was not given
to 45% of men treated with breast conservation surgery (31). In a SEER
database analysis of 382,030 women and 712 men with breast cancer from
1983 to 2009 who underwent a lumpectomy, men were found to receive
suboptimal oncologic care when compared to women. These authors found
gender disparities in the receipt of adjuvant radiation (69.8% of women and
35.4% of men) and axillary lymph node sampling (81.6% of women vs.
59.2% of men) following lumpectomy (33). Nonetheless, the use of PMRT
has been increasing over time in men from 1998 to 2013 in a study using the
SEER database (30).
CONCLUSIONS
Even though male breast cancer patients present at more advanced stages,
overall outcomes are similar to female breast cancer when compared stage by
stage. When reviewing relative survival rates of male and female breast
cancer from the SEER database, matched survival by stage is similar after
accounting for age of diagnosis and poorer life expectancy (2,38). Although
there are limited dedicated studies on male breast cancer, outcomes should
hopefully continue to improve as awareness improves and further dedicated
research comes forward.

REFERENCES

1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2019. CA Cancer J


Clin 2019;69(1):7–34.
2. Korde LA, Zujewski JA, Kamin L, et al. Multidisciplinary meeting on
male breast cancer: summary and research recommendations. J Clin
Oncol 2010;28(12):2114–2122.
3. Breast Cancer Linkage Consortium. Cancer risks in BRCA2 mutation
carriers. J Natl Cancer Inst 1999;91(15):1310–1316.
4. Abdelwahab Yousef AJ. Male breast cancer: epidemiology and risk
factors. Semin Oncol 2017;44(4):267–272.
5. Hultborn R, Hanson C, Kopf I, et al. Prevalence of Klinefelter’s
syndrome in male breast cancer patients. Anticancer Res
1997;17(6D):4293–4297.
6. Leon-Ferre RA, Giridhar KV, Hieken TJ, et al. A contemporary review
of male breast cancer: current evidence and unanswered questions.
Cancer Metastasis Rev 2018;37(4):599–614.
7. Nguyen C, Kettler MD, Swirsky ME, et al. Male breast disease: pictorial
review with radiologic-pathologic correlation. Radiographics
2013;33(3):763–779.
8. Iuanow E, Kettler M, Slanetz PJ. Spectrum of disease in the male breast.
AJR Am J Roentgenol 2011;196(3):W247–W259.
9. Giordano SH. A review of the diagnosis and management of male breast
cancer. Oncologist 2005;10(7):471–479.
10. Vermeulen MA, Slaets L, Cardoso F, et al. Pathological characterisation
of male breast cancer: Results of the EORTC
10085/TBCRC/BIG/NABCG International Male Breast Cancer
Program. Eur J Cancer 2017;82:219–227.
11. Fentiman IS. Surgical options for male breast cancer. Breast Cancer Res
Treat 2018;172(3):539–544.
12. Bateni SB, Davidson AJ, Arora M, et al. Is breast-conserving therapy
appropriate for male breast cancer patients? A national cancer database
analysis. Ann Surg Oncol 2019;26(7):2144–2153.
13. Boughey JC, Bedrosian I, Meric-Bernstam F, et al. Comparative
analysis of sentinel lymph node operation in male and female breast
cancer patients. J Am Coll Surg 2006;203(4):475–480.
14. Al-Kalla T, Komorowska-Timek E. Breast total male breast
reconstruction with fat grafting. Plast Reconstr Surg Glob Open
2014;2(11):e257.
15. Bamba R, Krishnan NM, Youn R, et al. The use of low-profile silicone
breast implants in male breast reconstruction. Plast Reconstr Surg
2018;141(2):324e–325e.
16. Spear SL, Bowen DG. Breast reconstruction in a male with a transverse
rectus abdominis flap. Plast Reconstr Surg 1998;102(5):1615–1617.
17. Niewoehner CB, Schorer AE. Gynaecomastia and breast cancer in men.
BMJ 2008;336(7646):709–713.
18. Chavez-Macgregor M, Clarke CA, Lichtensztajn D, et al. Male breast
cancer according to tumor subtype and race: a population-based study.
Cancer 2013;119(9):1611–1617.
19. Venigalla S, Carmona R, Guttmann DM, et al. Use and effectiveness of
adjuvant endocrine therapy for hormone receptor-positive breast cancer
in men. JAMA Oncol 2018;4(10):e181114.
20. Eggemann H, Ignatov A, Smith BJ, et al. Adjuvant therapy with
tamoxifen compared to aromatase inhibitors for 257 male breast cancer
patients. Breast Cancer Res Treat 2013;137(2):465–470.
21. Schulster M, Bernie AM, Ramasamy R. The role of estradiol in male
reproductive function. Asian J Androl 2016;18(3):435–440.
22. Zagouri F, Sergentanis TN, Chrysikos D, et al. Fulvestrant and male
breast cancer: a pooled analysis. Breast Cancer Res Treat
2015;149(1):269–275.
23. Di Lauro L, Vici P, Del Medico P, et al. Letrozole combined with
gonadotropin-releasing hormone analog for metastatic male breast
cancer. Breast Cancer Res Treat 2013;141(1):119–123.
24. Carmalt HL, Mann LJ, Kennedy CW, et al. Carcinoma of the male
breast: a review and recommendations for management. Aust N Z J Surg
1998;68(10):712–715.
25. McGreevy CM, Williams AD, Tchou JC, et al. Utility of oncotype dx in
male breast cancer patients and impact on chemotherapy administration
a comparative study with female patients. J Am Coll Surgeons
2018;227(4):S39–S39.
26. Massarweh SA, Sledge GW, Miller DP, et al. Molecular characterization
and mortality from breast cancer in men. J Clin Oncol
2018;36(14):1396–1404.
27. Sparano JA, Gray RJ, Makower DF, et al. Adjuvant chemotherapy
guided by a 21-gene expression assay in breast cancer. N Engl J Med
2018;379(2):111–121.
28. Bagley CS, Wesley MN, Young RC, et al. Adjuvant chemotherapy in
males with cancer of the breast. Am J Clin Oncol 1987;10(1):55–60.
29. Giordano SH, Perkins GH, Broglio K, et al. Adjuvant systemic therapy
for male breast carcinoma. Cancer 2005;104(11):2359–2364.
30. Abrams MJ, Koffer PP, Wazer DE, et al. Postmastectomy radiation
therapy is associated with improved survival in node-positive male
breast cancer: a population analysis. Int J Radiat Oncol Biol Phys
2017;98(2):384–391.
31. Cardoso F, Bartlett JMS, Slaets L, et al. Characterization of male breast
cancer: results of the EORTC 10085/TBCRC/BIG/NABCG
International Male Breast Cancer Program. Ann Oncol 2018;29(2):405–
417.
32. Chakravarthy A, Kim CR. Post-mastectomy radiation in male breast
cancer. Radiother Oncol 2002;65(2):99–103.
33. Cloyd JM, Hernandez-Boussard T, Wapnir IL. Poor compliance with
breast cancer treatment guidelines in men undergoing breast-conserving
surgery. Breast Cancer Res Treat 2013;139(1):177–182.
34. Fentiman IS, Fourquet A, Hortobagyi GN. Male breast cancer. Lancet
2006;367(9510):595–604.
35. Madden NA, Macdonald OK, Call JA, et al. Radiotherapy and male
breast cancer: a population-based registry analysis. Am J Clin Oncol
2016;39(5):458–462.
36. Cloyd JM, Hernandez-Boussard T, Wapnir IL. Outcomes of partial
mastectomy in male breast cancer patients: analysis of SEER, 1983–
2009. Ann Surg Oncol 2013;20(5):1545–1550.
37. Yu E, Suzuki H, Younus J, et al. The impact of post-mastectomy
radiation therapy on male breast cancer patients—a case series. Int J
Radiat Oncol Biol Phys 2012;82(2):696–700.
38. Giordano SH, Cohen DS, Buzdar AU, et al. Breast carcinoma in men: a
population-based study. Cancer 2004;101(1):51–57.
CHAPTER 20

Breast Cancer Recurrence—Strategies


for Risk Reduction
KIRSTEN EDMISTON
HISTORY
Breast cancer is the most common cause of cancer in women. Sixty-four
percent will have local stage disease, 27% will have regional disease at
presentation, both potentially curable (1). At a fundamental level, all the
facets of breast cancer care from surgery to adjuvant chemotherapy/endocrine
therapy and radiation are done to eradicate the tumor and minimize the risk of
recurrence. Surgery at its most elemental, physically removes the tumor. So
then, what surgical strategies can be used to further reduce the risk of
recurrence?
One can think about recurrence in terms of local (in-breast) recurrence,
regional recurrence (RR) with the ipsilateral axilla, and distant recurrence.
The risk of systemic recurrence varies greatly from patient to patient based
on:

1. Tumor biology
a. Individual tumor’s molecular profile with the presence or absence of
cellular estrogen receptors (ERs), progesterone receptors (PRs), HER-2
neu proteins (HER-2). The molecular subtypes are defined as hormone
receptor (either ER or PR) (HR)+/HER-2− (luminal A/B), HR+/HER-
2+ (luminal HER-2), HR−/HER-2+ (HER-2), and HR−/HER-2− (basal
or triple negative)
b. Grade
c. Proliferation index (KI67)
2. Genetic predisposition
3. Stage at presentation
4. Patient characteristics (menopausal status)
5. The treatment of the disease

The molecular subtype has been found to be an independent predictor of


recurrence-free survival and overall survival but not in-breast recurrence
(IBR) after mastectomy (Fig. 20-1) (2). Surgeons cannot control the tumor
biology and the patient’s germline mutations at the time of presentation and
only to a certain extent, the stage at presentation and patient characteristics.
The surgeon has the greatest impact on local and regional recurrence through
their surgical treatment.
MECHANISM OF IN-BREAST RECURRENCE
The risk of in-breast recurrence (IBR) after mastectomy is approximately
4.9% at 5 years (3). This is independent of whether the mastectomy is done
as a skin-sparing mastectomy (SSM) or nipple-sparing mastectomy (NSM).
The median time for the appearance of clinically overt local recurrence (LR)
is 2 to 4 years, depending on stage. Most recurrences occur on the
skin/subcutaneous tissue not the muscle. Unfortunately, LR after mastectomy
is rarely an isolated event with most eventually developing metastatic
disease. Failure of mastectomy to prevent IBR may be related to the minimal
yet irreducible percentage of residual breast tissue and lymphatics either in
the skin flaps, or chest wall. Additional breast tissue can be found outside the
confines of the mastectomy—above the clavicle, within the axilla, posterior
to the anterior axillary line, and extending down on the abdominal wall
through the inframammary fold.
PRESENTATION OF A LOCAL/REGIONAL RECURRENCE
An LR after breast-conserving surgery (BCS) may present in several different
ways. Patients most commonly present with a new palpable mass or area of
thickening in the breast or a new mass in the axilla. They may also present
with small superficial skin nodules, measuring from 3 to 5 mm on the chest
wall or an area of retraction in the skin or nipple. Patients may also be
asymptomatic with only mammographic or sonographic evidence of
malignancy (i.e., areas of architectural distortion, new microcalcifications, or
masses). Tragically, patients can present with fungating masses in the area of
a previous lumpectomy (Fig. 20-2). Patients who have undergone
mastectomy with autologous reconstruction may also present in similar
fashion with a palpable mass, skin nodules, areas of retraction, or new skin
erythema. The differential diagnosis in this patient population can include the
development of a recurrence, progressive fat necrosis, a chronic seroma, scar
tissue, fibrocystic change, breast edema, and idiopathic postmastectomy
vasculitis (Fig. 20-3). Biopsy of the mass or skin lesion is critical to
determine the nature of the lesion.

FIGURE 20-1 Association of molecular subtype and overall survival and


locoregional recurrence (LRR) in patients with T1–2 breast cancer and 1–3 positive
lymph nodes who underwent mastectomy without postmastectomy radiation
therapy. (Reprinted with permission from Moo TA, McMillan R,Lee M, et al. Impact of
molecular subtype on loco-regional recurrence in mastectomy patients with T1-2 breast
cancer and 1–3 positive lymph nodes. Ann Surg Oncol 2014;21:1569.)

In terms of timing, an LR, RR, or secondary primary tumor can occur at


any time after treatment. Patients with an LR or RR have a significantly
higher risk of developing distant disease and poorer overall survival as
compared to those without an LR or RR. Geurts et al. reviewed the
nationwide population-based Netherlands Cancer Registry cohort of women
who were treated with curative intent for breast cancer (4). They analyzed the
occurrence and timing of both the first recurrence and subsequent recurrences
in 9,342 patients. They also identified prognostic factors for both first and
subsequent recurrences. Lastly, they identified consequence of these patterns
for surveillance. Recurrence occurred in 1,853 women (20%). A total of
1,343 (72%) patients first presented with a distal recurrence while 362 (20%)
had LR and 148 (8%) had an RR. Subsequent recurrences were also most
commonly distant (Fig. 20-4). They identified that most commonly patients
locally recur during the second year after treatment. RR and distant
recurrences rates remain relatively constant through 10 years of follow-up
(Fig. 20-5A). The annual risk of LR peaked at 2 years (0.7% [95% CI 0.5 to
0.8]) and 8 years (0.4% [95% CI 0.2 to 0.5]). The annual risk of RR peaked at
2 years (0.3% [95% CI 0.2 to 0.4]) and then decline thereafter (Fig. 20-5B).
FIGURE 20-2 This is an 80-year-old who presented with a neglected local
recurrence. The patient had previously undergone breast-conservation surgery. The
diagnosis was confirmed with a shave biopsy.
FIGURE 20-3 This is a 71-year-old female who presented with diffuse erythema 5
years after a skin-sparing mastectomy with DIEP reconstruction. The differential
diagnosis was recurrence versus vasculitis versus infection. Punch biopsy
demonstrated a nonspecific vasculitic process.
FIGURE 20-4 Flow chart of first and subsequent recurrences. LR, local recurrence;
RR, regional recurrence; DM, distant metastasis. (Reprinted from Geurts YM,
Witteveen A, Bretveld R, et al. Patterns and predictors of first and subsequent recurrence
in women with early breast cancer. Breast Cancer Res Treat 2017;165(3):709–720.
http://creativecommons.org/licenses/by/4.0/. No changes were made.)
ESTIMATION OF RISK OF RECURRENCE

Invasive Breast Carcinoma


Traditionally, risk of recurrence and treatment decision were based on
clinical and pathologic staging, including tumor size, lymph node
involvement, and the presence/absence of metastatic disease (TNM staging).
Breast cancer (invasive and preinvasive) are now recognized to be
heterogeneous with the outcomes based more on the individual tumor’s
molecular profile with the presence or absence of cellular ERs, PRs, HER-2,
and multiple other gene mutations. The most recent AJCC Staging Manual
(8th edition) includes tumor characteristics, molecular biomarkers, and
multigene panels that have been validated to have critical prognostic
significance to prognostic staging beyond anatomic staging (5). With the
inclusion of these molecular biomarkers and multigene panels, patients may
undergo important and prognostic stage shifts. For example, in a subgroup
analysis base on HR status, those with stage I to III, and HR− disease have a
worse overall survival than those with HR+ disease (6). Overall, applying the
8th edition staging criteria resulted in a stage change for >35% of patients
diagnosed with invasive breast cancer and refined overall survival estimates
as compared to the 7th edition—6.8% were upstaged and 29.7% were
downstaged.
Multigene Assays
Multiple multigene assays have been developed to assess recurrence risk and
integrated into clinical care for both invasive breast cancer and DCIS. They
differ in how they classify patients, leading to potential differences in
treatment decision making and clinical utility.
Oncotype DX (Genomic Health, Redwood City CA) uses a 21-gene panel
to stratify recurrence risk in patients with ER+ tumors with both N0 and N1
lymph nodes. The test uses reverse transcriptase-polymerase chair reaction
(RT-PCR) to measure expression of 16 cancer-related genes and 5
housekeeping genes. The involved genes are related to proliferation,
invasion/metastases, ER, and HER-2 neu. Oncotype DX not only provides
prognostic information but also helps to identify patients who would not
benefit from chemotherapy. It has been incorporated in the American Society
of Clinical Oncology (ASCO) and National Comprehensive Cancer Network
(NCCN) and European Society of Medical Oncology (ESMO) guidelines
along with the St. Gallen Consensus, and the NICE Diagnostic Guidance.

FIGURE 20-5 Hazard of (A) all first recurrences and (B) first LR and RR during 10
years of follow-up. LR, local recurrence; RR, regional recurrence; DM, distant
metastasis. (Reprinted from Geurts YM, Witteveen A, Bretveld R. Patterns and predictors
of first and subsequent recurrence in women with early breast cancer. Breast Cancer Res
Treat 2017;165(3):709–720. http://creativecommons.org/licenses/by/4.0/. No changes
were made.)

Other assays that provide predictive information include MammaPrint that


is useful for early-stage breast cancers and has the capacity to assess the risk
of metastases to other body parts. Prediction analysis of microarrays 50
(PAM50) uses a 50-gene transcript to identify intrinsic breast cancer subtypes
with prognostic impact. This assay is also known as the Prosigna assay that
similarly uses intrinsic breast subtypes to determine a 10-year risk of distant
recurrence in patients with early-stage ER+ breast cancer.
Recurrence Risk for DCIS
DCIS accounts for approximately 20% of all breast cancers diagnosed in the
United States (7). The incidence of DCIS increased dramatically with the
expanded use of screening mammography in women age ≥50 from the late
1980s until about 1998. Screening mammography increased from 29% of
eligible women in 1987 to 70% in 2000. Since then, the incidence has
increased at a much slower rate. Currently, the annual incidence of DCIS
varies from 38 to 80/100,000 women, based on race, ethnicity, age, state
residence, and breast density (1). Most recently in 2012 to 2016, the DCIS
incidence rate is decreasing by 2.1% per year (8).
The current treatment for DCIS usually consists of BCS followed by
adjuvant radiation therapy. Mastectomy with reconstruction is an alternative
if BCS is contraindicated or otherwise elected. Recurrence rates for DCIS
treated with BCS with appropriate adjuvant treatment have decreased over
time. The Early Breast Cancer Trialists’ Collaborative Group overview of the
randomized trials of radiation in DCIS concluded that radiotherapy reduced
the absolute 10-year risk of any ipsilateral breast event (either recurrent DCIS
or invasive cancer) by 15.2% (12.9% vs. 28.1% 2P < 0.0001) over BCS alone
(9). They also concluded that it was effective regardless of the age at
diagnosis, extent of BCS, use of tamoxifen, method of DCIS detection,
margin status, focality, grade, comedonecrosis, architecture, or tumor size
(10).
Extent of Surgery
With the pioneering work of the National Surgical Adjuvant Breast and
Bowel Project (NSABP), Umberto Veronesi, MD and others in the 1970s,
breast-conserving therapy (BCT) has been well established as oncologically
safe, offering similar local control rates and equivalent long-term survival
rates compared with non-NSM (11).
Margins
DCIS
The management of DCIS remains controversial to minimize overtreatment
and undertreatment. Despite this, margin status is one of the most important
determinates in LR and clinical outcomes. The SSO/ASRO/ASCO Consensus
Guidelines on margins for DCIS, published in 2016, recommend at least 2-
mm margins to reduce the risk of IBR relative tor narrower negative margins
(1,2). Parenthetically, the multidisciplinary panel also noted that clinical
judgment was necessary to determine whether patients with smaller negative
margin widths (1 mm or less) require reexcision. They identified additional
factors important to consider prior to additional surgery including an
assessment of residual calcifications on postexcision mammogram, extent of
DCIS in proximity to margin, and which margin is close (anteriorly just
under the skin and posterior excised to the pectoral fascia vs. margins
associated with residual breast tissue). The routine practice of obtaining
negative margins widths wider than 2 mm is not supported by the evidence.
In a recent case control study, De Lorenzi et al. at the European Institute of
Oncology (IEO) compared oncoplastic breast surgery followed by radiation
(44 patients) and conservative breast surgery alone followed by radiation
(375 patients) (13). The primary end points were disease-free survival (DFS)
and ipsilateral breast tumor recurrence (IBTR). The tumor size was larger in
the oncoplastic group. This was expected as oncoplasty can manage the
resection of larger volumes of breast tissue. The average annual rates of
invasive IBTR were 1.6% and 1.0% for the oncoplastic and conservative
patients, respectively. The authors also found no difference in the rates of
contralateral breast cancer distant metastasis and contralateral breast cancer.
They observed similar rates of focally involved margins (focally ink on
DCIS) in 4.5% and 3.5%, respectively for the oncoplastic and conservative
patients. Close margins (<1 mm) were observed in 22.8% and 17.9%,
respectively. None of their patients underwent further surgery. They
concluded that oncoplastic breast surgery is a safe and valid treatment
component for patients with DCIS.
In a recent review of DCIS, Song et al. reviewed their experience at Emory
Healthcare System (14). Twenty-eight patients were included in the study.
Therapeutic mammoplasty was the definitive procedure in 64%. There were
10 patients (36%) that required reoperation: 9 for positive margins and 1 for
residual microcalcifications. Positive margin rates were independent of tumor
location. All 10 patients requiring completion mastectomy or reexcision had
intermediate- or high-grade disease. In addition, the women requiring
reoperation were younger (mean 45.6; median 43) as compared with those
who did not require reoperation (mean 57; median 57). The authors
concluded that oncoplastic reduction techniques are appropriate for DCIS
taking into account patient selection and improve confirmation of negative
margins. One strategy to minimize the incidence of positive margins is to
obtain a preoperative breast MRI imaging that is useful in determining the
extent of DCIS and establishing the boundaries for resection. Intraoperative
margin assessment can also reduce the risk of positive margins.

Invasive Ductal Carcinoma


Achieving negative margins is critical to minimize the risk of an LR after
breast-conservation surgery. Positive margins are associated with at least a
twofold increase in IBR. The optimal margin to minimize IBR was
historically unknown resulting in approximately one in four women
attempting breast conservation needing to go back for a reexcision. In 2014,
the ASCO, Society of Surgical Oncology, and American Society for
Radiation Oncology released their consensus guidelines on margins for BCS
with whole breast irradiation in stages I and II invasive breast cancer. After
an extensive review of the available data, the ASCO/SSO/ASTRO guidelines
concluded: that the use of no ink on tumor (i.e., no cancer cells adjacent to
any inked edge/surface of the specimen) as the standard for an adequate
margin invasive cancer in the era of multidisciplinary therapy is associated
with low rates of ipsilateral breast tumor recurrence and has the potential to
decrease reexcision rates, improve cosmetic outcomes, and decrease health
care costs (15).

Flap Thickness
The term SSM was introduced in 1991 to describe a total mastectomy with
preservation of as much skin as possible. The breast parenchyma, nipple
areolar complex (NAC), biopsy scar, and any involved skin are removed
(16). In contrast, an NSM is defined as removal of the breast parenchyma
with preservation of the NAC. The risk of recurrence after SSM is
approximately 4.8% at 5 years (3).The authors also found that this was less
than the 9.5% for historical non-SSMs. The technical challenge for both types
of mastectomies is to make the flaps as thin as possible to minimize the risk
of recurrence from residual breast tissue but not too thin so as to compromise
the vascular supply of the subdermal plexus, resulting in full-thickness
necrosis. This balance is particularly important in high–genetic risk but
otherwise healthy patients who are undergoing a prophylactic preventative
mastectomy to minimize their risk but preserve their breast appearance.
To determine the ideal flap thickness, anatomists have identified a
superficial (Camper fascia) and deeper layer (Scarpa fascia), which envelope
the breast parenchyma. Unfortunately, these defining layers are inconsistent
landmarks within the breast. Up to 44% of patients do not have a superficial
fascial layer (17). Beer et al. also found the minimum distance between the
dermis and the superficial fascia varied up to 0.2 to 0.4 mm, making it too
thin to ensure flap viability (18).
Larson et al. then tried to identify the relatively avascular layer of non–
breast-bearing subcutaneous tissue between the dermis of the breast skin and
the underlying parenchyma (19). After reviewing 76 breast mammoplasty
specimens, the authors did find a consistent and distinct layer of non–breast-
bearing subcutaneous tissue. The median thickness was 10 mm but the range
was 0 to 29 mm. This is consistent with the varying thickness in different
locations within the breast from behind the NAC to periphery of the breast
(Fig. 20-6). Fundamentally, there is no single universal thickness for
mastectomy skin flaps. The surgeon should rely on the patient’s physical
examination, imaging, location of the tumor, and other factors to determine
the flap thickness during both mastectomy and lumpectomies.
FIGURE 20-6 Varying distances between the skin and breast parenchyma.

Nipple-Sparing Mastectomy—Recurrence in the NAC


The biggest concern regarding an NSM is the risk of recurrence in the
retained NAC from occult nipple involvement. Wu et al. reviewed their
experience with 944 patients who underwent NSM and immediate breast
reconstruction with a median follow-up of 85 months. The 5-yr cumulative
incidence of cancer recurrence at the NAC was 3.5%. Multifocality or
multicentricity, HR- and HER-2 neu–positive subtype, high histologic grade,
and extensive intraductal component were independently associated with
cancer recurrence at the NAC on multivariate analyses. Most importantly, the
authors found that patients with and without cancer recurrence at the NAC as
the first event had no significant difference in terms of distant metastasis–free
survival and overall survival. Similarly, Lago et al. reviewed their 10-year
experience with NSM in DCIS and found a 1.4% rate of nipple
relapse/recurrence in 69 patients (20). From a technical perspective, they
avoid the use of electrocautery in favor of the scalpel or Metzenbaum scissors
to minimize nipple necrosis. They also core out tissue behind the NAC to
minimize residual tissue.
NSM has also been studied as an option for risk reduction in patients at
high risk for developing breast cancer. Jakub et al. reviewed the outcomes of
nine institutions’ experience with prophylactic NSM in patients with BRCA
mutations (21). A total of 346 patients (201 with BRCA1 and 145 with
BRCA2 mutations) underwent NSM and followed-up for 34 and 56 months,
respectively. No ipsilateral breast cancers occurred after prophylactic NSM.
Using risk models for BRCA1/2 mutation carriers, NSM prevented 22 new
primary breast cancers. They further concluded that NSM is oncologically
safe to minimize recurrence in patients with BRCA1/2 mutations.
RECONSTRUCTION
Breast reconstruction is an integral part of the surgical management of
patients undergoing mastectomy, either autologous or implant based.
Reconstruction can be performed in an immediate or delay manner. The
benefits of postmastectomy reconstruction include reducing psychological
distress after mastectomy while restoring self-image and improving quality of
life. Data would also suggest that women undergoing reconstruction have
reduced postmastectomy pain (22) and a lower breast cancer–related
lymphedema risk (23). The authors further identify that the lymphedema rates
were not statistically different between patients undergoing implant-based or
autologous reconstruction.
Despite these benefits, some patients and their providers have raised
questions regarding the oncologic safety of reconstruction. The theoretic risks
stem from the concern that reconstruction impairs the ability to detect a
recurrence in a timely manner, it delays the initiation of adjuvant
chemotherapy or and radiation, and decreases overall survival. These
concerns have not been validated in the literature. Siotos et al. reviewed their
experience at Johns Hopkins Hospital from 2003 to 2015 for 1,517 women
undergoing mastectomy with or without reconstruction. After adjusting for
various clinical and socioeconomic factors, the authors found an overall
survival benefit associated with breast reconstruction, however not
statistically significant. Both groups had a similar rate of recurrence (Fig. 20-
7) (24). The retrospective review of the 2004 to 2014 California Cancer
Registry data for 58,738 stage 0 to III breast cancer patients undergoing
mastectomy demonstrated similar results. Jabo et al. found that the median
time between diagnosis and surgery was higher for patients undergoing
reconstruction (49 days, interquartile range [IQR] 34 to 73) compared with
those without reconstruction (35 days [IQR 21 to 56], p < 0.001).
Reconstruction did not affect the interval from surgery to adjuvant
chemotherapy or radiation and did improve overall survival. The contributing
factors leading to the improved survival with reconstruction were
multifactorial. The authors did caution however that delays from the time of
diagnosis to surgery >120 days were associated with significantly lower
survival in <60-year-old women (25).
FIGURE 20-7 Kaplan–Meier curve for recurrence-free survival probability among
patients with or without breast reconstruction. (From Siotos C, Naska A, Bello RJ, et
al. Survival and disease recurrence rates among breast cancer patients following
mastectomy with or without breast reconstruction. Plast Reconstr Surg 2019;144(2):169e–
177e.)
FIGURE 20-8 Effect of radiotherapy (RT) after breast-conserving surgery (BCS) on
10-year risk of any (locoregional or distant) first recurrence and on 15-year risk of
breast cancer death in women with pathologically verified nodal status. pN0,
pathologically node negative; pN+, pathologically node positive; RR, rate ratio.
(From Early Breast Cancer Trialists’ Collaborative Group, 2011.)
ROLE OF RADIATION THERAPY
Radiation therapy plays an important role in BCT to decrease the risk of in-
breast recurrence and overall breast cancer death. BCS (lumpectomy/partial
segmental mastectomy, etc.) excises any identifiable macroscopic disease.
Radiation therapy is then used to treat any residual microscopic tumor thus
minimizing the risk of locoregional recurrence and/or life-threatening distant
metastatic disease. The Early Breast Cancer Trialists’ Collaborative Group
conducted a meta-analysis of 17 trials involving 10,801 women of
radiotherapy versus no radiotherapy after BCS with pathologically confirmed
node-negative (pN0) or node-positive (pN+) disease (9). Overall, the authors
found that radiotherapy reduced the 10-year risk of any (locoregional or
distant) first recurrence from 35% to 19.3% (with an absolute reduction of
15.7%, 95% CI, 13.7% to 17.7%, 2p < 0.00001) and reduced the 15-year risk
of breast cancer death from 25.2% to 21.4% (absolute reduction 3.8%, 1.6 to
6.0, 2p = 0.00005). This benefit was identified in both patients with pN0 and
pN+ disease (see Fig. 20-8). In patients with pN0 disease, radiation therapy
reduced the first recurrence risk from 31.0% to 15.6% (1) (absolute
recurrence reduction at 15.4%, 13.2 to 17.6, 2p < 0.00001), and the 15-year
risk of breast cancer mortality from 20.5% to 17.2% (absolute mortality
reduction 3.3%, 0.8 to 5.2, 2p = 0.005). For patients with pN0 disease, the
absolute recurrence reduction varied by age, grade, HR status, extent of
surgery, and tamoxifen. These characteristics further stratified large (>20%),
intermediate (10% to 19%), and lower (<10%) reductions in both 10-year
recurrence risk and 15-year mortality (26) (see Fig. 20-9).
FIGURE 20-9 Absolute reduction in 15-year risk of breast cancer death with
radiotherapy (RT) after breast-conserving surgery versus absolute reduction in 10-
year risk of any (locoregional or distant) recurrence in women with pN0 disease.
Sizes of dark boxes are proportional to amount of information. Dashed line: one
death from breast cancer avoided for every four recurrences avoided. (From Early
Breast Cancer Trialists’ Collaborative Group, 2011.)

REFERENCES

1. American Cancer Society. Cancer Facts and Figures—Special Section:


Breast DCIS. Accessed November 3, 2019 from American Cancer
Society. www.cancer.org
2. Moos T, McMillan R, Lee M, et al. Impact of molecular subtype on
locoregional recurrence in mastectomy patients with T1-T2 breast
cancer and 1–3 positive lymph nodes. Ann Surg Oncol
2014;21(5):1569–1574.
3. Carlson G, Bostwick J, Styblo T, et al. Ski-sparing mastectomy:
oncologic and reconstructive considerations. Ann Surg
1997;225(5):570–575; discussion 575–578.
4. Geurts Y, Witteveen A, Bretveld R, et al. Patterns and predictors of first
and subsequent recurrence in women with early breast cancer. Breast
Cancer Res Treat 2017;165(3):709–720.
5. American Joint Committee on Cancer. AJCC Cancer Staging Manual.
New York, NY: Springer International Publishing; 2016.
6. Plichta J, Ren Y, Thomas S, et al. Implications for breast cancer
restaging based on the 8th Edition AJCC Staging Manual. Ann Surg
2020;271(1):169–176.
7. Siegel R, Miller K, Jemal A. Cancer Statistics, 2015. CA Cancer J Clin
2015;65(1):5–29.
8. DeSantis C, Ma J, Gaudet M, et al. Breast cancer statistics 2019. CA
Cancer J Clin 2019;69:438–451.
9. Early Breast Cancer Trialists’ Collaborative Group (EBCTCG), McGale
P, Taylor C, et al. Effect of radiotherapy after mastectomy and axillary
surgery on 10 year recurrence and 20 year breast cancer mortality: meta-
analysis of individual patient data for 8135 women in 22 randomised
trials. Lancet 2014;383(9935):2127–2135.
10. Early Breast Cancer Trialists Collaborative Group (EBCTCG), Correa
C, McGale P, et al. Overview of the randomized trials of radiotherapy in
ductal carcinoma in situ of the breast. J Natl Cancer Inst Monogr
2010;2010(41):162–177.
11. Fisher B, Anderson S, Bryant J, et al. Twenty-year follow-up of a
randomized trial comparing total mastectomy, lumpectomy and
lumpectomy plus irradiation for the treatment of invasive breast cancer.
N Engl J Med 2002;347(16):1233–1241.
12. Morrow M, Van Zee K, Solin L, et al. Society of Surgical Oncology-
American Society for Radiation Oncology-American Society of Clinical
Oncology Consensus Guideline on margins for breast conserving
surgery with whole-breast irradiation in ductal carcinoma in situ. Ann
Surg Oncol 2016;23(12):3801–3810.
13. De Lorenzi F, Di Bella J, Mainsonneuve P, et al. Oncoplastic breast
surgery for the managment of ductal carcinoma in situ (DCIS): Is it
oncologically safe? A retrospective cohort analysis. Eur J Surg Oncol
2018;44(7):957–962.
14. Song H, Styblo T, Carlson G. The use of oncoplastic reduction
techniques to reconstruct partial mastectomy defects in women with
ductal carcinoma in situ. Breast J 2010;16(2):141–146.
15. Buchholz T, Somerfield M, Griggs J, et al. Margins for breast-
conserving surgery with whole-breast irradiation in stage I and II
invasive breast cancer: American Society of Clinical Oncology
endorsement of the Society of Surgical Oncology/American Society for
Radiation Oncology Consensus Guideline. J Clin Oncol 2014;32:1502–
1506.
16. Toth B, Lappert P. Modified skin incisions for mastectomy: the need for
plastic surgical input in preoperative planning. Plast Reconstr Surg
1991;87:1048–1053.
17. Beer G, Varga Z, Budi S, et al. Incidence of the superficial fascia and its
relevance in skin-sparing mastectomy. Cancer 2002;94:1619–1625.
18. Robertson S, Rusby J, Cutress R. Determinants of optimal mastectomy
skin flap thickness. Br J Surg 2014;101:899–911.
19. Larson D, Basir Z, Bruce T. In oncologic safety compatible with a
predictably viable mastectomy skin flap? Plast Reconstr Surg
2011;127:27–33.
20. Lago V, Maisto V, Gimenez-Climent J, et al. Nipple-sparing
mastectomy as treatment for patients with ductal carcinoma in situ: a 10
year follow-up study. Breast J 2018;24(3):298–303.
21. Jakub J, Peled A, Gray R, et al. Oncologic safety of prophylactic nipple-
sparing mastectomy in a population with BRCA mutations: a multi-
institutional study. JAMA Surg 2018;153(2):123–129.
22. Eltahir Y, Werners L, Dreise M, et al. Quality-of-life outcomes between
mastectomy alone and breast reconstruction: comparison of patient
reported Breast_Q and other health-related quality-of-life measures.
Plast Reconstr Surg 2013;132(2):201e–2019e.
23. Siotos C, Sebai M, Wan E, et al. Breast reconstruction and risk of arm
lymphedema development: a meta-analysis. J Plast Reconstr Aesthet
Surg 2018;71(6):807–818.
24. Siotos C, Naska A, Bello R, et al. Survival and disease recurrence rates
among breast cancer patients following mastectomy with or without
breast reconstruction. Plast Reconstr Surg 2019;144(2):169e–177e.
25. Jabo B, Lin A, Aljehani A, et al. Impact of breast reconstruction on time
to definitive surgical treatment, adjuvant therapy and breast cancer
outcomes. Ann Surg Oncol 2018;25(10):3096–3105.
26. Early Breast Cancer Trialists’ Collaborative Group (EBCTCG), Darby
S, McGale P. Effect of radiotherapy after breast-conserving surgery on
10-year recurrence and 15-year breast cancer death: meta-analysis of
individual patient data for 10,801 women in 17 randomized trials.
Lancet 2011;378(9804):1707–1716.
CHAPTER 21

Disease of the Breast, Benign to


Premalignant; Hyperplasia to DCIS
MICHELE L. B. LEY | JEFFREY A. SUGANDI

Pathology of the breast encompasses a wide variety of disorders, including


benign, premalignant, and malignant diseases, as well as disorders of
uncertain malignant potential. A variety of infections and systemic diseases
may affect the breast. This chapter presents a review of common breast
diseases including benign and carcinoma in situ diseases.
The functional unit of the breast is the terminal ductal lobular unit. This is
composed of small acini, which drain into a terminal duct. The terminal duct
is the first tributary of the ductal system of the breast, which functions to
extrude milk from the nipple. The entire lobular and ductal structure of the
breast is lined by two layers of cells, the inner epithelial layer and the outer
myoepithelial layer, which arises by preferential growth of the inner
epithelial layer. A useful corollary of this paradigm is that the demonstration
of the absence of myoepithelial cells by immunohistochemistry can be used
by the pathologist to determine the malignant potential of a lesion.
BENIGN DISORDERS
Fibrocystic change is the pathologic condition that correlates with the term
“lumpy, bumpy” breasts. This term is applied to a plethora of benign changes
in the breast, which are best categorized based on subsequent risk of
development of breast carcinoma. Dupont and Page (1,2) reviewed benign
breast biopsies from 3,000 women and used well-defined criteria to
categorize them into three groups: nonproliferative lesions, proliferative
lesions without atypia, and atypical hyperplasia. This clinically relevant
classification has been independently corroborated and sanctioned by a
Consensus Conference of the College of American Pathologists (3,4).
NONPROLIFERATIVE LESIONS
This is the most common category of breast disorders and includes cysts,
papillary apocrine change, mild hyperplasia of the usual type, and epithelial-
related calcifications.
Women with these lesions do not incur a higher risk of development of
breast carcinoma than women who had no breast biopsy (relative risk 0.89).
CYSTIC BREAST MASS
In the early 20th century Joseph Bloodgood described blue cysts in the breast
(blue-domed cysts of Bloodgood) (5). Haagensen noted that cysts may form a
palpable mass, and thus he termed them gross cysts (6). However, most cysts
are small and can be visualized only on microscopic examination (Fig. 21-1).
Breast cysts can be diagnosed with physical examination as palpable,
ballotable mass. Breast ultrasound can classify whether or not the cyst is
simple, complicated, or complex. Table 21-1 summarizes the characteristic
findings of cystic breast masses.
Simple breast cysts are benign and no surgical excision is indicated. They
are typically a well-circumscribed, anechoic mass with well-defined wall and
posterior enhancement and are categorized as BIRADS-2 (benign) on
imaging. Fine-needle aspiration (FNA) under ultrasound guidance can be
performed if there is concern for inflammation or infection or for
symptomatic relief. Turbid or purulent aspirate with concern for infection
should be sent for culture. If the cyst does not collapse, or there is any
suspicion of abnormality, for example, frankly bloody aspirate with solid
component, then core needle biopsy should be performed instead of cytology
to obtain tissue diagnosis. Patients with a simple breast cyst that collapses
after aspiration with concordant clinical findings do not need further workup
and may resume routine screening (7).
FIGURE 21-1 Fibrocystic change, nonproliferative type. Two cysts are filled with
inspissated secretions. Dense fibrosis is seen in the background with normal and
atrophic lobules.

TABLE 21-1 Characteristics Summary of Breast Cysts


Simple Cyst Complicated Cyst Complex Cyst
• Well • No solid elements, • Contains solid
circumscribed intracystic mass, thick component
• Oval or round wall/septa • Thick wall
• Anechoic with • May contain debris • Intracystic mass
posterior • Round, circumscribed • Both anechoic and
enhancement echogenic (solid)
components

Complicated cysts are considered a BIRADS-3 (probable benign) on


imaging and associated with a ∼2% risk of malignancy (8). Therefore they
require a short-term follow-up imaging and physical examination. Core
needle biopsy should be performed for any suspicion of malignancy or
increase in size.
Complex cysts have both cystic and solid components, thick walls, and/or
septa. These cysts are associated with a higher risk of harboring malignancy
(14% to 20%) and are categorized as BIRADS 4–5 (suspicious or highly
suggestive of malignancy) on imaging, therefore core biopsy is required.
PROLIFERATIVE LESIONS WITHOUT ATYPIA
Women with these lesions have a slight risk of development of breast
carcinoma, approximately 1.5 to 2 times that of the general population. This
category includes moderate or florid hyperplasia of the usual type, sclerosing
adenosis, small-duct papillomas, and fibroadenoma (1,9).

FIGURE 21-2 Sclerosing adenosis. An enlarged lobule has numerous acini in a


sclerotic, dense stroma with focal microcalcifications.

Sclerosing adenosis is the most common lesion and refers to expanded


lobular units with a proliferation of both acini and intervening stroma.
Microcalcifications are often seen in association with sclerosing adenosis and
frequently correspond to “benign calcifications” seen on mammography (Fig.
21-2). These lesions are also often identified on breast MRI mimicking the
nonmass enhancement of in situ lesions. MRI-guided biopsy can confirm the
diagnosis. Rarely, a clinically palpable mass may be formed by a large
number of lobules with cellular sclerosing adenosis and has been referred to
as an adenosis tumor. It is considered benign and no treatment or surgical
excision is needed for sclerosing adenosis.
Usual ductal hyperplasia, moderate or florid, is an epithelial proliferation
characterized by ducts that are more than four cells’ thick and having a slit-
like fenestrated pattern (Fig. 21-3). Solid and papillary patterns may also be
seen. The cells may overlap, show slight variability in shape and size, and
have a swirling or streaming pattern. No additional treatment is required for
usual ductal hyperplasia.
Small-duct papillomas arise in the peripheral duct system and tend to be
multiple. Microscopically, they are composed of fibrovascular papillae
covered with the two cell types of the ductal system, the inner epithelial and
the outer myoepithelial cells.

FIGURE 21-3 Usual ductal hyperplasia. The ducts are full of overlapping cells with
indistinct borders, forming a sieve-like pattern.
ATYPICAL HYPERPLASIAS
Atypical hyperplasias confer a risk of development of breast carcinoma that
is 3.5 to 5 times that of the reference population. This category includes both
atypical ductal hyperplasia (ADH) and atypical lobular hyperplasia (ALH)
(1,2).
These lesions are difficult diagnostic problems, with variable interobserver
agreement (10–12). Their morphologic features are midway between those of
usual hyperplasia and carcinoma in situ. Page et al. defined criteria for ADH
that are widely used and include nuclear monomorphism, regular cell
placement, and round, not fenestrated, spaces in part of the duct (Fig. 21-4)
(13). ALH refers to proliferation of lobular cells with distention of acini in no
more than half of a lobule and may include pagetoid spread into adjacent
ducts (14). Earlier studies showed that atypical hyperplasias do not have a
linear progression to carcinoma but they increase the risk of development of
breast carcinoma in both breasts (2,15). A recent retrospective analysis found
that the breast diagnosed with ALH is three times more likely to develop
invasive carcinoma than the contralateral breast (16). These data suggest that
ALH may lie somewhere between linear progression and generalized risk.
Columnar cell hyperplasia (CCH) with or without atypia is a newly
recognized morphologic entity. CCH without atypia is one of many
hyperplastic lesions that slightly increase the relative risk of development of
breast carcinoma and are grouped under fibrocystic change, proliferative type
(17). CCH are frequently associated with microcalcifications and may have
mild, moderate, or marked atypia. Severe atypia typically has micropapillary
architecture and may be indistinguishable from ductal carcinoma in situ
(DCIS). CCH has been noted to be associated with ALH, lobular carcinoma
in situ (LCIS), and tubular carcinoma (18). As with other atypical
proliferative lesions, there is a high level of interobserver variability among
pathologists in diagnosing CCH with atypia (19). Flat epithelial atypia is also
a newly recognized morphologic entity (18) where the columnar shaped
epithelial cells that layer the terminal duct show low-grade cytologic atypia.
Limited available data suggest that it has a very low risk of both local
recurrence and progression to invasive cancer (20).
FIGURE 21-4 Atypical ductal hyperplasia. The duct has two population of cells.
Monomorphic cells with distinct borders are arranged around sharply demarcated
round spaces. Overlapping cells are arranged around irregular spaces.

A diagnostic of an atypical lesion of any type as rendered on a core biopsy


is an indication for a surgical biopsy. Atypical lesions are diagnosed in 4.3%
to 6.7% patients who undergo a core biopsy for a mammographically
detected lesion, and the subsequent surgical biopsy reveals intraductal
carcinoma in 12.5% to 36% and invasive carcinoma in 0% to 14% of patients
(21–24). Magnetic resonance imaging (MRI) screening has been
recommended for women at high risk for development of breast carcinoma
(25).
Atypical lesions of the breast are a diagnostic challenge for the surgical
pathologist, and there is considerable interobserver variation among
pathologists in interpreting these lesions. The Susan G. Komen for the Cure
Foundation published a white paper on breast pathology (26) that
recommends that the accuracy of diagnosis of breast lesions can be enhanced
by specialty training, second opinions, and integration of pathologists into
clinical care teams.
RADIAL SCARS AND COMPLEX SCLEROSING LESIONS
Radial scars are typically small areas of scarring (<1 cm) surrounded by
glandular elements. Their stellate morphology mimics a classic scirrhous
carcinoma for both the mammographer and the pathologist. Typically they
are seen only on microscopy, which reveals an area of intense sclerosis in the
center, surrounded by dilated ducts, sclerosing adenosis, and apocrine
metaplasia (Fig. 21-5). Glands caught up in the central scirrhous zone may
mimic invasive carcinoma on high magnification. The overall architecture of
the lesion is critical in avoiding this pitfall, especially on frozen section.
Numerous sclerotic lesions do not have the classic morphology of a radial
scar but show varying degrees of sclerosis and ductal hyperplasia. These
lesions are commonly referred to as complex sclerosing lesions.
In a carefully performed case control study, it was shown that women with
biopsy-proven radial scars are at an increased risk for breast cancer. Women
with proliferative lesions with atypia associated with radial scar had a relative
risk of breast cancer of 3.0 (27). Surgical excision is recommended when
radial scar is diagnosed on core biopsy.
FIGURE 21-5 Radial scar. The central zone is sclerotic with a few compressed ducts.
Dilated ducts are seen at the periphery, some of which show usual ductal
hyperplasia.
BENIGN NEOPLASMS

Fibroadenoma
Fibroadenomas (FAs) typically present as painless, mobile, rubbery masses.
They are usually solitary but are occasionally multiple (28). They are most
often present in the upper outer quadrant and are slightly more common in
the left breast.
On gross examination, fibroadenomas are well-circumscribed smoothly
lobulated masses. On microscopic examination, fibroadenomas are biphasic
having epithelial and stromal components (Fig. 21-6). Occasionally, the
epithelial component is insignificant and the stromal component is
hypocellular and densely sclerotic. This variant, hyalinized fibroadenoma, is
invariably associated with coarse microcalcifications, which may be
worrisome to the mammographer.
Fibroadenomas usually present as palpable, well-defined, rubbery mobile
mass on physical examination. Imaging findings on ultrasound reveal well-
defined, lobulated solid mass. Diagnosis can be confirmed with core needle
biopsy and then followed with short-term follow-up within 3 to 6 months. In
asymptomatic patients, fibroadenomas can be left alone. If a fibroadenoma is
symptomatic or increases in size on follow-up, then surgical excision is
warranted. Cryoablation therapy under ultrasound guidance is an alternative
approach to management of fibroadenomas, once the diagnosis is confirmed
with core needle biopsy. It may take up to 12 months for the progressive
resolution of fibroadenomas treated with cryoablation (29,30).
FIGURE 21-6 Fibroadenoma. The tumor is circumscribed and covered by a
pseudocapsule. It is composed of numerous ducts in a background of cellular stroma.

Juvenile fibroadenoma is a variant seen in young girls, and these tumors


show both epithelial and stromal hypercellularity (31). They may be multiple,
grow rapidly, and cause venous dilation in the overlying skin. Tubular
adenoma is a subtype that has an abundance of small tubules on microscopic
examination and is also common in young women (32). Complex
fibroadenomas contain cysts larger than 3 mm, sclerosing adenosis, epithelial
calcifications, or papillary apocrine change. One study showed a higher risk
of breast cancer (33) in patients with such lesions.
Lactational adenomas are seen during pregnancy and in the postpartum
period and may represent lactational changes superimposed on an underlying
tubular adenoma or fibroadenoma. They present a well-circumscribed mass,
which on microscopy shows glands and ducts with secretory changes.
Infarction, pain, and tenderness may complicate fibroadenomas during
pregnancy.
There is an increased relative risk (between 1.2 and 3.0) of invasive
carcinoma in women with fibroadenoma (33). For this reason, fibroadenoma
has been included in the category of proliferative lesions without atypia by
some authors (34).
Phyllodes Tumor
Phyllodes tumor is a rare fibroepithelial breast tumor that accounts for less
than 1% of all breast neoplasms (35). This entity encompasses tumors that
run the gamut from benign to malignant but mostly fall into the category of
tumors of uncertain malignant potential (borderline). Conventionally,
phyllodes tumors have been referred to as cystosarcoma phyllodes.
On physical examination, phyllodes tumor can be indistinguishable from
fibroadenoma. A large breast mass >3 cm with rapid growth should prompt
suspicion for phyllodes tumor and requires core needle biopsy or surgical
excision. Microscopically, they have characteristic hypercellular stroma
around the ductal elements, which form a leaf-like pattern giving the lesion
its name (Fig. 21-7). A high mitotic count, nuclear pleomorphism, infiltrative
tumor margins, and stromal overgrowth are the main criteria used to assess
biologic behavior. Benign tumors are characterized by increased cellularity,
lack of stromal overgrowth, mild to moderate cellular atypia, circumscribed
margins, and low mitotic rate (<4 per 10 high power fields). Borderline
tumors are characterized by higher degree of cellularity and atypia, mitotic
rate of 4 to 9 mitoses per 10 high power fields, and microscopic infiltrative
borders. Malignant tumors have marked stromal cellularity, atypia,
infiltrative margins, stromal overgrowth, and more than 10 mitoses/10 high
power fields (36,37).
FIGURE 21-7 Phyllodes tumor, benign. The tumor has a frond-like architecture,
with compressed ducts lined by ductal and myoepithelial cells.

As with all stromal tumors, ample sampling is necessary because the


sarcomatous component may be small and limited to a small portion of the
tumor. Phyllodes tumors tend to have local recurrences and should be widely
excised (38,39). Wide excision with at least 1-cm margins is recommended
for management of borderline and malignant phyllodes tumor. Benign
phyllodes can be excised without additional margins. This recommendation is
based on data that showed that tumor size and surgical margins are the
prognostic determinant of local recurrence and distant metastases (40).
Axillary lymph node involvement is rare in phyllodes tumor, therefore
axillary surgery is usually not indicated.
Intraductal Papilloma
These tumors typically arise in a large duct in the subareolar region and
present with symptom of unilateral spontaneous bloody nipple discharge.
One nested case control study showed that papillomas with areas of ADH
within them have a risk of breast carcinoma at that site, which is similar to
the risk associated with ADH in the adjacent breast (41). On careful
dissection papillomas appear as pearly, small, white nodules.
Microscopically, they distend a duct and are composed of a stalk with
branching thick fibrovascular cores lined by myoepithelial and ductal cells
(Fig. 21-8). The proliferation of both cell types is an indicator of benign
nature. Complex growth patterns can make the distinction between a
papilloma and papillary carcinoma challenging for the pathologist.
Papillomas typically do not show significant pleomorphism, mitotic activity,
and necrosis (42,43).

FIGURE 21-8 Intraductal papilloma. A large duct contains a papillary structure


with thick fibrovascular cores lined by ductal and myoepithelial cells.

Papillomas with atypia have been shown to have pathologic upgrade up to


67% at the time of surgical excision, therefore surgical excision is
recommended. However, literature on pure papillomas without atypia is
mixed with little consensus on management (44–46). The available data
showed that the relative risk of breast cancer in papilloma without atypia is
2.0. The presence of atypia increases the relative risk to 5.1 (47). Therefore
current consensus guidelines issued by American Society of Breast Surgeons
recommend individualized decision to excise papillary lesion based on risk:
size, symptoms of palpability and nipple discharge, and breast cancer risk
factors (Table 21-2). Observed lesions should be closely followed with
imaging to establish stability (48).
Nipple Adenoma
Adenomas of the nipple present as ill-defined masses in the nipple region.
Microscopically, they are composed of gland-like spaces associated with
proliferation of ductal epithelium. The latter may show a pseudoinvasion
pattern and extension into the nipple, which may clinically mimic Paget
disease. The presence of both myoepithelial and epithelial layers in this lesion
is an indicator of benignity. Adenomas may be excised due to size but they
do not have malignant potential (49). These lesions should be examined in
their entirety because they have been reported in rare cases to be associated
with carcinoma (50,51).

TABLE 21-2 Summary of Borderline or High-Risk Breast Lesions With


Risks and Recommendations
Lesion Relative Recommendation Notes
Risk of
Breast
Cancer
Atypical 3.5–5.3 Surgical excision Completely excised on core
Hyperplasia needle biopsy may be
observed
Radial Scar 3.0 Surgical excision Completely excised on core
needle biopsy may be
observed
Fibroadenoma 1.2–3.0 Surgical excision
or observation
Papillary 2.0–5.1 Excision or close Incidental, benign papillary
Lesions imaging and lesions can be followed
follow-up
Phyllodes Surgical excision
Tumor
LCIS 2–8 Surgical excision Excision for discordant
or clinical and pathology, limited
imaging follow- sample, or presence of
up other high-risk lesion
Pleomorphic 2–8 Surgical excision
LCIS
LCIS, lobular carcinoma in-situ.

Miscellaneous Lesions
Lipoma is a benign entity in the breast composed of mature fat cells.
Clinically apparent masses sometimes yield only fat without any glandular
elements on excision and are diagnosed as lipoma.
Hamartoma is a benign lesion with varying amount of glandular, adipose,
and fibrous tissues. Hamartoma may present as discrete, painless masses or
may be found incidentally on screening mammogram (49).
Fibromatosis is a locally invasive neoplastic condition that afflicts
numerous sites in the body and is best recognized as desmoid tumor of the
abdominal wall. Microscopically, it consists of proliferation of benign-
appearing spindle-shaped cells, which invade breast parenchyma. Wide
excision is curative (52–55). Rosen described the entity mucocele-like lesion,
which consists of extravasated mucin from mucinous cysts and may present
as a mass (56). Pseudoangiomatous hyperplasia of the mammary stroma
(PASH) may clinically present as a mass. The proliferating fibroblasts line
slit-like spaces and mimic vascular proliferation (57–59). A variety of benign
stromal tumors may be seen in the breast, including leiomyoma,
neurofibroma, myofibroblastoma, and chondrolipoma.
INFLAMMATORY CONDITIONS

Fat Necrosis
Fat necrosis seen in the breast is most commonly iatrogenic. It has been
associated with history of radiation, prior oncoplastic surgery including flap
reconstruction, reduction mastopexy, and fat grafting after implant
reconstructive surgeries. However, it can mimic breast carcinoma both
clinically and on mammography, therefore biopsy may be necessary to
confirm diagnosis. In the early phase, microscopic examination shows a
cavity lined by histiocytes with a foamy cytoplasm with a smattering of
chronic inflammatory cells. With time, foreign body giant cells appear and
the lesion becomes sclerotic and may developed coarse microcalcifications,
which usually can be recognized as such by an experienced mammographer.
Once fat necrosis is diagnosed by core needle biopsy, excision is not
necessary and there is no increased risk of future malignancy.
Mammary Duct Ectasia
This disease typically presents as an ill-defined mass in the areolar lesion or
with spontaneous nipple discharge in a perimenopausal woman. The ducts in
this region are dilated and associated with chronic inflammation.
Occasionally, abundant plasma cells are seen (plasma cell mastitis), and this
condition has been described as a separated entity (60) but probably
represents a variant. It can mimic breast cancer (61–65). Duct ectasia does
not require surgical excision unless for symptom control of the discharge or
to rule out malignancy.
Granulomatous Mastitis
Granulomatous mastitis is a rare, benign, chronic inflammatory condition. It
was first described in 1972 by Kessler as a lesion that clinically mimicking a
carcinoma (66). Mammary tuberculosis is rare. Sarcoidosis can affect the
breasts on occasion and should be diagnosed only when all infectious agents
have been excluded (65). Idiopathic granulomatous mastitis may be
associated with microabscesses and responds to corticosteroid therapy (67).
Granulomatous mastitis is a diagnosis of exclusion once malignancy and
infectious etiology have been ruled out and histopathology confirms
noncaseating granuloma.
NONINVASIVE CARCINOMA

Lobular Carcinoma in Situ


Foote and Steward (68) introduced the concept of LCIS in 1941. They
observed that LCIS is a rare, multicentric entity that cannot be identified
clinically on gross examination; it is often an incidental finding on biopsy for
other abnormalities or presents as microcalcifications on mammography.
Women with LCIS are associated with an increased risk of developing
invasive breast cancer on both sides by four- to eightfold compared to general
population (69). The potential invasive carcinoma might be either ductal or
lobular. LCIS has been reported to have a variable incidence ranging from
0.5% to 3.6% (70–73). LCIS is more common in White, younger,
premenopausal women, and the mean age of diagnosis is 44 to 46 years
(65,74,75).
LCIS itself is considered a benign entity and treatment is not the same as
for noninvasive ductal carcinoma. Therefore it is no longer categorized as
tumor in situ (Tis) neoplasm under American Joint Committee on Cancer
(AJCC) TNM staging system (76).
Classic LCIS is defined as solid proliferation of small cells involving
terminal duct lobular units; the cells are typically uniform, with round–oval
nuclei, clear or eosinophilic cytoplasm, and cytologic dyshesion (Fig. 21-9).
Pleomorphic LCIS has a feature of larger cells with marked nuclear
pleomorphism otherwise similar cytologic dyshesion as classic LCIS.
Pleomorphic LCIS is associated with a higher risk of recurrence and
development of invasive carcinoma.
National Comprehensive Cancer Network (NCCN) Guidelines
recommends surgical excision for all cases of LCIS diagnosed by core needle
biopsy. If surgical excision shows classic LCIS, no further surgery is
indicated, even with presence of classic LCIS at the margin. If pleomorphic
LCIS is found on excisional biopsy, complete excision with negative margin
is recommended. After surgical excision, patients with LCIS should be
monitored with interval history and physical examination every 6 to 12
months and annual diagnostic mammogram (77).
FIGURE 21-9 Lobular carcinoma in situ. Lobules are distended with monomorphic
cells with moderate amount of cytoplasm and low-grade nuclei.

Ductal Carcinoma in Situ


DCIS of the breast is a noninvasive form of breast cancer. It is defined as a
heterogeneous group of lesions with neoplastic changes of the tissue confined
to breast ducts. According to the AJCC TNM Staging, DCIS is designated as
stage 0 (TisN0M0) based on its confinement within the ducts (76).
The incidence of DCIS in the United States saw a dramatic increase in the
last four decades from 5 per 100,000 women in the 1970s to 32 per 100,000
women in 2004 due to increased utilization of breast cancer screening
mammogram (78). Recent study done by Oseni et al. showed increased
incidence of DCIS diagnosis in Blacks, Hispanics, and Asians, but it
remained relatively unchanged in Whites over 25 years (79). DCIS currently
accounts for approximately 20% to 25% of all cases of diagnosed breast
neoplasm in the United States (80).
There are no specific clinical manifestations of DCIS. Most patients
diagnosed with DCIS will present without breast symptoms or findings on
physical examination.
DCIS usually presents with suspicious microcalcifications detected on
mammography in majority of patients (81). DCIS is clearly the precursor
lesion for most invasive breast cancers, but not all DCIS lesions have the
ability to become invasive breast cancer. The prognosis of DCIS is very
good, with 10-year survival rate of 97% to 98% (82,83).
The risk factors for DCIS are similar to invasive breast cancer and include
family history of breast cancer, increased breast density, obesity, nulliparity,
or late age at first birth, as well as genetic syndromes defined by mutations in
BRCA1 and BRCA2 genes (84,85).
WORKUP
Patients with abnormal imaging should undergo complete workups consisting
of history and physical examination, bilateral diagnostic mammogram, tissue
biopsy, determination of tumor estrogen receptor (ER) status, and MRI as
indicated.
IMAGING
The importance of quality mammography is of paramount importance.
Currently, most lesions are detected by mammography; therefore all patients
with suspected DCIS require diagnostic bilateral mammograms with
magnification. The most common findings in more than 80% DCIS patients
are microcalcifications, frequently clustered, linear and branching, and
generally without an associated soft tissue abnormality.
Currently, the use of MRI is not routinely indicated in the evaluation of
DCIS. Studies have shown that MRI has a high sensitivity of up to 98% for
DCIS, thus at the same time may result in overestimating the extent of the
disease (86–89). MRI may be helpful to identify the extent of DCIS,
multicentric disease and synchronous disease in the contralateral breast
(90,91). MRI however has not been shown to reduce reexcision rates or
decrease the rate of local recurrence (92). Currently breast MRI and MRI-
guided biopsy for evaluation of DCIS is indicated in certain circumstances
where additional information is warranted during the initial workup that may
alter surgical planning.
BIOPSY
If radiologic workup shows suspicious calcification lesion, the diagnosis of
DCIS is confirmed by stereotactic core needle biopsy. Open surgical
excisional biopsy may be used in conjunction with image-guided localization
if the lesion cannot be biopsied using minimally invasive techniques. This
should be a rare event with current image-guided biopsy techniques (93,94).
PATHOLOGIC CLASSIFICATION
Although there is no universally accepted histopathologic classification, most
pathologists classify DCIS into five major groups: comedo, cribiform,
micropapillary, papillary and solid (95–97).
Comedo DCIS is characterized by necrosis in the center of the lesion with
the calcified necrotic material typically seen as linear, branching
calcifications on mammograms (Fig. 21-10). The comedo type is frequently
associated with high nuclear grade, higher mitotic activity, HER-2/neu
expression, and clinically more aggressive behavior (98,99). Comedo
necrosis was the only factor found to be a predictor of ipsilateral recurrence
in a multivariate analysis (100).

FIGURE 21-10 Mammography imaging showing irregular branching calcifications.


Histopathology showed high-grade comedo ductal carcinoma in situ.

Cribiform DCIS is characterized by limited necrosis in only small clusters


of cells, uniform nuclei, and infrequent mitoses. Micropapillary DCIS shows
small groups of cells with projection into the lumina. Papillary subtype does
have true fibrovascular core papilla in contrast to micropapillary type. The
solid DCIS variant is defined by tumor cells that fill the involved space with
lack of significant necrosis, fenestrations, or papilla. Papillary and cribriform
types tend to be less aggressive (95–97,101).
Determination of ER and progesterone receptor status is beneficial in order
to determine the benefit of adjuvant endocrine therapy to reduce the risk of
subsequent invasive breast cancer as well as predict overall risk of local
recurrence. HER-2/neu expression is a worse prognostic indicator for
invasive breast cancer, however its significance as prognostic indicator for
DCIS has not been proven. Currently, there are no sufficient studies to
support the use of monoclonal antibody agent to human epidermal growth
factor receptor 2 (HER-2) in DCIS, therefore knowing the HER-2 status does
not alter management and is not required per NCCN Guidelines (77).
TREATMENT
The primary goal of treatment of DCIS is to prevent progression to invasive
breast carcinoma. Therapeutic modalities include surgery, radiation therapy,
and adjuvant endocrine therapy.
SURGERY
Patient with DCIS may be treated with breast-conserving surgery
(lumpectomy) followed by radiation therapy or mastectomy. An
observational study of more than 100,000 women with DCIS from 1988 to
2011 showed that lumpectomy with or without radiotherapy had a similar 10-
year breast cancer-specific mortality compared to mastectomy (100).
Therefore the choice of local treatment depends on the extent of disease and
an individual patient’s preference after considering the potential risks of and
benefits of each treatment as well as the associated risk of local recurrence.
BREAST-CONSERVING THERAPY
Breast-conserving therapy (BCT) usually includes lumpectomy to excise the
tumor with negative surgical margins followed by radiation therapy to
eradicate any residual microscopic disease. Sentinel lymph node biopsy is not
indicated for most patients undergoing lumpectomy for DCIS.
According to current guidelines recommended by Society of Surgical
Oncology (SSO), American Society for Radiation Oncology (ASTRO), and
American Society of Clinical Oncology (ASCO), excision with at least 2-mm
clear margins is adequate in DCIS patients treated with lumpectomy followed
by radiation therapy. This recommendation was based on meta-analysis of 20
studies and 7,883 patients with DCIS who underwent lumpectomy followed
by radiotherapy. Patients with margins of at least 2 mm were associated with
significantly reduced risk of ipsilateral breast tumor recurrence compared to
patients with margins <2 mm (12% vs. 24%). There was no evidence that
wider margins greater than 2 mm resulted in reduction of recurrence (102).
In situations where invasive breast cancer is present with DCIS,
SSO/ASTRO/ASCO guidelines recommend “no ink on tumor” as an
adequate margin for patients treated with lumpectomy followed by whole
breast radiation (103). This is based on meta-analysis of 33 studies including
more than 28,000 patients where positive margins (defined by ink on invasive
tumor) are associated with twofold increase in the risks of ipsilateral breast
tumor recurrence compared with negative margins. However, there was no
evidence that more widely clear margins were associated with decreased the
rate of recurrence (104).
In patients with microcalcifications seen in preoperative mammogram,
surgeons should obtain postexcision mammogram for lumpectomy patients
prior to radiation therapy to confirm that adequate excision of DCIS have
been achieved (105–107).
MASTECTOMY
Mastectomy is the most effective treatment available for DCIS. It has a high
rate of cure for DCIS with local recurrence rates of approximately 1%
(108,109). Mastectomy is indicated for patients with DCIS with evidence of
widespread disease that is unlikely to achieve clear margins or cosmetically
acceptable resection with breast-conserving surgery. However mastectomy is
an aggressive form of treatment for patients with DCIS with only local
recurrence benefit but lacking evidence of survival benefit as discussed
above. Mastectomy also has been associated with higher morbidity rates
(wound complications, bleeding, infections, and overall complications)
compared to lumpectomy (110). Radiation therapy is not routinely indicated
for DCIS post mastectomy.
Patients who meet the criteria for mastectomy may have higher likelihood
of harboring an occult invasive cancer compared to patients with smaller
focus of DCIS, therefore sentinel lymph node biopsy should be strongly
considered in the event that unexpected invasive cancer is found in the
mastectomy specimen. The rationale for this is due to permanent alteration of
the lymphatic drainage from the breast to the axilla, making it impossible to
perform accurate sentinel lymph node biopsy for staging postmastectomy
(78,111,112).
RADIATION THERAPY
Radiation therapy after lumpectomy has been shown to reduce the odds of
invasive and noninvasive recurrences in the breast but not associated with
survival advantage (82,101,113). In some patients with low-risk disease and
widely negative resected margins, it is reasonable to omit radiation therapy;
particularly in the setting of comorbidity, advanced age, or patient preference
(114). Preliminary data shows that gene expression assays such as the
Oncotype DX DCIS may be utilized as a helpful tool to stratify patients into
low, intermediate, or high risk of recurrence and therefore inform the
decision for postlumpectomy radiation (115,116).
SYSTEMIC TREATMENT
Systemic treatment for DCIS patients is available in the form of endocrine
therapy for chemoprevention in patients with ER-positive DCIS. The main
role of systemic treatment is to reduce risk of invasive breast cancer in
ipsilateral as well as in contralateral breast following local treatment. The
agent approved for used is tamoxifen. Anastrozole belongs to the class of
aromatase inhibitors, and is an acceptable alternative for postmenopausal
patients. Chemotherapy is not indicated for treatment of DCIS patients due to
its overall good prognosis and noninvasive nature of this disease.
POSTTREATMENT SURVEILLANCE
DCIS has an excellent long-term prognosis. ASCO Guidelines recommend
surveillance with history and physical examination every 3 to 6 months for
the first 3 years after primary therapy, then every 6 to 12 months for the next
2 years, and annually thereafter. Patients who underwent breast conserving
should obtained posttreatment mammogram within 6 months after radiation
therapy followed by every 12 months for surveillance. In addition, all patients
should be counseled for breast self-examination, regular pelvic examination,
and genetic counseling as indicated for high-risk women (117).

REFERENCES

1. Dupont WD, Page DI. Risk factors for breast cancer in women with
proliferative breast disease. N Engl J Med 1985;312(3):146–151.
2. Page DL, Dupont WD, Rogers LW, et al. Atypical hyperplastic lesions
of the female breast. A long-term follow-up study. Cancer
1985;55(11):2698–2708.
3. Is ‘fibrocystic disease’ of the breast precancerous? A Consensus Report
from the College of American Pathologists. Indiana Med
1986;79(9):753–754.
4. London, SJ, Connolly JL, Schnitt SJ, et al. A prospective study of
benign breast disease and the risk of breast cancer. JAMA
1992;267(7):941–944.
5. Bloodgood J. The pathology of chronic cystic mastitis of the female
breast, with special consideration of the blue-domed cyst. Arch Surg
1921;3:445.
6. Haagensen CD. The relationship of gross cystic disease of the breast and
carcinoma. Ann Surg 1977;185(3):375–376.
7. NCCN Guidelines Version 1.2019. Breast Cancer Screening and
Diagnosis. https://www.nccn.org/professionals/physician_gls/pdf/breast-
screening.pdf. Accessed on Sept 6, 2019.
8. Venta LA, Kim JP, Pelloski CE, et al. Management of complex breast
cysts. Am J Roentgenology 1999;173:1331–1336.
9. Jensen RA, Page DL, Dupont WD, et al. Invasive breast cancer risk in
women with sclerosing adenosis. Cancer 1989;64(10):1977–1983.
10. Rosai J. Borderline epithelial lesions of the breast. Am J Surg Pathol
1991;15(3):209–221.
11. Schnitt SJ, Connolly JL, Tavasoli FA, et al. Interobserver reproducibility
in the diagnosis of ductal proliferative breast lesions using standardized
criteria. Am J Surg Pathol 1992;16(12):1133–1143.
12. Bodian CA, Perzin KH, Lattes R, et al. Reproducibility and validity of
pathologic classifications of benign breast diseases and implications for
clinical applications. Cancer 1993;71(12):3908–3913.
13. Page DL, Schuyler PA, Dupont WD, et al. Atypical lobular hyperplasia
as a unilateral predictor of breast cancer risk: a retrospective cohort
study. Lancet 2003;361(9352):125–129.
14. Page DL, Dupont WD, Rogers LW. Ductal involvement by cells of
atypical lobular hyperplasia in the breast: a long-term follow-up study of
cancer risk. Hum Pathol 1988;19(2):201–207.
15. Marshall LM, Hunter DJ, Connolly JL, et al. Risk of breast cancer
associated with atypical hyperplasia of lobular and ductal types. Cancer
Epidemiol Biomarkers Prev 1997;6(5):297–301.
16. Page DL. Breast lesions, pathology and cancer risk. Breast J
2004;10(Suppl 1):S3–S4.
17. Hartmann LC, Sellers TA, Frost MH, et al. Benign breast disease and
the risk of breast cancer. N Engl J Med 2005;353(3):229–237.
18. Collins LC, Achacoso NA, Nekhlyudow L, et al. Clinical and pathologic
features of ductal carcinoma in situ associated with the presence of flat
epithelial atypia: an analysis of 543 patients. Mod Pathol
2007;20(11):1149–1155.
19. Tan PH, Ho BC, Selvarajan S, et al. Pathological diagnosis of columnar
cell lesions of the breast: are there issues of reproducibility? J Clin
Pathol 2005;58(7):705–709.
20. Schnitt SJ. The diagnosis and management of pre-invasive breast
disease: flat epithelial atypia—classification, pathologic features and
clinical significance. Breast Cancer Res 2003;5(5):263–268.
21. Brem RF, Behrndt VS, Sanow L, et al. Atypical ductal hyperplasia:
histologic underestimation of carcinoma in tissue harvested from
impalpable breast lesions using 11-gauge stereotactically guided
directional vacuum-assisted biopsy. AJR Am J Roentgenol
1999;172(5):1405–1407.
22. Moore MM, Hargett CW 3rd, Hanks JB, et al. Association of breast
cancer with the finding of atypical ductal hyperplasia at core breast
biopsy. Ann Surg 1997;225(6):726–731; discussion 731–733.
23. Gadzala DE, Cederbom GJ, Bolton JS, et al. Appropriate management
of atypical ductal hyperplasia diagnosed by stereotactic core needle
breast biopsy. Ann Surg Oncol 1997;4(4):283–286.
24. Burbank F. Stereotactic breast biopsy of atypical ductal hyperplasia and
ductal carcinoma in situ lesions: improved accuracy with directional,
vacuum-assisted biopsy. Radiology 1997;202(3):843–847.
25. Lehman CD, Gatsonis C, Kuhl CK, et al. MRI evaluation of the
contralateral breast in women with recently diagnosed breast cancer. N
Engl J Med 2007;356(13):1295–1303.
26. Perkins C, Balma D, Garcia R, et al. Why current breast pathology
practices must be evaluated. A Susan G Komen for the cure white paper:
June 2006. Breast J 2007;13(5):443–447.
27. Jacobs TW, Byrne C, Colditz G, et al. Radial scars in benign breast-
biopsy specimens and the risk of breast cancer. N Engl J Med
1999;340(6):430–436.
28. Dent DM, Cant PJ. Fibroadenoma. World J Surg 1989;13(6):706–710.
29. Littrup PJ, Freeman-Gibb L, Andrea A, et al. Cryotherapy for breast
fibroadenomas. Radiology 2005;234(1):63–72.
30. Kaufman CS, Littrup PJ, Freman-Gibb LA, et al. Office-based
cryoablation of breast fibroadenomas: 12-month followup. J Am Coll
Surg 2004;198(6):914–923.
31. Pike AM, Oberman HA. Juvenile (cellular) adenofibromas. A
clinicopathologic study. Am J Surg Pathol 1985;9(10):730–736.
32. Hertel BF, Zaloudek C, Kempson RI. Breast adenomas. Cancer
1976;37(6):2891–2905.
33. Dupont WD, Page DL, Parl FF, et al. Long-term risk of breast cancer in
women with fibroadenoma. N Engl J Med 1994;331(1):10–15.
34. Schnitt S, Connolly JL. Pathology of Benign Breast Disorders in
Diseases of Breast. 2nd ed. Philadelphia, PA: Lippincott Williams &
Wilkins; 2000.
35. Bernstein L, Deapen D, Ross RK. The descriptive epidemiology of
malignant cystosarcoma phyllodes tumors of the breast. Cancer
1993;71(10):3020–3024.
36. Norris HJ, Taylor HB. Relationship of histologic features to behavior of
cystosarcoma phyllodes. Analysis of ninety-four cases. Cancer
1967;20(12):2090–2099.
37. Page D, Anderson TJ, Johnson RL. Sarcomas of the Breast. Edinburgh,
UK: Churchill Livingstone; 1987.
38. Hajdu SI, Espinosa MH, Robbins GF. Recurrent cystosarcoma
phyllodes: a clinicopathologic study of 32 cases. Cancer
1976;38(3):1402–1406.
39. Lindquist KD, van Heerden JA, Weiland LH, et al. Recurrent and
metastatic cystosarcoma phyllodes. Am J Surg 1982;144(3):341–343.
40. Kapiris I, Nasiri N, A’Hern R, et al. Outcome and predictive factors of
local recurrence and distant metastases following primary surgical
treatment of high grade malignant phyllodes tumours of the breast. Eur J
Surg Oncol 2001;27(8):723–730.
41. Page DL, Salhany KE, Jensen RA, et al. Subsequent breast carcinoma
risk after biopsy with atypia in a breast papilloma. Cancer
1996;78(2):258–266.
42. Azzopardi JG. Problems in Breast Pathology. Philadelphia, PA: WB
Saunders; 1979.
43. Kraus FT, Neubecker RD. The differential diagnosis of papillary lesions
of the breast. Cancer 1962;(144):444.
44. Cyr AE, Novack D, Trinkaus K, et al. Are we overtreating papillomas
diagnosed on core needle biopsy? Ann Surg Oncol 2010;18:946–951.
45. Holley SO, Appleton CM, Farria DM, et al. Pathologic outcomes of
nonmalignant papillary breast lesions diagnosed at imaging-guided core
needle biopsy. Radiology 2012;265(2):379–384.
46. Foley NM, Racz JM, Al-Hilli Z, et al. An international multicenter
review of the malignancy rate of excised papillomatous breast lesions.
Ann Surg Oncol 2015;22(suppl 3):S385–S390.
47. Lewis JT, Hartmann LC, Vierkant RA, et al. An analysis of breast
cancer risk in women with single, multiple, and atypical papilloma. Am
J Surg Pathol 2006;30(6):665–672.
48. The American Society of Breast Surgeons Consensus Guideline on
Concordance Assessment of Image-Guided Breast Biopsies and
Management of Borderline or High-Risk Lesions 2018.
https://www.breastsurgeons.org/docs/statements/Consensus-Guideline-
on-Concordance-Assessment-of-Image-Guided-Breast-Biopsies.pdf.
Accessed Sept 14, 2019.
49. Guray M, Sahin AA. Benign breast diseases: classification, diagnosis,
and management. Oncologist 2006;11(5):435–449.
50. Rose PP, Caicco JA. Florid papillomatosis of the nipple. A study of 51
patients, including nine with mammary carcinoma. Am J Surg Pathol
1986;10(2):87–101.
51. Gudjonsdottir A, Hagerstrand I, Ostberg G. Adenoma of the nipple with
carcinomatous development. Acta Pathol Microbiol Scand A
1971;79(6):676–680.
52. Rosen Y, Papasozomenos SC, Gardner B. Fibromatosis of the breast.
Cancer 1978;31(3):1409–1413.
53. Rosen PP, Ernsberger D. Mammary fibromatosis. A benign spindle-cell
tumor with significant risk for local recurrence. Cancer
1989;63(7):1363–1369.
54. Ali M, Fayemi AO, Braun EV, et al. Fibromatosis of the breast. Am J
Surg Pathol 1979;3(6):501–505.
55. Hanna WM, Jambrosic J, Fish E. Aggressive fibromatosis of the breast.
Arch Pathol Lab Med 1985;109(3):260–262.
56. Rosen PP. Mucocele-like tumors of the breast. Am J Surg Pathol
1986;10(7):464–469.
57. Vuitch MF, Rosen PP, Erlandson RA. Pseudoangiomatous hyperplasia
of mammary stroma. Hum Pathol 1986;17(2):185–191.
58. Powell CM, Cranor ML, Rosen PP. Pseudoangiomatous stromal
hyperplasia (PASH). A mammary stromal tumor with myofibroblastic
differentiation. Am J Surg Pathol 1995;19(3):270–277.
59. Cohen MA, Morris EA, Rosen PP, et al. Pseudoangiomatous stromal
hyperplasia: mammographic, sonographic, and clinical patterns.
Radiology 1996;198(1):117–120.
60. Fletcher A, Margrath IM, Riddell RH, et al. Granulomatous mastitis: a
report of seven cases. J Clin Pathol 1982;35(9):941–945.
61. Dixon JM, Anderson TJ, Lumsden AB, et al. Mammary duct ectasia. Br
J Surg 1983;70(10):601–603.
62. Bundred NJ, Dixon JM, Lumsden AB, et al. Are the lesions of duct
ectasia sterile? Br J Surg 1985;72(10):844–845.
63. Dixon JM. Periductal mastitis/duct ectasia. World J Surg
1989;13(6):715–720.
64. Dixon JM, Ravisekar O, Chetty U, et al. Periductal mastitis and duct
ectasia: different conditions with different aetiologies. Br J Surg
1996;83(6):820–822.
65. Rosen PP, Kosloff C, Lieberman PH, et al. Lobular carcinoma in situ of
the breast. Detailed analysis of 99 patients with average follow-up of 24
years. Am J Surg Pathol 1978;2(3):225–251.
66. Kessler E, Wolloch Y. Granulomatous mastitis: a lesion clinically
simulating carcinoma. Am J Clin Pathol 1972;58(6):642–646.
67. DeHertogh DA, Rossof AH, Harris AA, et al. Prednisone management
of granulomatous mastitis. N Engl J Med 1980;303(14):799–800.
68. Foote FWJ, Stewart FW. Lobular carcinoma in situ: a rare form of
mammary carcinoma. Am J Pathol 1941;17:491–496.
69. Wong SM, King T, Boileau JF, et al. Population-based analysis of breast
cancer incidence and survival outcomes in women diagnosed with
lobular carcinoma in situ. Ann Surg Oncol 2017;24(9):2509–2517.
70. Wheeler JE, Enterline HT, Roseman JM, et al. Lobular carcinoma in situ
of the breast. Long-term followup. Cancer 1974;34(3):554–563.
71. Andersen JA. Lobular carcinoma in situ of the breast. An approach to
rational treatment. Cancer 1977;39(6):2597–2602.
72. Page DL, Kidd TE Jr, Dupont WD, et al. Lobular neoplasia of the
breast: higher risk for subsequent invasive cancer predicted by more
extensive disease. Hum Pathol 1991;22(12):1232–1239.
73. Haagensen C, Bodian C, Haagensen DE. Lobular neoplasia (Lobular
Carcinoma in Situ) Breast Carcinoma: Risk and Detection.
Philadelphia, PA: WB Saunders; 1981.
74. Newman W. In situ lobular carcinoma of the breast: report of 26 women
with 32 cancers. Ann Surg 1963;157:591–599.
75. Rosner D, Bedwani RN, Vana J, et al. Noninvasive breast carcinoma:
results of a national survey by the American College of Surgeons. Ann
Surg 1980;192(2):139–147.
76. Amin MB, Edge SB, Greene FL, et al., eds. AJCC (American Joint
Committee on Cancer) Cancer Staging Manual. 8th edition. Chicago,
IL: Springer; 2018.
77. NCCN Guidelines Version 3.2019 Breast Cancer
http://www.nccn.org/professionals/physician_gls/pdf/breast.pdf.
Accessed on Sept 6, 2019.
78. Virnig BA, Tuttle TM, Shamliyan T, et al. Ductal carcinoma in situ of
the breast: a systematic review of incidence, treatment, and outcomes. J
Natl Cancer Inst 2010;102(3):170–178.
79. Oseni TO, Zhang B, Coopey SB, et al. Twenty-five year trends in the
incidence of ductal carcinoma in situ in US women. J Am Coll Surg.
2019;228(6);932–939.
80. Kerlikowske K. Epidemiology of ductal carcinoma in situ. J Natl
Cancer Inst Monogr 2010;(41):139–141.
81. Dershaw DD, Abramson A, Kinne DW. Ductal carcinoma in situ:
mammographic findings and clinical implications. Radiology
1989;170(2):411–415.
82. Wapnir IL, Dignam JJ, Fisher B, et al. Long-term outcomes of invasive
ipsilateral breast tumor recurrences after lumpectomy in NSABP B-17
and B-24 randomized clinical trials for DCIS. J Natl Cancer Inst
2011;103(6):478–488.
83. Stuart KE, Houssami N, Taylor R, et al. Long-term outcomes of ductal
carcinoma in situ of the breast: a systematic review, meta-analysis and
meta-regression analysis. BMC Cancer 2015;15:890.
84. Claus EB, Stowe M, Carter D. Family history of breast and ovarian
cancer and the risk of breast carcinoma in situ. Breast Cancer Res Treat
2003;78(1):7–15.
85. Claus EB, Petruzella S, Matloff E, et al. Prevalence of BRCA1 and
BRCA2 mutations in women diagnosed with ductal carcinoma in situ.
JAMA 2005;293(8):964–969.
86. Allen LR, Lago-Torro CE, Hughes JH, et al. Is there a role for MRI in
the preoperative assessment of patients with DCIS? Ann Surg Oncol
2010;17:2395–2400.
87. Kuhl CK, Schrading S, Bieling HB, et al. MRI for diagnosis of pure
ductal carcinoma in situ: a prospective observational study. Lancet
2007;370:485–492.
88. Menell JH, Morris EA, Dershaw DD, et al. Determination of the
presence and extent of pure ductal carcinoma in situ by mammography
and magnetic resonance imaging. Breast J 2005;11(6):382–390.
89. Lee SG, Orel SG, Woo JJ, et al. MR imaging screening of the
contralateral breast in patients with newly diagnosed breast cancer;
preliminary results. Radiology 2003;226(3):773–778.
90. Brennan ME, Houssami N, Lord S, et al. Magnetic resonance imaging
screening of the contralateral breast in women with newly diagnosed
breast cancer: systematic review and meta-analysis of incremental
cancer detection and impact on surgical management. J Clin Oncol
2009;27(3):5640–5649.
91. Hwang ES, Kinkel K, Esserman LJ, et al. Magnetic resonance imaging
in patients diagnosed with ductal carcinoma-in-situ: value in the
diagnosis of residual disease, occult invasion and multicentricity. Ann
Surg Oncol 2003;10(4):381–388.
92. Pilewskie M, Olcese C, Eaton A, et al. Perioperative breast MRI is not
associated with lower locoregional recurrence rates in DCIS patients
treated with or without radiation. Ann Surg Oncol 2014;21:1552–1560.
93. Silverstein M, Lagios M, Recht A, et al. Image-detected breast cancer:
state of the art diagnosis and treatment. J Am Coll Surg 2005;201:586–
597.
94. Jeffries DO, Neal CH, Noroozian M, et al. Surgical biopsy is still
necessary for BI-RADS 4 calcifications found on digital mammography
that are technically to faint for stereotactic core biopsy. Breast Cancer
Res Treat 2015;154(3):557–561.
95. Lagios MD. Duct carcinoma in situ: pathology and treatment. Surg Clin
North Am 1990;70:853–871.
96. Page DL, Anderson TJ. Diagnostic Histopathology of the Breast.
Edinburgh: Churchill Livingstone; 1987.
97. Alfred C. Ductal carcinoma in situ. In: Harris JR, Lippman ME, Morrow
M, et al., eds. Diseases of the Breast. 4th ed. Philadelphia, PA:
Lippincott-Raven; 2009:321.
98. Van de Vijver M, Peterse J, Mooi WJ, et al. Neu-protein overexpression
in breast cancer: association with comedo-type ductal carcinoma in situ
and limited prognostic value in stage II breast cancer. N Engl J Med
1988;319:1239–1245.
99. Silverstein MJ, Waisman JR, Gamagami P, et al. Intraductal carcinoma
of the breast (208 cases). Clinical factors influencing treatment choice.
Cancer 1990;66(1):102–108.
100. Fisher ER, Dignam K, Tan-Chiu E, et al. Pathologic findings from the
National Surgical Adjuvant Breast Project (NSABP) eight-year update
of Protocol B-17: intraductal carcinoma. Cancer 1999;86(3):429–438.
101. Narod SA, Iqbal J, Giannakeas V, et al. Breast cancer mortality after a
diagnosis of ductal carcinoma in situ. JAMA Oncol 2015;1(17):888–896.
102. Morrow M, Van Zee KJ, Solin LJ, et al. Society of Surgical Oncology-
American Society for Radiation-Oncology-American Society of Clinical
Oncology Consensus Guideline on margins for breast-conserving
surgery with whole-breast irradiation in ductal carcinoma in situ. J Clin
Oncol 2016;34:4040–4046.
103. Moran MS, Schnitt SJ, Giuliano AE, et al. Society of Surgical
Oncology-American Society for Radiation Oncology consensus
guideline on margins for breast-conserving surgery with whole-breast
irradiation in stages I and II invasive breast cancer. J Clin Oncol
2014;32(14):1507–1515.
104. Houssami N, Macaskill P, Marinovich ML, et al. The association of
surgical margins and local recurrence in women with early-stage
invasive breast cancer treated with breast-conserving therapy: a meta-
analysis. Ann Surg Oncol 2014;21(3):717–730.
105. Waddell BE, Stomper PC, DeFazio JL, et al. Postexcision
mammography is indicated after resection of ductal carcinoma-in-situ of
the breast. Ann Surg Oncol 2000;7:665–668.
106. Gluck BS, Dershaw DD, Liberman L, et al. Microcalcifications on
postoperative mammograms as an indicator of adequacy of tumor
excision. Radiology 1993;188(2):469–472.
107. Grann A, Abdou JC, Dragman N, et al. The value of postexcision
preradiation mammography in patients with early-stage breast cancer.
Am J Clin Oncol 2004;27(3):285–288.
108. Swain S. Ductal carcinoma in situ—incidence, presentation, and
guidelines to treatment. Oncology 1989;3:25–42.
109. Hwang ES. The impact of surgery on ductal carcinoma in situ outcomes:
the use of mastectomy. J Natl Cancer Inst Monogr 2010;2010(41):197–
199.
110. Chatterjee A, Pyfer B, Czerniecky B, et al. Early postoperative outcomes
in lumpectomy versus simple mastectomy. J Surg Res 2015;198(1):143–
148.
111. Cody HS, Van Zee KJ. Point: sentinel lymph node biopsy is indicated
for patients with DCIS. J Natl Compr Canc Netw 2003;1:199–206.
112. Lyman GH, Giuliano AE, Somerfield MR, et al. American Society of
Clinical Oncology guideline recommendations for sentinel lymph node
biopsy in early-stage breast cancer. J Clin Oncol 2005;23:7703–7720.
113. Goodwin A, Parker S, Ghersi D, et al. Post-operative radiotherapy for
ductal carcinoma in situ of the breast—a systematic review of the
randomised trials. Breast 2009;18(3):143–149.
114. McCormick B, Winter K, Hudis C, et al. RTOG 9804: a prospective
randomized trial for good-risk ductal carcinoma in situ comparing
radiotherapy with observation. J Clin Oncol 2015;33(7):709–715.
115. Solin LJ, Gray R, Baehner FL, et al. A multigene expression assay to
predict local recurrence risk for ductal carcinoma in situ of the breast. J
Natl Cancer Inst 2013;105(10):701–710.
116. Rakovitch E, Nofech-Mozes S, Hanna W. Multigene expression assay
and benefit of radiotherapy after breast conservation in ductal carcinoma
in situ. J Natl Cancer Inst 2017:109(4).
117. Khatcheressian JL, Hurley P, Bantug E. Breast cancer follow-up and
management after primary treatment: American Society of Clinical
Oncology clinical practice guideline update. J Clin Oncol
2013;31(7):961–965.
CHAPTER 22

Breast Cancer Screening and


Management in the Transgender
Patient
DHIVYA R. SRINIVASA | ESTHER A. KIM
HISTORY
“Top surgery” encompasses both feminizing and masculinizing chest surgery
for transgender patients. Both procedures have undergone evolution as
gender-affirmation surgery (GAS) has come to the forefront of health
disparities’ discussions. With the institution of the Affordable Care Act,
insurance carriers were required to cover GAS, thereby creating a surge in the
number of these procedures performed. Accordingly, discussions surrounding
long-term outcomes and effects of these procedures have heightened.
Namely, the long-term incidence of breast cancer in both the transmale and
transfemale cohorts requires specific attention.
Transfemales are oftentimes on long-term feminizing hormone therapy.
The undue effects on breast tissue and the potential for dysplasia raise
concern about heightened breast cancer risk. For transmen, the underlying
patient protoplasm confers a baseline risk which may warrant an oncologic
mastectomy. Since masculinizing surgery does not routinely remove as much
breast tissue as an oncologic mastectomy, residual threat for developing
breast cancer is of concern in all patients, but especially those with a higher
baseline risk. This chapter reviews both surgical and screening practices with
respect to managing breast cancer in transwomen who undergo feminizing
augmentation and transmen who undergo mastectomy.
INDICATIONS

Transmales
Standard practice prior to performing a masculinizing mastectomy in
transmales is to review the patient’s personal and family history of breast and
other cancers. A detailed history should also include any previous breast
surgery, skin changes, nipple discharge, or palpable masses. Any account of
familial cancers should prompt referral to a geneticist for additional testing
and risk stratification. Essentially, the reconstructive surgeon should have a
comprehensive understanding of any predisposition to developing breast
cancer such that appropriate screening is performed. High-risk patients (i.e.,
BRCA positive) should meet with a breast surgeon to discuss whether a risk
reduction prophylactic mastectomy is indicated and further delineate long-
term monitoring. In patients with a lifetime risk of 20% or greater, the
American Society of Breast Surgeons recommends screening with MRI (1).
Therefore, transmen that meet this criterion would qualify for screening MRI
postoperatively from masculinizing chest surgery as well. This example
underscores the importance of including a breast surgeon and/or breast
oncologist in preoperative planning in high-risk individuals.
Additionally, the surgeon should comply with national guidelines for
breast cancer screening (2,3). Current recommendations include annual
mammography starting at 50 years of age in women with no additional risk
factors. However, certain high-risk patients qualify for earlier screening and
this should be evaluated on a case-by-case basis. Prior to performing
mastectomy, it is incumbent that appropriate screening is performed and
reviewed by the surgeon. Any abnormalities warrant further workup prior to
proceeding with GAS. In addition to screening for breast cancer, a detailed
breast and axillary examination is necessary in all patients to evaluate for
masses, skin changes, and/or nipple aberrancies. Any evidence of
abnormality warrants further evaluation by a breast oncology surgeon prior to
GAS.
Transfemales
The incidence of breast cancer in genetic males is quite low, around 0.1%.
Therefore, no specific screening recommendations are in place for detection
of breast cancer in males. However, transwomen are oftentimes on
feminizing hormone therapy including estrogen, progesterone, and
testosterone blockers. The surgeon should document all past history and
current medications, especially hormone therapy (including duration of
treatment and adverse effects). The long-term effects of these medications on
glandular development, specifically glandular dysplasia, warrant screening
guidelines for patients receiving hormone therapy (4,5). A Dutch study
published in May 2019 presented a significantly increased risk of breast
cancer in transwomen on hormone treatment. Specifically, a 46-fold
increased risk of breast cancer exists compared to cis-gender men. In this
cohort, the median duration of hormone therapy was 15 years and the
majority of tumors were both estrogen and progesterone sensitive, and of
ductal origin (6). These features suggest that although the increased risk of
breast cancer in transwomen is lower than cis-gender women, hormone
therapy likely plays a critical role in the pathogenesis of breast cancer in
transfemales.
To encompass both the risk of hormone therapy and general population
recommendations for cis-gender women, screening mammography for
transfemales is recommended every 2 years for patients older than 50
with at least 5 years of hormone therapy (7). As with cis-gender women,
additional risk factors may prompt lowering the age at which to initiate
screening. Family history or known mutations should warrant genetic
counseling to guide decisions on screening frequency and modality. Although
mammography is still the modal examination utilized, certain patients may
require an MRI (8). Lastly, it is important to note that transwomen although
have a lower incidence of breast cancer compared to cis-gender women, the
average age of disease is lower in the transwomen population (6). This data
warrants a discussion regarding lowering the age at which we recommend
screening mammography in patients on hormone therapy.
CONTRAINDICATIONS
Transmales should not undergo mastectomy without appropriate screening
mammography (9). What is considered “appropriate” varies per patient. Most
commonly, annual mammography is indicated in all women starting at age 50
(10). However, certain risk factors require earlier screening. Any suggestive
history or abnormalities in radiology or examination should be further
investigated prior to surgery.
Transfemales should not undergo feminizing augmentation if physical
examination suggests any breast masses or skin changes concerning for
breast cancer.
PREOPERATIVE PLANNING

Transfemales
Preoperative patient education regarding individual risk for developing breast
cancer is a necessary component of preoperative planning for top surgery. In
transwomen, it is incumbent to share that hormone therapy imposes an
increased risk of developing breast cancer. Seemingly, longer durations of
treatment are associated with increasing risk. Therefore, patients should be
urged to perform self-breast examinations and seek medical help should any
masses or skin changes arise.
A recent association between anaplastic large cell lymphoma (ALCL) and
textured breast implants has led to the recall of certain textured breast
prostheses. The authors suggest avoiding the use of textured implants for
feminizing augmentation due to at least two reported cases of breast implant
associated-anaplastic large cell lymphoma (BIA-ALCL) in transwomen who
received textured implants (11,12). If the surgeon chooses to place textured
implants, the authors recommend a preoperative conversation regarding the
risk of developing ALCL, inclusion of this risk in the consent form, as well
as appropriate documentation.
OPERATIVE TECHNIQUE
The specific operative technique should not be modified. The surgeon should
explain to transmale patients however, that although the term “mastectomy”
is used to describe the operation, the goal is to achieve the contour of a male
chest and not simply remove all breast tissue. In fact, breast tissue is often
left on the anterior skin flap to optimize the natural contour of the male chest
as opposed to leaving a concavity. This residual tissue does have the potential
to develop breast cancer.
No specific operative modifications are recommended to reduce the risk of
breast cancer for transfemales in performing a feminizing augmentation.
INTRAOPERATIVE CARE
All tissue removed during a GAS should be sent to pathology for permanent
section. Although it is not commonplace to remove any tissue during a
feminizing augmentation, should any specimens be removed, they should
also be sent to pathology for permanent section. Any abnormal pathology
should be referred to a breast surgeon for further management. In some cases,
transwomen have received off-label silicone injections. These silicone
granulomas can present as masses in the breast and should also be excised if
symptomatic.
POSTOPERATIVE CARE

Transwomen
Long-term post-operative follow-up is necessary to best detect potential
breast cancers that may arise in either transwomen who undergo feminizing
augmentation or transmen who undergo gender-affirming mastectomies.
Oftentimes, the primary care provider (PCP) follows the patient for longer
than the reconstructive surgeon. The authors recommend educating both the
patient and PCP regarding the potential risk for breast cancer development.
Self-examinations should be encouraged and patients should seek evaluation
should any masses develop. Transwomen should also be counseled on the
potential risk of breast cancer with hormone therapy. Feminizing
augmentation does not affect that risk, but hormone therapy duration likely
does. These patients should also be encouraged to perform self-breast
examinations and report any abnormalities to their PCP.
Transmen
Transmen should be educated on the differences bet-ween gender-affirming
mastectomies and an oncologic mastectomy, and that residual breast tissue is
left in situ that can potentially develop into breast cancer. Monitoring
transmen for breast cancer postoperatively poses a challenge since
mammography is often not technically feasible in a transmale patient after
masculinizing chest surgery (13). Rather, risk stratification using a patient’s
personal and family history is paramount. Therefore, high-risk patients
should be evaluated by genetics, and a multidisciplinary discussion is
necessary to decide on whether screening MRI is indicated and how often.
Self-examinations should be discussed with all patients since variable
amounts of breast tissue are left behind at the time of surgery.

CASES

CASE 1
A 49-year-old transgender male presents to clinic requesting top surgery.
He has been living as a male for over 22 years, but only started
testosterone 7 months ago as he reached menopause. Mammogram was
obtained preoperatively, and was negative. His family history reveals a
paternal grandmother with breast cancer. He undergoes a double-incision
mastectomy. The right breast specimen pathology shows multiple foci of
atypical ductal hyperplasia and one 2-mm focus of low-grade DCIS. Of
note, the specimen was also studied with mammogram to rule out other
lesions. The left breast pathology showed benign breast parenchyma.
Challenges Moving Forward
In general, patients who have DCIS who undergo mastectomy also
receive a sentinel lymph node biopsy at the same time. The reasoning
behind this is to secure that lymph nodes are sufficiently sampled for
metastasis in case the final pathology shows an invasive component. In
patients who undergo mastectomy, it is not possible to obtain an accurate
sentinel node, therefore it is performed as a precautionary measure along
with the mastectomy. In this patient, the breast surgeon will be unable to
perform a sentinel lymph node biopsy. Given that the entire specimen
only shows DCIS, and the lesion was only 2 mm, the chances of
metastasis are exceedingly low. The other challenge is whether the
patient needs further surgery. A double-incision mastectomy for the
purposes of gender affirmation is not the same operation as an oncologic
mastectomy; accordingly, residual breast tissue still carries the risk of
cancer and the patient needs to decide whether he wants another
operation for further risk reduction. If not, the discussion should include
risk stratification to best determine if MRI is warranted for screening
moving forward.

CASE 2

A 54-year-old transmale has been living as a male for 2 years, during


which he has also been on testosterone therapy. Preoperative
mammogram was negative for concerning lesions. He has no known
family history. Per standard protocol, bilateral specimens from his
double-incision mastectomy were sent for permanent section. Pathology
of the right breast revealed a 1-mm focus of invasive ductal carcinoma
with a close posterior margin (<0.01 cm).
Challenges Moving Forward
This patient has an invasive cancer and therefore requires a sentinel
lymph node biopsy. For the same reasons outlined in case 1, this patient
is now unable to obtain a proper sentinel lymph node biopsy. With sub-
centimeter lesions, lymph node metastasis is unlikely, but still reported.
Further, this patient also needs to understand that his surgery is not
oncologic in nature, so if he wants optimal surgical risk reduction,
additional breast tissue should be removed. Potentially, an MRI could
help delineate the amount of retained breast tissue and guide any
potential benefit of further surgery. Lastly, this patient has a close
posterior margin. However, there are no clips to mark where the lesion
was, and therefore, targeted radiation therapy to this area would not be
possible. This case highlights the importance of detecting lesions
preoperatively; appropriate cancer management becomes severely limited
in the postoperative setting.
CONCLUSION
The authors recommend the reconstructive surgeon provide a letter to the
patient’s PCP regarding the nature of their surgery and overall risk for breast
cancer. For transfemales undergoing feminizing augmentation, patients
should be aware of the effects of progesterone and estrogen therapy with a
likely increased risk for breast cancer with longer-term hormone therapy.
Screening in an otherwise normal-risk individual should start at 50 years of
age and after 5 years of hormone therapy. The authors feel that the discussion
regarding lowering the initial age for screening in transwomen is necessary
due to the younger age of onset in patients taking hormone therapy. For
transmen who undergo masculinizing chest surgery, long-term risk of breast
cancer is unknown. Most tumors are found at the time of surgery.
Accordingly, the patient’s history and risk factors should guide
individualized recommendations regarding screening.
As is, numerous health disparities afflict the transpopulation with several
studies reflecting significant untoward effects on overall health. One such
study of over 1,000 transgender women at an urban center showed that
transfemales are less likely to obtain recommended mammograms (after 5
years of hormone therapy) compared to cis females (14). The authors feel that
a concerted effort to educate both patients and PCPs on breast cancer
screening in transindividuals can alleviate some of the existing barriers to
care.

REFERENCES

1. The American Society of Breast Surgeons. Consensus Guideline on


Diagnostic and Screening Magnetic Resonance Imaging of the Breast.
ASBS Research Committee Meeting. 2017. Available at
www.breastsurgeons.org.
2. American College of Obstetricians-Gynecologists. Practice bulletin no.
122: breast cancer screening. Obstet Gynecol 2011;118(2 Pt 1):372–382.
3. Final Update Summary: Breast Cancer: Screening. U.S. Preventive
Services Task Force. May 2019.
https://www.uspreventiveservicestaskforce.org/Page/Document/UpdateSummaryFina
cancer-screening
4. Gooren LJ, van Trotsenburg MA, Giltay EJ, et al. Breast cancer
development in transsexual subjects receiving cross-sex hormone
treatment. J Sex Med 2013;10:3129–3134.
5. Brown GR, Jones KT. Incidence of breast cancer in a cohort of 5,135
transgender veterans. Breast Cancer Res Treat 2015;149:191–198.
6. de Blok CJM, Wiepjes CM, Nota NM, et al. Breast cancer risk in
transgender people receiving hormone treatment: nationwide cohort
study in the Netherlands. BMJ 2019;365:l1652.
7. Sonnenblick EB, Shah AD, Goldstein Z, et al. Breast imaging of
transgender individuals: a review. Curr Radiol Rep 2018;6(1):1.
8. Weyers S, Villeirs G, Vanherreweghe E, et al. Mammography and
breast sonography in transsexual women. Eur J Radiol 2010;74(3):508–
513.
9. Phillips J, Fein-Zachary VJ, Mehta TS, et al. Breast imaging in the
transgender patient. AJR Am J Roentgenol 2014;202:1149–1156.
10. Eismann J, Heng YJ, Fleischmann-Rose K, et al. Interdisciplinary
management of transgender individuals at risk for breast cancer: case
reports and review of the literature. Clin Breast Cancer 2019;19:e12–
e19.
11. Ali N, Sindhu K, Bakst RL. A rare case of a transgender female with
breast implant–associated anaplastic large cell lymphoma treated with
radiotherapy and a review of the literature. J Investig Med High Impact
Case Rep 2019;7:2324709619842192.
12. Kadin M, Glicksman C. Commentary on: breast implant-associated
anaplastic large-cell lymphoma in a transgender woman. Aesthet Surg J
2017;37(8):NP88–NP89.
13. Grynberg M, Fanchin R, Dubost G, et al. Histology of genital tract and
breast tissue after long-term testosterone administration in a female-to-
male transsexual population. Reprod Biomed Online 2010;20:553–558.
14. Bazzi AR, Whorms DS, King DS, et al. Adherence to mammography
screening guidelines among transgender persons and sexual minority
women. Am J Public Health 2015;105(11):2356–2358.
CHAPTER 23

Shared Decision Making: Patient


Choice and Satisfaction
SUNNY MITCHELL
HISTORY
Shared decision making complements informed consent and aims to educate
the patient on all evidence-based treatment options while incorporating their
own preferences. This practice brings the patient into the decision-making
process, encouraging active participation in the choice(s) of specific
treatment they will undergo. This differs markedly from an era when the
physician made the treatment choice for the patient. An era of enhanced
breast cancer knowledge, advanced surgical techniques, and a more
thoughtful consideration of quality of life (QOL) and satisfaction have
merged to make shared decision making the standard of care within the
informed consent process. This becomes even more imperative as the
majority of women diagnosed and treated for breast cancer will complete
their therapies and continue to live past the time of diagnosis and treatment.
Ideally, the effects of surgery and other treatment-related modalities for
breast cancer, including chemotherapy and radiation therapy should leave as
minimal a lasting footprint as possible and interfere as little as possible with
QOL and satisfaction, allowing the individual treated for breast cancer to
move on with their lives.
How is shared decision making implemented within the informed consent
process? Components include a thoughtful, well-informed conversation with
the patient that offers all evidence-based treatment modalities applicable for
the individual and addresses patient expectations, while respecting autonomy
and personal preferences. Incorporation of additional education tools in paper
or electronic format, conversations with all members of the multidisciplinary
breast cancer treatment team, and adequate follow-up time to answer any
additional questions is imperative.
PATIENT CHOICE
Patient choice may be influenced by many factors, including unfortunately
lack of choice. Various, sometimes conflicting findings are reported in the
literature, highlighting the complexity and individual nature of patient
thought and the decision-making process. It is important to identify and
address the complexities and expectations which may help form the patient’s
choice. Patients may experience a false sense of urgency, make decisions
based on fear, value different opinions, and/or make choices secondary to a
variety of factors.
Sense of Urgency and Insufficient Time for Decision Making
In order to adequately participate in treatment choice, time must be allotted
for adequate decision making. Women may perceive a false sense of urgency
while choosing type of breast surgery (1), and have inadequate time for
decision making during fertility treatment consultation (2), or reconstruction
options (3), within the decision-making process. It is imperative to address
this head on while navigating the patient through the decision-making
process by assuring patients that they have the time to learn about, discuss,
consider, and actively participate in making the best choice for them.
Decisions Made From a Sense of Fear
Fear of recurrence may drive a woman’s choice toward mastectomy instead
of breast conservation surgery (BCS) (4,5). Fear (6–8) followed by desires
for symmetry (6,8), and the opinions of others (7), were the noted influencer
of patients opting to undergo a contralateral prophylactic mastectomy (CPM).
Even women who anticipate a “very large” financial burden compared to
unilateral therapeutic mastectomy may opt for CPM (9). Women with a
BRCA mutation, enrolled in an MRI-based screening program were more
likely to undergo prophylactic mastectomies when a high perception of
personal breast cancer risk and a history of breast cancer in a first-degree
relative existed (10). Presumably fear is addressed by adequate education and
support.
Whose Opinion Matters?
Whose opinion of best treatment is most valuable may vary from patient to
patient. Women may value their own opinion, defer to their surgeon, value
both theirs and their surgeons, or try to perceive what their physician thinks is
best. A prospective study in the Netherlands assessing predictors of patients’
surgical choices found patient’s concerns and their perception of the
treatment preferences of their physicians were important factors in the
patients’ decision-making process (11). Women opting for lumpectomy over
mastectomy were found to place similar weight on their own and surgeon’s
input (12). When opting for mastectomy, patients may value their own
opinion most (12,13), or a combination of personal choice and surgeon’s
advice (14). Another study (15) suggested surgeons attempt to identify the
patients preferred degree of participation in decisions and tailor the decision-
making process to them.
A multicentered study examining how women had elected for or against
immediate breast reconstruction with mastectomy revealed decision making
was influenced by the perceived importance of alternatives, prevailing
“norms” regarding surgical practice within each hospital system, and
interactions with health professionals (16). A survey of patients who
underwent bilateral prophylactic mastectomy (BPM) and reconstruction
found patients were strongly influenced by their physicians and less so by
other means (media, internet, etc.) (17).
A 2016 study out of Memorial Sloan Kettering Cancer Center noted that
despite hours of education from surgeons on lack of survival benefit and risks
associated with bilateral surgery, patients determined to pursue a CPM will
sometimes change surgeons or hospitals to have the CPM (13). A study
evaluating breast reconstruction noted most patients reported a desire to
know “everything” regarding their reconstruction surgery and to be “very
involved” (18). Potential financial concerns may influence patient decision
and should be queried and addressed as actual financial burden may not
equate to patient’s assumptions (19). Presumably, adequate information and
communication are essential to base treatment decisions on realistic concerns,
and the treatment preferences of the patient (11).
Older Patients
A study of women >70 years old found a complexity of factors influencing
the decision-making process including: treatment characteristics, personal
goals/beliefs, patient characteristics, physician’s recommendation, and
personal/family experience (20). A study of women ≥67 years old found
greater patient–physician communication to be associated with a sense of
choice (21). Contrarily, women over 70 years old in the United Kingdom
were noted to utilize passive information seeking and were noted to rely
heavily on “expert” decision making; their main concern was not social
support or age but rather QOL and independence (19). Older patient age
should not correlate to an inherent bias of surgeons as to a presumption of
thoughts or desires, each individual should be counseled on an individual
basis regardless of age.
Patient Expectations
An important component of choice in the decision-making process is
addressing patient expectations. Experiences of reconstructive surgery may
fail to match patient’s presurgical expectations and the process of adjusting to
the impact of surgery may continue past the postop period and throughout the
following year (16). Recommendation of a routine preoperative checklist in
preop consultations was the result of a literature review delineating a need for
accurate and consistent measures of patient-reported expectations, and
education of both of patients and health practitioners on the importance of
informed discussion about treatment options, for women facing a choice
about breast reconstruction, a major breast cancer survivorship decision (22).
High-risk women may be more likely to opt for prophylactic surgery
secondary to the expectation of an aesthetically acceptable result from nipple-
sparing mastectomy (NSM) and reconstruction (23). Patient expectations
should be directly addressed within the shared decision-making process.
Reconstruction
A study performed in the United Kingdom noted lack of information and/or
time, involvement in decision making, and issues relating to the evolution
and organization of reconstructive services as potential explanations of
inequalities noted in breast reconstruction (3). A survey of patients who had
undergone BPM and reconstruction found multiple factors influenced
decision making with the ultimate choice in reconstruction involving tissue
availability, appearance of implant reconstructions, total amount of surgery
required, and extent of visible scars (17).
The potential prevalence of cancer-related fatigue and depression may be
implicated in a patient’s desire to undergo less extensive reconstructive
surgery (24). Factors influencing type of, timing of, or desire for lack of
reconstruction should stem from a fully informed patient.
“No Best Option”
Incorporating a shared decision-making model between patient and physician
has inherent complexities in treatment of the breast. A study evaluating
patient perceptions on shared decision making demonstrated a potential
undermining of the patient’s interest of a guarantee of the best care available,
in this era of medical authority shifting and perceived differences between
decision making, participation, and information (25). Advances in breast
cancer treatment have led to multiple options within and between treatment
disciplines such as: type of breast surgery; reconstruction type, timing/ or
lack thereof; neoadjuvant or adjuvant chemotherapy; radiation therapy, etc.
All of which are expected to be communicated to the patient. When patients
are presented with treatment options where “no clear best choice based on
outcome evidence” exists, this communication of “uncertainty” was found to
negatively relate to decision satisfaction in breast cancer treatment, but not in
preventative treatment (26). Informational needs have been reported as very
important by patients in making breast cancer treatment decisions (27).
Limited Information
In a survey of women who underwent delayed mastectomy reconstruction,
only 51% reported discussing immediate reconstruction prior to their delayed
reconstruction and 41% reported no discussions regarding advantages or
disadvantages of reconstructive options (28). Some women have reported no
option given for immediate reconstruction (29). A large population based
sample of 1,844 women diagnosed with breast cancer in metropolitan Los
Angeles and Detroit between 2001 and 2003, demonstrated the majority of
women had inadequate knowledge to make informed decisions about their
breast cancer surgical treatment (30). Information on surgical options should
be complete and thorough to allow for appropriate decision making.
SATISFACTION
Patient satisfaction of breast cancer treatment has been measured utilizing a
multitude of variables in a variety of ways. Many factors may influence an
individual patient’s satisfaction.
Role of Decision Making and Feeling Informed
Patients who wanted and participated in an active decision-making role
(15,31), or made the treatment decisions themselves (32), have reported
greater satisfaction with their treatment choice. In women who made an
informed choice of either BCS or mastectomy after making an informed
choice of surgical options reported satisfaction with their choice when
queried prior to and 6 months after surgery (33). Many women who had
surgery for breast cancer reported not feeling completely informed about their
surgical options (1,30). The role of decision making, and feeling informed
can correlate directly with satisfaction and stems from a fully informed
patient.
Role of Physician/Team Communication and Decisional
Conflict
A study of women ≥67 years old found greater patient–physician
communication to be associated with satisfaction with care (21). A pilot
randomized control trial assessing the feasibility and effect of a
preconsultation educational group intervention on the decision-
making process for breast reconstruction found a reduction of decisional
conflict and improvement in patients’ shared decision-making quality
compared to routine preoperative patient education (34). Physician and breast
cancer treatment team communication can directly affect patient satisfaction
and reduce decisional conflict.
Role of Body Image
Women who underwent a lumpectomy or mastectomy have reported
decreased comfort levels with partners seeing their chest (12). A significant
reduction in comfort with one’s partner has been reported after mastectomy,
more so than lumpectomy (12). Older women undergoing mastectomy with
immediate reconstruction may have better sexual well-being postoperatively
and better acceptance of their body image (35). Body image including sexual
well-being may be affected by surgical intervention and should be taken into
consideration preoperatively within surgical choice and patient expectations.
Role of Scars
In questionnaires filled out by women who had breast cancer surgery at two
large centers in Ireland 61% referred that their partners’ opinion of scars were
important (36). A nationwide survey highlighted scars from lumpectomy
and/or mastectomy are not merely “cosmetic” but have a substantial impact
on the lives and well- being of women (37). Breast scars may affect a
patient’s well-being and satisfaction. Preoperative discussions on potential
incision (scar) placement can optimize incision placement and inform
expectations.
Role of Personality
Specific personality traits have been reported to potentially play a role in the
patient’s choice of a reconstructive option (38) and their overall postoperative
satisfaction. Women with an anxious personality have been reported to
potentially experience worse QOL after BCS than mastectomy (39).
Thorough patient evaluation entails consideration of concomitant mental
health diagnoses and personality traits to better serve patients.
Role of Surgical Options
Oncoplastic BCS, regardless of XRT, was correlated to better psychosocial
and self-rated satisfaction with breast appearance and return to work and
function (40). Direct-to-implant breast reconstruction advantages such as lack
of secondary surgery, faster recovery, better QOL, good outcomes, and
patient satisfaction rates have been reported (41). Specific surgical
procedures may correlate to patient satisfaction and should be optimized
whenever feasible.
Role of Radiation Therapy
Radiation therapy has been correlated to lower satisfaction (35), as well as
positive satisfaction (42), and no effect on patient satisfaction (40).
Appropriate education pretreatment choice should be optimized to account
for expectations.
Role of Contralateral Prophylactic Mastectomy
Of women who consider CPM, limited data is available between those who
undergo CPM and those who do not (8). Reported reasons for dissatisfaction
after CPM are adverse or diminished body image, poor cosmetic result,
complications, diminished sense of sexuality, emotional issues, and perceived
lack of education regarding alternative surveillance/CPM efficacy (8), as well
as a prolonged psychological impact 3 years after the procedure (43). In the
setting of opting for a CPM, a cohort of Chinese women demonstrated similar
results to their Caucasian counterparts in being reluctant to confront possible
sexual problems at the decision-making stage; the physical and psychological
impact inevitably emerged right after the procedure (43). Thoughtful
discussion highlighting the risks and benefits of a CPM should facilitate
patient education and address satisfaction.
Role of Decision Aids
Decision aids have been reported to reduce anxiety and increase satisfaction
with treatment choice (44), increase readiness to make a decision (45), reduce
decisional conflict (51) and decision regret (18), correlate with no difference
in anxiety, depression, or QOL outcomes (18), and make no significant
improvement of knowledge (45). When utilized with high-risk women
undergoing decision making regarding reconstruction with prophylactic
mastectomies, decision aids have been correlated to reduced decisional
conflict and improved knowledge with greater satisfaction of information
(46). Decision aids have been shown to enhance the patient experience in
choice and satisfaction.
Role of Regret Over Time
Patients with early-stage breast cancer reported no difference in change in
decision regret over time by surgery type at 9 months and 4 years
postoperatively, a new diagnosis of breast cancer was associated with an
increase in regret over time (47). Presumably, a fully educated patient
engaged in the shared decision-making process should have lower degrees of
treatment regret.
Discussion
The decision-making process is continuously being addressed and optimized.
Ongoing efforts continue to develop, evaluate, and adapt decision aid scales
(44,45,48–51). The helpfulness of decision aids is demonstrated in patient use
correlating to less decisional conflict, higher satisfaction with the decision
made and the decision process, and higher knowledge levels (52). An
argument for better decision aids was highlighted when surveying a group of
women on reconstruction decision revealed that despite using similar
informational content, sources, and similar influential factors, some women
referred no option given for immediate reconstruction (29).
The majority of women undergoing breast reconstruction will be long-term
breast cancer survivors; the decisions they make about reconstructive surgery
are likely to have long-lasting effects on their QOL, emphasizing the
importance of making high-quality decisions (3). The goal, after successful
removal of the breast cancer, is to provide reconstruction that the patient feels
whole from a psychosocial perspective, self-perception or imaging, and
sexual well-being (53). Long-term effects of modern breast cancer surgery,
that is, from lumpectomy, oncoplastic lumpectomy, mastectomy, mastectomy
with reconstruction, and likewise, depend heavily on reasonable surgical
recommendations and should be discussed for specific oncologic and
reconstructive surgical plans (53).
An inherent component to shared decision making is the onus of
responsibility on the surgeon to be up to date on current-era breast surgeries
such as oncoplastic lumpectomies, nipple-sparing mastectomies, and both
breast conservation and mastectomy options that minimize or hide scarring
and optimize aesthetic outcome. The variety of currently available
reconstructive surgery options should all be a part of the plastic surgeons’
armamentarium, allowing for treatment to be tailored to the individual patient
(54). An example of surgical progress in both therapeutic and prophylactic
mastectomy is the NSM, attributed with a lessened psychological burden
(13). In the setting of postmastectomy reconstruction, patient satisfaction and
QOL are the most significant outcome variables when evaluating surgical
success (55). As breast reconstructive procedures continue to change and
advance, additional studies on reconstructive procedures to determine the
impact on women’s short- and long-term psychosocial adjustments should be
undertaken (56).
Efforts to address optimizing patient decision making have been
undertaken within the United States and globally:
In attempts to understand and reduce significant regional differences in
immediate reconstruction within Sweden, a national study found that
patient participation in decision making, availability of plastic surgery
services, and patient information were independent predictors of
immediate breast reconstruction, leading to recommendations to focus on
oncoplastic and reconstructive training and improve collaboration
between breast and plastic surgeons (57).
A study evaluating disparity of local and regional immediate
reconstruction in the United Kingdom noted most reconstruction was
implant based and autologous perforator flaps more likely to be offered in
specialty institutions, leading to recommendations of plastic surgeons to
not become deskilled in techniques such as a latissimus dorsi (LD) flap
(58).
The significance of preoperative patient expectation management when
undergoing risk-reducing procedures was demonstrated in a comparison
of patient satisfaction using the BREAST-Q questionnaire on women who
underwent bilateral mastectomy and reconstruction in the Cambridge
Breast Unit, finding the therapeutic group with higher patient satisfaction
than the risk-reducing group across most domains including breast,
outcome, psychosocial, sexual, physical and information, in direct
contrast to the BRCA gene–positive group which scored the lowest (59).
Potential cultural differences may help form the decision-making process
and factor into levels of satisfaction (60).
Time spent and utilization of education tool(s) in surgical consultation at
the time of a new cancer diagnosis was explored in a 2012 survey (N =
2,818) of the membership of the American Society of Breast Surgeons
(ASBrS), revealing 89% of respondents were utilizing education tools
and 90% of surgeons spent more than 30 minutes meeting with a patient
with a new cancer diagnosis (61).
An ASBrS Consensus Statement on CPM recommended counseling
should include discussions of CPM, risks of CPM, rates of contralateral
breast cancer, ensure patients are engaged in the decision making, and
making decisions that are concordant with their treatment preferences and
personal values (62).
The most relevant content and format of a psychological consult prior to
risk reducing or CPM was defined as: patient understanding of the
procedure and cancer risk, potential physical/emotional impact of
surgery, informed decision making, and past/current psychological issues
(anxiety and body image) by a consensus of experts in Australia
(psychologists, surgeons, nurses, oncologists, genetic specialists, and
researchers) (63).
The shared decision-making process continues past the initial treatment
decision time period and includes perioperative decisions as highlighted
by a consensus statement from the ASBrS, recommending decisions
regarding reexcision in the setting of ductal carcinoma in situ (DCIS).
BCS should optimally involve multidisciplinary input and shared decision
making with the patient (64).
An example of the need for optimizing shared decision making is
highlighted in the results of a population-based sample of 1,844 women
diagnosed with breast cancer in metropolitan Los Angeles and Detroit
2001 and January 2003, demonstrating the majority of women had
inadequate knowledge with which to make informed decisions
about breast cancer surgical treatment, and recommending fundamental
changes in patient education including an increase in the use
of decision aids and in decreasing the speed at which treatment decisions
are made (30).
The need for thorough education on cancer risk and realistic expectations
was demonstrated in a study of a cohort of Chinese women, BRCA
positive, who subsequently opted for prophylactic CPM (43).
A multimodality cancer team and sufficient preop time for discussion are
helpful components of providing comprehensive treatment options for all
women with breast cancer (14).
Throughout the shared decision-making process, autonomy must be
considered and respected. Promoting the exercise of autonomy needs to go
beyond the conception of autonomy as rational individuals making their own
decision, and clinicians need to work with an understanding of autonomy as
relational in order to better involve women in their care (65).
CONCLUSION
Inherent components of the shared decision making process are patient
choice and satisfaction. A prerequisite of choice is full consent including
shared decision making. Legitimate shared decision making implies the
patient must be fully informed and offered all potential options that are best
for the individual as per current era evidence-based medicine.
Multidisciplinary tumor boards, educational aids, thoughtfulness of QOL and
well-being, sufficient decision-making time, education on all current era
evidence-based treatment options, while respecting patient autonomy are
components of the shared decision-making process.

REFERENCES

1. Mitchell S, Gass J, Hanna M. How well informed do patients feel about


their breast cancer surgery options? Findings from a nationwide survey
of women after lumpectomy and/or mastectomy. J Am Coll Surg
2018;226:134–146.
2. Hill KA, Nadler T, Mandel R, et al. Experience of young women
diagnosed with breast cancer who undergo fertility preservation
consultation. Clin Breast Cancer 2012;12(2):127–132.
3. Potter S, Mills N, Cawthorn S, et al. Exploring inequalities in access to
care and the provision of choice to women seeking breast reconstruction
surgery: a qualitative study. Br J Cancer 2013;109:1181–1191.
4. Nold RJ, Beamer RL, Helmer SD, et al. Factors influencing a woman’s
choice to undergo breast-conserving surgery versus modified radical
mastectomy. Am J Surg 2000;180(6):413–418.
5. Ballinger RS, Mayer KF, Lawrence G, et al. Patients’ decision-making
in a UK specialist centre with high mastectomy rates. Breast
2008;17(6):574–579.
6. Buchanan PJ, Abdulghani M, Waljee JF, et al. An analysis of the
decisions made for contralateral prophylactic mastectomy and breast
reconstruction. Plast Reconstr Surg 2016;138(1):29–40.
7. Soran A, Ibrahim A, Kanbour M, et al. Decision making and factors
influencing long-term satisfaction with prophylactic mastectomy in
women with breast cancer. Am J Clin Oncol 2015;38(2):179–183.
8. Ager B, Butow P, Jansen J, et al. Contralateral prophylactic mastectomy
(CPM): a systematic review of patient reported factors and
psychological predictors of influencing choice and satisfaction. Breast
2016;28:107–120.
9. Huang J, Chapgar A. Impact of anticipated financial burden on patient
decision to undergo contralateral prophylactic mastectomy. Surgery
2018;164(4):856–865.
10. Haroun I, Graham T, Poll A, et al. Reasons for risk-reducing
mastectomy versus MRI-screening in a cohort of women at high risk of
breast cancer. Breast 2011;20(3):254–258.
11. Molenaar S, Oort F, Sprangers M, et al. Predictors of patients’ choices
for breast-conserving therapy or mastectomy: a prospective study. Br J
Cancer 2004;90:2123–2130.
12. Kwait RM, Pesek S, Onstad M, et al. Influential forces in breast cancer
surgical decision making and the impact on body image and sexual
function. Ann Surg Oncol 2016;23(10):3403–3411.
13. Manning AT, Sacchini VS. Conservative mastectomies for breast cancer
and risk-reducing surgery: the Memorial Sloan Kettering Cancer Center
Experience. Gland Surg 2016;5(1):55–62.
14. Fancher TT, Palesty JA, Thomas R, et al. A woman’s influence to
choose mastectomy as treatment for breast cancer. J Surg Res
2009;153(1):128–131.
15. Keating NL, Guadagnoli E, Landrum MB, et al. Treatment decision
making in early-stage breast cancer: should surgeons match patients
desired level of involvement? J Clin Oncol 2002;20(6):1473–1479.
16. Harcourt D, Rumsey N. Mastectomy patients’ decision-making for or
against immediate breast reconstruction. Psychooncology
2004;13(2):106–115.
17. Nelson JA, Tchou J, Domchek S, et al. Breast reconstruction in bilateral
prophylactic mastectomy patients: factors that influence decision
making. J Plast Reconstr Aesthet Sug 2012;65(11):1481–1489.
18. Luan A, Hui KJ, Remington AC, et al. Effects of a noel decision aid for
breast reconstruction: a randomized prospective trial. Ann Plast Surg
2016;76 (Suppl 3):S249–S254.
19. Smith JR, Jaffe J, Pruitt J, et al. The effect of contralateral prophylactic
mastectomy on breast related charges: a 5 yr analysis. J Surg Oncol
2018;118(1):212–220.
20. Angarita FA, Elmi M, Zhang Y, et al. Patient-reported factors
influencing the treatment decision-making process of older women with
non-metastatic breast cancer: a systematic review of qualitative
evidence. Breast Cancer Res Treat 2018;171(3):545–564.
21. Liang W, Burnett CB, Rowland JH, et al. Communication between
physicians and older women with localized breast cancer: implications
for treatment and patient satisfaction. J Clin Oncol 2002;20(4):1008–
1016.
22. Flitcroft K, Brennan M, Spillane A. Women’s expectations of breast
reconstruction following mastectomy for breast cancer: a systematic
review. Support Care Cancer 2017;25(8):2631–2661.
23. Lewis RS, George A, Rusby JE. Nipple-sparing mastectomy in women
at high risk of developing breast cancer. Gland Surg 2018;7(3):325–336.
24. Ter Louw RP, Patel KM, Sosin M, et al. Patient centered decision
making in breast reconstruction utilizing the delayed-immediate
algorithm. J Plast Reconstr Aesthet Surg 2014;67(4):477–482.
25. Durif-Bruckert C, Roux P, Morelle M, et al. Shared Decision making in
medical encounters regarding breast cancer treatment: the contribution
of methodological triangulation. Eur J Cancer Care (Engl)
2015;24(4):461–472.
26. Politi MC, Clark MA, Ombao H, et al. Communicating uncertainty can
lead to less decision satisfaction: a necessary cost of involving patients
in shared decision making? Health Expect 2011;14:84–91.
27. Spittler CA, Pallikathayil L, Bott M. Exploration of how women make
treatment decisions after a breast cancer diagnosis. Oncol Nurs Forum
2012;39(5):E425–E433.
28. Nelson JA, Fischer JP, Radecki MA, et al. Delayed autologous breast
reconstruction: factors which influence patient decision making. J Plast
Reconstr Aesthet Surg 2013;66(11):1513–1520.
29. Begum S, Grunfeld EA, Ho-Asjoe M, et al. An exploration of patient
decision-making for autologous breast reconstructive surgery following
mastectomy. Patient Educ Couns 2011;84(1):105–110.
30. Fagerlin A, Lakhani I, Lantz PM, et al. An informed decision? Breast
cancer patients and their knowledge about treatment. Patient Educ
Couns 2006;64(1–3):303–312.
31. Deadman JM, Leinster SJ, Owens RG. Taking responsibility for cancer
treatment. Soc Sci Med 2001;53(5):669–677.
32. Chang JT, Chen CJ, Lin YC, et al. Health-related quality of life and
patient satisfaction after treatment for breast cancer in northern Taiwan.
Int J Radiat Oncol Biol Phys 2007;69(1):49–53.
33. Lacovara JE, Arzouman J, Kim CJ, et al. Are patients with breast cancer
satisfied with their decision making? A comparison over time. Clin J
Oncol Nurs 2011;15(3):320–323.
34. Causarano N, Platt J, Baxter NN, et al. Pre-consultation educational
group intervention to improve shared decision-making for
postmastectomy breast reconstruction: a pilot randomized controlled
trial. Support Care Cancer 2015;23(5):1365–1375.
35. Meshulam-Derazon S, Shay T, Lewis S, et al. Immediate breast
reconstruction: comparative outcome study of one-stage direct-to-
implant and two-stage/tissue expander techniques. Isr Med Assoc J
2018;20:340–344.
36. Joyce CW, Murphy S, Murphy S, et al. Scar wars: preferences in breast
surgery. Arch Plast Surg 2015;42(5):596–600.
37. Gass J, Mitchell S, Hanna M. The Psychosocial Impact of Surgical Scars
on Breast Cancer Survivorship: Findings from a Nationwide Survey of
Women who Reported Lumpectomy and/or Mastectomy. 2017 San
Antonio Breast Cancer Symposium, Abstract #1263, Dec 9, 2017.
38. Offodile AC, Prigerson H, Craft RO, et al. Impact of personality traits
on choice and perceptions of autologous breast reconstruction. J
Reconstr Microsurg 2015;31(2):139–144.
39. van der Steeg AFW, De Vries J, Roukema JA. Anxious personality and
breast cancer: possible negative impact on quality of life after breast
conserving therapy. World J Surg 2010;34:1453–1460.
40. Kelsall JE, McCulley SJ, Brock L, et al. Comparing oncoplastic breast
conserving surgery with mastectomy and immediate breast
reconstruction: case-matched patient reported outcomes. J Plast
Reconstr Aesthet Surg 2017;70(10):1377–1385.
41. Bertozzi N, Pesce M, Santi P, et al. One-stage immediate breast
reconstruction: a concise review. BioMed Res Int 2017;2017:6486859.
42. El Sabawi B, Ho AL, Sosin M, et al. Patient centered outcomes of breast
reconstruction in the setting of post mastectomy radiotherapy: a
comprehensive review of the literature. J Plast Reconstr Aesthet Surg
2017;70(6):768–780.
43. Kwong A, Chu ATW. What made her give up her breasts: a qualitative
study on decisional considerations for contralateral prophylactic
mastectomy among breast cancer survivors undergoing BRCA 1/2
genetic testing. Asian Pac J Cancer Prev 2012;13:2241–2247.
44. Heller L, Parker PA, Youssef A, et al. Interactive digital education aid in
breast reconstruction. Plast Reconstr Surg 2008;122(3):717–724.
45. Sivell S, Edwards A, Manstead AS, et al. Increasing readiness to decide
and strengthening behavioral intentions: evaluating the impact of a web-
based patient decision aid for breast cancer treatment options (BresDex).
Patient Educ Couns 2012;88(2):209–217.
46. Sherman KA, Kilby CJ, Shaw LK, et al. Facilitating decision making in
women undergoing genetic testing for hereditary breast cancer:
BRECONDA randomized controlled trial results. Breast 2017;36:79–85.
47. Martinez KA, Li Y, Resnicow K, et al. Decision regret following
treatment for localized breast cancer: is regret stable over time? Med
Decis Making 2015;35(4):446–457.
48. Stalmeier PF, Roosmalen MS, Verhoef LC, et al. The decision
evaluation scales. Patient Educ Couns 2005;57(3):289–293.
49. Stalmeier PF, Roosmalen MS. Concise evaluation of decision aids.
Patient Educ Couns 2009;74(1):104–109.
50. Fuzesi S, Cano SJ, Klassen AF, et al. Validation of the electronic
version of the BREAST-Q in the army of women study. Breast
2017;33:44–49.
51. Collins ED, Moore CP, Clay KF, et al. Can women with early stage
breast cancer make an informed decision for mastectomy? J Clin Oncol
2009;27(4):519–525.
52. O’Leary KA, Estabrooks CA, Olson K, et al. Information acquisition for
women facing surgical treatment for breast cancer: influencing factors
and selected outcomes. Patient Educ Couns 2007;69(1–3):5–19.
53. Chatterjee A. Long term effects of modern breast cancer surgery. Gland
Surg 2018;7(4):366–370.
54. Gardani M, Bertozzi N, Grieco MP, et al. Breast reconstruction with
anatomical implants: a review of indications and techniques based on
current literature. Ann Med Surg (Lond) 2017;21:96–104.
55. Pirro O, Mestak O, Vindigni V. Comparison of patient-reported
outcomes after implant versus autologous tissue breast reconstruction
using the BREAST-Q. Plast Reconstr Surg Glob Open 2017;5:e1217.
56. Parker PA. Breast Reconstruction and psychosocial adjustment: what
have we learned and where do we go from here? Semin Plast Surg
2004;18(2):131–138.
57. Frisell A, Lagergreen J, de Boniface J. National study of the impact of
patient information and involvement in decision-making on immediate
breast reconstruction rates. Br J Surg 2016;103:1640–1648.
58. Leff DR, Bottle A, Mayer E, et al. Trends in immediate postmastectomy
breast reconstruction in the United Kingdom. Plast Reconstr Surg Glob
Open 2015;3:e507.
59. Kazzazi F, Haggie R, Forouhi P, et al. A comparison of patient
satisfaction (using the BREAST-Q questionnaire) with bilateral beast
reconstruction following risk-reducing or therapeutic mastectomy. J
Plast Reconstr Aesthet Surg 2018;71(91):1324–1331.
60. Lillie SE, Janz NK, Friese CR et al. Racial and ethnic variation in
partner perspectives about the breast cancer treatment decision making
experience. Oncol Nurs Forum 2014;41(1):13–20.
61. Schubart JR, Dominici LS, Farnan M, et al. Shared decision making in
breast cancer: a national practice pattern of surgeons. Ann Surg Oncol
2013;20(10):3323–3329.
62. Boughey JC, Attai DJ, Chen SL, et al. Contralateral prophylactic
mastectomy consensus statement from the American Society of Breast
Surgeons: additional considerations and a framework for a shared
decision making. Ann Surg Oncol 2016;23:3106–3111.
63. Braude L, Kirsten L, Gilchrist J, et al. The development of a template
for psychological assessment of women considering risk-reducing or
contralateral prophylactic mastectomy: a national Delphi consensus
study. Psychooncology 2018;27(10):2349–2356.
64. Landercasper J, Attai D, Atisha D, et al. Toolbox to reduce lumpectomy
reoperations and improve cosmetic outcome in breast cancer patients:
The American Society of Breast Surgeons Consensus Conference. Ann
Surg Oncol 2015;22:3174–3183.
65. Twomey M. Autonomy and reason: treatment choice in breast cancer. J
Eval Clin Pract 2012;18(5):1045–1050.
CHAPTER 24

Team Approach to Nipple-Sparing


Mastectomy
ALLEN GABRIEL | MAURICE Y. NAHABEDIAN | TONI STORM | G. PATRICK MAXWELL
HISTORY
Surgical management of breast cancer has evolved in the past 50 years
toward a more minimally invasive approach with better aesthetic outcomes,
but without compromising oncologic safety. With the realization of the
contribution of the quality of the mastectomy skin envelope to aesthetic
outcome, mastectomy techniques have evolved from radical mastectomies
where all of the breast tissue, including the skin, nipple, and areola, as well as
the axillary lymph nodes are removed to skin-sparing mastectomies (SSMs)
where breast tissue, including the nipple areolar complex (NAC), are
removed but the breast skin is preserved as much as possible to nipple-
sparing mastectomies (NSMs), which is a SSM with preservation of the
NAC.
Preserving the NAC has aesthetic benefits as immediate breast
reconstruction following NSM allows for better cosmetic results compared
with other forms of mastectomy (1). The nipple is a key defining visual
feature of the breast and is the point at which the most natural convexity of
the breast occurs. Although staged nipple reconstruction and areola tattooing
can potentially achieve similar aesthetic results, they are often short-lived as
loss of projection and fading, respectively, is common over time (2). NSM
aims to create an aesthetic result that is closer to the natural state than breast
reconstruction techniques.
Preserving the NAC is also associated with improved patient satisfaction,
psychological benefit, and quality of life after breast reconstruction compared
with non-NSMs (3). All postmastectomy patients are fraught with distress
brought on by the diagnosis of breast cancer and suffer a severe alteration of
body image and the resultant adverse psychological consequences (4,5).
Preservation of the NAC can be an extremely vital part of their rehabilitation
in the sense that it visually transforms the mastectomy skin into a breast
immediately following breast reconstruction.
NSM was attempted in the 1980s as a treatment for breast cancer (6) but
never gained popularity due to the controversies surrounding oncologic
safety, which persist to this day. However, better tumor detecting
technologies are creating support for the return of this concept in recent years
in the therapeutic setting. In the risk-reducing setting, NSM has become a
well-established practice (7).
RISK-REDUCTION NSM
NSM was first described in the 1960s for breast cancer risk reduction in
patients with benign breast lesions (8). The concept did not gain popularity
because the outcomes were inconsistent and unimpressive, the complication
rate was high, and most importantly efficacy in risk reduction could not be
demonstrated because of a lack of selection criteria. Thirty years later, the
seminal work of Hartmann changed the perception of risk-reduction NSM. In
women with a family history of breast cancer, prophylactic NSM was
demonstrated to be associated with a reduction in the incidence of breast
cancer of at least 90% (9). Subsequently, the efficacy of NSM was
demonstrated in patients with BRCA1 and BRCA2 gene mutations where a
90% to 100% risk reduction was reported (10). Similarly, in women with a
personal and family history of breast cancer, contralateral prophylactic
mastectomy was shown to result in a 94% risk reduction in premenopausal
women and a 96% risk reduction in postmenopausal women (11).
The indications for risk-reducing NSM have evolved over the past 25
years. Initially, NSM was primarily indicated in women with a strong family
history and/or a personal history of high-risk breast lesions such as lobular
carcinoma in situ or atypical hyperplasia (9). In more recent time periods, the
indications have shifted to primarily those with genetic mutations (12).
However, NSM can be considered virtually in all prophylactic cases after
ruling out malignancy and discussing with patients all risk-reducing
strategies. Preoperative evaluation for NSM should include complete imaging
studies, preferentially breast magnetic resonance imaging (MRI).
THERAPEUTIC NSM

Increasing Trends of NSM


In carefully selected patients, NSM as a treatment for breast cancer has been
increasingly performed in the last decade. A recent analysis of the National
Cancer Database indicates an 800-fold increase in NSM among women who
underwent treatment for stage 0–III breast cancer followed by reconstruction
from 2005 to 2015 (from 1.7% to 14.3%) (13). By 2015, NSM was
performed in 15.3% of mastectomies with reconstruction for ductal
carcinoma in situ (DCIS), 14.3% of mastectomies with reconstruction for
stage I–II breast cancer, and 10.7% of mastectomies with reconstruction for
stage III breast cancer.
Oncologic Safety of NSM
Current evidence suggests that in appropriately selected patients, NSM is
associated with an acceptable rate of locoregional cancer recurrence. Recent
systematic reviews of published studies place the recurrence rate at 1.8% to
2.3% (14–16). The recurrence rate with NSM has been shown to be
comparable to conventional mastectomy (17–19), breast-conserving surgery
(20), and SSM (21). Despite the acceptable recurrence rate, concerns still
exist that occult malignancy could remain within residual glandular breast
tissue left behind underneath the skin envelope (7). According to the SKINI-
trial, residual breast tissue is commonly observed after SSM and NSM, in
about half of the cases (22). However, invasive or in situ carcinomas are
rarely found in the skin envelope. In the SKINI-trial, 99 SSM and 61 NSM
were performed. Of biopsies from the skin envelope (10 biopsies per SSM,
14 biopsies per NSM), residual disease was detected in 3 biopsies.
Oncologic Indications/Contraindications for NSM
The indications for therapeutic NSM have evolved and expanded over time,
thus, allowing a wider population of patients to benefit from this procedure.
Previous oncologic criteria for NSM included tumor size <3 cm, tumor-to-
nipple distance >2 cm, clinically negative axillary nodes, no skin
involvement or inflammatory cancer, and possible preoperative MRI to
exclude nipple involvement (23). These criteria were based on published
studies at that time that investigated the relationships between oncologic
parameters and nipple involvement. A systematic review of these studies, has
summarized the significant findings (15). Essentially, reduced tumor-to-
nipple distance, lymph node metastasis, lymphovascular invasion, HER-2
positivity, grade 3 tumor, multicentricity, and retroareolar location were
found to increase the incidence of occult nipple malignancy. In addition, the
four most common tumor types (invasive ductal carcinoma, invasive lobular
carcinoma, DCIS, invasive ductal carcinoma/DCIS) were found to have
similar nipple involvement rates, ranging from 15% to 17%.
Currently, nipple involvement, inflammatory breast cancer, skin
involvement, and bloody nipple discharge (but not clear nipple discharge) are
absolute contraindications for NSM (7). Tumor size and tumor-to-nipple
distance no longer factor as oncologic criteria but rather the primary focus
has shifted to nipple margin status. Because a negative retroareolar margin
may exclude occult nipple involvement with a high negative predictive value
even in patients at high risk of occult nipple involvement before surgery, such
as patients with a tumor nipple distance ≤1 cm or tumors >3 cm in diameter
(24), thus, the current strategy of treating the nipple margin like any other
margin. While clinical signs of nipple involvement and R1 resection at the
nipple margin have traditionally been considered to be contraindications to
nipple preservation (25), the clinical relevance of a positive retroareolar
margin in an individual patient is, however, unknown (7). Moreover, while a
positive retroareolar margin would require the excision of the nipple, there is
no clear consensus on whether the areolar can be preserved. Areolar
involvement is of low occurrence even in the presence of nipple involvement.
This was shown in a retrospective study of 217 mastectomy patients where
nipple involvement was seen in 10.6% of patients and areolar involvement in
0.9% of patients (26). It should be noted that on rare occasions nipple
involvement can occur as a late event after NSM. A retrospective study of
861 patients reported 7 cases of local recurrence in the nipple on an average
of 32 months after surgery. NAC was completely removed in all cases and no
further recurrences were noted at an average follow-up of 47.4 months (27).
Inflammatory breast cancer is an absolute contraindication for skin sparing
even after neoadjuvant chemotherapy and complete remission of all skin
changes (7). This is because at diagnosis, inflammatory breast cancer is
always at a locally advanced stage (at least stage III) as breast cancer cells
have grown into the skin. Further, even without redness, edema of the skin
with enhancement on imaging is also a contraindication to skin sparing.
While skin involvement is an absolute contraindication, opinion varies
regarding whether cT4b and cT4c breast cancers limited to a 1 × 1 cm area of
skin ulceration should be a contraindication to skin preservation. In addition,
there is no clear consensus on whether the absence of any distance between
tumor and skin on preoperative imaging, even in the absence of clinical signs
of skin infiltration, or a histologic margin of less than 1 mm should be
contraindications to skin preservation.
NSM and Breast Irradiation
Premastectomy breast irradiation was once considered to be a
contraindication to NSM because of concerns of nipple ischemia from a
compromised bloody supply to the breast. Further, irradiation also has
deleterious effects on the skin eventually leading to skin fibrosis. A recent
retrospective analysis of 605 NSMs (517 no radiation, 43 premastectomy
radiation, and 45 postmastectomy radiation) followed by immediate
reconstruction, however, reported a nipple retention rate of 90% in patients
who had radiation therapy (pre- or postmastectomy). Nipple removal
secondary to malposition or positive oncologic margins in patients with
radiation did not differ significantly from those without radiation (28). In
another retrospective analysis of 982 NSMs, 816 with no radiation, 67 with
preoperative radiation, and 97 with postmastectomy radiation, experienced
nipple loss at 0.9%, 4.3%, and 4.1%, respectively. Although nipple loss was
significantly higher in irradiated breasts, the retention rate was greater than
95% (29). Both these studies demonstrate that NSM can be successfully
performed in the setting of breast irradiation.
NSM and Neoadjuvant Chemotherapy
Locally advanced breast cancer was once considered to be a contraindication
for NSM. Patients with locally advanced breast cancer can now be offered
NSM after downsizing of their tumors and obtaining negative margins with
neoadjuvant chemotherapy (7). Downsizing of tumors with neoadjuvant
chemotherapy prior to NSM has been found to be oncologically safe. A
propensity score–matched study found no significant difference in the rate of
NAC involvement after neoadjuvant chemotherapy followed by NSM versus
NSM without neoadjuvant chemotherapy (9.8% vs. 13.3%). Four-year local
disease-free survival also did not differ significantly between the groups (30).
Another study found that patients with locally advanced breast cancer are
most at risk for distant rather than local recurrence. In this study, the local
recurrence rate was 5% and the distant recurrence rate was 15.1% after
neoadjuvant chemotherapy and NSM. None of the local recurrences involved
the preserved NAC (31).
NSM AND HIGH BODY MASS INDEX, LARGE BREASTS, OR PTOTIC
BREASTS
NSM was once considered a contraindication in patients with high body mass
index (BMI; >30 kg/m2), large breasts (>500 g), and/or ptotic breasts because
of concerns of an increased risk of complications, including nipple necrosis
(32). These contraindications have changed in the last decade with the
demonstration that excellent outcomes can be achieved in these patients. In
women with high BMI and/or large breasts, several authors have shown that
with careful preoperative planning, acceptable nipple necrosis rates can be
achieved, ranging from 0.2% to 6.0% (33–35).
In women with ptotic breasts, several approaches have been described to
manage the redundant skin and minimize the risk of nipple necrosis,
including skin-reduction techniques with NAC pedicles during NSM, free
nipple grafting, staged NSM, and surgical delay of the NAC. The Wise
pattern is the most well-known of the skin-reduction pedicle techniques. The
“autoderm” technique is another skin-reduction technique in which excess
skin is de-epithelialized to preserve the dermal vessels and imbricated to
reduce the skin envelope following mastectomy (36).
The free nipple graft breast reduction is an alternative to the NAC pedicle
technique that is useful in severe macromastia, when large, bulky pedicles
may impede adequate reduction and optimal contour (37). In this technique,
the nipple is harvested as a full-thickness skin graft, preserving the complete
thickness of the dermis, and then grafted back onto the breast after reduction
mammaplasty.
In staged NSM, a reduction mammaplasty or mastopexy is performed as a
first stage followed by NSM as a second stage (38). In prophylactic cases, the
second stage is performed at least 3 months after the first stage. In therapeutic
cases, the first stage involves oncoplasty with tumor resection and lymph
node biopsy followed by reduction mammaplasty or mastopexy. Second-
stage NSM was initially performed 1 month later to avoid delays in cancer
treatment but later extended to 10 to 12 weeks later to allow for an extended
recovery (39).
Surgical delay of the NAC involves radially undermining 5 cm from the
nipple in a circumferential fashion using sharp dissection (40). The skin and
subcutaneous tissue is severed from the underlying breast parenchyma with
disruption of the pectoral/intercostal perforators. The NAC now has to rely
on peripheral vessels for its blood supply which may help the NAC to better
survive after NSM. NSM is usually performed 1 to 3 weeks later.
NSM AND NIPPLE NECROSIS
Compared with traditional mastectomy techniques, NSM is associated with
an elevated risk for nipple and mastectomy flap ischemia or necrosis. The
published literature reports a partial or full nipple necrosis rate ranging from
1.8% to 58% (average 15%) and a partial- or full-thickness flap necrosis rate
ranging from 3% to 11% (average 3.4%) (21). The elevated risk of nipple and
flap necrosis is inherent to NSM because with the preservation of the
majority or entirety of the skin envelope a larger surface area needs to be
adequately perfused. Further, patient-related factors such as BMI, breast
morphology (breast size, mastectomy weight, and ptosis), and smoking as
well as treatment-related factors such as radiation, chemotherapy, incision
pattern, and mastectomy flap thickness can also increase the risk of nipple
and skin ischemia (29,41,42).
TECHNICAL ASPECTS OF NSM

Flap Quality
Optimizing mastectomy flap thickness and perfusion is one of the most
important technical aspects of NSM. Communication between breast
surgeons and plastic surgeons is critical for ensuring the delivery of an
optimized mastectomy skin flap with preservation of the entire skin and
subcutaneous fat thickness of the breast superficial to the breast fascia as well
as their vascularity while at the same time ensuring maximal oncologic
resection. Because breast subcutaneous layer and skin thickness superficial to
the fascia are variable by nature, there is no single universal flap thickness
and optimal flap thickness varies by patient (7,43,44).
Patient factors such as BMI and breast size appear to influence flap
thickness, including the overall, as well as the anterior, middle, and posterior,
flap thickness (44). A study found that the average ideal flap thickness
increased with increasing BMI (<25 kg/m2, 25 to 30 kg/m2, and >30 kg/m2)
or mastectomy weight (<400 g, 400 to 799 g, and ≥800 g) categories (44). An
understanding of the inter- as well as intrapatient variability in mastectomy
flap thickness is important to guide patient-specific optimal anatomic NSM
flap dissection at the level of the superficial breast fascia.
It is also of importance to understand the blood supply of the breast to
ensure that adequate flap perfusion is achieved. After NSM, the perfusion of
the flap and NAC is dependent on the superficial vasculature in the
subcutaneous and subdermal levels. More than 60% of the blood supply is
from the internal mammary perforators, and overresection and crossing of the
lateral edge of the sternum will sacrifice this crucial blood supply. All
inferomedial and superomedial incisions should therefore be avoided.
Decreasing dissection medially beyond the lateral border of the sternum and
beyond the lateral border of the latissimus dorsi maximizes the retention of
the blood supply to the mastectomy flap. Careful dissection with a face lift
scissor or scalpel should be performed around the NAC to maximize the
blood supply. Sharp dissection with tumescence also appears to lower the risk
of mastectomy flap necrosis compared with standard electrocautery (45).
Additionally, periareolar incisions, especially from 6 to 12 o’clock positions,
should be avoided. Periareolar incisions are associated with a dramatic
increase in the risk of flap necrosis in contrast to inframammary incisions
(46). The use of intraoperative indocyanine green angiography for the
assessment of flap viability during flap trimming may further help ensure
perfusion and reduce the risk of ischemia (47).
Incision Location
Incisions for NSM, whether on the lateral or vertical breast, inframammary
fold, former biopsy site, or reduction pattern, should never compromise the
efficacy of the oncologic resection (Fig. 24-1). All incisions should be an
option and the best should be chosen to achieve maximal safe resection while
keeping the aesthetic goals in mind.

FIGURE 24-1 Incision options. EIMF, extrainframammary fold; IMF,


intramammary fold; LB, lateral breast; NSRM, nipple-sparing reduction
mastectomy; VB, vertical breast. (From Allen G, Nahabedian MY, Sigalove SR, G.
Maxwell P. Prepectoral Techniques in Reconstructive Breast Surgery. 1st ed.
Philadelphia, PA: Wolters Kluwer; 2019.)

When deciding to choose the incision, the size of the breast and degree of
ptosis are the two most important factors. Regardless of the etiology of
ptosis, a useful tool for the surgeon is to classify patients by the degree of
ptosis present. It is important to clarify with the patient at this time what their
goals are in terms of the final appearance of the breast. Regnault
classification system should be used to grade the extent of ptosis (48,49). The
amount of preoperative ptosis can be used as a guide to selecting the
operation necessary to achieve correction and symmetrization (Fig. 24-2).
FIGURE 24-2 A–D: Preoperative views of a 23-year-old woman, BRCA positive
desiring risk-reducing mastectomy. E–I: Postoperative views 18 months following
nipple-sparing mastectomy and two-stage breast reconstruction with form-stable, gel
implants, acellular dermal matrix, and fat injection.

For patients with small and medium-sized nonptotic breasts,


inframammary (IMF) incision can be chosen safely (Fig. 24-3 and Table 24-
1). The other extreme would be patients with larger and more significantly
ptotic breasts, for whom a nipple-sparing reduction mastectomy (NSRM) can
be performed to excise all breast tissue. There are two factors to consider
here. First, with larger breasts IMF incision may not allow for complete
excision superiorly, and therefore alternative incisions should be planned.
Second, with more ptotic breasts and patient desire for a smaller breast, a
reduction of the skin envelope will be necessary. This can be done in a
vertical component only or combined with a variant-size horizontal
component (see Table 24-1). We prefer the combination of vertical and
horizontal components for skin envelope reduction as it is more predictable
than the vertical component alone. With NSRM the NAC is excised and
banked over the mastectomy flap. If a concurrent autologous reconstruction is
performed, then this can be banked over the new tissue. The precise
dissection and retention of the blood flow to the mastectomy flaps will be
crucial for the graft to completely take over the mastectomy flap. If there is
concern about the mastectomy flaps, the NAC can be banked at another site
until the vascularity of the mastectomy flaps is confirmed. Other incision
options are based again on breast size and degree of ptosis as described in
Table 24-1 and shown in Figure 24-4.
NAC Anatomy
Detailed knowledge about NAC microanatomy is essential for understanding
the technical challenges encountered when considering its preservation. In a
series of papers, Rusby et al. delineated the configuration of the central breast
duct bundle as well as duct microvasculature in relation to position of duct
bundles, both of which have been instrumental in providing a strategy for
performing NSM where a balance between preservation of blood supply and
excision of a large percentage of duct bundles needs to be achieved.
Prior to Rusby et al.’s study, little was known about the spatial location of
ducts, their size, and their relationship to orifices on the surface, although the
variation in the number of ducts was known. Rusby et al. showed that many
ducts share a few common openings onto the surface of the nipple, explaining
the observed discrepancy between number of ducts and number of orifices
(50). Neither duct diameter nor position predicted whether a duct system will
terminate close to the nipple or pass deeper into the breast. They also showed
that the majority of ducts form a central bundle within the papilla. Up to two-
thirds of the cross-sectional area of the papilla is taken up by the central
bundle. The central bundle narrows to form a “waist” before the ducts
disperse and widen into the breast parenchyma. In cases where all ductal
tissue needs to be removed, as in DCIS, an understanding of the central
bundle configuration would be important to its excision. Of the 129 nipples
that were examined in this study, 17% contained lobular tissue, which
highlights the importance of excising the duct core even in prophylactic
mastectomies.
FIGURE 24-3 A–C: Preoperative views of a 61-year-old woman with right ductal
carcinoma in situ. D–F: Twenty-four months following bilateral nipple-sparing
mastectomy/R sentinel lymph node biopsy and two-stage breast reconstruction with
form-stable, gel implants, acellular dermal matrix, and fat injection.

TABLE 24-1 Surgical Techniques

Nipple viability is a concern following coring of the ducts. In another


study, Rusby et al. investigated nipple microvessels and their position relative
to ducts (51). They found that 29% of vessels are located in the duct bundle.
A 2-mm rim of nipple tissue contains 50% of vessels and a 3-mm rim
contains 66%. Thus, leaving a rim of nipple tissue when excising ducts would
leave a large proportion of microvessels intact. At the same time, leaving a 2-
or 3-mm rim of peripheral nipple tissue would ensure complete duct excision
in 96% and 87% of sections, respectively.
In yet another study, Rusby et al. demonstrated the surgical technique for
the safe excision of the duct bundle (52). The precise identification of the
duct margin directly beneath the nipple proves to be difficult once the duct
bundle has been divided. In this ex-vivo series, successful retroareolar margin
identification was achieved by grasping the duct bundle with atraumatic
forceps as soon as it became exposed. A cut made below and above the
forceps resulted in a full cross-section of the duct bundle and a more
complete excision of duct tissue.
FIGURE 24-4 A–E: Preoperative view of a 56-year-old woman with left ductal
carcinoma in situ. F: Postoperative view 7 days following lumpectomy and
reconstruction on left and reduction on right for matching with incisional NPT.
G–K: Postoperative view 1 week following bilateral nipple-sparing mastectomy and
placement of 133 FV expanders with incisional NPT. Case 3 post operative:
Postoperative views 14 months following nipple-sparing mastectomy and two-stage
breast reconstruction with silicone implants, acellular dermal matrix, and fat
injection.
CONCLUSION
NSM improves aesthetic outcomes and quality of life for patients undergoing
mastectomy. The indications for NSM have expanded over the last decade,
allowing more patients to experience the benefits of this procedure. In
properly selected patients, NSM is oncologically safe. A detailed knowledge
of NAC microanatomy and institution of measures to optimize mastectomy
flap thickness and perfusion are critical to successful performance of this
procedure.

REFERENCES

1. Mota BS, Riera R, Ricci MD, et al. Nipple- and areola-sparing


mastectomy for the treatment of breast cancer. Cochrane Database Syst
Rev 2016;11:CD008932.
2. Lee HC, Eom JS, Kim EK, et al. Does the sequence of tattooing and
nipple reconstruction affect nipple projection? Ann Plast Surg
2017;79:430–432.
3. Bailey CR, Ogbuagu O, Baltodano PA, et al. Quality-of-life outcomes
improve with nipple-sparing mastectomy and breast reconstruction.
Plast Reconstr Surg 2017;140:219–226.
4. Carreira H, Williams R, Müller M, et al. Associations between breast
cancer survivorship and adverse mental health outcomes: a systematic
review. J Natl Cancer Inst 2018;110:1311–1327.
5. Heidari M, Ghodusi M. The relationship between body esteem and hope
and mental health in breast cancer patients after mastectomy. Indian J
Palliat Care 2015;21:198–202.
6. Kissin MW, Kark AE. Nipple preservation during mastectomy. Br J
Surg 1987;74:58–61.
7. Weber WP, Haug M, Kurzeder C, et al. Oncoplastic Breast Consortium
consensus conference on nipple-sparing mastectomy. Breast Cancer Res
Treat 2018;172:523–537.
8. Freeman BS. Subcutaneous mastectomy for benign breast lesions with
immediate or delayed prosthetic replacement. Plast Reconstr Surg
Transplant Bull 1962;30:676–682.
9. Hartmann LC, Schaid DJ, Woods JE, et al. Efficacy of bilateral
prophylactic mastectomy in women with a family history of breast
cancer. N Engl J Med 1999;340:77–84.
10. Hartmann LC, Sellers TA, Schaid DJ, et al. Efficacy of bilateral
prophylactic mastectomy in BRCA1 and BRCA2 gene mutation carriers.
J Natl Cancer Inst 2001;93:1633–1637.
11. McDonnell SK, Schaid DJ, Myers JL, et al. Efficacy of contralateral
prophylactic mastectomy in women with a personal and family history
of breast cancer. J Clin Oncol 2001;19:3938–3943.
12. Grobmyer SR, Pederson HJ, Valente SA, et al. Evolving indications and
long-term oncological outcomes of risk-reducing bilateral nipple-sparing
mastectomy. BJS Open 2018;3:169–173.
13. Wong SM, Chun YS, Sagara Y, et al. Oncoplastic Breast Consortium
consensus conference on nipple-sparing mastectomy. Ann Surg Oncol
2019;26:3194–3203.
14. Endara M, Chen D, Verma K, et al. Breast reconstruction following
nipple spring mastectomy: a systematic review of the literature with
pooled analysis. Plast Reconstr Surg 2013;132:1043–1054.
15. Mallon P, Feron JG, Couturaud B, et al. The role of nipple-sparing
mastectomy in breast cancer: a comprehensive review of the literature.
Plast Reconstr Surg 2013;131:969–984.
16. Headon HL, Kasem A, Mokbel K. Oncological safety of nipple-sparing
mastectomy: a systematic review of the literature with a pooled analysis
of 12,358 procedures. Arch Plast Surg 2016;43:328–338.
17. Seki T, Jinno H, Okabayashi K, et al. Comparison of oncological safety
between nipple sparing mastectomy and total mastectomy using
propensity score matching. Ann R Coll Surg Engl 2015;97:291–297.
18. Huang J, Mo Q, Zhuang Y, et al. Oncological safety of nipple-sparing
mastectomy in young patients with breast cancer compared with
conventional mastectomy. Oncol Lett 2018;15:4813–4820.
19. Lee SB, Lee JW, Son BH, et al. Oncologic safety of skin-sparing
mastectomy followed by immediate reconstruction in young patients
with breast cancer. Asian J Surg 2019;42:274–282.
20. Sakurai T, Suzuma T, Yoshimura G, et al. J Clin Oncol
2014;32(15Suppl):e12030–e12030.
21. Agha RA, Al Omran Y, Wellstead G, et al. Systematic review of
therapeutic nipple-sparing versus skin-sparing mastectomy. BJS Open
2018;3:135–145.
22. Papassotiropoulos B, Güth U, Chiesa F, et al. Prospective evaluation of
residual breast tissue after skin- or nipple-sparing mastectomy: results of
the SKINI-Trial. Ann Surg Oncol 2019;26:1254–1262.
23. Willey SC, Spear SL, Hammond DC, et al. Surgery of the Breast:
Principles and Art. Philadelphia, PA: Lippincott Williams & Wilkins;
2011.
24. Brachtel EF, Rusby JE, Michaelson JS, et al. Occult nipple involvement
in breast cancer: clinicopathologic findings in 316 consecutive
mastectomy specimens. J Clin Oncol 2009;27:4948–4954.
25. Veronesi U, Stafyla V, Petit JY, et al. Conservative mastectomy:
extending the idea of breast conservation. Lancet Oncol
2012;13(7):e311–e317.
26. Simmons RM, Brennan M, Christos P, et al. Analysis of nipple/areolar
involvement with mastectomy: can the areola be preserved? Ann Surg
Oncol 2002;9(2):165–168.
27. Lohsiriwat V, Martella S, Rietjens M, et al. Paget’s disease as a local
recurrence after nipple-sparing mastectomy: clinical presentation,
treatment, outcome, and risk factor analysis. Ann Surg Oncol
2012;19(6):1850–1855.
28. Reish RG, Lin A, Phillips NA, et al. Breast reconstruction outcomes
after nipple-sparing mastectomy and radiation therapy. Plast Reconstr
Surg 2015;135:959–966.
29. Tang R, Coopey SB, Colwell AS, et al. Nipple-sparing mastectomy in
irradiated breasts: selecting patients to minimize complications. Ann
Surg Oncol 2015;22:3331–3337.
30. Agresti R, Sandri M, Gennaro M, et al. Evaluation of local oncologic
safety in nipple–areola complex-sparing mastectomy after primary
chemotherapy: a propensity score-matched study. Clin Breast Cancer
2017;17:219–231.
31. Peled AW, Wang F, Foster RD, et al. Expanding the indications for total
skin-sparing mastectomy: is it safe for patients with locally advanced
disease? Ann Surg Oncol 2016 23:87–91.
32. Tousimis E, Haslinger M. Overview of indications for nipple sparing
mastectomy. Gland Surg 2018;7:288–300.
33. Coopey SB, Tang R, Lei L, et al. Increasing eligibility for nipple-sparing
mastectomy. Ann Surg Oncol 2013;20:3218–3222.
34. de Alcantara Filho P, Capko D, Barry JM, et al. Nipple sparing
mastectomy for breast cancer and risk-reducing surgery: the Memorial
Sloan-Kettering Cancer Center experience. Ann Surg Oncol
2011;18:3117–3122.
35. Jensen JA, Orringer JS, Giuliano AE. Nipple-sparing mastectomy in 99
patients with a mean follow-up of 5 years. Ann Surg Oncol
2011;18:1665–1670.
36. Dietz J, Fedele G. Skin reduction nipple-sparing mastectomy. Ann Surg
Oncol 2015;22:3404.
37. Colen SR. Breast reduction with use of the free nipple graft technique.
Aesthet Surg J 2001;21:261–271.
38. Spear SL, Rottman SJ, Seiboth LA, et al. Breast reconstruction using a
staged nipple-sparing mastectomy following mastopexy or reduction.
Plast Reconstr Surg 2012;129:572–581.
39. Economides JM, Graziano F, Tousimis E, et al. Expanded algorithm and
updated experience with breast reconstruction using a staged nipple-
sparing mastectomy following mastopexy or reduction mammaplasty in
the large or ptotic breast. Plast Reconstr Surg 2019;143:688e–697e.
40. Jensen JA, Lin JH, Kapoor N, et al. Surgical delay of the nipple-areolar
complex: a powerful technique to maximize nipple viability following
nipple-sparing mastectomy. Ann Surg Oncol 2012;19:3171–3176.
41. Frey JD, Choi M, Karp NS. The effect of neoadjuvant chemotherapy
compared to adjuvant chemotherapy in healing after nipple-sparing
mastectomy. Plast Reconstr Surg 2017;139:10e–19e.
42. Salibian AA, Frey JD, Bekisz JM, et al. Ischemic complications after
nipple-sparing mastectomy: predictors of reconstructive failure in
implant-based reconstruction and implications for decision-making.
Plast Reconstr Surg Glob Open 2019;7:e2280.
43. Robertson SA, Rusby JE, Cutress RI. Determinants of optimal
mastectomy skin flap thickness. Br J Surg 2014;101:899–911.
44. Frey JD, Salibian AA, Choi M, et al. Optimizing outcomes in nipple-
sparing mastectomy: mastectomy flap thickness is not one size fits all.
Plast Reconstr Surg Glob Open 2019;7:e2103.
45. Ng T, Knowles S, Brackstone M, et al. Mastectomy flap necrosis after
nipple-sparing mastectomy and immediate implant-based reconstruction:
an evaluation of tumescence and sharp dissection technique on surgical
outcomes. Breast J 2019;25(6):1079–1083.
46. Colwell AS, Tessler O, Lin AM, et al. Breast reconstruction following
nipple-sparing mastectomy: predictors of complications, reconstruction
outcomes, and 5-year trends. Plast Reconstr Surg 2014;133:496–506.
47. Gorai K, Inoue K, Saegusa N, et al. Prediction of skin necrosis after
mastectomy for breast cancer using indocyanine green angiography
imaging. Plast Reconstr Surg Glob Open 2017;5:e1321.
48. Regnault P. Breast ptosis. Definition and treatment. Clin Plast Surg
1976;3:193–203.
49. Regnault P. The hypoplastic and ptotic breast: a combined operation
with prosthetic augmentation. Plast Reconstr Surg 1966;37:31–37.
50. Rusby JE, Brachtel EF, Michaelson JS, et al. Breast duct anatomy in the
human nipple: three-dimensional patterns and clinical implications.
Breast Cancer Res Treat 2007;106:171–179.
51. Rusby JE, Brachtel EF, Taghian A, et al. George Peters award.
Microscopic anatomy within the nipple: implications for nipple-sparing
mastectomy. Am J Surg 2007;194:433–437.
52. Rusby JE, Kirstein LJ, Brachtel EF, et al. Nipple-sparing mastectomy:
lessons from ex vivo procedures. Breast J 2008;14:464–470.
SECTION II

The Axilla and Lymphedema


25 Basic Science and Management of Postsurgical Lymphedema and
Vascularized Lymph Node Transplant
26 Sentinel Node Biopsy and Axillary Dissection
27 Postneoadjuvant Axillary Assessment and Management
28 Alternative Methods for Axillary Sentinel Lymph Node Dissection
29 Axillary Surgery Versus Radiation as Treatment of Regional Nodes:
AMAROS Trial and Beyond
30 Conservative Management of Postsurgical Lymphedema
31 Selection of Vascularized Lymph Node Donor Sites for Upper
Extremity Lymphedema Surgery and Strategies to Minimizing
Complications
32 Liposuction as a Viable Treatment for End-Stage Upper Extremity
Lymphedema
CHAPTER 25

Basic Science and Management of


Postsurgical Lymphedema and
Vascularized Lymph Node Transplant
JOSEPH H. DAYAN
HISTORY
Lymphedema continues to be a common and debilitating disease affecting
millions of women with breast cancer worldwide. Managing lymphedema
can be onerous with lifelong compression, massage, and
physiotherapy. Despite 100% compliance, lymphedema often
progresses. Many patients experience a delay in referral because mild
swelling may not appear very impressive on physical examination. However,
these patients often experience poor quality of life because they have an
incurable disease, avoid many activities they enjoy, and are committed to
hours of daily care. Additionally, approximately one-third of patients develop
cellulitis which can spread rapidly and lead to sepsis (1).
While there are clear guidelines for breast cancer screening, surveillance
for lymphedema in high-risk patients (axillary dissection and radiotherapy) is
not yet standard practice. It is also not uncommon for mild limb swelling to
be observed as opposed to immediate referral for lymphedema
therapy. Waiting for a 10% or greater difference in limb volume is akin to
waiting for a heart attack to diagnose coronary artery disease. Lymphatic
dysfunction starts before visible swelling. Symptoms of pain, heaviness, and
transient swelling are best referred early to a certified lymphedema therapist.
Fortunately, there has recently been significant interest in lymphedema,
improved understanding of the disease, and promising treatments. Surgery
has become a viable option not only for appropriately selected patients with
lymphedema but also for those patients undergoing axillary dissection who
are at risk. Effective medical therapies for lymphedema may soon become a
reality. This chapter does not cover the entirety of this subject, but aims to
provide a modern and practical understanding of lymphedema, and describe
the current role of lymphatic surgery. Undoubtedly, the indications and
surgical options for this disease will evolve significantly in years to come.
PATHOPHYSIOLOGY OF LYMPHEDEMA
A common misconception about lymphedema is that it is purely a plumbing
issue: removal of axillary lymph nodes causes a mechanical obstruction that
leads to backup of lymph and swelling of the upper limb. While there is
certainly an initial mechanical obstruction, not all patients develop
lymphedema immediately after axillary dissection. Most develop
lymphedema months or years later, so there is something else that happens in
addition to the surgical injury. Another peculiarity of lymphedema is that
over 80% of patients develop some degree of fibrofatty accumulation, and
one-third of patients have more fat than fluid in their limb (2). These bizarre
manifestations of this disease are a result of the immune response to the
lymphatic injury which can result in this chronic and progressive
condition. One current hypothesis proposed is that the initial
lymphadenectomy leads to lymph stasis, creating an inflammatory
environment which then leads to scarring of the lymphatics, compounding the
lymph stasis which continues to amplify the inflammatory process (3).
Authors have demonstrated that a lymphatic injury–induced inflammatory
cascade leads to increased levels of IL-4 and IL-13, in turn leading to
lymphatic vessel injury and lymphedema (4). Administering antibodies
specific to cytokines which promote T helper 2 cell differentiation associated
with IL-4 and IL-13 production effectively reversed lymphedema in a mouse
model (4). It still remains a mystery why some patients have a fluid-dominant
limb while others have a fat-dominant limb, some have intractable cellulitis
and others have never had a single episode. These different patterns of
lymphedema are not on the same continuous spectrum. Medical therapies
have aimed to target the inflammatory cascade and block it, or to stimulate
lymphangiogenesis (5–7).
DIAGNOSIS OF LYMPHEDEMA
Lymphedema is most commonly diagnosed by clinical examination. Upper
limb swelling is typically first evaluated with duplex ultrasound to rule out
deep vein thrombosis, and if negative, the patient is referred for lymphedema
therapy. Historically, a 10% difference in limb volume was diagnostic for
lymphedema. However, significant swelling is a late finding of lymphatic
compromise. Patient symptoms of heaviness, transient swelling, and pain
typically precede swelling and should be referred for lymphedema
therapy. There are technologies that may improve early detection of
lymphedema. Bioimpedance spectroscopy (BIS) is a noninvasive test that can
detect abnormally high extracellular volume in a limb, consistent with
lymphedema. Imaging of the lymphatic system is traditionally performed
with lymphoscintigraphy. While not particularly sensitive, a finding of
dermal backflow in the limb is diagnostic (1).
More recently and currently off-label but commonly used among
lymphatic surgeons, is indocyanine green (ICG) lymphography (8). This
involves subdermal injection of ICG which is taken up by the lymphatic
vessels and using a near-infrared camera, a high-resolution image of the
lymphatic system itself is seen. Abnormalities of the lymphatic vessels are
directly and clearly visualized. A complete absence of lymphatic vessels of
the lymphatic system is seen in Figure 25-1. Imaging studies are best used to
confirm a diagnosis in cases which are unclear or in preparation for lymphatic
surgery. In summary, patient-reported symptoms often present much earlier
than visible swelling and should prompt referral for lymphedema
therapy. Screening with symptoms and/or BIS at the patient’s postop
oncologic follow-up appointment every 6 months is a reasonable starting
point for lymphedema surveillance in high-risk patients.
FIGURE 25-1 Clinical photo compared to ICG lymphangiography demonstrating
advanced lymphedema with no lymphatic vessels visualized. Not an ideal candidate
for lymphovenous bypass.
INDICATIONS FOR LYMPHATIC SURGERY
Our understanding of which lymphatic procedure is appropriate for which
patient continues to evolve. Currently, the three most common procedures are
lymphovenous bypass (LVB), lymph node transplant, and liposuction (9–13).
The first two aim to provide an exit for lymph, while liposuction is reserved
for the more advanced cases of lymphedema which are fat dominant. These
procedures can also be combined in patients who have a significant degree of
both fluid and fat accumulation.
LVB is a minimally invasive outpatient procedure where an obstructed
lymphatic vessel is divided and anastomosed to a neighboring vein through
one or several small incisions (Fig. 25-2). These vessels are typically 0.3 to
0.8 mm in diameter making LVB technically challenging. In general, distal
LVB is most effective in patients with early lymphedema evidenced by
presence of linear lymphatics on ICG. An LVB performed on a heavily
scarred lymphatic vessel is not going to be as effective. More recently,
immediate lymphatic reconstruction with LVB in the axilla at the time of
lymphadenectomy is being performed in the hopes of reducing the risk of
lymphedema (Fig. 25-3) (14). Data in this field is still preliminary and also
under study protocol at our institution.
FIGURE 25-2 Distal lymphovenous bypass demonstrating patent anastomosis with
clear lymph flowing into the vein.
FIGURE 25-3 Immediate lymphatic reconstruction at the time of axillary dissection
with lymphovenous bypass of several lymphatic vessels telescoped into the
thoracoepigastric vein.

In contrast, a vascularized lymph node transplant (VLNT) only requires an


arterial and venous anastomosis and does not depend on the state of the
lymphatic vessels. This allows one to perform a viable VLNT in someone
with not only mild but also moderate lymphedema. However, there is no data
to guide us regarding which patients are most likely to respond to this
procedure. VLNT depends on the lymphangiogenic growth factors within the
transplanted nodes which have been shown to induce ingrowth of lymphatic
vessels (15). The proposed mechanism includes shunting of lymph into the
venous system through interconnections between the lymphatic sinuses and
venules within the lymph node (16).
A variety of donor sites have been described including groin, axillary,
supraclavicular, and intra-abdominal lymph nodes (17–20). One of the
concerns regarding this procedure, particularly for groin and axillary-based
lymph node transplant is the risk of donor-site lymphedema (21,22). Dayan et
al. first described reverse lymphatic mapping for VLNT to significantly
reduce these risks (17,23). Currently, we favor the omentum based on the
right gastroepiploic vessels because it eliminates any risk of donor-site
lymphedema and also provides abundant lymphatic tissue with consistent
anatomy. In our practice, lymph node transplant to the axilla is indicated in
patients who already have secondary issues such as axillary contracture, pain,
or axillary vein stenosis. If there is profound swelling in the hand and
forearm and there is no migration of ICG above the elbow, then a distal
lymph node transplant or two lymph nodes transplants (one placed in the
wrist or forearm and the other placed in the axilla) are offered (19). Our
group will also perform VLNT at the time of axillary dissection in select
cases where the axilla is expected to be radiated in addition to the chest
wall. This is done not only to reconstruct the lymphatic system but also
replace the soft tissue to mitigate potentially significant contracture and pain.
Finally, liposuction is reserved for patients with a large fat-dominant limb
and advanced lymphatic disease. Patients must already be in compliance with
24/7 compression and have no pitting edema to be a good candidate (12).
Liposuction alone without full compliance to around-the-clock compression
is often unsuccessful.
CONTRAINDICATIONS
Although the body mass index (BMI) cutoff may vary among surgeons,
patients with a BMI greater than 30 would benefit from preoperative
optimization with weight loss first. High BMI impairs lymphatic function,
and surgery is not without risk or with guarantee (24). Patients with severe
axillary stenosis may not respond to lymph node transplant if the axillary
vein is not adequately decompressed. Extensive prior abdominal surgery is a
relative contraindication to omentum VLNT. Noncompliant patients or those
with unrealistic expectations are not good candidates. Realistic expectations
are vital, as lymphatic surgery is not a cure for lymphedema, most patients
still require some form of compression, and there is still a risk of disease
progression.
PREOPERATIVE PLANNING
At the initial visit, all patients have limb volume, bioimpedance, and a
validated patient-reported outcome such as the ULL-27 and LLIS recorded
(1). Limb volume measurements alone are inadequate because they are
significantly affected by many factors such as change in compression,
temperature, and salt intake. The most basic assessment would include limb
volume and a patient-reported outcome questionnaire.
Work-up for lymphatic surgery varies among surgeons but the following is
a basic framework. These are the four components of the work-up: (1) assess
the lymphatic system, (2) assess the fluid/fat composition of the limb, (3)
assess the venous system, and (4) check for oncologic recurrence. In our
practice, this work-up involves ICG lymphography, lymphoscintigraphy, and
magnetic resonance angiography (MRA). ICG is performed in the office with
two injections in each hand: first, 0.2 mL of 1% plain lidocaine followed by
0.1 mL of ICG in the first and third webspace. Images are acquired using a
near-infrared camera immediately after injection to identify intact lymphatic
vessels that abruptly end. If they are present, then the patient is likely a good
candidate for LVB. If there is significant axillary contracture or more
advanced disease, then VLNT may be an option.
Lymphoscintigraphy is performed to determine if there are any residual
functional lymph nodes in the axilla. This is critical when performing lymph
node transplant to the axilla as one must avoid injury to those lymph nodes
during recipient-site exposure. In this situation, filtered technetium is injected
into the hand the morning of surgery. With the guide of a gamma probe,
functional axillary nodes can be identified and avoided during exposure of
the axillary recipient site.
Finally, MRA tells us if there is axillary vein stenosis, reveals the fat/fluid
composition, and may identify an occult recurrence or metastatic lesion.
Patients with significant fat accumulation are notified of this feature as the
limb volume is unlikely to reduce significantly with a physiologic procedure
alone and may require liposuction. All patients are referred to a certified
lymphedema therapist for preoperative decongestive therapy to optimize the
limb and weight loss if appropriate.
OPERATIVE TECHNIQUE
VASCULARIZED OMENTUM LYMPHATIC TRANSPLANT HARVEST
A two-team approach is used in the supine position with one surgeon
harvesting the omentum while the other surgeon is preparing the axilla.
Vascularized omentum lymphatic transplant (VOLT) can be harvested open,
laparoscopically, or robotically. The author currently prefers an open
approach through a limited epigastric incision to allow for the use of finer
instruments not available laparoscopically and fine bipolar
cautery. Alternatively, some plastic surgeons have a general surgery
colleague harvest the omentum.
The patient is given a light bowel prep of MiraLAX 2 days prior to
VOLT. A subcutaneous injection of 40 mg of prophylactic enoxaparin is
given the morning of surgery as well as alvimopan 12 mg orally to minimize
the risk of ileus.
A 6- to 8-cm midline epigastric incision is made depending on
subcutaneous thickness. The preperitoneal fat is encountered after incising
the linea alba after which the peritoneum is opened and the abdominal cavity
is exposed. A Balfour retractor is placed to maximize exposure. The
omentum is then visualized and delivered into the field along with the
transverse colon (Fig. 25-4). The stomach is also identified for orientation. In
cases where only a small portion of omentum is required, one can start
dissection superior to the transverse colon and enter the lesser sac directly. In
most cases, however, a portion of the greater omentum is required to fill in
the axillary defect.
The omentum is then retracted upward toward the ceiling while the
transverse colon is retracted inferiorly toward the patient’s feet. This key
maneuver allows the surgeon to enter the plane safely between the transverse
mesocolon and the omentum. The very thin film of tissue connecting the
omentum to the transverse colon is then carefully divided. The critical portion
of this case is to avoid the transverse mesocolon which carries the blood
supply to the colon. If violated this could lead to ischemia of a portion of the
colon. These blood vessels appear somewhat tortuous and deeper compared
to the very long and linear segmental vessels of the omentum. The correct
plane is avascular and once entered quite easy to develop.
FIGURE 25-4 Initial exposure of the omentum. In this case, performed during
bilateral DIEP flap harvest after elevating the abdominal apron.

Dissection then proceeds up the left side of the omentum directly to the
greater curvature of the stomach. The left gastroepiploic vessels are then
divided and the remaining right gastroepiploic pedicle is mobilized from the
stomach. The very fragile short gastric vessels are divided using a LigaSure
or similar device for efficiency. The gastroepiploic pedicle will then diverge
from the stomach and the dissection is complete (Fig. 25-5). While there are
more prominent lymph nodes more proximally, dissection should not
continue to the point where the pancreas is visualized.
PREPARATION OF THE AXILLA AND ANASTOMOSIS
A high transverse axillary incision is made from the pectoralis major muscle
to the latissimus dorsi muscle. Dissection proceeds laterally, where the
axillary vein is exposed. The deep surface of the latissimus muscle is then
exposed and medially the thoracodorsal vessels are identified and prepared
for anastomosis. In previously radiated patients, these vessels are often
displaced and adherent against the lateral chest wall. Occasionally, these
vessels may not be available in which case dissection continues proximally to
expose the circumflex scapular artery and vein. Great care is taken to remove
any dense axillary scar and fully decompress the length of the axillary vein if
it is narrowed (Fig. 25-6).
Because the omentum may be prone to venous hypertension, two recipient
veins are used for anastomosis to both the proximal right gastroepiploic vein
and the distal end of the gastroepiploic vein. A “Y” branch of the
thoracodorsal vein, the circumflex scapular vein, or a vein in the upper arm
can be used for the second venous anastomosis (Fig. 25-7).
FIGURE 25-5 Isolation of a portion of the omentum lymphatic transplant on the
right gastroepiploic vessels.
FIGURE 25-6 Exposure of the axillary recipient bed with decompression of the
axillary vein and preparation of the thoracodorsal vessels.
FIGURE 25-7 VOLT anastomosed to the thoracodorsal artery (red arrow),
thoracodorsal vein proximally, and a second recipient vein distally in the axilla (blue
arrows).

The flap is completely buried and inset with a few 3-0 Monocryl sutures to
ensure the entire axillary vein is covered and the omentum spans the entire
defect from the lateral chest wall to the upper arm. The axilla is closed over a
closed suction drain after injecting liposomal bupivacaine for pain relief. The
abdominal wall is closed with a running PDS barbed suture and the skin is
closed without a drain.
POSTOPERATIVE CARE
Patients typically stay in the hospital for 3 days with Doppler probe
monitoring through the overlying skin. Patients are started on sips of clears
but can have a regular diet once flatus is present, typically within 24
hours. Patients ambulate on the first postoperative day. Shoulder abduction is
limited between 30 and 90 degrees for 2 weeks after which full range of
motion exercises are performed without restriction.

CASES

CASE 1

Case 1 is a patient with a fat-dominant limb and significant hand swelling


in around-the-clock compression preoperatively (Fig. 25-8). She had no
visible lymphatic vessels for bypass on ICG and no ICG migration above
the elbow. A VOLT was performed to the forearm to offload fluid
buildup and 1 year later liposuction was performed to reduce the fat
component. Notably, her hand swelling resolved, attributed to the lymph
node transplant as liposuction is not performed in the hand. She has a
stable and significant reduction in limb volume 3 years postoperatively
and remains in compression.
FIGURE 25-8 Preoperative photo (left) compared to 3-year postoperative
result (right) following VOLT to the forearm and liposuction 1 year later.

CASE 2

Case 2 is a patient with moderate lymphedema and no migration of ICG


above the elbow who had three severe episodes of cellulitis requiring IV
antibiotics (Fig. 25-9). Preoperatively she was in compression around the
clock. She underwent vascularized groin lymph node at that time to the
wrist (uncommon for us to do this today) with a stable improvement at 9
years post op. Notably, she typically no longer wears compression unless
flying or doing strenuous activity. She has had only one episode of
cellulitis treated with oral antibiotics during this period.
FIGURE 25-9 Preoperative photo (left) compared to 9-year postoperative
result (right). Patient was in continuous compression and had multiple
episodes of severe cellulitis preoperatively. She underwent VLNT to the wrist
and only occasionally wears compression with only one episode of cellulitis
during this long follow-up period.
RISKS
Risks of VLNT in general include the possibility that there is no
improvement in lymphedema and in rare cases, the lymphedema
worsens. Lymph node transplants harvested from the groin and axilla, and
rarely, supraclavicular region carry a risk of donor-site lymphedema. Chyle
leak may occur particularly on the left side when harvesting supraclavicular
lymph nodes. Specific to VOLT, there are very small risks of hernia, bowel
obstruction, prolonged ileus, pancreatitis, and rarely, injury to intra-
abdominal structures.
OUTCOMES
Outcomes in lymphedema are challenging to assess as there is no single
metric that can adequately reflect the multiple dimensions of this disease. The
majority of current published data reports improved quality of life and
reduced limb volume and circumference following VLNT. A total of 300
patients in four studies compared VLNT to physiotherapy alone
demonstrating reduced limb circumference and improved quality of life
(11,25–27). Specifically, pain, heaviness, and functional status generally
improve following surgery. Most studies demonstrate a reduction in the
incidence of cellulitis. Our institution is currently in the midst of a
prospective controlled long-term outcomes’ study on lymphatic surgery
versus physiotherapy alone.
CONCLUSION
VLNT has evolved significantly in terms of technique and indications. VLNT
has become a safe and established option for patients with early to
moderately advanced lymphedema. Lymphedema is still a frontier and as our
understanding of this disabling disease improves, so will our approach to
treating and preventing it.

REFERENCES

1. Wiser I, Mehrara BJ, Coriddi M, et al. Preoperative assessment of upper


extremity secondary lymphedema. Cancers (Basel) 2020;12:E135.
2. Dayan JH, Wiser I, Verma R, et al. Regional patterns of fluid and fat
accumulation in patients with lower extremity lymphedema using
magnetic resonance angiography. Plast Reconstr Surg 2020;145:555–
563.
3. Dayan JH, Ly CL, Kataru RP, et al. Lymphedema: pathogenesis and
novel therapies. Annu Rev Med 2018;69:263–276.
4. Ly CL, Nores GDG, Kataru RP, et al. T helper 2 differentiation is
necessary for development of lymphedema. Transl Res 2019;206:57–70.
5. Gardenier JC, Kataru RP, Hespe GE, et al. Topical tacrolimus for the
treatment of secondary lymphedema. Nat Commun 2017;8:14345.
6. Tervala TV, Hartiala P, Tammela T, et al. Growth factor therapy and
lymph node graft for lymphedema. J Surg Res 2015;196:200–207.
7. Rockson SG, Tian W, Jiang X, et al. Pilot studies demonstrate the
potential benefits of antiinflammatory therapy in human lymphedema.
JCI Insight 2018;3:123775.
8. Narushima M, Yamamoto T, Ogata F, et al. Indocyanine green
lymphography findings in limb lymphedema. J Reconstr Microsurg
2016;32:72–79.
9. Becker C, Assouad J, Riquet M, et al. Postmastectomy lymphedema:
long-term results following microsurgical lymph node transplantation.
Ann Surg 2006;243:313–315.
10. Mihara M, Hara H, Hayashi Y, et al. Upper-limb lymphedema treated
aesthetically with lymphaticovenous anastomosis using indocyanine
green lymphography and noncontact vein visualization. J Reconstr
Microsurg 2012;28:327–332.
11. Cheng MH, Chen SC, Henry SL, et al. Vascularized groin lymph node
flap transfer for postmastectomy upper limb lymphedema: flap anatomy,
recipient sites, and outcomes. Plast Reconstr Surg 2013;131:1286–1298.
12. Hoffner M, Ohlin K, Svensson B, et al. Liposuction gives complete
reduction of arm lymphedema following breast cancer treatment—a 5-
year prospective study in 105 patients without recurrence. Plast
Reconstr Surg Glob Open 2018;6:e1912.
13. Chang DW, Suami H, Skoracki R. A prospective analysis of 100
consecutive lymphovenous bypass cases for treatment of extremity
lymphedema. Plast Reconstr Surg 2013;132:1305–1314.
14. Boccardo F, Valenzano M, Costantini S, et al. LYMPHA technique to
prevent secondary lower limb lymphedema. Ann Surg Oncol
2016;23:3558–3563.
15. Huang JJ, Gardenier JC, Hespe GE, et al. Lymph node transplantation
decreases swelling and restores immune responses in a transgenic model
of lymphedema. PLoS One 2016;11:e0168259.
16. Ito R, Zelken J, Yang CY, et al. Proposed pathway and mechanism of
vascularized lymph node flaps. Gynecol Oncol 2016;141:182–188.
17. Dayan JH, Dayan E, Smith ML. Reverse lymphatic mapping: a new
technique for maximizing safety in vascularized lymph node transfer.
Plast Reconstr Surg 2015;135:277–285.
18. Maldonado AA, Chen R, Chang DW. The use of supraclavicular free
flap with vascularized lymph node transfer for treatment of
lymphedema: a prospective study of 100 consecutive cases. J Surg
Oncol 2017;115:68–71.
19. Kenworthy EO, Nelson JA, Verma R, et al. Double vascularized
omentum lymphatic transplant (VOLT) for the treatment of
lymphedema. J Surg Oncol 2018;117:1413–1419.
20. Nguyen AT, Suami H, Hanasono MM, et al. Long-term outcomes of the
minimally invasive free vascularized omental lymphatic flap for the
treatment of lymphedema. J Surg Oncol 2017;115:84–89.
21. Vignes S, Blanchard M, Yannoutsos A, et al. Complications of
autologous lymph-node transplantation for limb lymphoedema. Eur J
Vasc Endovasc Surg 2013;45:516–520.
22. Demiri E, Dionyssiou D, Tsimponis A, et al. Donor-site lymphedema
following lymph node transfer for breast cancer-related lymphedema: a
systematic review of the literature. Lymphat Res Biol 2018;16:2–8.
23. Dayan JH, Dayan E, Kagen A, et al. The use of magnetic resonance
angiography in vascularized groin lymph node transfer: an anatomic
study. J Reconstr Microsurg 2014;30:41–45.
24. Mehrara BJ, Greene AK. Lymphedema and obesity: is there a link?
Plast Reconstr Surg 2014;134:154e–160e.
25. Dionyssiou D, Demiri E, Tsimponis A, et al. A randomized control
study of treating secondary stage II breast cancer-related lymphoedema
with free lymph node transfer. Breast Cancer Res Treat 2016;156:73–
79.
26. Engel H, Lin CY, Huang JJ, et al. Outcomes of lymphedema
microsurgery for breast cancer-related lymphedema with or without
microvascular breast reconstruction. Ann Surg 2018;268:1076–1083.
27. Lin CY, Liu HE, Cheng MH. Factors associated with professional
healthcare advice seeking in breast cancer-related lymphedema. J Surg
Oncol 2020;121:67–74.
CHAPTER 26

Sentinel Node Biopsy and


Axillary Dissection
HIRAM S. CODY III

In the pregenomic era, axillary lymph node status was the most important
prognostic factor for patients with operable breast cancer and consequently
the goals of axillary surgery have been (1) staging/prognostication, (2) local
control, and (3) arguably, a small survival benefit. For these purposes,
axillary lymph node dissection (ALND) has been the gold standard for most
of the 20th century, but since the mid-1990s has largely given way to sentinel
lymph node biopsy (SLNB). Here we will review the historic background of
ALND and SLNB, the indications for each procedure, and the operative
techniques.
HISTORY
Jean Louis Petit (1674 to 1750), director of the French Surgical Academy,
was probably the first surgeon to articulate a unified concept for breast cancer
surgery (1). He emphasized the importance of an en bloc resection of the
breast and axillary nodes, but his insight came too early: Although breast
cancer had been considered surgically incurable for most of the 19th century,
Halsted’s landmark 1894 (2) and 1907 (3) reports of his meticulous technique
for “radical mastectomy” (RM)—including removal of the breast, pectoral
muscles, and axillary contents—demonstrated a reduction in local recurrence
(LR) and apparent cure for about one-third of patients. The concept that
minimizing LR would maximize survival made RM the standard operation
for the next 70 years despite later reports of more radical (extended RM) (4)
or less radical (modified RM) (5) techniques. In the “Halstedian” era, the goal
was to maximize cure by minimizing local failure.
In the 1970s, Fisher proposed that breast cancer was a systemic disease
from the outset and that survival was largely a function of tumor biology, not
extent of surgery (6). The “Fisher hypothesis” was first tested in the National
Surgical Adjuvant Breast and Bowel Project (NSABP) B-04 randomized trial
(1971 to 1974). At 25 years’ follow-up (7), variations in extent of axillary
surgery for mastectomy patients with clinically node-positive breast cancer
(RM vs. total mastectomy/radiotherapy [RT]) or clinically node-negative
disease (RM vs. total mastectomy/RT vs. total mastectomy alone) yielded no
differences in any category of survival. B-04 did confirm the overwhelming
prognostic significance of axillary node metastasis, and ALND was
incorporated into all subsequent NSABP trials for invasive breast cancer,
including NSABP B-06, in which survival at 20 years (8) was comparable for
mastectomy versus breast-conserving surgery. In the “Fisher” era, the
primary goal of ALND was prognostication to guide systemic therapy, a
secondary objective was local control, and a survival benefit was unproved.
We now know that both Halsted and Fisher were right. A remarkable
series of meta-analyses from the Early Breast Cancer Trialists’ Collaborative
Group (EBCTCG) confirms that breast cancer is a family of diseases with a
wide spectrum of behavior (9), ranging from predominantly local (Halsted) to
predominantly systemic (Fisher) phenotypes. First, the EBCTCG showed that
local control and survival are related (42,000 women in 78 randomized trials)
and estimated that for every four LRs prevented, one life would be saved
(10). Second, they confirmed that there is no survival advantage for more
radical versus less radical versions of mastectomy (3,400 women in nine
trials) or for mastectomy versus breast conservation (3,100 women in seven
trials) (11). Finally, they demonstrated an incremental survival benefit from
the addition of systemic adjuvant therapy (chemo- or hormonal) to local
treatment (8,000 to 33,000 women in six separate meta-analyses comprising
194 trials) (12). These results highlight the multidisciplinary nature of
contemporary breast cancer treatment and the importance of collaboration
among the disciplines of surgical, medical, and radiation oncology.
The SLN concept, first articulated by Cabanas in 1977 (13) for penile
cancer and independently by Morton et al. in 1992 (14) for melanoma, is that
(a) the first—or first few—regional lymph nodes draining a tumor site could
predict the status of that regional node basin, (b) these nodes could be
reliably mapped by injections of radiotracer and/or dye, and (c) SLN-negative
patients might thereby avoid the added morbidity of regional node dissection.
Krag et al. (15) in 1993 (using isotope mapping) and Giuliano et al. (16) in
1994 (using blue dye) were the first to report SLNB for breast cancer. Since
then, an extensive literature covering all aspects of the procedure and
including seven randomized trials comparing SLNB with ALND has
confirmed that the morbidity of SLNB is less than that of ALND, that staging
accuracy is at least equivalent, and that for SLN-negative patients survival
and other disease-related adverse events are comparable on long-term follow-
up (17). It is now also clear that many patients with positive SLN do not
require ALND; in the landmark ACOSOG Z0011 trial (18), patients with
cT1–2N0 breast cancers, 1–2 hematoxylin and eosin (H&E)–positive SLN,
and treated with breast conservation including whole-breast RT were
randomized to SLNB alone versus SLNB plus ALND. At 10 years follow-up
(19) there were no differences in any category of survival or in the rates of
local, regional node or distant recurrence, even though additional positive
nodes were found in 27% of ALND specimens. The International Breast
Cancer Study Group (IBCSG) Trial 23–01 (20) similarly randomized patients
with SLN micrometastases to SLNB versus SLNB with ALND, and at 10
years found no advantage for ALND.
CASE SELECTION FOR SLNB
Early in the SLN era there were many putative contraindications to the
procedure and much concern about the “learning curve” during which one’s
early experience with SLNB should be validated by a planned “backup”
ALND. It is now clear that SLNB is suitable for virtually all patients with
cN0 operable invasive breast cancers and that—using standardized
techniques—the “learning curve” is as short as one case (21). SLNB is also
indicated for patients with ductal carcinoma in situ (DCIS) who require
mastectomy (or for whom invasion is suspected based on the presence of a
mass) and for patients with clinically suspicious nodes but a nondiagnostic
needle biopsy. SLNB is indicated for patients who are cN0 but node positive
on FNA or core biopsy, 50% of whom in our own experience (22) had 1 to 2
positive SLNs, meeting Z0011 criteria and avoiding ALND. SLNB is
indicated for patients who are cN0 following neoadjuvant chemotherapy,
whether they were node negative (23) or node positive, upfront (24). SLNB is
reasonable but admittedly very low yield for prophylactic mastectomy, where
invasive cancer will be found in a few percent of patients. SLNB is feasible
in patients with locally recurrent breast cancer and prior axillary surgery (25),
especially if fewer than 10 nodes were removed in a prior SLNB or ALND,
but the benefit of “reoperative SLNB” is unproved (26). Finally, prior
aesthetic breast surgery, augmentation or reduction, is not a contraindication
to SLNB (27,28).
TECHNIQUE OF SLNB
SLNB requires close collaboration among the disciplines of nuclear
medicine, surgery, and pathology and although SLNB works well with a
variety of techniques, each institution will want to develop its own specialty-
specific consensus protocols. The following represents the SLNB literature as
a whole and our own institutional experience with more than 25,000
procedures since 1995.
Nuclear Medicine
The success of SLNB is maximized, and the false-negative rate is minimized,
by the combination of radioisotope and blue dye, but radioisotope accounts
for the greatest proportion of this success, and with experience the marginal
benefit of blue dye diminishes (29,30). The isotope of choice is technetium
(Tc99m) bound to a variety of carriers, most commonly sulfur colloid (United
States), colloidal albumin (Europe), and antimony (Australia). Novel carriers
and nonradioactive techniques (fluorescence, ultrasound microbubbles, and
magnetic particles) (31) report mapping success comparable to legacy agents.
There is no standardization of isotope dose, particle size, volume of
injectate, timing of injection, or site of injection, and many methods appear to
work well. Our preference (32) is to inject 0.1 mCi (3.7 MBq) of unfiltered
Tc99m–sulfur colloid on the morning of surgery or 0.5 mCi (18.5 MBq) the
day before. With this protocol, which allows for radioactive decay (the half-
life of Tc99m is 6 hours) we have observed equivalent results with same-day
or day-before isotope (33). It appears that the performance of unfiltered and
filtered isotope preparations is similar.
We inject a volume of 0.05 cc; this has the advantage of leaving a very
small “hot spot” on the breast, so as not to overshadow the axilla in patients
with upper outer quadrant tumors. We inject intradermally at a single site
over the tumor, having found this technique superior to parenchymal or
peritumoral injection. These results have been independently confirmed in a
randomized trial by Povoski et al. (34) and in the large multicenter Louisville
Sentinel Node Trial (35): superficial injections (intradermal, subdermal, or
subareolar) were more successful than parenchymal (peritumoral) injection or
dye-only techniques. Across the SLNB literature the false-negative rate of all
methods was similar, suggesting that the lymphatics of the entire breast
usually drain to the same few SLNs (36).
Although preoperative lymphoscintigraphy (LSG) is essential in SLNB for
melanoma, its role in breast cancer is debatable. LSG does not improve the
identification of axillary SLN, other than to alert the surgeon that more than
one axillary SLN is present. Even when the LSG is negative, a hand-held
gamma probe will usually identify “hot” SLN at surgery. LSG can identify
nonaxillary lymphatic drainage (primarily to the internal mammary nodes) in
a minority of patients, but the impact of this information on treatment, local
control, or survival is unproved.
Surgery
For breast conservation we perform SLNB under local anesthetic with
intravenous (IV) sedation and for mastectomy under general anesthesia.
Before starting surgery, we inject 1 to 5 cc of isosulfan blue dye subdermally
in the breast, (a) at a single site over the tumor, (b) just superolateral to a
surgical biopsy site, or (c) in the subareolar area. Using a hand-held gamma
probe, we identify and mark the isotope injection site in the breast, any focal
hot spots in the axilla, and any intervening hot spots that might suggest the
presence of intramammary SLN.
SLNB is best done prior to the breast operation—while the lymphatics are
still intact—and through a separate transverse skin line incision in the axilla.
Even tumors high in the axillary tail will be further from the axilla than they
appear, and one should avoid the temptation to do the entire operation
through a single incision except perhaps for mastectomy done through a
single oblique incision, where SLNB is easily done through the axillary end
of the incision prior to proceeding with the mastectomy.
SLNB is best done under direct vision and with adequate exposure, as
inadvertent division of sensory nerves probably accounts for most of the
reported morbidity of SLNB. As dissection is deepened through the axillary
fascia, any blue lymphatics are left intact and traced proximally into the
axilla, blue nodes are identified, and the gamma probe is used to identify any
“hot” nodes. SLN are usually found low in level I, but in about 25% of cases
they are found at other locations: posteriorly along the latissimus muscle,
higher in the axilla near the axillary vein, beneath the pectoralis minor in
levels II to III, and (much less often) as Rotter (interpectoral) or
intramammary SLN. The gamma probe is very useful throughout this
dissection and is indispensable in the very large or fatty axilla where
identification of blue lymphatics/nodes can be challenging.
All blue and/or “hot” nodes are removed, typically a median of 2 to 3 per
patient. When multiple hot SLNs (or a diffusely hot axilla) are found, we
make every effort to remove the hottest SLN, which will be positive in 80%
of SLN-positive patients (37). We do not in general submit large numbers of
SLN, having found that 98% of positive SLN are identified within the first
three SLNs and 99% within the first four SLNs submitted (38). Another
useful guideline is the “10% rule,” in which all nodes with counts ≥10% of
the hottest node are submitted as SLN. For patients who were node positive
prior to neoadjuvant chemotherapy, the false-negative rate of SLNB is
minimized by using dual tracers (blue dye plus isotope) and by removing at
least three SLNs (39–41).
A final and critical element in SLNB is careful palpation of the axilla and
the submission of any palpably suspicious nodes as SLN. In our initial
experience with SLNB (42), we reported that a false-negative rate of 14%
defining the SLNs as blue and/or hot was reduced to 4.6% by defining the
SLNs as blue and/or hot and/or palpable.
The axillary incision after SLNB is closed routinely without drainage. The
morbidity of SLNB is less than that of ALND but is not zero. Patients may
experience pain, seroma, hematoma, or infection. Blue dye may cause
transient bluish-green discoloration of the skin and urine, blue urticaria in
<1%, and anaphylactic reactions in <0.5% of patients (43).
Pathology
Our previous practice of intraoperative SLN frozen section and consent to
proceed with ALND if SLN positive is now limited to patients outside the
Z0011 selection criteria, largely those having a mastectomy or SLNB after
neoadjuvant chemotherapy.
Axillary nodes have typically been examined by a single H&E–stained
section, despite evidence that additional study (serial sections and/or
immunohistochemical [IHC] stains for cytokeratins) could identify missed
nodal metastases in a significant fraction of patients (44). These enhanced
techniques—prohibitive for the examination of an entire ALND specimen—
became feasible for SLNB and promised more accurate staging and selection
of treatment. We now know from two large prospective trials (45,46) in
which all treatment was based on the results of routine H&E staining that
subsequent serial sectioning and IHC staining upstaged 10% to 16% of
patients to SLN positive but that survival among those converted to node
positive—90% of whom has already received systemic adjuvant therapy—
was unaffected. One must conclude that SLN “ultrastaging” beyond routine
H&E may result in overtreatment without affecting outcome.
CASE SELECTION FOR ALND
In the simplest sense, ALND would seem to be indicated for any patient with
a contraindication to SLNB. In fact, as noted above, most of the putative
“contraindications” to SLNB have been disproved, and SLNB is suitable for
virtually all patients with cT1–3N0 invasive cancers. The role of ALND
continues to diminish but there are still clear indications to perform it (Table
26-1).
Clinically Positive Axilla
The literature on SLNB is largely limited to patients with cN0 disease, so
ALND makes sense for the clinically positive axilla, but with significant
qualifications. First, clinical axillary examination is equally subject to false-
negative and false-positive results, and in our early experience with SLNB
25% of cN1 axillae proved to be benign (47). The cN1 axilla requires
histologic confirmation by FNA or core biopsy prior to ALND. Second,
neoadjuvant chemotherapy makes sense for any patient with biopsy-proven
cN1–2 disease, and dependent on tumor subtype achieves a pathologic
complete response (pCR) in 20% to >90% of axillae (48), allowing these
patients—if SLN negative—to avoid ALND.

TABLE 26-1 Indications for SLNB and ALND


Indications for SLNB Indications for ALND
cT1–3N0 invasive breast cancer cN1 axilla, positive FNA/core
biopsy, not a candidate for
neoadjuvant chemotherapy
cN1 axilla but negative FNA/core Clinically positive axilla or positive
biopsy SLNB after neoadjuvant chemo
cN0 axilla but positive FNA/core Inflammatory breast cancer
biopsy
cN0 axilla after neoadjuvant Failed/unavailable SLNB
chemotherapy
DCIS requiring mastectomy (or with Prior inadequate ALND
a mass)
Ipsilateral invasive breast recurrence Isolated axillary local recurrence
(ipsilateral or contralateral)
Prophylactic mastectomy (optional)

SLN Positive Outside the Z0011 Selection Criteria


This category includes (a) all patients with more than two positive SLNs, (b)
SLN-positive patients treated by mastectomy, (c) SLN-positive patients
having breast conservation without whole-breast RT, and (d) all patients
found at surgery to have matted (cN2) nodes or unexpectedly extensive
axillary disease.
Clinically Node Positive or SLN Positive Following
Neoadjuvant Chemotherapy
After neoadjuvant chemotherapy patients who remain clinically node positive
require ALND, as do patients who are cN0 but SLN positive. A new trial—
Alliance 11202—by randomizing SLN-positive patients to ALND versus no
further surgery is asking whether ALND needs to be routine in this setting.
Inflammatory Breast Cancer
The safety of SLNB has not been established for patients with inflammatory
breast cancer and following neoadjuvant chemotherapy ALND remains
standard care. SLNB for inflammatory breast cancer only makes sense in the
setting of a clinical trial including a backup ALND to performance
characteristics, especially the false-negative rate.
Prior Inadequate ALND
In the NSABP B-04, Fisher et al. (49) found that the proportion of cN0
patients with positive axillae was the same whether 3 to 5, 6 to 10, 11 to 15,
or 16 to 20 nodes had been removed (i.e., the removal of relatively few nodes
was sufficient to establish axillary node status), but that the proportion with
≥4 nodes positive was highest when ≥26 nodes had been removed (i.e., a
more complete node dissection was necessary to correctly determine the
degree of node involvement). Of note, there were no cases of subsequent
axillary LR if ≥6 nodes had been removed. ALND makes sense for any
patient in whom a recent “ALND” removed few nodes, most of which were
positive, suggesting a high risk of residual disease.
Failed SLNB
With increasing experience, the success rate of SLNB approaches but does
not equal 100%. For that small fraction of failed SLNB procedures or for a
SLN procedure that is technically unsatisfactory in any other way, it is
reasonable to perform ALND, especially if node status is required to
determine subsequent treatment.
Unavailability of SLNB
SLNB is not universally available, especially in developing nations, where
the added logistics and cost may prove to be excessive. Since the potential
impact of SLNB worldwide is substantial (many patients with clinically
diagnosed breast cancers are still node negative), the challenge will be to find
ways to minimize the cost of SLNB while maintaining accuracy. Where
SLNB is not available, ALND should remain standard care.
Isolated Locoregional Recurrence
Axillary LR after a negative SLNB is infrequent and comparable to that after
ALND, about 1% at 10 years. As for ALND, most axillary recurrences are
early events, virtually all within the first 5 years (50). Many axillary masses
that appear after SLNB are benign, but for those that are malignant, ALND is
indicated. ALND also makes sense for those patients who relapse in the
contralateral axilla and do not have other distant sites of disease.
TECHNIQUE OF ALND
The axillary contents lie within a complex space best described as an
eccentrically shaped pyramid. Viewed through a transverse section (Fig. 26-
1), the axilla is a triangular space bounded by the chest wall medially, the
subscapularis posteriorly, the latissimus posterolaterally, and the pectoralis
major and minor muscles anteriorly. Viewed from the front through a coronal
section (Fig. 26-2), the triangle is bounded by the axillary vein superiorly, the
latissimus laterally, and the chest wall medially.

FIGURE 26-1 The anatomic boundaries of axillary lymph node dissection, as seen in
a transverse section through the midportion of the axilla, showing the pectoralis
major and minor anteriorly, the serratus medially, and the latissimus and
subscapularis posteriorly.

The axillary contents are arbitrarily divided into three “levels”: Level I lies
lateral to, level II lies posterior to, and level III lies medial to the pectoralis
minor muscle (see Fig. 26-2). Level I comprises the largest volume of
axillary tissue and the largest proportion of the axillary nodes (perhaps 70%),
with level II comprising perhaps 20% and level III 10% or less. The anatomic
distinction between axillary levels I and II is somewhat arbitrary, while level
III is more anatomically distinct. Historically, breast cancer prognosis was
related to the “highest level” of axillary node involvement, but since about
1970 the number of positive nodes and not the level has emerged as the
prognostically relevant variable.

FIGURE 26-2 The anatomic extent of axillary lymph node dissection, with levels I,
II, and III designated as lying lateral to, behind, or medial to the pectoralis minor
muscle, respectively.
Extent of Procedure
The extent of ALND is formally classified as level I, level I to II, or level I to
III (“complete ALND”). While axillary node metastases usually proceed
sequentially from levels I to II to III, a large literature addresses the subject of
“skip metastases,” that is, disease at levels II or III with level I negative. At
present, “skip metastases” are best viewed simply as level II or III SLN,
receiving drainage directly from the breast. Nothing is being “skipped,” and
these nodes should be readily identified by lymphatic mapping and submitted
as SLN. In our practice, ALND is typically a level I to II dissection, extended
to level III if required for removal of all gross disease.
Choice of Incision
The possible incisions for ALND are either separate from (Fig. 26-3, panels
1, 2, and 4) or contiguous with (Fig. 26-3, panels 3 and 5) the incision used
for the breast operation. A separate incision is best done transversely, gently
curved following a skin line, about two-finger breadths inferior to the axillary
skin crease. Separate axillary and breast incisions are almost always
cosmetically superior to contiguous ones, especially in the setting of skin-
sparing mastectomy with immediate reconstruction (Fig. 26-3, panel 2) and
for patients with upper outer quadrant tumors having breast conservation
(Fig. 26-3, panel 4). Here the temptation to perform a single incision (Fig.
26-3, panel 5) is the strongest, but the tumor may be deceptively far from the
axilla, requiring resection of a large volume of intervening tissue.
FIGURE 26-3 Incisions for sentinel lymph node biopsy and/or axillary lymph node
dissection for mastectomy or breast-conserving surgery.

A contiguous incision is perfectly reasonable for patients having


mastectomy without reconstruction (Fig. 26-3, panel 3) and for patients
having breast conservation for tumors very high in the axillary tail (Fig. 26-3,
panel 5). In either case, SLNB is easily done through the axillary end of the
incision prior to proceeding with the breast operation.
Beginning the Operation
For patients with severe comorbidity, ALND can be done under local
anesthesia with sedation, but it is best done under general anesthesia. The
ipsilateral chest and arm should be prepped, with a sterile sleeve covering the
arm to allow changes in position during surgery. The operation is begun with
a transverse skin line incision starting behind the lateral border of the
pectoralis major and carried back toward the latissimus. The incision should
be sufficient for good exposure and extended laterally as needed.
Flap Elevation
The first and foremost technical element of ALND is complete dissection of
the skin flaps to their anatomic limits prior to entering the axilla. This point
cannot be emphasized enough: Virtually all technical difficulties with ALND
stem from inadequate flap elevation at the outset of the procedure. The
second key technical element of ALND is to have adequate countertraction
(“tissue under tension, surgeon at ease”). As the flap dissection deepens,
Richardson retractors are placed at each end of the field and traction
constantly applied parallel to the line of dissection.
Flap thickness should be uniform and depends on the patient’s body
habitus. For thin patients, I dissect in the areolar plane just beneath the
axillary sweat glands, but otherwise I leave 2 to 5 mm of fatty tissue on the
flap. Ectopic axillary breast tissue, often visible preoperatively, should be
encompassed by the skin flaps as well. Flaps of uniform thickness will mold
smoothly into the axillary defect at the end of the procedure, with a good
cosmetic result.
Flaps are elevated to the pectoralis major medially, the serratus inferiorly,
and the latissimus laterally. Dissection is carried cephalad along the anterior
border of the latissimus to its tendinous portion (the “white tendon”) and to
the axillary vein, which crosses the operative field anteriorly at about this
level. The final step in flap elevation is to identify the axillary vain
superiorly. By retracting the pectoralis major superomedially and the axillary
contents inferiorly, the clavipectoral fascia is seen as a flat, translucent layer
of tissue passing anterior to the axillary vein, artery, and brachial plexus
before inserting on the coracobrachialis muscle. As the clavipectoral fascia
passes medially it splits to encompass the minor anteriorly and posteriorly
before again fusing into a single layer medial to the minor. The clavipectoral
fascia is carefully incised just anterior to the axillary vein, and with this step
the axillary contents are easily mobilized inferiorly, completely exposing the
axillary vein. This step completes the flap elevation and allows the operator
to proceed confidently with the axillary vein in full view.
Dissection of the Medial Pectoral Nerve
The medial pectoral nerve (named for its origin from the medial cord of the
brachial plexus) lies lateral to the pectoral muscles, coursing anteriorly and
inferiorly as it curls around the lateral borders of the minor and major. It
innervates the lower one-third of the pectoralis major, should be preserved
whenever possible, and if injured causes muscle atrophy, which is strikingly
visible after mastectomy, especially with implant breast reconstruction. The
accompanying medial pectoral vessels give off small side branches which
pass inferolaterally into the axillary contents, and only after these are
carefully ligated and divided can the dissection be deepened beneath the
pectoralis minor to reach the level II nodes. At this point, retractors can be
placed deep to the pectoralis minor, and by retracting the major and minor
medially, level II of the axilla is exposed. Adduction of the arm facilitates
this step and will often allow exposure of level III as well.
Mobilizing Levels II and III
With levels II and III exposed, the clavipectoral fascia is carefully incised as
far medially as possible. Having already incised the clavipectoral fascia
superiorly along the axillary vein, this step allows the axillary contents to be
mobilized laterally off the chest wall in full view of the axillary vein. Any
small side branches of the axillary vein are divided and ligated.
If gross axillary disease is palpable in levels II to III and if retraction of the
minor provides inadequate exposure, then the pectoralis minor should be
divided. This is done by dividing and ligating the medial pectoral
neurovascular bundle, bluntly entering the plane between the major and
minor, adducting the arm, and retracting the major anteriorly. This step may
require the division of one or more small pectoral nerve branches that pass
through the body of the minor. The major is retracted anteriorly, exposing
and preserving the lateral pectoral nerve and thoracoacromial vessels running
along the underside of the major, as well as any interpectoral (Rotter) nodes
lying on either side of this neurovascular bundle. Grossly involved Rotter
nodes are easily removed at this point. The clavipectoral fascia is incised
along the medial border of the minor (taking care to avoid the neurovascular
bundle) and the minor is then encircled and retracted anteriorly by the
surgeon’s finger. The muscle is divided over the surgeon’s finger at the level
of the axillary vein. This widely exposes levels II and III, and following
incision of the clavipectoral fascia superomedially, the entire axillary
contents can then be mobilized laterally from “Halsted ligament” (the
tendinous portion of the subclavius muscle where it inserts on the first rib,
marking the highest extent of level III). In this setting, I usually excise the
denervated pectoralis minor along with the axillary contents, although the
muscle can be left in place.
Identifying the Intercostobrachial Nerve
As the axillary contents are mobilized laterally off the chest wall, the side
branches of the axillary vein are serially divided and ligated. As the
dissection proceeds laterally, the intercostobrachial nerve (ICBN, a sensory
branch of T2) is encountered running laterally and tethering the axillary
contents to the chest wall. I usually sacrifice the ICBN, since most often it
will already have been divided laterally in the axilla during the dissection up
the anterior border of the latissimus to the axillary vein. Division of the ICBN
frees up the axillary contents further and allows exposure of the long thoracic
nerve (which always lies posterior to the ICBN). The T3 and (if necessary)
T4 sensory nerve roots are similarly divided to further free the axillary
contents from the lateral chest wall. Preservation of the ICBN and other
sensory nerves is possible but may require fragmentary excision of the
axillary contents and may not reduce sensory morbidity, which usually
resolves within 1 to 2 years regardless.
Identifying the Long Thoracic Nerve
As the dissection continues laterally, the largest side branch of the axillary
vein (“thoracoepigastric”) is divided and ligated. As the axillary contents are
retracted laterally to look for the long thoracic nerve, the first “white line”
one sees is usually a thin fold of fascia enclosing the serratus muscle and not
the nerve. The long thoracic nerve is usually visible lateral to this, running
just beneath the thin layer of fascia encompassing the medial aspect of the
axillary contents. After carefully incising this layer, the nerve is easily
separated from the axillary contents by placing both index fingers into the
space just lateral to the nerve and simultaneously sweeping superiorly and
inferiorly. This frees and exposes the nerve along most of its length and
prevents injury later on.
Identifying the Thoracodorsal Nerve
Most side branches of the axillary vein, including the thoracoepigastric, enter
the vein along roughly the same plane. In contrast, the thoracodorsal
neurovascular bundle is angulated about 45 degrees posteriorly. Once all the
anteriorly located side branches have been ligated, the thoracodorsal
neurovascular bundle is identified by simply retracting the axillary contents
inferiorly. The thoracodorsal nerve is easily identified, lying just medial to
the artery and vein, by sweeping a finger inferiorly along, and just medial to,
the thoracodorsal bundle.
Completing the Axillary Dissection
This intervening bridge of level I tissue between the two nerves is then
clamped as close to the vein as possible, divided distal to the clamp, and
ligated proximally. The clamp should be applied carefully, with the axillary
vein and both nerves under direct vision at all times. If the long thoracic
nerve has not been swept completely free of the axillary tissue at this level or
if the thoracodorsal nerve is crossing the axilla diagonally and has not been
fully exposed, then either nerve could easily “sneak” into the clamp and be
cut during this maneuver. Once the bridge of tissue has been cut, the
specimen is swept inferiorly, exposing the subscapularis muscle posteriorly
and leaving a clean operative field between the two nerves. As the axillary
contents are mobilized inferolaterally, dissection is carried directly along the
thoracodorsal nerve, and the small side branches of the thoracodorsal vessels
are easily identified and ligated. As the thoracodorsal bundle begins to curve
back toward the chest wall, the operation is completed by dividing the few
remaining soft tissue attachments inferolateral to the bundle and removing the
specimen. For more extensive dissections I orient the specimen with sutures
or metal tags before handing it off.

FIGURE 26-4 The operative field of a completed axillary lymph node dissection
(ALND). The ligated side branches of the axillary vein lie superiorly, the side
branches of the thoracodorsal bundle laterally, and the cut stumps of the
intercostobrachial (T2), T3, and T4 sensory nerves medially. Not every ALND will
require the sacrifice of the intercostal sensory nerves, and depending on the patient’s
anatomy, some or even all of them can be preserved.

Closing
Figure 26-4 shows the field of the completed ALND. The axillary vein (with
its ligated side branches) is visible superiorly, the cut ends of the T2 (ICBN),
T3, and T4 sensory nerves are visible medially, and the long thoracic nerve
and the thoracodorsal neurovascular bundle (with its ligated side branches)
are seen posteriorly. After inspecting the field for hemostasis, a flat 7-mm
Jackson–Pratt drain is placed through a stab wound in the lower skin flap and
the skin incision is closed and confirmed to be airtight by applying suction to
the drain. A dressing of gauze, fluffs, and surgical bra is applied, and the
patient is awakened and returned to the recovery room.
Postoperative Care
Patients having ALND with breast conservation are normally discharged the
day of surgery and those having mastectomy (with or without implant
reconstruction) on the first postoperative day. All patients are instructed in
wound care (I normally allow showering the day after surgery), given a log
book to record their wound drainage (we remove drains when the 24-hour
drainage is less than 30 cc), and a program of postoperative shoulder
exercises (which they can usually begin immediately).
COMPLICATIONS OF SLNB AND ALND

Lymphedema
Lymphedema is the single complication of greatest concern to patients and is
the subject of an extensive but problematic literature, with wide variation in
definition, assessment, patient characteristics, extent of surgery/RT, and
length of follow-up. In a Cochrane meta-analysis of 26 randomized trials
(17), the odds of lymphedema—compared to ALND—were less for no
axillary surgery (10 trials), for axillary sampling (6 trials), and for SLNB (7
trials). In the ALMANAC trial of SLNB versus SLNB/ALND (51), the
patient-reported incidence of moderate or severe lymphedema at 12 months
was less with SLNB than ALND (5% vs. 13%), and in a careful prospective
study of our own (52), measurable lymphedema 5 years after SLNB versus
ALND was 5% versus 16%, respectively. Of note, a separate trial—
AMAROS (53)—observed that for SLN-positive patients randomized to
axillary RT versus ALND, the morbidity of axillary RT was half that of
ALND and a consistent finding in many studies is that the risk of
lymphedema is greatest following ALND plus RT.
Longstanding recommendations to patients for the “prevention of
lymphedema” (avoidance of trauma/injury, infection, arm constriction,
venipuncture, IVs, injections, heavy lifting, repetitive motions) have little
basis in fact (54). Meta-analyses show no adverse effect of exercise (25
studies) (55) or breast reconstruction (19 studies) (56), and no clear benefit
from manual lymphatic drainage (10 trials) (57) or axillary reverse mapping
(preservation of arm lymphatics during SLNB—24 studies) (58).
Lymphedema cannot be cured but it can be treated with various combinations
of elastic compression garments, compression pumps, bandaging, exercise,
and complex physiotherapy, but in general requires lifelong compression
garments to maintain any therapeutic gains. New surgical techniques
(lymphatic–venous anastomosis, free lymphatic transfer) are promising but
supported at present by low-certainty evidence (59).
Axillary Web Syndrome
“Axillary web syndrome” (AWS)—long observed by surgeons—was named
and described by Moskovitz et al. (60) in 2001. AWS is the appearance 1 to 8
weeks after ALND (or SLNB) of a “web” of tender subcutaneous lymphatic
cords running from the lateral axilla down the upper inner aspect of the arm,
associated with pain and limitation of arm movement. Affecting 6% of their
750 patients, the cause is surgical disruption of veins or lymphatics
proximally at the level of the axilla. AWS is a benign and self-limited
condition that should not be confused with lymphedema and does not require
treatment.
Sensory Morbidity
The sensory sequelae of both SLNB and ALND are largely related to the
division of sensory nerves, most notably the ICBN, a cutaneous sensory
branch of T2 that innervates the upper inner arm, axilla, and superolateral
breast. Technical modifications of ALND that allow preservation of the
ICBN are the subject of an enthusiastic but anecdotal literature. In the single
randomized trial comparing ICBN preservation versus division, ICBN
preservation reduced the size of the sensory deficit, but there were otherwise
no differences between groups in pain, shoulder movement, arm
circumference, or presence of neuromas on either 3-month (61) or 3-year
follow-up (62).
Three of the seven randomized trials report less sensory morbidity with
SLNB versus ALND. These and other studies confirm that (a) the sensory
morbidity of SLNB is not zero and (b) the sensory morbidity of both
operations diminishes over time.
Shoulder Function
Limitation in shoulder range of motion (ROM) is a side effect of ALND, with
two randomized trials reporting less limitation for SLNB versus ALND.
These and other studies confirm that shoulder ROM improves rapidly over
time, and recommend exercises to restore shoulder ROM are an essential
element of postoperative care.
Infection
Cellulitis of the arm, chest wall, or breast is a well-recognized but relatively
infrequent side effect of ALND, affecting about 10% of patients. Cellulitis
can arise de novo or following a nonsterile skin break but—as above—there
is no evidence that sterile skin punctures cause cellulitis or that avoidance is
preventive of either infection or lymphedema. Repeated episodes of infection
may increase the risk of lymphedema, and prompt treatment with oral or IV
antibiotics makes sense.
CONCLUSION
Looking ahead, the role of axillary surgery will continue to decline. First—
regarding prognostication—with the emergence of genomic profiling axillary
node status is no longer paramount; both the MINDACT (63) and Plan B (64)
trials demonstrate comparably high survival rates for node-negative and
node-positive patients with low genomic risk scores. Second—regarding
local control—with increasing use of neoadjuvant chemotherapy and
increasingly effective agents, SLNB will continue to displace ALND, and
rates of axillary recurrence will continue to decline. Finally, low-risk patients
may not need axillary staging at all: In the CALGB 9343 trial (65)—a
randomization of women over age 70 with low-risk breast cancers to breast
conservation with versus without breast RT—two-thirds did not have any
axillary staging, with no effect on 10-year survival and axillary LR in only
3%. In summary, more patients can avoid any axillary staging, SLNB will
continue to play a role where node status remains essential for planning local
and systemic therapy, and ALND will be fewer and more difficult—
increasingly limited to the salvage of chemotherapy-resistant and locally
recurrent disease.

REFERENCES

1. Power SD. The history of the amputation of the breast to 1904.


Liverpool Med Chir J 1934;52:49–56.
2. Halsted WS. I. The results of operations for the cure of cancer of the
breast performed at the Johns Hopkins hospital from June, 1889, to
January, 1894. Ann Surg 1894;20(5):497–555.
3. Halsted WS. I. The results of radical operations for the cure of
carcinoma of the breast. Ann Surg 1907;46(1):1–19.
4. Urban JA. Radical excision of the chest wall for mammary cancer.
Cancer 1951;4(6):1263–1285.
5. Patey DH, Dyson WH. The prognosis of carcinoma of the breast in
relation to the type of operation performed. Br J Cancer 1948;2(1):7–13.
6. Fisher B. Laboratory and clinical research in breast cancer—a personal
adventure: the David A. Karnofsky memorial lecture. Cancer Res
1980;40(11):3863–3874.
7. Fisher B, Jeong JH, Anderson S, et al. Twenty-five-year follow-up of a
randomized trial comparing radical mastectomy, total mastectomy, and
total mastectomy followed by irradiation. N Engl J Med
2002;347(8):567–575.
8. Fisher B, Anderson S, Bryant J, et al. Twenty-year follow-up of a
randomized trial comparing total mastectomy, lumpectomy, and
lumpectomy plus irradiation for the treatment of invasive breast cancer.
N Engl J Med 2002;347(16):1233–1241.
9. Hellman S, Weichselbaum RR. Oligometastases. J Clin Oncol
1995;13(1):8–10.
10. Early Breast Cancer Trialists’ Collaborative Group (EBCTCG). Effects
of chemotherapy and hormonal therapy for early breast cancer on
recurrence and 15-year survival: an overview of the randomised trials.
Lancet 2005;365(9472):1687–1717.
11. Early Breast Cancer Trialists’ Collaborative Group. Effects of
radiotherapy and surgery in early breast cancer. An overview of the
randomized trials. N Engl J Med 1995;333(22):1444–1455.
12. Clarke M, Collins R, Darby S, et al. Effects of radiotherapy and of
differences in the extent of surgery for early breast cancer on local
recurrence and 15-year survival: an overview of the randomised trials.
Lancet 2005;366(9503):2087–2106.
13. Cabanas RM. An approach for the treatment of penile carcinoma.
Cancer 1977;39(2):456–466.
14. Morton DL, Wen DR, Wong JH, et al. Technical details of
intraoperative lymphatic mapping for early stage melanoma. Arch Surg
1992;127(4):392–399.
15. Krag DN, Weaver DL, Alex JC, et al. Surgical resection and
radiolocalization of the sentinel lymph node in breast cancer using a
gamma probe. Surg Oncol 1993;2(6):335–339; discussion 340.
16. Giuliano AE, Kirgan DM, Guenther JM, et al. Lymphatic mapping and
sentinel lymphadenectomy for breast cancer. Ann Surg
1994;220(3):391–398; discussion 398–401.
17. Bromham N, Schmidt-Hansen M, Astin M, et al. Axillary treatment for
operable primary breast cancer. Cochrane Database Syst Rev
2017;1:CD004561.
18. Giuliano AE, Hunt KK, Ballman KV, et al. Axillary dissection vs no
axillary dissection in women with invasive breast cancer and sentinel
node metastasis: a randomized clinical trial. JAMA 2011;305(6):569–
575.
19. Giuliano AE, Ballman KV, McCall L, et al. Effect of axillary dissection
vs no axillary dissection on 10-year overall survival among women with
invasive breast cancer and sentinel node metastasis: the ACOSOG
Z0011 (alliance) randomized clinical trial. JAMA 2017;318(10):918–
926.
20. Galimberti V, Cole BF, Viale G, et al. Axillary dissection versus no
axillary dissection in patients with breast cancer and sentinel-node
micrometastases (IBCSG 23-01): 10-year follow-up of a randomised,
controlled phase 3 trial. Lancet Oncol 2018;19(10):1385–1393.
21. Clarke D, Newcombe RG, Mansel RE. The learning curve in sentinel
node biopsy: the ALMANAC experience. Ann Surg Oncol 2004;11(3
Suppl):211S–215S.
22. Pilewskie M, Mautner SK, Stempel M, et al. Does a positive axillary
lymph node needle biopsy result predict the need for an axillary lymph
node dissection in clinically node-negative breast cancer patients in the
ACOSOG Z0011 era? Ann Surg Oncol 2016;23(4):1123–1128.
23. van Deurzen CH, Vriens BE, Tjan-Heijnen VC, et al. Accuracy of
sentinel node biopsy after neoadjuvant chemotherapy in breast cancer
patients: a systematic review. Eur J Cancer 2009;45(18):3124–3130.
24. van Nijnatten TJ, Schipper RJ, Lobbes MB, et al. The diagnostic
performance of sentinel lymph node biopsy in pathologically confirmed
node positive breast cancer patients after neoadjuvant systemic therapy:
a systematic review and meta-analysis. Eur J Surg Oncol
2015;41(10):1278–1287.
25. Maaskant-Braat AJ, Voogd AC, Roumen RM, et al. Repeat sentinel
node biopsy in patients with locally recurrent breast cancer: a systematic
review and meta-analysis of the literature. Breast Cancer Res Treat
2013;138(1):13–20.
26. Ugras S, Matsen C, Eaton A, et al. Reoperative sentinel lymph node
biopsy is feasible for locally recurrent breast cancer, but is it
worthwhile? Ann Surg Oncol 2016;23(3):744–748.
27. Sado HN, Graf RM, Canan LW, et al. Sentinel lymph node detection
and evidence of axillary lymphatic integrity after transaxillary breast
augmentation: a prospective study using lymphoscintography. Aesthetic
Plast Surg 2008;32(6):879–888.
28. Munhoz AM, Ferreira MC. Re: implications of transaxillary breast
augmentation: lifetime probability for the development of breast cancer
and sentinel node mapping interference. Aesthetic Plast Surg
2007;31(4):320–321.
29. Cody HS 3rd, Fey J, Akhurst T, et al. Complementarity of blue dye and
isotope in sentinel node localization for breast cancer: univariate and
multivariate analysis of 966 procedures. Ann Surg Oncol 2001;8(1):13–
19.
30. Derossis AM, Fey J, Yeung H, et al. A trend analysis of the relative
value of blue dye and isotope localization in 2,000 consecutive cases of
sentinel node biopsy for breast cancer. J Am Coll Surg
2001;193(5):473–478.
31. Ahmed M, Purushotham AD, Douek M. Novel techniques for sentinel
lymph node biopsy in breast cancer: a systematic review. Lancet Oncol
2014;15(8):e351–e362.
32. Cody HS 3rd, Borgen PI. State-of-the-art approaches to sentinel node
biopsy for breast cancer: study design, patient selection, technique, and
quality control at Memorial Sloan-Kettering Cancer Center. Surg Oncol
1999;8(2):85–91.
33. McCarter MD, Yeung H, Yeh S, et al. Localization of the sentinel node
in breast cancer: identical results with same-day and day-before isotope
injection. Ann Surg Oncol 2001;8(8):682–686.
34. Povoski SP, Olsen JO, Young DC, et al. Prospective randomized clinical
trial comparing intradermal, intraparenchymal, and subareolar injection
routes for sentinel lymph node mapping and biopsy in breast cancer.
Ann Surg Oncol 2006;13(11):1412–1421.
35. Chagpar AB, Martin RC, Scoggins CR, et al. Factors predicting failure
to identify a sentinel lymph node in breast cancer. Surgery
2005;138(1):56–63.
36. Pesek S, Ashikaga T, Krag LE, et al. The false-negative rate of sentinel
node biopsy in patients with breast cancer: a meta-analysis. World J
Surg 2012;36(9):2239–2251.
37. Martin RC, Derossis AM, Fey J, et al. Intradermal isotope injection is
superior to intramammary in sentinel node biopsy for breast cancer.
Surgery 2001;130(3):432–438.
38. McCarter MD, Yeung H, Fey J, et al. The breast cancer patient with
multiple sentinel nodes: when to stop? J Am Coll Surg
2001;192(6):692–697.
39. Boughey JC, Suman VJ, Mittendorf EA, et al. Sentinel lymph node
surgery after neoadjuvant chemotherapy in patients with node-positive
breast cancer: the ACOSOG Z1071 (Alliance) clinical trial. JAMA
2013;310(14):1455–1461.
40. Kuehn T, Bauerfeind I, Fehm T, et al. Sentinel-lymph-node biopsy in
patients with breast cancer before and after neoadjuvant chemotherapy
(SENTINA): a prospective, multicentre cohort study. Lancet Oncol
2013;14(7):609–618.
41. Boileau JF, Poirier B, Basik M, et al. Sentinel node biopsy after
neoadjuvant chemotherapy in biopsy-proven node-positive breast
cancer: the SN FNAC study. J Clin Oncol 2015;33(3):258–264.
42. Hill AD, Tran KN, Akhurst T, et al. Lessons learned from 500 cases of
lymphatic mapping for breast cancer. Ann Surg 1999;229(4):528–535.
43. Montgomery LL, Thorne AC, Van Zee KJ, et al. Isosulfan blue dye
reactions during sentinel lymph node mapping for breast cancer. Anesth
Analg 2002;95(2):385–388.
44. Tan LK, Giri D, Hummer AJ, et al. Occult axillary node metastases in
breast cancer are prognostically significant: results in 368 node-negative
patients with 20-year follow-up. J Clin Oncol 2008;26(11):1803–1809.
45. Giuliano AE, Hawes D, Ballman KV, et al. Association of occult
metastases in sentinel lymph nodes and bone marrow with survival
among women with early-stage invasive breast cancer. JAMA
2011;306(4):385–393.
46. Weaver DL, Ashikaga T, Krag DN, et al. Effect of occult metastases on
survival in node-negative breast cancer. N Engl J Med 2011;364(5):412–
421.
47. Specht MC, Fey JV, Borgen PI, et al. Is the clinically positive axilla in
breast cancer really a contraindication to sentinel lymph node biopsy? J
Am Coll Surg 2005;200(1):10–14.
48. Mamtani A, Barrio AV, King TA, et al. How often does neoadjuvant
chemotherapy avoid axillary dissection in patients with histologically
confirmed nodal metastases? Results of a prospective study. Ann Surg
Oncol 2016;23(11):3467–3474.
49. Fisher B, Wolmark N, Bauer M, et al. The accuracy of clinical nodal
staging and of limited axillary dissection as a determinant of histologic
nodal status in carcinoma of the breast. Surg Gynecol Obstet
1981;152(6):765–772.
50. van der Ploeg IM, Nieweg OE, van Rijk MC, et al. Axillary recurrence
after a tumour-negative sentinel node biopsy in breast cancer patients: a
systematic review and meta-analysis of the literature. Eur J Surg Oncol
2008;34(12):1277–1284.
51. Goyal A, Newcombe RG, Chhabra A, et al. Morbidity in breast cancer
patients with sentinel node metastases undergoing delayed axillary
lymph node dissection (ALND) compared with immediate ALND. Ann
Surg Oncol 2008;15(1):262–267.
52. McLaughlin SA, Wright MJ, Morris KT, et al. Prevalence of
lymphedema in women with breast cancer 5 years after sentinel lymph
node biopsy or axillary dissection: objective measurements. J Clin
Oncol 2008;26(32):5213–5219.
53. Donker M, van Tienhoven G, Straver ME, et al. Radiotherapy or surgery
of the axilla after a positive sentinel node in breast cancer (EORTC
10981–22023 AMAROS): a randomised, multicentre, open-label, phase
3 non-inferiority trial. Lancet Oncol 2014;15(12):1303–1310.
54. Cemal Y, Pusic A, Mehrara BJ. Preventative measures for lymphedema:
separating fact from fiction. J Am Coll Surg 2011;213(4):543–551.
55. Singh B, Disipio T, Peake J, et al. Systematic review and meta-analysis
of the effects of exercise for those with cancer-related lymphedema.
Arch Phys Med Rehabil 2016;97(2):302–315.e13.
56. Siotos C, Sebai ME, Wan EL, et al. Breast reconstruction and risk of
arm lymphedema development: a meta-analysis. J Plast Reconstr
Aesthet Surg 2018;71(6):807–818.
57. Huang TW, Tseng SH, Lin CC, et al. Effects of manual lymphatic
drainage on breast cancer-related lymphedema: a systematic review and
meta-analysis of randomized controlled trials. World J Surg Oncol
2013;11:15.
58. Han C, Yang B, Zuo WS, et al. The feasibility and oncological safety of
axillary reverse mapping in patients with breast cancer: a systematic
review and meta-analysis of prospective studies. PLoS One
2016;11(2):e0150285.
59. Markkula SP, Leung N, Allen VB, et al. Surgical interventions for the
prevention or treatment of lymphoedema after breast cancer treatment.
Cochrane Database Syst Rev 2019;2:CD011433.
60. Moskovitz AH, Anderson BO, Yeung RS, et al. Axillary web syndrome
after axillary dissection. Am J Surg 2001;181(5):434–439.
61. Abdullah TI, Iddon J, Barr L, et al. Prospective randomized controlled
trial of preservation of the intercostobrachial nerve during axillary node
clearance for breast cancer. Br J Surg 1998;85(10):1443–1445.
62. Freeman SR, Washington SJ, Pritchard T, et al. Long term results of a
randomised prospective study of preservation of the intercostobrachial
nerve. Eur J Surg Oncol 2003;29(3):213–215.
63. Cardoso F, van’t Veer LJ, Bogaerts J, et al. 70-Gene signature as an aid
to treatment decisions in early-stage breast cancer. N Engl J Med
2016;375(8):717–729.
64. Gluz O, Nitz UA, Christgen M, et al. West German Study Group phase
III plan B trial: first prospective outcome data for the 21-gene recurrence
score assay and concordance of prognostic markers by central and local
pathology assessment. J Clin Oncol 2016;34(20):2341–2349.
65. Hughes KS, Schnaper LA, Bellon JR, et al. Lumpectomy plus tamoxifen
with or without irradiation in women age 70 years or older with early
breast cancer: long-term follow-up of CALGB 9343. J Clin Oncol
2013;31(19):2382–2387.
CHAPTER 27

Postneoadjuvant Axillary Assessment


and Management
CHRISTINA A. MINAMI | MELISSA L. PILEWSKIE
HISTORY
Standards in the surgical management of breast cancer were initially set in
landmark trials focused on upfront surgery. Over the years, however, studies
have demonstrated equivalent survival outcomes when comparing
neoadjuvant chemotherapy (NAC) with adjuvant chemotherapy (1), and have
highlighted the potential for NAC to limit the extent of surgery in the breast
and axilla (2–4). Moreover, a survival advantage has been shown with the
addition of adjuvant chemotherapy in certain patient populations who are
unable to achieve a pathologic complete response (pCR) after NAC (5),
resulting in a potential expansion in the utilization of NAC in women with
operable breast cancer. As the use of NAC in breast cancer patients grows, so
do the questions surrounding optimal management of the axilla.
In this chapter, we will discuss the feasibility, timing, and optimization of
sentinel lymph node biopsy (SLNB) after NAC in both initially clinically
node-negative (cN0) and clinically node-positive (cN+) patients. In addition,
we will address the optimal sequencing of treatment to avoid axillary lymph
node dissection (ALND), the prognostic implications of residual disease after
NAC, current indications for ALND, relative contraindications to SLNB, and
ongoing clinical trials in this area.
AXILLARY SURGERY IN CLINICALLY NODE-NEGATIVE PATIENTS

Feasibility and Timing of Sentinel Lymph Node Biopsy After


Neoadjuvant Chemotherapy
Initial concerns regarding the use of SLNB after NAC focused on the
theoretical lymphatic alterations secondary to treatment-related fibrosis and
the possibility of non-uniform therapeutic response in the axilla. These
factors would render the sentinel node an unreliable indictor of axillary nodal
status and result in an unacceptably high false-negative rate (FNR) (6). The
feasibility of SLNB, however, has been demonstrated in multiple early
studies (7), and while certain small studies demonstrated FNRs up to 33%
(8–10), larger studies have affirmed the accuracy of SLNB following NAC.
Hunt et al. (6) performed a large, single-center retrospective analysis of 3,746
cT1-3N0 patients who underwent SLNB from 1994 to 2007. Using blue dye,
Tc-labeled sulfur colloid, or a combination of the two, surgeons performed
sentinel lymph node (SLN) surgery after NAC in 575 (15.3%) of patients.
Successful identification of the SLN was slightly lower in the NAC group
when compared to the surgery-first group (97.4% vs. 98.7%, respectively [p
= 0.02]). There was no significant difference in the FNR between the two
groups, with an FNR of 4.1% in the surgery-first group, and 5.9% FNR in the
NAC group (p = 0.39). Prospective, multicenter data are also available from
the GANEA trial (11), which enrolled 195 patients, the majority of whom
had T2 or T3 disease, and included both cN0 and cN1 patients. After NAC,
the detection rate among the cN0 patients was 94.6%, with the FNR just
under 10% (9.4%). High identification rates coupled with low FNRs have
also been borne out in large meta-analyses, with identification rates ranging
from 90% to 94% and FNRs ranging from 7% to 12% among cN0 patients
undergoing SLNB following NAC (12–15).
With the feasibility of SLNB after NAC established, the timing of SLNB
has also been questioned. It has been argued that pre-NAC SLNB provides
accurate axillary staging, separating node-negative patients who can avoid
ALND and axillary radiation, from node-positive patients, who may benefit
from adjuvant radiation therapy (RT). Negative SLNB prior to NAC has been
shown to accurately predict a pathologically negative axilla after NAC (16),
but performing SLNB prior to NAC has several drawbacks: patients are
subjected to an additional surgical procedure, NAC would be delayed to
allow for wound healing, and, perhaps most importantly, a positive pre-NAC
SLNB obviates the possible avoidance of an ALND in the setting of a
complete axillary response.
Nodal Positivity Rates and Axillary Recurrences After NAC
Studies consistently report lower rates of nodal positivity among cN0 patients
undergoing axillary surgery following NAC when compared to upfront
surgery, highlighting the ability of NAC to downstage microscopic axillary
disease. The National Surgical Adjuvant Breast and Bowel Project (NSABP)
B-18 trial enrolled almost 1,100 cN0 patients to compare preoperative versus
postoperative chemotherapy (doxorubicin and cyclophosphamide [AC]),
finding 33% of patients were pathologically node positive after NAC
compared to 48% of women undergoing upfront surgery (p < 0.001) (17).
Similarly, NSABP B-27, which examined the addition of preoperative or
postoperative docetaxel (T) to preoperative AC, found 40% nodal positivity
in the group undergoing preoperative ACT versus 49% nodal positivity in the
group undergoing preoperative AC and postoperative T (p < 0.001) (18).
Hunt et al. also reported a significant decrease in nodal positivity rates after
NAC versus upfront surgery in cN0 patients in their single-center experience,
although the greatest benefit was seen in patients with T2 and T3 tumors (6%
decrease in T1 tumors, 16% decrease in T2 tumors, 21% in T3 tumors)
(Table 27-1) (6).
SENTinel NeoAdjuvant (SENTINA), a multicenter randomized clinical
trial, included both cN0 and node-positive patients. Patients who were
initially cN0 underwent SLNB (with radiocolloid alone, blue dye alone, or
both) prior to NAC; those found to be pathologically node negative did not
undergo any further axillary surgery (n = 662), while those with a positive
SLNB underwent a repeat SLNB and ALND after NAC (n = 360). In stark
contrast to results from a previous smaller study, which demonstrated a
detection rate of 97% and an FNR of 4.5% (19), the repeat-SLNB arm after
NAC had a disappointing overall SLN detection rate of 60.8% and an FNR of
51.6% (20), results too poor to support attempts at repeat SLNB among those
with an upfront microscopically positive SLN. The latest edition of the
National Comprehensive Cancer Network (NCCN) guidelines recommends
that in cN0 patients, SLNB should preferably be performed after preoperative
systemic therapy (21).

TABLE 27-1 Nodal Positivity Rates Among cN0 Patients Undergoing


Upfront Surgery Versus Post-NAC
Study Upfront Surgery NAC (%) P-value
(%)
NSABP B-18 48 33 <0.001
(17)
NSABP B-27 49 40 <0.001
(18)
University of 0.04
Texas MD
Anderson
Cancer Center
study (6)
T1 19 13
T2 37 21
T3 51 30
NAC, neoadjuvant chemotherapy; NSABP, National Surgical Adjuvant Breast and Bowel Project.

While these data speak to the technical feasibility and optimal timing of
SLNB, the oncologic safety and possible sequelae of a false-negative SLNB
must also be considered. It stands to reason that a false-negative SLNB
following NAC may have differing oncologic repercussions compared to
patients treated with upfront surgery, given that axillary disease left in situ
following NAC is uniquely chemotherapy resistant. Existing studies,
however, have failed to bear out this concern. Hunt et al. found a 1.2%
regional recurrence rate at a median follow-up of 47 months in node-negative
patients undergoing SLNB alone after NAC, as compared to a 0.9%
recurrence rate in patients undergoing SLNB prior to NAC (6). Smaller
studies following cN0 women treated with SLNB alone after NAC have also
failed to note any axillary recurrences at a median follow-up of more than 4
years (22,23). These data support the use of SLNB alone following NAC in
patients who are both clinically and pathologically node negative. The
standard of care remains to proceed with a completion ALND for any
positive SLN identified after NAC.
Strategies to Avoid Axillary Lymph Node Dissection
Use of NAC is now one strategy to minimize the likelihood of requiring an
ALND among early-stage breast cancer patients. Axillary downstaging has
been well documented in large studies, with rates ranging from 35% to 63%
(24–26), although given variable nodal response to chemotherapy by receptor
profile, the ability to downstage microscopic axillary disease expectedly
differs by tumor subtype. Table 27-2 shows rates of nodal pCR among
women with biopsy-proven nodal metastases broken down by tumor receptor
profile. The highest rates of nodal pCR are seen in HER2+ tumors (65% to
97%), while the lowest rates are in HR+/HER2- cancers (21%), with triple
negative pCR rates in between (47% to 49%) (24,27).
To minimize the risk of ALND in early-stage breast cancer patients,
practitioners should understand how this differential response to NAC by
disease subtype can affect surgical decision making. In a retrospective
analysis of a Memorial Sloan Kettering Cancer Center cohort of cT1-2N0
patients, factors associated with the likelihood of undergoing ALND in
patients who received upfront surgery (breast-conserving surgery [BCS] or
mastectomy) or NAC were examined (30). As per American College of
Surgeons Oncology Group (ACOSOG) Z0011 criteria, patients in the upfront
BCS cohort underwent ALND if they had ≥3 positive SLNs. In the upfront
mastectomy group, patients underwent ALND for any axillary micro- or
macrometastases, but not for isolated tumor cells (ITCs). In the post-NAC
group, ALND was indicated for any evidence of nodal disease, including
ITCs, and if ≥3 negative SLNs were not identified. Rates of ALND were
found to be lower in estrogen receptor (ER)+/progesterone receptor (PR)+
HER2 patients undergoing upfront BCS versus those who underwent NAC
(15% vs. 34% respectively, p < 0.001), given the low rate of nodal pCR
experienced in patients with this tumor profile. However, when comparing
management with upfront mastectomy to NAC, patients with triple-negative
breast cancer (TNBC) or HER2+ disease, subtypes with a much greater
likelihood of achieving a nodal pCR, ALND rates were significantly lower
following NAC. This speaks against the use of NAC for early-stage
ER+/PR+, HER2- tumors solely for microscopic nodal downstaging, while
supporting its use in appropriate patients with TNBC and HER2+ tumors.

TABLE 27-2 Nodal pCR Rates After NAC: Overall and by Tumor Subtype
AXILLARY SURGERY IN CLINICALLY NODE-POSITIVE PATIENTS

Feasibility and Optimization of SLNB Following NAC


Lymphedema rates are substantially lower following SLNB compared to
ALND (5% vs. 15% to 30%, respectively) (31,32). Given this substantial
difference in surgical morbidity, there has been growing interest in
identifying patient populations who could safely be managed with an SLNB
alone. Although historical management of cN+ disease involved an ALND,
studies have shown that 35% to 50% of these patients convert to being
pathologically node negative, and may be spared the morbidity of a
dissection (see Table 27-2).
Studies have thus sought to leverage the benefits of systemic therapy to de-
escalate axillary surgery. An early study of SLNB after NAC in cN+ patients
reported an identification rate of 93%, but an unacceptably high FNR of 25%
(33). However, three prospective, multi-institutional trials, primarily
including cN1 patients, have subsequently reported on the feasibility and
accuracy of SLNB following NAC: the SENTINA trial, the ACOSOG Z1071
trial, and the Sentinel Node Biopsy Following Neoadjuvant Chemotherapy
(SN-FNAC) trial (Table 27-3). SENTINA, as previously discussed, had both
clinical node-negative and node-positive trial arms. Node-positive (defined as
cN1 or cN2, as determined by examination and imaging—histologic
confirmation was not required) patients who converted to cN0 after NAC
underwent SLNB and ALND (n = 592), while those who remained cN+
underwent ALND alone (n = 123). The overall SLN detection rate was
relatively low at 80.1%, but differed significantly by mapping techniques:
detection was 77.4% with radiocolloid alone, while it was 87.8% with
radiocolloid and blue dye. The overall FNR was 14.2%, but dual-tracer
mapping resulted in an FNR of 8.6% versus 16.0% for radiocolloid alone. An
FNR of 7.3% was reported if ≥3 SLNs were identified. On multivariate
analysis, the use of dual tracer was significantly associated with a higher
detection rate (p = 0.05). On multivariate analysis of factors associated with
FNR, dual tracer did not result in significantly lower FNR rates (p = 0.15),
but number of SLNs taken did (p = 0.01) (20).
TABLE 27-3 Post-NAC SLN Identification Rates and False-Negative Rates
in Post-NAC Patients
ACOSOG Z1071 SN-FNAC (25) SENTINA (20)
(34) (%) (%) (%)
Overall 92.7 87.6 80.1
Identification
Rate
Overall FNR 12.6 13.3 14.2
FNR by
Mapping
Method
Single Tracer 20.3 16.0 16.0
Dual Tracer 10.8 5.2 8.6
FNR by Number
of SLNs
Removed
1 SLN Removed N/A 18.2 24.3
2 SLNs Removed 21.1 4.9a 18.5
≥3 SLNs 9.1 N/A 7.3
Removed
aFNR with ≥2 SLNs removed.
NAC, neoadjuvant chemotherapy; SLN, sentinel lymph node; ACOSOG, American College of
Surgeons Oncology Group; SN-FNAC, Sentinel Node Biopsy Following Neoadjuvant Chemotherapy;
SENTINA, SENTinel NeoAdjuvant; FNR, false-negative rate.

ACOSOG Z1071 also aimed to assess the use of SLNB in post-NAC


patients, with slightly different inclusion criteria (35). Patients could have
cT0–4 disease, and nodal disease had to be confirmed by fine-needle
aspiration (FNA) or core needle biopsy. A total of 663 women with cN1
disease and 38 women with cN2 disease underwent NAC followed by
surgery. After NAC, patients underwent SLNB and ALND regardless of
clinical nodal status, with 83% of patients converting to cN0 while 13%
remained cN+ with palpable adenopathy (4% had unknown post-NAC
clinical axillary status). The overall detection rate of at least one SLN was
92.7%. To be included in the FNR calculation, patients had to have at least
two SLNs removed. Overall FNR was 12.6% (failing to meet the predefined
10% threshold), but in exploratory analyses, dual-tracer mapping resulted in
10.8% FNR as compared to 20.3% with single-agent mapping. If three or
more SLNs were removed, the FNR fell to 9.1%. Number of SLNs removed
(2 vs. ≥3) remained the only significant factor associated with a lower FNR
on multivariate analysis.
SN-FNAC was a phase II trial that included cT0–3 patients with biopsy-
proven cN1–2 disease who underwent post-NAC physical examination and
axillary ultrasound; conversion to node-negative status was not required (25).
All sentinel nodes underwent hematoxylin and eosin (H&E) staining and, if
negative, immunohistochemistry (IHC) was required. Sample size was based
on an expected FNR of 10%, but the trial closed early after interim analysis
results were found to be comparable to results of the similarly designed
ACOSOG Z1071 trial, which were reported when SN-FNAC was at 51%
accrual. A total of 153 patients were ultimately included in the final analysis,
with an overall detection rate of 87.6%. The overall FNR was 13.3%,
although when ITCs were considered positive, the FNR fell to 9.6%. This
trial underscored the fact that the size of residual nodal disease in the SLNB
after NAC is not necessarily indicative of the burden of residual disease, as
57% of patients with only ITCs in the SLN had positive non-SLNs. Similar to
the aforementioned trials, SN-FNAC also found that the number of SLNs
removed had a significant bearing on the FNR, reporting an FNR of 4.9%
when ≥2 SLNs were removed.
Despite the fact that these trials had overall FNRs exceeding 10%, the
decrease in FNRs when specific criteria were applied (i.e., the use of dual-
tracer mapping and removal of at least three SLNs) suggests that SLNB after
NAC is feasible with an acceptable FNR with certain technical
considerations.
Other techniques have been suggested to optimize post-NAC SLNB, such
as clipping or tattooing of the positive axillary node at the time of initial
FNA, followed by localizing techniques using wires or radioactive seeds to
aid in ensuring removal of the marked node at the time of surgery. Excising
clipped nodes may reduce the FNR, as studies have shown that the clip is not
in an SLN in up to 24% of cases (36,37). Excising the clipped node in the
ACOSOG Z1071 population resulted in a 6.8% FNR. Caudle et al. also
demonstrated a reduction in the FNR from 10.0% to 1.4% with the addition
of the clipped node in the SLNB specimen (37). Using a 125I-labeled
radioactive seed, Diego et al. found that 9% of clipped nodes did not have
any blue dye or radioactive colloid. Their group was able to localize 29 of 30
clipped nodes, finding that all patients with residual axillary disease had
disease in their clipped nodes (26). Wire localization has also been proposed
(38), as one study found that wire localization in patients who had undergone
NAC resulted in a 97% rate of clipped lymph node (LN) removal as
compared to 83% of non–wire-localized clipped LNs.
Tattooing the positive LN at the time of biopsy, which does not require an
additional localizing procedure, has also been explored. In a single-institution
study using Spot® (GI Supply, Camp Hill, PA), all 12 patients who had
undergone NAC and who were tattooed at the time of biopsy had their
tattooed node successfully identified. The tattooed node corresponded to an
SLN in all post-NAC patients (29). In a study of 20 patients in Korea, all
charcoal-tattooed LNs were excised and 2 patients had a positive charcoal-
tattooed node in the absence of positive SLNs (29).
Although excision of the biopsy-proven positive marked axillary node is
attractive in principle, there are several drawbacks that emerge in practice.
The additional localization procedure can represent significant challenges,
particularly with displaced or non-visualized clips within the axilla at the
time of the localization procedure (40). Furthermore, there is questionable
incremental benefit to retrieval of a clipped node when additional techniques
(for example, removal of three or more SLNs) are utilized during the SLNB
procedure. Identification of treatment effect within an SLN represents an
additional strategy to ensure retrieval of a previously positive LN. Rates of
nodal treatment effect from SLNB performed following NAC are high
without preoperative nodal marking (88% in patients with ≥3 SLNs
retrieved); however, up to 3% of patients who undergo ALND have no
treatment effect seen (41).
The above-mentioned techniques represent methods to optimize the SLNB
procedure when performed in women who have converted from cN1 to cN0
following NAC. Use of these techniques can 1) minimize the FNR and 2)
potentially spare patients without residual nodal disease the morbidity of an
ALND. Mamtani et al. (27) quantified rates of axillary downstaging by tumor
subtype in 195 patients with biopsy-proven cN1 disease treated with NAC.
Those who were cN0 after neoadjuvant treatment were eligible for SLNB.
ALND was performed in patients who failed to map, had fewer than three
negative SLNs retrieved, or had any axillary disease on pathologic review. A
total of 85% of the node-positive patients in this cohort became eligible for
SLNB after NAC, and, overall, 48% of patients avoided ALND. Pathologic
compete response rates differed significantly by tumor subtype: ER+/HER2−
(21%), ER+/HER2+ (70%), ER−/HER2+ (97%), and ER−/HER2− (47%)
(see Table 27-2).
Management of Residual Nodal Disease
It is well established that in the upfront surgery setting, not all residual
disease manifests as clinically significant recurrences, and despite FNRs of
up to 10%, SLNB alone in patients with limited axillary disease results in
axillary failure rates of <1% (42–44). Rates of axillary failure in patients who
undergo SLNB alone after conversion from being cN1 to cN0 after NAC
have yet to be fully determined. Data from small retrospective studies report
similar, low axillary failure rates in this population (23,45), but more robust
follow-up data are necessary. Recurrence data are not available from the
aforementioned large prospective trials that have determined SLNB FNRs in
the post-NAC setting, as all patients underwent ALND.
While long-term data are lacking on the recurrence rates of women who
obtain a nodal pCR, it is known that the presence of residual nodal disease
post-NAC is associated with worse outcomes and higher rates of locoregional
recurrence (LRR). Data from NSABP B-18 and B-27 show that residual
disease in the breast and axilla after NAC is a greater predictor of LRR than
pretreatment stage. In a review of 3,088 women from these trials, among
those who were cN0 treated with BCS following NAC, 10-year regional
recurrence rates were ≤2% regardless of final pathologic status. Among cN+
patients, those who achieved a pCR had similar low regional recurrence rates
of <2%, but those with residual nodal disease had regional recurrence rates
approaching 9%. Among mastectomy patients, failure to achieve nodal pCR
was the strongest predictor of 10-year LRR (hazard ratio [HR] 4.5, 95%
confidence interval [CI] 1.6 to 12.2, p < 0.001) (46). These results support the
use of more-aggressive locoregional therapy among women with residual
nodal disease following NAC.
Omitting axillary dissection in patients with microscopic disease in an
SLNB after NAC has thus far not been supported by existing data. SN-FNAC
showed that the burden of disease in the SLN was not indicative of volume of
disease in non-SLNs. Fifty-seven percent of patients with ITCs, 38% of
patients with micrometastases, and 56% of patients with macrometastases
had disease in at least one non-SLN (25). Similarly, a retrospective study of
702 patients undergoing SLNB after NAC found 17% of patients with ITCs,
64% with micrometastases, and 62% of those with macrometastases had
additional non-SLN metastases on ALND (47). While the numbers of
patients with SLN ITCs alone in these studies were small (6 and 7,
respectively), the high rates of non-SLN positivity in patients with
micrometastases and macrometastases support completion ALND in the
setting of residual low-volume nodal disease after NAC. Ongoing trials will
further evaluate the appropriate axillary management among women with
microscopic nodal disease identified in the post-NAC setting.
CURRENT INDICATIONS FOR ALND AFTER NAC
While the treatment paradigm is shifting in the management of patients who
convert from cN1 to cN0 following NAC, patients with persistently positive
axillary nodes by clinical evaluation, those with any residual nodal
metastasis, or those who fail to map should proceed with an ALND for
axillary staging. ALND also remains appropriate in situations in which an
optimal SLNB has not been achieved, either through failure to retrieve three
or more SLNs, or a clipped node.
The majority of data examining the use of SLNB after NAC applies only to
patients presenting with cT1-3N0-1 disease. Only a small percentage of cN2
patients were included in the prospective trials evaluating SLNB in node-
positive patients (6% in SN-FNAC, 5% in ACOSOG Z1071). Extrapolating
the results of these studies to N2/N3 patients should thus be avoided, and
ALND should be undertaken in this population. In addition, cT4 and
inflammatory breast cancers have been excluded from all major trials, and
convincing evidence that SLNB may be feasible and accurate in locally
advanced cancers is currently lacking. Data will be forthcoming from a
prospective study examining accuracy of SLNB in patients with cT4 and/or
cN2/N3 disease with excellent response to chemotherapy and conversion to a
clinically negative axillary examination following NAC (48).
ONGOING STUDIES
Although full discussion of regional axillary nodal RT is beyond the scope of
this chapter, the future management of the post-NAC axilla requires
exploration of the optimal combination of both RT and surgery. While the
European Organisation for Research and Treatment of Cancer AMAROS trial
demonstrated that axillary nodal RT represents a safe alternative to ALND in
cT1–2 patients with one or two positive SLNs with primary surgery (49), it is
unclear what role axillary nodal RT should play in the post-NAC axilla. Data
from two ongoing randomized trials will help to answer this question.
The NSABP B-51 trial is a randomized phase III study examining the
impact of nodal RT in cT1-3N1 patients with biopsy-proven nodal metastases
who undergo NAC. Patients who have definitive surgery post-NAC and those
with pathologically negative nodes (by either ALND or SLNB +/− ALND)
are eligible. Women are then randomized to regional nodal RT versus no
regional nodal RT. The primary aim of this study is to evaluate the impact of
regional nodal RT on breast cancer events in patients who convert from node
positive to node negative following NAC (50).
The role of ALND and RT among persistently node-positive patients is the
focus of Alliance A011202, a randomized phase III trial comparing ALND
and regional nodal RT to axillary nodal RT alone in patients presenting with
cT1-3N1 disease. Women who convert from cN+ to cN0 but who have a
pathologically positive SLN after NAC are enrolled. The primary outcome is
invasive breast cancer recurrence-free interval, with secondary outcomes
including overall survival, ipsilateral/local/regional invasive breast cancer
recurrence, and development of arm and breast lymphedema (51).
CONCLUSION
Among cN0 patients, SLNB following NAC is feasible, has FNRs
comparable with those in patients undergoing upfront surgery, and, if
negative, is associated with a low rate of nodal recurrence. In patients who
convert from cN1 at presentation to cN0 following NAC, an optimized SLNB
is being used with increasing frequency in attempts to avoid ALND among
those with a complete nodal response. Long-term follow-up is necessary to
document nodal recurrence rates among patients who achieve a nodal pCR
following NAC and managed with SLNB alone. Ongoing trials are assessing
the optimal use of axillary surgery and nodal RT to better personalize axillary
management and minimize treatment-related harm.

REFERENCES

1. Rastogi P, Anderson SJ, Bear HD, et al. Preoperative chemotherapy:


updates of national surgical adjuvant breast and bowel project protocols
B-18 and B-27. J Clin Oncol 2008;26:778–785.
2. Golshan M, Cirrincione CT, Sikov WM, et al. Impact of neoadjuvant
chemotherapy in stage II-III triple negative breast cancer on eligibility
for breast-conserving surgery and breast conservation rates: surgical
results from CALGB 40603 (Alliance). Ann Surg 2015;262:434–439;
discussion 438–439.
3. Wolmark N, Wang J, Mamounas E, et al. Preoperative chemotherapy in
patients with operable breast cancer: nine-year results from national
surgical adjuvant breast and bowel project B-18. J Natl Cancer Inst
Monogr 2001;(30):96–102.
4. van der Hage JA, van de Velde CJ, Julien JP, et al. Preoperative
chemotherapy in primary operable breast cancer: results from the
European Organization for Research and Treatment of Cancer trial
10902. J Clin Oncol 2001;19:4224–4237.
5. Masuda N, Lee SJ, Ohtani S, et al. Adjuvant capecitabine for breast
cancer after preoperative chemotherapy. N Engl J Med 2017;376:2147–
2159.
6. Hunt KK, Yi M, Mittendorf EA, et al. Sentinel lymph node surgery after
neoadjuvant chemotherapy is accurate and reduces the need for axillary
dissection in breast cancer patients. Ann Surg 2009;250:558–566.
7. Geng C, Chen X, Pan X, et al. The feasibility and accuracy of sentinel
lymph node biopsy in initially clinically node-negative breast cancer
after neoadjuvant chemotherapy: a systematic review and meta-analysis.
PLoS One 2016;11:e0162605.
8. Nason KS, Anderson BO, Byrd DR, et al. Increased false negative
sentinel node biopsy rates after preoperative chemotherapy for invasive
breast carcinoma. Cancer 2000;89:2187–2194.
9. Piato JR, Barros AC, Pincerato KM, et al. Sentinel lymph node biopsy
in breast cancer after neoadjuvant chemotherapy. A pilot study. Eur J
Surg Oncol 2003;29:118–120.
10. Kinoshita T. Sentinel lymph node biopsy is feasible for breast cancer
patients after neoadjuvant chemotherapy. Breast Cancer 2007;14:10–15.
11. Classe JM, Bordes V, Campion L, et al. Sentinel lymph node biopsy
after neoadjuvant chemotherapy for advanced breast cancer: results of
Ganglion Sentinelle et Chimiotherapie Neoadjuvante, a French
prospective multicentric study. J Clin Oncol 2009;27:726–732.
12. Xing Y, Foy M, Cox DD, et al. Meta-analysis of sentinel lymph node
biopsy after preoperative chemotherapy in patients with breast cancer.
Br J Surg 2006;93:539–546.
13. van Deurzen CH, Vriens BE, Tjan-Heijnen VC, et al. Accuracy of
sentinel node biopsy after neoadjuvant chemotherapy in breast cancer
patients: a systematic review. Eur J Cancer 2009;45:3124–3130.
14. Kelly AM, Dwamena B, Cronin P, et al. Breast cancer sentinel node
identification and classification after neoadjuvant chemotherapy—
systematic review and meta analysis. Acad Radiol 2009;16:551–563.
15. Tan VK, Goh BK, Fook-Chong S, et al. The feasibility and accuracy of
sentinel lymph node biopsy in clinically node-negative patients after
neoadjuvant chemotherapy for breast cancer—a systematic review and
meta-analysis. J Surg Oncol 2011;104:97–103.
16. Schrenk P, Tausch C, Wolfl S, et al. Sentinel node mapping performed
before preoperative chemotherapy may avoid axillary dissection in
breast cancer patients with negative or micrometastatic sentinel nodes.
Am J Surg 2008;196:176–183.
17. Fisher B, Brown A, Mamounas E, et al. Effect of preoperative
chemotherapy on local-regional disease in women with operable breast
cancer: findings from National Surgical Adjuvant Breast and Bowel
Project B-18. J Clin Oncol 1997;15:2483–2493.
18. Bear HD, Anderson S, Brown A, et al. The effect on tumor response of
adding sequential preoperative docetaxel to preoperative doxorubicin
and cyclophosphamide: preliminary results from National Surgical
Adjuvant Breast and Bowel Project Protocol B-27. J Clin Oncol
2003;21:4165–4174.
19. Khan A, Sabel MS, Nees A, et al. Comprehensive axillary evaluation in
neoadjuvant chemotherapy patients with ultrasonography and sentinel
lymph node biopsy. Ann Surg Oncol 2005;12:697–704.
20. Kuehn T, Bauerfeind I, Fehm T, et al. Sentinel-lymph-node biopsy in
patients with breast cancer before and after neoadjuvant chemotherapy
(SENTINA): a prospective, multicentre cohort study. Lancet Oncol
2013;14:609–618.
21. EORTC Breast Cancer Cooperative Group; EORTC Radiotherapy
Group; Bijker N, Meijnen P, Peterse JL, et al. Breast-conserving
treatment with or without radiotherapy in ductal carcinoma-in-situ: ten-
year results of European Organisation for Research and Treatment of
Cancer randomized phase III trial 10853—a study by the EORTC Breast
Cancer Cooperative Group and EORTC Radiotherapy Group. J Clin
Oncol 2006;24:3381–3387.
22. Dauphine C, Nemtsev D, Rosing D, et al. Axillary recurrence after
sentinel lymph node biopsy for breast cancer. Am Surg 2010;76:1127–
1129.
23. Nogi H, Uchida K, Mimoto R, et al. Long-term follow-up of node-
negative breast cancer patients evaluated via sentinel node biopsy after
neoadjuvant chemotherapy. Clin Breast Cancer 2017;17:644–649.
24. Boughey JC, McCall LM, Ballman KV, et al. Tumor biology correlates
with rates of breast-conserving surgery and pathologic complete
response after neoadjuvant chemotherapy for breast cancer: findings
from the ACOSOG Z1071 (Alliance) Prospective Multicenter Clinical
Trial. Ann Surg 2014;260:608–614; discussion 614–616.
25. Boileau JF, Poirier B, Basik M, et al. Sentinel node biopsy after
neoadjuvant chemotherapy in biopsy-proven node-positive breast
cancer: the SN FNAC study. J Clin Oncol 2015;33:258–264.
26. Diego EJ, McAuliffe PF, Soran A, et al. Axillary staging after
neoadjuvant chemotherapy for breast cancer: a pilot study combining
sentinel lymph node biopsy with radioactive seed localization of pre-
treatment positive axillary lymph nodes. Ann Surg Oncol 2016;23:1549–
1553.
27. Mamtani A, Barrio AV, King TA, et al. How often does neoadjuvant
chemotherapy avoid axillary dissection in patients with histologically
confirmed nodal metastases? Results of a prospective study. Ann Surg
Oncol 2016;23:3467–3474.
28. Enokido K, Watanabe C, Nakamura S, et al. Sentinel lymph node biopsy
after neoadjuvant chemotherapy in patients with an initial diagnosis of
cytology-proven lymph node-positive breast cancer. Clin Breast Cancer
2016;16:299–304.
29. Choy N, Lipson J, Porter C, et al. Initial results with preoperative
tattooing of biopsied axillary lymph nodes and correlation to sentinel
lymph nodes in breast cancer patients. Ann Surg Oncol 2015;22:377–
382.
30. Pilewskie M, Morrow M. Axillary nodal management following
neoadjuvant chemotherapy: a review. JAMA Oncol 2017;3:549–555.
31. McLaughlin SA, Wright MJ, Morris KT, et al. Prevalence of
lymphedema in women with breast cancer 5 years after sentinel lymph
node biopsy or axillary dissection: objective measurements. J Clin
Oncol 2008;26:5213–5219.
32. Ashikaga T, Krag DN, Land SR, et al. Morbidity results from the
NSABP B-32 trial comparing sentinel lymph node dissection versus
axillary dissection. J Surg Oncol 2010;102:111–118.
33. Shen J, Gilcrease MZ, Babiera GV, et al. Feasibility and accuracy of
sentinel lymph node biopsy after preoperative chemotherapy in breast
cancer patients with documented axillary metastases. Cancer
2007;109:1255–1263.
34. Boughey JC, Suman VJ, Mittendorf EA, et al. Factors affecting sentinel
lymph node identification rate after neoadjuvant chemotherapy for
breast cancer patients enrolled in ACOSOG Z1071 (Alliance). Ann Surg
2015;261:547–552.
35. Boughey JC, Suman VJ, Mittendorf EA, et al. Sentinel lymph node
surgery after neoadjuvant chemotherapy in patients with node-positive
breast cancer: the ACOSOG Z1071 (Alliance) clinical trial. JAMA
2013;310:1455–1461.
36. Boughey JC, Ballman KV, Le-Petross HT, et al. Identification and
resection of clipped node decreases the false-negative rate of sentinel
lymph node surgery in patients presenting with node-positive breast
cancer (T0-T4, N1-N2) who receive neoadjuvant chemotherapy: results
from ACOSOG Z1071 (Alliance). Ann Surg 2016;263:802–807.
37. Caudle AS, Yang WT, Krishnamurthy S, et al. Improved axillary
evaluation following neoadjuvant therapy for patients with node-positive
breast cancer using selective evaluation of clipped nodes:
implementation of targeted axillary dissection. J Clin Oncol
2016;34:1072–1078.
38. Plecha D, Bai S, Patterson H, et al. Improving the accuracy of axillary
lymph node surgery in breast cancer with ultrasound-guided wire
localization of biopsy proven metastatic lymph nodes. Ann Surg Oncol
2015;22:4241–4246.
39. Park S, Koo JS, Kim GM, et al. Feasibility of charcoal tattooing of
cytology-proven metastatic axillary lymph node at diagnosis and
sentinel lymph node biopsy after neoadjuvant chemotherapy in breast
cancer patients. Cancer Res Treat 2017;3:801–812.
40. Hartmann S, Reimer T, Gerber B, et al. Wire localization of clip-marked
axillary lymph nodes in breast cancer patients treated with primary
systemic therapy. Eur J Surg Oncol 2018;44:1307–1311.
41. Barrio AV, Mamtani A, Edelweiss M, et al. How often is treatment
effect identified in axillary nodes with a pathologic complete response
after neoadjuvant chemotherapy? Ann Surg Oncol 2016;23:3475–3480.
42. Morrow M, Van Zee KJ, Patil S, et al. Axillary dissection and nodal
irradiation can be avoided for most node-positive Z0011-eligible breast
cancers: a prospective validation study of 793 patients. Ann Surg
2017;266:457–462.
43. Giuliano AE, Hunt KK, Ballman KV, et al. Axillary dissection vs no
axillary dissection in women with invasive breast cancer and sentinel
node metastasis: a randomized clinical trial. JAMA 2011;305:569–575.
44. Galimberti V, Cole BF, Viale G, et al. Axillary dissection versus no
axillary dissection in patients with breast cancer and sentinel-node
micrometastases (IBCSG 23-01): 10-year follow-up of a randomised,
controlled phase 3 trial. Lancet Oncol 2018;19:1385–1393.
45. Kang YJ, Han W, Park S, et al. Outcome following sentinel lymph node
biopsy-guided decisions in breast cancer patients with conversion from
positive to negative axillary lymph nodes after neoadjuvant
chemotherapy. Breast Cancer Res Treat 2017;166:473–480.
46. Mamounas EP, Anderson SJ, Dignam JJ, et al. Predictors of
locoregional recurrence after neoadjuvant chemotherapy: results from
combined analysis of National Surgical Adjuvant Breast and Bowel
Project B-18 and B-27. J Clin Oncol 2012;30:3960–3966.
47. Moo TA, Edelweiss M, Hajiyeva S, et al. Is low-volume disease in the
sentinel node after neoadjuvant chemotherapy an indication for axillary
dissection? Ann Surg Oncol 2018;25:1488–1494.
48. Vargas C, Kestin L, Go N, et al. Factors associated with local recurrence
and cause-specific survival in patients with ductal carcinoma in situ of
the breast treated with breast-conserving therapy or mastectomy. Int J
Radiat Oncol Biol Phys 2005;63:1514–1521.
49. Donker M, van Tienhoven G, Straver ME, et al. Radiotherapy or surgery
of the axilla after a positive sentinel node in breast cancer (EORTC
10981–22023 AMAROS): a randomised, multicentre, open-label, phase
3 non-inferiority trial. Lancet Oncol 2014;15:1303–1310.
50. Standard or comprehensive radiation therapy in treating patients with
early-stage breast cancer previously treated with chemotherapy and
surgery. https://clinicaltrials.gov/ct2/show/NCT01872975.
51. Cutuli B, Cohen-Solal-le Nir C, de Lafontan B, et al. Breast-conserving
therapy for ductal carcinoma in situ of the breast: the French Cancer
Centers’ experience. Int J Radiat Oncol Biol Phys 2002;53:868–879.
CHAPTER 28

Alternative Methods for Axillary


Sentinel Lymph Node Dissection
STEPHANIE A. VALENTE | STEPHEN R. GROBMYER
HISTORY
Axillary lymphatic mapping for sentinel node (SN) biopsy is the standard
procedure for the surgical staging of patients with early-stage breast cancer.
Sentinel lymph node (SLN) biopsy has been shown to be safe, accurate, and
limits the need for traditional axillary dissection in most patients (1).
Conventionally, SLN lymphatic mapping for breast cancer has involved the
use of colloid radiotracer labelled with technetium 99 (2), visible blue dye
(methylene blue or isosulfan blue) (3), or a combination of both (4). Best
mapping results are achieved with periareolar, subdermal injection of the
tracer (5,6). SLNs are defined as axillary lymph nodes in which there is the
accumulation of one or more of these tracers or dyes above defined
thresholds (7). Studies have demonstrated that there is surgeon-associated
variation in both the number of SLNs removed and in the likelihood of
finding a positive SLN (8). In large studies involving experienced surgeons,
the SN detection rate using dual mapping with Tc and a visible dye is
approximately 99%, therefore, use of both methods combined is
recommended by some to achieve the highest accuracy of SLN biopsy and to
reduce the false-negative rate (1,9).
Both traditional mapping techniques also have drawbacks that may limit
their routine use (10). 99mTc-labeled radiotracer injection requires nuclear
medicine licensing, radioactive material handling regulations, and patient
inconvenience with painful periareolar injections typically occurring before
surgery. Although there are reports of surgeons performing Tc injections in
the operating suite, this still requires regulatory resources and is not common
(11). Blue dye injections can be performed during surgery, but risk skin
necrosis with methylene blue injection, inhibiting its use for nipple-sparing
mastectomies, and there is a risk of anaphylaxis with isosulfan blue dye
injection (12,13).
Alternative techniques including indocyanine green (ICG) dye, and
superparamagnetic iron oxide (SPIO) have been utilized for SLN mapping in
an effort to overcome some of the limitations of traditional methods.
Indocyanine Green (ICG)
ICG is a fluorescent dye with moderate optical properties that can be detected
using near-infrared (NIR) cameras. ICG has been used in humans for over 50
years and has an excellent safety profile (14). There are many uses for ICG
during image-guided surgery. After intravenous injection, it can be used for
NIR angiography of blood vessels, skin flap perfusion for mastectomies,
identification of the extrahepatic bile ducts, and identification of oncologic
tumor metastases (15). ICG also has been reported by numerous authors to be
safely used for subcutaneous injection and sentinel node (SN) mapping in
gastrointestinal cancer (16), melanoma (17), and breast cancer (18–21). The
use of ICG for lymphatic mapping and SLN identification offers many
potential advantages over the use of other lymphatic mapping techniques
including the ability to inject the material while the patient is in the operating
room under anesthesia, the ability to use NIR to directly, instantly visualize
lymphatic anatomy and flow, with no special material handling required, and
low cost (20,22).
Recent studies have demonstrated high concordance in the number of
breast cancer SLN identified between ICG and traditional Tc or blue dye
mapping techniques, signifying the benefit of NIR-guided SN biopsy for
standard use (21,23–27). In the modern treatment of breast cancer, the
importance of SLN biopsy has focused on appropriately staging patients in
order to customize adjuvant treatment recommendations.
Superparamagnetic Iron Oxide (SPIO)
SPIO is the newest described lymphatic mapping tracer which consists of a
dextran-coated magnetic nanoparticle that is injected subareolar into the
breast and travels to the SLNs within minutes and can last for up to 30 days
(28). The injected material is identified in the SLNs with the use of a hand-
held magnetometer as well as visualized on a preoperative MRI (29).
INDICATIONS

Indocyanine Green (ICG)


NIR guided, ICG SLN mapping can be performed in breast cancer patients
undergoing SLN either primarily or after neoadjuvant chemotherapy
(27,30,31). ICG SN mapping has been compared to either Tc, blue dye, or
both and consistently been found to be just as effective with rates over 95%
(18,19,21,23,24,26,27,32–38). Specifically, ICG safely performs similarly to
traditional SLN mapping in regard to the number of SNs identified, rate of
failed mapping, and identification of pathologically positive SNs (27).
If the surgeon desires dual tracer, ICG can safely be used in combination
with Tc or blue dye. Alternatively, in experienced hands, ICG could be used
as a sole SLN mapping tracer, similar to Tc and blue dye uses.
Superparamagnetic Iron Oxide (SPIO)
Studies have shown that after injection of SPIO, preoperative MRI can
accurately identify the location and number of SLNs to be excised, similar to
utility of a lymphoscintogram (29). Additionally, SPIO MRI has the ability to
give the surgeon the spatial vision and anatomy of the SLN location (29).
Studies have shown that intraoperative use of the magnometer SPIO SLNs
yields a 94.4% to 98.8% positive identification rate and can be performed
either with blue dye or radiocolloid (28,39).
CONTRAINDICATIONS

Indocyanine Green (ICG)


The ICG SN detection method is known to safe and be associated with very
few side effects. Since ICG contains iodine, patients with thyroid disease or
iodine allergies should not have ICG used. ICG has been reported to be more
difficult to perform in patients with higher BMI due to lower visibility of
axillary lymphatics. NIR penetrates tissue to a maximum depth of 2 cm. A
slightly longer ICG transit time (from injection to SLN visualization in the
axilla) and lower sensitivity has been reported in patients with a BMI over 40
(32). Use of the axillary “image enhancer” device to help compress the
axillary tissue and attenuate ICG signals, is particularly helpful in obese
patients (27,37).
Superparamagnetic Iron Oxide (SPIO)
There have been no reported adverse outcomes with interstitial injection of
the SPIO tracer. It does create a small brown discoloration of the skin where
it was injected that can be long term (28). Patients with dextran allergies,
pacemakers, or other implantable devices not compatible with MRI will not
be able to undergo the SPIO MRI (28). Use of metal instruments and
retractors in the operative filed are prohibited, as the metal creates
interference with the magnometer probe.
PREOPERATIVE PLANNING

Indocyanine Green (ICG)


Use of ICG requires preparation of a mixture of a 25 mg vial of ICG mixed
with 5 ml sterile water to create a 0.5% ICG solution (27). Since ICG
produces NIR fluorescence, undetectable by human eyes, an appropriate
intraoperative detection system to identify the ICG transcutaneously is
required. Due to the emergence of NIR-guided image surgery utilized in a
variety of operations, the NIR detection devices are becoming more common
and widely available for use in operating rooms (16,17,22).
Superparamagnetic Iron Oxide (SPIO)
A 2 ml of magnetic tracer mixed with 3 ml of normal saline is injected into
the breast and massaged for 5 minutes. If preoperative MRI is planned, the
patient undergoes a breast MRI to evaluate the number and location of lymph
nodes to be excised. Alternatively, if MRI is not being performed, this can be
performed in the operating suite or the day prior. Similar to other SLNB
techniques, use of dual tracer is used, and either blue dye or nuclear medicine
in injected (39,40).
OPERATIVE TECHNIQUE

Indocyanine Green (ICG)


At the time of operation, after the induction of anesthesia, 0.5 to 1 cc of 0.5%
ICG mixture, is injected subdermally into the breast lateral subareolar region
(23,24,27). ICG movement into the periareolar lymphatics can be facilitated
by manual massage and immediately observed with NIR fluorescence
imaging. ICG lymphatic drainage is quickly detected and monitored real time
by NIR device. Once the ICG dye reaches the axillary basin, transcutaneous
imaging can be facilitated by use of a translucent “image enhancer,” which
compresses the axillary subcutaneous tissue and allows for visualization of
the ICG avid lymph nodes (Fig. 28-1) (27). This precise spot of fluorescence
in the axilla is marked for incision placement for the SN biopsy procedure.
With assistance of the NIR camera, the fluorescent lymphatic channels are
meticulously dissected and followed to the first ICG avid lymph node. The
afferent and efferent lymphatic channels are precisely clipped and ligated so
that ICG leakage into the dissection field is avoided.
FIGURE 28-1 Use of the “image enhancer” to help identify indocyanine green (ICG)
sentinel lymph nodes in the axilla. A: Image enhancer is used to visualize lymphatic
drainage and ICG avid lymph nodes in the axilla using the near infrared camera. B:
Site of node is marked using the image enhancer. C: Fluorescent node in the axillary
nodal basin. (From Valente SA, Al-Hilli Z, Yanda C, et al. Prospective trial of near
infrared fluorescent lymph node mapping with indocyanine green in breast cancer
patients. J Am Coll Surg 2019;228(4):672–678.)

Fluorescent lymph nodes (ICG positive) are then methodically,


sequentially identified and removed. SLN removal continues until no residual
fluorescence SLN are visible in the axilla. All SLNs are then sent for
pathologic analysis as per standard surgical practice.
Superparamagnetic Iron Oxide (SPIO)
Periareolar or upper outer quadrant breast glad injection of the SPIO material
is performed usually the day prior to surgery. At surgery, nonmetal
instruments are used during the SLN portion of the surgery. The hand-held
magnometer is used to audibly confirm identify the SLN. Upon dissection the
SLNs will also be stained a brown-black color from the SPIO material, giving
visual confirmation.
INTRAOPERATIVE CARE

Indocyanine Green (ICG)


ICG offers advantages of real-time imaging, ease of handling, low cost, and
rapid localization of the SLN. The median lymphatic transit time from ICG
injection to start of SN excision of just 5 to 15 minutes.
Superparamagnetic Iron Oxide (SPIO)
Use of traditional metal operating instruments cannot be used with the
magnometer, and therefore special plastic-made operating instruments need
to be used when performing the SLNB to avoid interference with the
magnometer. The magnometer machine does require repeat calibration to
reset the baseline magnetic level (28).
POSTOPERATIVE CARE

Indocyanine Green (ICG)


There have been no reported adverse outcomes to the use of ICG for
lymphatic mapping.
Superparamagnetic Iron Oxide (SPIO)
SPIO has been shown to stay in the lymph nodes for up to 3 weeks after the
injection (40). This could be useful in preoperative injection timing.
Additionally, it has been suggested to have utility when performing a
mastectomy for ductal carcinoma in situ, subsequently allowing for SLNB as
a delay procedure, only if final pathology shows an invasive carcinoma
where SLNB would be indicated.
RISKS OF THE PROCEDURE

Indocyanine Green (ICG)


Removal of unnecessary nodes during the SN procedure is not desirable, as
upper extremity morbidity risk increases with increasing removal of SLN. A
concern raised in some studies is the excessive number of SN identified using
the ICG technique (19,41). However, others have shown no statistical
difference in the median SLN removed between techniques (27). It is
proposed the mechanism by which ICG dye identifies more SNs than with Tc
or blue dyes is that the ICG molecule is smaller than the Tc bound to albumin
and therefore travels faster (23). Studies have suggested that ICG mixture
concentration, quantity injected, and procedure timing play a role in the
appropriate number of SLNs identified, however the optimal formula is yet to
be determined (26). The recommendation is to start the SLN procedure
immediately after the ICG is seen reaching the axilla, thereby performing the
SLN portion as the first part of the operation.
Superparamagnetic Iron Oxide (SPIO)
There have been no reported adverse reactions. Injection of the material
should be avoided in patients with a dextran intolerance, as SPIO is part of a
dextran mixture. Subsequent MRI after injection of the material into the
breast has been reported to show refraction caused by the SPIO at the breast
injection site and movement in breast lymphatic channels which may make it
difficult to interpret imaging details of the breast tissue (29).
As with ICG mapping, studies have shown that a slightly higher number of
SLNs has been removed with the SPIO technique, with an average of four
lymph nodes (39).
CONCLUSION

Indocyanine Green (ICG)


ICG with NIR fluorescence imaging can be safely and efficiently used for
real time intraoperative lymphatic mapping in breast cancer patients. The
ICG NIR imaging method is an efficient, convenient, and equivalent
intraoperative method of SN detection compared to the traditional mapping
techniques.
Superparamagnetic Iron Oxide (SPIO)
ICG with NIR fluorescence and imaging can be safely and efficiently used
for real time intraoperative lymphatic mapping in breast cancer patients.
Additionally, SPIO with MRI permits preoperative visualization of SLNs;
subsequent use of a magnometer in the axilla allows accurate SLN
localization. The ICG NIR and SPIO imaging techniques are efficient,
convenient, and equivalent intraoperative methods of SN detection compared
to the traditional mapping techniques.

REFERENCES

1. Krag DN, Anderson SJ, Julian TB, et al. Sentinel-lymph-node resection


compared with conventional axillary-lymph-node dissection in clinically
node-negative patients with breast cancer: overall survival findings from
the NSABP B-32 randomised phase 3 trial. Lancet Oncol
2010;11(10):927–933.
2. Krag DN, Weaver DL, Alex JC, et al. Surgical resection and
radiolocalization of the sentinel lymph node in breast cancer using a
gamma probe. Surg Oncol 1993;2(6):335–339; discussion 340.
3. Giuliano AE, Kirgan DM, Guenther JM, et al. Lymphatic mapping and
sentinel lymphadenectomy for breast cancer. Ann Surg
1994;220(3):391–398; discussion 398–401.
4. Kelley MC, Hansen N, McMasters KM. Lymphatic mapping and
sentinel lymphadenectomy for breast cancer. Am J Surg
2004;188(1):49–61.
5. McMasters KM, Wong SL, Martin RC 2nd, et al. Dermal injection of
radioactive colloid is superior to peritumoral injection for breast cancer
sentinel lymph node biopsy: results of a multiinstitutional study. Ann
Surg 2001;233(5):676–687.
6. Klimberg VS, Rubio IT, Henry R, et al. Subareolar versus peritumoral
injection for location of the sentinel lymph node. Ann Surg
1999;229(6):860–864; discussion 864–865.
7. Martin RC 2nd, Edwards MJ, Wong SL, et al. Practical guidelines for
optimal gamma probe detection of sentinel lymph nodes in breast
cancer: results of a multi-institutional study. For the University of
Louisville Breast Cancer Study Group. Surgery 2000;128(2):139–144.
8. Larson KE, Valente SA, Tu C, et al. Surgeon-associated variation in
breast cancer staging with sentinel node biopsy. Surgery
2018;164(4):680–686.
9. Koukouraki S, Sanidas E, Askoxilakis J, et al. Is there any benefit from
sentinel lymph node biopsy using the combined radioisotope/dye
technique in breast cancer patients with clinically negative axilla? Nucl
Med Commun 2009;30(1):48–53.
10. Kelley LM, Holmes DR. Tracer agents for the detection of sentinel
lymph nodes in breast cancer: current concerns and directions for the
future. J Surg Oncol 2011;104(1):91–96.
11. Thompson M, Korourian S, Henry-Tillman R, et al. Intraoperative
radioisotope injection for sentinel lymph node biopsy. Ann Surg Oncol
2008;15(11):3216–3221.
12. Efron P, Knudsen E, Hirshorn S, et al. Anaphylactic reaction to
isosulfan blue used for sentinel node biopsy: case report and literature
review. Breast J 2002;8(6):396–399.
13. Thevarajah S, Huston TL, Simmons RM. A comparison of the adverse
reactions associated with isosulfan blue versus methylene blue dye in
sentinel lymph node biopsy for breast cancer. Am J Surg
2005;189(2):236–239.
14. Hope-Ross M, Yannuzzi LA, Gragoudas ES, et al. Adverse reactions
due to indocyanine green. Ophthalmology 1994;101(3):529–533.
15. Schaafsma BE, Mieog JS, Hutteman M, et al. The clinical use of
indocyanine green as a near-infrared fluorescent contrast agent for
image-guided oncologic surgery. J Surg Oncol 2011;104(3):323–332.
16. Kusano M, Tajima Y, Yamazaki K, et al. Sentinel node mapping guided
by indocyanine green fluorescence imaging: a new method for sentinel
node navigation surgery in gastrointestinal cancer. Dig Surg
2008;25(2):103–108.
17. Korn JM, Tellez-Diaz A, Bartz-Kurycki M, et al. Indocyanine green
SPY elite-assisted sentinel lymph node biopsy in cutaneous melanoma.
Plast Reconstr Surg 2014;133(4):914–922.
18. Abe H, Mori T, Umeda T, et al. Indocyanine green fluorescence imaging
system for sentinel lymph node biopsies in early breast cancer patients.
Surg Today 2011;41(2):197–202.
19. Aoyama K, Kamio T, Ohchi T, et al. Sentinel lymph node biopsy for
breast cancer patients using fluorescence navigation with indocyanine
green. World J Surg Oncol 2011;9:157.
20. Troyan SL, Kianzad V, Gibbs-Strauss SL, et al. The FLARE
intraoperative near-infrared fluorescence imaging system: a first-in-
human clinical trial in breast cancer sentinel lymph node mapping. Ann
Surg Oncol 2009;16(10):2943–2952.
21. Sugie T, Kinoshita T, Masuda N, et al. Evaluation of the clinical utility
of the ICG fluorescence method compared with the radioisotope method
for sentinel lymph node biopsy in breast cancer. Ann Surg Oncol
2016;23(1):44–50.
22. Papathemelis T, Jablonski E, Scharl A, et al. Sentinel lymph node
biopsy in breast cancer patients by means of indocyanine green using the
Karl Storz VITOM(R) fluorescence camera. Biomed Res Int
2018;2018:6251468.
23. Ballardini B, Santoro L, Sangalli C, et al. The indocyanine green method
is equivalent to the 99mTc-labeled radiotracer method for identifying the
sentinel node in breast cancer: a concordance and validation study. Eur J
Surg Oncol 2013;39(12):1332–1336.
24. Sugie T, Ikeda T, Kawaguchi A, et al. Sentinel lymph node biopsy using
indocyanine green fluorescence in early-stage breast cancer: a meta-
analysis. Int J Clin Oncol 2017;22(1):11–17.
25. Takeuchi M, Sugie T, Abdelazeem K, et al. Lymphatic mapping with
fluorescence navigation using indocyanine green and axillary surgery in
patients with primary breast cancer. Breast J 2012;18(6):535–541.
26. Verbeek FP, Troyan SL, Mieog JS, et al. Near-infrared fluorescence
sentinel lymph node mapping in breast cancer: a multicenter experience.
Breast Cancer Res Treat 2014;143(2):333–342.
27. Valente SA, Al-Hilli Z, Radford DM, et al. Near infrared fluorescent
lymph node mapping with indocyanine green in breast cancer patients: a
prospective trial. J Am Coll Surg 2019;228(4):672–678.
28. Man V, Wong TT, Co M, et al. Sentinel lymph node biopsy in early
breast cancer: magnetic tracer as the only localizing agent. World J Surg
2019;43(8):1991–1996.
29. Pouw JJ, Grootendorst MR, Bezooijen R, et al. Pre-operative sentinel
lymph node localization in breast cancer with superparamagnetic iron
oxide MRI: the SentiMAG Multicentre Trial imaging subprotocol. Br J
Radiol 2015;88(1056):20150634.
30. Shilad S, Cakmakoglu C, Schwarz G, et al. Triple mapping to optimize
axillary management in breast cancer patients after neoadjuvant therapy.
Ann Surg Oncol 2018;25(10):3106.
31. Tsuyuki S, Yamaguchi A, Kawata Y, et al. Assessing the effects of
neoadjuvant chemotherapy on lymphatic pathways to sentinel lymph
nodes in cases of breast cancer: usefulness of the indocyanine green-
fluorescence method. Breast 2015;24(3):298–301.
32. Grischke EM, Rohm C, Hahn M, et al. ICG fluorescence technique for
the detection of sentinel lymph nodes in breast cancer: results of a
prospective open-label clinical trial. Geburtshilfe Frauenheilkd
2015;75(9):935–940.
33. Samorani D, Fogacci T, Panzini I, et al. The use of indocyanine green to
detect sentinel nodes in breast cancer: a prospective study. Eur J Surg
Oncol 2015;41(1):64–70.
34. Tong M, Guo W, Gao W. Use of fluorescence imaging in combination
with patent blue dye versus patent blue dye alone in sentinel lymph node
biopsy in breast cancer. J Breast Cancer 2014;17(3):250–255.
35. Guo W, Zhang L, Ji J, et al. Evaluation of the benefit of using blue dye
in addition to indocyanine green fluorescence for sentinel lymph node
biopsy in patients with breast cancer. World J Surg Oncol 2014;12:290.
36. Xiong L, Gazyakan E, Yang W, et al. Indocyanine green fluorescence-
guided sentinel node biopsy: a meta-analysis on detection rate and
diagnostic performance. Eur J Surg Oncol 2014;40(7):843–849.
37. Zhang X, Li Y, Zhou Y, et al. Diagnostic performance of indocyanine
green-guided sentinel lymph node biopsy in breast cancer: a meta-
analysis. PLoS One 2016;11(6):e0155597.
38. Wishart GC, Loh SW, Jones L, et al. A feasibility study (ICG-10) of
indocyanine green (ICG) fluorescence mapping for sentinel lymph node
detection in early breast cancer. Eur J Surg Oncol 2012;38(8):651–656.
39. Rubio IT, Diaz-Botero S, Esgueva A, et al. The superparamagnetic iron
oxide is equivalent to the Tc99 radiotracer method for identifying the
sentinel lymph node in breast cancer. Eur J Surg Oncol 2015;41(1):46–
51.
40. Douek M, Klaase J, Monypenny I, et al. Sentinel node biopsy using a
magnetic tracer versus standard technique: the SentiMAG multicentre
trial. Ann Surg Oncol 2014;21(4):1237–1245.
41. Sugie T, Sawada T, Tagaya N, et al. Comparison of the indocyanine
green fluorescence and blue dye methods in detection of sentinel lymph
nodes in early-stage breast cancer. Ann Surg Oncol 2013;20(7):2213–
2218.
CHAPTER 29

Axillary Surgery Versus Radiation as


Treatment of Regional Nodes:
AMAROS Trial and Beyond
AMANDA AMIN | MELISSA MITCHELL
HISTORY

Impact of Extensive Surgery on Clinical Outcome


Historically, breast cancer was theorized to spread contiguously through
lymph nodes prior to metastatic spread. Therefore, surgical removal of the
draining axillary lymphatics was recommended to prevent distant disease
progression and improve survival. In the early days of breast surgery, even
patients with minimal disease underwent radical mastectomy with complete
axillary dissection. Ultimately, many of these patients still developed distant
disease. One theory was that additional nodal disease in the internal
mammary nodal chain was contributing to disease spread. Randomized
studies were performed to assess the utility of an extended procedure to
remove the internal mammary nodes. Results from a large multicenter trial of
1,453 patents with T1-3N0-1 disease showed no statistically significant
survival benefit of extended surgical resection to include the internal
mammary nodes (1). With clear evidence that comprehensive nodal surgery
beyond axillary lymph node dissection (ALND) does not improve breast
cancer survival, the need for axillary dissection was also brought into
question.
Bernard Fisher was one of the first physicians to question whether ALND
was truly therapeutic or only prognostic. He theorized that systemic control
was of greater importance than extensive surgery. The first trial to assess the
necessity of axillary dissection was NSABP B04 (2). On this study, 1,079
clinically node-negative women were randomized to one of three different
treatment regimens: radical mastectomy, simple mastectomy with local–
regional irradiation, or simple mastectomy with no irradiation. In the third
arm, axillary dissection was only performed if patients became clinically
positive. Local control was superior in the group that received simple
mastectomy with radiation over radical mastectomy. There was no difference
in overall survival (OS) between the three groups. Forty percent of patients
undergoing radical mastectomy were found to have positive lymph nodes,
thus 40% of patients in the simple mastectomy-alone group would be
expected to have positive nodes. However, only 18% of these patients with
simple mastectomy alone developed an axillary recurrence that required
ALND. Only 3% of patients with simple mastectomy and radiation developed
an axillary recurrence, as compared to 1% in patients who underwent ALND.
There was no survival advantage for any of the three arms, suggesting that
ALND could be reserved for patients who develop a clinically apparent
recurrence (2).
A study by the Institute Curie performed in the era prior to sentinel lymph
node biopsy (SLNB) randomized cT1-2N0 breast cancer patients to axillary
dissection versus radiation to the axilla (3). All patients underwent
lumpectomy followed by radiation to the breast and axilla. In the dissection
group, 21% of patients were found to have metastatic lymph nodes. At 15
years, there was no significant difference between the two groups in OS
(75.5% vs. 73.8%) or local recurrence (7.2% vs. 7.1%). There was increased
risk of isolated axillary recurrence, though it was very low, and similar to
NSABP B04 (1% vs. 3%, p = 0.04).
In the current era, systemic therapy is becoming more effective as
treatments are tailored for tumor biology. Studies suggest that improved
systemic therapy impacts not only distant tumor control, but also local
control for breast cancer patients (4). As a result, less emphasis is being
placed on the need for aggressive surgery that may cause significant long-
term morbidity. This has caused a rapid pendulum shift in the surgical
management of patients with locally advanced breast cancer. This chapter
will review the most recent studies assessing omission of ALND for node-
positive disease, with details provided in Table 29-1. It should be noted that
this topic is rapidly evolving, and therefore currently accruing trials that will
define the standard of care in the future for this population of patients will
also be reviewed.

TABLE 29-1 Characteristics of Recent Trials of Sentinel Lymph Node


Biopsy Alone in Node-Positive Breast Cancer
Trials of Sentinel Lymph Node Biopsy Versus Axillary
Dissection in Node-Positive Patients
The American College of Surgeons Oncology Group (ACOSOG) Z0011 trial
is a more recent study of de-escalation of axillary surgery (5). This trial
enrolled 891 patients with T1–T2 clinically node-negative breast cancer and
one or two positive sentinel nodes. All patients were planned for lumpectomy
and whole breast radiation. Patients were randomized to completion ALND
after SLNB or SLNB alone. This study demonstrated similar 10-year OS in
ALND and SLNB-alone arms (83.6% vs. 86.3%, HR 0.85, p = 0.02). There
was no difference in 10-year cumulative incidence of locoregional
recurrences between the two arms (6.2% for ALND, 5.3% for SLNB alone; p
= 0.36). It is theorized that the incidental axillary radiation from whole breast
radiotherapy may have improved local control in the axilla for patients
randomized to SLNB.
Similar to the Z0011 study, the International Breast Cancer Study Group
(IBCSG) 23-01 trial randomly assigned 931 patients with cT1–T2N0 breast
cancer and a positive SLNB to completion ALND or SLNB alone (6). Unlike
Z0011, this trial only allowed micrometastases seen on SLNB (pN1mi),
making this a lower-risk population. IBCSG 23-01 allowed inclusion of
patients undergoing mastectomy, though this was a small minority of the
cohort (9%). IBCSG 23-01 found no significant difference in disease-free
survival (DFS) or OS between the ALND and SLNB-alone groups. There
was significantly less lymphedema (13% vs. 3%, p < 0.0001) and neuropathy
(8% vs. 3%, p < 0.0004) in the SLNB-alone arm.
A multicenter randomized trial, AATRM, was conducted in Spain on
patients with cT1-2N0 disease who were found to have micrometastatic
disease at the time of SLNB (7). A total of 233 patients were randomized to
ALND versus no further surgery. In patients undergoing lumpectomy, care
was taken to avoid excess radiation to the axilla. As in IBCSG 23-01, only a
small minority of patients underwent mastectomy (8%) and these patients did
not receive postmastectomy radiation therapy (PMRT). The incidence of
additional positive nonsentinel nodes was low in the ALND group (13%).
There was no significant difference in local recurrence between the SLNB
and ALND groups (2.5% vs. 1%, p = 0.348).
Trials of Sentinel Lymph Node Biopsy and Targeted Radiation
Versus Axillary Dissection in Node-Positive Patients
The Optimal Treatment Of the Axilla-Surgery Or Radiotherapy (OTOASOR)
trial was a single-center phase III study with 474 evaluable patients
randomized to completion ALND versus radiation directed to the axilla (8).
Patients were enrolled prior to surgery, and clinical tumor size was required
to be ≤3 cm. However, patients were found to have larger tumors at surgical
excision, with 21 patients having pT3 disease. There was an imbalance of
tumor size in the randomized arms, with significantly more pT2 and pT3
disease in the ALND arm (57% vs. 40%, p = 0.003). In the radiation group,
60.4% of patients had macrometastatic disease. In the ALND arm, 38.5% of
patients had additional positive nonsentinel nodes, and 22% were upstaged to
pN2 or pN3. Only 23.3% of the ALND patients received regional nodal
irradiation (RNI). All patients in the radiation arm received radiation to the
level I to III axilla and supraclavicular region. Patients in the ALND arm only
received radiation if they had ≥ pN2 disease or additional risk factors putting
them at high risk of recurrence. With a mean follow-up of 97 months, axillary
recurrence was not significantly different between the radiation and ALND
arms (1.7% vs. 2%, p = 1.0). Eight-year OS was not significantly different
(84.8% vs. 77.9%, p = 0.06).
The European Organization for Research and Treatment of Cancer
(EORTC)’s After Mapping of the Axilla: Radiotherapy Or Surgery?
(AMAROS) was a multicenter randomized trial of 1,425 cT1-T2N0 patients
with a positive SLNB. As in OTOASOR, the two arms were completion
ALND versus no further axillary surgery. The SLNB arm required directed
radiation toward the level I and II axilla (9). Arms were better balanced than
OTOASOR, with pT2 disease in 18% of patients in the ALND arm versus
21% in the SLNB arm. In the SLNB arm, 62% of patients had
macrometastatic disease and 5% had ≥3 positive nodes. In the ALND group,
8% of patients were found to have ≥4 positive nonsentinel nodes. Regional
radiation was delivered in the ALND group for patients with ≥4 positive
nodes. As in Z0011, IBCSG 23-01, and OTOASOR, completion ALND
failed to significantly impact 5-year axillary recurrence (0.43% vs. 1.19%,
noninferior), 5-year DFS (86.9 vs. 82.7%, p = 0.18), or 5-year OS (93.3% vs.
92.5%, p = 0.34), when compared to the SLNB alone.
Development of breast cancer–related lymphedema (BCRL) was a
secondary end point of AMAROS. The group undergoing SLNB had
significantly less BCRL at all posttreatment time points. Clinical BCRL at 5
years was seen in 11% of patients randomized to SLNB and radiation, as
compared to 23% of patients with ALND (p < 0.001). Objective BCRL,
measured as 10% increase in arm circumference at 5 years, was 6% for the
SLNB group as compared to 13% for ALND (p = 0.0009).
Z0011, AMAROS, OTOASOR, and IBCSG 23-01 have been practice
changing. The 2016 American Society of Clinical Oncology (ASCO)
guidelines state that ALND should not be recommended for women with
cT1–T2 (≤5-cm) breast cancer who have one or two sentinel lymph node
metastases and are planned for lumpectomy with adjuvant whole breast
radiation therapy (10). In early-stage patients with cN1 disease undergoing
mastectomy, ALND is often recommended unless it is micrometastatic
disease or there are clear indications for postmastectomy radiation, which
will be discussed below. For patients with larger tumors (cT3), those
undergoing neoadjuvant systemic therapy, and those with ≥2 positive sentinel
nodes, axillary dissection is still routinely recommended. However, even in
these higher-risk populations, the clinical benefit of surgically reducing the
axillary disease burden remains a subject of debate. Multiple ongoing trials,
which will be discussed below, will help to further define the population of
patients who need more aggressive local therapy.
INDICATIONS FOR AXILLARY DISSECTION VERSUS TARGETED RADIATION
TO THE AXILLA

Surgery First
Lumpectomy patients, cT1-2N0, ≤2 nodes found on SLNB, no gross
ECE: In clinically node-negative patients with T1–2 tumors undergoing
upfront surgery with lumpectomy and planned for whole breast radiation,
sentinel node biopsy is sufficient, as described in the previous section. The
radiation oncologist should ensure that the entire level I and II axilla is
encompassed in the radiation tangent portal, as shown in Figure 29-1. The
decision for extended radiation to include the supraclavicular and internal
mammary nodes, RNI, should be made based on careful review of patient and
tumor characteristics, such as patient age, tumor size, and tumor biology, as
described in the cases below.
Lumpectomy patients, cT2N0, ê3 nodes found on SLNB or gross ECE:
These patients were not included on the Z0011 trial, and only 5% of patients
on AMAROS and OTOASOR had ≥3 positive sentinel nodes. As these
patients were not well represented in randomized trials of SLNB alone, the
standard of care is to proceed with ALND in patients with >2 positive nodes
or gross ECE. These patients should receive RNI in addition to whole breast
radiotherapy.
Exploratory data exists for both ALND and SLNB alone in this population.
A retrospective review at Memorial Sloan Kettering Cancer Center
(MSKCC) suggests that patients with gross ECE or >2 positive nodes are
very high risk for additional nodal disease (11). They changed their standard
practice to routinely omit ALND in patients who met strict criteria for
eligibility for Z0011. However, patients with ≥3 positive lymph nodes, gross
ECE, or matted adenopathy were still recommended for completion ALND.
In patients meeting these exclusion criteria and recommended for ALND,
72% had additional positive nodes. With a median follow-up of 13 months,
distant metastatic disease developed in 7% of the patients recommended for
ALND, highlighting the competing distant disease risk in this population of
patients with more aggressive tumor biology.
FIGURE 29-1 Radiation tangent field design for patients with a positive sentinel
node not undergoing ALND. The Radiation Therapy Oncology Group breast cancer
contouring atlas should be used to contour axillary levels I and II. A: A
representative axial slice shows a contour of the level I and II axilla in purple, with
lymphatic space contoured medial to the pectoralis minor and including the
pectoralis minor. Using a standard tangent angle (yellow) may miss the posterior
axilla. A steeper tangent angle (red) can improve coverage of the axilla target, while
still sparing lung. B: Standard tangent fields encompass the breast alone with 1-cm
superior and inferior margins on the breast tissue. C: Modified tangent fields are
shown, with a raised superior border and posterior extension of the upper portion of
the tangent field to include the axilla contour (shown in purple) in the radiation port.
Dashed blue line depicts extension of standard tangents to the level of the humeral
head “high tangent” and how a high tangent would encompass less of the axilla than
3D conformal radiation targeting this area.

In support of omitting ALND, a SEER analysis was performed to assess


outcomes for pT1–T2 patients with ≥3 positive lymph nodes found on SLNB
(12). There was no difference in OS in patients undergoing completion
ALND versus SLNB alone when adjusted for age, use of radiation, tumor
size, hormone status, or tumor grade. As the data to support this practice is
limited, omission of ALND in patients with three positive nodes or gross
ECE is cautionary outside of a clinical trial, and should only be considered in
the setting of low disease burden, such as low nomogram scores (13).
Lumpectomy patients, cT3N0: While OTOASOR included some T3
patients, they represented a very small portion of the population. As
AMAROS and Z0011 did not include cT3 tumors, the standard of care for
these patients is ALND. These patients will all require adjuvant radiation
therapy to the breast and RNI.
Recommendations for ALND in this group stem from a high risk of
additional nodal disease in studies of SLNB followed by completion ALND
for T3 patients, in the range of 57% to 80%. Routine substitution of radiation
for ALND in T3 patients should not be performed off trial until additional
data is obtained. Cautious use can be considered in patients who are low risk
for additional disease based on nomograms (13). All of these patients will be
at high risk for distant disease, thus systemic therapy should be optimized.
Mastectomy patients, pT1–2N1mi: Z0011 excluded patients undergoing
mastectomy as the primary breast surgery, and therefore this trial is not
applicable to patients proceeding with mastectomy. Although both IBCSG
23-01 and AATRM included patients proceeding with mastectomy, this
population was a small minority of the entire cohort (9%). Furthermore, only
pN1mi patients were included (6,7). Patients with pN0(i+) or pN1mi disease
may be considered for SLNB alone, even if PMRT is not planned, in the
setting of biologically favorable disease. Patients with highly unfavorable
features, such as young age, unfavorable tumor biology, large primary tumor,
should be treated similar to patients with macrometastatic disease (pN1).
Further data to support this practice includes a retrospective study from
MSKCC that reviewed outcomes of node-positive patients undergoing
mastectomy and SLNB alone, no radiation (14). The majority of mastectomy
patients in this study had isolated tumor cells (ITCs) at SLNB (54%, pN0[i+])
and 37% had pN1mi disease. Only 9% had pN1 macrometastatic disease.
Almost all of the patients (99%) were pT1–2. Patients included in this study
had low risk of additional axillary nodal involvement, with a median risk of
nonsentinel axillary nodal metastasis of 9% per the MSKCC nomogram.
None of the patients with pN0(i+) disease developed an axillary recurrence.
Excluding those with ITCs, the 4-year local and regional recurrence rates in
this study were very low for node-positive mastectomy patients with pN1mi
and pN1 disease (1.2% and 2.5%, respectively).
Mastectomy patients, pT1-2N1: The decision to perform ALND in N1
macrometastatic mastectomy patients is more complex, and closely
intertwined with the decision for PMRT. All patients in AMAROS,
OTOASOR, and Z0011with pN1 disease received radiation (whole breast
radiation or PMRT) as a component of their care. However, not all pN1
patients who undergo mastectomy will require PMRT. While RNI is standard
for patients with ≥4 positive lymph nodes, radiation is not routinely
recommended for patients with one to three positive nodes (15). A meta-
analysis from EBCTCG suggested that PMRT improved survival in patients
with pN1 disease (16). However, patients treated in the older trials included
in this analysis had large, grossly abnormal nodes. In the modern era, many
patients with pN1 disease have disease found only on serial thin sectioning of
sentinel nodes, yet they are similarly categorized as pN1. Multiple factors
should therefore be considered when making a decision on PMRT in pN1
patients, including patient age, primary tumor size, hormone receptor status,
Oncotype Dx recurrence score, histologic grade, tumor location, and presence
of lymphovascular space invasion (LVSI) or extracapsular extension (ECE)
(15,17). Patient preferences on exposure to radiation and its associated risks
or reconstruction desires can also affect treatment decisions, as described
below. In patients with multiple high-risk factors that sufficiently justify
PMRT, the patient can proceed to PMRT and avoid completion ALND. In
patients with low-risk disease, ALND should be performed and radiation
avoided.
Surgery After Neoadjuvant Chemotherapy
For patients presenting with clinically node-positive disease or aggressive
tumor biology (triple negative or HER2 amplified), neoadjuvant
chemotherapy is often recommended. One of the many reasons for this
change in order of therapy from a surgery-first approach is the goal to
downstage the axilla and reduce unnecessary ALND (18).
Originally, standard of care was to perform ALND for axillary staging
after completion of neoadjuvant chemotherapy, even in cN0 disease. Several
recent studies have proven the appropriately low false-negative rate with
SLNB in patients undergoing neoadjuvant chemotherapy, allowing this to be
standard of care for cN0 disease. The Sentinel Node biopsy aFter
NeoAdjuvant Chemotherapy study (SN FNAC) was a multicenter
prospective study of 153 patients with pT0-3N1-2 disease treated with
neoadjuvant chemotherapy, who underwent SLNB followed by ALND (19).
They found that use of mandatory immunohistochemical evaluation on
pathologic review helped to reduce their false-negative rate, which was 8.4%
when patients with ypN0(i+) disease were included.
Sentinel-lymph-node biopsy in patients with breast cancer before and after
neoadjuvant chemotherapy (SENTINA) was a multicenter European trial
with the purpose of investigating the detection rate and false-negative
detection rate of SLNB after neoadjuvant chemotherapy for patients with cN1
disease that convert to ycN0. Of the 592 women that underwent SLNB after
neoadjuvant chemotherapy, the detection rate was 80.1% and the false-
negative rate was 14.2%. Authors concluded that SLNB was a reliable
diagnostic method before chemotherapy, but the SLNB had a lower detection
rate and higher false-negative rate after neoadjuvant chemotherapy (20).
The larger Alliance ACOSOG Z1071 trial similarly assessed the false-
negative rate in a population of 649 patients who underwent neoadjuvant
chemotherapy followed by SLNB and completion ALND (21). The overall
false-negative rate was found to be unacceptably high at 12.6%. However,
with use of dual tracer and removal of a minimum of three nodes, the false-
negative rate fell under the acceptable threshold of 10%. Building on this,
more contemporary studies have suggested that use of a clip placed at the
time of percutaneous biopsy into the clinically positive lymph node, and
documented retrieval of the clipped node at the time of SLNB, can lower the
false-negative rate to 1.4% (21,22).
cN0 patients undergoing neoadjuvant chemotherapy followed by
surgery with ypN+ SLNB: These patients should all undergo axillary
dissection. Unfortunately, past and ongoing trials have focused on the
management of patients with documented cN1 disease before neoadjuvant
chemotherapy, and those that have cN0 have been excluded. This population
of patients should therefore continue to receive ALND as standard of care.
cN1 patients who convert to ypN0 at SLNB: These patients do not need
completion ALND. However, these patients should still be assessed for the
need for radiation to the axilla and other draining lymphatics. De-escalation
of radiation in this population is currently being assessed in by RTOG
1304/NSABP B-51, which will be discussed below in beyond AMAROS
(23).
cN1 patients, who convert to ycN0, who undergo SLNB and are still
ypN1: These patients should all proceed with completion ALND unless
enrolled on a clinical trial. Alliance A011202 is currently assessing the role
of SLNB without completion ALND in this population (24).
CONTRAINDICATIONS
Advanced stage disease: Outside of a clinical trial, patients with any sentinel
node involvement after neoadjuvant chemotherapy (ypN+) should undergo
completion ALND. As noted above, for patients with cT3/4 or pN2/3 disease,
the standard of care continues to be ALND until additional trials mature. The
population of patients suitable for SLNB alone is likely to grow as studies
increasingly suggest that effective systemic therapy and targeted radiation
therapy can provide similar local control even in higher-risk patients.
Radiotherapy contraindications: Absolute and relative contraindications
to radiation should be considered when making decisions regarding local
therapy. ALND should be chosen over targeted radiation with SLNB in
patients with scleroderma, active lupus, prior therapeutic radiation to the
chest, active pregnancy, and Li–Fraumeni syndrome (25).
PREOPERATIVE PLANNING
All patients with a breast abnormality (BI-RADS 4 or 5) should be assessed
with mammogram and targeted ultrasound (US) of the breast, in addition to
an axillary US on the side of the breast abnormality. Breast MRI should be
used selectively when a cancer diagnosis has been made. The American
Society of Breast Surgeons Choosing Wisely Campaign endorses the
statement “Don’t routinely order breast MRI in new breast cancer patients”
(26). Multiple studies confirm an association between receipt of breast MRI
and increased ipsilateral and contralateral mastectomy rates, as well as
increased time to treatment, without improved survival, decreased local
recurrence, or decreased re-excision rates.
If MRI has already been obtained, or it was needed for further assessment,
obtaining a dedicated axillary US to specifically assess the lymph nodes does
not appear to be necessary. MRI is equivalent to axillary US in detecting
lymph node metastases (27,28).
For patients who are surgery first that meet Z0011 criteria (cT1-2N0 and
desires breast conservation) and axillary US demonstrates only one to two
abnormal lymph nodes, axillary staging should be performed in the operating
room with SLNB. If >2 abnormal lymph nodes on US or large tumor size (>5
cm), or if the tumor markers are such (triple negative or HER2 amplified) that
patient will receive neoadjuvant chemotherapy, percutaneous biopsy should
be performed of the most abnormal lymph node. Most patients with biopsy-
proven axillary disease, even if hormone receptor positive, should receive
neoadjuvant chemotherapy, in attempt to downstage the axilla. During
percutaneous biopsy, a clip should be placed to reduce the false-negative rate
at the time of future SLNB (22).
BCRL is a chronic, progressive disease that results from breast cancer
treatment and nodal surgery. Node-positive patients often receive treatment
with taxane-based chemotherapy, ALND, and RNI, all of which contribute
incrementally to the risk of developing BCRL. Baseline measurements with
bioimpedance spectroscopy (BIS) are recommended before initiation of any
of these therapies. Patients are then followed and interventions are started if
changes are seen clinically or on BIS measurements. This has been shown to
significantly improve patient outcomes and decrease risk of persistent BCRL
(29).
For patients undergoing mastectomy, preoperative consultation with
radiation oncology and discussion at tumor conference can help to identify
patients who will require PMRT regardless of pathologic lymph node status.
Factors considered in making the decision for PMRT include patient age,
primary tumor size, hormone receptor status, Oncotype Dx recurrence score,
histologic grade, tumor location, and presence of LVSI or ECE (15,17).
Presence of multiple high-risk features increases the risk of local recurrence
enough to justify radiation therapy. Patient desire for reconstruction and the
type of reconstruction may also influence the decision for PMRT in patients
who are at intermediate risk. For patients at high risk for local recurrence,
who will definitely require PMRT, a preoperative discussion may be useful
between radiation oncology and plastic surgery to determine the optimal
timing and type of reconstruction.
INTRAOPERATIVE TECHNIQUE
For patients who go to surgery first with lumpectomy, sentinel lymph nodes
should be sent for routine pathology. Consideration is made to return to the
operating room for completion ALND if >2 positive nodes or gross ECE, per
Z0011 criteria (3). For those who have surgery first and have mastectomy,
sentinel lymph nodes should be sent for frozen section analysis. Completion
ALND is performed for even one positive sentinel lymph node unless they
have clear indications for PMRT defined preoperatively (10). Those without
a clear need for PMRT at the time of surgery should be managed with frozen
section identification and completion ALND if the intraoperative assessment
of the sentinel nodes is positive. If the sentinel lymph node is found to be
negative on frozen section analysis, but positive on final processing, a
multidisciplinary conversation at tumor board is warranted to discuss the pros
and cons of returning to the operating room for completion ALND over
PMRT. Discussion with the patient on goals of treatment can also influence
the decision of how to proceed in the setting of a positive node detected
postoperatively.
Many have quickly adopted omission of completion ALND for positive
sentinel lymph nodes in mastectomy patients based on the above mentioned
AMAROS and IBCSG (6,9). Patients undergoing mastectomy were an
underrepresented minority of the study population totaling only 332 patients
between AMAROS (18%, n = 248) and IBCSG 23-01 (9%, n = 84). In
addition, many of these patients had small volume disease, N1mi, and thus
were not representative of most N1 patients. Thus, for macroscopic nodal
disease, ALND or PMRT is required for these patients.
For those who receive neoadjuvant chemotherapy and are cN0, SLNB
should be performed using dual tracer, with the goal to retrieve at least three
sentinel lymph nodes, per Z1071 (21). Sentinel lymph nodes should be sent
for frozen section analysis and completion ALND is performed for any
positive lymph nodes. For those who were cN1, received neoadjuvant
chemotherapy, and have converted to ycN0, SLNB should be performed
using dual tracer in addition to localization of the previously biopsied and
clipped lymph node. Retrieval and documentation of the removal of the
previously biopsied lymph node, in addition to frozen section assessment of
all sentinel nodes should be performed. If all sentinel nodes are ypN0, then
no additional nodal procedure is performed. However, if there is persistent
nodal disease (ypN+), completion ALND is standard of care outside of
participation in Alliance A011202 (24).
POSTOPERATIVE CARE

Radiation Guidelines in Patients With pN1 Disease Not


Undergoing ALND
The noninferiority of SLNB to completion ALND for node-positive patients
from Z0011 was surprising. One theory for the similar outcome was that
radiation oncologists intentionally manipulated fields in the SLNB arm to
improve nodal coverage. A secondary analysis of the treatment portals
assessed the proximity of the upper border of the radiation field to the
humeral head as a surrogate for axillary coverage (30). Patients were
considered to be treated with “high tangents” if the treatment portal was
within 2 cm of the humeral head. There was no statistically significant
difference between the two arms, suggesting that radiation oncologists did
not intentionally alter the field for patients undergoing SLNB alone.
It has been reported that standard breast tangents encompass approximately
50% of levels I and II of the axilla with 95% of the prescription dose (31).
Increasing the height of the radiation portal with “high tangents” will increase
the percentage of treated axilla. However, there is still a portion of the axilla
that will remain out of the treatment field, as shown in Figure 29-1.
Therefore, in patients with a positive SLNB who do not have completion
ALND, the radiation oncologist should contour an axillary target volume
rather than merely raising the border of the radiation portal. It is imperative
that the radiation oncologist thoroughly review the operative reports when
developing treatment fields. This volume should encompass the entire level I
and II axilla that would normally be targeted by ALND. With tailoring of the
gantry angle and 3D conformal radiation portals, the entire axilla can easily
be included in the treatment field (31). Addition of the entire axilla to the
breast treatment portal has minimal added morbidity for the average patient
and does not preclude her from treatment with hypofractionated radiation.
FIGURE 29-2 Radiation supraclavicular third field design for patients with a
positive sentinel node with SLNB alone versus ALND. Supraclavicular nodes
(orange), level III axilla (cyan), level II axilla (yellow), and level I axilla (magenta) are
shown. A: The lateral border of the supraclavicular field should be extended past the
level I contour, oftentimes this is several centimeters beyond the lateral border of the
humeral head. B: In patients undergoing completion dissection, the lateral border of
the supraclavicular field will block the level I and a portion of the level II axilla,
placing the border at approximately the medial edge of the humeral head.

Decisions regarding the administration of radiotherapy to other regional


nodes (supraclavicular, infraclavicular, internal mammary) in patients with
pT1-2N1 disease are more complex. Factors to consider include young age,
hormone-negative tumors, high grade, LVSI, or large tumor burden at the
primary site or in the nodes (15). There is also data to support use of radiation
to the internal mammary nodes for high-risk patients. The National Cancer
Institute of Canada MA.20 trial randomly assigned lumpectomy-treated
patients mainly with one to three positive nodes (although 10% were high-
risk node negative and 5% had >3 positive nodes) to WBRT +/− RNI. This
trial demonstrated a significant improvement with addition of RNI in 10-year
locoregional recurrence-free survival (HR 0.59, p = 0.009, absolute
improvement of 3%), DFS (HR 0.76, p = 0.01, absolute improvement of 5%),
and distant DFS (HR 0.76, p = 0.03, absolute improvement of 4%), but not in
OS (81.8% vs. 82.8%, p = 0.38) (32). EORTC 22922 included lumpectomy
and mastectomy patients with primarily N0 or N1 disease and similarly
showed significant improvement in DFS (HR 0.89, p = 0.04, absolute
improvement of 3%), distant DFS (HR 0.86, p = 0.02, absolute improvement
of 3%), and breast cancer–specific mortality (HR 0.82, p = 0.02, absolute
improvement of 1.9%) with addition of RNI to radiation to the breast/chest
wall (33). Similar to the results of the MA.20 trial, EORTC 22922 showed no
improvement in OS.
In the setting of a patient with indications for RNI who has had a
completion ALND, the radiation field should not specifically target the level I
axilla. The difference in treatment of the level III axilla and supraclavicular
region as compared to the level I to III axilla and supraclavicular region is
shown in Figure 29-2. Placement of surgical clips at the superior edge of the
axillary dissection for patients undergoing ALND can help guide the target
contouring for the radiation oncologist. Avoiding increased radiation to the
dissected axilla may help to reduce BCRL.

CASES

CASE 1

35-year-old female who undergoes lumpectomy for a 1.5-cm grade I IDC,


luminal A type tumor and SLNB showing one of four nodes involved with
5 mm of metastatic breast cancer.
This patient, while younger than the average patient on Z0011 or
AMAROS, meets criteria for these studies and is appropriate for
omission of completion ALND. Due to young age, comprehensive
radiation would likely be recommended. Radiation portals would be
similar to Figures 29-1C and 29-2A.

CASE 2

60-year-old female who undergoes mastectomy for a grade I, hormone-


positive pT1N1 breast cancer and SLNB showing one node involved with
5 mm of metastatic breast cancer on final pathology. There is no LVSI or
ECE. She has a tissue expander in place and is planning for implant-
based reconstruction.
This patient does not have high-risk features that would prompt
comprehensive PMRT. ALND should be performed. If no additional
positive nodes are found, the patient can forego radiation therapy, which
would make implant-based reconstruction more successful. With only
one sentinel node assessed, which is a macrometastasis, the patient is not
a good candidate for omission of both radiation and axillary lymph node
dissection.

CASE 3

55-year-old female undergoes neoadjuvant chemotherapy for HER2-


positive breast cancer, cT2N1. She converts to ycN0 and undergoes
lumpectomy and sentinel lymph node biopsy. Frozen section of the
sentinel nodes is negative, but final pathologic review shows 1 mm of
residual invasive disease in one of three sentinel lymph nodes.
Any persistent nodal disease after neoadjuvant chemotherapy should
be managed with completion ALND and RNI to the undissected nodal
basins. She would be a candidate for enrolling in Alliance A011202 if she
desired avoiding ALND (24).

CASE 4

45-year-old female who undergoes bilateral mastectomy for a 1.8-cm


grade II hormone-positive, HER2-negative IDC and SLNB showing one
of four nodes positive for metastatic breast cancer on frozen section.
Other than her age, this patient does not have high-risk features that
would prompt comprehensive PMRT. Completion ALND should be
performed unless she enrolls on trial. If no additional positive lymph
nodes are identified, no LVSI or ECE, she could consider enrolling in
MA.39, to use Oncotype Dx recurrence score to decide about the need for
PMRT rather than completion dissection (34).
RISKS OF AXILLARY DISSECTION VERSUS RADIATION
In patients undergoing lumpectomy, radiation is already a component of their
care, and the inclusion of the level I/II axilla in the radiation portal presents
minimal excess risk. For patients undergoing mastectomy, however, there are
many factors to be considered, and patient preferences should also play a role
in the decision making (15). The main benefit for PMRT over axillary
dissection is reduced BCRL, as seen in AMAROS (9). However, this benefit
for reduced BCRL is countered by a risk of radiation-induced cardiac or
pulmonary toxicity. Radiation can also significantly impact cosmesis in
patients undergoing reconstruction after mastectomy. There is markedly
reduced success of implant-based reconstruction, which can lead to more
invasive procedures with autologous reconstruction. Furthermore, many
patients desiring mastectomy have chosen this more aggressive surgery with
the goal to avoid radiation therapy. Therefore, in pN1 patients with favorable
features, who would otherwise not be recommended for PMRT, ALND
should still be performed.
BEYOND AMAROS
In the published studies of SLNB versus ALND in early-stage breast cancer,
IBCSG 23, AMAROS, Z11, and OTOASOR, the patients had relatively low
burden of disease. Most patients had T1 tumors, and a significant proportion
had micrometastatic disease in the lymph nodes. Furthermore, most patients
underwent lumpectomy. None of the published trials allowed neoadjuvant
chemotherapy. Several ongoing trials are aimed to assess patients with higher
disease burden, mastectomy, and/or neoadjuvant chemotherapy, as detailed in
Table 29-2.
The POsitive Sentinel NOde: adjuvant therapy alone versus adjuvant
therapy plus Clearance or axillary radiotherapy (POSNOC) study is aimed at
assessing the role of local therapy in a population of patients similar to
AMAROS and Z11 (35). Eligible patients will have cT1-2N0 disease, with
one to two positive nodes on SLNB. Unlike the former trials, only
macrometastatic disease is allowed. This study assumes equivalence of
ALND versus SLNB with radiation, either of which can be utilized in the
control arm. Patients in the experimental arm are not allowed to receive
axillary radiation. They will undergo radiation to the breast or chest wall
only. The primary end point of the POSNOC trial is axillary recurrence.
Similar to POSNOC, the Sentinel Node biopsy in breast cancer: OMission
of Axillary Clearance (SENOMAC) trial aims to assess the effect of axillary
dissection in cN0 patients with macrometastatic N1 breast cancer on SLNB
(36). For this trial, patients are randomized to ALND versus SLNB alone.
Patients on both arms will receive the same radiation treatment; radiation is
not allowed to target the level I axilla in the SLNB arm. This trial also
includes patients who have received neoadjuvant chemotherapy. The primary
end point for SENOMAC is breast cancer specific survival.

TABLE 29-2 Characteristics of Ongoing Trials of Sentinel Lymph Node


Biopsy Alone in Node-Positive Breast Cancer
The Tailored AXIllary Surgery (TAXIS) trial is a multinational
randomized trial of ALND versus targeted axillary dissection and targeted
radiation in patients with clinically node-positive disease (37). Patients with
suspicious nodes on clinical examination or imaging undergo axillary lymph
node biopsy with clip placement. Eligible patients will have a pathologically
positive axillary biopsy at diagnosis. Patients are stratified by use of
neoadjuvant chemotherapy versus upfront surgery. Targeted axillary
dissection is defined as SLNB and removal of palpable axillary nodes, as well
as verified removal of the previously placed biopsy clip during the biopsy
procedure. All patients receive radiation to the breast or chest wall,
undissected axilla, supraclavicular, and internal mammary nodes. Primary
end point is DFS.
A pair of ongoing trials, Alliance A011202 and RTOG-1304/NSABP-B51,
truly test the theory that effective systemic therapy is essential for local
control (23,24). Eligible patients will have clinically node-positive disease at
the time of diagnosis, confirmed by lymph node biopsy. Patients who then
convert to cN0 after neoadjuvant chemotherapy are taken for surgery with
SLNB. Patients with a pathologic complete response in the biopsied nodes
are randomized to regional nodal radiation or no nodal radiation. Patients
with lumpectomy still receive breast tangent radiation, but mastectomy
patients receive no radiation. Patients with persistent positive nodal disease at
the time of SLNB are randomized to ALND versus targeted radiation to the
level I and II axilla. All patients with persistent nodal disease receive
radiation to the breast/chest wall, supraclavicular nodes, level III axilla, and
internal mammary nodes. The primary end point for both trials is invasive
breast cancer recurrence-free interval.
CONCLUSION
While the need for axillary dissection has been questioned for decades, newly
published trials and ongoing studies are truly challenging the theory that
residual axillary disease contributes to disease control and survival. In light
of the IBSCG and AATRM trials, any patient with micrometastatic nodal
disease can be considered for SLNB alone, even in the setting of mastectomy
without radiation. In patients with macroscopic nodal disease, and ≤2 nodes,
ALND can be omitted if radiation is planned, after either lumpectomy or
mastectomy. The radiation oncologist should take care to target the level I
and II axilla specifically, as per AMAROS. For the select group of N1
mastectomy patients who are eligible for ALND or targeted radiation to the
axilla, presentation at a multidisciplinary tumor conference can be helpful.
Discussion should also ensue with the patient of the risks and benefits of the
two approaches. The patient should be involved in the decision making
process to achieve the best outcomes. For patients with higher nodal disease
burden, T3–4 disease, clinically palpable nodes, or persistent positive nodes
after neoadjuvant chemotherapy, axillary dissection should continue to be
performed unless the patient is enrolled on trial, until data is available from
the ongoing studies.

REFERENCES

1. Lacour J, Le M, Caceres E, et al. Radical mastectomy versus radical


mastectomy plus internal mammary dissection. Ten year results of an
international cooperative trial in breast cancer. Cancer
1983;51(10):1941–1943.
2. Fisher B, Redmond C, Fisher ER, et al. Ten-year results of a randomized
clinical trial comparing radical mastectomy and total mastectomy with
or without radiation. N Engl J Med 1985;312(11):674–681.
3. Louis-Sylvestre C, Clough K, Asselain B, et al. Axillary treatment in
conservative management of operable breast cancer: dissection or
radiotherapy? Results of a randomized study with 15 years of follow-up.
J Clin Oncol 2004;22(1):97–101.
4. Mannino M, Yarnold JR. Local relapse rates are falling after breast
conserving surgery and systemic therapy for early breast cancer: can
radiotherapy ever be safely withheld? Radiother Oncol 2009;90(1):14–
22.
5. Giuliano AE, Ballman K, McCall L, et al. Locoregional recurrence after
sentinel lymph node dissection with or without axillary dissection in
patients with sentinel lymph node metastases: long-term follow-up from
the American College of Surgeons Oncology Group (Alliance)
ACOSOG Z0011 randomized trial. Ann Surg 2016;264(3):413–420.
6. Galimberti V, Cole BF, Zurrida S, et al. Axillary dissection versus no
axillary dissection in patients with sentinel-node micrometastases
(IBCSG 23–01): a phase 3 randomised controlled trial. Lancet Oncol
2013;14(4):297–305.
7. Sola M, Alberro JA, Fraile M, et al. Complete axillary lymph node
dissection versus clinical follow-up in breast cancer patients with
sentinel node micrometastasis: final results from the multicenter clinical
trial AATRM 048/13/2000. Ann Surg Oncol 2013;20(1):120–127.
8. Savolt A, Peley G, Polgar C, et al. Eight-year follow up result of the
OTOASOR trial: the optimal treatment of the axilla—surgery or
radiotherapy after positive sentinel lymph node biopsy in early-stage
breast cancer: A randomized, single centre, phase III, non-inferiority
trial. Eur J Surg Oncol 2017;43(4):672–679.
9. Donker M, van Tienhoven G, Straver ME, et al. Radiotherapy or surgery
of the axilla after a positive sentinel node in breast cancer (EORTC
10981–22023 AMAROS): a randomised, multicentre, open-label, phase
3 non-inferiority trial. Lancet Oncol 2014;15(12):1303–1310.
10. Lyman GH, Somerfield MR, Bosserman LD, et al. Sentinel lymph node
biopsy for patients with early-stage breast cancer: American Society of
Clinical Oncology clinical practice guideline update. J Clin Oncol
2017;35(5):561–564.
11. Dengel LT, Van Zee KJ, King TA, et al. Axillary dissection can be
avoided in the majority of clinically node-negative patients undergoing
breast-conserving therapy. Ann Surg Oncol 2014;21(1):22–27.
12. Bonneau C, Hequet D, Estevez JP, et al. Impact of axillary dissection in
women with invasive breast cancer who do not fit the Z0011 ACOSOG
trial because of three or more metastatic sentinel lymph nodes. Eur J
Surg Oncol 2015;41(8):998–1004.
13. Van Zee KJ, Manasseh DME, Bevilacqua JLB, et al. A nomogram for
predicting the likelihood of additional nodal metastases in breast cancer
patients with a positive sentinel node biopsy. Ann Surg Oncol
2003;10(10):1140–1151.
14. Milgrom S, Cody H, Tan L, et al. Characteristics and outcomes of
sentinel node-positive breast cancer patients after total mastectomy
without axillary-specific treatment. Ann Surg Oncol 2012;19(12):3762–
3770.
15. Recht A, Comen EA, Fine RE, et al. Postmastectomy radiotherapy: an
American Society of Clinical Oncology, American Society for Radiation
Oncology, and Society of Surgical Oncology focused guideline update.
Ann Surg Oncol 2017;24(1):38–51.
16. EBCTCG (Early Breast Cancer Trialists’ Collaborative Group); McGale
P, Taylor C, Correa C, et al. Effect of radiotherapy after mastectomy and
axillary surgery on 10-year recurrence and 20-year breast cancer
mortality: meta-analysis of individual patient data for 8135 women in 22
randomised trials. Lancet 2014;383(9935):2127–2135.
17. Mamounas EP, Liu Q, Paik S, et al. 21-gene recurrence score and
locoregional recurrence in node-positive/ER-positive breast cancer
treated with chemo-endocrine therapy. J Natl Cancer Inst 2017;109(4).
18. Kuerer HM, Sahin AA, Hunt KK, et al. Incidence and impact of
documented eradication of breast cancer axillary lymph node metastases
before surgery in patients treated with neoadjuvant chemotherapy. Ann
Surg 1999;230(1):72–78.
19. Boileau JF, Poirier B, Basik M, et al. Sentinel node biopsy after
neoadjuvant chemotherapy in biopsy-proven node-positive breast
cancer: the SN FNAC study. J Clin Oncol 2015;33(3):258–264.
20. Kuehn T, Bauerfeind I, Fehm T, et al. Sentinel-lymph-node biopsy in
patients with breast cancer before and after neoadjuvant chemotherapy
(SENTINA): a prospective, multicentre cohort study. Lancet Oncol
2013;14(7):609–618.
21. Boughey JC, Suman VJ, Mittendorf EA, et al. Sentinel lymph node
surgery after neoadjuvant chemotherapy in patients with node-positive
breast cancer: the ACOSOG Z1071 (Alliance) clinical trial. JAMA
2013;310(14):1455–1461.
22. Caudle AS, Yang WT, Krishnamurthy S, et al. Improved axillary
evaluation following neoadjuvant therapy for patients with node-positive
breast cancer using selective evaluation of clipped nodes:
implementation of targeted axillary dissection. J Clin Oncol
2016;34(10):1072–1078.
23. National Cancer Institute. Standard or comprehensive radiation therapy
in treating patients with early-stage breast cancer previously treated with
chemotherapy and surgery.
http://www.cancer.gov/clinicaltrials/search/view?
cdrid=750327&version=Health Professional. Accessed May 23, 2019.
24. National Cancer Institute. Comparison of axillary lymph node dissection
with axillary radiation for patients with node-positive breast cancer
treated with chemotherapy.
http://www.cancer.gov/clinicaltrials/search/view?
cdrid=751211&version=HealthProfessional. Accessed May 23, 2019.
25. Dilaveri CA, Sandhu NP, Neal L, et al. Medical factors influencing
decision making regarding radiation therapy for breast cancer. Int J
Womens Health 2014;6:945–954.
26. Consensus Guideline on Diagnostic and Screening Magnetic Resonance
Imaging of the Breast.
https://www.breastsurgeons.org/docs/statements/Consensus-Guideline-
on-Diagnostic-and-Screening-Magnetic-Resonance-Imaging-of-the-
Breast.pdf. Accessed May 23, 2019.
27. Assing MA, Patel BK, Karamsadkar N, et al. A comparison of the
diagnostic accuracy of magnetic resonance imaging to axillary
ultrasound in the detection of axillary nodal metastases in newly
diagnosed breast cancer. Breast J 2017;23(6):647–655.
28. Almerey T, Villacreses D, Li Z, et al. Value of axillary ultrasound after
negative axillary MRI for evaluating nodal status in high-risk breast
cancer. J Am Coll Surg 2019;228(5):792–797.
29. Kilgore LJ, Korentager SS, Hangge AN, et al. Reducing breast cancer-
related lymphedema (BCRL) through prospective surveillance
monitoring using bioimpedance spectroscopy (BIS) and patient directed
self-interventions. Ann Surg Oncol 2018;25(10):2948–2952.
30. Jagsi R, Chadha M, Moni J, et al. Radiation field design in the
ACOSOG Z0011 (Alliance) trial. J Clin Oncol 2014;32(32):3600–3606.
31. Reed DR, Lindsley SK, Mann GN, et al. Axillary lymph node dose with
tangential breast irradiation. Int J Radiat Oncol Biol Phys
2005;61(2):358–364.
32. Whelan TJ, Olivotto IA, Parulekar WR, et al. Regional nodal irradiation
in early-stage breast cancer. N Engl J Med 2015;373(4):307–316.
33. Poortmans PM, Collette S, Kirkove C, et al. Internal mammary and
medial supraclavicular irradiation in breast cancer. N Engl J Med
2015;373(4):317–327.
34. Alliance for Clinical Trials in Oncology; Eastern Cooperative Oncology
Group; NRG Oncology; Southwest Oncology Group. Regional
radiotherapy in biomarker low risk node positive breast cancer
(TAILOR RT). Clinicaltrials.gov. Accessed January 22, 2020.
35. Goyal A, Mann B, Thompson AM; group Ptm. POSNOC: Positive
sentinel node—Adjuvant therapy alone versus adjuvant therapy plus
clearance or axillary radiotherapy. J Clin Oncol
2018;36(15_suppl):TPS600.
36. de Boniface J, Frisell J, Andersson Y, et al. Survival and axillary
recurrence following sentinel node-positive breast cancer without
completion axillary lymph node dissection: the randomized controlled
SENOMAC trial. BMC Cancer 2017;17(1):379.
37. Henke G, Knauer M, Ribi K, et al. Tailored axillary surgery with or
without axillary lymph node dissection followed by radiotherapy in
patients with clinically node-positive breast cancer (TAXIS): study
protocol for a multicenter, randomized phase-III trial. Trials
2018;19(1):667.
CHAPTER 30

Conservative Management of
Postsurgical Lymphedema
MICHELLE LEE HSIA | CHRISTOPHER PHAM | KETAN M. PATEL
HISTORY
Lymphedema is a distressing long-term health problem that many breast
cancer survivors must manage. Cancer-related lymphedema is referred to as
secondary lymphedema and usually involves traumatic injury to the native
lymphatic circulation. Trauma can occur from surgical incisions, lymph node
dissections (sentinel or axillary), radiation, or advanced cancer that
compresses lymphatic structures. Approximately 5% to 20% of women
develop upper extremity lymphedema after sentinel lymph node biopsy
(SLNB) and axillary lymph node dissection (ALND), respectively, with the
risk of those rates of increasing up to 2 years post surgery (1,2). Because of
the higher risk of developing lymphedema after ALNDs compared to SLNBs,
surgeons will try to perform SLNBs whenever appropriate. However, there
are additional risk factors that can raise one’s risk, such as type of breast
surgery (mastectomy vs. lumpectomy), number of lymph nodes removed,
subsequent breast surgeries, radiation, and obesity (2,3). Because of these
covariates, the true incidence of upper extremity lymphedema after surgery is
ill defined.
Most patients who have lymphedema report onset of symptoms within the
first 3 years of surgery (4). However, lymphedema has been reported to occur
within days and up to 30 years after breast cancer treatment (5).
Unfortunately, there is varying data on the incidence and prevalence of
lymphedema after breast cancer, primarily due to differences in diagnosis,
inability to compare different patient populations, and inadequate follow-
up/delayed reporting by patients (4).
Due to the ambiguity of lymphedema incidence rates, patient education
that focuses on risk factors and symptoms of lymphedema should be
integrated in their care. A focus group exploring patients’ experiences with
breast cancer–related lymphedema and its treatments found four substantive
themes (6):
1. Patients felt there was a lack of information on lymphedema provided
before, during, and after cancer treatment.
2. Patients reported common symptoms and triggers. Patients were able to
recall specific triggers that marked the onset of their lymphedema and
common activities that exacerbated their symptoms. These common
symptoms were described as numbness, heaviness, tingling, aching,
tightness, and burning (6).
3. Patients reported difficulty accessing care and resources. Finding
therapists certified in lymphedema is difficult and insurance often limited
the number of visits and compression garments covered.
4. Patients reported that lymphedema had a detrimental impact on quality of
life. Patients commonly reported being unable to participate in day-to-day
activities (either at home or at work) due to pain, limited range of motion,
and/or strength. They also report an inability to enjoy leisure or social
activities because of body image concerns, difficulty finding appropriate
clothing, and disappointment in their performance of activities (6,7).
The optimal treatment of lymphedema likely lies in multidisciplinary care
consisting of surgeons, oncologists, primary care physicians, occupational
therapists, and physical therapists. Traditional and nontraditional therapies
are outlined in this chapter to describe ways to treat and manage breast
cancer-related upper extremity lymphedema. For most patients, a physician is
required to make a referral to a lymphedema-certified occupational therapist
or physical therapist. If a patient does seek services without a referral, it is
still advisable for the rehabilitative team to consult and communicate with the
patient’s oncologist or primary care physician.
RISK REDUCTION EDUCATION
Since there is a lack of understanding and research on why lymphedema
occurs with some patients and not with others who are medically treated
identically, there is also no consensus on how to prevent it from occurring.
Preventative strategies that are given to patients lack scientific evidence and
follow a “common sense” approach (8). The National Lymphedema
Network’s (NLN’s) position paper on Risk Reduction Practices suggest
precautions patients should take after their surgeries to reduce the likelihood
of developing lymphedema (Table 30-1).

TABLE 30-1 NLN Recommendations for Risk Reduction Practicesa


People at Risk for Developing Lymphedema Should Consider:
Reporting any changes in their at-risk limb to their health care provider (i.e.,
changes in size, sensation, color, temperature, or texture)
Maintain normal body weight
Exercise
Be fitted with a compression garment; which is to be worn if any symptoms
start
Maintain good skin care to reduce incidence of infection. Treat any signs of
infection with their medical provider
Avoid trauma when possible (i.e., falls, fractures, burns, venipuncture,
scratches)
Avoid limb constriction of the at-risk limb
Avoid exposure to extreme temperatures
If surgery is needed for the at-risk limb, informing the medical provider of
the risk of lymphedema
Precautionary measures when flying (wearing compression garment,
moving the limb)

aAdapted for upper extremity precautions.


TRADITIONAL THERAPY

Complete Decongestive Therapy


Dynamic insufficiency, also known as high-volume insufficiency, is when the
lymphatic load (amount of lymph fluid) exceeds the ability of an intact
lymphatic system to transport (9). Mechanical insufficiency, known as low-
volume insufficiency, is the reduction in transport capacity of the lymph fluid
due to functional causes, such as surgery, radiation, trauma, or inflammation.
In the case of combined dynamic and mechanical insufficiency, there is a
simultaneous reduction in transport capacity and an increase in lymphatic
load.
Once lymphedema is diagnosed, there is no cure. The primary goal of
treatment is to return lymphedema to a latent and/or manageable stage
through optimizing and utilizing intact lymphatic structures.
Complete decongestive therapy (CDT) (Fig. 30-1) is considered the
standard treatment for lymphedema and consists of a combination of manual
lymphatic drainage (MLD), skin care, compression, and decongestive
exercise.

FIGURE 30-1 Complete decongestive therapy.

Manual Lymphatic Drainage


MLD is a manual treatment technique developed by Emil Vodder (1896–
1986). What initially started as manipulation of swollen lymph nodes for
patients with chronic colds and sinus infections, transformed into an
evidence-based practice of massaging the lymphatic system to drain lymph
fluid. MLD consists of four basic “Vodder strokes” that work due to the
working and resting phase of the strokes.
During the working phase of a stroke, a manual stretch is applied to the
subcutaneous tissue, resulting in the manipulation of the anchoring filaments
of lymph capillaries and the smooth musculature in the wall of the
lymphangions (9). The stroke is applied directionally, with the purpose of
redirecting lymph toward lymph nodes for drainage. The pressure is enough
to stretch the subcutaneous tissues against the underlying fascia, however not
to the extent of damaging the anchoring filaments or other lymphatic
structures (Fig. 30-2) (9).
The resting phase of the stroke is the pressure being released. It is pressure
free, with the elasticity of the skin moving the therapist’s hand passively back
to the starting position. It is during this phase that initial lymph vessels
absorb tissue fluid from the interstitial spaces.

Preparation Pathways and Manual Techniques


Using MLD, therapists are identifying healthy lymphatic areas to serve as
facilitators to drain the protein-rich lymph fluid in the interstitial spaces.
These pathways and lymphatic structures are used to reroute the lymph fluid
from blocked or damaged areas in the swollen arm and breast back to the
venous system. In the example of unilateral, secondary upper extremity
lymphedema after breast cancer, the therapist manipulates lymph nodes and
collectors in healthy adjacent quadrants, including the ipsilateral
supraclavicular (to stimulate return of lymph fluid into the venous system)
and inguinal areas and the contralateral axillary area. The purpose is to
increase lymphangiomotoricity—the working phase of stretching the
subcutaneous tissue—to result in a “suction effect” of the lymph fluid in the
affected area (9).

FIGURE 30-2 Manual stroke. A: Working phase—skin stretch surface area. B:


Working phase—skin stretch proximal direction. C: Resting phase—release stretch,
return to previous position.
Despite lymphatic “watersheds” that separate quadrants in our bodies,
some lymph fluid can cross watershed through lymph capillaries (Fig. 30-3).
Areas with high lymph fluid accumulation cause the lymphatics to dilate in
that area, with that pressure forcing lymph back into the lymph capillaries
(dermal backflow) and across a watershed. After lymph nodes are
manipulated or “activated,” manual strokes of redirecting fluid from a
congested area to a healthy area are continued. Fluid travels from the affected
axilla across the watershed to the contralateral axilla (interaxillary
anastomoses) and ipsilateral inguinal area (axilloinguinal anastomoses). The
initial preparation of lymph nodes and adjacent pathways can initiate a
decrease in limb volume without the manipulation of the limb.
After the preparation of the lymphatic system, the working and resting
strokes of MLD on the affected limb or breast/trunk are performed. Working
manual strokes are completed against the lymph vessels natural flow patterns,
redirecting fluid up to the lymph nodes (toward the axilla in our example).
These manual strokes are applied in quadrants, starting at the shoulder and
upper arm (Fig. 30-4). Each section is “drained” by applying traveling
strokes distal to proximal, to clear and promote lymph movement in that area.
The follow quadrants are the elbow joint, forearm, wrist, and hand/fingers.
The purpose being each proximal section has been activated and cleared by
the manual strokes, therefore as distal sections are being worked on, lymph
fluid is encouraged to move within the pathways promoted up the arm.
When scar tissue obstructs lymphatic circulation, lymphostatic fibrosis can
develop. Due to congestion within the structures, lymph fluid pools and
attracts fat cells that bind in the surrounding tissues. The lymph fluid hardens
and the tissues become denser. The inclusion of fibrosis-breaking techniques
are added to MLD by providing a more intense “kneading” or “s-shape”
maneuver to the skin that is intended to soften and break up areas of fibrosis
(9). This should only be applied once decongestion of the lymphatic system
has begun.
While generally safe, there are some considerations before performing
MLD in patients with active oncologic disease. If a patient has active
malignancies, working with the referring physician is advised. While there is
no conclusive evidence that MLD would accelerate the spread of active
malignancies to other parts of the body, there is reason to be cautious (9).
MLD is contraindicated while patients are actively receiving radiation
therapy because of issues regarding the sensitivity and integrity of the skin.
MLD may be considered after radiotherapy once the skin has healed.
Comorbidities (such as congestive heart failure, renal failure, deep vein
thrombosis, etc.) that affect the lymphatic system should be considered
before performing MLD and should be discussed with the referring physician
before performing any maneuvers.

Self-Care
The lymphatics play a role in immunologic function and the removal of
lymph nodes or damage to the native lymphatic structures increases the risk
of soft tissue infection. Lymph nodes filter bacteria and toxins that invade our
bodies and the immune system works to prevent or stop infection. If the
remaining lymphatic structures cannot keep up with the lymphatic fluid that
needs to filter to fight infection, the protein-rich environment can serve as an
environment for bacteria to grow and spread (9).
As stated previously, the NLN advocates maintaining good skin care and
addressing infections as urgent medical care. Based on expert opinion and
physiologic principles, it is encouraged that patients avoid aggressive skin
care, needle punctures, or blood draws on the affected arm, and monitor for
cuts and scratches secondary to their impaired lymphatic transport ability
(10,11). Any damage to the skin, trauma or heat, can serve as an entrance to
bacteria. During CDT, skin care is performed, and patients are educated on
ways to integrate proper techniques into their daily routines. After proper
cleaning, moisturizing is integral to maintain healthy and intact skin (to
prevent dry and cracked skin). Patients should be comfortable inspecting their
skin for any wounds or signs of infection (redness, tenderness, warmth). If a
patient incurs a wound or blister in their upper extremity, they should follow
basic hygiene protocols of cleaning with soap and water, applying an over-
the-counter antimicrobial ointment, and covering it with a clean, dry bandage
(9). While patients are at an increased risk of infection, not every injury will
result in infection. Educating patients and making them active participants in
their care is crucial.
FIGURE 30-3 Watersheds/lymphatic system; green—lymphatic pathways; red—
anastomoses pathways; red dividing lines—watersheds. (Courtesy of Klose Training.)

FIGURE 30-4 Arm sections for decongestion. A: upper arm quadrant. B: elbow
joint. C: forearm quadrant. D: wrist joint. E: hand/fingers.

During CDT, it is important for patients and therapists to participate in skin


care before and after bandaging. Prior to administering compression
bandaging/stockings, extremities are cleansed and moisturized to prepare the
skin for prolonged periods of coverage. After the patient removes their
compression bandages/stockings, they should also wash their extremity and
apply moisturizer. Moisturizers should be fragrance free, hypoallergenic, and
formulated with a neutral pH.

Compression Therapy
Compression therapy increases the internal pressure inside tissues, including
blood and lymphatic vessels. In most cases of lymphedema, the elastic fibers
in the skin tissues are damaged by the accumulation of fluid and become
unable to provide sufficient resistance against the musculature working
underneath (9). The external pressure forces fluid reabsorption and provides
continued force, which prevents reaccumulation. “Short stretch” compression
bandages have braided cotton fibers that are woven to achieve a certain
degree of elasticity (∼60% extensibility of the bandage’s original length) (9).
The working pressure of a bandage is the resistance the bandage sets
against the working musculature. It is temporary and is dependent on active
muscle contraction. A bandage’s active working pressure increases the tissue
pressure, which contributes to the return of fluids within the venous and
lymphatic vessels. The lower the elasticity, the higher the working pressure.
For example, short-stretch bandages exert less working pressure than “long-
stretch” bandages, which have more than 140% extensibility (vs. ∼60% seen
in short-stretch bandages).
In contrast to working pressure, resting pressure is the pressure the
bandage exerts when there is no muscle contraction. Short-stretch bandages
have both higher working and lower resting pressures than long-stretch
bandages. Short-stretch bandages are more conducive to long periods of wear
time and accommodate most lifestyles and activities, which make them useful
for lymphedema management.

FIGURE 30-5 Compression bandages on the arm.


For CDT, short-stretch bandages are applied after skin care and MLD to
maintain the decongestive effect achieved from MLD. Depending on the
severity of lymphedema, different levels of foam padding can be incorporated
into bandaging to bolster surfaces (i.e., bony structures) or to increase
pressure over areas of fibrosis. Short-stretch bandages are multilayered,
which creates an increasing pressure gradient distally that then tapers as it is
applied proximally (Fig. 30-5). The pressure gradient created by the
bandages then promotes unidirectional drainage.

Therapeutic Exercise
Some lymphedema experts advise the use of compression garments during
vigorous exercise (12). The combination of muscle contraction and
relaxation, working in tandem with the compression, helps to increase venous
and lymphatic return to the circulatory system (lymphangiomotoricity) and
facilitates movement out of the interstitial space. Abdominal breathing
exercises are important to incorporate into treatment to stimulate the deep
lymphatic structures; since the lymphatic system does not have an active
pump to move fluid (like the heart and circulatory system) it is dependent on
active muscle and joint activity. The NLN recommends the following types
of exercises to be safe for lymphedema patients, with oversight from a
certified lymphedema therapist to prevent exacerbation of the swelling:

Remedial Exercises
Remedial exercises are completed during the intensive phase of treatment
when the goal is to reduce the size of the limb as aggressively as possible
(Fig. 30-6). It involves active, repetitive, nonresistive motion (12).
FIGURE 30-6 Remedial exercises example. A: Shoulder shrug. B: Shoulder rolls. C:
Shoulder flexion. D: Shoulder abduction. E: Elbow flexion. F: Finger flexion.

Remedial exercises in the intensive phase focus on draining fluid through


muscle contractions from proximal to distal in the affected limb. For the
upper extremity, after MLD is completed, patients are educated on how to
perform range of motion and joint exercises that promote muscle movement
(see Fig. 30-6). Exercises should be performed proximal to distal, draining
each section of their arm to allow for decongested pathways for lymph fluid.
Starting with the shoulder down to the hand and finger joints, movements
should be done slowly and purposefully, activating specific muscles’
contractions. Patients should be encouraged to perform remedial exercises
daily alongside compression therapy. In addition, patients should also
perform diaphragmatic breathing alongside their exercises in order to create a
negative pressure in the thoracic cavity that facilitates lymphatic return to the
venous system.

Stretching and Flexibility


Stretching activities are important to allow muscle and connective tissue to
move within their full range. Oncology treatments, such as surgery or
radiation, can cause the development of fibrous scar tissue, resulting in
muscle contractures and other joint restrictions. Stretching during treatment
can minimize skin scarring and contractures and simultaneously prevent
lymphatic obstructions. Flexibility exercises should be performed slowly and
progressed gradually.
It is important to note that stretching is not a treatment for lymphedema
(i.e., will not result in limb size reduction) but may reduce the severity of any
joint and muscle limitations. For example, axillary web syndrome (AWS) is a
possible complication after SLNB or ALND and has a reported incidence rate
of 20% and 72%, respectively (13). Although there is no gold standard
treatment for AWS, the mainstay of treatment typically focuses on stretching
and improving flexibility. Patients with AWS should be referred to an
occupational or physical therapist since stretching and increased flexibility
may optimize lymphatic function and help treat symptoms of this condition
(12).

Resistance Exercise
Resistance exercise may reduce limb volume when used as an adjunct to
compression therapy. The two most common forms of resistance exercise are
isotonic and isometric exercises.
Isotonic resistance exercise is the most common form of strength training.
It consists of moving the joint through a range of motion with a constant
weight, typically with a free weight (such as dumbbells or barbells).
Examples of common isotonic resistance exercises used for women with
breast cancer–related upper extremity lymphedema are triceps extensions,
biceps curls, wall push-ups, and pulley exercises.
Isometric resistance exercises involve muscle actions in which the length
of the muscle does not change and there is no visible movement at the joint.
Examples of isometric exercises are shoulder blade squeezes, palms pressed
together with shoulders level, and holding the plank position. The goal
number of repetitions and sets will depend on the patient’s baseline activity
level, oncologic treatment timeline, and lymphedema severity. Resistance
exercise regimens should be set with an occupational or physical therapist,
who can work with the patient on endurance and strength and plan gradual
increases in treatment.
A 2016 systematic review of breast cancer–related upper extremity
lymphedema showed that resistance training could be used to elicit increases
in strength without triggering changes to lymphedema status (14). In
addition, Bok et al. used ultrasound measurements to show that adherence to
a regimen of resistance exercise significantly increased muscle thickness of
the affected arm, while significantly decreasing subcutaneous tissue thickness
(15).
Phases of Care (Fig. 30-7)
Intensive Phase (First Phase)
MLD, skin care, compression therapy, and exercise are the main components
of the first phase of CDT, the intensive/decongestive phase. Traditionally,
patients are seen daily however due to insurance and reimbursement
limitations and the high demand on therapists, this frequency will vary by
clinic. Due to the inability to see patients daily, the importance of patient
education and ability to carry over practices at home is critical. The duration
of the intensive phase will vary depending on the severity of the
lymphedema, patient response, and compliance. Early-stage lymphedema can
be treated and transferred to self-management/home programs in as little as 2
weeks. The intensive phase of therapy for severe cases of lymphedema can
take up to 8 weeks. It is common for lymphedema patients to follow up
annually with their therapists, but this may be sooner if symptoms are
exacerbated due to poor compliance, infection, or other medical
complications.
FIGURE 30-7 Phases of care.

Lymphedema, if caught early, can return to latency with the first phase of
CDT. However, chronic lymphedema is irreversible, and patients typically
struggle with the strict guidelines of MLD and constant compression. Results
will vary based on patient participation, response to different bandages and
compression foam, and the ability to maintain practices independently. While
symmetry between the affected and unaffected limb is unlikely to be
achieved, patients may report feeling “less heavy,” clothes fitting better,
and/or increased satisfaction with their body image (16,17). And this can help
them start to transition to the second phase of CDT, self-management.

Self-Management Phase (Second Phase)


In the second phase, the provision of MLD is transitioned from the therapist
to the patient/home caretaker (family member, home nurse, etc.). Throughout
the first phase, it is emphasized that the patient will be an active participant in
self-MLD, with guided practice performed during therapy and educational
handouts to be used at home. It is recommended that patients perform MLD
(in conjunction with deep diaphragmatic breathing) at least twice daily. We
note that skin-care principles are continued through both phases.
During the second phase, compression therapy changes from compression
bandaging to compression garments. The purpose of compression bandages
in the intensive phase is to provide a constant yet changing compression to
reinforce fluid drainage. Patients are being seen multiple times a week and
rebandaged to prevent reaccumulation changing such that at each visit the
bandages may be reapplied to create a smaller limb circumference.

FIGURE 30-8 Compression garment examples. A: Compression bra. B: Velcro


sleeve. C: Compression sleeve and glove. D: Lymph pads. E: Night compression
sleeves.

As the volume change slows down over time or plateaus, patients are
measured for a compression garment. A compression garment serves as a
maintenance item that will provide enough force to maintain a baseline
circumference rather than providing further reductions in limb circumference.
Many therapists use the analogy that compression garments should be
considered similar to glasses or hearing aids (9). Because there is no cure for
lymphedema, a patient in the second phase of therapy may reach a
manageable level of edema that should be considered their baseline. At that
time, the compression garments should be considered a necessity to everyday
activities of daily living. If patients choose not to wear a compression
garment and maintain this baseline, their lymphedema may reaccumulate
over time and they may require intensive CDT again (phase one).
Compression garments are available for almost any body part. For breast
cancer–related upper extremity lymphedema, there are gloves and gauntlets,
sleeves, bras, and shirts (for trunk compression). Alternatively, from standard
compression sleeves and gloves, there are options for those who need
additional compression or who are unable to don the sleeves independently
(Fig. 30-8). There are also lightweight, breathable, and moisture-wicking
materials that allow patients to wear their garments overnight.
Garments lose efficacy over time due to natural wear to the elasticity and
patients can experience reaccumulation of lymphedema despite proper wear.
If compression garments are worn daily, they need to be replaced every 6 to 9
months. Patients should follow up with their therapists either biannually or
annually for assessment.

Maintenance and Timeline


Dependent on the severity of the initial lymphedema, the functional
performance of the patient, and other possible medical conditions,
lymphedema patients can be “frequent fliers” for therapy care. It is not
uncommon for patients to return for care weeks or months later due to
episodes of infection/cellulitis, exacerbation of swelling from a fall or
strenuous activity, and/or from noncompliance. These patients may need to
start in the intensive phase again dependent on the severity of their
exacerbation or just need a few “refresher” treatments to assist in their self
management..
Patients should follow up at least once a year for measurements and
assistance with new garments. After they complete their therapy, patients can
work with compression garment vendors directly if their lymphedema status
is stable. It is important to educate and reinforce with patients, that their
lymphedema is a disease, that will require lifelong management.
ALTERNATIVE THERAPIES
While CDT is considered the standard treatment for lymphedema treatment,
there are different modalities on the market that are building evidence to their
efficacy. Because CDT is time consuming, labor intensive, and costly,
alternative treatments are being investigated. These alternative modalities can
be less time consuming, performed at home independently, and do not subject
the patient to wear bulky or visible compression therapy. However, currently
there is no evidence that these modalities can effectively be done as a
standalone treatment, but in combination with CDT or paired with one or two
of its principles (i.e., exercise and/or compression bandaging).
Low-Level Laser Therapy
Low-level laser therapy (LLLT), also known as photo biomodulation (PBM)
therapy, is a nonpharmalogic treatment modality for breast cancer–related
lymphedema. It is a noninvasive form of phototherapy that utilizes light
wavelengths (that range from 650 to 1,000 nm) to deliver low irradiance to
the target tissue through a small, hand-held device (Fig. 30-9). It is effective
for reducing inflammation, promoting lymph vessel regeneration, improving
lymphatic motility, and preventing tissue fibrosis (18,19). Small studies have
reported reductions in limb volume, breakdown in scar tissue, and increases
in range of motion.
Storz et al. (2017) found that LLLT did not significantly improve quality
of life, pain scores, grip strength, and limb volume compared to a double-
blind placebo control trial, after 8 weeks of treatment (20). Carati et al.
(2003) found no differences in limb volume directly after treatment with
LLLT, but 31% of subjects had clinically significant reduction in limb
volume 1 to 3 months of follow-up after 2 cycles of LLLT (21). Piller and
Thelander (1998) studied LLLT for 10 weeks and found 19.3% volume
reduction and progressive improvements in subjective symptoms (22). They
did a 2.5-year follow-up with these patients and found that there were
continued reductions in arm volume and reported arm tightness 6 months
after treatment had stopped. In a systematic review of nine studies, Smoot
(2015) found that with LLLT added to CDT reduced limb volume greater
than CDT alone (23). While LLLT has potential as an alternative treatment, it
not been shown to be superior to CDT when used alone (LLLT only) (23).
FIGURE 30-9 Low level laser therapy (LLLT).

Taping
Kinesio taping is a common technique used by therapists that involves
applying elastic bandages to provide muscle support without limiting
movement. Tapes can be left on for 3 for 5 days, with an interval of 24 hours
between applications. While not a primary therapeutic method for
lymphedema, it has been used to complement CDT.
Taping is performed by stretching the skin and allowing the skin to elevate
and produce space between the dermis and epidermis, creating small folds
known as “convolutions.” Creating convolutions is believed to reduce
intradermal pressure, enabling lymph in the interstitial space to travel from
high-pressure to lower-pressure areas. Applying tape on the affected limb in
conjunction with physical activity is believed to increase connective tissue
flexibility, forming a path for lymph to move through the connective tissue
(Fig. 30-10).
A meta-analysis by Gatt et al. (2017) on the effectiveness of Kinesio taping
for cancer-related lymphedema showed that both compression bandaging and
Kinesio taping, when combined with CDT, led to improvements in limb
volume (24). However, compression bandaging-alone yielded greater results.
When Kinesio tape is applied alone, upper limb functionality can improve but
no difference in limb volume has been found (25). Patients and therapists
reported that Kinesio tape was preferred in hot and humid conditions when
compression bandaging was too bulky or uncomfortable. Compared to
compression, Kinesio tape was better accepted and the benefits included
longer wear time, less difficulty in usage, and increased comfort and
convenience (25). In addition, Kinesio taping can be less painful for
management throughout the day and has less impact on the activities of daily
living (less movement restrictions and psychosocial concerns on body
image). Bosman et al. (2014) found that Kinesio taping, in conjunction with
CDT, could be used to promote lymphatic movement across watershed areas
of drainage and could be strategically used on body structures not appropriate
for bandaging (i.e., across the chest to connect axilla to axilla or down the
trunk to connect axilla to inguinal lymph nodes) (Fig. 30-10) (26).

FIGURE 30-10 Kinesio tape. A: Kinesio tape connecting interaxillary anatomoses. B:


Kinesio tape dorsum of hand and fingers.
Intermittent Pneumatic Compression Device
Intermittent pneumatic compression devices (PCD) are home units that
deliver external pneumatic compression through multiple inflatable
components (chambers) and a calibrated, gradient compressor. The number
of chambers can vary, settings are easily adjustable and customizable for
individual use. PCDs have been used to treat lymphedema but the evidence
surrounding its practice varies. Johansson et al. (1998) studied PCDs in
lymphedema by providing 2 hours of pump therapy, 5 days a week for 2
weeks and found no significant reductions in arm volume (27). In addition,
patients reported continued tension and heaviness. A systematic review and
meta-analysis of PCDs for lymphedema by Shao et al. (2014) showed no
significant differences in the percent of volume reduction and reported
symptoms between the PCD + CDT and CDT-alone groups (28).
It is important to highlight that PCDs are used to supplement CDT
therapies and are not meant to be stand-alone treatments. PCDs are beneficial
to patients who are unable to perform self-management of MLD or who are
unable to regularly wear compression bandages or garments. For example,
patients who complain of pain with regular compression bandages or
garments may benefit from PCD therapy. PCDs can be used during the
intensive phase of CDT and/or as part of a home self-management program
to maintain results. Specific to breast cancer–related lymphedema, PCDs are
able to address both upper-extremity limb edema and truncal edema via a
vest.
PREHABILITATION
Knowing that there is no cure for lymphedema and patients who undergo an
SLNB or ALND are at risk of developing lymphedema, how do we best serve
our patients? Prehabilitation is the process of optimizing physical and
psychological functionality preoperatively to enable the individual to
maintain a normal level of function during and after surgery. By establishing
a baseline functional level, identifying impairments and providing
interventions that promote physical and psychological health, the aim is to
reduce incidence and/or severity of future impairments (29). By referring
patients to an occupational or physical therapist prior to their breast surgery,
patients can benefit from:
Lymphedema risk reduction strategies related to activity
Skin care principles
Early compression sleeve measurements to facilitate early therapy
postoperatively
Preoperative stretching and exercise programs to optimize range of
motion and strength
Patients who decline prehabilitation should, at minimum, be educated on
recognizing the signs and symptoms of upper extremity lymphedema after
breast cancer surgery in order to facilitate early detection and treatment.

REFERENCES

1. McLaughlin SA, Bagaria S, Gibson T, et al. Trends in risk reduction


practices for the prevention of lymphedema in the first 12 months after
breast cancer surgery. J Am Coll Surg 2013;216(3):380–389.
2. Michelotti A, Invernizzi M, Lopez G, et al. Tackling the diversity of
breast cancer related lymphedema: perspectives on diagnosis, risk
assessment, and clinical management. Breast 2019;44:15–23.
3. Ribeiro Pereira ACP, Koifman RJ, Bergmann A. Incidence and risk
factors of lymphedema after breast cancer treatment: 10 years of follow-
up. Breast 2017;36:67–73.
4. PDQ® Supportive and Palliative Care Editorial Board. PDQ
Lymphedema. Bethesda, MD: National Cancer Institute.
https://www.cancer.gov/about-cancer/treatment/side-
effects/lymphedema/lymphedema-hp-pdq. Accessed January 20, 2019.
5. Brennan M, Weitz J. Lymphedema 30 years after radical mastectomy.
Am J Phys Med Rehabil 1992;71(1):12–14.
6. Thomas-MacLean R, Miedema B, Tatemichi S. Breast cancer-related
lymphedema: women’s experiences with an underestimated condition.
Can Fam Physician 2015;51:246–247.
7. Tobin MB, Lacey HJ, Meyer L, et al. The psychological morbidity of
breast cancer related arm swelling. Psychological morbidity of
lymphoedema. Cancer 1993;72(11):3248–3252.
8. Cemal Y, Pusic A, Mehrara BJ. Preventative measures for lymphedema:
separating fact from fiction. J Am Coll Surg 2011;213(4):543–551.
9. Zuther J, Norton S, Armer J. Lymphedema Management: The
Comprehensive Guide for Practitioners. 3rd ed. Stuttgart: Thieme; 2013.
10. NLN Medical Advisory Committee. Position Statement of the National
Lymphedema Network: Lymphedema Risk Reduction Practices. New
York: National Lymphedema Network. Updated December 2011.
Available at https://lymphnet.org/position-papers/. Accessed January 1,
2019.
11. McLaughlin S, Bagaria S, Gibson T, et al. Trends in risk reduction
practices for the prevention of lymphedema in the first 12 months after
breast cancer surgery. J Am Coll Surg 2013;216(3);380–389; quiz 511–
513.
12. NLN Medical Advisory Committee. Position Statement of the National
Lymphedema Network: Exercise. New York: National Lymphedema
Network. Updated December 2011. Available at
https://lymphnet.org/position-papers/. Accessed January 19, 2019.
13. Leidenius M, Leppänen E, Krogerus L, et al. Motion restriction and
axillary web syndrome after sentinel node biopsy and axillary clearance
in breast cancer. Am J Surg 2013;185(2):127–130.
14. Nelson NL. Breast cancer–related lymphedema and resistance exercise:
a systematic review. J Strength Cond Res 2016;30(9):2656–2665.
15. Bok SL, Jeon Y, Hwang PS. Ultrasonographic evaluation of the effects
of progressive resistive exercise in breast cancer related lymphedema.
Lymphat Res Biol 2016;14:18–24.
16. Williams A, Vadgama A, Franks P, et al. A randomized controlled
crossover study of manual lymphatic drainage therapy in women with
breast cancer-related lymphoedema. Eur J Cancer Care (Engl)
2012;11(4):254–261.
17. Moseley AL, Carati CJ, Piller NB. A systematic review of common
conservative therapies for arm lymphoedema secondary to breast cancer
treatment. Ann Oncol 2007;18(4):639–646.
18. Baxter G, Liu L, Tumilty S, et al. Low level laser therapy for the
management of breast cancer-related lymphedema: a randomized
controlled feasibility study. Lasers Surg Med 2018;50(9);924–932.
19. Baxter G, Liu L, Petrich S, et al. Low level laser therapy
(photobiomodulation therapy) for breast cancer-related lymphedema: a
systematic review. BMC Cancer 2017;17(1):833.
20. Storz M, Gronwald B, Gottschling S, et al. Photobiomodulation therapy
in breast cancer-related lymphedema: a randomized placebo-controlled
trial. Photodermatol Photoimmunol Photomed 2017;33(1):32–40.
21. Carati C, Anderson S, Gannon B, et al. Treatment of postmastectomy
lymphedema with low-level laser therapy: a double blind, placebo-
controlled trial. Cancer 2013;98(6):1114–1122.
22. Piller NB, Thelander A. Treatment of chronic postmastectomy
lymphedema with low level laser therapy: a 2.5 year follow-up.
Lymphology 1998;31(2):74–86.
23. Smoot B, Chiavola-Larson L, Lee J, et al. Effect of low-level laser
therapy on pain and swelling in women with breast cancer-related
lymphedema: a systematic review and meta-analysis. J Cancer Surviv
2015;9(2):287–304.
24. Gatt M, Willis S, Leuschner S. A meta-analysis of the effectiveness and
safety of kinesiology taping in the management of cancer-related
lymphoedema. Eur J Cancer Care (Engl) 2017;26(5).
25. Martins J, Aguiar SS, Fabro EA, et al. Safety and tolerability of
Kinesio® Taping in patients with arm lymphedema: medical device
clinical study. Support Care Cancer 2016;24(3):1119–1124.
26. Bosman J. Lymphtaping for lymphoedema: an overview of the treatment
and its uses. Br J Community Nurs 2014; Suppl:S12, S14, S16–S18.
27. Johansson K, Lie E, Ekdahl C, et al. A randomized study comparing
manual lymph drainage with sequential pneumatic compression for
treatment of postoperative arm lymphedema. Lymphology 1998;31:56–
64.
28. Shao Y, Qi K, Zhou Q, et al. Intermittent pneumatic compression pump
for breast cancer-related lymphedema: a systematic review and meta-
analysis of randomized controlled trials. Oncol Res Treat
2014;37(4):170–174.
29. Carli F, Gillis C, Scheede-Bergdahl C. Promoting a culture of
prehabilitiation for the surgical cancer patient. Acta Oncol
2017;56(2):128–133.
CHAPTER 31

Selection of Vascularized Lymph Node


Donor Sites for Upper Extremity
Lymphedema Surgery and Strategies
to Minimizing Complications
ANNA C. HOWELL | DANIEL J. GOULD | KETAN M. PATEL

Lymphedema is a debilitating disease. Between 140 and 250 million people


worldwide suffer from lymphedema (1). While the majority of those with this
disease have primary lymphedema, it has been postulated that between 20%
and 50% of women who survive breast cancer will develop unilateral breast
cancer–related lymphedema (BCRL) (2,3). Moreover, women who undergo
axillary lymph node dissection are four times more likely to develop
ipsilateral BCRL when compared to those who undergo axillary lymph node
biopsy alone (2).
LYMPHATIC SYSTEM AND LYMPHEDEMA
The lymphatic system is an important biologic system that regulates
metabolism of lipids, fluid homeostasis, and immune mechanics. Its
mechanics rely on networks of lymphatic vessels and lymph nodes to
transport extracellular fluid, immune cells, as well as molecules and
macromolecules, which may be packaged into a variety of carriers.
This afferent (prenodal) lymph fluid enters lymphatic capillaries, drains
into lymph nodes, and then is transported via efferent (postnodal) lymphatic
vessels. The systemic efferent lymphatic vessels meet at either the thoracic
duct, which then drains into the venous system via the junction of the left
internal jugular and subclavian veins, or the right lymphatic duct, which
drains into the right subclavian vein (4,5).
Flow in the thoracic duct is about 100 mL per hour, and total body flow of
lymph is around 4 to 5 L per day (6). Given the incredible volume of flow,
any disruption can easily lead to edema.
Lymphedema is the pathologic process by which this transport and
drainage of proteinaceous lymph fluid is deranged. This lymphostasis creates
lymphatic vessel hypertension and dilation, which can lead to lymphatic
leakage into the interstitial compartment and, ultimately, dermal backflow
and lymphedema. Primary lymphedema usually becomes apparent within the
first 2 years of life, and occurs when there are structurally or physiologically
abnormal lymphatics (7–9). Secondary lymphedema occurs due to physical
injury of the lymphatic system. Globally, the most common cause of
secondary lymphedema is filariasis (10); in the United States, secondary
lymphedema is usually secondary to ablative cancer treatments.
The International Society of Lymphology has defined a classification
system to describe the progression of lymphedema (11). Stage 0 is a
subclinical or latent condition, defined as the impairment of lymphatic fluid
transportation without any clinical manifestations of lymphedema. Stages I to
III describe the progression of lymphedema. Stage I is defined as the early
accumulation of edema which resolves with elevation of the affected
extremity. Pitting edema may occur at this early stage. Stage II represents
continued limb edema that rarely improves with limb elevation alone and
pitting is present. Stage III describes limb edema classified as lymphostatic
elephantiasis, wherein pitting can be absent and certain skin changes, such as
fibrosis, increased skin thickness, fat deposition, and acanthosis are present.
Interestingly, an affected limb may exhibit more than one stage of
lymphedema, which demonstrates the complicated nature of this disease.
Moreover, further clinical descriptions of lymphedema exist. The extent of
lymphedema and frequency of erysipelas, an infection of the superficial
lymphatic system and the upper dermis, may be factored into the clinical
description of lymphedema. Likewise, the circumference or volume (11) of
the affected limb may be measured and compared to unaffected limbs. Using
the above staging classification system, minimal lymphedema is considered
when limb volume is between 5% and 20% greater than the unaffected side.
A 20% to 40% volumetric increase in affected limb volume is considered
moderate lymphedema, and severe lymphedema is seen when the limb
volume is more than 40% of the unaffected side.
By taking disease progression and clinical manifestations of lymphedema
into account, clinicians can usually diagnose lymphedema by history and
physical examination. If, however, diagnosis is difficult to make on account
of confounding factors such as obesity or other causes of extremity edema
including cardiac or renal failure, or if further information about the affected
limb is otherwise useful in treatment or staging of the disease, imaging
modalities may be warranted.
Multiple studies have demonstrated that BCRL has a negative impact on
quality of life (12–20). BCRL has been shown to cause impairments in the
glenohumeral joint, and has been associated with rotator cuff tendonitis (21).
Despite the overall diminished quality of life in patients with lymphedema,
the severity of clinical lymphedema does not seem to have a direct effect on
the impact on one’s quality of life (22).
TREATMENT OF LYMPHEDEMA
The treatment of lymphedema may be surgical or nonsurgical. Many patients
will start conservative therapy prior to undergoing a surgical procedure (23).
Conservative therapy consists of multiple modalities, usually employed over
several months. Decongestive therapy is one such modality, which aims to
decrease the interstitial fluid burden on the affected limb. Compression
therapy may include customized garments, bandages, and wraps. Some will
also employ intermittent pneumatic compression devices to the affected limb.
Supervised exercise regimens have also proven to be helpful in the
conservative treatment of lymphedema.
Alternatively, surgical treatment may be the best option for some patients.
Surgical treatment may include reductive or debulking procedures, such as
liposuction and direct excision, or may change the physiology of the
lymphedematous limb, in the case of lymphaticovenous bypass or lymph
node transplant. Vascularized lymph node transplant (VLNT) moves lymph
nodes from a donor site as a flap, via their artery and vein, to the
lymphedematous limb, where the microsurgical anastomoses are created. The
remainder of this chapter will focus on VLNT, specifically in regard to the
treatment of upper extremity lymphedema.
No one treatment algorithm exists, so timing of surgical intervention varies
widely. Some surgeons argue that surgical intervention should be employed
when lymphedema is refractory to conservative treatment or causes severe
deformity or physical impairment (24,25). Alternatively, others will prefer to
offer surgical treatment, such as VLNT, prior to the onset of permanent
fibrosis (26–29). Still yet, others advocate for preventative surgical
intervention with lymphaticovenous shunt at the time of breast cancer
extirpation (30). Preventative surgical intervention has not yet become
widespread because of the concern over iatrogenic donor site lymphedema,
and because all those at risk for lymphedema will not develop the disease.
MECHANISM OF ACTION OF VLNT
The mechanism of action of VLNT is based on two physiologic hypotheses:
improved lymphatic drainage, whereby bringing in new, nondiseased lymph
tissue decreases interstitial pressure within the affected area, and
lymphangiogenesis, which describes the growth of new lymphatic channels
in the affected area.
The action of a lymphatic pump system has been proposed (31). High
pressure inflow from the donor artery creates a favorable environment from
which the donor vein drains. New, healthy lymph nodes and associated
lymphatic capillaries from the VLNT provide low pressure within the flap,
and excess lymphatic fluid from the hypertensive surrounding interstitial
fluid is then recruited into the new flap via the high-pressure artery. This fluid
is then mobilized into the venous drainage system via the native
lymphaticovenous connections within the transplanted flap itself. Overall,
this decreases the pressure in the affected area, and will allow for old and
damaged lymph channels to reopen. Long-term evidence has demonstrated,
clinically and via indocyanine green (ICG) imaging, that this physiologic
lymphatic pump system remains functional as long as the venous and arterial
anastomoses remain patent (32,33).
Likewise, the theory of a lymphatic sink has also been described (34).
Akin to arterial and venous pumping of lymphatic fluid, it is proposed that
the new, healthy lymphatic tissue brought with the VLNT flap creates a low-
pressure system into which the surrounding lymphatic fluid may drain. As
such, the lymph nodes within the VLNT flap provide a lymphatic sink for the
surrounding hypertensive interstitial compartment of the lymphedematous
limb. Imaging studies have shown this to be the case: ICG is immediately
taken up into the transplanted lymph node and is then distributed into the
venous system (35).
Lastly, the idea of lymphangiogenesis, or the creation of new lymphatic
channels in the affected area, has been described as a possible mechanism of
action of VLNT. Lymph nodes secrete a human lymphangiogenic growth
factor, vascular endothelial growth factor C (VEGF-C), which has been
shown to be an instrumental growth factor in lymphatic channel creation in
the embryonic stage (36–38). This VEGF-C, which is secreted from the
newly transplanted lymph nodes, may help create connections between the
transplanted new lymphatic channels and the diseased lymph channels in the
recipient tissue. This theory is promoted by imaging with MR lymphography
and lymphoscintigraphy, which have demonstrated that transplanted lymph
nodes become incorporated into the recipient site postoperatively (26).
DONOR SITE OPTIONS
Multiple potential donor sites for VLNT exist. Choosing the most appropriate
donor site for each individual patient requires the surgeon to weigh donor site
starring against the risk of iatrogenic lymphedema. Potential donor sites for
upper extremity lymphedema include the groin (39), supraclavicular (40,41)
and submental (42–44) lymph node basins, as well as omental (45–47) and
jejunal (48) lymph node basins. The use of contralateral axillary lymph nodes
has also been described (49). Importantly, the patient may also have
preferences about donor site which may drive the decision making.
Groin Flap
The lymphatic groin flap (Figs. 31-1 to 31-3), based off of the superficial
circumflex iliac artery, is a workhorse flap in the transfer of lymph nodes.
This flap is generally favorable due to its hidden or concealable scar in the
groin crease. However, it may confer disadvantages owing to the possibility
of iatrogenic lymphedema of the operated extremity. For this reason, careful
dissection is key and reverse lymphatic mapping is advocated.
FIGURE 31-1 The lymphatic groin flap in situ prior to surgical harvest. Markings
demonstrate the borders of the flap, as well as the lymph nodes which drain the
abdomen (within the ellipse) and those that drain the lower extremity, marked
“SLN.”
FIGURE 31-2 The lymphatic groin flap after harvest. The yellow clip marks the
artery, while the green clip marks the vein.
FIGURE 31-3 Recipient site options. A: Proximal forearm recipient site markings,
with the radial artery (labelled “RA”) clearly delineated. B: Proximal forearm
recipient site prepared for vascularized lymph node transplantation. C: Distal
forearm recipient site prepared for vascularized lymph node transplantation.
MRI may be used to locate the lymph nodes in the groin. One study
demonstrated that the lymph nodes are located one-third the distance from
pubic tubercle to the anterior superior iliac spine (50). Ultrasound can also be
employed to localize groin lymph nodes (51). It is important to note that the
suprafascial groin lymph nodes located laterally drain the abdominal wall and
the suprailiac region, whereas the lymph nodes located medially drain the
lower extremity (52,53).
The groin flap is harvested by making an elliptical skin incision below the
inguinal ligament and medial to the sartorius. A skin paddle 10 cm by 5 cm
may be harvested with this flap. The flap is elevated from lateral to medial in
a plane just superficial to the sartorius fascia. The pedicle length is
approximately 2.5 cm and its diameter is 1.5 mm. This flap usually carries
three to four lymph nodes. The majority of lymph nodes are found 3 cm
perpendicularly below this line between the pubic tubercle and the anterior
superior iliac spine. Care is taken near the saphenous vein bulb and junction
with the deeper femoral vein. Superficial lymphatics from the lower
extremity exist within this area and can be inadvertently damaged when
separating the medial portion of the flap.
Outcome studies have demonstrated that limb circumference is improved
when compared to physical therapy alone. There was approximately a 40%
reduction rate in circumference compared to physical therapy alone, which
conferred an 8% circumferential reduction (39). In another study, upper
extremity circumference returned to normal in 10/24 patients, decreased by
more than 50% in 6/24 patients, decreased by less than 50% in 6/24 patients,
and only 2 patients had no change in limb circumference (33). Likewise, no
patients required postoperative physiotherapy or compression garments (39).
Supraclavicular Flap
One of the two commonly utilized lymphatic flaps in the cervical area, the
supraclavicular lymph node flap is based off of the transverse cervical artery.
This flap is favored by some surgeons owing to its concealable scar and low
risk of causing iatrogenic lymphedema. However, the flap may still cause
lymphocele and seroma, and its anatomy can be less consistent.
Preoperative workup usually is performed via CT angiography or
ultrasound, depending on surgeon preference. Most surgeons will prefer to
harvest the right side in order to avoid potential iatrogenic injury to the
thoracic duct. Either an ellipse, if a skin paddle is desired, or an S-shaped
incision, is made between the borders of the clavicle, the sternocleidomastoid
muscle, the trapezius muscle, and the external jugular vein. The inferior
border of the flap is incised first and dissection is begun in a subplatysmal
plane from lateral to medial. The omohyoid is encountered and often must be
divided in order to proceed with dissection in order to encounter the
transverse cervical artery and its vein, which lies between the omohyoid and
the anterior scalene muscles. Dissection is continued to the thyrocervical
trunk posteriorly as it tracks toward the trapezius muscle. Skin perforators are
identified and maintained if skin paddle is desired. Larger lymph nodes are
usually visible and palpable above the anterior scalene muscle. The anatomy
of the transverse cervical artery may be somewhat inconsistent: 80% of the
time, it originates from the thyrocervical trunk and 17% of the time, it
originates directly from the mammary or the subclavian arteries (54). The
pedicle is usually 4 to 5 cm in length and its diameter is 1.5 to 2.5 cm. The
lymph nodes that are carried on this flap are the level V nodes found within
the posterior triangle of the neck. There are usually one to three lymph nodes
that may be harvested with the flap.
Multiple studies have demonstrated favorable outcomes with regard to
subjective outcomes such as overall satisfaction with the surgery and quality-
of-life outcomes. Improvement in limb circumference was found to be
between 14% and 16% at the distal most portion of the limb in one study
(55).
Submental Flap
The next of the cervical flaps, the submental flap, is based off of the
submental artery perforators. It has been viewed favorably for VLNT due to
its very low rate of donor site complications and no chance of donor site
iatrogenic lymphedema. However, it leaves behind a visible scar on the face
which may be intolerable to those with poor scarring. Likewise, dissection
proceeds in close proximity to the marginal mandibular nerve, so careful flap
elevation is essential.
Preoperative workup is usually performed with ultrasound, however this
may vary depending on surgeon preference. The dissection of this flap starts
with a skin paddle designed as an ellipse from the angle of the mandible to
the mandibular symphysis. The submental artery is found as a branch off of
the facial artery and traverses 1 cm below the angle of the mandible. The
pedicle then travels anteriorly toward the mandibular symphysis; the anterior
belly of the digastric may need to be divided in order to preserve perforators
to the skin. Pedicle length is usually less than 1 cm and its diameter is 1 to 2
mm. Level 1a and 1b lymph nodes are carried on the submental flap, which
have approximately three to four per side. Outcome studies have been
favorable. One study demonstrated a mean reduction in upper and lower limb
circumference of 41.4% (35).
Gastroepiploic Flap
One of the two commonly discussed intra-abdominal flaps, the omental, or
gastroepiploic, flap is based off of the right gastroepiploic artery. This is a
favorable flap for VLNT owing to its very few donor site complications when
compared to the groin and supraclavicular donor sites (56) and no chance of
conferring iatrogenic lymphedema. The disadvantages of this flap are owed
to its intra-abdominal location: dissection proceeds in close proximity to the
gastrointestinal tract and may therefore need to be harvested in concert with
an intra-abdominal surgeon if necessary. Additionally, the takeoff of the right
gastroepiploic artery from the right gastroduodenal artery may be as close as
1 cm, so careful dissection is of utmost importance.
Preoperative workup for this flap has been demonstrated to usually be a
CT angiogram in order to carefully elucidate exactly the location of the
lymph nodes in proximity to the pedicle. Dissection of this flap may be
performed laparoscopically or via an open technique. Once in the abdomen,
dissection starts along the greater curvature of the stomach. The lesser sac is
then entered and dissection is continued to the pylorus in order to mobilize
the antrum. The antrum is reflected superiorly in order to visualize the right
gastroepiploic artery origin off of the gastroduodenal artery. Dissection is
then continued along the gastrocolic ligament in order to create the flap,
which is usually 3 cm in width. Once the recipient site is prepared, the artery
and vein are clipped, ligated, and delivered extracorporeally to the limb of
interest. The pedicle is usually 4 cm in length; however, as mentioned
previously, it is of utmost importance to note that the pedicle may be as short
as 1 cm, so careful dissection at and around the pedicle is critical. The pedicle
diameter is 1.5 to 3 mm, and the flap has three lymph nodes on average.
Outcome studies have demonstrated subjective improvement in
lymphedema in 83% and volumetric improvement in 22% (57). The double
gastroepiploic VLNT yielded improvement in limb circumference of 44% in
one study (58).
Jejunal Mesenteric Lymph Node Flap
The next intra-abdominal flap that has been used for VLNT is the jejunal
mesenteric lymph node flap. It confers no risk of iatrogenic lymphedema, a
small and concealable scar, and reliable anatomy. As with the gastroepiploic
flap, the jejunal mesenteric lymph node flap is in close proximity to the
gastrointestinal tract and may require harvest with a laparoscopic surgeon in
order to avoid iatrogenic bowel injury during dissection.
The flap may be harvested via an open or laparoscopic technique. Incision
in the open technique may be made either as a short upper midline incision 3
to 5 cm in length or via an abdominoplasty incision if following autologous
abdominally based breast reconstruction. The proximal one-third of the
jejunum is identified and its mesentery is inspected extracorporeally via
palpation and transillumination to determine an area with a cluster of lymph
nodes. The peritoneum is then incised distally and the mesentery is ligated
distally to proximally toward the root of the mesentery until a vascular
pedicle of appropriate caliber is encountered. All major branches to the
jejunum are maintained to avoid ischemic bowel. Likewise, bowel continuity
is maintained. The pedicle is usually 3 to 5 cm in length and 1 to 2 mm in
diameter. There are an average three lymph nodes per flap (59).
Preliminary outcomes for this flap thus far have been favorable. One study
(59) demonstrated that 12/15 patients who received the jejunal mesenteric
lymph node flap reported subjective improvement and 7/10 patients had
objective improvement in limb circumference at 1 month. Further studies are
necessary over a longer period of time to further demonstrate the efficacy of
this flap.
Lateral Thoracic Lymph Node Flap
Based off of the lateral thoracic artery, this axillary lymph node flap has been
used for VLNT. Advantages of the flap include consistent anatomy, long
pedicle, and an inconspicuous scar. Concerns over this flap lie mostly in the
possibility of iatrogenic lymphedema of the donor site extremity, which may
be as high as 18%. Due to this high risk of iatrogenic lymphedema of the
operated extremity, reverse lymphatic mapping is necessary in order to avoid
this complication.
Preop workup of this area has been described to be ultrasound in order to
identify the pedicle and surrounding lymph nodes. Dissection proceeds with a
skin paddle of approximately 10 cm × 5 cm between the anterior and
posterior axillary lines. Suprafascial dissection is continued to the lateral
border of the 2nd intercostal brachial nerve and the pectoralis minor muscle.
Dissection follows inferiorly along the lateral thoracic artery until sufficient
arterial caliber is encountered. It is important to only harvest level 1 nodes
below the pectoralis minor in order to avoid iatrogenic lymphedema. Pedicle
length is usually 3 to 4 cm and its diameter is 1 to 2 mm. Eleven to fifteen
lymph nodes are found within this flap.
Preliminary outcomes have demonstrated favorable outcomes in 100% of
seven patients, but these were transferred to lower extremity, not upper
extremity. Further longitudinal studies are necessary in order to further
examine the outcomes of this lymphatic flap.
REVERSE LYMPHATIC MAPPING
The concept of reverse mapping (Fig. 31-4) has become a mainstay technique
for harvest of lymph nodes at the base of an extremity (i.e., lateral thoracic
and groin sites) (60,61). The technique involves differential identification of
harvestable lymph nodes and those draining the extremity. The two dyes used
for this include T99 and ICG. Technetium is typically injected into the distal
extremity in order to identify key nodes at the base of the extremity.
Conversely, ICG is injected in the lymphosome of interest. For the groin
VLNT, ICG is injected in to the lower abdomen. For the lateral thoracic
VLNT, ICG is injected in to the lateral chest region. Using a combination of
the near-infrared camera and gamma probe, selective isolation of “safe”
harvestable lymph nodes can be performed from these two sites.
FIGURE 31-4 The concept of reverse lymphatic mapping. A: Technicium-99 (T99) is
injected into the distal extremity and the gamma probe is used to identify key and
sentinel nodes that drain the extremity. B: The sentinel lymph node draining the
extremity is marked “SLN.” This group of lymph nodes is found below the lower
border of the groin flap. C: Indocyanine green (ICG) is injected into the lower
abdomen. D: Once the flap is elevated, the gamma probe is again used to verify that
the flap is not being harvested with any lymph nodes that took in T99. This allows
the safe harvest of the flap without removing any lymph nodes that drain the lower
extremity. E: The flap is examined under near-infrared camera to identify key
lymph nodes that will be transplanted to the lymphedematous limb.
DISCUSSION
Lymphatic surgery continues to grow in popularity. As a result, new
techniques are being described that better stratify patients to an optimal
treatment pathway. Vascularized lymph node transfer techniques have
become an integral part of most surgeons’ armamentarium for the surgical
treatment of moderate- and later-stage lymphedema. Several donor sites exist
when considering VLNT for BCRL. A thorough understanding of the
surgical techniques is imperative to prevent perioperative complications.
Reverse mapping is a critical component when considering surgery at the
base of an extremity. In addition, thorough patient counselling as to the
potential risks of surgery and realistic expectations will help to provide
consistent and reliable patient satisfaction.

REFERENCES

1. Nitti M, Hespe GE, Cuzzone D, et al. Definition, incidence, and


pathophysiology of lymphedema. In: Cheng MH, Chang DW, Patel KM,
eds. Principles and Practice of Lymphedema Surgery. Edinburgh:
Elsevier; 2016.
2. DiSipio T, Rye S, Newman B, et al. Incidence of unilateral arm
lymphedema after breast cancer: a systematic review and meta-analysis.
Lancet Oncol 2013;14:500–515.
3. McLaughlin SA, Wright MJ, Morris KT, et al. Prevalence of
lymphedema in women with breast cancer 5 years after sentinel lymph
node biopsy or axillary dissection: objective measurements. J Clin
Oncol 2008;26:5213–5219.
4. Chin CS, Shahani R. Anatomy of the thorax. In: Sabiston and Spencer
Surgery of the Chest. 9th ed. Amsterdam, NL: Elsevier; 2016.
5. Smith ME, Riffat F, Jani P. The surgical anatomy and clinical relevance
of the neglected right lymphatic duct: review. J Laryngol Otol
2013;127(2):128–133.
6. Hall JE. The microcirculation and lymphatic system: capillary fluid
exchange, interstitial fluid, and lymph flow. In: Hall JE. Guyton and
Hall Textbook of Medical Physiology. 13th ed. Amsterdam, NL:
Elsevier; 2016.
7. Lee B, Laredo J, Lee T, et al. Terminology and classification of
congenital vascular malformations. Phlebology 2007;22:249–252.
8. Lee BB, Laredo J, Seo JM, et al. Treatment of lymphatic malformations.
In: Hemangiomas and Vascular Malformations. New York, NY:
Springer; 2009:231–250.
9. Cheng MH, Chang DW, Patel KM. Principles and Practice of
Lymphedema Surgery. Elsevier Health Sciences; 2015.
10. Babu S, Nutman TB. Immunopathogenesis of lymphatic filarial disease.
Semin Immunopathol 2012;34(6):847–861.
11. Executive Committee. The diagnosis and treatment of peripheral
lymphedema: 2016 consensus document of the International Society of
Lymphology. Lymphology 2016;49(4):170–184.
12. Ahmed RL, Prizment A, Lazovich D, et al. Lymphedema and quality of
life in breast cancer survivors: the Iowa Women’s Health Study. J Clin
Oncol 2008;26(35):5689–5696.
13. Coster S, Poole K, Fallowfield LJ. The validation of a quality of life
scale to assess the impact of arm morbidity in breast cancer patients
post-operatively. Breast Cancer Res Treat 2001;68(3):273–282.
14. Kwan W, Jackson J, Weir LM, et al. Chronic arm morbidity after
curative breast cancer treatment: prevalence and impact on quality of
life. J Clin Oncol 2002;20:4242–4248.
15. Mak SS, Mo KF, Suen JJ, et al. Lymphedema and quality of life in
Chinese women after treatment for breast cancer. Eur J Oncol Nurs
2009;13:110–115.
16. Hayes SC, Rye S, Battistutta D, et al. Upper-body morbidity following
breast cancer treatment is common, may persist longer-term and
adversely influences quality of life. Health Qual Life Outcomes
2010;8:92.
17. Beaulac SM, McNair LA, Scott TE, et al. Lymphedema and quality of
life in survivors of early-stage breast cancer. Arch Surg 2002;137:1253–
1257.
18. Ridner SH. Quality of life and a symptom cluster associated with breast
cancer treatment-related lymphedema. Support Care Cancer
2005;13:904–911.
19. Pinto M, Gimigliano F, Tatangelo F, et al. Upper limb function and
quality of life in breast cancer related lymphedema: a cross-sectional
study. Eur J Phys Rehabil Med 2013;49(5):665–673.
20. Park JE, Jang HJ, Seo KS. Quality of life, upper extremity function and
the effect of lymphedema treatment in breast cancer related lymphedema
patients. Ann Rehabil Med 2012;36(2):240–247.
21. Herrera JE, Stubblefield MD. Rotator cuff tendonitis in lymphedema: a
retrospective case series. Arch Phys Med Rehabil 2004;85:1939–1942.
22. Lee TS, Morris CM, Czerniec SA, et al. Does lymphedema severity
affect quality of life? Simple question. Challenging answers. Lymphat
Res Biol 2018;16(1):85–91.
23. Szolnoky G, Dobozy A, Kemény L. Towards an effective management
of chronic lymphedema. Clin Dermatol 2014;32(5):685–691.
24. Allen RJ Jr, Cheng MH. Lymphedema surgery: patient selection and an
overview of surgical techniques. J Surg Onc 2016;113:923–931.
25. Granzow JW, Soderberg JM, Kaji AH, et al. Review of current surgical
treatments for lymphedema. Ann Surg Oncol 2014;21:1195–1201.
26. Becker C, Vasile JV, Levine JL, et al. Microlymphatic surgery for the
treatment of iatrogenic lymphedema. Clin Plast Surg 2012;39:385–398.
27. Becker C. Autologous lymph node transfers. J Reconstr Microsurg
2016;32:28–33.
28. Koshima I, Narushima M, Yamamoto Y, et al. Recent advancement on
surgical treatments for lymphedema. Ann Vasc Dis 2012;5:409–415.
29. Suami H, Chang DW. Overview of surgical treatments for breast
cancer–related lymphedema. Plast Reconstr Surg 2010;126:1853–1863.
30. Boccardo FM, Casabona F, Friedman D, et al. Surgical prevention of
arm lymphedema after breast cancer treatment. Ann Surg Oncol
2011;18:2500–2505.
31. Lin CH, Ali R, Chen SC, et al. Vascularized groin lymph node transfer
using the wrist as a recipient site for management of postmastectomy
upper extremity lymphedema. Plast Reconstr Surg 2009;123:1265–
1275.
32. Patel KM, Lin CY, Cheng MH. From theory to evidence: long-term
evaluation of the mechanism of action and flap integration of distal
vascularized lymph node transfers. J Reconstr Microsurg.
2015;31(1):26–30.
33. Becker C, Assouad J, Riquet M, et al. Postmastectomy lymphedema:
long-term results following microsurgical lymph node transplantation.
Ann Surg 2006;243:313–315.
34. Cheng MH, Huang JJ, Nguyen DH, et al. A novel approach to the
treatment of lower extremity lymphedema by transferring a vascularized
submental lymph node flap to the ankle. Gynecol Oncol 2012;126:93–
98.
35. Patel KM, Lin CY, Cheng MH. From theory to evidence: long-term
evaluation of the mechanism of action and flap integration of distal
vascularized lymph node transfers. J Reconstr Microsurg 2015;31:26–
30.
36. Saaristo AM, Niemi TS, Viitanen TP, et al. Microvascular breast
reconstruction and lymph node transfer for postmastectomy
lymphedema patients. Ann Surg 2012;255:468–473.
37. Jeltsch M, Kaipainen A, Joukov V, et al. Hyperplasia of lymphatic
vessels in VEGF-C transgenic mice. Science 1997;276:1423–1425.
38. Karkkainen MJ, Haiko P, Sainio K, et al. Vascular endothelial growth
factor C is required for sprouting of the first lymphatic vessels from
embryonic veins. Nat Immunol 2004;5:74–80.
39. Cheng MH, Chen SC, Henry SL, et al. Vascularized groin lymph node
flap transfer for postmastectomy upper limb lymphedema: flap anatomy,
recipient sites, and outcomes. Plast Reconstr Surg 2013;131(6):1286–
1298.
40. Althubaiti GA, Crosby MA, Chang DW. Vascularized supraclavicular
lymph node transfer for lower extremity lymphedema treatment. Plast
Reconstr Surg 2013;131(1):133e–135e.
41. Constantinescu T, Patel KM, Visconti G, et al. Supraclavicular lymph
node flap for lymphedema: early experience and technical refinements.
Plast Reconstr Surg 2015;136(4 Suppl):108.
42. Cheng MH, Huang JJ, Huang JJ, et al. A novel approach to the treatment
of lower extremity lymphedema by transferring a vascularized
submental lymph node flap to the ankle. Gynecol Oncol
2012;126(1):93–98.
43. Cheng MH, Lin CY, Patel KM. A prospective clinical assessment of
anatomic variability of the submental vascularized lymph node flap. J
Surg Oncol 2017;115(1):43–47.
44. Tzou CH, Meng S, Ines T, et al. Surgical anatomy of the vascularized
submental lymph node flap: anatomic study of correlation of submental
artery perforators and quantity of submental lymph node. J Surg Oncol
2017;115(1):54–59.
45. Constantinescu T, Patel KM, Visconti G, et al. Single-stage, dual
gastroepiploic lymph node flaps for the surgical treatment of
lymphedema. Plast Reconstr Surg 2015;136:136–137.
46. Nguyen AT, Suami H. Laparoscopic free omental lymphatic flap for the
treatment of lymphedema. Plast Reconstr Surg 2015;136:114–118.
47. Howell AC, Gould DJ, Mayfield C, et al. Anatomical basis of the
gastroepiploic vascularized lymph node transfer: a radiographic
evaluation using computed tomographic angiography. Plast Reconstr
Surg 2018;142(4):1046–1052.
48. Coriddi M, Skoracki R, Eiferman D. Vascularized jejunal mesenteric
lymph node transfer for treatment of extremity lymphedema.
Microsurgery 2017;37(2):177–178.
49. Gerety PA, Pannucci CJ, Basta MN, et al. Lymph node content of
supraclavicular and thoracodorsal-based axillary flaps for vascularized
lymph node transfer. J Vasc Surg Venous Lymphat Disord
2016;4(1):80–87.
50. Dayan JH, Dayan E, Kagen A, et al. The use of magnetic resonance
angiography in vascularized groin lymph node transfer: an anatomic
study. J Reconstr Microsurg 2014;30(1):41–45.
51. Patel KM, Chu SY, Huang JJ, et al. Preplanning vascularized lymph
node transfer with duplex ultrasonography: an evaluation of 3 donor
sites. Plast Reconstr Surg Glob Open 2014;2(8):e193.
52. Tanis PJ, Nieweg OE. The anatomy and physiology of lymphatic
circulation. In: Atlas of Lymphoscintigraphy and Sentinel Node
Mapping. New York, NY: Springer; 2013:1–5.
53. van der Ploeg IM, Kroon BB, Olmos RAV, et al. Evaluation of
lymphatic drainage patterns to the groin and implications for the extent
of groin dissection in melanoma patients. Ann Surg Onc 2009;16:2994–
2999.
54. Cordova A, D’Arpa S, Pirrello R, et al. Anatomic study on the
transverse cervical vessels perforators in the lateral triangle of the neck
and harvest of a new flap: the free supraclavicular transverse cervical
artery perforator flap. Surg Radiol Anat 2009;31:93–100.
55. Sapountzis S, Singhal D, Rashid A, et al. Lymph node flap based on the
right transverse cervical artery as a donor site for lymph node transfer.
Ann Plast Surg 2014;73(4):398–401.
56. Ciudad P, Manrique OJ, Date S, et al. A head-to-head comparison
among donor site morbidity after vascularized lymph node transfer:
pearls and pitfalls of a 6-year single center experience. J Surg Oncol
2017;115(1):37–42.
57. Nguyen AT, Hiroo S, Hanasono MM, et al. Long-term outcomes of the
minimally invasive free vascularized omental lymphatic flap for the
treatment of lymphedema. J Surg Oncol 2017;115:84–89.
58. Ciudad P, Manrique OJ, Date S, et al. Double gastroepiploic
vascularized lymph node transfers to middle and distal limb for the
treatment of lymphedema. Microsurgery 2017;37:771–779.
59. Coriddi M, Wee C, Meyerson J, et al. Vascularized jejunal mesenteric
lymph node transfer: a novel surgical treatment for extremity
lymphedema. J Am Coll Surg 2017;225(05):650–657.
60. Dayan JH, Dayan E, Smith ML. Reverse lymphatic mapping: a new
technique for maximizing safety in vascularized lymph node transfer.
Plast Reconstr Surg 2015;135:277–285.
61. Scaglioni MF, Suami H. Lymphatic anatomy of the inguinal region in
aid of vascularized lymph node flap harvesting. J Plast Reconstr Aesthet
Surg 2015;68:419–427.
CHAPTER 32

Liposuction as a Viable Treatment for


End-Stage Upper Extremity
Lymphedema
JAUME MASIÀ | CRISTHIAN D. POMATA | PATRÍCIA MARTÍNEZ-JAIMEZ
HISTORY
Lymphedema is a disabling progressive chronic disease that carries
significant physical, functional, and economic consequences which impairs
the patient’s quality of life (1). The upper extremity lymphedema, secondary
to mastectomy, axillary node dissection, or biopsy, and postoperative
irradiation, is a common complication after breast cancer treatment (2).
Prospective cohort studies show that 21.4% of women develop lymphedema
after breast cancer treatment, but the incidence varies considerably, ranging
from 5% to 30% (3).
At the beginning of secondary lymphedema, the obstruction or disruption
of the lymphatic system causes accumulation of fluid and plasma proteins in
the superficial interstitial space. Later, as the lymph stasis persists, the
chronic inflammation response produces fat deposition and fibrosis inducing,
a permanent edematous state with sclerotic changes in the subcutaneous
tissue, altering progressively the remaining functioning lymphatic channels
(4,5). The swelling may generate pain, heaviness, tightness, impaired limb
mobility, body image alteration, and anxiety (6).
The clinical management in early breast cancer–related lymphedema
involves a wide variety of strategies. Initially, patients are treated by
conservative methods such as decongestive lymphatic therapy (DLT)
including manual lymphatic drainage, multilayer bandaging, compression
garments, lymph-reducing exercises and skincare (7,8).
Over the last five decades, microsurgical techniques such as lymphatic–
venous shunt, lymphaticovenous–lymphatic bypass, lymph vessel
transplantation, and lymphatic node transfer, have emerged to reconstruct the
damaged lymphatic system in early stages of lymphedema (9–13). However,
no standardized protocol for lymphedema surgical procedure has been well
established.
Despite the revolutionary concept of restoring the lymphatic system
functionality is gaining popularity, none of these microsurgical procedures
provide a complete reduction of the excess volume in later stages of
lymphedema due to the persistence of the fibrotic and hypertrophied adipose
tissue that occurs in response to the chronic lymph stasis and inflammation.
Therefore, reductive surgical procedures to remove the excess subcutaneous
adipofibrotic tissue are necessary to achieve a complete reduction of the
swelling and reach similar measures to the healthy contralateral arm.
The excisional technique consisting of circumferential massive resection of
skin, subcutaneous fat tissues, and sometimes deep fascia, resurfaced by free
split-thickness or full-thickness skin graft, was first reported by Charles
(1912). It was first applied to the upper limb, by Macey (1940) and
posteriorly, was initially performed in cases of postmastectomy lymphedema
by Bunnel (1948), Watson (1953), and McCormack (1954). However, this
highly invasive “debulking” procedure may result in pain, wound-healing
complications, infections, lymph fistulas, and bizarre cosmetic appearance
(14).
Moreover, the modern liposuction method to remove the excess fat tissue,
via blunt cannulas attached to a suction machine, was first described by
Giorgio and Arpad Fischer in 1976, as a dry technique (15), instead, Illouz is
known for developing the wet technique in 1977 (16). Despite, liposuction is
the most performed aesthetic surgery in the world, in the late nineties,
Brorson introduced the use of liposuction for late breast cancer–related upper
extremity lymphedema, reporting favorable overall results in prospectively
followed patients, achieving a reduction of 83% at 1 month, 98% at 6
months, and 104% at 1 year; with excellent long-term results (17).
INDICATIONS
A surgical approach to remove the hypertrophied fibroadipose tissue is
suitable when a complete reduction of the excess volume of the arm has not
been achieved by conservative treatment or microsurgical lymphatic
procedures. The main indication for selective liposuction as the treatment of
upper extremity lymphedema is the presence of nonpitting lymphedema.
Nevertheless, every patient is rigorously independently evaluated based on
the clinical examination of the lymphedema stage according to the
International Society of Lymphedema (ISL) (Table 32-1) (18), and the results
of the preoperative indocyanine green (ICG) lymphography assessment (19).
There are two predominant circumstances:

TABLE 32-1 Staging of Lymphedema of the International Society of


Lymphology
ISL Stage Features
0/IA Latent or subclinical condition where
swelling is not yet evident despite
impaired lymph transport.
I Early accumulation of fluid relatively
high in protein content which
subsides with limb elevation.
Pitting may occur.
II Limb elevation alone rarely reduces
the tissue swelling and pitting is
manifest. In late stage II, the limb
may not pit as excess
subcutaneous fat and fibrosis
develop.
III Lymphostatic elephantiasis where
pitting can be absent and trophic
skin changes such as acanthosis,
alteration in skin character and
thickness, further deposition of fat
and fibrosis, and warty
overgrowths have developed.

a. Primary selective liposuction is indicated in cases of volume excess,


nonpitting lymphedema ISL stage III, and nonfunctioning lymphatic
channels by ICG lymphography assessment.
b. Secondary selective liposuction is indicated in cases of volume excess,
nonpitting lymphedema in late ISL stage II, and functioning lymphatic
system by ICG lymphography assessment; in patients with previous
microsurgical lymphatics’ derivation, reconstruction, or transplantation
techniques.
Also, the lymphoscintigraphy is a standardized preoperative imaging test
that gives a global evaluation of the functionality of the lymphatic system,
always recommended before any intervention. Even if it is not essential for
the surgical decision, it provides comparative information used in the
postoperative assessment (19).
PREOPERATIVE CARE
In this stage, the main objective is to remove the accumulated lymph keeping
the affected arm without signs of fovea, therefore with nonpitting
lymphedema, as the liposuction is a method to remove fat, not fluid. To
achieve this goal, a complex DLT is necessary for a minimum of 7 to 15
intensive days before surgery.
The Godoy manual lymph drainage technique, consisting of linear motion
along the path of lymphatic vessels toward the corresponding lymph nodes, is
highly recommended (20). This effective therapy option is performed in the
last 4 days for 4 hours, before surgery, to allow an optimal state before the
intervention.
The patient must not take aspirin or salicylates and preparations containing
vitamin E within 10 days before surgery. If some analgesic therapy is
necessary, paracetamol will be a good choice. Alcoholic beverages and
tobacco should be reduced or eliminated. Nevertheless, supplements with
vitamin C and antioxidants are authorized.
The night before surgery, the prophylactic anticoagulant therapy starts
using enoxaparin sodium 20 to 40 mg.
On the surgery day, the measurements of the circumference of the upper
extremities are calculated, starting from point 0, at the olecranon and
continuing toward the proximal and distal part of the arm, measuring and
marking every 5 cm. The wrist (styloid process of the ulna) and hand
(circumference from the base of the thumb) measurements are always taken
independently (Fig. 32-1) (21). In the same way, the whole arm is divided
into quadrants to facilitate symmetric liposuction and precise quantification
of fat removal. If distal functional lymphatics were previously identified by
diagnostic imaging techniques, ICG lymphography is performed before
surgery marking the active lymphatic channels’ trajectory in order to be
careful during liposuction.
FIGURE 32-1 Upper extremity measurement.
FIGURE 32-2 Arm divided into quadrants and tourniquet placement.

The prophylactic antibiotic therapy with Cefazolin 1 g is administrated 1


hour before surgery.
SURGICAL TECHNIQUE
Under general anesthesia, liposuction is performed using power-assisted
liposuction with a vibrating cannula that makes easier the fibroadipose tissue
suction.
The dry technique is performed in the distal segment of the arm (wrist–
elbow) employing a tourniquet pressure of 250 mm Hg (Fig. 32-2) with the
previous exsanguination using Esmarch bandages, to minimize blood loss
(22).
The liposuction is carried out following the technique described by
Brorson (23), through 10 to 15, 3-mm-long incisions, using 15- and 25-cm-
long cannulas with diameters of 3 and 4 mm, respectively. It is executed
circumferentially, step by step, from the distal to proximal arm, removing the
hypertrophied fat as completely as possible using previously measured
circumferences of the healthy arm as a control.
The liposuction with the least damage to the lymphatic system is that
performed longitudinally, parallel to the brachial axis (Fig. 32-3). It always is
preferable to make all the required incisions to avoid transverse or oblique
maneuvers that can destroy the functioning lymphatic channels. Furthermore,
the aspiration should be carried out by delicate cannula movements, in the
superficial subcutaneous plane with the openings towards the deep plane, to
avoid subdermal plexus damage.

FIGURE 32-3 The dry technique in the distal segment of the arm using power-
assisted liposuction always with longitudinal cannula orientation, parallel to the
brachial axis.
FIGURE 32-4 Subcutaneous infiltration of saline solution containing low-dose
adrenaline and lidocaine to perform the wet liposuction technique.

When the distal part of the arm is treated, the incisions are left open to
drain. A sterilized made-to-measure compression sleeve is applied to the arm
to stem bleeding and reduce postoperative edema, utilizing a sterilized Easy-
Slide to facilitate putting on the garment. Then, a sterilized standard interim
glove, in which the tips of the fingers have been cut to facilitate gripping, is
put on the hand, and the tourniquet is removed. Special attention should be
taken with the ischemia time (120 minutes) to avoid skeletal muscle injury or
neuro-vascular problems (24).
Successively, the proximal segment of the arm (elbow–shoulder) is treated
using the tumescence technique, which involves subcutaneous infiltration of
1 to 2 L of saline containing low-dose adrenaline and lidocaine (Fig. 32-4).
The same liposuction technique, described above, with a vibrating cannula, is
performed; however, water-assisted liposuction can also be used. Finally, the
compression sleeve already put on in the distal segment of the arm is pulled
up to compress the whole upper limb, then is lightly wrapped with a large
absorbent compress, keeping the arm at heart level on a large pillow.
In general, the operating time is about 2–3 hours and more than 2 liters of
fat in excess could be effectively removed by liposuction (25). Nevertheless,
the total aspirate volume varies according to the excess of hypertrophied fat
compared to the contralateral arm.
POSTOPERATIVE CARE
After surgery, it is opportune to examine the color, temperature, and
sensitivity of distal areas of the arm and possible bleeding through the open
incisions.
Effective postoperative analgesic therapy is essential to pain control.
The prophylactic anticoagulant therapy with enoxaparin sodium 20 to 40
mg/day continues for 7 days, instead, the prophylactic antibiotic therapy is
maintained with cefazolin 1 mg until discharge and continues with
ciprofloxacin 500 mg every 12 hours for 10 days.
The morning after surgery, the patient is allowed to get up and walk. The
garments are removed 48 hours after surgery, at which moment, the patient
can take a shower. The skin should be lubricated with lotion and the other set
of garments is put on, taking care of the correct placement avoiding wrinkles
or folds formations that produce local pain. It is convenient to put
hydrocolloid dressing between the index finger and thumb, and brachial
plexus. The used set of sleeves, gauntlets, and interim glove, are washed and
dried. The patient repeats this on the fourth postoperative day before
discharge.
The patient changes the garments by herself two or three times a week
until she does not feel pain, always after showering and lubricating the arm,
alternating the two or three sets.
When it is possible for the patient to handle the pain, the garments are
changed every day after being washed. Washing “activates” the garments by
increasing the compression due to shrinkage.
The arm is measured at the 1–6–12 months after surgery. The set of
garments can be renewed three or four times during the first year, increasing
the compression progressively. After the first year, the patient will follow-up
with the doctor every 6 months.
To maintain the effect of liposuction, the compression garment must be
worn continuously.
TREATMENT OUTCOMES
When liposuction is performed to an appropriate candidate, the procedure
should not cause major or minor postoperative complications, not even
further alteration of the lymphatic function (25). To achieve this goal, the
procedure should be performed by a qualified surgeon trained in liposuction
for lymphedema, and supported by a well-prepared team that manages the
pre- and postsurgical care (26).
A progressive postoperative reduction, becoming more symmetrical to the
contralateral arm, is achieved at 6 months, with a good skin retraction
without the need for skin excision (Fig. 32-5). Therefore, all of these
outcomes are translated into successive functional, cosmetical, and quality-
of-life improvements.
In addition, the incidence of erysipelas decrease due to the improved blood
flow in the skin (27), and consequently, the less stagnant lymph and lower
physical compression of the fibrotic-adipose tissue, allow the possibility of a
small improvement on lymphatic function. However, the prevention of
recurrence of lymph accumulation in patients with nonfunctioning lymphatic
system requires life-long management with decongestive therapy and
compression garment.
FIGURE 32-5 Preoperative (left) and postoperative (right) images. A: Advanced
lymphedema of the left arm with nonpitting and nonfunctional lymphatic channels
who underwent primary selective liposuction. B: Patient with nonpitting
lymphedema of the left arm and previous lymphatic–venous anastomosis surgery,
who underwent selective liposuction as a secondary treatment.

Some negative side effects are skin numbness, pain, skin irritation caused
by the compression garment, infection, and bleeding. Nevertheless, all of this
can be well handled without any complications.
CONTRAINDICATIONS
Like all surgical procedures, certain established conditions would exclude
patients from being candidates for selective upper extremity liposuction.
As a specific contraindication, liposuction should never be performed on
patients who are preoperatively not treated in a maximally conservative
manner as it is almost certain that the clinical features will show pits on
pressure, indicating the presence of excess lymph fluid a no the real volume
excess of hypertrophied fat tissue (23).
Other general contraindications comprise patients with an active infection
(lymphangitis, erysipelas), metastatic cancer, open wounds, an active
anticoagulation treatment, a medical or familiar history of coagulation
disorders, not physically fit to undergo surgery, and patients who refuse to
wear compression garments continuously after surgery (23).
CONCLUSION
Nowadays, liposuction is the gold standard treatment to remove the fat
hypertrophy caused by chronic lymphedema. When the procedure is
performed following the steps described, liposuction is a very reliable and
safe technique. Nevertheless, there are some potential complications that one
should always have in mind such as vascular problems due to the tourniquet
ischemia over time, soft tissue necrosis due to aggressive liposuction, and
possible lymphangitis or cellulitis due to the use of the not clean garment.

REFERENCES

1. Ahmed RL, Prizment A, Lazovich D, et al. Lymphedema and quality of


life in breast cancer survivors: the Iowa Women’s Health Study. J Clin
Oncol 2008;26(35):5689–5696.
2. Tsai RJ, Dennis LK, Lynch CF, et al. The risk of developing arm
lymphedema among breast cancer survivors: a meta-analysis of
treatment factors. Ann Surg Oncol 2009;16(7):1959–1972.
3. DiSipio T, Rye S, Newman B, et al. Incidence of unilateral arm
lymphoedema after breast cancer: a systematic review and meta-
analysis. Lancet Oncol 2013;14(6):500–515.
4. Warren AG, Brorson H, Borud LJ, et al. Lymphedema: a comprehensive
review. Ann Plast Surg 2007;59(4):464–472.
5. Brorson H, Ohlin K, Olsson G, et al. Breast cancer-related chronic arm
lymphedema is associated with excess adipose and muscle tissue.
Lymphat Res Biol 2009;7(1):3–10.
6. Fu MR, Ridner SH, Hu SH, et al. Psychosocial impact of lymphedema:
a systematic review of literature from 2004–2011. Psychooncology
2013;22(7):1466–1484.
7. Lasinski BB, McKillip Thrift K, Squire D, et al. A systematic review of
the evidence for complete decongestive therapy in the treatment of
lymphedema from 2004 to 2011. PMR 2012;4(8):580–601.
8. Ezzo J, Manheimer E, McNeely ML, et al. Manual lymphatic drainage
for lymphedema following breast cancer treatment. Cochrane Database
Syst Rev 2015;(5):CD003475.
9. O’Brien BM, Sykes P, Threlfall GN, Browning FS.
Microlymphaticovenous anastomoses for obstructive lymphedema. Plast
Reconstr Surg 1977;60(2):197–211.
10. Baumeister RG, Siuda S. Treatment of lymphedemas by microsurgical
lymphatic grafting: what is proved? Plast Reconstr Surg 1990;85(1):64–
74; discussion 75–76.
11. Ho LCY, Lai MF, Yeates M, et al. Microlymphatic bypass in obstructive
lymphoedema. J Plast Reconstr Aesthet Surg 1988;41(5):475–484.
12. Koshima I, Inagawa K, Urushibara K, et al. Supermicrosurgical
lymphaticovenular anastomosis for the treatment of lymphedema in the
upper extremities. J Reconstr Microsurg 2000;16(6):437–442.
13. Becker C, Assouad J, Riquet M, et al. Postmastectomy lymphedema:
long-term results following microsurgical lymph node transplantation.
Ann Surg 2006;243(3):313–315.
14. Thompson N. The surgical treatment of chronic lymphoedema of the
extremities. Surg Clin North Am 1967;47(2):445–503.
15. Fischer A, Fischer G. First surgical treatment for molding body’s
cellulite with three 5 mm incisions. Bull Int Acad Cosmet Surg
1976;3:35.
16. Illouz YG. Body contouring by lipolysis: a 5-year experience with over
3000 cases. Plast Reconstr Surg 1983;72(5):591–597.
17. Brorson H, Svensson H. Complete reduction of lymphoedema of the
arm by liposuction after breast cancer. Scand J Plast Reconstr Surg
Hand Surg 1997;31(2):137–143.
18. Executive Committee. The diagnosis and treatment of peripheral
lymphedema: 2016 consensus document of the International Society of
Lymphology. Lymphology 2016;49(4):170–184.
19. Akita S, Mitsukawa N, Kazama T, et al. Comparison of
lymphoscintigraphy and indocyanine green lymphography for the
diagnosis of extremity lymphoedema. J Plast Reconstr Aesthetic Surg
2013;66(6):792–798.
20. de Godoy JMP, de Godoy ACP, Maria de FGG. Evolution of Godoy &
Godoy manual lymph drainage. Technique with linear Movements. Clin
Pract 2017;7(4):1006.
21. Yamamoto T, Yamamoto N, Hara H, ey al. Upper extremity
lymphedema index: a simple method for severity evaluation of upper
extremity lymphedema. Ann Plast Surg 2013;70(1):47.
22. Wojnikow S, Malm J, Brorson H. Use of a tourniquet with and without
adrenaline reduces blood loss during liposuction for lymphoedema of
the arm. Scand J Plast Reconstr Surg Hand Surg 2007;41(5):243–249.
23. Brorson H. Liposuction in lymphedema Treatment. J Reconstr
Microsurg 2016;32:56–65.
24. Fletcher IR, Healy TE. The arterial tourniquet. Ann R Coll Surg Engl
1983;65(6):409–417.
25. Hoffner M, Ohlin K, Svensson B, et al. Liposuction gives complete
reduction of arm lymphedema following breast cancer treatment—a 5-
year prospective study in 105 patients without recurrence. Plast
Reconstr Surg Glob Open 2018;6(8):e912.
26. Boyages J, Kastanias K, Koelmeyer LA, et al. Liposuction for advanced
lymphedema: a multidisciplinary approach for complete reduction of
arm and leg swelling. Ann Surg Oncol 2015;22(3):1263–1270.
27. Lee D, Piller N, Hoffner M, et al. Liposuction of postmastectomy arm
lymphedema decreases the incidence of erysipelas. Lymphology
2016;49(2):85–92.
SECTION III

Oncoplastic Techniques and Breast Reduction


33 Oncoplastic Breast Surgery and Shared Decision Making
34 Oncoplastic Techniques in Breast Conservation Therapy—The Plastic
Surgeon’s Perspective
35 Local Flaps for Partial Mastectomy Defects
36 Local Flaps for Breast-Conserving Surgery Defects
37 Avoiding Pitfalls in Symmetry Procedures Following Unilateral
Autologous Versus Implant-Based Reconstruction
38 Breast Reduction and Mastopexy After Massive Weight Loss
39 Vertical Breast Reduction and Rereduction
40 Reduction Mammoplasty With Inverted-T Incision
41 Secondary Breast Reduction
42 Management of Complications in Breast Reduction: The Displaced
NAC
43 Male Breast Reduction: Liposuction Versus Excision
CHAPTER 33

Oncoplastic Breast Surgery and


Shared Decision Making
MAURIZIO BRUNO NAVA | NICOLA ROCCO | GIUSEPPE CATANUTO
HISTORY
Surgical treatment of breast cancer has moved from a simple unique decision
(Halsted mastectomy) to a high number of possible techniques. Multiple
biologic, topographic, and morphologic elements drive the final decision.
Moreover, surgery should integrate with other treatments such as
radiotherapy (RT) and systemic drugs (1–3). Finally, all these elements
should be discussed with the patient and a shared decision should be reached.
Notably, in our previous report we demonstrated that our decisions’ pathway
receives the highest amount of information from the patient. We also proved
that every decision can be adapted to personal and disease-related necessities
(4,5).
SHARED DECISIONS AND BREAST CANCER
Medical decisions have become even more complex nowadays. Very often,
several different therapies can be offered to treat the same disease. These may
be associated to various side effects that can be temporary or irreversible.
Surgery, by definition, determinates irreversible changes. In similar
conditions, the participation of patients in the decision process becomes
mandatory and this is the case of breast cancer surgery (5). Mastectomy, for
example, is a permanent mutilation of an apparently useless organ. For this
reason, some patients refuse complex treatments and still consider this
technique the most simple and suitable decision.
Patients affected by breast cancer requiring surgery may benefit the most
from the shared decision approach, as decisions are particularly complex and
multifactorial. The breast is the most important landmark of female identity
and therefore any scar, mutilation, or amputation needs to be discussed and
managed according to personal values (6).
Not only patients but also the healthcare system benefits from shared
decision making (SDM) with an increase in its efficiency (7). Legare (8) who
confirmed that 20% of patients who participated in SDM choose less-
invasive surgical options proved this. Another study from the Group Health
(9) demonstrated that decision aids determined about 32% less surgery for
hip and knee replacement with consistent savings across 6 months (10,11).
A study from Budden (12) concluded that women not involved in the SDM
were also less likely to be satisfied with the decision process (assessed using
the Treatment Decision Satisfaction Questionnaire and the Brief Symptom
Inventory-18). There is a demonstrated link in this study between
psychological distress and somatization and poor participation in SDM. The
relationship between patient’s involvement and outcomes was analyzed also
by Janz (13).
An active role was associated to higher satisfaction with decision, a higher
education level generated a more active role, and patients who had more self-
efficacy in communication had more influence in the decision process. Some
studies investigated the role of SDM strictly according to surgical strategies.
More mastectomies were associated to a higher patient’s involvement by
Katz in a subanalysis of the Surveillance, Epidemiology, and End Results
(SEER) database (14). Despite it being clear that surgeons supported breast-
conserving surgery, well-informed patients surprisingly decided to remove
the entire gland. The authors speculated that this decision might be
conditioned by fear of recurrence and by the preference for avoiding radiation
treatment. More recent information from evidence at high level can be used
to reassure patients about these issues and encourage breast conservation
whenever is possible (15). Regarding breast reconstruction, it is interesting to
note that this choice is also associated to levels of beneficial interaction
between patients and doctors (16).
GENERAL CONCEPTS OF SDM APPLIED TO ONCOPLASTIC BREAST
SURGERY
The model proposed by Elwyn (17) for SDM translates complex
conceptualization into a practical tool for everyday clinical work. A three-
step process is designed to let the patients move “from initial preference” to
“informed decision.” In the original work by Elwyn the step one of the
clinical tool is called “choice talk.”
During this phase the physician communicates about the diagnosis, the
characteristics of the disease, the amount of known information related to the
actual condition, its prognosis, and the possibility to be treated in several
ways. At this stage, the patients should know that different treatments may
have different consequences and that some of these might matter more to
them than to other people. Moreover, side effects are variable on individual
basis and treatments may be unsuccessful. Before starting an interaction at
this stage, it may be helpful to check reactions and prevent the request of an
immediate and premature closure of the entire process.
The second stage of the process is called “option talk.” During this an
investigation of the actual level of patient’s knowledge about various options
should be performed. A list of possible alternative solutions can be offered
and these should be evaluated in details in terms of harms and benefits. After
a brief summary the final phase will start.
The “decision talk” should focus on preferences of the patients. At this
stage, a preference could be elicited bearing in mind that a backup option
should be available. After this, we can move to a decision although the doctor
should always keep a door open to any change.
This original model was criticized because of possible overlap in the first
two phases. The first phase (choice talk) was then changed in 2017 (18) and
denominated “team talk.” During this phase patients and doctors discuss and
deliberate an alliance to make a final perfectly suitable decision. During the
following phase, each possible alternative has to be discussed in terms of
harms and benefits. An active comparison in view of patient’s principles is
expected at this stage. After discussion of possible options a decision has to
be taken.
PRELIMINARY PHASE
To adapt the three talks model to the oncoplastic work, we added a
preliminary phase in which we collect factual, objective information on
disease and patients’ characteristics.
Patient’s Personal History and Morphologic Characteristics
Several aspects of personal history affect the final surgical decisions. For
instance, patients with a family history of breast cancer, when a gene
mutation is demonstrated (19) can be offered a bilateral mastectomy for
prophylactic purpose. This may happen even in case of small unifocal lesions
otherwise treated by breast-conserving surgery.
General conditions, age, and comorbidities play a role in options’
selection. For example, elderly patients with hormone-responsive disease not
candidate for surgery under general anesthesia, whose lesions are too wide to
allow local anesthesia can be candidate to preoperative systemic endocrine
treatment and surgery can be delayed until this can be performed in safer
conditions (20).
Other conditions may interfere with surgery, for instance, heavy smokers
may risk necrotic complications (21) as well obese patients and diabetic (22).
Previous surgical procedures may interfere with autologous reconstructions
whereas any other surgery to the breast followed by RT could increase the
complication rates and interfere with therapeutic decisions.
During the first consultation, before communicating the diagnosis and
treatment plans, patient’s morphology has to be assessed. The original
oncoplastic workflow included only breast volume and ptosis, but with more
generalized use of autologous tissue and fat transplantation, we advise to
estimate distribution of fat in other regions of the body, morphology of the
lower abdomen, and presence of scars.
Regarding breast volume, we do not use any quantitative estimation. This
can be rather intrusive (except for 3D photography that is poorly validated
and expensive) thus we prefer to rely on bra cup size. Ptosis is classified
according to Regnault classification (23).
Assessment of body mass index can partially assist in identification of risk
factors and surgical choice. In this phase modern imaging can provide useful
information not only for diagnosis and staging of disease, but also for
surgical planning. We use digital mammography to anticipate thickness of
mastectomy flaps and risk of necrotic complications during nipple areolar
complex (NAC)–sparing mastectomy and direct-to-implant (DTI) breast
reconstructions (24,25). Other studies demonstrate that pattern of skin
vascularity (as observed during contrast-enhanced MRI) may provide useful
information for the safe surgical planning of breast reconstructions (26).
Assessment of Disease Characteristics
Breast cancer is a heterogeneous disease. A very basic histologic
classification identifies in situ and invasive cancers. Intraductal cancers are
generally treated with primary surgery. This can be breast conservation or
mastectomy according to extension of disease. Excisions in this case should
be planned in order to leave 1 to 2 mm of free margins (27).
Post–breast-conservation RT has proven to be beneficial in reducing
invasive recurrence (28,29). There are no randomized trials comparing
breast-conserving surgery to mastectomy in this setting. The need of post–
breast-conservation RT could be avoided in selected conditions and this
should be communicated to the patient. Invasive cancers, by definition
require systemic treatment. Generally, this is planned according to a surrogate
classification of molecular subtypes or using gene-based recurrence score
(such as Oncotype Dx) (30) that indicate risk of recurrence and benefit from
chemotherapy (31,32). The information on surrogate subtypes should be
available before surgery as this can indicate primary systemic therapy
(chemotherapy+/− target therapies or hormonal therapy in selected
conditions).
Some trials in the past demonstrated that systemic treatment before surgery
can downsize unifocal cancers and allow breast-conserving surgery or can
allow radical surgery in locally advanced breast cancers. Some authors (33)
demonstrated that despite a higher chance of pathologic complete response
with modern therapies breast-conservation rates are not increasing. For these
reasons patients should be informed properly on the purpose of systemic
therapies administered before surgery.
Clearly the most important driver for surgical decision is the local staging
of disease. Cochrane et al. demonstrated (34) that there is a clear relationship
between tumor size, location, and cosmetic results. This is expressed by a
ratio that can be calculated using digital mammography. Clearly not all
lesions are unifocal, some may be extended to other quadrants, or may be
associated to microcalcifications. All this information should be addressed
before any final decision and should be derived from clinical examination
and imaging including MRI scans. In any case surgical removal has to be
designed with radical intent.
The combination of biologic, morphologic, and topographic information
generates multiple therapeutic choices with an expected equal oncologic
outcome but different side effects. The patient is invited to select the strategy
that better fulfills her needs and expectations.
Before calling for decisions, the surgeon still needs to identify subsets in
which a mastectomy is invariably required (extended DCIS, locally advanced
breast cancer, multicentric or multifocal disease not suitable for breast
conservation due to poor tumor-to-breast ratio). It is debatable if in borderline
conditions breast-conserving surgery has to be offered as in the form of
therapeutic mammoplasties (35) or in any kind of breast-conserving surgery
with uncertain radical intent or with positive margins.
It is advisable to have a defined plan before starting the three steps of the
SDM.
SHARED DECISION MAKING BEFORE ONCOPLASTIC PROCEDURES

Team Talk
During the step one of the SDM the surgeon seeks an alliance with the
patient. In this phase we explain that breast cancer is a very curable disease
especially at early stage. Survival is not really threatened by surgical
decisions provided that surgery is radically performed. Thus life after
diagnosis and treatment in most of the cases is not in threat, on the contrary
quality of life (QoL) is likely to be influenced by poor initial decisions on
treatment. During the initial talk the physicians should involve the other
caregivers provided that the patient is keen to accept support from them in the
decision process. We find it determinant in this phase that doctors should use
a very easy language. Sometimes even well-educated patients can find
medical terminologies hard to understand. In this phase we should inform
patients about uncertainties related to every kind of treatment (i.e., treatment
of breast cancer is multidisciplinary; multiple pathways of treatment may
reach the same goal, each treatment has different consequences; sometimes
treatments are not effective or may generate side effects of different
magnitude). The doctors should be able to check patients’ reactions and avoid
premature closures. Several barriers become evident during this phase. Until
recently for instance, patients still believe that they should do what doctors
think is best.
Once the alliance has been established the doctor becomes entitled to
investigate patients’ values before introducing surgical options. We used a
graphic scale as suggested by Platt and Causarano (36,37).
Option Talk
The proper information burden to patients:

The information on oncologic effects of surgical procedures: The wider


the resection the better the oncologic outcome: False! Inform patients
that wider resections are not required for therapeutic purposes.

Despite surgery still being the most practiced primary treatment of early-
stage breast cancer, systemic and local–regional therapies are effective in
reducing significantly the disease recurrence (local or systemic) and
minimizing extensive resections.
For these reasons, wide free margins for invasive cancers have been
replaced by the no-ink-on-tumor policy for invasive cancer and narrow
margins for DCIS. This policy is a widespread standard for breast
conservation nowadays (38).
Patients should be informed that extensive resections or mastectomies for
unifocal early-stage breast cancer are mainly dictated by their requests and
not by therapeutic needs. Mastectomies are required only when other
techniques cannot be performed on free margins.
THERAPEUTIC MAMMOPLASTIES AND UNCERTAINTIES
Bilateral mammoplasties do not have a therapeutic effect but may have
impact on patient’s QoL and may reduce the need for reoperations for
involved margins (39).
However, side effects and uncertainties can be associated to this technique
and patients should be properly informed. One of these is the timing of
contralateral adjustments. The surgical safety of more complex procedures
seems confirmed by a recent cohort series (40), but the impact on QoL and on
efficiency of healthcare systems of bilateral procedures is still unknown.
It should be stated that the incidence of positive margins may be reduced
and that adjuvant treatments are not delayed after oncoplastic bilateral
resections (41) except for a minor delay in RT administration. A recent
systematic review revealed that even if positive margins can be lowered by
therapeutic mammoplasties, the secondary mastectomy rate can increase (42).
Uncertainties are also present about tumor bed localization for boost of RT
and some authors believe that poor information is available through current
evidence (43). Nonetheless it is not clear if an intraoperative beam of
radiations can be administered on the tumor bed. It is also unknown whether
these techniques can be used as an alternative to mastectomies for
multicentric disease. A trial is ongoing (35) to answer this question. Although
the TEAM study did not investigate QoL some authors (44) demonstrated an
improvement in postsurgery QoL after oncologic mastopexies and reductions.
According to other authors some advantages may be associated with better
administration of RT to smaller breast (45), but information after therapeutic
mammoplasties is still inconsistent.
Patients that after a complete information process, including data on
potential impairment of QoL (46), still require a mastectomy for lesions that
can be easily removed with breast conservation are still entitled to do this. In
fact, the most advanced guidelines still consider total breast removal a gold
standard even in this setting (47).
BREAST RECONSTRUCTION TECHNIQUES AND INFORMATION TO PATIENTS
There is a critical paucity of good-quality evidences for breast reconstruction
(48) and therefore the creation of a reliable information burden for patients
can be troublesome.
For sure patients should be aware about morbidity associated to these
procedures, impact on timing of adjuvant treatments, and effects on QoL.
Data on QoL in breast reconstruction can be partially derived from the
large American cohort study from the Mastectomy Reconstruction outcomes
consortium (MROC) that reveals a significant advantage for patients
undergoing autologous flaps using the validated four-domain breast-Q
questionnaire (49). In the medium-term patients who underwent autologous
reconstructions (2 years), patients who underwent autologous reconstruction
were more satisfied with their breasts and had greater psychosocial well-
being and sexual well-being than did those who underwent implant
reconstruction. Although the authors claim that this information can provide
further support in the decision-making process we do not concur with their
opinion. We recommend extreme caution in conveying these data into
standard clinical practice straightforward for several reasons. The
characteristics of the two cohorts are not largely comparable; a relevant
proportion of cases in the implants group received bilateral mastectomies and
the BMI was significantly higher for women in the autologous group Women
with higher BMI may benefit from receiving an abdominoplasty or a breast
reduction. Patients were treated in a time frame in which more modern one-
stage DTI procedures were not widespread and this certainly may impact on
final results, as well as preservation of the pectoralis major in some cases.
Nipple saving after mastectomy in conjunction with DTI breast
reconstructions may significantly improve levels of QoL (50) and prevent
more scars or lengthier operations.
Such conclusions therefore cannot be extrapolated to current practice and
to populations from other areas who normally bears lower rates of bilateral
procedure and BMI values.
Another report from the Mastectomy Reconstruction Outcomes
Consortium (MROC) (51), based on the same population, evaluated the
complication rates in implant-based versus autologous tissue-based
reconstructions. A very low failure rate was associated to autologous
reconstructions: 1.3% for deep inferior epigastric perforator (DIEP) flaps
versus 7.1% for DTI and two-stage implant-based reconstructions. Clearly a
failure of a major microvascular procedure cannot be compared to that of a
simple procedure like an implant-based reconstruction.
On the other side, once again the nearly doubled complication rate of
autologous only–based procedures (15.5 EI vs. 29.2 DIEP reoperative
complications) is certainly affected by the significantly higher BMI in the
DIEP population. A higher risk of reoperative complications using
autologous tissue, as reported by the MROC, may impact on the timing of
adjuvant procedures. Concerns in this regard are hypothesized by a recent
retrospective series that stated that patients bearing one of the following risk
factors—older age, diabetes, and autologous flap—had a 74% chance of
experiencing delay in chemotherapy initiation (51).
The MROC itself stating a nearly doubled chance of complications
requiring reintervention, envisaged the risk of a delayed access to adjuvant
treatments.
Implant-based reconstruction and DTI breast reconstruction seems a
reasonable alternative option to autologous-based reconstructions.
Surprisingly, one of the few RCTs available on breast reconstruction
contradicts this assumption. The BRIOS RCT (52,53) in its first report
compared immediate one-stage techniques to conventional two stages and
reported a significantly higher risk of complications for DTI breast
reconstructions (including removal of implant, acellular dermal matrix, or
both) than two-stage reconstructions. In a subsequent report published in
2018 no advantages in terms of QoL between the comparators were
identified. Finally the last report, published in 2019 denied advantages in
terms of cost-effectiveness of this technique (53).
This information threatens a promising technique and may compromise a
safe communication process with patients. The BRIOS trial was severely
criticized several times. For instance, Kovacs (54) commented that the
complication rates are too high in this series compared to current quality
standards and poor results maybe the effects of a poor learning curve of the
involved surgical team. Similar comments from Potter (55) highlight that
probably the trial was performed prematurely and that the technique deserves
more preliminary work before being discarded. Potter claims also that the
IDEAL criteria for experimental studies are not entirely observed in this
work. We concur with this viewpoint and we confirmed (56) that a thorough
preoperative assessment of patients’ morphologic characteristics such as
breast ptosis, breast size, and thickness of mastectomy flaps should be taken
into account. Moreover, the dissection of mastectomy flaps should be very
accurately performed to prevent flap ischemia, contamination, and
devascularization. The usefulness of DTI breast reconstructions was in the
past assessed by some lower-evidence studies that in our opinion, can be
considered reasonably reliable.
Some patients may require autologous reconstructions to avoid implants.
Good communication skills are required in this case.
Recently several doubts about the safety of silicone breast implants have
been highlighted in relation to the extremely rare development of breast
implant–associated anaplastic large cell lymphoma (BIA-ALCL).
BIA-ALCL is a distinctive type of T-cell lymphoma arising around breast
implants (57). The first case of BIA-ALCL was described in 1997 (58),
almost four decades after the introduction of silicone breast implants. Since
the first described case, the number of reported cases of BIA-ALCL has
increased, likely as a result of increased awareness.
Data from a U.S. population-based study showed an incidence of BIA-
ALCL of 2.03 per million women per year, with a lifetime prevalence of 1 in
30,000 for women with textured implants (59). Recent data from Australia
and New Zealand would have revealed a rise in the frequency of BIA-ALCL
with an estimated incidence rising from 1 in 300,000 to 1 in 1,000 to 10,000
patients (60). These data suggested a potential association between textured
implants and the development of BIA-ALCL, even though no specific risk
estimates could be calculated because we actually do not know the exact
global breast implants’ sales data, that implies we do not know the
denominators to consider when calculating specific relative risks (i.e., total
number of textured and smooth breast implants) and no data showing a
definitive association between texturization and BIA-ALCL can be derived
from published literature, specifically long-term follow-up large cohort
studies.
Many surgeons around the world are looking for alternatives to implants
for breast reconstruction, myocutaneous pedicled and muscle-sparing free
flaps being the first considered alternatives to silicone implants.
However, according to several studies, breast reconstruction with
autologous tissue flaps is not free from complications and high rates of
reinterventions and the flap surgical procedures are time consuming and
expensive (when compared to implant-based reconstruction).
The MROC study, a prospective multicenter trial, recruited patients
undergoing breast reconstruction (implant based and autologous tissue based)
following mastectomy from 11 centers across North America from February
2012 to July 2015. The results of this trial in terms of patient-reported
outcomes and postoperative complications have been presented in several
reports (49,51). Reported 2-year complications’ rate following autologous
tissue-based reconstruction is 47% versus 26.6% with implant-based
techniques, reported reoperation rates are 27.4% with autologous tissues
versus 15.5% with implants. These data must be taken into account when
considering autologous flaps as alternatives to silicone implants for breast
reconstruction.
The MROC data are extremely relevant also when considering a breast
reconstruction in the radiotherapic setting.
Increasingly, surgical options in women requiring postmastectomy
radiotherapy (PMRT) are immediate autologous procedures, or immediate
mesh-assisted implant reconstructions with the latter comprising either one-
or two-stage procedures, various anatomic locations of implants (either
subpectoral or prepectoral), and biologic or synthetic meshes. Currently,
these various options are unsubstantiated by high-quality clinical evidence
(61,62).
The MROC study showed significantly fewer surgical complications and
improved patient-reported QoL outcomes after immediate autologous breast
reconstruction compared to immediate implant-based reconstruction and
PMRT at 2 years following mastectomy (49). A meta-analysis similarly
concluded reduced levels of morbidity following autologous breast
reconstruction compared to implant procedures in the RT setting (63).
Studies have historically reported a higher incidence of fat necrosis and
flap contracture in women undergoing immediate versus delayed autologous
reconstructions, with PMRT significantly exacerbating surgical morbidity
(64,65). Potential support for the efficacy and tolerability of autologous tissue
to radiation treatment comes from “proof of principle” studies evaluating
chest wall microvascular perforator tissue replacement flaps (thoracodorsal
artery perforator [TDAP], lateral intercostal artery perforator [LICAP], lateral
thoracic artery perforator [LTAP] flaps) after partial mastectomy and RT
(66–68).
The use of autologous tissue is the “standard of care” for delayed breast
reconstruction in the irradiated patient. The optimal timing for a delayed
autologous tissue-based reconstruction in the setting of RT remains uncertain
and is supported only by level IV clinical evidence. Studies are conflicting in
terms of reduction in rates of free abdominal flap loss when breast
reconstruction is performed at 12 months or more after PMRT compared to
earlier interventions (69,70).
CONCLUSION

Messaging to Patients
List of simplified messages for patients:

Oncologic messaging
Breast conservation with postop radiation is safe
Mastectomy per se is not a cure but may be required to provide safe
removal of disease
Resections with wider free margins are no more required
Systemic therapies cure the disease also locally
Primary systemic therapies are safe and may reduce the extent of
surgery
Local recurrence rates are very low and not dissimilar among breast-
conserving surgery and mastectomy
Reconstructive messaging
Bilateral therapeutic mammoplasties can reduce the needs for
reoperation for positive margins but may increase the secondary
mastectomy rate and delay adjuvant treatments
The timing of contralateral reductions is not clear (immediate or
delayed after RT)
Breast reconstruction with implants in one stage can be accomplished
when specific characteristics occur
Two-stage breast reconstructions can be suitable for patients with large
and ptotic breast at risk of poor vascularity
Fat grafting increases cosmetic results of implant-based
reconstructions
Some preliminary and experimental evidence proved a regenerative
effect of fat grafting in after radiation–induced damage
ALCL is a rare complication related to use of implants
Other immune system disease may arise in association to implants, but
they are still very rare
Autologous reconstructions require long-lasting operations and
excellent surgical skills. The complication rate is higher and this may
compromise the access to adjuvant therapies
Higher rates of QoL can be provided by autologous reconstruction
when compared with implant-based techniques
Physical morbidity may be increased by myocutaneous pedicled flaps
that should be discarded in favor of more preservative fasciocutaneous
microvascular flaps (DIEP etc.)
Thin patients, diabetics, and obese women are not good candidates for
autologous reconstructions
Autologous tissue-based techniques represent the first reconstructive
choice for radiotreated patients, as a delayed option
Autologous reconstruction can be a reasonable alternative after
multiple failures with implants

Assessment of Patients’ Values


Patients’ values are directly connected to the final surgical decision. These
can be assessed in several ways. However, the exercise model tested by
Causarano (37) is used in our current practice. We ask the patient to rate their
personal values (1 to 5) regarding:

Minimal scars on other part of the body


Shortest hospital stay
Avoid foreign body in my body
Lowest risk for very serious complications
Natural looking and feeling when naked
Smallest number of future surgeries

Once assessed, patients’ values are translated into three subgroups of possible
techniques.
Possible Techniques
Minimal aggressiveness
Maximum reshape
Mastectomy

These were created according to a qualitative classification of complexity


based on:

Length of scars: a single linear segment; two segment (like comma-


shaped, j-shaped mammoplasties or vertical scars); Wise pattern, more
scars outside the breast
Number of anatomical sites involved in the surgical procedure (one
breast vs. both; other donor sites outside the breast such as back,
abdomen, thigh, etc.)
Length of procedure
Mastectomy and reconstruction: with or without reconstruction
Reconstruction in one or two stages with implants or autologous or both
with or without contralateral adjustment

From the combination of these characteristics, we identified three possible


subgroups according to mastectomy or breast conservation (patients are
candidates of breast-conserving surgery according to local staging of
disease):

1. Minimal aggressiveness: techniques included in the first subgroup can


be offered to patients seeking the lowest surgical impact: less scars,
short inpatients, no drains, and minimal complications; willing to accept
minimal bilateral asymmetries or even deformities. Following to our
previous investigation we may add to this subgroup, patients who may
not be concerned by deformities and those may require very simple
procedure even if this may generate a distorted breast shape. This can be
the condition of elderly women or patients with comorbidities who may
seek quick surgery under local anesthetics.
2. Maximum reshape: In subgroup 2 we include bilateral therapeutic
mammoplasties; this can be offered to patients who request the
maximum reshape and are not prepared to accept any kind of
asymmetric result. These maybe more prepared to undergo lengthier
operations, postop drains, or sometimes according to surgeon’s
preferences, undergo a delayed contralateral procedure.
3. Mastectomy: Option three may be suitable for patients those despite
breast-conserving surgery can be performed still require a mastectomy.
Clearly this subgroup may gather women who refuse breast
reconstruction or those who prefer to save as much as possible the
cutaneous envelope (including the NAC) but not the glandular tissue.

Patients who are invariably candidates for mastectomy are offered the most
simple reconstruction (one stage with implants without contralateral
symmetry procedures) for minimal aggressiveness. These patients should be
prepared to get a moderate/major degree of asymmetry. The most reasonable
goal for this surgery is wearing a bra without any visible damage to the social
aspect of the breast.
The second subgroup maximum “reshape” includes those interested in
getting symmetric results as much as possible. To these patients we may offer
two-stage, or one-stage breast reconstruction with contralateral procedures.
This subgroup may include autologous reconstruction.
The third subgroup includes patients who desire only breast removal
without breast reconstruction.

REFERENCES

1. Fisher B, Wolmark N, Redmond C, et al. Findings from NSABP


Protocol No. B-04: comparison of radical mastectomy with alternative
treatments. II. The clinical and biologic significance of medial central
breast cancers. Cancer 1981;48(8):1863–1872.
2. Fisher B, Anderson S, Redmond CK, et al. Reanalysis and results after
12 years of follow-up in a randomized clinical trial comparing total
mastectomy with lumpectomy with or without irradiation in the
treatment of breast cancer. N Engl J Med 1995;333(22):1456–1461.
3. Rastogi P, Anderson SJ, Bear HD, et al. Preoperative chemotherapy:
updates of National Surgical Adjuvant Breast and Bowel Project
Protocols B-18 and B-27. J Clin Oncol 2008;26:778–785.
4. Catanuto G, Khan A, Ursino V, et al. De-escalation of complexity in
oncoplastic breast surgery: case series from a specialized breast center.
Breast 2019;46:12–18.
5. Catanuto G, Pappalardo F, Rocco N, et al. Formal analysis of the
surgical pathway and development of a new software tool to assist
surgeons in the decision making in primary breast surgery. Breast
2016;29:74–81.
6. Gerteis M, Edgman-Levitan S, Daley J, et al. Through the Patient’s
Eyes. San Francisco: Jossey-Bass; 1993.
7. Agrawal S, Goel AK, Lal P. Participation in decision making regarding
type of surgery and treatment-related satisfaction in North Indian
women with early breast cancer. J Cancer Res Ther 2012;8(2):222–225.
8. Légaré F, Adekpedjou R, Stacey D, et al. Interventions for increasing
the use of shared decision making by healthcare professionals. Cochrane
Database Syst Rev 2018;7:CD006732.
9. Arterburn D, Wellman R, Westbrook E, et al. Introducing decision aids
at Group Health was linked to sharply lower hip and knee surgery rates
and costs. Health Off (Milwood) 2012;31(9):2094–2104.
10. Mahmoodi N, Sargeant S. Shared decision-making rhetoric and reality:
women’s experiences and perceptions of adjuvant treatment decision-
making for breast cancer. J Health Psychol 2019;24(8):1082–1092.
11. de Mik SML, Stubenrouch FE, Balm R, et al. Systematic review of
shared decision-making in surgery. Br J Surg 2018;105(13):1721–1730.
12. Budden LM, Hayes BA, Buettner PG. Women’s decision satisfaction
and psychological distress following early breast cancer treatment: a
treatment decision support role for nurses. Int J Nurs Pract
2014;20(1):8–16.
13. Janz NK, Wren PA, Copeland LA, et al. Patient-physician concordance:
preferences, perceptions, and factors influencing the breast cancer
surgical decision. J Clin Oncol 2004;22(15):3091–3098.
14. Katz SJ, Lantz PM, Janz NK, et al. Patient involvement in surgery
treatment decisions for breast cancer. J Clin Oncol 2005;23(24):5526–
5533.
15. Buchholz TA, Tucker SL, Erwin J, et al. Impact of systemic treatment
on local control for patients with lymph node-negative breast cancer
treated with breast-conservation therapy. J Clin Oncol 2001;19(8):2240–
2246.
16. Ananian P, Houvenaeghel G, Protière C, et al. Determinants of patients’
choice of reconstruction with mastectomy for primary breast cancer. Ann
Surg Oncol 2004;11(8):762–771.
17. Elwyn G, Frosch D, Thomson R, et al. Shared decision making: a model
for clinical practice. J Gen Intern Med 2012;27(10):1361–1367.
18. Elwyn G, Durand MA, Song J, et al. A three-talk model for shared
decision making: multistage consultation process. BMJ 2017;359:j4891.
19. Metcalfe K, Lynch HT, Ghadirian P, et al. Contralateral breast cancer in
BRCA1 and BRCA2 mutation carriers. J Clin Oncol 2004;22(12):2328–
2335.
20. Spring LM, Gupta A, Reynolds KL, et al. Neoadjuvant endocrine
therapy for estrogen receptor-positive breast cancer: a systematic review
and meta-analysis. JAMA Oncol 2016;2(11):1477–1486.
21. Goodwin SJ, McCarthy CM, Pusic AL, et al. Complications in smokers
after postmastectomy tissue expander/implant breast reconstruction. Ann
Plast Surg 2005;55(1):16–19; discussion 19–20.
22. Robertson SA, Jeevaratnam JA, Agrawal A, et al. Mastectomy skin flap
necrosis: challenges and solutions. Breast Cancer (Dove Med Press)
2017;9:141–152.
23. Regnault P. Breast ptosis. Definition and treatment. Clin Plast Surg
1976;3(2):193–203.
24. Rancati A, Angrigiani CH, Hammond D, et al. Direct to implant
reconstruction in nipple sparing mastectomy: patient selection by
preoperative digital mammogram. Plast Reconstr Surg Glob Open
2017;5(6):e1369.
25. Frey JD, Salibian AA, Choi M, et al. Mastectomy flap thickness and
complications in nipple-sparing mastectomy: objective evaluation using
magnetic resonance imaging. Plast Reconstr Surg Glob Open
2017;5(8):e1439.
26. Bahl M, Pien IJ, Buretta KJ, et al. Can vascular patterns on preoperative
magnetic resonance imaging help predict skin necrosis after nipple-
sparing mastectomy? J Am Coll Surg 2016;223(2):279–285.
27. Morrow M, Van Zee KJ, Solin LJ, et al. Society of Surgical Oncology-
American Society for Radiation Oncology-American Society of Clinical
Oncology Consensus Guideline on margins for breast-conserving
surgery with whole-breast irradiation in ductal carcinoma in situ. Ann
Surg Oncol 2016;23(12):3801–3810.
28. Early Breast Cancer Trialists’ Collaborative Group (EBCTCG), Correa
C, McGale P, et al. Overview of the randomized trials of radiotherapy in
ductal carcinoma in situ of the breast. J Natl Cancer Inst Monogr
2010;2010(41):162–177.
29. McCormick B, Winter K, Hudis C, et al. RTOG 9804: a prospective
randomized trial for good-risk ductal carcinoma in situ comparing
radiotherapy with observation. J Clin Oncol 2015;33(7):709–715.
30. Tang G, Cuzick J, Costantino JP, et al. Risk of recurrence and
chemotherapy benefit for patients with node-negative, estrogen receptor-
positive breast cancer: recurrence score alone and integrated with
pathologic and clinical factors. J Clin Oncol 2011;29(33):4365–4372.
31. Park KU, Chen Y, Chitale D, et al. Utilization of the 21-gene recurrence
score in a diverse breast cancer patient population: development of a
clinicopathologic model to predict high-risk scores and response to
neoadjuvant chemotherapy. Ann Surg Oncol 2018;25(7):1921–1927.
32. Soran A, Bhargava R, Johnson R, et al. The impact of Oncotype DX®
recurrence score of paraffin-embedded core biopsy tissues in predicting
response to neoadjuvant chemotherapy in women with breast cancer.
Breast Dis 2016;36(2–3):65–71.
33. Criscitiello C, Curigliano G, Burstein HJ, et al. Breast conservation
following neoadjuvant therapy for breast cancer in the modern era: are
we losing the opportunity? Eur J Surg Oncol 2016;42(12):1780–1786.
34. Cochrane RA, Valasiadou P, Wilson AR, et al. Cosmesis and
satisfaction after breast-conserving surgery correlates with the
percentage of breast volume excised. Br J Surg 2003;90(12):1505–1509.
35. Winters ZE, Benson JR; MIAMI (Multiple Ipsilateral breast conserving
surgery versus mastectomy) Trial Management Group. Surgical
treatment of multiple ipsilateral breast cancers. Br J Surg
2018;105(5):466–468.
36. Platt J, Baxter N, Jones J, et al. Pre consultation educational group
intervention to improve shared decision-making in postmastectomy
breast reconstruction: study protocol for a pilot randomized controlled
trial. Trials 2013;14:199.
37. Causarano N, Platt J, Baxter NN, et al. Pre-consultation educational
group intervention to improve shared decision-making for
postmastectomy breast reconstruction: a pilot randomized controlled
trial. Support Care Cancer 2015;23(5):1365–1375.
38. Havel L, Naik H, Ramirez L, et al. Impact of the SSO-ASTRO margin
guideline on rates of re-excision after lumpectomy for breast cancer: a
meta-analysis. Ann Surg Oncol 2019;26(5):1238–1244.
39. O’Connell RL, Baker E, Trickey A, et al; TeaM Steering Group;
Mammary Fold Academic and Research Collaborative. Current practice
and short-term outcomes of therapeutic mammaplasty in the
international TeaM multicentre prospective cohort study. Br J Surg
2018;105(13):1778–1792.
40. Di Micco R, O’Connell RL, Barry PA, et al. Bilateral mammoplasty for
cancer: surgical, oncological and patient-reported outcomes. Eur J Surg
Oncol 2017;43(1):68–75.
41. Di Micco R, O’Connell RL, Barry PA, et al. Standard wide local
excision or bilateral reduction mammoplasty in large-breasted women
with small tumours: surgical and patient-reported outcomes. Eur J Surg
Oncol 2017;43(4):636–641.
42. Losken A, Dugal CS, Styblo TM, et al. A meta-analysis comparing
breast conservation therapy alone to the oncoplastic technique. Ann
Plast Surg 2014;72(2):145–149.
43. Gardfjell A, Dahlbäck C, Åhsberg K. Patient satisfaction after unilateral
oncoplastic volume displacement surgery for breast cancer, evaluated
with the BREAST-Q™. World J Surg Oncol 2019;17(1):96.
44. Down SK, Jha PK, Burger A, et al. Oncological advantages of
oncoplastic breast-conserving surgery in treatment of early breast
cancer. Breast J 2013;19(1):56–63.
45. The European Organization for Research and Treatment of Cancer
(EORTC), Breast Cancer Co-operative Group (BCCG), Curran D, van
Dongen JP, et al. Quality of life of early-stage breast cancer patients
treated with radical mastectomy or breast-conserving procedures: results
of EORTC Trial 10801. Eur J Cancer 1998;34(3):307–314.
46. https://www.nccn.org/professionals/physician_gls/default.aspx. Last
Accessed in September 2019.
47. Rocco N, Rispoli C, Moja L, et al. Different types of implants for
reconstructive breast surgery. Cochrane Database Syst Rev 2016;
(5):CD010895.
48. Santosa KB, Qi J, Kim HM, et al. Long-term patient-reported outcomes
in postmastectomy breast reconstruction. JAMA Surg
2018;153(10):891–899.
49. Casella D, Di Taranto G, Marcasciano M, et al. Nipple-sparing bilateral
prophylactic mastectomy and immediate reconstruction with TiLoop®
Bra mesh in BRCA1/2 mutation carriers: a prospective study of long-
term and patient reported outcomes using the BREAST-Q. Breast
2018;39:8–13.
50. Bennett KG, Qi J, Kim HM, et al. Comparison of 2-year complication
rates among common techniques for postmastectomy breast
reconstruction. JAMA Surg 2018;153(10):901–908.
51. Kontos M, Lewis RS, Lüchtenborg M, et al. Does immediate breast
reconstruction using free flaps lead to delay in the administration of
adjuvant chemotherapy for breast cancer? Eur J Surg Oncol
2010;36(8):745–749.
52. Dikmans RE, Negenborn VL, Bouman MB, et al. Two-stage implant-
based breast reconstruction compared with immediate one-stage
implant-based breast reconstruction augmented with an acellular dermal
matrix: an open-label, phase 4, multicentre, randomised, controlled trial.
Lancet Oncol 2017;18(2):251–258.
53. Negenborn VL, Young-Afat DA, Dikmans REG, et al. Quality of life
and patient satisfaction after one-stage implant-based breast
reconstruction with an acellular dermal matrix versus two-stage breast
reconstruction (BRIOS): primary outcome of a randomised, controlled
trial. Lancet Oncol 2018;19(9):1205–1214.
54. Kovacs T, Charalampoudis P, Hout BAI, et al. Results from the BRIOS
randomised trial. Lancet Oncol 2017;18(4):e190.
55. Potter S, Wilson RL, Harvey J, et al. Results from the BRIOS
randomised trial. Lancet Oncol 2017;18(4):e189.
56. Catanuto G, Dumitru D, Rancati A, et al. Quality of life after breast
reconstruction—the BRIOS study. Lancet Oncol 2018;19(11):e578.
57. Swerdlow AH, Campo E, Pileri SA, et al. The 2016 revision of the
World Health Organization classification of lymphoid neoplasms. Blood
2016;127 (20):2375–2390.
58. Keech JA Jr, Creech BJ. Anaplastic T-cell lymphoma in proximity to a
saline-filled breast implant. Plast Reconstr Surg 1997;100:554–555.
59. Doren EL, Miranda RN, Selber JC, et al. U.S. epidemiology of breast
implant-associated anaplastic large cell lymphoma. Plast Reconstr Surg
2017;139:1042–1050.
60. Magnusson M, Beath K, Cooter R, et al. The epidemiology of breast
implant-associated anaplastic large cell lymphoma in Australia and New
Zealand confirms the highest risk for grade 4 surface breast implants.
Plast Reconstr Surg 2019;143(5):1285–1292.
61. Davila AA, Mioton LM, Chow G, et al. Immediate two-stage tissue
expander breast reconstruction compared with one-stage permanent
implant breast reconstruction: a multi-institutional comparison of short-
term complications. J Plast Surg Hand Surg 2013;47:344–349.
62. Vandeweyer E, Deraemaecker R. Radiation therapy after immediate
breast reconstruction with implants. Plast Reconstr Surg 2000;106:56–
58; discussion 59–60.
63. Barry M, Kell MR. Radiotherapy and breast reconstruction: a meta-
analysis. Breast Cancer Res Treat 2011;127:15–22.
64. Tran NV, Chang DW, Gupta A, et al. Comparison of immediate and
delayed free TRAM flap breast reconstruction in patients receiving
postmastectomy radiation therapy. Plast Reconstr Surg 2001;108:78–82.
65. Kelley BP, Ahmed R, Kidwell KM, et al. A systematic review of
morbidity associated with autologous breast reconstruction before and
after exposure to radiotherapy: are current practices ideal? Ann Surg
Oncol 2014;21:1732–1738.
66. Kim JB, Kim DK, Lee JW, et al. The usefulness of pedicled perforator
flap in partial breast reconstruction after breast conserving surgery in
Korean women. Arch Plast Surg 2018;45(1):29–36.
67. Ho W, Stallard S, Doughty J, et al. Oncological outcomes and
complications after volume replacement oncoplastic breast
conservations—the Glasgow experience. Breast Cancer (Auckl)
2016;10:223–228.
68. McCulley SJ, Schaverien MV, Tan VK, et al. Lateral thoracic artery
perforator (LTAP) flap in partial breast reconstruction. J Plast Reconstr
Aesthet Surg 2015;68(5):686–691.
69. Baumann DP, Crosby MA, Selber JC, et al. Optimal timing of delayed
free lower abdominal flap breast reconstruction after postmastectomy
radiation therapy. Plast Reconstr Surg 2011;127:1100–1106.
70. Momoh AO, Colakoglu S, de Blacam C, et al. Delayed autologous
breast reconstruction after postmastectomy radiation therapy: is there an
optimal time? Ann Plast Surg 2012;69:14–18.
CHAPTER 34

Oncoplastic Techniques in Breast


Conservation Therapy—The Plastic
Surgeon’s Perspective
ALBERT LOSKEN | BRIAN PETTITT-SCHIEBER
HISTORY
Breast-conserving therapy (BCT) continues to rise as a treatment for women
with breast cancer, and we have subsequently become more aware of poor
cosmetic results following radiation therapy and long term. Up to 30% of
women will have a residual deformity following BCT that may require
surgical correction (1), which is often challenging following radiation therapy
(2). The oncoplastic approach is subsequently becoming more popular,
whereby partial breast reconstruction is performed often at the time of tumor
resection, to minimize or prevent these deformities. In a review of 10,607
breast cancer surgeries, the oncoplastic approach was the one procedure with
the biggest increase of nearly fourfold from 2007 to 2014 (3). Werner
Audretsch is credited for his pioneering work in the field of oncoplastic
breast surgery, an approach which was initially more popular in Europe and
the United Kingdom, and has recently gained acceptance and popularity
worldwide. The oncoplastic terminology will be used in this chapter as it
applies to the immediate reconstruction of the partial mastectomy defect. This
field has clearly been driven by both patient demands, as well as the
development of combined surgical techniques, made possible through greater
interaction between specialties. Patients like the oncoplastic approach
because it often allows them to undergo BCT, and often without a deformity,
breast surgeons like the ability to resect a generous amount without concerns
about the cosmesis, and plastic surgeons bring an eye for aesthetic results and
enjoy performing breast reconstruction.
The Plastic Surgeon’s Perspective
The plastic surgeon’s role in the oncoplastic approach is critically important
as the initial driving force was over the minimization or correction of BCT
deformities and the sole focus from their perspective is one of reconstruction.
With the appropriate training and qualifications, this approach can be offered
by a single surgeon; however for now in the United States, the combined
team with a resective surgeon and reconstructive surgeon remains the most
popular. There remains inconsistency in how this is offered in various parts
of the world. In the United Kingdom, the interest in oncoplastic surgery has
increased over the last 5 years with significantly more breast surgeons
performing reduction techniques and latissimus dorsi flaps (4). A survey in
Canada demonstrated that surgeons that were predominately focused on
breast surgery were more likely to use the oncoplastic technique and involve
plastic surgeons. Those not performing oncoplastic procedures cited a lack of
training and access to plastic surgeons as a significant barrier (5). In a survey
in the United States, both breast and plastic surgeons agreed that complex
partial reconstructions were best performed using the team approach and that
margin concerns were a major concern and aesthetic benefits were a major
driving force in both groups (6). The plastic surgeon has been an integral part
of the refinements in partial breast reconstruction and will likely continue to
push the envelope in terms of new techniques and improved outcomes.
Reconstruction is a major part of the oncoplastic definition, being volume
replacement versus volume displacement. Further division in the definition
for oncoplastic surgery separates volume displacement oncoplastic surgery
into levels 1 and 2. Specifically, level 1 volume displacement oncoplastic
surgery involves reconstruction of the breast with subsequent local tissue
rearrangement designs for reconstruction. Such designs would involve
undermining of breast tissue, creation of glandular shelves, and are often
performed by the resective surgeon. Level 2 volume displacement
oncoplastic surgery involves more complex reconstruction often performed
by the reconstructive surgeon and includes mastopexy or reduction
mammoplasty designs to reconstruct the large volume defects with
contralateral symmetry breast mastopexy or reduction mammoplasty
operations. The goals of the oncoplastic approach are (1) avoid the BCT
deformity, minimize positive margins, broaden indications for BCT, avoid
full mastectomy, and preserve shape.
INDICATIONS
The two main reasons to reconstruct partial mastectomy defects are:

1. to increase the indications for BCT making breast conservation practical


in patients who otherwise might require a mastectomy, and
2. to minimize the potential for a poor aesthetic result (Table 34-1). The
decision is typically based on tumor characteristics, breast shape, and
size.

Based on these factors contributing to a poor aesthetic outcome, the


oncoplastic approach is indicated whenever the potential for a poor
cosmetic result exists, or patients with tumors in whom a standard
lumpectomy would lead to breast deformity or gross asymmetry. In
particular, this includes women with large tumors and women with large
breasts. The tumor to breast ratio is one of the most important factors when
predicting the potential for a poor outcome. In general, when more than 20%
of the breast is excised with partial mastectomy, the cosmetic result is likely
to be unfavorable (7). Women with central or lower quadrant tumors have
also been shown to have a worse cosmetic outcome because of tumor
location, especially when a significant amount of skin is removed. Lower
quadrant lumpectomies have been shown to reduce cosmesis by 50% when
compared to other quadrants. A recent study of 350 patients demonstrated
that the maximal volumes of tissue resected with lumpectomy without
resulting in unacceptable aesthetic and functional outcomes of decreased
quality of life (QOL) were 18% to 19% in the upper-outer quadrant, 14% to
15% in the lower quadrant, 8% to 9% in the upper-inner quadrant, and 9% to
10% in the lower-inner quadrant (8).

TABLE 34-1 Indications for Immediate Partial Mastectomy Reconstruction


Cosmetic Reasons Oncologic Reasons
High tumor to breast ratio (>20%) Concern about clear margins
Tumor location—Central, inferior, Wide excision required
medial
Macromastia Poor candidate for mastectomy and
reconstruction (i.e., age, breast
size)
Large tumor Patient desires BCT
Patient desires smaller breasts
Significant ptosis, or breast
asymmetry

Factors in addition to cosmetic reasons as an indication for this


approach include oncologic issues. Important indications include situations
where the surgeon is concerned about the potential for involved margins with
standard resection, and based on initial pathology or breast imaging studies
needs to perform a wider excision in order for the patient to be a candidate
for breast-conserving surgery (BCS). Other more aggressive and higher-
staged breast cancers are also amenable to oncoplastic resections and
subsequently, the oncoplastic approach broadens the indications for BCT, as
these patients might otherwise have required a mastectomy. Additional
indications include women who desire breast conservation despite potential
adverse conditions, as well as older women with large ptotic breasts in whom
mastectomy and reconstruction would be difficult.
CONTRAINDICATIONS
Contraindications to the immediate oncoplastic technique include those
patients not candidates for BCS, prior history of chest wall irradiation, diffuse
multicentric breast disease, inflammatory breast cancer, and those patients
without sufficient breast tissue remaining to warrant BCS. If significant
resection is required and little breast tissue is anticipated, then either a flap
reconstruction would be required or the need for mastectomy should be
discussed.
PREOPERATIVE PLANNING
If the oncoplastic approach is deemed necessary for the previously mentioned
indications, it is important that the ablative surgeon and reconstructive
surgeon communicate and understand the various perspectives. The ablative
surgeon must recognize the concept of breast shape, symmetry, and aesthetics
and anticipate an unfavorable result without intervention as well as the
reconstructive options. It is equally important that the reconstructive surgeon
not compromise the oncologic tenets of cancer management in an attempt to
improve breast shape. In an attempt to anticipate the defect size and location
relative to the nipple-areolar complex, it is helpful to review the films
following wire placement and further discuss the plan with the breast surgeon
in terms of the best approach and incision location. Members of the surgical
team examine the patient, identify her expectations and desires, and evaluate
breast size, shape, and tumor characteristics. A contralateral breast procedure
is often required when volume preservation techniques such as flap
reconstructions are not used.
It is important to decide the best time to do partial breast reconstruction.
When indicated, it is better to perform immediate reconstruction at the time
of tumor resection (see Table 34-1). This has the benefits of operating on a
nonirradiated or surgically scarred breast, resulting in lower complication
rates and improved aesthetic results (9,10). This is often preferred since it is
only one procedure performed on the breast prior to radiation therapy.
Reduction techniques prior to radiation therapy result in significantly lower
complication rates when compared to performing reductions after completion
of radiation therapy (21% vs. 57%, p < 0.001) and Kronowitz has shown
similar results (24% vs. 50%) (10). The main concern with immediate
reconstruction is the potential for positive margins. When this concern does
exist, the reconstruction can be delayed until final confirmation of negative
margins (delayed-immediate reconstruction). This then allows the benefits
of reconstruction prior to radiation therapy with the luxury of clear margins.
The main disadvantage is the need for a second procedure, which might be
unnecessary in most cases. When a flap reconstruction is required, we prefer
to confirm final margin status prior to partial breast reconstruction. There are
situations where poor results are encountered years after following radiation
therapy, which then require correction (delayed reconstruction). Since the
delayed approach requires operating on an irradiated breast, this often has
higher postoperative complications, increased need for flap reconstruction,
and poorer aesthetic outcomes.
OPERATIVE TECHNIQUE
The decision as to which procedure is more appropriate is multifactorial,
however, is ultimately determined by breast size, tumor size, and tumor
location (Table 34-2). Other factors are also important including patient risks
and desires, tumor biology, and surgeon comfort level with the various
techniques. Being familiar with the various reconstructive tools will allow
reconstruction of almost any partial mastectomy defect.
Volume Displacement Techniques
The breast reshaping procedures all essentially rely on advancement, rotation
or transposition of a large area of breast to fill a small- or moderate-sized
defect. This absorbs the volume loss over a larger area. Perhaps the most
popular and versatile breast reshaping options that involve reconstructive
surgeons are the mastopexy or reduction techniques. The ideal patient is one
where the tumor can be excised within the expected breast reduction
specimen, in medium to large or ptotic breasts where sufficient breast
parenchyma remains following resection to reshape the mound (type 2b
defects). Any moderate to large breast can be reconstructed using these
techniques unless a skin deformity exists beyond the standard Wise pattern
(type 2a defect).
In women with large or ptotic breasts, the numerous reduction patterns or
pedicle designs will invariably allow remodeling of a defect in any location
and any size, as long as sufficient breast tissue and skin is available.
Preoperative markings are important, and a decision is made on pedicle
design depending on tumor location. Typically, if the pedicle points to or can
be rotated into the defect, it can be used. The Wise pattern markings are more
versatile allowing tumor resection in any breast quadrant. The breast surgeon
often performs the lumpectomy through an incision within the Wise pattern
markings. Once the resection is performed, the cavity is inspected paying
attention to the defect location in relation to the nipple, as well as the
remaining breast tissue. The reconstructive goals include:

1. preservation of nipple viability,


2. filling the tumor defect and closing the dead space, and
3. reshaping the breast mound.
TABLE 34-2 Partial Mastectomy Reconstruction Techniques
Volume Displacement Techniques Volume Replacement Techniques
Parenchymal remodeling, volume Adjacent or distant tissue transfer,
shrinkage volume preserving
Primary closure Implant augmentation: rare
Mirror biopsy/excision Local flaps
Batwing mastopexy Fasciocutaneous
Breast flap advancement technique Perforator flaps
Latissimus dorsi musculocutaneous
flap
Nipple-areolar centralization
Reduction mastopexy techniques Distant flaps
Other
Stem cells, fat injections
Omentum

Once a decision has been made as to the most appropriate pedicle for
nipple preservation, and it has been determined how to fill the lumpectomy
cavity, only then should additional tissue be removed to reduce and shape the
breast mount. The contralateral procedure is performed using a similar
technique. The ipsilateral side is typically kept about 10% to 15% larger to
allow for radiation fibrosis. When the partial defect cannot be filled with the
standard breast reduction techniques in women with smaller ptotic breasts or
more peripheral defects, then autoaugmentation techniques can be utilized.
These include either extending the primary nipple pedicle to fill the defect or
creating a secondary independent pedicle to fill the defect. These techniques
have been shown to further broaden the indications for the oncoplastic
technique without increasing complications.
Volume Replacement Techniques
Women with large tumor to breast ratios and women with small to moderate
breasts who have insufficient residual breast tissue for rearrangement require
partial reconstruction using nonbreast local or distant flaps. Volume is
preserved and a contralateral procedure is often not required.
Small lateral defects (less than 10% of breast size) can be closed with local
fasciocutaneous flaps. Clough described using the subaxillary area as a
transposition flap (11), and Munhoz has more recently demonstrated how the
lateral thoracodorsal flap (LTDF) is ideal for lateral defects (12). The
latissimus dorsi musculocutaneous flap is a common local option for lateral,
central, and even medial defects (13). It has excellent blood supply and
provides both muscle for filling of glandular defects and skin for cutaneous
deficiencies. A denervated and radiated LD will undergo postoperative
atrophy. To compensate for the expected loss in muscle volume, a flap much
larger than the defect should be harvested, possibly preserving sub-Scarpa fat
on the muscle. Hamdi introduced the concept of pedicled perforator flaps for
partial breast reconstruction (14,15). A similar skin island to the classical LD
musculocutaneous flap can be raised as a perforator flap either from the
thoracodorsal or intercostal vessels. By sparing the underlying muscles, the
donor site morbidity is less, with less seroma formation. The thoracodorsal
artery perforator (TDAP) flap can easily reach defects in the lateral,
superolateral, and central regions of the breast. If no suitable perforators are
found, the flap is easily converted to a muscle-sparing TDAP or LD flap. The
lateral intercostal artery perforator (LICAP) flap is another alternative to
the TDAP flap for lateral and inferior breast defects. The LICAPs are found
at 2.7 to 3.5 cm from the anterior border of the LD muscle. The anterior
intercostal artery perforator (AICAP) flap is similar to the random-
designed thoracoepigastric skin flap; the skin paddle can be harvested as an
AICAP flap. The AICAP is based on perforators originating from the
intercostal vessels through the rectus abdominis or the external oblique
muscles. Since it has a short pedicle, the AICAP flap is suitable to close
defects that extend over the inferior or medial quadrants of the breast. The
superior epigastric artery perforator (SEAP) flap is based on perforators
arising from the superior epigastric artery or its superficial branch. It has the
same indications as the AICAP flap; however, the SEAP flap has a longer
vascular pedicle and therefore it can cover more remote defect in the breast.
Large medial defects are more difficult to reconstruct. The superficial inferior
epigastric artery free flap has been described for this location (16).
POSTOPERATIVE CARE
Most patients have minimal postoperative care. One important difference
from the plastic surgeon’s perspective is the importance of reviewing the
pathology and margin status and being involved in the decision process and
procedure if reexcision is planned. It is also important to manage
complications appropriately and in a timely fashion so as not to delay
initiation of adjuvant therapies. Another area of involvement postoperatively
is with surveillance. The reconstructive surgeon will occasionally need to
educate the radiologist in terms of what was done and how this might impact
breast imaging down the line. Oncoplastic reduction techniques and flap
reconstruction techniques have not been shown to interfere with the ability to
screen for postoperative tumor recurrence (17,18).

CASES

CASE 1

This is a 50-year-old female (Fig. 34-1) with a left lower pole breast
cancer. She underwent a generous 120-g tumor resection including breast
tissue and skin. When the defect is below the Wise pattern markings and
a reduction is planned, a generous resection is possible. If additional
resection is performed by the reconstructive surgeon during the reduction,
it is important to mark the specimen appropriately since this would
potentially be a new margin if the original margins are positive. A lower
pole defect can be reconstructed using any oncoplastic reduction
technique except an inferior pedicle. A superomedial pedicle was chosen
because it is a relatively short pedicle and a total of 320 g was resected on
the left including the lumpectomy specimen. The cavity was marked with
clips prior to closure. A superomedial reduction was performed on the
contralateral side with 360 g removed. It is common to overresect the
contralateral side in anticipation of irradiation fibrosis with time. Her
result is shown 5 months postoperatively and prior to irradiation therapy.
FIGURE 34-1 Left lower pole breast cancer.

CASE 2

A 49-year-old woman with macromastia and right-sided breast cancer


(Fig. 34-2A,B). She is marked preoperatively with standard (Fig. 34-2C)
Wise pattern markings. Her defect is shown following lumpectomy with
positive margins superiorly (Fig. 34-2D). She was taken to the operating
room in a delayed-immediate fashion, and additional tissue was resected,
ensuring negative margins (Fig. 34-2E). An inferior pedicle was
deepithelialized (Fig. 34-2F). However, given the potential for volume
void above the nipple-areolar reconstruction, the breast parenchyma was
plicated above the nipple to create volume and fill the defect (Fig. 34-
2G–I). Her result is shown 1 year following completion of radiation
therapy (Fig. 34-2J,K).
FIGURE 34-2 Right-sided breast cancer.
CASE 3

This is a 41-year-old female (Fig. 34-3) with breast ptosis and moderate
volume who presented with a 1.5-cm infiltrating ductal carcinoma in the
upper outer quadrant IDC. A decision was made to undergo breast
conservation therapy and given the size of the anticipated defect, she was
referred for reconstruction of the partial defect given concern for a poor
cosmetic result. A preoperative decision was made to perform a tissue
rearrangement technique given sufficient anticipated breast volume
following resection. She underwent wire localization and partial
mastectomy removing a 100-g specimen from the upper outer quadrant.
The access incision for the tumor resection was within the proposed
mastopexy reduction markings. After examining the defect, it was felt
that a standard inferior or central mound reduction or mastopexy would
not get enough tissue into the upper outer defect. A decision was made to
perform a vertical oncoplastic mastopexy-type procedure using an
extended autoaugmentation technique for the defect. A superomedial
pedicle was deepithelialized to keep the nipple alive, and the lower pole
tissue was also deepithelialized down to the IMF in between the vertical
markings. The medial and lateral pillars were created and the extended
pedicle was lifted off the chest wall only enough to allow sufficient
rotation of the pedicle. The nipple was then rotated into the proposed
nipple location and the extended pedicle was rotated to the fill the defect.
This provided vascularized tissue into the tumor cavity. No additional
tissue was removed. The medial and lateral pillars were plicated and the
breast was shaped and closed in a mastopexy fashion. A contralateral
reduction 105 g was performed using a superomedial pedicle and
removing the lower pole tissue. She has decent shape and symmetry 1.5
years following completion of radiation therapy.
FIGURE 34-3 Breast ptosis and moderate volume.

CASE 4

This is a 50-year-old female (Fig. 34-4) with a right medial breast cancer
who underwent a 100-g partial mastectomy. There was concern about
getting a clear margin and so a decision was made to proceed with
delayed-immediate reconstruction. Once margin confirmation was
cleared, she was taken back to the OR for reconstruction 2 weeks later.
The breast was slightly more edematous, however, with the luxury of
clear margins and before irradiation therapy. Given that she did not have
large breasts and that the defect was along the cosmetically sensitive,
medial aspect of the breast, the decision was made to perform a
superolateral pedicle for the nipple-areolar complex in which the primary
pedicle was extended in an autoaugmentation fashion by deepithelializing
the pedicle down to the inframammary fold. Medial and lateral pillars
were created and no additional tissue was removed. The pedicle was
released off the chest wall only as much as was needed to rotate the
glandular tissue into the medial tumor defect. This provided vascularized
tissue into the tumor cavity. No additional tissue was removed. The
medial and lateral pillars were plicated and the breast was shaped and
closed in a mastopexy fashion. A contralateral reduction of 105 g was
performed using a superomedial pedicle and removing the lower pole
tissue. She is shown shortly after finishing irradiation therapy on the right
with a swollen reddened breast. This all resolves and she is shown with a
soft breast and decent shape and symmetry 1.5 years following
completion of radiation therapy.

FIGURE 34-4 Right medial breast cancer.

CASE 5
This is a 44-year-old patient (Fig. 34-5) who presented with a T2 tumor
in the left breast. She will require a quadrantectomy-type resection and
has small nonptotic breasts. An immediate breast reconstruction was
planned because of the expected unaesthetic result after tumor resection
in such small-sized breast. A decision was made to use a pedicled
thoracodorsal artery perforator (TDAP) flap to minimize donor site
morbidity. Perforators were mapped preoperatively by unidirectional
Doppler and the skin island was drawn large enough to be rotated on the
pedicle to fill the upper lateral quadrant defect without too much tension.
The TDAP flap is raised on a single perforator and tunneled into the
defect. The inset is under no tension in anticipation of radiation therapy.
She is shown 1 year after completion of irradiation therapy with
preservation of the lateral breast contour and nipple-areolar position.

FIGURE 34-5 T2 tumor in the left breast. (Case courtesy Moustapha Hamdi,
MD.)
CASE 6

This 68-year-old patient (Fig. 34-6) with large ptotic breasts has a left
medial breast cancer. This is a very cosmetically sensitive area and a
large 63-g resection was performed. A decision was made to perform an
inferior pedicle for nipple transfer. This alone would not have filled the
medial defect. The entire lower pole was deepithelialized as was the
tissue above the nipple for autoaugmentation. An additional 295 g was
removed on that side. The medial portion was back cut and rotated to fill
the defect. It was sutured to the upper portion of the pedicle to provide
volume. An additional 295 g was removed on that side. The left side was
purposely kept larger intraoperatively with 362 g removed. She is shown
1 year postoperatively with good symmetry.
FIGURE 34-6 Left medial breast cancer.

CASE 7

A 34-year-old woman (Fig. 34-7A,B) who had previously had a breast


reduction and subsequently required a partial mastectomy in the upper
quadrant. Initial margins were positive, and she was taken back for
reexcision. Once confirmation of negative margins was obtained
following the second resection, she already had a significant contour
deformity (Fig. 34-7C–E). In order to fill the volume void, a latissimus
dorsi myofascial flap was harvested through a minimally invasive
approach and transferred into the defect (Fig. 34-7F,G). Her shape and
symmetry are preserved 6 months postoperatively (Fig. 34-7H,I).

FIGURE 34-7 Partial mastectomy in the upper quadrant. (From A. Losken,


M. Hamdi, eds. Partial Breast Reconstruction: Techniques in Oncoplastic
Surgery. St. Louis, MO: QMP; 2009.)

CASE 8

A 40-year-old woman (Fig. 34-8A,B) with infiltrating ductal cancer and


ductal carcinoma in situ on the lateral aspect of her right breast. She has
macromastia and was scheduled for an oncoplastic reduction with partial
mastectomy. Location of the tumor and margin status necessitated
resection of parenchyma and skin from above the proposed Wise
markings (Fig. 34-8C). The weight of the specimen was 500 g. An
inferior pedicle was created leaving skin laterally on the pedicle to
replace the resected breast skin (Fig. 34-8D,E). A total of 1,290 g of
breast tissue was removed from the right, and a contralateral reduction
was performed. She is shown at completion of radiation therapy to the
right breast with reasonable shape and symmetry (Fig. 34-8F,G)
removing 1,650 g.
FIGURE 34-8 Infiltrating ductal cancer and ductal carcinoma in situ on the
lateral aspect of her right breast.
OUTCOMES
As the various oncoplastic techniques are fairly well established in the
literature, we are now seeing more papers focusing on outcomes and patient
satisfaction.
Complications
It is important that complications resulting from oncoplastic techniques do
not interfere with the initiation of adjuvant therapy. Overall complications
following oncoplastic surgeries range between 15% and 30% (19). Volume
displacement techniques report complications on average 16% of the time
and include delayed wound healing (3% to 15%), fat necrosis (3% to 10%),
and infection (1% to 5%). Overall complications following volume
replacement techniques are slightly higher (range 2% to 77%) and this is
likely due to the addition of donor site complications and potential flap loss
issues. Munhoz recently reported a 33% complication rate using the
latissimus dorsi technique for partial mastectomy defects, 65% of which was
related to the donor site (13). The most common complication was dorsal
seroma, which occurred in 20% of their patients (50% of their
complications). While complications do exist, they are often managed with
conservative treatment and do not delay initiation of adjuvant treatment.
When compared to mastectomy and immediate reconstruction, oncoplastic
procedures have lower complication rates and quicker recovery, especially in
obese women (20,21). When compared to BCT alone, the complication rate
is slightly higher in the oncoplastic group. Oncoplastic surgery in one study
did not delay the time to delivery of adjuvant chemotherapy (29 days) when
compared to lumpectomy alone (29.5 days) and mastectomy with immediate
reconstruction (31 days). In patients who have complications following
oncoplastic surgery, it has been shown to delay the initiation of radiation
therapy in 8.2% of patients (22), and another study showed that the time to
radiation therapy is significantly longer in patients with complications (72
days) compared to no complication (55 days) (23). Although the impact this
might have on oncologic outcomes is unknown, it stresses the importance of
minimizing complications as much as possible.
An National Surgical Quality Improvement Project (NSQIP) evaluation
comparing 75,972 BCS patients to 1,363 patients who had oncoplastic
surgery with soft tissue transfer showed no increased risk of complication in
the oncoplastic group despite longer operating room time in that group (24).
Margins
Positive margins following oncoplastic surgery range from 1.8% to 19%
(Table 34-3). One of the strengths of the oncoplastic approach is the ability to
resect widely and subsequently obtain a lower positive margin rate at 10%,
compared to 20% to 40% for standard lumpectomy (25,26). This translates to
far fewer reexcisions and secondary operations and occurs because the breast
surgical oncologist has the option to remove a greater section of breast tissue
since reconstruction would follow. Fewer secondary operations means that
adjuvant treatment in the form of chemotherapy and radiation is not delayed.
We also showed fewer surgical reexcisions (12.0% vs. 25.9%, p = 0.01), and
wider margins from the tumor when oncoplastic surgery was performed (4.3
vs. 2.8 mm, p = 0.01) (27). The recent meta-analysis also found a reduction in
the positive margin rate for both invasive and in situ disease from 21% with
BCT alone to 12% (19).

TABLE 34-3 Classification of the Partial Mastectomy Defect With


Potential Outcome and Treatment Options
Description Potential Treatment
Outcome
Type 1 Small, peripheral Breast shape is Primary closure,
(favorable) defect preserved with breast tissue
Large or small acceptable advancement
breasts symmetry flap
Type 2 Medium to large Size and shape
(unfavorable) defect deficiency with
Central defects noticeable
distortion and
asymmetry
Type 2a Small breasts, Volume
with or replacement
without ptosis procedures
type 2b
Medium to large Quadrantectomy Volume
breasts, with defect outside replacement
or without standard Wise technique
ptosis pattern
Any lumpectomy
defect
Quadrantectomy Volume
defect within displacement
standard Wise techniques
pattern
Type 3 Extensive Major deficiency Mastectomy and
(unfavorable) resection with reconstruction
little
remaining
breast tissue
Large or small
breasts
From Losken A, Hamdi M. Partial breast reconstruction: current perspectives. Plast Reconstr Surg
2009;124(3):722–736.

Positive margins in oncoplastic reductions have been associated with larger


biopsy size, larger tumor size (>2.00 cm), and ER positivity (27). Reexcision
rate of 30% has been associated with being overweight, microcalcifications,
and tumor multifocality (28). While important to minimize reexcision and
positive margins, a recent study has shown that mastectomy rate (34% vs.
15%) and reexcision rate (32% vs. 18%) are significantly lower in the
oncoplastic groups compared to BCT (29).
Patient-Reported Outcomes
When it comes to patient-reported outcomes and satisfaction, the oncoplastic
reduction technique has been shown to fare favorable compared to BCT alone
and compared to mastectomy and reconstruction for women with
macromastia. While we often at best wish to preserve satisfaction and QOL
when performing breast reconstruction, this approach does often show
improvement. Likely because of the benefit to reduction mammoplasty, these
patients in our series reported improvement in body acceptance, feelings of
attractiveness, satisfaction with how their breasts looked unclothed, and
satisfaction with sex life. Their improvement in emotional health is likely due
to the breast cancer being managed and behind them. Veiga et al. showed a
positive impact on QOL and self-esteem when comparing patients who had
oncoplastic surgery compared to BCT alone (30). Hart et al. has similarly
shown that oncoplastic reduction patients reported an unexpected increase in
their ability to wear sexually provocative clothing and in their partner’s
perception of them as womanly (31). While not typically a driving force
behind the selection of the oncoplastic reduction for women with
macromastia and breast cancer, the QOL improvements are a definite benefit
of this technique. Others have similarly found that self-reported body image
scores and patient-reported outcome measures significantly favored
oncoplastic surgery to mastectomy with immediate reconstruction (implant or
flap) (32). In a recent large series of oncoplastic patients at over 1-year
follow-up, women reported increased emotional health (3.73 → 4.18, p =
0.019), body acceptance (3.41 → 4.50, p = 0.050), feelings of attractiveness
(3.07 → 3.88, p = 0.064), satisfaction with how their breasts looked
unclothed (2.53 → 3.38, p = 0.075), and satisfaction with sex life (3.16 →
3.48, p = 0.068) (31). When comparing oncoplastic reduction techniques to
lumpectomy alone in large-breasted patients with small (<3-cm) tumors,
despite worse prognostic factors and more surgery in the oncoplastic group,
these patients reported slightly better satisfaction and physical functioning
and fewer adverse effects of the radiation therapy (32).
Outcomes studies have been performed with preliminary results suggesting
cost-effectiveness for oncoplastic surgery (33). However, compared to other
cancer operations, oncoplastic surgery is relatively young and additional
future randomized controlled trials with regard to locoregional recurrence
rates, role for adjuvant radiation in certain early-stage cancers, etc., in
addition to patient-centered outcomes data with regard to aesthetic self-
perceptions are needed.
Recurrence
The benefits oncoplastic procedures might have on recurrence are all related
to generous resection and wider margins. Longer-term follow-up studies
showed local recurrence to be 8.7% at 10 years and the overall survival rate
was 82.2% (34), and another study of 545 patients had a 6.7 recurrence rate at
an average follow-up of 7 years with a comparable survival at 91% compared
to BCT alone (35,36). Whether wider margins truly translate into lower
recurrence remains to be seen and has not been demonstrated in the
oncoplastic data (34). In an effort to evaluate the oncologic safety of
oncoplastic surgery, a recent comparison in 980 patients demonstrated similar
5-year recurrence rates with 3.4% in the lumpectomy group, 2% in the
oncoplastic group, and 2.6% in the mastectomy with immediate
reconstruction group (37). The groups all had similar histologic variables.
Another comparison in 801 patients between oncoplastic reduction and
lumpectomy demonstrated longer operating time and higher tissue necrosis in
the oncoplastic reduction group, with no difference in reexcision or
mastectomy rate (38). They did report improvement in patient satisfaction
and QOL in the reduction group with equivalent overall 10-year survival, but
higher local recurrence rates in that group. The oncoplastic approach has also
been found to be safe compared to mastectomy in tumors larger than 2 cm
with similar overall survival rates (87.3 vs. 87.1% at 10 years) (36).
CONCLUSION
The oncoplastic approach from the plastic surgeon’s perspective is one of
knowing the indications for partial breast reconstruction, working with a
breast surgeon, being comfortable performing the various reconstructive
techniques, and understanding the importance of aesthetic outcomes
especially in the setting of radiation therapy, minimizing complications and
subsequently ensuring high levels of patient satisfaction.

REFERENCES

1. Clough KB, Cuminet J, Fitoussi A, et al. Cosmetic sequelae after


conservative treatment for breast cancer: classification and results of
surgical correction. Ann Plast Surg 1998;41(5):471–481.
2. Kronowitz SJ, Feledy JA, Hunt KK, et al. Determining the optimal
approach to breast reconstruction after partial mastectomy. Plast
Reconstr Surg 2006;117(1):1–11; discussion 12–14.
3. Carter SA, Lyons GR, Kuerer HM, et al. Operative and oncologic
outcomes in 9861 patients with operable breast cancer: single-institution
analysis of breast conservation with oncoplastic reconstruction. Ann
Surg Oncol 2016;23(10):3190–3198.
4. Challoner T, Skillman J, Wallis K, et al. Oncoplastic techniques:
attitudes and changing practice amongst breast and plastic surgeons in
Great Britain. Breast 2017;34:58–64.
5. Maxwell J, Roberts A, Cil T, et al. Current practices and barriers to the
integration of oncoplastic breast surgery: a Canadian perspective. Ann
Surg Oncol 2016;23(10):3259–3265.
6. Losken A, Kapadia S, Egro FM, et al. Current opinion on the
oncoplastic approach in the USA. Breast J 2016;22(4):437–441.
7. Anderson BO, Masetti R, Silverstein MJ. Oncoplastic approaches to
partial mastectomy: an overview of volume-displacement techniques.
Lancet Oncol 2005;6(3):145–157.
8. Pukancsik D, Kelemen P, Újhelyi M, et al. Objective decision making
between conventional and oncoplastic breast-conserving surgery or
mastectomy: an aesthetic and functional prospective cohort study. Eur J
Surg Oncol 2017;43(2):303–310.
9. Patel KM, Hannan CM, Gatti ME, et al. A head-to-head comparison of
quality of life and aesthetic outcomes following immediate, staged-
immediate, and delayed oncoplastic reduction mammaplasty. Plast
Reconstr Surg 2011;127(6):2167–2175.
10. Kronowitz SJ, Kuerer HM, Buchholz TA, et al. A management
algorithm and practical oncoplastic surgical techniques for repairing
partial mastectomy defects. Plast Reconstr Surg 2008;122(6):1631–
1647.
11. Clough KB, Kroll SS, Audretsch W. An approach to the repair of partial
mastectomy defects. Plast Reconstr Surg 1999;104(2):409–420.
12. Munhoz AM, Montag E, Arruda EG, et al. The role of the lateral
thoracodorsal fasciocutaneous flap in immediate conservative breast
surgery reconstruction. Plast Reconstr Surg 2006;117(6):1699–1710.
13. Munhoz AM, Montag E, Fels KW, et al. Outcome analysis of breast-
conservation surgery and immediate latissimus dorsi flap reconstruction
in patients with T1 to T2 breast cancer. Plast Reconstr Surg
2005;116(3):741–752.
14. Hamdi M, Van Landuyt K, de Frene B, et al. The versatility of the inter-
costal artery perforator (ICAP) flaps. J Plast Reconstr Aesthet Surg
2006;59(6):644–652.
15. Hamdi M, Van Landuyt K, Monstrey S, et al. Pedicled perforator flaps
in breast reconstruction: a new concept. Br J Plast Surg 2004;
57(6):531–539.
16. Spiegel AJ, Khan FN. An intraoperative algorithm for use of the SIEA
flap for breast reconstruction. Plast Reconstr Surg 2007; 120(6):1450–
1459.
17. Losken A, Schaefer TG, Newell M, et al. The impact of partial breast
reconstruction using reduction techniques on postoperative cancer
surveillance. Plast Reconstr Surg 2009;124(1):9–17.
18. Mele S, Wright D, Paramanathan N, et al. Long-term effect of
oncoplastic breast-conserving surgery using latissimus dorsi miniflaps
on mammographic surveillance and the detection of local recurrence. J
Plast Reconstr Aesthet Surg 2017;70(9):1203–1209.
19. Losken A, Dugal CS, Styblo TM, et al. A meta-analysis comparing
breast conservation therapy alone to the oncoplastic technique. Ann
Plast Surg 2014;72(2):145–149.
20. Tong WM, Baumann DP, Villa MT, et al. Obese women experience
fewer complications after oncoplastic breast repair following partial
mastectomy than after immediate total breast reconstruction. Plast
Reconstr Surg 2016;137(3):777–791.
21. Losken A, Pinell XA, Eskenazi B. The benefits of partial versus total
breast reconstruction for women with macromastia. Plast Reconstr Surg
2010;125(4):1051–1056.
22. Hillberg NS, Meesters-Caberg MAJ, Beugels J, et al. Delay of adjuvant
radiotherapy due to postoperative complications after oncoplastic breast
conserving surgery. Breast 2018;39:110–116.
23. Kapadia SM, Reitz A, Hart A, et al. Time to radiation after oncoplastic
reduction. Ann Plast Surg 2019;82(1):15–18.
24. Cil TD, Cordeiro E. Complications of oncoplastic breast surgery
involving soft tissue transfer versus breast-conserving surgery: an
analysis of the NSQIP database. Ann Surg Oncol 2016;23(10):3266–
3271.
25. Fitoussi AD, Berry MG, Famà F, et al. Oncoplastic breast surgery for
cancer: analysis of 540 consecutive cases [outcomes article]. Plast
Reconstr Surg 2010;125(2):454–462.
26. Losken A, Hart AM, Broecker JS, et al. Oncoplastic breast reduction
technique and outcomes: an evolution over 20 years. Plast Reconstr
Surg 2017;139(4):824e–833e.
27. Losken A, Pinell-White X, Hart AM, et al. The oncoplastic reduction
approach to breast conservation therapy: benefits for margin control.
Aesthet Surg J 2014;34(8):1185–1191.
28. Amabile MI, Mazouni C, Guimond C, et al. Factors predictive of re-
excision after oncoplastic breast-conserving surgery. Anticancer Res
2015;35(7):4229–4234.
29. Crown A, Wechter DG, Grumley JW. Oncoplastic breast-conserving
surgery reduces mastectomy and postoperative re-excision rates. Ann
Surg Oncol 2015;22(10):3363–3368.
30. Veiga DF, Veiga-Filho J, Ribeiro LM, et al. Quality-of-life and self-
esteem outcomes after oncoplastic breast-conserving surgery. Plast
Reconstr Surg 2010;125(3):811–817.
31. Hart AM, Pinell-White X, Egro FM, et al. The psychosexual impact of
partial and total breast reconstruction: a prospective one-year
longitudinal study. Ann Plast Surg 2015;75(3):281–286.
32. Kelsall JE, McCulley SJ, Brock L, et al. Comparing oncoplastic breast
conserving surgery with mastectomy and immediate breast
reconstruction: case-matched patient reported outcomes. J Plast
Reconstr Aesthet Surg 2017;70(10):1377–1385.
33. Asban A, Homsy C, Chen L, et al. A cost-utility analysis comparing
large volume displacement oncoplastic surgery to mastectomy with
single stage implant reconstruction in the treatment of breast cancer.
Breast 2018;41:159–164.
34. Emiroglu M, Salimoglu S, Karaali C, et al. Oncoplastic reduction
mammoplasty for breast cancer in women with macromastia:
oncological long-term outcomes. Asian J Surg 2017;40(1):41–47.
35. De Lorenzi F, Hubner G, Rotmensz N, et al. Oncological results of
oncoplastic breast-conserving surgery: long term follow-up of a large
series at a single institution: a matched-cohort analysis. Eur J Surg
Oncol 2016;42(1):71–77.
36. De Lorenzi F, Loschi P, Bagnardi V, et al. Oncoplastic breast-
conserving surgery for tumors larger than 2 centimeters: is it
oncologically safe? A matched-cohort analysis. Ann Surg Oncol
2016;23(6): 1852–1859.
37. Mansell J, Weiler-Mithoff E, Stallard S, et al. Oncoplastic breast
conservation surgery is oncologically safe when compared to wide local
excision and mastectomy. Breast 2017;32:179–185.
38. Acea-Nebril B, Cereijo-Garea C, García-Novoa A, et al. The role of
oncoplastic breast reduction in the conservative management of breast
cancer: complications, survival, and quality of life. J Surg Oncol 2017;
115(6):679–686.
CHAPTER 35

Local Flaps for Partial Mastectomy


Defects
MOUSTAPHA HAMDI | IBRAHIM AL BASSAM
HISTORY
Perforator flaps have been described and used since the mid-1990s.
Harvesting a flap without any muscle sacrifice as well as sparing the
functional motor nerves to the underlying muscle has expanded the horizons
of reconstructive breast surgery, minimizing donor-site morbidity (1).
There are two basic types of surgical techniques in partial breast
reconstruction: volume displacement and volume replacement techniques (2).
Volume displacement techniques with the concept of breast tissue
rearrangement will be described more in details in another chapter. Volume
replacement techniques are used in small to moderate-sized breasts or when
the tumor/breast ratio is large and the residual breast tissue is insufficient for
the reshaping and the replacement of the defect. Volume replacement is
performed with nonbreast local or distant flaps offering both tissue for the
filling of the glandular defect and the skin deficiency of the reconstructed
breast. The use of local flaps as a volume replacement technique are the main
focus of this chapter.
Local perforator flaps are commonly utilized in our department for partial
breast reconstruction. The thoracodorsal (TD) and intercostal (IC) arteries
provide many perforators to the area adjacent to the breast with minimum
donor-site morbidity, unlike the latissimus dorsi (LD) muscle or
musculocutaneous flap which has an increased risk for donor-site morbidity
(1).
INDICATIONS
Patients often require surgery after partial mastectomy to correct volume
discrepancy, contour deformity, and nipple malposition (3). The resection of
more than 15% to 20% of the breast parenchyma in a small-volume (A or B
cup) breast and more than 30% in larger breast will result in volumetric
deformities and bilateral asymmetries (Fig. 35-1). Patients with small or
nonptotic breasts could require volume replacement. In addition, radiotherapy
distorts the shape of the breast, initially causing breast edema and skin
erythema and eventually causing parenchymal fibrosis, retraction, skin
atrophy, hyper/hypopigmentation, and telangiectasia. The long-term results
of radiation are unpredictable but usually stabilize 1 to 3 years after radiation
(4). In these patients, partial breast reconstruction with flaps could be
considered as an important part of whole breast cancer treatment.

FIGURE 35-1 Partial breast reconstruction: a decision-making process.


FIGURE 35-2 Indications of partial breast reconstruction flaps.

The main indication for pedicled flaps is immediate or delayed partial


breast reconstruction when volume replacement is necessary. However, these
flaps can be utilized as a salvage procedure after partial/total previous free
flap loss for breast reconstruction or as soft tissue coverage of the thoracic
area after radical excision. Moreover, these flaps can be combined with
implants in breast reconstruction as well when reconstructing larger-volume
breasts (Fig. 35-2).
CONTRAINDICATIONS
Perforator flaps are considered very meticulous surgeries that require
sufficient training in microsurgery; lack of adequate training would be a
contraindication to perform such procedure. As local pedicled flaps these
flaps have limitation when it comes to the site of the defect and it will be
difficult to reconstruct inferomedial defects of the breast with such flaps.
Planning partial breast reconstruction for large breasts or larger defects with
these local flaps won’t give sufficient volume for the reconstruction.
Previous axillary or thoracic surgery with damage to the TD vessels is a
contraindication for LD flap or thoracodorsal artery perforator (TDAP) flap
but these patients may still be candidates for a lateral intercostal artery
perforator (LICAP) flap. Previous scars and irradiation to the area may be
considered as relative contraindications of local pedicled perforator flaps as
they also might result in damaging the perforator complex (1). In the end,
when breast deformity after partial mastectomy and radiotherapy is severe,
the optimal choice is to perform a complete mastectomy and autologous
reconstruction with a free flap transfer.
PREOPERATIVE PLANNING
Preoperative evaluation of the patient must be standardized and detailed. Any
previous breast surgery should be taken into account. Different body types,
skin laxity, and fat distribution are important factors in the decision-making
process. Breast physical examination must include the evaluation of breast
skin elasticity and thickness, scars, and any defining marks such as tattoos,
stretch marks, and contour irregularities. Breast shape, grade of ptosis, and
size are determinants of success in surgical treatment. The base and width of
the breast, the width of the nipple areolar complex (NAC), the height of the
nipple, and the distance from the sternal notch, midline, and inframammary
fold (IMF) must be documented in detail. Any natural breast asymmetry
should be pointed out to the patient before surgery. Furthermore, palpation
for masses or abnormalities in the breast parenchyma, nipple examination,
and detailed documentation of breast sensation are mandatory.
In planning the approach to treat the partial mastectomy defect, the primary
decision that must be made is whether reconstructive surgery will be needed
after the tumor excision. Poor cosmetic outcomes after partial mastectomies
can occur from both the amount of breast tissue removed and/or the site of
the cancer. Partial breast reconstruction with flaps depends on the size of the
tumor, its anatomical location, the need for skin excision, and the amount of
tissue resection required to achieve free margins in relation to the volume of
the breast.
When volume replacement is necessary, the decision of which technique
will be used is determined mostly by the surgeon’s experience, the location of
the tumor, and the size of the defect in relation to the size of the remaining
breast. The nonbreast locoregional flaps offer extra tissue required in large
tumor excisions/quadrantectomies for the replacement of the breast volume,
however they can be more demanding procedures and associated with donor-
site and flap morbidity. Small lateral defects can be easily repaired with skin
rotation flaps or lateral thoracic axial flaps. However, most of these
fasciocutaneous flaps may be unavailable in patients who have had axillary
lymph node dissection. The LD muscle or musculocutaneous flaps have been
very popular as a method of choice in partial breast reconstruction (4). On the
other hand, local pedicled perforator flaps have allowed surgeons to replace
large defects with the minimum donor-site morbidity. Fasciocutaneous
perforator flaps offer sufficient soft tissue coverage while sparing the muscle
and tend to have a lower seroma rate.
RELEVANT SURGICAL ANATOMY
Both breast and plastic surgeons must have a thorough understanding of
breast anatomy, physiology, and the standards of aesthetically pleasing breast
shape. Oncoplastic surgeons should consider the aesthetic breast subunits
when planning both cosmetic quadrantectomies and reconstructions (Table
35-1) (4,5).
The Latissimus Dorsi Flap
The LD flap has the advantage of having a constant anatomy (6). The blood
supply of the LD comes from the TD artery, a terminal branch of the
subscapular artery. The subscapular artery runs about 5 cm before splitting
into the scapular circumflex and the TD arteries. The TD artery is about 2 to
4 mm in diameter and it courses along the posterior axillary fold for about 8
to 14 cm before piercing the LD on its costal surface. The TD artery gives off
one or two branches to the serratus anterior muscle and one branch to the
overlying skin. The basic pattern of the TD bundle (artery, nerve, and one to
two venae comitantes) branches into a lateral (vertical) and a medial
(horizontal) branch. The lateral branch follows a course parallel to the muscle
fibers, 1 to 4 cm medial to the free lateral border of the muscle and gives off
perforating vessels that supply the skin. The smaller medial branch diverges
at an angle of 45 degrees and travels medially. There are perforating vessels
from the IC and lumbar arteries which supply the muscle and overlying skin
as well (6).

TABLE 35-1 Aesthetic Subunits of the Breast


• The breast skin to the areola
• The areola to the nipple
• The breast skin to the chest wall at the inframammary fold
• The anterior axillary line
• The breast to the sternal skin
Different aesthetic breast subunits have been proposed according to the tissue, color and texture
differences.
From Losken A, Hamdi M. Partial Breast Reconstruction—Techniques in Oncoplastic Surgery. New
York: Thieme Medical Publishers Inc; 2017.
The TDAP Flap
The TDAP flap is based on the perforators from the descending (vertical) or
horizontal branches of the TD vessels. Anatomic studies on cadavers showed
the presence of two to three musculocutaneous perforators from the vertical
branch. The proximal perforator enters in the subcutaneous plane obliquely 8
to 10 cm below the axillary fold and 2 to 3 cm posterior to the lateral border
of the muscle. The second perforator is located 2 to 4 cm distally to the first
one. Occasionally, a direct cutaneous perforator arising from the TD vessel
passes around the lateral border of the muscle, making flap harvesting easier.
Due to anatomical variations, there may not be always a single reliable
perforator for the TDAP flap (7). In this case the surgeon must be aware and
be prepared to modify the flap dissection intraoperatively into a muscle-
sparing LD flap.
The TDAP flaps are classified as follows (1):

Standard TDAP flap, when no muscle component is included in the flap.


MS-LD-TDAP I, where a small piece of LD muscle (4 × 2 cm) is
incorporated within the flap.
MS-LD-TDAP II, where a larger segment of up to 5 cm width is
designed along the lateral border of the LD muscle.
MS-LD-TDAP III, where a larger area of LD muscle is harvested (Fig.
35-3).

The ICAP Flap


The intercostal artery perforator (ICAP) flap is based on perforators arising
from the IC vessels. The IC vessels provide an arcade between the aorta and
the internal mammary vessels and are classified in four segments: vertebral,
IC, intermuscular, and rectus segments (8).
The ICAP flaps are classified as follows:

Dorsal intercostal artery perforator (DICAP) flap: The flap is based on


perforators from the vertebral segment of the IC vessels.
The lateral intercostal artery perforator (LICAP) flap, based on
perforators arising from the IC segment.
Anterior intercostal artery perforator (AICAP) flap: The nutrient
perforators of this flap arise from the muscular or rectus segment.
The IC is the longest (12-cm) segment and it is very important because it
gives five to seven musculocutaneous perforators. The LICAP, commonly
used in breast surgery, originates from the costal segment of the IC vessels.
The largest perforator is most frequently found in the sixth IC space, from 0.8
to 3.5 cm from the lateral border of the LD muscle. The pedicle has adequate
length, allowing the rotation of the flap up to 180 degrees without tension and
without the need to extend the dissection into the costal groove. An IC nerve
may be included in the harvesting if a sensate ICAP flap is needed. For small
defects, the LICAP is designed on the lateral aspect of the thorax and for
moderate to large defects the distal limit of the skin pad can reach the
posterior thoracic region, planned in a fashion similar to the skin pad of an
LD flap.
FIGURE 35-3 TDAP anatomy. (Adapted from Hamdi M, Salgarello M, Barone-Adesi
L, et al. Use of the thoracodorsal artery perforator [TDAP] flap with the implant in breast
reconstruction. Ann Plast Surg 2008;61[2]:143–146.)

FIGURE 35-4 The ICAP flap. (Adapted from Hamdi M, Van Landuyt K, de Frene B, et
al. The versatility of the inter-costal perforator [ICAP] flaps. J Plast Reconstr Aesthet
Surg 2006;59[6]:644–652.)

The AICAP flap is outlined over the upper abdomen, so that the final scar
will be hidden under the bra strap. The donor site can be closed primarily if it
is up to 6 cm wide (preoperative pinch test) or in a reversed abdominoplasty
fashion (Fig. 35-4).
OPERATIVE TECHNIQUE
PREOPERATIVE MARKINGS
Perforator mapping simplifies flap marking and can be performed using a
portable ultrasound system. To localize the TD perforators, a unidirectional
handheld Doppler (8-Hz) ultrasonography examination is performed in the
planned skin flap area. However, although this device is handy, it has the
disadvantage of generating both false-negative and false-positive perforators
and provides less detailed anatomic vessel information. This is due to the
misleading background signal from the TD vessels, which can be confusing
and difficult to distinguish from the perforator signal. To avoid this, during
the test, the patient is positioned in the lateral surgical position with 90
degrees of shoulder abduction and 90 degrees of elbow flexion. Preoperative,
CTA scan can be also used to accurately identify the perforators (9). The
patient is preferably marked the day before surgery. In immediate
reconstruction, the breast and the tumor size and location as well as the final
defect size are estimated. The skin incisions of the partial mastectomy are
planned both for oncologic and aesthetic purposes. The TDAP flap, planned
for the partial breast reconstruction, is designed to include the traced
perforators (one or more) at the proximal part if feasible, in the directions of
relaxed skin lines, under the bra line, or even horizontally according to the
patient’s preference. The pinch test estimates the skin laxity and fat excess in
the lateral thorax and back area. The size of the flap is determined by the
need for defect coverage and averages 20 × 8 cm. The skin marking is
performed at first with the patient in an upright position and the lateral border
of the LD muscle is palpated and also marked. Then the patient is placed in a
lateral decubitus position, with the reconstruction side facing upward, for the
perforator mapping and the flap design. The skin island is always extended
over the lateral border of the LD to include the premuscular perforators if
present. The proximal border of the flap approximates the IMF. If the defect
is more medial, the flap is designed more distally, further onto the back. The
LICAP flap design follows the same rules, however the flap is placed more
anteriorly, toward the breast. When AICAP flaps are chosen for partial breast
reconstruction, these flaps are usually designed under the IMF along the rib.
SURGICAL EXPOSURE AND DETAILS OF PROCEDURE
The patient is prepped and positioned in supine position for the partial breast
mastectomy. When the lumpectomy/quadrantectomy is completed, clips are
placed in the wound bed in order to mark the area for radiation therapy. If the
reconstructive plan provides for a TDAP or LICAP flap, the patient is
positioned and prepped again in lateral position as for LD flap dissection.
Otherwise, for AICAP flaps the patient remains in the supine position. The
flap harvesting starts with skin incisions. A posterior approach is usually used
in the TDAP flap. The surgeon continues dissection down to the LD in the
suprafascial plane, while beveling away from the flap in order to recruit as
much tissue as possible. Harvesting proceeds from the back toward the
axillary region. The dissection continues meticulously, under loupe
magnification, until the perforator vessel is encountered.
If the perforator has a visible pulsation and is adequate in caliber (>0.5
mm) the dissection continues along the perforator course up to the TD
pedicle. If a longer pedicle length is required, the TD vessels can be dissected
up to their subscapular vessel origin and included in the flap. If the perforator
has an intramuscular course, the dissection is achieved in the direction of the
muscle fibers and any nerves that come across should be carefully preserved.
All the perforator side branches within the muscle fibers are either ligated or
coagulated. If two perforators are found along the same row, they can both be
included within the flap, without sacrificing any muscle fibers. In case of
inadequate perforator size, the flap is converted to a muscle-sparing LD,
preserving a small cuff of muscle attached to the posterior wall of the
perforators, sacrificing only few fibers and, most important, preserving the
muscle innervation. This adjustment is also useful when the flap is planned
for the medial breast reconstruction, because it protects the perforators from
tension. The flap harvesting carries on, with the skin incisions continued
proximal to the axilla and lateral to the LD and the dissection proceeds
anteriorly, until the flap is freed from the donor site and left connected only
to the vascular pedicle.
The flap is passed through a subcutaneous tunnel in the axilla–lateral
thoracic area to the recipient breast area, avoiding any injury to the pedicle.
The donor site is closed in three anatomical layers, a drain is placed, and the
patient is returned again to the supine position. Before the final insetting, the
flap can be partially or totally de-epithelialized and folded if needed to give
extra projection to the reconstructed breast mound. In LICAP flap dissection,
an anterior approach is performed from the breast toward the lateral border of
LD muscle. Perforator dissection is done within the serratus muscle until
reaching its origin from the costal groove. Further dissection is usually not
needed.
INTRAOPERATIVE CARE

The patient is positioned carefully to prevent brachial plexus traction


injuries by avoiding inadvertent overabduction or traction of the
shoulder joint especially with inexperienced surgeons as the procedure
could be lengthy in the beginning.
Use antiembolism stockings or mechanical calf compression boots.
Keep the operating room warm as any drop in the body temperature can
cause vasoconstriction.
Local use of Papaverine irrigation can be useful in case of intraoperative
vessel vasoconstriction as it relieves the spasm of the vessels.
Intraoperative handheld Doppler can be used to confirm the perforator
location.
ICG can be used after harvesting the flap to map the vascularity of the
flap and avoid partial flap or fat necrosis.
POSTOPERATIVE CARE
Postoperatively, standard perforator flap monitoring protocol is followed.
Patients receive low–molecular-weight heparin (LMWH) during the relative
immobilization time. The arm is held in 45-degree abduction. Arm stretching
is restricted for a week.
Patients treated for BCT with pedicled perforator flaps have a short
recovery course and can be discharged home once the drains are removed,
usually 3 to 5 days postoperatively, and physiotherapy can be started. Most
patients require 9 to 14 sessions of shoulder physiotherapy. Adjuvant breast
radiation therapy can be started 6 weeks postoperatively, and chemotherapy,
if indicated, can start before radiotherapy at 3 weeks postoperatively.

CASES

CASE 1

A 44-year-old patient with a ductal carcinoma over the junction of the


lateral quadrants of the right breast. The patient underwent a lumpectomy
with nipple areola centralization by the breast surgeon (Fig. 35-5).
Unfortunately, the margins were involved. The patient was a good
candidate for further resection and immediate partial breast
reconstruction with a pedicled perforator flap.
The perforators were located by the Doppler examination. Two
perforators were localized, the closest one to the defect was presumed to
be an intercostal and the other one was presumed to be a thoracodorsal
perforator (Fig. 35-6A). A skin paddle was modified upward to include
both perforators at the lateral thoracic area (Fig. 35-6B). The flap was
extended posteriorly with two versions, a short one if the intercostal
perforator was chosen and a longer one if the thoracodorsal perforator
was chosen during the surgery (Fig. 35-6C). The oncologic resection was
done in lateral position of the patient and then the intercostal perforators
were first explored by anterior approach (Fig. 35-7A). The short version
flap was then incised (Fig. 35-7B). The LICAP flap was dissected from
the underlying LD muscle (Fig. 35-7C). The flap was turned in 180
degrees to reach the defect (Fig. 35-7D). The skin was de-epithelialized
leaving a small skin paddle (Fig. 35-7E). Postoperative views are shown
(Fig. 35-8).

FIGURE 35-5 A 44-year-old patient with a ductal carcinoma over the


junction of the lateral quadrants of the right breast. Frontal view (A), oblique
view (B) and lateral view (C).

FIGURE 35-6 Preoperative markings.


FIGURE 35-7 Operative technique.
FIGURE 35-8 Postoperative views: frontal (A), oblique (B) lateral (C, D), and
back (E).

CASE 2

A 42-year-old patient with a ductal carcinoma within the superolateral


quadrant of the left breast. The tumor was close to the skin. Since the
patient was slim, a piece of latissimus dorsi (LD) muscle was included in
the flap (Fig. 35-9).
A muscle-sparing latissimus dorsi flap was harvested. The skin
incision was made (Fig. 35-10A). The flap was based on the descending
branch of the thoracodorsal vessels (Fig. 35-10B). This technique spares
more than 80% of the LD muscle. The flap was transferred to the defect
and the patient was turned into supine position (Fig. 35-10C). Figure 35-
11 shows 1-year postoperative results.

FIGURE 35-9 A, B: Preoperative views with the amount of skin resection


including the underlying tumor, and (C) the surgical markings with a skin
paddle measuring 20 × 8.5 cm was designed.
FIGURE 35-10 Operative technique.
FIGURE 35-11 One-year postoperative result of partial breast reconstruction
with muscle-sparing LD flap (A, B) and the donor site (C).

CASE 3

A patient undergoing a quadrantectomy for a tumor of the superolateral


quadrant of the right breast. The quadrantectomy specimen weighed 195
g. Reconstruction is with a completely de-epithelialized thoracodorsal
artery perforator (TDAP) flap based on one perforator (Fig. 35-12).
FIGURE 35-12 A–C: Preoperative views. D: The flap design with the
Doppler-located perforators marked. E: The dissection of the perforator
through the split latissimus dorsi (LD) muscle. The thoracodorsal nerve is
preserved. F, G: The TDAP flap is passed through the split LD muscle and
then through the axilla. H: The LD muscle is left intact. I–K: Postoperative
views. L: Donor site.
COMPLICATIONS
The average complication rate was 14% in oncoplastic flap reconstruction
cases. The complication rate of breast conservation therapy (BCT) alone was
25.9%, although early complication rates were not routinely reported (1).
Donor-site morbidity in partial breast reconstruction is reduced to a minimum
using locoregional pedicled perforator flaps. Seroma is the most common
donor-site complication. According to a recent study, the seroma rate in MS-
LD-TDAP II flaps is 5.5%, while there are no seromas in perforator flaps.
Seromas are usually treated conservatively with aspiration.
Other postoperative complications observed were wound dehiscence (4%),
infection (2%), and hematoma (2%). Partial or total flap losses are rare. Fat
necrosis of the flap has been observed and might be suspicious on several
radiologic imaging modalities. In case of a suspicious lesion, biopsy with
fine-needle aspiration, core biopsy, or excisional biopsy might be necessary
to rule out tumor recurrence (up to 25%). When the necrosis is minimal it can
be treated, if necessary, by excision and primary closure or reconstruction
with another local flap. In those cases of extensive necrosis, a mastectomy
with total breast reconstruction might be indicated (10). Pathologic scars, flap
contractures, and volume loss are rare sequelae and may need secondary
procedures.
Some patients who undergo reconstruction with a TDAP flap encounter an
initial decrease in forward arm elevation and passive abduction, which
recovers over time.
Partial breast reconstruction with flaps may give a “plugged-in”
appearance, which seems to be slightly improved after radiation therapy.
OUTCOMES
It is hard to calculate the long-term outcomes of partial breast reconstruction
with pedicled perforator flaps due to the unpredictable impact of radiation
therapy on the final result. Breast asymmetry due to the different aging
process between the two breasts can be observed because the nonirradiated
side may become more ptotic when compared to the irradiated side. The
irradiated breast may also atrophy. When the breast asymmetry is noticeable,
fat grafting and/or contralateral breast reshaping is indicated.
CONCLUSION
BCT is considered the gold standard in the treatment of early-stage breast
cancer. The main indication for pedicled flaps is immediate or delayed partial
breast reconstruction when volume replacement is necessary. The harvesting
of a local perforator flap has a long learning curve, requiring a sufficient
knowledge of the anatomy of the area. Secondary procedures such as breast
lipofilling and contralateral breast reshaping may be required to reach breast
symmetry.

REFERENCES

1. Hamdi M. Pedicled perforator flaps in breast reconstruction. In: Spear


SI, Willey SC, Robb GI, et al., eds. Surgery of the Breast: Principles
and Art. Philadelphia, PA: Lippincott-Raven; 2010:757–769.
2. Noguchi M, Yokoi-Noguchi M, Ohno Y, et al. Oncoplastic breast
conserving surgery: volume replacement vs. volume displacement. Eur J
Surg Oncol 2016;42(7):926–934.
3. Delay E, Guerid S, Meruta AC. Indications and controversies in
lipofilling for partial breast reconstruction. Clin Plast Surg
2018;45(1):101–110.
4. Munhoz AM, Montag E, Gemperli R. Oncoplastic breast surgery:
indications, techniques and perspectives. Gland Surg 2013;2(3):143–
157.
5. Losken A, Hamdi M. Partial Breast Reconstruction—Techniques in
Oncoplastic Surgery. New York: Thieme Medical publishers Inc; 2017.
6. Griffin JM. Latissimus dorsi musculocutaneous flap. In: Strauch B,
Vasconez LO, Hall-Finley EJ, et al., eds. Grabb’s Encyclopedia of
Flaps. Vol. 3. 3rd ed. Philadelphia, PA: Lippincott Williams &
Wilkins/Wolter Kluwer; 2009:1026.
7. Hamdi M, Van Landuyt K, Hijjawi JB, et al. Surgical technique in
pedicled thoracodorsal artery perforator flaps: a clinical experience with
99 patients. Plast Reconstr Surg 2018;121(5):1632–1641.
8. Hamdi M, Van Landuyt K, de Frene B, et al. The versatility of the inter-
costal artery perforator (ICAP) flaps. J Plast Reconstr Aesthet Surg
2006;59(6):644–652.
9. Hamdi M, Van Landuyt K, Van Hedent E, et al. Advances in
autogenous breast reconstruction: the role of preoperative perforator
mapping. Ann Plast Surg 2007;58(1):18–26.
10. Hamdi M. Oncoplastic and reconstructive surgery of the breast. Breast
2013;22(suppl 2):S100–S105.
CHAPTER 36

Local Flaps for Breast-Conserving


Surgery Defects
DOUGLAS R. MACMILLAN | STEPHEN J. MCCULLEY
HISTORY
Oncoplastic techniques for the immediate reconstruction of breast-conserving
surgery (BCS) defects broadly fall into three categories: simple local
parenchymal mobilization; breast reduction/mastopexy; and volume
replacement (1). Several methods of volume replacement have been reported;
in this chapter we describe the use of local flaps.
Volume replacement is of most use in the small-/moderate-sized breast that
does not have a simple or reduction/mastopexy option (or this is not desired).
The aim is to preserve breast appearance with minimal, if any scarring visible
from the front and replace volume with well-vascularized breast-like
subcutaneous adipose tissue capable of tolerating radiotherapy.
Local perforator flaps harvested from the chest wall around the breast
utilize the various adjacent options for vascularization and take advantage of
lax lateral chest wall subcutaneous tissue. Their reliability has long been
established and their anatomical basis has been well described (2–4). For
partial breast reconstruction, these flaps have largely superseded the
previously described latissimus dorsi (LD) muscle flap with its attendant
morbidity loss of function and potential to atrophy (5–8). They keep donor-
site morbidity to a minimum and preserve the option of LD flap
reconstruction should it ever be required for salvage or total reconstruction.
In addition, the scarring resulting from harvesting tissue lateral or inferior to
the breast can usually be hidden in the bra line and these flaps can provide a
good-sized skin island if required.
Flaps local to the boundaries of the breast can be classified according to
their nutrient vessel:

Intercostal artery perforator flap—lateral (LICAP flap), anterior


(AICAP flap), and medial (MICAP flap)

This flap is based on perforators from the vascular arcade formed by the
posterior and anterior intercostal arteries in the upper 6–7 intercostal spaces.
Anatomical studies have shown that there are multiple such perforators in and
around the breast footprint on the chest wall and between the lateral border of
the breast and the anterior border of the LD, particularly in the 4th–6th
intercostal spaces. Our experience has shown many of these perforators are
closely related to the lateral breast border and are very common in certain
locations—they can almost always be found in a triangle created by the
lateral and inferior breast creases. As the vascular basis are the perforators
there is no movable pedicle with these flaps. The perforators are therefore the
fixed or “pivot” point in the movement of these flaps, hence those closer to
the breast are more useful. The flap can be delivered into the breast as either a
turnover flap (often with a line of perforators) or as a rotation/propeller
technique (usually with a single or close cluster of perforators). The plethora
of perforators allows these flaps to be placed where donor volume exists and
they can usually be based on more than one perforator. If the defect is more
medial, the breast tissue lateral to defect will need removing to allow access
for the flap.

Lateral thoracic artery perforator (LTAP) flap

The lateral thoracic vessels usually arise from the axillary artery, although
may arise from the subscapular or thoracodorsal artery. They are always
visualized and routinely divided as part of an axillary node clearance
procedure. As they course down the lateral border of the breast they give off
perforators that allow them to be used for pedicled flaps. Alternatively, they
can augment intercostal perforator-based flaps as a turnover flap. Of note, the
distal course of the lateral thoracic vessels is variable and occasionally there
is no descending branch lateral to the breast and the vessels enter the breast
directly just below the axilla. In addition, the descending branch rarely
reaches the level of the inframammary fold and in the axilla the vessels are
usually closely related to the sentinel node. However, when available, these
transposition flaps provide an easy option to fill lateral defects and have the
potential to reach medially. As these flaps have a true vascular pedicle they
allow transposition of the flap into the breast and can allow breast tissue
lateral to a central defect to be preserved.

Thoracodorsal artery perforator (TDAP) flap

The TDAP flap is pedicled flap usually based on perforators of the


descending branch on the thoracodorsal artery and only occasionally
indicated for immediate reconstruction of defects from BCS. However, it has
the potential for large volume and long reach. It can be raised on a single
perforator with splitting of the muscle, however it is most easily raised with a
muscle patch including more than one perforator on an anterior branch of the
main descending branch. The thoracodorsal nerve and hence function of the
LD muscle is preserved. It is a slightly more technically demanding flap to
raise.
LOCATING THE PERFORATORS
The perforators are identified using an 8-MHz handheld Doppler. Only
perforators within 2 to 3 cm of the lateral breast crease and within 1 to 2 cm
of the inframammary fold are of value in allowing easy delivery of the flap
into the breast. In our experience and on the basis of a perforator mapping
study, there are common sites for intercostal perforators as shown in Figure
36-1.
Perforators of the thoracodorsal vessels are well described (9,10). For the
purpose of reconstruction of partial breast defects, to give reach and keep the
donor-site scar in the inframammary fold, TDAP flap is best raised on a
muscle patch using more distal perforators at the level of the bra line as
described in the section that follows.
FIGURE 36-1 Common sites for perforators.
PLANNING A LOCAL PERFORATOR FLAP
Although all these flaps can be planned to reach a defect anywhere in the
breast, the ideal (and easiest) case is a small nonptotic breast with a laterally
sited cancer. However, from our experience of over 500 cases (11), we have
found the following to be common solutions to frequently encountered
clinical scenarios as noted in Figures 36-2 and 36-3.
For more central defects in the upper half of the breast, including those
behind the nipple, a pedicled LTAP flap is ideal. Alternatively, a LICAP flap
can be extended and intervening breast tissue excised. If neither of these
options is possible then a TDAP flap can be used. If a skin-bearing flap is
required (e.g., if the nipple is required to be excised) then an LTAP flap again
is ideal or alternatively a TDAP flap (Figs. 36-4 and 36-5).
In the lower breast, central defects can be filled with LICAP flaps based on
perforators at the lateral end of the inframammary fold. Alternatively, they
can be filled with a bilobed “gullwing” flap based on intercostal perforators
near the breast meridian on the inframammary fold (Figs. 36-6 and 36-7).
FIGURE 36-2 Lower lateral defect filled with a turnover LICAP flap usually based
on two or three perforators.
FIGURE 36-3 Lateral defect filled with turnover LICAP flap supplemented with
LTAP vessels. The LTAP vessels augment the flap without hindering flap delivery.
FIGURE 36-4 Upper central defect filled with an LTAP flap.
FIGURE 36-5 Upper central defect filled with an extended LICAP flap. Here the
tissue lateral to the defect needs to be excised to allow for flap delivery.
FIGURE 36-6 Lower central defect filled with LICAP flap.
FIGURE 36-7 Lower central defect filled with AICAP flap.
FIGURE 36-8 Upper medial defect filled with an LTAP flap.

Medial defects always represent a challenge, whatever technique is used.


In the upper half of the breast they are most easily filled with a pedicled
LTAP flap, turned over, and transposed. In the lower half of the breast a flap
based on a medial intercostal perforator can be used in those who have some
tissue laxity below the inframammary fold (Figs. 36-8 and 36-9).
FIGURE 36-9 Upper medial defect filled with an extended MICAP flap.
FIGURE 36-10 Lower medial defect filled with a MICAP flap.

Medial defects in the lower half of the breast are easily reached by a flap
based on medial intercostal perforators (Fig. 36-10).
Lateral flaps are usually designed as a leaf pattern with the aim of keeping
the scar close to the curvature of the breast or inframammary fold and within
the bra line as much as possible. Flap width can be planned by assessing skin
laxity by superior and inferior tissue stretch, avoiding excessive horizontal
tension, which may lateralize the breast. Flap size will depend on volume of
subcutaneous tissue available/required and the necessary reach. In our
experience intercostal perforator flaps should be planned with the skin island
directly over the vessels, the arborization being visible as multiple bleeding
points directly over the perforator at deepithelialization, and the subdermal
plexus being an important conduit for flap vascularization. It is for this reason
we consider keeping the dermis is essential as opposed to a pure adipofascial
flap, which we consider to be less reliable. LTAP flaps, on the other hand,
can have a degree of superior adipofascial extension toward the vessels to
keep the scar low but usually have to be sited slightly higher than LICAP
flaps due to the location of these vessels.
Most flaps are performed simultaneous with cancer excision as a day case
procedure. In a few cases, where certainty regarding clear margins is desired
before commitment to the flap and its scar, the operation can be planned as
two stage with an initial wide local excision and the flap performed as a
secondary procedure. For such cases the wide local excision cavity can be
maintained for 2 to 3 weeks with water instillation. At the subsequent flap
insertion, it is important to “freshen up” the margins of the cavity to prevent
encapsulation of the flap.
OPERATIVE TECHNIQUE
LICAP/LTAP FLAPS
For all the lateral chest wall flap procedures, the patient is positioned supine
with a 3-L pressure bag partially inflated below the ipsilateral hemithorax to
tilt the torso. This provides good access to the lateral chest wall and breast,
and deflation of the pressure bag after flap harvest and closure of the wound
posteriorly allows for insetting with the patient supine or sitting up if
necessary. Local anesthetic with adrenaline is infiltrated around the planned
wide local excision and used as a means of hydrodissection of the
subcutaneous tissue overlying the cancer. It is also infiltrated around the flap,
carefully avoiding the marked LICAP perforators and the LTAP territory.
For LICAP and LTAP flaps, the initial part of the procedure is to locate, if
present, the LTAP vessels. These lie below Scarpa fascia just above the
Serratus fascia and are usually 1 to 3 cm from the lateral curvature of the
breast. Once identified, or if not present, the wide excision of the cancer is
performed via the upper anterior marking of the flap design. Care is
obviously required to avoid damage to any LTAP vessels or LICAP
perforators mapped behind the flap design. As with all oncoplastic BCS, a
generous margin of excision is planned, to maximize the likelihood of
achieving clear histologic margins. Care is taken not to extend subcutaneous
or submammary dissection beyond the defect created by the wide local
excision, the principle being to create a hand-in-glove scenario when the
defect is filled with the flap.
The sequence for raising the flap starts with circumferential dissection
down to the muscular fascial plane, beveling slightly away from the flap
slightly to increase volume, particularly deep to Scarpa fascia. The lower
medial part of the incision can be left until the perforators have been
visualized as this maintains the option of isolating the flap at least partly on a
dermal bridge, particularly in scenarios illustrated in Figures 36-2, 36-3, 36-
6, 36-7, 36-9, and 36-10 above. The flap can then be raised posterior to
anterior in the premuscular fascial plane to meet the identified perforators to
complete the dissection. If LTAP vessels are confirmed and clearly consisting
of an artery and vein then a decision may be made to isolate the entire flap on
these vessels at this stage, expediting any further dissection. If not present
(sometimes only a vein is identified) or their course is not favorable, the flap
dissection would proceed by raising the flap from posterior to anterior toward
mapped intercostal perforators. Once the flap is elevated anterior to the
border of the LD, dissection continues on a much more cautious basis. This
may be achieved with cutting diathermy on a low setting or with fine
scissors, and bipolar diathermy as required. As the “fall-back” vascular
source of the LICAP flap is usually the TDAP vessels or converting the flap
to a more random one based on the inferior dermal attachments (in turn
derived from more caudally located perforators), both of these areas are
worth some consideration during their respective parts of the dissection. In
practice, if LICAP perforators are clearly identified preoperatively then these
“fall-back” options can be confidently sacrificed early in the dissection. The
level of dissection moving medially from the LD border is just superficial to
the Serratus fascia. Perforating vessels are readily identified and preserved
according to their suitability to be part of the overall flap design and plan for
flap movement, either rotation or turnover. Commonly the flap reaches a
point of mobility where it can be “turned over” or rotated into the defect
without formally fully exposing the perforators. Often a “mesentery” of tissue
including more than one perforator can be preserved at the lateral border of
the breast. As the flap turns over, the lateral curvature and breast shape is
naturally reconstructed.
In some cases, anatomical variants of the chest wall vessels, such as a long
subcutaneous branch of the thoracodorsal vessels, a cutaneous branch of the
serratus branch of the thoracodorsal vessels, or a subcutaneous branch of a
vessel accompanying the long thoracic nerve are serendipitously found and
used. Due to the rich diversity of options available to vascularize a chest wall
flap, the learning curve for this operation includes developing a sense of
when one “ideal” source of vascularization has been identified such that
others can be sacrificed. In this regard, any visibly pulsatile vascular bundle
can be considered adequate. This can usually be supplemented with other
contributory vessels without compromising flap mobility.
Axillary surgery is usually performed via the LICAP incision and a
separate incision is used for AICAP and MICAP procedures. It is easier to
raise the flap before performing a sentinel node biopsy or axillary node
clearance due to the access that is then afforded. As an axillary dissection
usually involves division of the lateral thoracic vessels, planning an LTAP
flap in this setting is a less suitable option. If desired, the LTAP vessels can
be dissected through the axilla, although this is time consuming due to
multiple branches encountered. Care needs to be taken during sentinel node
biopsy in LTAP flap procedures due to the course of these vessels being very
closely related to the most common sentinel node site. For this reason, a final
decision on which flap perforators are preserved may be best taken after
performing the sentinel node biopsy.
The breast cavity is then washed thoroughly, a drain placed, and the flap
inserted into the defect. Flaps are deepithelialised, preserving the subdermal
plexus. A principle of flap deployment is that it is sutured to prevent the flap
falling out of the defect rather than being sutured in. Thus, if any sutures are
necessary to maintain flap position they are usually placed between the flap
and deep subcutaneous or breast tissue at the very peripheral part of the
breast. Sutures to the chest wall are avoided. The wound is then closed in
layers with sutures to the deep fascia, deep dermis, and subcutis.
TDAP FLAP
As stated above, the indications for a TDAP flap in the immediate
reconstruction of BCS defects are few. They are indicated primarily when a
large-volume flap is required or in delayed partial breast reconstruction after
radiotherapy. Due to the fact that a TDAP flap usually renders impossible the
subsequent raising of an LD flap, our preference is always to perform a
LICAP or LTAP flap in preference to a TDAP flap if both options are
available. In addition, for this reason, a two-stage approach is often used with
an initial wide local excision of the cancer and sentinel node biopsy followed
by a TDAP flap 1 to 3 weeks later once clear histologic margins are
confirmed. If axillary node clearance is indicated, this would be performed at
the second stage.
Classically, the TDAP flap is planned around a single primary perforator
located approximately 10 cm below the posterior axillary fold. However, this
confers limited reach for partial mastectomy defects. More caudal perforators
are readily found, but due to the extra length of proximal dissection of the
pedicle that is necessary, flap harvest is modified from the classical
description to incorporate a muscle patch, which simplifies the dissection and
greatly reduces operative time.
Under general anesthetic, the patient is positioned lateral with the arm
flexed to 90 degrees. Local anesthetic with adrenaline is infiltrated around the
flap. Dissection starts with circumferential dissection down to LD and
serratus fascia, beveling outward to increase volume, particularly deep to
Scarpa fascia. The anterior part of the flap is then raised to the anterior border
of the LD, which in turn is elevated for a few centimetres from the underlying
serratus and chest wall such that the undersurface of the lateral border of LD
is visualized. In almost all cases, an anterior branch of the descending branch
of the thoracodorsal vessels is identified and these (and its undissected
perforators) are used as the basis of the flap.
A myotomy is then created just medial to this anterior branch of the
descending thoracodorsal vessel and continued caudally along the width of
the flap. The flap is then raised medial to lateral to this level and the distal
end of the vessels ligated and overlying muscle divided. The anterior branch
is then dissected proximally until the main descending branch of the
thoracodorsal vessels is encountered. At this point the distal continuation of
the descending branch is ligated and the thoracodorsal nerve preserved. Also
at this point, the muscle overlying the pedicle is divided, thus isolating the
flap on its perforators protected by a small patch of muscle, usually
measuring approximately 2/3 cm × 6/8 cm. The vessels are then dissected
proximally, according to the length of pedicle required separating and
preserving the nerve en route. In most cases for BCS this would include
division of the transverse branch of the thoracodorsal vessels. The flap is then
tunneled into the breast defect and the wound closed in layers with a drain
(Fig. 36-11).
FIGURE 36-11 TDAP flap with muscle patch, preserving thoracodorsal nerve and
LD function. A: Illustration. B–E: Sequence one through four of technique.
FIGURE 36-12 A–F: A small volume LICAP flap rotated into a lower outer
quadrant defect.
FIGURE 36-13 A–F: A large LTAP/LICAP flap turned over into an upper outer
quadrant defect.
CONCLUSION
The location and consistency of tissue from the lateral chest wall makes it
ideal for use as immediate reconstruction of partial defects. Local perforator
flaps fill a breast cavity with breast-like subcutaneous adipose tissue and can
provide a good-sized skin island if required. Because these flaps do not
compromise an option for total breast reconstruction, they are very suitable
for one-stage reconstruction at the same time as wide local excision of the
cancer. Knowing that the defect is to be filled allows confidence to take a
“wide” margin around a cancer, thus reducing the incidence of positive
margins. The long scar from the donor site is the main limitation of these
procedures but sited in lines of tension and within the bra line as much as is
possible, they are not visible from the front and very well accepted in our
experience.
Flap size can vary from small volume flaps adjacent to a small lateral
defect (see Fig. 36-12A–F), to large volume flaps replacing either a large
defect or a more medial one (Fig. 36-13A–F).
In thin women, long flaps are often required to obtain sufficient volume.
The defect locations that lend themselves most readily to local flaps are those
in the outer third of the breast (Figs. 36-14A–F and 36-15A–F). However,
with careful planning these flaps have the potential to fill a defect at any site.
Volume replacement in BCS may be an underutilized form of oncoplastic
surgery and its increased use may enable more women to be offered this
option as a better alternative to mastectomy and breast reconstruction.
FIGURE 36-14 A lower outer quadrant defect in a thin patient filled with a turnover
LICAP flap, before and after radiotherapy. A–C: Preop patient. D–F: Postop
patient.
FIGURE 36-15 An outer defect filled with an LTAP flap, before and after
radiotherapy. A, B: Preop patient. C–E: Postop patient.

REFERENCES

1. Macmillan RD, McCulley SJ. Oncoplastic breast surgery: what, when


and for whom? Curr Breast Cancer Rep 2016;8:112–117.
2. Bhattacharya S, Bhagia SP, Bhatnagar SK, et al. The anatomical basis of
the lateral thoracic flap. Eur J Plast Surg 1990;13:238–240.
3. Hamdi M, Van Landuyt K, de Frene B, et al. The versatility of the inter-
costal artery perforator (ICAP) flaps. J Plast Reconstr Aesthetic Surg
2006;59:644–652.
4. Hamdi M, Spano A, Van Landuyt K, et al. The lateral intercostal artery
perforators: anatomical study and clinical application in breast surgery.
Plast Reconstr Surg 2008;121:389–396.
5. Dixon JM, Venizelos B, Chan P. Latissimus dorsi mini-flap: a technique
for extending breast conservation. Breast 2002;11:58–65.
6. Noguchi M, Saito Y, Mizukami Y, et al. Breast deformity, its correction,
and assessment of breast conserving surgery. Breast Cancer Res Treat
1991;18:111–118.
7. Rainsbury RM, Paramanathan N. Recent progress with breast-
conserving volume replacement using latissimus dorsi miniflaps in UK
patients. Breast Cancer 1998;5:139–147.
8. McCulley SJ, Schaverien MV, Tan VKM, et al. Lateral thoracic artery
perforator (LTAP) flap in partial breast reconstruction. J Plast Reconstr
Aesthetic Surg 2015;68:686–691.
9. Heitmann C, Guerra A, Metzinger SW, et al. The thoracodorsal artery
perforator flap: anatomic basis and clinical application. Ann Plast Surg
2003;51:23–29.
10. Mun GH, Lee SJ, Jeon BJ. Perforator topography of the thoracodorsal
artery perforator flap. Plast Reconstr Surg 2008;121:497–504.
11. Macmillan RD, McCulley SJ. Oncoplastic breast conserving surgery. In:
Dixon JM, Barber MD. Breast Surgery: A Companion to Specialist
Surgical Practice. 6th ed. UK: Elsevier; 2018.
CHAPTER 37

Avoiding Pitfalls in Symmetry


Procedures Following Unilateral
Autologous Versus Implant-Based
Reconstruction
MICHELE A. SHERMAK
HISTORY
Breast reconstruction is performed in women post lumpectomy or
mastectomy for breast cancer treatment. Over 100,000 breast reconstruction
procedures are performed annually (1). Unilateral acquired defects are more
common than bilateral presentations, and initial reconstruction is focused on
creating an aesthetic breast post partial or total mastectomy, in an immediate,
delayed, or staged fashion. To achieve symmetry with the reconstructed
breast, plastic surgical procedures are often necessary for the contralateral,
otherwise unaffected breast, particularly with implant reconstruction. In 1998
President Clinton mandated that insurance companies cover reconstructive
surgery on both breasts in breast cancer patients, even with unilateral cancer,
so more women are able to pursue contralateral symmetry surgery since
insurance covers it. This mandate also came at a time when breast
reconstruction outcomes were providing more superb aesthetic results not
only in clothing but undressed and more women were opting to undergo
reconstruction, encouraged by other cancer survivors and their treating
physicians. Breast reconstruction prevalence has increased almost 30% since
2000 (1). Pedicled TRAMs were routine in the 1990s, and perforator flaps
were starting to join the mainstream. Over time, less-invasive mastectomy
approaches have allowed improved aesthetic outcomes, such as skin-sparing
patterns, ultimately followed by nipple-sparing techniques (2,3). Women are
experiencing greater aesthetic results of their reconstructed breast, often
surpassing their preoperative appearance, so the need for the opposite breast
to match and look as good as the reconstructed breast became increasingly
accepted and expected.
The best option for the best match is undergoing contralateral prophylactic
mastectomy (CPM) with symmetrical mastectomy and reconstructive
procedures. This practice is controversial in that the risk of contralateral
cancer has proven to be low while the risk of complications associated with
contralateral mastectomy and reconstruction are considerable (4,5). It has
been demonstrated that the 10-year cumulative risk of developing a
contralateral breast cancer in women who were initially diagnosed with
unilateral disease is 6% to 7%, and that the 20-year incidence is 9% (6,7).
While CPM is recommended for patients with genetic or treatment-based
(Mantle radiation) predisposition for breast cancer, the application of CPM to
achieve symmetry is a standard some centers follow, but not most (8).
As CPM is not universally accepted, symmetry procedures after unilateral
mastectomy reconstruction have become the necessary challenge to meet.
Contralateral procedures for symmetry are more necessary after implant-
based reconstruction relative to autologous techniques, as the main goal of
autologous breast reconstruction is to maintain the volume, shape, and
dimensions of the breast undergoing mastectomy (9). With microsurgical
techniques gaining greater prevalence over pedicled reconstructions, greater
volumes of tissue may be more safely transferred, and skin-sparing
mastectomy approaches have also resulted in reduced need for contralateral
symmetry procedures (2,6). Despite improved outcomes in autologous
reconstruction, implant reconstruction rates are growing due to acceptance of
nipple-sparing mastectomy (NSM), acellular dermal matrices, and greater
implant options (10). With the shift in higher utilization of implant
reconstruction, there is an even greater need currently for contralateral
symmetry procedures.
It is understood that contralateral breast surgery should not impair
screening for breast cancer, and this is supported by data. It has been
determined that mammographic accuracy, sensitivity, and specificity are not
affected by the glandular rearrangement (11).
While contralateral surgery may be performed immediately at the time of
cancer resection and reconstruction, when performed at a second stage,
symmetry is better guaranteed, allowing the breast reconstruction to fully
heal and settle. The best long-term result is the one that settles least, and
breast implant reconstruction has resulted in the best outcomes through
objective testing. Breast lift and breast reduction techniques change most
over time with age, weight changes, and medications necessary for cancer
treatment, with increasing ptosis and size, leading to less predictability over
the long term relative to implant reconstruction. Over time, the literature has
focused greater interest on the “if” over the “what” with regard to
contralateral symmetry procedure: patient satisfaction versus what procedure
to do. Symmetry is the key to long-term successful outcome and patient
satisfaction after breast cancer treatment (12,13).
The toolbox for contralateral breast symmetry surgery includes implants
and/or breast lift, or breast reduction. Fat transfer also may be incorporated in
the reconstructive strategy.
INDICATIONS

Implants
Implant placement in the contralateral breast may be performed when the
woman undergoing mastectomy and reconstruction decides she wants to aim
for a higher volume, fuller breast post mastectomy reconstruction. This is
common for women who are younger, thinner, postpartum, and/or have
deflated breasts without significant ptosis. Optimal patients for contralateral
implant procedures include those who undergo NSM with immediate
prepectoral reconstruction, non-NSM with expander reconstruction above or
below the pectoralis major with later conversion to a breast implant, or
autologous reconstruction.
In women who hope to achieve a final breast volume comparable to
baseline, reconstruction with shaped textured implants particularly in the
prepectoral position may achieve acceptable symmetry to the contralateral
breast; however, due to the greater documented risk of BIA-ALCL with
textured implants, more implant-based reconstructions include smooth round
implants which provide more upper pole volume, and a need to match this
with an implant or fat on the uninvolved breast (14).
Breast Lift
Breast lift of the contralateral breast is performed in women with ptosis who
have satisfactory volume match, or in women whose contralateral breast
becomes relatively more ptotic after radiation treatment which results in more
fibrosis, scarring, and a tighter breast envelope on the cancer side. Breast lift
may be performed with an implant and/or fat transfer to achieve better
volume symmetry and to obtain more optimal upper pole fullness which
better matches the upper pole on the reconstructed side, more common with
implant reconstruction. It is important for the patient to understand that breast
lift may not provide symmetry over the long term and future adjustments may
be necessary for breast changes secondary to weight gain, aging, and
decreased tissue strength leading to future ptosis.
Breast Reduction
Contralateral breast reduction more often applies to women who are older,
have a larger BMI and/or a large breast size with ptosis, or in women who
have undergone lumpectomy and radiation for breast conservation which
does not conserve symmetry. Breast reduction pairs well with a staged
implant reconstruction associated with total mastectomy in which the nipple
cannot be spared; autologous reconstruction with a volume reduced from
baseline; or lumpectomy and oncoplastic reconstruction followed by
radiation therapy. Breast reduction helps achieve three-dimensional
symmetry, including width, length, contour, and volume of the mastectomy
reconstruction. As with breast lift, patients need to be informed of changes
anticipated in the reduced breast over time that may require revision surgery
to restore symmetry, particularly with implant reconstruction of the cancer
side.
Fat Transfer
While fat transfer is a useful tool for reconstruction post mastectomy, filling
in defects left unfilled by implants, camouflaging rippling under thin skin
flaps, or smoothing transition of the reconstructive border with flaps or
implants, fat is also an ideal adjunct to enhancing the contralateral breast,
improving volume and size, as well as creating upper pole fullness, with
autologous tissue properties that avoid the need for foreign material. Fat
transfer optimization is an active area of study that will continue to evolve to
allow greater success with larger volumes of fat and improvement of survival
with reduction of absorption.
CONTRAINDICATIONS
Contraindications to symmetry procedures hinge on the cancer status,
personal preference, and medical comorbidities of women undergoing breast
cancer treatment. Women might not opt for contralateral surgery due to
aversion to noncritical surgical procedures, relying on special bras and
prosthetic inserts to achieve a more symmetrical appearance in clothing.
Women with aggressive breast cancer requiring adjuvant therapies and
particularly poor prognosis should delay contralateral surgery, but these
issues, which previously were total contraindications, have become relative
contraindications. Women with medical issues such as severe
cardiopulmonary diseases are not candidates for elective symmetry surgical
procedures. High BMI, dependence on blood thinners, and tobacco use
present relative contraindications to any surgical procedure. Scarring and
prior surgery on the contralateral breast may limit options regarding
techniques used for symmetry.
PREOPERATIVE PLANNING
Reconstructive planning accounting for the goal of symmetrical breasts may
take place at the time of initial consultation, even if staging is necessary.
Plans must be made in conjunction with the breast oncologic surgeon.
Decisions impacting reconstructive planning depend on whether the nipple
areolar complex (NAC) may be spared; if lumpectomy or mastectomy is
mandated; if oncoplastic approach is possible; if there are plans for adjuvant
chemo- or radiation therapy, either before or after mastectomy; and the
prognosis of the patient. Reconstructive planning for contralateral surgery
depends on patient acceptance of contralateral surgery versus attempting to
create the best match to the native breast, most possible with autologous
reconstruction. Surgical plans for the contralateral breast may evolve after
mastectomy and reconstruction, depending on the degree of asymmetry and
patient acceptance of this. There is no specific time surgery must be done on
the opposite breast: contralateral breast surgery may be performed
immediately at the time of mastectomy; delayed 4 to 6 months after
mastectomy and reconstruction; or beyond that if the patient needs more time
to recover from adjuvant treatments or does not feel ready for contralateral
surgery.
Reconstructing the contralateral breast in a later stage is beneficial for
optimizing aesthetic outcome and symmetry. Delaying contralateral surgery
to a second stage allows for healing and settling of the reconstructed breast;
and dealing with any wound-healing complications or scarring fibrosis after
mastectomy and reconstruction. The patient also may be stronger for second-
stage surgery over performing single-stage surgery. If there is a need for
additional contralateral volume, women may be sized with implants or with
three-dimensional imaging to best plan for a matching implant.
Measurements are also more reliable in considering delayed contralateral
breast reduction or lift, depending on how the reconstructed breast settles
after mastectomy/reconstruction. Radiation therapy may be required in
treatment, and allowing for contraction of breast dimensions will afford better
contralateral symmetry as well.
If the patient is undergoing oncoplastic surgery with contralateral reduction
performed in a single stage, then planning should allow for preservation of a
larger skin envelope on the cancer side due to predictable contraction of the
skin envelope with radiation therapy. The patient should be informed that
with radiation, achieving symmetry is more challenging and often not
possible, with the goal of reaching the best possible match.
OPERATIVE TECHNIQUE
Timing is important when considering surgery to match a reconstructed
breast. While the contralateral breast may be reconstructed immediately at the
time of contralateral mastectomy/reconstruction, the match is best assured
with a second-stage procedure. This allows for the reconstructed breast to
settle. This also allows for the possibility of any wound healing or tissue
perfusion issues on the reconstructed side that might result in a smaller or
more compact breast. If radiation therapy is determined to be necessary on
the cancer side, then even more time might be considered to time the second
stage. The earliest time to perform second-stage symmetry surgery would fall
at 4 months, and after that, any amount of time would be fine: the longer the
time, the better the match. After radiation therapy, more time might be
necessary for the reconstructed side to settle. Skin pigmentation resolution
may serve as a guide. At least 4 months should be allowed, but 6 months may
be more optimal.
Implant Reconstruction
An implant is chosen importantly considering chest width measurement.
Implants of various profiles in that width range may be placed in a bra and
the best match is chosen. Three-dimensional imaging can alternatively be
used to choose a symmetrical implant.
Augmentation of the contralateral breast is performed utilizing an
inframammary incision. Incision placement is marked to best match the
opposite breast, matching the distance from the nipple to the inframammary
crease on the opposite side. Placing the implant under the pectoralis muscle
decreases the risk of capsular contracture and reduces the risk of ptosis from
the weight of the implant behind the breast tissue. Intraoperatively, implant
sizers aid in most accurately simulating the outcome with any given implant.
The patient should be sat up on the OR table to assess symmetry of the
implant volume and the pocket, considering the IMF position. The implant
pocket is closed, first approximating the fold to the chest wall with
absorbable or permanent suture, to reduce risk of inferior implant
malposition. The pocket is then closed with absorbable braided suture and the
incision is closed.
Breast Lift/Breast Reduction
Measurements comprise the most critical aspect of this procedure. Wise
pattern allows for symmetrically accurate dimensions. The pedicle may be
inferior, superior, or central, depending on breast size and degree of ptosis. In
smaller breasts, superior and central mounds techniques are easier, while in
larger breasts, an inferior pedicle tends to be easier. Measuring against a
reconstructed nipple–sparing mastectomy mandates that the nipple-to-sternal
notch and nipple-to-fold distances match. On the Wise pattern, the angle
between the limbs that become the nipple-to-IMF distance should allow for a
width to match the reconstructed side. Distance from the nipples to midline
should also match. Measuring the Wise pattern is a little more challenging
when matching a reconstructed breast without a nipple in patients who may
later undergo tattoo or no nipple reconstruction. In order to design the
contralateral breast pattern, virtual nipple location should be marked on the
cancer side. Typically this will be 21 cm +/− 2 cm from the clavicle,
approximately 7 cm from the sternal notch. Ideal nipple position on the
cancer side may be used to guide an actual nipple reconstruction at that time
with any variety of nipple flap/grafting techniques.
Intraoperatively the patient should be sat up on the OR table to compare
sides and make adjustments utilizing tailor-tacking techniques.
Fat Transfer
There is a range of techniques used to harvest and process fat for breast
reconstruction, and there is little data to support the most optimal technique.
Liposuction techniques that are less traumatic protect adipocytes, and
isolating and transferring isolated adipocytes without tumescent solution,
interstitial fluids, or oil will allow for the least absorption and lower the risk
for development of fat cysts and inflammation. Nonaugmented technology
suction-assisted lipectomy (SAL) with a cannula of at least 4 mm applies the
least trauma to adipocytes, as does lower pressure suction. The most optimal
fat donor sites include areas easily visible and accessible during breast
surgery, such as the abdomen, waist, and inner thighs. Studies have not
demonstrated which donor sites are more optimal for fat survival. Fat should
be separated from the additional fluids and traumatized cells in the
lipoaspirate, through cleaning with saline or lactated ringers to remove blood
and oils, and gravitational separation. Commercial systems may include
vibration or hand-powered rotation to optimize separation of the layers. Fat
may then be drawn up into 60-cc syringes and passed through a cannula at
least 3 mm in diameter with a large opening, passing the fat slowly in a
layered fashion. Fat is best placed in the subcutaneous space, but with breast
reconstruction or shaping the contralateral breast, fat may also be layered into
pectoralis muscle or breast tissue. Typically absorption will result in a loss of
20% to 30% of the volume transferred, so overgrafting beyond symmetry is
recommended.
INTRAOPERATIVE CARE
Measures are taken during surgery to reduce the risk of complications. At the
start sequential compression devices are turned on to reduce risk of venous
thromboembolism (VTE) and antibiotic is infused intravenously prior to
incision to cover gram-positive bacteria. Antibiotic-containing fluids should
be used for irrigation of the breast and implants. The patient should be
warmed to reduce the risk of infection and VTE as well. Careful padding is
applied to all pressure surfaces. The arms may be positioned against the body
or perpendicular to the body, depending on surgeon preference, and the arms
need to be secured to avoid motion and potential stretch and associated
neuropathies. A belt should be placed around the patient to prevent mobility
as well, particularly when sitting the patient up on the OR table to assess
symmetry. Pain should be addressed proactively, using intraoperative
numbing medication on the chest wall and in the incisions, and pain
management may be further optimized with premedication prior to surgery
with nonnarcotic pain relievers and muscle relaxers.
POSTOPERATIVE CARE
Delayed symmetry procedures are typically performed as an outpatient, with
follow-up arranged within a week of surgery. Dressings applied may remain
in place until follow-up, or bathing instructions should be provided if bathing
is allowed. Pain management is focused on nonnarcotic medications
including nonsteroidal anti-inflammatories, acetaminophen, and muscle-
relaxant medications. Narcotics are used as needed. A soft bra is
recommended for the first month or two to avoid pressure against incisions,
and compression garments and foam padding may be recommended for
liposuction donor sites. Upper body physical exertion is limited for a month
after surgery.
Over the long term, scar management becomes the focus, and the surgeon
needs to work with the patient on scar optimization techniques that may
include massage and topical agents, such as those that include silicone.

CASES

CASE 1

Delayed latissimus/implant breast reconstruction with nipple


reconstruction and contralateral breast lift. This 64-year-old woman
originally presented with a right total mastectomy defect that was
radiated and not reconstructed (Fig. 37-1A–D). Latissimus myocutaneous
pedicled flap was used to reconstruct her right chest defect, in
conjunction with a tissue expander. Contralateral breast lift with a Wise
pattern and inferior pedicle was performed concurrently with the
latissimus flap procedure. Postoperatively the expander was filled. The
patient was taken back to surgery 7 months later to exchange her
expander to a 470-cc smooth round gel implant, add 180 cc of fat from
her abdomen to enhance the reconstructed breast border, and reconstruct
her NAC with a skate flap and full-thickness skin graft from the lower
abdomen for areolar reconstruction. Contralateral fat transfer of 240 cc
was performed at that time to symmetrically augment the left breast. She
is photographed 1 year after her second procedure (Fig. 37-1E–H).
FIGURE 37-1 A–D: Preoperative photos of woman who underwent delayed
latissimus/tissue expander breast reconstruction and immediate contralateral
Wise pattern breast lift, with second-stage exchange of tissue expander for gel
implant and nipple reconstruction and bilateral fat transfer. E–H:
Postoperative photos were taken 1 year after the second stage of her
reconstruction.

CASE 2

Immediate prepectoral-shaped gel implant of nipple-sparing


mastectomy (NSM) with delayed contralateral smooth round gel
implant reconstruction. This 55-year-old woman had left breast cancer
requiring NSM (Fig. 37-2A–C). She desired a fuller breast reconstruction
and was initially reconstructed immediately with a 395-cc mentor-shaped
textured implant in the prepectoral position. Postoperatively she was
sized with implants in a bra to determine an optimal implant to use for
her right breast for symmetry. Five months later a 320-cc smooth round
gel implant was placed subpectorally in her right breast and 115 cc of fat
was transferred to the left breast to smooth the borders of her
reconstruction and reduce visible rippling. She is photographed 10
months after her second procedure (Fig. 37-2D–F).

FIGURE 37-2 A–C: Preoperative photos of woman who underwent NSM


with immediate prepectoral round gel implant reconstruction, with second-
stage contralateral breast augmentation with shaped textured gel implant 5
months later. D–F: Postoperative photos were taken 10 months after the
second-stage symmetry procedure of her reconstruction.

CASE 3

Revision reconstruction with fat transfer of reconstructed radiated


breast and contralateral mastopexy/revision of implant and scaffold
to reinforce IMF. This 41-year-old woman had history of right breast
cancer initially treated with NSM and prepectoral expander. She
underwent exchange from expander to shaped implant with fat transfer,
and contralateral augmentation mastopexy. She then underwent radiation
therapy. She presented with complaints of contracture and implant
malposition of her right breast, and unhappiness with her left breast
which she thought was too large (Fig. 37-3A–C). She underwent
exchange of both of her implants to smooth round gels, 560 cc on the
right and 360 cc on the left, with revision mastopexy on the left and
acellular dermal matrix sling to support her IMF. She was photographed
1 year after her revision surgery (Fig. 37-3D–F).

FIGURE 37-3 A–C: Preoperative photos of woman who presented


dissatisfied after her initial reconstruction with contracture and implant
malposition of her reconstructed radiated right breast and a contralateral
breast that was too large and ptotic. D–F: Postoperative photos were taken 15
months after her reconstruction.
OUTCOMES
The literature has evolved from addressing questions of the safety of
performing surgery on the contralateral breast in a breast cancer patient, to
methods of achieving symmetry to a unilateral breast reconstruction,
diverting to investigation of the safety of CPM to achieve the most optimal
symmetrical reconstruction, to actual data describing outcomes with
unilateral reconstruction and contralateral symmetry techniques over time.
Breast cancer risk is elevated in women with a history of breast cancer.
The 10-year cumulative risk of developing a contralateral breast cancer in
women initially diagnosed with unilateral disease is 6% to 7%, and that the
20-year incidence is 9% (6). Breast cancer risk is statistically significantly
elevated in women with the BRCA gene and in women who have undergone
Mantle radiation therapy. Risk is relatively elevated with genetic mutation in
the CHEK2/PTEN/p53/PALB2/CDH1 gene (8). CPM is offered to women
with clearly elevated risk of cancer in the contralateral breast, but softer
indications more often lead to CPM, such as patient fear of recurrence and
decreased need for long-term surveillance, as well as the clear aesthetic
advantage, as a desire for symmetry is commonly reported as a motivation for
undergoing CPM. Since 1998, CPM has increased from approximately 5% to
20% among all women undergoing mastectomy for unilateral breast cancer.
A study by Alba et al. investigated pathology of the contralateral breast and
safety of performing bilateral mastectomy and reconstruction. From 2013 to
2018, of 244 patients, 176 (72.1%) underwent CPM. Surgical pathologic
results of the prophylactic breast revealed occult ductal carcinoma in situ or
invasive cancer in 13 patients (7.3%) and lobular carcinoma in situ in 8
patients (4.6%). Incidence of complications was similar between groups
(unilateral mastectomy, 19.12% (n = 13); CPM, 13.07% (n = 23); p = 0.234)
(4). Crosby et al. reviewed the MD Anderson patient population to address
safety of CPM, and found that the risk of complication in the prophylactic
breast is almost the same as complications emanating from the cancer side.
They studied 497 consecutive patients undergoing immediate
postmastectomy bilateral reconstruction for an index breast cancer combined
with a CPM between 2005 and 2010. Of the 154 patients who developed
complications, 42 (27.3%) developed a complication in the prophylactic
breast (5). With a lack of data supporting the cancer benefit in CPM
combined with the risk of performing CPM, the majority of breast centers
discourage performance of CPM, unless motivated by the benefit of
symmetry.
With regard to answering the question of safety of combining
reconstruction with simultaneous contralateral symmetry procedure including
mastopexy, breast reduction, and implant placement, Cooney et al. utilized
the 2005 to 2012 American College of Surgeons National Surgical Quality
Improvement Program databases and found that preoperative comorbidities
and other patient-related factors may have a larger influence on postoperative
morbidity than the addition of a contralateral matching procedure alone (15).
Nava et al. noted that surveillance screening is not impaired by performing
contralateral breast surgery, despite the findings of parenchymal distortions,
skin thickening, and stromal edema (11).
Authors have reported their experience with contralateral symmetry
procedures, describing their approaches. The interesting aspect of these
studies is their timeline, as different approaches to breast reconstruction were
more in vogue in different decades, from pedicled to free flaps, from staged
implant reconstruction and nipple sacrifice to NSM, and from flaps to
implants. Losken et al. first reviewed the incidence of contralateral
procedures from 1975 to 1999 at Emory that included 1,394 women who
underwent unilateral mastectomy and reconstruction. A contralateral
procedure was performed in 67% of delayed reconstructions and in 22% of
immediate reconstructions. Implant-based reconstruction resulted in a higher
incidence of contralateral operations (89% delayed and 57% immediate)
compared with pedicled TRAM flap reconstruction (59% delayed and 18%
immediate). Breast reduction was the most common contralateral symmetry
procedure to match autologous reconstruction (57%) and contralateral
implant was most commonly performed after implant reconstruction (41%)
(9). In 2005, Nahabedian studied 382 women who underwent unilateral
breast reconstruction from 1998 to 2002 (7). The results of his study
demonstrated that ipsilateral revision procedures are more common than
contralateral procedures to obtain symmetry by a factor of four, which
Nahabedian believed was due to the fact that with the more current technique
of free tissue transfer, larger volumes of skin and fat could be transplanted to
achieve initial volume symmetry. In a later paper, Nahabedian reported that
breast reduction was the most common operation performed to match an
autologous reconstruction (57%) and implant placement was the most
common operation after implant-based reconstruction (41%), looking at data
from 1997 to 2007. Of the 665 women who had a unilateral mastectomy, the
type of reconstruction included autologous tissues in 457 women (68.7%) and
implants in 208 women (31.3%). Contralateral procedures occurred with
greater frequency after delayed reconstruction (24.3%) and were followed by
autologous (16.8%), prosthetic (16.3%), and immediate reconstruction
(12.6%). The most common contralateral procedures included breast
reduction (8.6%) followed by mastopexy (5.6%), and implant augmentation
(2.3%) (6).
More contemporary literature has shifted in reporting techniques used to
achieve symmetry to objective outcomes from the actual symmetry
procedure, understanding that contralateral procedures are often pursued with
an expectation to achieve the highest possible aesthetic level after
mastectomy. Razdan et al. at Memorial Sloan Kettering used the BREAST-Q,
a validated Breast Reconstruction (BR)–specific instrument used to
investigate long-term patient-reported outcomes (PROs) such as patient-
reported satisfaction and health-related quality of life (HRQoL). Considering
that the majority of breast reconstructions are implant based, they studied 553
patients who underwent implant reconstruction from 2011 to 2015. Of this
group, 67 (12%) underwent contralateral augmentation, 68 (12%) mastopexy,
93 (17%) reduction, and 325 (59%) were controls. Mean follow-up time was
52 months. Satisfaction and outcome scores were higher in the augmentation
group relative to the control group (p = 0.01). On multivariable analysis,
augmentation remained an independent predictor of satisfaction (p = 0.04).
Physical well-being scores were lower for contralateral mastopexy and
reduction compared with the controls. Contralateral breast reduction and
mastopexy demonstrated equivalent satisfaction compared with controls, but
were associated with lower physical well-being. These findings suggested
that the best symmetry technique for breast reconstruction with an implant is
an implant, replacing like with like, and that outcomes of current mastopexy
and reduction techniques may be impaired by aging effects that are
particularly magnified when the reconstructed breast is comprised of a static
and stable implant (13). Barone argued that the aesthetic outcome of breast
reconstruction, specifically determined by symmetry, is more important in
determining patient satisfaction and well-being after postmastectomy
reconstruction than the patient’s overall extirpative and reconstructive
experience. From 1997 to 2017, 582 patients comprising three cohorts were
compared: 235 patients underwent contralateral management with an implant,
178 with breast reduction, and 169 with mastopexy without implants.
BREAST-Q BR- postoperative module was administered to evaluate breast
perception and patient satisfaction, and surgeon-rated aesthetic outcomes
were measured using the Kroll Scale, an itemized aesthetic tool. This study
demonstrated greater satisfaction with contralateral implant for symmetry as
measured with Breast Q, relative to reduction and mastopexy. From the
analysis of the Kroll Scale, the group of implant-based contralateral
management received the highest score for symmetry (p = 0.001), shape (p =
0.001), and aesthetic result overall (p = 0.001). This study was limited by not
reporting what kind of reconstruction had been performed on the cancer side
(12).
CONCLUSION
A great deal of evolution has occurred over methods of reconstruction after
mastectomy, as well as mastectomy techniques, over the past four decades.
One of the greatest challenges is creating a symmetrical, aesthetically
pleasing result after unilateral breast reconstruction, particularly if the
reconstruction is radiated. Techniques to achieve symmetry in the
contralateral breast include implant placement, breast lift with possible
implant placement, breast reduction, and fat transfer. Techniques are offered
to achieve symmetry, and the literature has borne out that breast cancer
patients are increasingly undergoing contralateral procedures to successfully
achieve better outcomes aesthetically and emotionally.

REFERENCES

1. https://www.plasticsurgery.org/documents/News/Statistics/2018/plastic-
surgery-statistics-full-report-2018.pdf. Accessed July 17, 2019.
2. Hidalgo DA. Aesthetic refinement in breast reconstruction: complete
skin-sparing mastectomy with autogenous tissue transfer. Plast Reconstr
Surg 1998;102(1):63–70; discussion 71–72.
3. Colwell AS, Christensen JM. Nipple-sparing mastectomy and direct-to-
implant breast reconstruction. Plast Reconstr Surg 2017;140(5S
Advances in Breast Reconstruction):44S–50S.
4. Alba B, Schultz BD, Cohen D, et al. Risk-to-benefit relationship of
contralateral prophylactic mastectomy: the argument for bilateral
mastectomies with immediate reconstruction. Plast Reconstr Surg
2019;144(1):1–9.
5. Crosby MA, Garvey PB, Selber JC, et al. Reconstructive outcomes in
patients undergoing contralateral prophylactic mastectomy. Plast
Reconstr Surg 2011;128(5):1025–1033.
6. Nahabedian M. Managing the opposite breast: contralateral symmetry
procedures. Cancer J 2008;14(4):258–263.
7. Nahabedian MY. Symmetrical breast reconstruction: analysis of
secondary procedures after reconstruction with implants and autologous
tissue. Plast Reconstr Surg 2005;115(1):257–260.
8. Wright FC, Look Hong NJ, Quan ML, et al. Indications for contralateral
prophylactic mastectomy: a consensus statement using modified Delphi
methodology. Ann Surg 2018;267(2):271–279.
9. Losken A, Carlson GW, Bostwick J 3rd, et al. Trends in unilateral breast
reconstruction and management of the contralateral breast: the Emory
experience. Plast Reconstr Surg 2002;110(1):89–97.
10. Albornoz CR, Bach PB, Mehrara BJ, et al. A paradigm shift in U.S.
breast reconstruction: increasing implant rates. Plast Reconstr Surg
2013;131(1):15–23.
11. Nava MB, Rocco N, Catanuto G, et al. Impact of contra-lateral breast
reshaping on mammographic surveillance in women undergoing breast
reconstruction following mastectomy for breast cancer. Breast
2015;24(4):434–439.
12. Barone M, Cogliandro A, Signoretti M, et al. Analysis of symmetry
stability following implant-based breast reconstruction and contralateral
management in 582 patients with long-term outcomes. Aesthetic Plast
Surg 2018;42(4):936–940.
13. Razdan SN, Panchal H, Albornoz CR, et al. Impact of contralateral
symmetry procedures on long-term patient-reported outcomes following
unilateral prosthetic breast reconstruction. J Reconstr Microsurg
2019;35(2):124–128.
14. Magnusson M, Beath K, Cooter R, et al. The epidemiology of breast
implant-associated anaplastic large cell lymphoma in Australia and New
Zealand confirms the highest risk for grade 4 surface breast implants.
Plast Reconstr Surg 2019;143(5):1285–1292.
15. Cooney CM, Sebai ME, Ogbuagu O, et al. Matching procedures at the
time of immediate breast reconstruction: an American College of
Surgeons national surgical quality improvement program study of
24,191 patients. Plast Reconstr Surg 2016;138(6):959e–968e.
CHAPTER 38

Breast Reduction and Mastopexy After


Massive Weight Loss
FRANCESCO M. EGRO | J. PETER RUBIN
HISTORY
The prevalence of morbid obesity continues to grow at an alarming rate. To
reduce the rate of obesity-related complications, many people seek to lose
weight through diet, exercise, or bariatric surgery. Massive weight loss
(MWL) is defined as weight loss greater than 50 lb, and breasts are
significantly affected by these changes. The loss of parenchymal volume
combined to skin redundancy and loss of elasticity, leads to a flattened,
deflated, and ptotic breast appearance. Furthermore, the skin redundancy
produces a roll of skin and fat on the lateral border of the breast that extends
onto the chest wall. This lateral roll blurs the lateral curve of the breast and
often forms one continuous roll of soft tissue, greatly affecting the aesthetics
of the breast (1). Correction of breast deformities remains a high priority for
women who have undergone MWL, and this book chapter explores the
anatomic changes observed in the breast after MWL and provides an
overview of the preoperative evaluation, operative technique, and
postoperative care to achieve an aesthetically pleasing result.
INDICATIONS
Given the wide variety of breast deformities seen in MWL patients, each
consultation must be individualized to determine the most appropriate plan to
pursue. Many breast contouring techniques following MWL have been
described (2–9) and several factors will determine which procedure is most
appropriate: (a) severity of the breast deformities, (b) desired breast size, and
(c) the surgeon’s experience.
Inadequate Breast Volume
Patients who have undergone significant breast involution or who do not have
sufficient lateral skin and fat rolls for selective breast autoaugmentation will
require breast implants if they desire larger breasts. Most of the patients that
fall into this category are young women with good skin tone. These patients
can be considered for an isolated breast augmentation if there is inadequate
breast volume in combination with minimal ptosis and skin redundancy. Our
preferred approach to breast augmentation is with an inframammary fold
(IMF) incision. Patients who fall into this category represent less than 2% of
MWL patients who require breast contouring. Description of this technique
can be found in another section of this text dealing with augmentation
mammaplasty.
Patients with inadequate volume associated with grade 2 or 3 ptosis,
significant skin redundancy, an enlarged nipple areolar complex (NAC),
and/or an inadequate lateral skin fold on physical examination will require a
mastopexy in addition to augmentation mammaplasty. In select patients we
perform an augmentation-mastopexy through a vertical incision extending
beneath the NAC. After submuscular placement of the implant, we tailor tack
the skin envelope to correct nipple position and control the redundant skin
envelope. It is not uncommon to extend the incision along the IMF to control
the skin redundancy. The patient must be made aware of this potential scar
burden preoperatively. In complicated cases in which there is significant
asymmetry or a loose IMF, we prefer to perform a staged augmentation-
mastopexy to optimize the aesthetic outcome and minimize the risks for
complication. In some cases, the patients have been satisfied with their breast
size following the mastopexy, obviating the need for later augmentation.
Excessive Breast Volume
Approximately 20% of patients presenting for breast surgery have excessive
breast volume necessitating a breast reduction. Our preferred technique is a
Wise-pattern reduction mammaplasty using either a medial or inferior
pedicle. The decision as to which pedicle is used will depend in part on the
nipple-to-fold distance and on the experience of the surgeon. These
techniques are described also in another section dealing with reduction
mammaplasty and mastopexy. Although the procedure is performed in a
similar manner as for non-MWL patients, there are special preoperative
considerations and modification to the markings that may need to be
addressed. Some patients have significant medialization of the NAC. In these
patients, it may be difficult to adequately rotate the pedicle to its new position
on the breast meridian. If we believe that this might be an issue, then we
choose an inferior pedicle. Since these patients may also have a considerable
lateral skin fold, the posterior extension and width of the lateral excision can
be significantly larger than for non-MWL patients. It is important to come out
of the breast crease laterally when performing the markings to prevent a
“boxy” appearance to the breast. The width of the lateral excision can be
estimated with a pinch test. Liposuction of the lateral skin fold may be useful
to further contour the lateral fold of the breast. This is best performed after
the skin resection has been performed and the skin has been temporarily
closed with staples.
Short-scar techniques in the MWL may result in a large inferior dog-ear
due to the excessive skin redundancy and poor skin tone. This dog ear will
require a horizontal excision to remove the redundancy. A pitfall of the short-
scar technique would be to chase the dog ear inferiorly, which would leave an
unsightly scar below the IMF. In addition, short-scar techniques will have
minimal impact on the lateral skin and fat roll that is present in the majority
of MWL patients.
Adequate Breast Volume
Although many of the women presenting after MWL feel that they need a
breast reduction, the majority of these woman have adequate volume to give
them the size and shape they desire. Careful examination of the breast
parenchyma will determine whether there is sufficient parenchymal volume.
The lateral skin and fat roll is also evaluated to assess how much tissue can
be recruited into the breast for selective autoaugmentation. In patients who
have adequate parenchymal volume, severe ptosis, and a significant lateral
skin and fat roll, our preferred technique is dermal suspension with total
parenchymal reshaping and selective autologous augmentation from the
lateral chest wall (2–4). This technique provides reliable results with the
ability to intraoperatively individualize the size and shape of the breast. Since
the parenchymal reshaping and the amount of tissue recruited for autologous
augmentation can be customized for each breast, this technique allows for the
correction of difficult breast asymmetries often encountered in these patients.
CONTRAINDICATIONS
In our practice, the only absolute contraindication for dermal suspension
mastopexy and parenchymal reshaping with selective autoaugmentation
includes active smoking because of potential of blood supply compromise to
the flaps. Relative contraindications include BMI over 35, diffuse fibrocystic
disease, prior breast scars, active intertrigo, and inadequate parenchymal or
lateral roll volume to mobilize and build a breast mound.
PREOPERATIVE PLANNING
A thorough history and physical examination is performed (10). The surgeon
should ask about weight loss, nutritional status, bariatric surgery, personal or
family history of venous thromboembolic event or breast cancer, and
smoking status. The patient should have maintained a stable weight,
preferably with a BMI under 30, for at least 3 months (no more than a 5-lb
change per month). Surgeons should assess for breast masses, scars, skin
quality, parenchymal volume, NAC position, and the presence/size of lateral
roll of skin and fat. All patients should undergo mammography in accordance
with the American Cancer Society guidelines (11). Patients should stop
medications that promote bleeding. Current smokers should be instructed to
avoid smoking at least 1 month prior to surgery and should undergo a
cotinine urine test before surgery. Informed consent should be obtained, and
postoperative care should be discussed. Throughout the consultation, the
patient’s goals should be gauged to ensure the expectations are realistic and
can be met.
OPERATIVE TECHNIQUE
INTRAOPERATIVE CARE

Markings
The procedure is based on an extended Wise pattern with preservation of
both a central and an inferior pedicle (Fig. 38-1). A new breast meridian in
marked in the center of the breast mound that ignores the medial position of
the nipple. The new nipple position is transposed from the level of the IMF
along the breast meridian. The top of the NAC is marked 2 cm above the new
nipple position. A keyhole pattern with 5-cm vertical limbs is drawn. The
lateral portion of the Wise pattern extends posteriorly to encompass the
lateral skin and fat roll. The robust blood supply through the lateral thoracic
perforators allows for sufficient tissue to be rotated into the breast for
autologous augmentation. This lateral extension can be used in its entirety or
can be trimmed, depending on the desired size and degree of asymmetry.
Technique
The areola is marked using a 42-mm cookie cutter. The skin within the entire
Wise pattern is then deepithelialized. The dermis is completely incised except
for a pedicle base width of approximately 10 cm inferiorly along the IMF.
The lateral and medial extent of this pedicle will correspond to the
approximated pivot points for the medial and lateral parenchymal flaps. The
entire breast is then degloved by raising skin flaps with a thickness of 1 to 1.5
cm. This dissection is carried down to the pectoralis fascia and then extends
in a cephalad direction to the level of the inferior border of the clavicle. The
nipple will survive on a healthy central pedicle. Preservation of the
attachments to the sternum is essential during medial dissection or symmastia
may result. The medial and lateral flaps are then elevated down to the level of
the chest wall fascia taking care to preserve any perforating vessels at the flap
base (Fig. 38-2). Dissection should be limited to the minimal amount
necessary to rotate the flaps to obtain the desired shape. The extent of the
lateral flap will vary depending on the amount of volume needed to obtain the
desired size, as well as on the degree of asymmetry that needs to be corrected.
When dealing with large lateral extended flaps, the flap margins should be
checked for healthy bleeding prior to rotation. Once the breast has been
degloved, the next step is to suspend the breast parenchyma to the chest wall.
The central dermal extension is suspended to the periosteum of either the 2nd
or 3rd rib along the new breast meridian. To safely perform this maneuver,
the fingers of the nondominant hand are used to palpate the rib and guide the
needle pass. The level of suspension will depend on which rib allows the
nipple to lie in the intended final position. Braided 1-0 nylon is used (Fig. 38-
3). The lateral breast flap is then rotated and fixated most often to the 3rd rib
periosteum. The level of fixation should be where the suspension provides
good lateral curvature to the breast parenchyma. The size of the lateral flap
can be adjusted prior to this maneuver to obtain the desired volume of
autologous augmentation. The medial flap is then rotated superiorly, most
commonly to the fourth rib, and fixated to the periosteum in a similar manner
(Fig. 38-4). During suspension of the parenchymal flaps, it is helpful to
continuously redrape the skin flaps to assess the shape and volume of the
breast. If the suspension does not provide the desired nipple position or breast
shape, it should be removed and repeated. Following the dermal suspension,
the parenchyma is plicated into its final shape. The dermis of the lateral flap
is plicated to the central pedicle dermis using 2-0 absorbable polyglactin
sutures. This is performed with the medial flap in similar fashion (Fig. 38-5).
If suturing the dermis of the medial and central flaps distorts the medial
breast contour, we simply approximate the deep breast parenchyma of these
two flaps. The final plication is performed inferiorly. The desired distance
from the IMF to the NAC is 5 cm. Plication is performed inferiorly to achieve
this distance, which also helps to increase nipple projection. The sequence of
dermal suspension and parenchymal reshaping is best performed
simultaneously on both breasts while the patient is in the sitting position. As
the patterns of suspension and plication cannot be predicted preoperatively, it
is easier to achieve symmetry if each step is performed synchronously. In
addition to the three main rows of dermal plication, additional individual
sutures or rows can be added to contour the final parenchymal shape.
Constant redraping of the skin flaps will assist in any minor adjustments. To
further improve nipple projection and add definition to the lateral sweep of
the breast, the lateral dermal edge from the lateral parenchymal flap is
sutured to the chest wall fascia (Fig. 38-6). This will also prevent lateral
herniation of the parenchyma. The lateral flap is not sutured to the periosteum
in this position to minimize the risk of injury to the long thoracic nerve and
the thoracodorsal nerve and pedicle. Prior to closure, the skin flaps are
redraped for a final time to ensure that the desired breast shape has been
achieved and to assess final symmetry. Closure begins with a 0-
polypropylene half-buried stitch tied over a Xeroform bolster to secure the
medial and lateral skin flaps to the IMF. A single drain is placed laterally that
wraps around the pedicle. The vertical and horizontal skin incisions are
closed with a combination of absorbable buried interrupted and running
sutures in the dermis. It may be necessary to release the dermis around the
NAC to bring it into its final desired position (Fig. 38-7). It is safe to release
the dermis over one-half of the circumference of the NAC, given the robust
central pedicle blood supply. If the dermis is not released in these cases, the
nipple may have a retracted appearance postoperatively. The NAC is secured
to the skin flaps with absorbable buried dermal sutures. Cyanoacrylate glue is
used along all incisions. For preoperative and postoperative photographs, see
Figures 38-8 to 38-10.

FIGURE 38-1 A: A diagrammatic representation of the extended Wise pattern. The


new breast meridian is drawn to correct the medialized nipple position. The total
area within the Wise pattern will be deepithelialized. B: The lateral extension will be
designed to encompass the lateral skin fold. The amount of lateral skin
deepithelialized will depend on the autologous volume needed to achieve the desired
breast size. Any remaining portion of the lateral roll is discarded.
FIGURE 38-2 The breast parenchyma is degloved to the level of the clavicle by
raising 1-cm-thick flaps. Medial and lateral parenchymal flaps are elevated off the
chest wall.
FIGURE 38-3 The central dermal extension is fixated to the 2nd or 3rd rib in the
plane of the new breast meridian using braided nylon sutures. The rib utilized is
determined by which position suspends the nipple to the desired final position.
FIGURE 38-4 The lateral breast flap is then medially rotated to recreate the lateral
curvature of the breast. The size of this flap is determined by the amount of tissue
required for autologous augmentation. This flap is often sutured adjacent to the first
fixation point. The dermis of the medial flap is then fixated to the chest wall, most
commonly to the fourth rib periosteum. The dermis of the medial and lateral flaps is
sutured to the central dermal extension using a running suture.
FIGURE 38-5 The dermis of the inferior pole is then plicated to shorten the nipple to
inframammary fold distance. Additional plication sutures can be placed to optimize
the breast shape.
FIGURE 38-6 The lateral aspect of lateral breast flap is sutured to the chest wall to
prevent the breast parenchyma from “herniating” laterally. This maneuver will also
increase nipple projection.
FIGURE 38-7 The skin flaps are redraped and reapproximated. The dermis around
the nipple can be scored around half of its circumference to prevent a tethered
appearance of the nipple.
POSTOPERATIVE CARE
Gauze fluffs are placed over all incision lines, and the chest is wrapped with
an elastic bandage. The dressing is taken down on postoperative day 4 or 5,
and the patient is placed in a sports bra for 4 to 6 weeks. The bolster suture is
removed at 1 week, and the drains are removed once the daily output is less
than 30 cc. The patients are instructed not to lift anything heavier than 10 lb
for the 3 weeks, after which they can slowly increase their activity.
Underwire bras are to be avoided for at least 6 weeks. If mastopexy is
performed as an isolated procedure, the patient can be discharged the same
day.

CASES

CASE 1

A 57-year-old woman after a 130-lb weight loss developed severe ptosis,


parenchymal volume loss with flattening of the breast, inelastic and
redundant skin envelope, NAC medialization, and rolls of skin and fat on
the lateral border of the breast. Patient elected to undergo mastopexy with
dermal suspension and parenchymal reshaping technique with selective
autoaugmentation, as well as abdominoplasty. Preoperative and
postoperative photographs are shown in Figure 38-8.
FIGURE 38-8 A,B: A 57-year-old woman after a 130-lb weight loss. The
markings demonstrate the extended Wise pattern that encompasses the
lateral skin fold and moves the nipple to a more medial position along the
new breast meridian. C: Intraoperative view demonstrating the suspension
and breast shape control achieved with parenchymal reshaping. D–F:
Preoperative views. G–I: Postoperative views 2 years after mastopexy using
dermal suspension and total parenchymal reshaping. The patient also
underwent abdominoplasty.

CASE 2

A 40-year-old woman following a 135-lb weight loss developed severe


ptosis, parenchymal volume loss with flattening of the breast, inelastic
and redundant skin envelope, NAC medialization, and rolls of skin and
fat on the lateral border of the breast. Patient elected to undergo
mastopexy with dermal suspension and parenchymal reshaping technique
with selective autoaugmentation, as well as abdominoplasty. Preoperative
and postoperative photographs are shown in Figure 38-9.
FIGURE 38-9 A,B: A 40-year-old woman following a 135-lb weight loss. The
lateral markings demonstrate how varying amount of tissue from the lateral
skin fold can be used for volume augmentation and the remaining skin fold
tissue is discarded. C–E: Preoperative views. F–H: Postoperative views 6
months after surgery. The patient also underwent abdominoplasty.

CASE 3

A 43-year-old woman 18 months after a Roux-en-Y gastric bypass with a


weight loss of 110 lb, developed severe ptosis, parenchymal volume loss
with flattening of the breast, inelastic and redundant skin envelope, NAC
medialization, and small rolls of skin and fat on the lateral border of the
breast. Patient elected to undergo mastopexy with dermal suspension and
parenchymal reshaping technique with selective autoaugmentation, as
well as abdominoplasty. Preoperative and postoperative photographs are
shown in Figure 38-10.
FIGURE 38-10 A 43-year-old woman 18 months after a Roux-en-Y gastric
bypass with a weight loss of 110 lb. Her preoperative body mass index was 26
kg/m2. A–C: Preoperative views. D–F: Postoperative views 2 years following
mastopexy with dermal suspension and total parenchymal reshaping. This
patient had a small lateral fold allowing the lateral scar to be shorter. The
patient also had a concurrent abdominoplasty.
OUTCOMES
This procedure has proven to be very durable and safe when performed alone
or in combination with other body contouring procedures. Patient satisfaction
with the procedure has been very high. Patients can expect mild pain, edema,
and ecchymosis. Our study showed that out of 108 MWL patients requiring
breast reshaping, 91 patients (182 breasts) underwent a dermal suspension,
parenchymal reshaping mastopexy with selective autoaugmentation, alone or
in combination with other procedures. Breast complications were very rare
and included seroma (n = 3), dehiscence (n = 3), or skin flap necrosis (n = 2).
Only 3 patients required a revision (3.3%), but none were related to the breast
reshaping procedure. Wound issues can often be treated with local wound
care. We have seen no cases of partial or total NAC necrosis, breast flap loss,
or significant fat necrosis.
CONCLUSION
Breasts are significantly affected by MWL and breast reshaping is especially
challenging in these patients because of the loss of volume, skin redundancy,
loss of elasticity, ptosis, and lateral rolls. Careful analysis will determine
which procedure is most appropriate. The most severe and challenging cases
benefit from skin resection coupled with dermal suspension, parenchymal
reshaping, autoaugmentation, and suture plication. This technique has proven
to be safe and durable, allowing to produce excellent outcomes.

REFERENCES

1. Song AY, Jean RD, Hurwitz DJ, et al. A classification of contour


deformities after bariatric weight loss: the Pittsburgh rating scale. Plast
Reconstr Surg 2005;116:1535–1544; discussion 1545–1546.
2. Rubin JP. Mastopexy in the massive weight loss patient: dermal
suspension and total parenchymal reshaping. Aesthet Surg J
2006;26:214–222.
3. Beidas OE, Rubin JP. Breast reshaping after massive weight loss. Clin
Plast Surg 2019;46(1):71–76.
4. Rubin JP, Gusenoff JA, Coon D. Dermal suspension and parenchymal
reshaping mastopexy after massive weight loss: statistical analysis with
concomitant procedures from a prospective registry. Plast Reconstr Surg
2009;123:782–789.
5. Hurwitz DJ, Agha-Mohammadi S. Postbariatric surgery breast
reshaping: the spiral flap. Ann Plast Surg 2006;56:481–486; discussion
486.
6. Graf RM, Mansur AE, Tenius FP, et al. Mastopexy after massive weight
loss: extended chest wall-based flap associated with a loop of pectoralis
muscle. Aesthet Plast Surg 2008;32(2):371–374.
7. Losken A, Holtz DJ. Versatility of the superomedial pedicle in
managing the massive weight loss breast: the rotation-advancement
technique. Plast Reconstr Surg 2007;120:1060–1068.
8. Hamdi M, Van Landuyt K, Blondeel P, et al. Autologous breast
augmentation with the lateral intercostal artery perforator flap in
massive weight loss patients. J Plast Reconstr Aesthet Surg 2009;62:65–
70.
9. Kwei S, Borud LJ, Lee BT. Mastopexy with autologous augmentation
after massive weight loss: the intercostal artery perforator (ICAP) flap.
Ann Plast Surg 2006;57:361–365.
10. Rubin JP, Nguyen V, Schentker A. Perioperative management of the
post-gastric bypass patient presenting for body contour surgery. Clin
Plast Surg 2004;31:601–610.
11. American Cancer Society. Detailed guide: breast cancer. Available
online at http://www.cancer.org/docroot/CRI/CRI_2_3x.asp?d=5.
Accessed July 12, 2009.
CHAPTER 39

Vertical Breast Reduction and


Rereduction
ELIZABETH J. HALL-FINDLAY | GUSTAVO JIMENEZ MUñOZ LEDO
HISTORY
Vertical breast reduction was initially slow to achieve widespread popularity.
Many surgeons are still concerned about the learning curve and having to
revise the pucker that can occur at the lower end of the vertical incision.
Surgeons realize, however, that patients who are preoperatively informed are
willing to accept that some time is necessary for the results to settle in most
plastic surgery procedures. This is no different in breast reduction surgery
than it is in rhinoplasty, facelift, or liposuction surgery.
Although most surgeons can accept that there is a certain revision rate
inherent in most plastic surgery procedures, for some reason they find it more
difficult to accept in breast reduction. Perhaps this is because the problems
(lateral and medial dog-ears, boxy shape, and bottoming out) with the
inverted T, inferior pedicle (1,2) procedures were so difficult to correct that
the revision rate remained low. Despite the development of the vertical
approach by Marchac (3) and also by Lassus (4), not many surgeons were
willing to try to reduce scarring when they had a method (inverted T, inferior
pedicle) that they believed to be safe and reliable.
Madeleine Lejour (5) popularized vertical breast reduction, but surgeons
found the technique difficult and the complication rate too high. The most
common comment that we get from surgeons who try the true superomedial
pedicle vertical breast reduction is that they find it so easy and predictable.
The senior author initially had problems insetting the superior pedicle, so she
tried the lateral pedicle (6). The assumption was that the lateral pedicle would
have better sensation, but it turned out that the medial pedicle actually gave
better shape and surprisingly better sensation. The problem with the lateral
pedicle is that the base of the pedicle is the same tissue that we want to use as
the lateral pillar (7), and it results in a shape that has excess lateral fullness.
We now almost exclusively use a true superomedially based pedicle (8)
where the base is carried lateral to breast meridian so that it has a dual axial
blood supply. The medial pedicle is easy to inset, is full thickness, has
reliable circulation, and has good sensation. The superomedial pedicle is a bit
more difficult to inset but it has a better blood supply.
The results are best when the inferior border of the medial pedicle becomes
the medial pillar, when the inferior and lateral breast tissue is removed, and
when the vertical incision is not cinched or gathered (9). Since the mid-
1990s, many of the problems with the vertical approach have been addressed,
and consistency of results can be achieved. Surgeons who have adopted this
approach are often surprised at how fast the learning curve can be.
Those who resist the vertical approach can still be heard saying that it
becomes a choice of scars over shape. However, once surgeons incorporate
the vertical approach for the breast reduction and mastopexy patients, they
realize that both the scars and the shape—both short and long term—are
significantly improved. The skin (which unfortunately stretches) is no longer
used as a brassiere. Instead, the parenchyma is reshaped and the skin is
allowed to redrape. By either removing the glandular ptosis (breast reduction)
or moving it (mastopexy), gravity is less likely to damage the shape over
time.
PRINCIPLES
The superomedial pedicle vertical breast reduction technique is less about
scarring than it is about concepts. Most inverted T type approaches remove a
horizontal ellipse of skin and breast tissue which when closed leave a medial
and a lateral dog-ear. Most vertical type approaches remove an inferior
vertical ellipse of skin and breast tissue and when closed leave a superior and
an inferior dog-ear. The removal of an inferior vertical wedge of breast tissue
allows the surgeon to narrow and cone the breast. It also removes the heavy
inferior breast tissue and leaves behind the superior breast tissue, thereby
resisting the negative effects of gravity.
The breast tissue is removed where it is in excess—inferior and lateral.
After the inferior vertical wedge of breast tissue is removed, the excess is
then removed from under the lateral flap.
There are numerous vertical approaches and numerous pedicle choices. We
prefer the (true) superomedial pedicle because it has a dual axial blood
supply, it rotates easily into position without kinking or compression, and it
has sensation which is equivalent to the other pedicles available. The inferior
border of the medial pedicle becomes the medial pillar so that as it rotates
into position, it leaves an elegant curve to the lower pole of the breast.
FIGURE 39-1 The Wise pattern is used to determine the shape of the parenchyma
that is left behind instead of being used to design a skin brassiere. The inferior
glandular ptosis is removed leaving the superior breast tissue attached to the
superior skin flaps. Removal of the inferior vertical wedge permits the result to resist
the effects of gravity.

An important concept to understand is that the superomedial pedicle


vertical breast reduction uses the Wise pattern (10) as a good breast
(brassiere) design for the pattern of the parenchyma which should be left
behind rather than for the skin resection pattern (Fig. 39-1A,B). Once the
inferior vertical wedge of skin and breast tissue is removed, breast tissue
under the lateral flap is removed, and the breast coned, then all breast tissue
inferior to the Wise pattern is removed both directly and with liposuction.
The skin is then allowed to redrape over the newly shaped breast mound.
The idea that surgeons need to choose between scars and shape is not true.
The superomedial pedicle vertical breast reduction not only results in reduced
scars but also maintains a good, long-lasting shape. The procedure takes less
time, the blood loss is less, and the recovery is faster. In our experience the
complications are also significantly less frequent with vertical breast
reductions than with inverted T inferior pedicle breast reductions. There are
more pucker revisions (about 5%) with the vertical approach, but they’re
easily corrected under local anesthesia.
The advantages are in the reduced scarring and the better shape but, when
surgeons realize that they do not need any tension on the skin closure, wound
healing problems and complications are dramatically reduced.
A true superomedial pedicle has a better blood supply than a medial
pedicle but it is a bit more difficult to inset (11). Both pedicles, however, can
be safely debulked of deep parenchyma because the blood supply is
superficial. Sensation in the medially based pedicles is excellent because the
innervation of the nipple is both medially and laterally based.
Nipple necrosis is the complication that surgeons fear the most. We believe
that there are four main arterial supplies to the breast and sometimes only
three of the four are dominant. We cannot make a preoperative determination
of which pedicle will be safe. We believe that nipple necrosis is inevitable in
a large-volume practice and it is more likely to be a statistical occurrence
rather than bad surgery. A true superomedial pedicle is the safest because it
has a dual axial blood supply (Fig. 39-2).
FIGURE 39-2 True superomedial pedicle has a dual axial vascular supply which is
superficial in the subcutaneous tissue. It is a safe pedicle even when an inverted T
skin resection is needed.

The other advantage is that the concept of the superomedial pedicle and the
vertical and lateral parenchymal resection can be used in much larger breast
reductions even when an inverted T skin resection pattern is needed to reduce
the redundant skin. Skin does not need to be removed as often as surgeons
think, but some patients have far too much skin or too much skin of poor
quality. The advantages of the superomedial pedicle with the inferior
resection can still be preserved even when the final closure has increased
scarring with a “T,” a “J,” or an “L.”
ANATOMY
The breast is an ectodermal-derived subcutaneous structure which is attached
loosely to the skin (and firmly at the nipple). It is only very loosely
“attached” to the chest wall. Those attachments are easily swept away during
a subglandular breast augmentation. The breast is held in place by skin fascial
fibers inferiorly (the inframammary fold [IMF]) and medially (over the
sternum).
The only artery (and venae comitantes) that travels through the breast
parenchyma to the nipple enters the breast directly from the chest wall at the
4th interspace and travels to the nipple areolar complex (Fig. 39-3). Although
there are lateral branches (which are enclosed in a loose layer which is
described as a breast septum by Wuringer (12), there are no other arteries that
course through the parenchyma to the nipple. There are, of course, vessels
that supply the breast parenchyma itself, but they do not course through the
parenchyma to the nipple. This chest wall–based artery and vein supply an
inferior (and central) pedicle.
The blood supply to the breast is therefore mainly superficial—the arteries
and veins are in the subcutaneous tissue that is pushed outward as the breast
develops. Most of the blood supply comes from the internal thoracic (internal
mammary) system via the second to sixth perforators. There is some supply
from the superficial branch of the lateral thoracic artery, but the
thoracoacromial system provides only minimal additional blood supply (and
none to the nipple areolar complex).
FIGURE 39-3 The only blood supply that travels through the breast parenchyma to
the nipple comes from the 4th intercostal branches of the internal mammary
(thoracic) system. This artery and venae comitantes (along with some lateral
branches) are enclosed in a thin cranial and caudal septum described by Elisabeth
Wuringer. The rest of the blood supply to the nipple is in the superficial
subcutaneous tissue.
FIGURE 39-4 Blood supply for superior and true superomedial pedicles. A: The
arterial supply to a superior pedicle comes from the descending artery of the internal
mammary (thoracic) system at the 2nd interspace. B: A true superomedial pedicle
has a dual axial blood supply that includes both the artery supplying a pure medial
pedicle, which comes from the 3rd interspace, along with the excellent blood supply
to a superior pedicle. When a pure medial pedicle is created, the artery from the
superior pedicle is transected—it is a strong vessel which is included in a true
superomedial pedicle.

The artery to a superior pedicle (Fig. 39-4A) comes from the 2nd (usually)
intercostal space and it descends and enters the nipple area just medial to
breast meridian and it is always about 1 cm deep to the skin—it bleeds with
significant force when it is cut during creation of a pure medial pedicle (it can
be traced with a pencil doppler preoperatively). The artery to the medial
pedicle also comes from the internal mammary system (usually from the 3rd
intercostal space) and it curves around the sternum, penetrates the pectoralis,
and is pushed outward in the subcutaneous tissue as the breast develops.
A true superomedial pedicle (Fig. 39-4B) includes both arteries from the
2nd and 3rd interspaces. It became apparent when creating a purely medial
pedicle that the strong descending artery from the 2nd interspace was being
sacrificed. Why not keep it? The true superomedial pedicle then incorporates
the blood supply to both a superior and a medial pedicle making it very safe.
The only problem is that a true superomedial pedicle (the base of which then
extends lateral to the breast meridian) is more difficult to inset. But when the
surgeon understands that there is no blood supply to the nipple coming
through the parenchyma (it is all superficial) then the surgeon can safely
debulk as much deep parenchyma as needed to facilitate an easier pedicle
inset.
The 5th and 6th intercostals from the internal mammary system also enter
the breast just above the IMF and they add extra security to an inferior
pedicle. This is typical for other zones of adherence in the body. Many of
these lower vessels are cut during creation of a central pedicle.
The only other blood supply is the superficial branch of the lateral thoracic
artery and it can be seen curling around the pectoralis muscle and entering the
lateral aspect of the breast. It supplies a lateral pedicle but it may enter the
breast at a more inferior level than the standard lateral pedicle design.
It is interesting that the veins do not accompany the arteries except for the
deep perforator—they can be seen just under the dermis and they drain
mainly superomedially. That is why we no longer infiltrate the incision lines
because the infiltrating needle can puncture the superficial veins, causing
small subcutaneous hematomas.
Although the main innervation to the nipple may come from the lateral
branch of the 4th intercostal nerve, there is no question that good innervation
comes from all quadrants of the breast (13). It appears that all the pedicles—
lateral, medial, superior, inferior, and central—have acceptable sensation.
With the medial pedicle, about 85% of patients will recover normal to near-
normal sensation, but that is reduced to about 76% with a lateral pedicle and
only 67% with a superior pedicle (7). The medial and inferior pedicles appear
to have similar recovery of sensation.
Most of the glandular breast tissue is concentrated deep to the nipple and
areolar complex and laterally in the upper outer quadrant. The medial aspect
of the breast has some glandular tissue but a higher proportion of fat.
It is important to understand the concept of the breast footprint (14). Some
patients are high breasted and some are low breasted. This is a very important
fact to point out to patients to better manage their expectations. There are
only minimal changes that a surgeon can make to the footprint. The upper
breast border of the footprint may start quite low on the chest wall and this
cannot be changed with a breast reduction. The vertical dimension of the
footprint can be quite short even in large, heavy breasts. The variation in the
vertical dimension can be from 3 to 15 cm. The IMF (the lower breast border)
can be quite different from one breast to the other in the same patient. The
horizontal dimensions of the footprint can also vary considerably with the
medial breast border determining whether a woman has a wide or narrow
breast cleavage. The lateral breast border usually extends to or just past the
anterior axillary line with most patients having an ideal horizontal breast base
diameter of 11 to 14 cm. The borders of the footprint can be expanded with
the addition of an implant or fat, and they can be reduced with the removal of
either parenchyma or an implant.
INDICATIONS AND CONTRAINDICATIONS
The best candidates for a superomedial pedicle vertical breast reduction are
young healthy patients who need a small to moderate-sized breast reduction
(usually up to 600 g or more). There is more of a learning curve for the larger
reductions but the method is still excellent; the superomedial pedicle can be
used for larger breast reductions even when an inverted T is needed to reduce
the skin envelope.
Very large reductions or reductions in massive–weight-loss patients are
often best performed with a superomedial pedicle because it allows the
surgeon to remove the heavy inferior breast tissue. Adding a T excision to the
skin is rarely needed unless the vertical incision is longer than about 13 to 15
cm. It has been shown that adding a horizontal skin excision does not alter
the revision rate (15). It may, in fact, be surprising to learn that it is difficult
to know where to actually place the horizontal scar because the IMF rises
with the removal of breast weight.
One of the hardest things for surgeons new to this technique to accept is
that a vertical incision of more than 5 cm is far from negative. A longer
vertical scar is both necessary and desirable to accommodate the extra
projection that occurs with the vertical techniques. It is also important to
understand that gathering the vertical incision does not result in a shorter
scar; gathering or cinching actually instead leads to wound healing problems
(9).
In some very large–breasted women any of the pedicles chosen will be
long. Theoretically the blood supply stretches with the breast as it grows and
becomes ptotic but the reality is that nipple necrosis is more likely with the
longer pedicles. The other problem with excessively long pedicles is the
sheer volume of the pedicle itself, which limits the size of the reduction and
increases the weight of the breast in the lower pole. This extra weight can be
sutured up onto the chest wall but it will tend to bottom out with time.
Some patients who have large breasts, good nipple position, good skin
elasticity, and a large proportion of fat to gland may be better candidates for
liposuction only. Some young patients (rarely) may have such a good shape
that the reduction can be performed through an inframammary incision only.
PREOPERATIVE ASSESSMENT
The key ingredient to a successful breast reduction is patient education. It is
important to make the patients understand the limits of what can and what
cannot be achieved. We make sure that patients understand the concept of
“high” and “low” breasted (Fig. 39-5) and that we cannot change the breast
footprint—or where the breast sits on the chest wall. It is important for us as
surgeons to understand patient expectations and determine if we can achieve
them or not; it is better not to operate on patients who cannot accept our
limitations.
We find that taking photographs during the consultation and marking them
for the patient is very helpful. Patients often see more in their photographs
than they see in the mirror. It’s very important to point out the footprint on
each patient and to emphasize the differences between both breasts (Fig. 39-
6).
Our examination consists of assessing the breast footprint—the upper,
lateral, medial, and inferior breast borders and then the third dimension of
how the breast sits on that footprint. Does the patient have good upper pole
fullness? If so, they can achieve a better cosmetic result. If a patient has a
great deal of ptosis and a poor upper pole it will be futile to try to push the
excess inferior breast tissue into the upper pole because it will just drop down
again.
We can visualize how long the pedicle might be and if we need to warn
them about a possible free nipple graft (very rare). We will assess the skin
quality and skin excess and again determine if we need to warn the patient
that a “hockey stick” or inverted T scar might need to be added to their
vertical scar. It is important to decide preoperatively approximately how
much tissue will need to be removed.
FIGURE 39-5 Variability in the breast footprint. Not only do both patients need to
be approached differently surgically but they also need to have very different
expectations. A: This patient is “high breasted” and has good upper pole fullness.
She has a high upper breast border but a low inframammary fold level. She has a
high breast footprint but one which is long vertically. B: This patient is “low
breasted” and has poor upper pole fullness. She has a low upper breast border but a
high inframammary fold level. She has a low breast footprint but one which is short
vertically.
FIGURE 39-6 Drawings are made on the patient’s preoperative consultation. The
footprint is pointed out (cross-hatched) and a larger and smaller breast reduction
result is drawn. Note that the patient is shown that the upper breast border does not
change—all of the reduction is performed inferiorly and laterally. Note how close
these drawings are to what was achieved in surgery (see Fig. 39-17).

We also warn the patients that we often cannot make their breast as small
as either of us would like. We cannot achieve as significant a reduction with
the vertical approaches as we could when we performed inverted T inferior
pedicle reductions. The photographs taken during the consultation are also
useful for pointing out any asymmetries and warning the patients that
symmetry is a goal but impossible to achieve. Patients are also warned that
breasts will change with time, gravity, pregnancy, and weight gain and
weight loss.
The teenagers are well aware that their breasts might grow as they continue
to develop and that a rereduction might be indicated. We believe that this is
far better for many teenagers than having them suffer until they are older
because they tend to withdraw and stop participating in sports and other
activities. As long as the teenager understands the procedure and its
limitations then we are fully prepared to perform the surgery when it is
physically indicated. The same applies to the older patients. It is not age that
matters; it is health and psychologically maturity of the patient.
PREOPERATIVE PLANNING

Determination of New Nipple Position


The new nipple position is often placed at the level of the IMF but in some
patients the IMF can be very misleading. What we have found is that the
upper breast border (the junction of the top of the breast with the chest wall)
is the most static and reliable landmark. Since the upper breast border does
not change with a breast reduction, it is a good landmark to determine new
nipple position. The nipple is usually best located about one-third to one-half
the distance up the final breast mound. This point is usually 8 to 11 cm below
the upper breast border in an average C cup breast. The new nipple position
should be determined in relationship to the existing breast upper breast border
and not at some arbitrary distance from the suprasternal notch (Fig. 39-7).

Marking the Upper Breast Border


The upper breast border is at the junction of the chest wall and the breast.
This is very clear in some patients, with a definite demarcation line, and it is
blurred in other patients, where the breast slopes gently away from the chest
wall. The upper breast border is at the junction of the preaxillary fold and the
breast and it can be quite low in some very low–breasted patients. The upper
breast border is often (but not always) at the level of the upper edge of the
stretch marks. Patients need to understand that the breast footprint cannot be
lifted on the chest wall, and if their breasts are attached at a low level, they
will remain at that level. Surgeons also need to understand that pushing the
breast up and suturing it to pectoralis fascia does not work in raising the
footprint (7).

Marking the Level of the IMF


This level is becoming less important in determining the new nipple position,
but it is important in deciding how aggressive the surgeon can be in resecting
tissue at the fold in order to elevate the fold itself. Sometimes the IMF can be
at quite different levels on the same patient. The surgeon can thus be more
aggressive with the resection of the lower fold.

Marking the Breast Meridian


The breast meridian should not be drawn through the existing nipple but at
the desired level. Although it does not matter where the line starts, it is easier
to draw it beginning at the clavicle and then making the mark down the breast
bisecting it. The nipple looks best slightly lateral to the midline and it is
therefore better to err on the side of marking the meridian slightly more
lateral.

Marking the New Nipple Position


The new nipple can then be marked at the intersection of the vertical mark (8
to 11 cm from the upper breast border) and the new breast meridian (8 to 11
cm from the midline of the sternum). This position will often be at the level
of the IMF but not always. It is important at this stage for the surgeon to
stand back and visualize the result to make sure that the nipple is designed at
a good level both horizontally and vertically.
The surgeon has more flexibility with nipple position in patients with a
very full upper pole, but he or she should place the nipple lower in a patient
who has a ski-jump type of slope to the upper half of the breast. Nipples can
always be raised if a revision is needed, but they cannot be lowered. If there
is significant asymmetry, the new nipple position should be placed up to 1 cm
or so lower on the larger breast. Not only is the larger breast heavier, but
closure of a wider vertical ellipse in the larger breast will push the nipple
further up than it will on the smaller breast.
Design of the Skin Resection Pattern
Areolar Opening
The top of the areola is then marked 2 cm above the new nipple position.
This accommodates most areolar diameters of 4 to 5 cm. The areola is then
drawn so that it will close as a circle. It does not actually need to be mosque
shaped since it is probably better to take out more distance vertically than
horizontally. The original Wise-pattern design (10) was 14 cm in
circumference, and this matches a 4.5-cm diameter areola. A large paperclip
can be used as a template because it is 16 cm in length and this matches a 5-
cm-diameter areola. If the areola is not a “perfect” circle at the end of the
procedure, it is quite simple to make the appropriate adjustments. It is
important to make sure that there is symmetry in the design from one breast
to the other.

FIGURE 39-7 Markings. A: The upper breast border is marked with a dotted line at
the junction of the chest wall and the breast. This patient is “high breasted,” with a
short distance between her clavicle and the top of her breast. The breast meridian is
marked. The meridian should not be drawn through the existing nipple position but
through the desired nipple position. In this patient the meridian is marked at 9.5 cm
from the chest midline (through the “air,” not around the skin). The new nipple
position is marked at the intersection of the breast meridian. The nipple should be
marked at a lower level on the larger breast, so in this patient it is marked at 8 cm
down from the upper breast border on the smaller breast and 9 cm on the larger
breast. Note that the nipple is marked 0.5 cm lower on the larger left breast. B: The
medial markings for the areolar opening are then made. The medial markings need
to be “ideal” and symmetrical. C: The lateral markings for the areolar opening are
more flexible because they will be more mobile and they often need to be wide
enough so that areolar skin is not left behind. The new areola is marked at 2 cm
above the new nipple position. It is drawn freehand so that when closed it will
complete a circle. It is drawn with a circumference of 14 to 16 cm to match a 4.5- to
5-cm-diameter areola. Then new nipple position is marked at 21 cm on the right and
at 21.5 cm on the larger left side. This is measured from the suprasternal notch but is
not determined at some arbitrary distance but as measured from the top of the
upper breast border. D: The true superomedial pedicle is then marked about 4 cm
below the areolar opening medially and then up around and just lateral to the breast
meridian. E: The vertical limbs are designed much as one would with an inverted T
approach. Instead of carrying the vertical limbs of the Wise pattern medially and
laterally, they are curved around and joined about 2 to 4 cm above the
inframammary fold. The surgeon can pinch the skin to make sure that not too much
skin is being removed. The skin closure is not used to hold the breast, so this should
be designed for a loose, tension-free closure. If the skin pattern is carried down to the
fold, the scar will extend down onto the chest wall. F: The blood supply to a true
superomedial pedicle is shown. A pure medial pedicle has a base which is about 4 cm
below the areolar opening and about 4 cm above the areolar opening. In order to
include the descending branch of the artery from the 2nd interspace, the true
superomedial pedicle is extended up and just lateral to the breast meridian. The
pedicle then has a dual axial blood supply.

It is important to draw the medial side of the areolar opening first. It should
be “ideally shaped” and symmetrical from one breast to the other. The lateral
part of the breast is more mobile and it can tolerate a wider design (which is
often necessary in order to completely remove all remaining areolar skin).

Skin Resection Opening


The lateral and medial breast limbs are much the same as with the Wise
pattern. The breast can be rotated laterally and medially to match up the
breast limbs with the breast and chest wall meridians. Instead of extending
these limbs at 5 cm laterally and medially, the limbs are curved down as a
“V” and joined about 2 to 4 cm above the IMF. We originally described a
“U”-shaped skin resection pattern in order to encourage surgeons to remove
enough subcutaneous tissue to prevent the formation of a pucker. These
puckers needed to be corrected because of too much excess subcutaneous
tissue that was left behind rather than too much skin.
It is important to recognize that the superomedial pedicle vertical breast
reduction does not rely on the skin as a brassiere, and the skin flaps can (and
should) be loose enough so that there is no tension on the closure. The
surgeon can pinch the skin both with the patient standing and again supine in
the operating room to gauge the closure and tension. It is important to leave
enough fat attached to the dermis of the skin so that scar contracture does not
occur.
Postoperative puckers are more a problem of excess subcutaneous tissue
than they are a problem of excess skin.
It is important to stay well above the IMF (average 4 cm) because the fold
itself will rise and because closure of a vertical ellipse will result in longer
skin limbs and the scar could easily cross the IMF. It is important to match
the markings on both sides to achieve symmetry.
Surgeons will initially have trouble with the idea of a vertical limb that
exceeds 5 to 7 cm, but if ideal breasts are analyzed, an ideal B cup breast will
have a distance of 7 cm from the bottom of the areola to the IMF, an ideal C
cup breast will have a distance of 9 cm from the bottom of the areola to the
IMF, and an ideal D cup breast will have a distance of 11 cm from the bottom
of the areola to the IMF. The parenchymal limbs can be about 7 cm, but the
skin then tucks up around and behind the puckers (Fig. 39-8).
DESIGN OF A MEDIALLY AND SUPEROMEDIALLY BASED PEDICLE

Design of a Medially Based Pedicle


The medially based pedicle will often appear to be “superomedially” based
when a patient is standing up, but when a patient is lying down the true
medial nature of the base can be seen. The blood supply is medial, whereas a
true superomedial pedicle has both a medial and a superior blood supply. The
best way to design a medially based pedicle that is easy to inset is to place
half of the base of the pedicle in the areolar opening and half of the base in
the vertical limb of the skin resection pattern. When surgeons perform a pure
medial pedicle they end up cutting the strong descending artery from the 2nd
interspace. It makes more sense to include this artery in order to then create a
true superomedial pedicle which has a dual axial arterial supply.
FIGURE 39-8 The superomedial vertical breast reduction has good projection
because the breast is coned after removal of an inferior vertical wedge of skin and
breast tissue. The pillars are about 7 cm in length once closed and the vertical skin
length can be longer because the skin tucks up around and behind the pillars.

The veins can usually be seen just below the skin, and it would be ideal to
try to include one of the visible veins within the base design. The artery to the
medial pedicle comes from the internal mammary system at the level of the
3rd interspace. It is deep as it comes around the sternum and then proceeds up
in the subcutaneous tissue toward the areola. The descending artery from the
2nd interspace usually enters the pedicle about the level of the breast
meridian. Both arteries travel about 1 cm deep to the skin and they travel
separately from the veins.
The inferior border of the medial pedicle becomes the medial pillar as the
pedicle is rotated up into position.
Design of a Superomedially Based Pedicle
A true superomedially based pedicle may be a good choice for the longer
pedicles since it will include both the medial and superior arteries. It will,
however, be more difficult to inset. Because we know that the descending
branch of the artery from the 2nd interspace almost always enters the areolar
opening just medial to the breast meridian and almost always within 1 cm
below the skin surface, we can create a wider base superiorly and then
remove deeper tissue (that has minimal blood vessels) in order to make it
easier to inset the pedicle.
OPERATIVE TECHNIQUE
POSITIONING
The patient is supine on the operating table with the arms angled outward.
For surgeons who wish to sit the patient up at the end of the procedure the
arms should be carefully wrapped and the patient positioned on the table so
that the back can go up in the right position. We do not usually consider this
maneuver necessary, because we know where we want the new nipple
position during the preoperative markings.
INFILTRATION
We no longer infiltrate the incision lines because we want to preserve any
veins which are found just below the dermis because this is the main venous
drainage. We will infiltrate the areas to be suctioned with either a tumescent
type of fluid (Ringers lactate 1 L with 1 cc of 1/1,000 epinephrine and 20 cc
of 2% plain lidocaine) or lidocaine with epinephrine (20 cc of 1% with
1/200,000 epinephrine diluted with 60 cc of saline). We use about 300 to 500
cc of tumescent fluid per side or about 40 cc of the lidocaine with
epinephrine per side. Most of the infiltration is placed in the lateral chest
wall, preaxillary areas and just above the IMF. These are the areas where
most of the liposuction is performed.
PEDICLE CREATION
The pedicle is deepithelialized in the usual fashion by placing a lap pad
around the base of the breast and holding it with a Kocher clamp. This puts
the skin under tension and allows it to be removed more easily. The
superomedial pedicle is much easier to deepithelialize than an inferior pedicle
(Fig. 39-9). A cuff of tissue is left around the new areola using the
Schwartzman maneuver.
Even when the nipple is high and contained within the areolar opening, we
still prefer a medially based pedicle rather than a superior pedicle. This not
only allows us better access to the excess lateral breast tissue but it also
maintains the elegant curve to the lower pole of the breast because the
inferior border of the medial pedicle becomes the medial pillar. The pedicle is
then cut straight down to chest wall to create a full-thickness pedicle but it
can be debulked because the blood supply to the nipple does not go through
the parenchyma. The blood supply is superficial but keeping it full thickness
allows preservation of sensation and ductal tissue.
Note that the pedicle is incised ending up just lateral to the breast meridian.
The whole area is deepithelialized to leave a platform of dermis left attached
to the areolar opening so that it can help prevent postoperative areolar
retraction.
An inferior wedge of skin and breast tissue is removed (Fig. 39-10). The
excision is carried up lateral to the superomedial pedicle to allow the surgeon
to remove parenchyma under the lateral flap (Fig. 39-11).
INSETTING OF THE PEDICLE
It is easiest to close the base of the areola before insetting the pedicle (Fig.
39-12). A single 3-0 Monocryl is used in the dermis of the pedicle and the
dermis of the opposite side. No undermining of the dermis in the pedicle is
needed. Once this suture is in place, the pedicle is then rotated up into
position. The areola will sit easily into the new opening. The whole base of
the pedicle rotates, which means that the areola sits into position with little
tension or compression. The inferior border of the medial pedicle becomes
the medial pillar. This is one of the most important aspects during the
insetting of the pedicle, if it doesn’t fit correctly we can excise deep breast
tissue on the pedicle to allow an easier inset.
If there is any resistance to insetting of the pedicle, then the deep
parenchyma should be debulked. There is no blood supply through the
parenchyma to the nipple of the superomedial pedicle; the blood supply is in
the subcutaneous tissue. It is therefore safe to debulk the pedicle as much as
might be necessary for an easy inset.
CLOSURE OF THE PILLARS
The pillars are closed with interrupted 3-0 Monocryl. The best way to
visualize the correct pillar closure is to pull the pedicle in a cephalad
direction and the pillars will fall together. It is important to place the first
pillar suture inferiorly so the pedicle is completely rotated into position. The
first suture is placed right at the base of the pedicle inferiorly, but this is only
about 7 cm below the areolar opening. The pillars only extend about halfway
down the skin opening. The first suture should not be deep. There is no point
in pulling on the lateral breast tissue to try to move it medially; there should
be no tension on the pillar closure. Tension on the breast tissue will
eventually stretch, and any lateral tissue pulled inward will eventually slide
back out. Sutures do not need to be deep but should only catch enough
fibrous type of breast tissue so that fibrous tissue can heal to fibrous tissue.
CLOSURE OF THE DERMIS
The dermis is closed with interrupted 3-0 Monocryl Plus. It is not necessary
to suture the dermis up onto the breast parenchyma. Such sutures will
actually delay resolution of the shape. Surgeons should resist the temptation
to excise more skin. The skin does not contribute to the shape, and too much
tension will just delay healing. The breast should have a good curve to the
lower pole and not be pushed up into a concave type of shape. With this
technique we want to achieve an aesthetically curved inferior pole and it
should be on average about 9 to 11 cm long.
FIGURE 39-9 Pedicle creation. The whole pedicle is usually deepithelialized but the
pedicle itself is cut along the initial design in order to leave a lateral platform of
tissue to help support the lateral aspect of the nipple areolar complex. A: The whole
pedicle is deepithelialized. B: The inferior vertical wedge of skin and breast tissue is
visible. C: The pedicle is incised up to and lateral to the breast meridian while
leaving the extra lateral deepithelialized skin as a platform to prevent areolar
retraction laterally.
FIGURE 39-10 Parenchymal resection. The vertical wedge of inferior breast tissue is
removed initially and then the extra breast tissue is removed where it is in excess—
mainly under the lateral flap. A: Even though a lateral platform of dermis is left in
the areolar opening, it is still important to excise any extra breast tissue in that area
as a superior extension (held in the forceps) of the inferior vertical wedge of skin and
breast tissue. B: The shape of the inferior vertical wedge of skin and breast tissue.
Note how some of the lateral excess is removed.
FIGURE 39-11 Resection of parenchyma from under the lateral flap. A: Note that
the superomedial pedicle is being pulled out of the way and the thickness of the
lateral pillar is marked in purple. B: The lateral pillar is left about 2 cm thick and the
excess is removed parallel to the skin with the cutting cautery. C: The extent of the
resection is shown. The inferior vertical wedge of skin and breast tissue has been
removed, as has the excess parenchyma under the lateral flap. The cross-hatched
areas are marked where more excess is removed. Parenchyma needs to be directly
excised and the excess fat can be contoured out with liposuction. The purple arrows
mark the inferior extent of the pillars. D: Any excess parenchyma laterally needs to
be removed. If it is mainly fatty tissue, it can be removed with liposuction but in
young women (such as this patient) the parenchyma is white glandular tissue that
needs to be directly excised. If this parenchyma is not removed, the breast will end
up with a boxy shape with too much lateral fullness. E: The black arrows point to the
crisscrossing inframammary fold fibers. The inframammary fold is a zone of
adherences consisting of skin fascial fibers that cover a vertical distance of a few
centimeters. It is not a ligament. If forceps are used to pull on these individual white
fibers, it can be seen that they all pull on the skin at the IMF.
FIGURE 39-12 Insetting of the superomedial pedicle. A: The base of the areola is
closed initially to make it easier to inset the pedicle. This also allows the surgeon to
assess the extent of the resection. B: Once the pedicle is inset, it can be pulled up to
show how the pillars fall together. The inferior border of the medial pedicle becomes
the medial pillar. The lower end of the pillars is at the level of the arrows marked on
the skin. The pillars are about 7 cm long. The pillars do not extend to the lower end
of the skin opening or to the inframammary fold. The inferior aspect of the pillars is
shown about halfway down the skin opening. C: The first suture in the pillars is
placed inferiorly. Deep sutures are not used. The goal is to have the pillars touch so
that they can heal together.

The best way to decide whether an inverted T skin resection should be


added is to lift the breast off the chest wall while pushing it caudally (Fig. 39-
13). If the lower aspect of the skin tucks up nicely, then no more skin needs
to be removed.
LIPOSUCTION
Liposuction is then used to refine the shape (Fig. 39-14). The subcutaneous
tissue above the IMF needs to be removed—all except a layer under the skin
to prevent contractures or adhesions. Some of the more fibrous tissue will
need to be directly excised, but the area can be easily tailored and shaped by
using liposuction. It is especially important not to leave excess subcutaneous
tissue just above the IMF laterally; postoperative puckers are more of a
problem of excess subcutaneous tissue and less of a problem of excess skin.
Liposuction is also used to reduce fullness in the preaxillary area and to
reduce excess fat along the lateral chest wall.

FIGURE 39-13 The best method to determine if a short T skin excision is needed. A:
The breast is lifted off the chest wall and pushed down. If the pucker tucks up as
shown then a T skin excision is not needed. B: Just pushing the breast caudally will
make it look as if a T is needed. The breast needs to be lifted off the chest wall and
then pushed caudally.
CLOSURE OF THE SKIN
The areola is closed with four interrupted stay sutures of 3-0 or 4-0 Monocryl
Plus. The circumference is then closed with a running subcuticular Monocryl
Plus suture. The skin is closed with a running subcuticular 3-0 Monocryl Plus
suture (Fig. 39-15). It is important not to take deep constricting bites of
dermis. The skin closure should be loose and without tension. It is tension in
the closure that leads to wound healing problems.
Initially it was believed that gathering the skin closure would promote
wound retraction; however, excessive gathering not only delays healing, but
it also delays resolution of the shape. Measurements at surgery and each
follow-up visit showed that the vertical distance not only stretched back out
(9), but unfortunately, sometimes a scar contracture with pleated skin
resulted.
This shortening was performed because surgeons mistakenly believed that
the vertical incision should be no longer than 5 to 7 cm. A longer vertical
incision is actually desired to accommodate both the increased projection and
the curve to the lower pole of the breast (Fig. 39-16). It may be tempting to
either excise the excess skin inferiorly or even to suture it down to the chest
wall. An added horizontal excision will only be necessary when the vertical
incision exceeds about 12 to 14 cm or in postbariatric patients with poor
quality skin.
It can be tempting to suture the pucker down to the chest wall but it can
end up being adherent permanently. The IMF should be able to slide and
suturing the pucker down will result in an indentation that needs to be
released postoperatively.
INTRAOPERATIVE AND POSTOPERATIVE CARE

Drains
Drains are rarely used because they do not prevent either a hematoma or a
seroma. Good hemostasis is essential; the surgeon should understand the
blood supply to secure the transected blood vessels. This is especially
important in the chest wall–based perforators that can retract and then bleed
later.
Bandaging and Taping
The incisions are covered with paper tape. It is best to use 3M Micropore
paper tape because it has a good adhesive that works well and does not cause
irritation. We do not use Steri-Strips because they can cause blisters.
The patients are placed in a noncompressive brassiere just to provide
support for about 2 weeks. They are not required to wear the brassiere but
most patients will wear some form of support for 2 to 3 weeks night and day.
FIGURE 39-14 The areas for liposuction so that the final result can be tailored. A:
The crosshatched areas for liposuction are marked. Note that the arrows mark the
lower end of the pillars. B: The liposuction has been performed. The power of the
inferior vertical wedge excision of skin and breast tissue in controlling the horizontal
base diameter can be seen. C: The breast can be lifted up in the same manner for
judging whether an inverted T might be needed and this will demonstrate any areas
of tissue excess. The pinch test can also be used to make sure that there will not be
any subcutaneous tissue excess left that will contribute to a pucker. D: The pinch test
is performed medially as well. It is important to leave enough fat on the
undersurface of the dermis to prevent postoperative scar contracture. It is important
not to suture the pucker down to the chest wall.
FIGURE 39-15 Comparison of preoperative and postoperative photos. A: Patient
prior to breast reduction. B: Patient at the end of the procedure.

Patients are encouraged to shower the next day and the paper tape forms a
good cover and bandage. The tape is actually difficult to remove before 3 to 4
weeks and it is easier to remove dry than in the shower.
Recovery
Most patients understand that it takes about 1 to 2 weeks to get back to
normal activities and 3 to 4 weeks to get back to sporting activities. They can
walk during the first week or so to maintain fitness and they can walk uphill
if they want to maintain an aerobic training level. They are advised to start
with something like a stationary bicycle and then with time to progress to
jogging. They can use lower body weights initially but they should hold off
on upper body weights for a few weeks. Patients are not restricted in their
arm movement or in driving (as shown in Fig. 39-17).
RISKS

Scarring
The vertical scar approaches can avoid the often-unsightly IMF scar. The
lateral and medial puckers (dog-ears) are replaced by an inferior pucker that
usually resolves and is easy to correct. The vertical scar is usually the best
scar with the circumareolar scar being somewhat more visible. When there is
significant skin redundancy and an inverted T skin resection is required, it
can often be kept fairly short. It is the more medial and lateral aspects of the
inframammary scar that become more hypertrophic.

FIGURE 39-16 This illustrates how a longer vertical length from the bottom of the
areola to the inframammary fold is actually desirable. A 5-cm vertical length results
in a flattened breast with very little projection.
FIGURE 39-17 Pre- and 2-week postoperative photos of the patient shown in the
marking and procedure photos. She was 16, 5′2″ and weighed 135 lb. She had 200 g
removed from the right breast and 300 g from the left breast. Another 60 cc of fat
was removed with liposuction. This was a small breast reduction but it shows the
principles of marking and surgery. There will be further resolution of the shape with
time but this shows that it is not necessary to wait for months for a good shape. A:
Preoperative frontal view. B: Preoperative lateral view. C: Preoperative arms-up
view. D: Two-month postoperative frontal view. E: Two-month postoperative lateral
view. F: Two-month postoperative arms-up view.

Sensation
Eighty-five percent of patients recover normal to near-normal sensation with
the medial and superomedial pedicle. A self-reported patient questionnaire
(7) showed that only 76% of patients recovered similar sensation with the
lateral pedicle and only 67% with the superior pedicle.
Breastfeeding
Dr Norma Cruz-Korchin (16) conducted an interesting study that showed that
the incidence of breastfeeding difficulties was the same after breast reduction
as it was in large-breasted women who had not had a reduction. About 60%
of the patients in both groups were able to breastfeed and one-fourth of those
patients had to supplement with formula.
COMPLICATIONS

Nipple and Areolar Necrosis


This is one of the most feared complications (Fig. 39-18). We need to
remember that breast reduction is a blood supply–reducing operation. It is
inevitable that some pedicles are going to lose circulation. The problem is in
deciding whether and when to intervene. It may be clear if there is obvious
venous congestion that removing some sutures or taking the patient back to
the operating room to correct any compression may be indicated.
In our experience, the problem is rarely one of venous congestion. Usually,
the nipple and areola look pale and dusky. There is nothing that can be done
about a lack of arterial input, except conversion to free nipple grafts.
However, this is rarely a good solution because the majority of nipples will
recover. Some may develop some edge necrosis or blistering, but the final
result will still be better than a free nipple graft. Free nipple grafts can have
healing problems of their own, especially if delayed. The nipples lack
projection, do not recover sensation, preclude breastfeeding, and frequently
develop patchy areas of depigmentation. We believe that it is better to
reconstruct the few patients who develop complete necrosis than to subject a
significant number of patients to a reoperation that has a low chance of
success, with or without conversion to free nipple grafts.
FIGURE 39-18 A true superomedial pedicle is less likely to result in nipple necrosis
because it has a dual axial blood supply. Often the recommendation is to remove the
nipple and perform a free graft, but it is important to understand that there are
consequences to action just as there are consequences to inaction. The areola tends to
be a privileged area and watchful waiting can be the best course of action. A:
Preoperative view. B: When a patient has this type of necrosis during the recovery
period, they will often push for an intervention. It is best to leave it alone. C: Once
the necrosis becomes well demarcated, it can be debrided. In this case, it was left
alone. D: No intervention or debridement was performed in this patient and the final
result was clearly better than either free nipple grafts or overaggressive early
treatment.

Hematoma
Drains will not prevent or treat a hematoma. The best way to prevent a
hematoma is to ensure that all known arteries are secured. This is especially
important when vasoconstrictors are used. The vessels may not be obvious,
but once the vasoconstrictor has worn off postoperatively, the artery may
open up and cause a hematoma. The only treatment for a substantial
hematoma is to take the patient back to surgery (Fig. 39-19). Knowledge of
the anatomy can help in searching for these vessels prior to closure.
Seroma
Drains do not prevent seromas either. Seromas can develop even after drains
have been left in for several days. It is interesting that breast seromas behave
differently from those in the abdomen. They usually eventually resorb.

FIGURE 39-19 This patient developed a hematoma on her right breast in the first 24
hours after surgery (she still has the prep solution showing). This is a large-enough
hematoma that the patient should be taken back to surgery for an evacuation.
Surgeons who are learning the vertical approach will frequently check their
patients postoperatively and will find a significant number of seromas. They
may be more common than realized but are perhaps best left alone.
Infection
We now use one intraoperative dose of cephalosporins and antibacterial (not
antibiotic) sutures for closure. The Monocryl Plus suture is impregnated with
triclosan. Many spitting sutures are the result of a low-grade infection and we
have found that using the antibacterial sutures has reduced this wound
healing problem.
The other key to avoiding healing problems is to avoid tension in the
closure of both the parenchyma and the skin. The superomedial pedicle
vertical breast reduction does not require skin tension to shape the breast, and
the skin repair is best left fairly loose.
Wound Healing Problems
Wound healing problems are usually the result of poor circulation and/or
infection. There is no question in our practice that wound healing problems
are more common in the larger breast reductions and more common in obese
patients. The inverted T is notorious for problems in healing where skin
tension is the greatest—at the T itself. As long as the vertical incision is
sutured loosely and without tension, then wound healing problems are
minimized. We no longer gather the vertical incision, but when we did, we
were very careful not to backtrack and constrict the circulation to the skin
margins.
Puckers
There are two puckers or dog-ears that develop with the inverted T procedure
at the lateral and medial extent of the inframammary scar. This is the
expected result after closing a horizontal ellipse.
There are two puckers or dog-ears that develop with the vertical
approaches to breast reduction. The excision of skin and parenchyma is
performed as a vertical ellipse with both upper and lower dog-ears. The upper
dog-ear is absorbed by the areola. The lower dog-ear has created a huge
controversy and resistance to the vertical technique. It is the reason that there
is a higher revision rate (about 5%) with the vertical approaches. However, is
there is a higher revision rate because we can actually do something about the
problem? There is really no good way to treat the lateral and medial dog-ears
with the inverted T, and therefore the revision rate remains artificially low.
We warn all our patients about the puckers, yet we need to fix only about
5%. Patients also know that we will not consider any revision for a full year
because most puckers will disappear on their own. The revision of a pucker,
when it’s needed, is easily performed under local anesthesia. If the pucker is
above the IMF, it is corrected with a small vertical incision along with a
horizontal resection of subcutaneous tissue. If the pucker extends below the
IMF, it is corrected with a horizontal excision of skin and subcutaneous
tissue.
Underresection and Bottoming Out
It is important to adhere to the preoperative assessment of the volume that
needs to be removed. The breasts look smaller on the table with the vertical
approaches than they do with the inverted T. It is important to remove extra
parenchyma underneath the lateral flap, and occasionally some tissue will
need to be removed superiorly. If a patient does not have much upper pole
fullness, it is important to leave as much superior tissue as possible.
Bottoming out is invariably the result of underresection. We can correct
the bottoming out with this vertical technique by removing inferior
parenchyma without removing any skin and without any attempt to reposition
the IMF. The complication of bottoming out is not the fault of the procedure,
but it has always been our fault in not removing enough breast tissue
inferiorly.
Asymmetry
When the breasts are asymmetric, it is important to design the new nipple
position lower on the larger breast. There are two reasons for this. One reason
is that the skin may be stretched more on the larger breast and the marking
will rise up when the extra breast weight is removed. The other reason is that
closure of the vertical ellipse (both skin and breast parenchyma) on the larger
side will push up the superior end even further.
The asymmetry can be sometimes better assessed in the arms-up position.
It is interesting that the IMF on the larger breast is not necessarily lower than
on the smaller breast. Note should be made of these differences while
planning the surgery. The fold can be raised to some degree by removing
tissue just above the IMF, either directly or with liposuction for tailoring.

CASES

CASE 1

In Figure 39-20, a 20-year-old woman underwent a superomedial vertical


breast reduction. She had 495 g removed from the right breast and 455 g
removed from the left breast. Another 150 cc of fat was removed with
liposuction. She was 5’5” tall and weighed 125 lb.
FIGURE 39-20 A, B: Preoperative frontal and lateral views. C, D:
Postoperative frontal and lateral views at 1.5 years. No horizontal scar was
needed.

CASE 2

A 36-year-old woman who underwent a superomedial vertical breast


reduction with removal of 180 g on the right and 170 g on the left (Fig.
39-21A–E). She had 350 cc of fat removed with liposuction. She is
shown postoperatively at 14 months (Fig. 39-21F–J).
FIGURE 39-21 A–E: Preoperative views (frontal, 3/4 and lateral views). F–J:
14 months postoperative views (frontal, 3/4, lateral views). (Courtesy of Dr
Gustavo Jiménez Muñoz Ledo.)

CASE 3

This patient underwent bilateral breast reduction with superomedial


pedicle with more than 1000 g removed from each breast.
FIGURE 39-22 A, B: Preoperative view. C: Intra operative view. D–F:
Postoperative view at 9 months.
FIGURE 39-23 This patient is shown at 1 year after her breast rereduction. No new
pedicle was created. The areola was reduced and elevated with deepithelialization
only. Note how much the inframammary fold was elevated without reopening the
horizontal scar. When the weight above the bottomed-out inframammary fold is
removed, the fold elevates on its own without the need of any sutures. A, B:
Preoperative. C, D: Postoperative at 1 year.
BREAST REREDUCTION
Women presenting for breast rereduction surgery can pose a surgical
challenge. Problems requiring correction include glandular hypertrophy,
nipple position, descent of the IMF, and glandular ptosis.
It is important to understand that a new pedicle cannot be used after a
previous breast reduction (17). Creation of the original pedicle has damaged
the blood supply to any other pedicle. Recreating the old pedicle may seem
like a good idea, but it has a high complication rate. It is best to accept that
there is a good random pattern blood supply to the nipple if the area around it
is just deepithelialized (Figs. 39-23 and 39-24). A review of 90 breast
rereductions showed that some edge necrosis occurred in one patient where
the nipple was elevated 6 cm.
Breast rereductions can often be performed safely when the nipples are in a
relatively good position. The problem is usually glandular ptosis and
bottoming out of the IMF. When the nipple areolar complex does not need to
be moved, an inferior wedge of skin and parenchyma can be safely removed
because this is unlikely to affect the blood supply to the nipple areolar
complex. The excess tissue is removed where it is in excess—inferiorly.
FIGURE 39-24 A–C: This patient had a rereduction removing 230 g on the right
breast and 220 g on the left breast. She had 525 cc of fat removed with liposuction.
Note that no new pedicle was created. The area around the areola was
deepithelialized only and the blood supply was random pattern. D–F: The patient is
shown at 10 years postoperatively and she wanted a further rereduction. This time
there was no need to elevate the nipples. G–I: This patient is shown a full year after
another rereduction. She had 120 g removed from the right breast and 100 g from
the left breast. This time another 1,050 cc of fat was removed with liposuction. J, K:
In neither case was the old inframammary scar reopened. The inframammary fold is
elevated by performing liposuction between the bottomed-out IMF and the
horizontal scar.

Breast rereduction can be performed safely if the surgeon follows the


following principles: (1) maintain the nipple areolar complex on a random
pattern blood supply by deepithelializing only, and not creating a new pedicle
or even recreating the original pedicle; (2) correct the excess glandular ptosis
by removing a vertically oriented inferior wedge of breast tissue even if it
contains the original pedicle; (3) elevate the IMF by removing the weight that
pushes it down (this is best achieved by liposuction and direct excision
between the bottomed-out IMF and the original horizontal scar); (4) do not
remove skin horizontally because the skin between the horizontal scar and the
bottomed-out IMF needs to be reverted to chest wall skin. If there is
redundant skin on the breast, it should be removed above the IMF scar.
When there is too much redundant skin in a patient who presents for a
rereduction, it is important to remove that skin above the IMF scar (Figs. 39-
25 and 39-26). It might be tempting to remove an ellipse of skin below the
fold, but this will actually pull the fold down.
FIGURE 39-25 This patient had unrecognized Cushing disease for 3 years.
Unfortunately, that meant that the inframammary fold fibers lost their strength and
she ended up with a very low footprint. She was well informed of that before her
rereduction so she was pleased with the final result. The extra skin was removed
from above the inframammary fold. The black arrow shows a mole for reference.
The skin between the bottomed-out inframammary fold and the horizontal scar
should not be removed. That skin needs to be returned to chest wall skin so that the
fold can rise. A, B: Preoperative view. C, D: Postoperative view. E: The skin AB
became breast skin but it originated as chest wall skin and should be returned back
to the chest wall. Sutures are not needed; removing the weight is enough.

FIGURE 39-26 Principles of breast rereduction. A: No new pedicle is created in a


rereduction. The skin is deepithelialized around the areola and an inferior vertical
wedge of skin and breast tissue (which includes the inferior pedicle if that was used
originally) is removed. Liposuction is used between the bottomed-out inframammary
fold and the horizontal scar to remove the weight and to allow the fold to rise. B: If
there is redundant skin, it should be removed from above the inframammary fold. It
is a mistake to remove an ellipse of skin below the inframammary scar because it will
just pull the scar down. Removing weight will allow the fold to rise without the need
to add sutures.

REFERENCES

1. Robbins TH. A reduction mammaplasty with the areola-nipple based on


an inferior pedicle. Plast Reconstr Surg 1977;59:67.
2. Courtiss EH, Goldwyn RM. Reduction mammaplasty by the inferior
pedicle technique. An alternative to free nipple and areola grafting for
severe macromastia or extreme ptosis. Plast Reconstr Surg 1977;59:500.
3. Marchac D, de Olarte G. Reduction mammaplasty and correction of
ptosis with a short inframammary scar. Plast Reconstr Surg 1982;69:45–
55.
4. Lassus C. A 30-year experience with vertical mammaplasty. Plast
Reconstr Surg 1996;97:373–380.
5. Lejour M. Vertical Mammaplasty and Liposuction of the Breast. St
Louis, MO: Quality Medical Publishing; 1993.
6. Hall-Findlay EJ. A simplified vertical reduction mammaplasty:
shortening the learning curve. Plast Reconstr Surg 1999;104:748.
7. Hall-Findlay EJ. Aesthetic Breast Surgery, Principles and Techniques.
St Louis, MO: Quality Medical Publishing; 2010.
8. Hall-Findlay EJ, Shestak KC. Breast reduction CME article. Plast
Reconstr Surg 2015;136(4):531e–544e.
9. Matthews JLK, Oddone-Paolucci E, Lawson DM, et al. Vertical scar
breast reduction: does gathering the incision matter? Ann Plast Surg
2016;77(1):25–31.
10. Wise RJ. A preliminary report on a method of planning the
mammaplasty. Plast Reconstr Surg 1956;17:367.
11. Hall-Findlay EJ. Invited discussion, Deventer: blood supply of the breast
revisited. Plast Reconstr Surg 2016;137:1398–1400.
12. Wuringer E, Mader N, Posch E, et al. Nerve and vessel supplying
ligamentous suspension of the mammary gland. Plast Reconstr Surg
1998;101:1486.
13. Schlenz I, Kuzbari R, Gruber H, et al. The sensitivity of the nipple-
areola complex: an anatomic study. Plast Reconstr Surg 2000;105:905–
909.
14. Hall-Findlay EJ. The three breast dimensions: analysis and effecting
change. Plast Recon Surg 2010;125(6):1632–1642.
15. Berthe JV, Massaut J, Greuse M, et al. The vertical mammaplasty: a
reappraisal of the technique and its complications. Plast Reconstr Surg
2003;111:2192–2199.
16. Cruz-Korchin N, Korchin L. Breast-feeding after vertical mammaplasty
with medial pedicle. Plast Reconstr Surg 2004;114(4):890–894.
17. Mistry RM, MacLennan SE, Hall-Findlay EJ, Principles of breast re-
reduction: a reappraisal. Plast Reconstr Surg 2017;139(6):1313–1322.
CHAPTER 40

Reduction Mammoplasty With


Inverted-T Incision
ETHAN E. LARSON | MAURICE Y. NAHABEDIAN | SHILIANG CHANG
INTRODUCTION
The evolution of reduction mammoplasty has been witness to a variety of
techniques, principles, and concepts. Many of these have been related to skin
pattern design, parenchymal reshaping, and pedicle orientation. Skin pattern
designs can include short-scar techniques such as the vertical and horizontal
incisions as well as the inverted-T or Wise incision. Parenchymal reshaping
can be achieved using internal sutures or reliance of the skin envelope.
Pedicle orientation can essentially be in any direction and includes superior,
superomedial, medial, inferior, lateral, or central. Each of these techniques
and modifications can be a topic unto itself. This chapter, however, focuses
on Wise pattern or inverted-T skin incision in reduction mammoplasty.
ANATOMY
The anatomy of the breast is complex but relatively constant. The borders of
the breast typically extend vertically from the second to the sixth rib, and
horizontally between the lateral sternal border and the anterior axillary line.
The breast is composed of numerous lobules and ductules that lead to the
nipple areolar complex (NAC). There is a superficial fascia layer, the breast
capsule surrounding the breast to provide its shape and contour.
When considering a reduction mammoplasty, a thorough knowledge of the
vascularity and innervation of the breast and NAC is important. There are
several sources of blood supply to the breast. The perforating branches of the
internal mammary, the lateral thoracic artery, the perforating branches from
the pectoral vessels, and the intercostal vessels (Fig. 40-1). Studies on the
vascular territories of the breast and NAC have demonstrated the internal
mammary artery to be the dominant blood supply in 70% of patients (1). The
innervation to the breast and NAC includes the medial and lateral branches of
the intercostal nerves between the second and sixth vertebrae. The dominant
innervation to the nipple is derived from the lateral cutaneous branch of the
fourth intercostal nerve. Studies on the innervation of the NAC have
demonstrated nerve branches from both the anterior (medial) and lateral
fourth, fifth, and sixth intercostal nerves (1–3).
HISTORY OF THE INFERIOR PEDICLE
Wise described his inverted T skin incision for reduction mammoplasty in
1956. Back then, Strombeck breast reduction technique utilizes
deepithelialized horizontal bipedicle flap to reposition the NAC. In 1962,
Paul McKissock rotated the pedicle design 90 degrees and performed the first
vertical bipedicle flap for reduction mammoplasty. Later in 1977, Robbins
described the inferior pedicle breast reduction (4–6).

FIGURE 40-1 The principal blood supply to the breast includes perforating
branches from the internal mammary and lateral thoracic systems.
FIGURE 40-2 Anteroposterior (A) and lateral (B) view of the typical posture seen in
patients with symptomatic macromastia.
INDICATIONS
Women with excessively large breasts who seek breast reduction often
experience chronic pain and tension in their neck, shoulders, and upper back.
Symptoms generally worsen later in the day. Associated symptoms include
recurrent intertriginous skin irritations along the inframammary fold (IMF)
and shoulder grooves from the pressure of supportive brassiere straps. Due to
the excess breast tissue weight that pulls the shoulders forward, trapezius
muscles may hypertrophy to compensate (Fig. 40-2).
PREOPERATIVE CONSIDERATIONS
As with all breast reductions, a standard medical history and examination of
the pertinent systems should be performed (7). Special attention should be
given to any history of bleeding disorders and conditions affecting wound
healing, including tobacco use and diabetes. Problems arising from mammary
hypertrophy, including back and neck pain, shoulder grooving, and
intertriginous skin rashes or ulceration, need to be documented. The patient’s
preoperative weight, height, cup size, and bra size should be noted and goals
discussed for her ideal postoperative size. Deep vein thrombosis risk should
be assessed, along with a history of contraceptive use or hormone
replacement. Subjective nipple sensitivity should also be documented.
Findings on physical examination, family history of breast cancer, and
patient’s age determine the need for screening mammogram. A preoperative
mammogram is recommended for any woman younger than 50 years of age
with a family or personal history of breast cancer. Otherwise, a biennial
screening mammogram is recommended for women between age 50 and 74
years according to the U.S. Preventive Services Task Force guidelines
released in 2016 (8). The incidence of occult breast cancer found during
pathologic examination of breast reduction specimens is reported as 0.06% to
2.4% (9–12).
A set of measurements can be useful as guidelines to design the pedicle
width and estimate the resection breast volume. These include the nipple-to-
sternal notch distance, the nipple-to-IMF distance, and the nipple-to-nipple
distance. Several methods have been used to estimate resection breast volume
including the Schnur, Appel, Descamps, and Galveston scales (13–15). The
Schnur sliding scale estimates resection weight based on the patient’s body
surface area. On the other hand, Descamps method estimates resection
volume based on a regression analysis using breast measurements such as the
nipple-to-sternal notch distance and nipple-to-IMF distance. Appel scale uses
a combination of breast measurements and body mass index to estimate the
resected volume. Galveston scale adds age into the regression analysis of
breast measures and body mass index (15).
When the breast size is massive with a pedicle length of more than 16 cm,
the possibility of conversion to a free nipple graft increases. Requirement of a
free nipple areolar graft will be determined intraoperatively (16). Patients
with a larger body habitus should be counseled preoperatively regarding the
additional possible problems with wound healing and the likely emergence of
their lateral axillary bra roll and large abdomen as possible aesthetic
problems in the future.
PATIENT MARKINGS: INVERTED-T TECHNIQUE
The Wise pattern or inverted-T skin reduction incision can be applied to any
pedicle, including a superior, superomedial, medial, inferior, lateral, and
central mound pedicle. The skin reduction pattern and the pedicle type used
in reduction mammoplasty are independent variables. Most common pedicle
used with inverted-T skin reduction pattern is the inferior pedicle due to its
reproducible result, straightforward techniques, and easily taught in
residency.

FIGURE 40-3 Standard preoperative markings include the sternal midline, breast
meridians, and the inframammary folds.

The patient is marked in the standing position. Standard breast landmarks


include the sternal midline, suprasternal notch, breast meridians, and breast
borders (Fig. 40-3). Lateral mammary fold is marked along the anterior to
midaxillary lines. The lateral mammary fold can be easily identified with the
patient’s arms in a raised position. The anticipated nipple position is marked
at the level of IMF along the breast meridian. The actual distance of the NAC
to the sternal notch is variable and usually ranges from 22 to 26 cm. The
vertical limbs of the Wise pattern are marked by moving the breast to either
side of its meridian. The length of the vertical limb ranges from 7 to 9 cm
depended on the width of the breast. The apical angle of the vertical limbs
ranges from 50 to 70 degrees. The horizontal limb of the inverted-T skin
reduction pattern extends from the medial point of IMF to the inferior point
on the medial vertical limb, and from the inferior point of lateral vertical limb
straight across to the lateral mammary fold. These marking are typically
drawn in the preoperative holding area (Fig. 40-4). The remaining markings
are made in the operating room.

FIGURE 40-4 Standard inverted-T markings. The new nipple areolar complex
position is located at the level of the inframammary fold. The horizontal limbs
extend to the apices of the inframammary fold.
In the operating room, the patient is placed in the supine position. The
inferior pedicle is designed with a base width that ranges from 8 to 10 cm
(Fig. 40-5). A 1-cm triangle is designed at the T junction to prevent wound
complications.

FIGURE 40-5 A: A preoperative view of a woman with severe mammary


hypertrophy. B: The inverted-T pattern. C: The typical markings for an inferior
pedicle. D: The inferior pedicle with a base width of 10 cm.
OPERATIVE TECHNIQUE
INFERIOR PEDICLE
Following the markings, the patient is placed in the supine position under
general anesthesia. The patient’s arms are usually extended at about 75
degrees from the operating table to allow for access to the soft tissues along
the anterior and midaxillary line. The chest is then prepared in the
standardized surgical fashion. Local anesthesia consisting of diluted lidocaine
and epinephrine may be used to minimize bleeding from the initial incisions.
The areola is marked with an appropriate nipple sizer and sharply incised to
the level of the dermis. Areolar incisions are performed bilaterally at the start
of the case to minimize size change over the course of the procedure. The
inferior pedicle is then incised and deepithelialized, leaving the nipple and
incised areola intact. It is recommended to maintain the dermal layer as much
as possible to avoid injury to the underlying subdermal plexus (16). The
pedicle is harvested with care to avoid undermining and maintaining
posterior–inferior attachments to the chest wall. Toward the base of the
pedicle, dissection should be flared out to maximize blood supply.
Dermoglandular wedge excisions are performed, with the majority of tissue
coming from medial, superior, and lateral compartments. The dissection is
carried along the breast capsule to provide an even-thickness mastectomy
flap. The medial and lateral inframammary incisions are beveled upward to
preserve IMF and avoid delayed bottoming-out phenomena. A thin layer of
fat is preserved on the pectoralis fascia to minimize seroma rate and
postoperative pain. Care must be taken during lateral resection not to pull too
hard to separate the tissues from the chest wall. Trauma in this region can
injure the pectoralis or serratus fascia and possibly compromise nerve supply
to the NAC. These excisions can be performed en bloc or segmentally,
depending on the size of the breast and the volume of resection. Following
the resection, the inferior pedicle is assessed for bleeding at the distal aspects
to ensure perfusion to the NAC. Absence of bleeding may indicate a need for
conversion to a free nipple graft, particularly if the pedicle length is long.
Following irrigation and hemostasis, a temporary trifurcation suture is
placed at the caudal portion of the vertical limbs and at the meridian of the
breast at the tip of the triangle. The skin edges are temporarily stapled, and
the patient is sat upright to assess volume, symmetry, and nipple position.
The patient is then returned to the supine position, and minor adjustments are
made. The NAC is marked approximately 5 cm above the IMF along the
breast meridian, usually at the most projected portion of the breast. The NAC
is exteriorized by excising the apical skin and fat from the apex of the vertical
limbs. All sutures and staples are then removed, and final hemostasis is
achieved. The triple point is approximated with a 2-0 Vicryl suture. The IMF
incision is closed in layers with 3-0 V-loc for dermis in a simple running
fashion and with 4-0 Biosyn for skin in a running subcuticular fashion. A
drain may be placed in the breast based on surgeon’s preference. Closed
suction drains often cause increased postoperative discomfort without proven
benefits (17–20).
Lateral bra roll can be surgically excised or treated with liposuction at the
time of reduction mammoplasty for better cosmetic result. Sterile dressings
are then applied with a supportive, nonunderwire postoperative bra selected
to provide comfort. Typically, the patient is ready to return home on the day
of the procedure. Drains are typically removed at 24 hours but may remain
longer if necessary. Figure 40-6 illustrates preoperative and postoperative
views following reduction mammaplasty using an inferior pedicle.

FIGURE 40-6 A: A preoperative view of a woman with moderate mammary


hypertrophy. B: The final appearance following inferior pedicle reduction
mammaplasty at 8-month follow-up. The resection volume was 1,400 g from the
right breast and 1,328 gm from the left breast.
CONCLUSION
The inverted-T skin reduction pattern can be utilized with any types of
pedicle. Skin reduction and parenchymal reshaping can be independent from
each other. A multicenter Breast Reduction Assessment: Values and
Outcomes analysis reviewed reduction mammoplasty results in 179 patients
performed using various techniques with majority of patients having
undergone Wise pattern inferior pedicle technique (21). The overall
complication rate was 37% with Wise-pattern reduction, with delayed healing
in 20%, spitting sutures in 6%, hematoma in 3%, fat necrosis in 2%, nipple
necrosis in 1.4%, and seroma in 1.4%. Other studies have reported similar
complication rates (22,23). Complication rates increase with increasing
resection weight of breast tissue and elevated body mass index.
The inferior pedicle reduction combined with an inverted-T skin technique
provides reproducible, predictable, and reliable results. It is also the easiest
technique to master.

REFERENCES

1. Palmer JH, Taylor GI. The vascular territories of the anterior chest wall.
Br J Plast Surg 1986;39:287–299.
2. Jaspars JJ, Posma AN, van Immerseel AA, et al. The cutaneous
innervation of the female breast and nipple-areola complex: implications
for surgery. Br J Plast Surg 1997;50:249–259.
3. Sarhadi NS, Shaw Dunn J, Lee FD, et al. An anatomical study of the
nerve supply of the breast, including the nipple and areola. Br J Plast
Surg 1996;49:156–164.
4. McKissock PK. Reduction mammaplasty with a vertical dermal flap.
Plast Reconstr Surg 1972;49:245–252.
5. Robbins TH. A reduction mammoplasty with the areolar-nipple based
on an inferior dermal pedicle. Plast Reconstr Surg 1977;59(1):64–67.
6. McKissock PK. Color atlas of mammaplasty. In: Goin JM, ed.
Operative Techniques in Plastic Surgery. New York: Thieme Medical
Publishers; 1991.
7. Nahai FR, Nahai F. MOC-PS CME article: breast reduction. Plast
Reconstr Surg 2008;121:1–13.
8. Carlos RC, Fendrick M, Kolenic G, et al. Breast screening utilization
and cost sharing among employed insured women after the affordable
care act. J Am Coll Radiol 2019;16(6):788–796.
9. Demirdover C, Geyik A, Vayvada H, et al. Is histological evaluation of
reduction mammaplasty specimens worthwhile? Aesthet Surg J
2019;39(6):NP178–NP184.
10. Waldner M, Klein HJ, Kunzi W, et al. Occurrence of occult
malignancies in reduction mammoplasties. Front Surg 2018;5:17.
11. Colwell AS, Kukreja J, Breuing KH, et al. Occult breast carcinoma in
reduction mammaplasty specimens: 14-year experience. Plast Reconstr
Surg 2004;113(7):1984–1988.
12. Clark CJ, Whang S, Paige KT. Incidence of precancerous lesions in
breast reduction tissue: a pathologic review of 562 consecutive patients.
Plast Reconstr Surg 2009;124(4):1033–1039.
13. Schnur PL, Hoehn JG, Ilstrup DM, et al. Reduction mammaplasty:
cosmetic or reconstructive procedure? Ann Plast Surg 1991;27(3):232–
237.
14. Descamps MJ, Landau AG, Lazarus D, et al. A formula determining
resection weights for reduction mammaplasty. Plast Reconstr Surg
2008;121(2):397–400.
15. Boukovalas S, Padilla PL, Spratt H, et al. Redefining the role of
resection weight prediction in reduction mammoplasty and breaking the
“one-scale-fits-all” paradigm. Plast Reconstr Surg 2019;144(1):18e–
27e.
16. Al-Shaham A. Pedicle viability as the determinant factor for conversion
to free nipple graft. Can J Plast Surg 2010;18(1):e1–e4.
17. Collis N, McGuiness CM, Batchelor AG. Drainage in breast reduction
surgery: a prospective randomised intra-patient trail. Br J Plast Surg
2005;58(3):286–289.
18. Corion LU, Smeulders MJ, van Zuijlen PP, et al. Draining after breast
reduction: a randomised controlled inter-patient study. J Plast Reconstr
Aesthet Surg 2009;62(7):865–868.
19. Wrye SW, Banducci DR, Mackay D, et al. Routine drainage is not
required in reduction mammaplasty. Plast Reconstr Surg
2003;111(1):113–117.
20. Hansen J, Chang S. Overview of breast reduction. UpToDate. Last
updated April 30, 2019.
21. Cunningham BL, Gear AJ, Kerrigan CL, et al. Analysis of breast
reduction complications derived from the BRAVO study. Plast Reconstr
Surg 2005;115:1597–1604.
22. Oqunleye AA, Leroux O, Morrison N, et al. Complications after
reduction mammoplasty: a comparison of Wise pattern/inferior pedicle
and vertical scar/superomedial pedicle. Ann Plast Surg 2017;79(1):13–
16.
23. Hammond DC, O’Connor EA, Knoll GM. The short-scar periareolar
inferior pedicle reduction technique in severe mammary hypertrophy.
Plast Reconstr Surg 2015;135(1):34–40.
CHAPTER 41

Secondary Breast Reduction


PATRICK J. BUCHANAN | RICHARD J. GRECO
HISTORY
Breast reduction is one of the most common plastic surgical procedures
performed in the United States with over 100,000 cases performed each year.
A very small portion of these patients will suffer enough regrowth of their
breast to have a recurrence of their symptoms and create secondary
macromastia. There are many techniques described for the initial reduction
operation, but many plastic surgeons have been wary of performing a
secondary reduction because of the fear of nipple areolar complex (NAC)
necrosis in the secondary operation. Historically, it has been taught and
documented in the literature that the same pedicle must be used for all
subsequent reductions to avoid NAC ischemia. Documented complication
rates from subsequent reductions are between 20% and 60% (1–5). Free
nipple graft techniques have been the mainstay of treatment for secondary
reductions and are functional but leave the patient with no sensation, no
potential ability to breastfeed, and hypopigmentation, frequently. Knowledge
of the cause of the “recurrent” macromastia, the previous pedicle technique,
and the relative position of the NAC will help to determine the best solution
for the patient.
INDICATIONS
The indications for a secondary breast reduction are the same as for the
primary procedure and include back and neck pain, breast pain, shoulder
pain, headaches, shoulder grooves, intertrigo, and numbness and tingling in
the arm or fingers associated with significantly enlarged breasts.
CONTRAINDICATIONS
Secondary breast reductions can definitely improve the symptoms of a patient
with recurrent symptomatic macromastia, but at the risk of poor healing and
possible loss of the NAC because of inadequate blood supply. Therefore, it is
very important to take into account the patient’s comorbidities including, but
not limited to a history of significant nicotine use, diabetes, morbid obesity,
other surgical scars that could potentially reduce the bloody supply to the
NAC, poor oxygenation due to heart or pulmonary issues, and any other
vascular disorders (i.e., scleroderma, vasculitis, etc.) that may add to the
present risk of loss of NAC before proceeding forward with the secondary
breast reduction.
PREOPERATIVE PLANNING
Preoperative planning for a secondary breast reduction should be similar to
that of a primary breast reduction. Per the American Cancer Society
guidelines, all patients over the age of 50 should have a screening
mammogram within 1 year of the scheduled surgery. Once imaging is
obtained, if warranted, the next decision is type of secondary reduction to
perform. As stated previously, if the initial vascular pedicle is known then the
secondary reduction should incorporate that pedicle in its design. However, if
the initial pedicle is not known, then the surgeon must look at the NAC
position.
When the NAC Is Already in the Correct/Ideal Position
In this group of patients we evaluate whether there has been a “bottoming
out”/stretching of the lower pole of the breast or just an overall enlargement
of a well-shaped breast. If the patient has a full, but well-shaped breast,
liposuction of the breast alone could be an excellent option to reduce the size
and symptoms while maintaining the overall shape and correct nipple areolar
position. If the NAC is in the correct position, but the breast has bottomed
out: a resection of the lower pole of the breast in a transverse only or a
vertical and horizontal resection is used to reduce the size of the breast and
improve the shape of the breast.
Previous Operation Was Free Nipple Graft Technique
This group of patients does not have a definable previous pedicle of blood
supply to the NAC. If the position of the NAC is correct, decide procedure as
above. If the NAC is in the incorrect position, utilization of a secondary free
nipple graft technique is an excellent choice.
Previous Pedicle of the NAC Is Known
If the previous pedicle is known, we would definitely include the blood
supply in any procedure we design.
Previous Pedicle of the NAC Is Unknown
In patients where there is no operative report available and no way to know
the actual blood supply to the nipple areolar complex from the previous
surgery, we attempt to include as many potential significant blood supplies to
the NAC as possible through our modified central mound (MCM) technique
or free nipple graft technique.
OPERATIVE TECHNIQUE
The surgical approach to the patient will depend on the present shape and size
of the patient’s breasts, the relative position of the NAC, the desired size
reduction, and the previous blood supply left intact to the NAC. For purposes
of this chapter, we will only highlight the techniques used when the initial
NAC pedicle is not known.
When the NAC Is Already in the Correct/Ideal Position
Liposuction
It is performed when the NAC is in the correct position, the initial NAC
vascular pedicle is unknown, and the overall breast shape is ideal. Use a
standard super-wet or tumescent liposuction technique. Ensure that the entire
breast is addressed to avoid areas of over- or undertreatment, which can lead
to breast distortion and asymmetries.

Inferior Pole Resection


This is performed when the NAC is in the correct position, but the breast
itself has a “bottomed out” appearance with stretching of the inferior pole. In
a horizontal scar–only technique, the inferior breast is marked and excised.
The scar is then placed directly in the IMF, thereby leaving the NAC in its
natural position. If excess skin remains, a vertical incision just below the
NAC can be made to reduce the excess skin and breast tissue in the
horizontal dimension.
When the Initial Breast Reduction Used a Free Nipple Graft
Since the initial reduction used a free nipple graft, there is no vascular pedicle
to the NAC that needs to be protected. Therefore, any style of secondary
reduction can be performed and a secondary free nipple graft is used if the
NAC needs to be repositioned.
Initial NAC Pedicle Is Unknown and the NAC Needs to Be
Repositioned
One such secondary reduction technique when the initial pedicle is unknown
is to perform an MCM reduction. Although similar to the McKissock
technique, the MCM reduction respects the vascular supply to the NAC by
preserving the remaining vascularity that is present in the horizontal septum
as described by Wuringer, while simultaneously preserving the vascularity in
the superior and inferior vascular pedicles (6). However, unlike the
McKissock technique, an MCM reduction leaves the superior aspect of the
bipedicle intact and it is not elevated off of the pectoralis fascia. As illustrated
in Figure 41-1, a Wise-pattern skin incision is made, superior and inferior
dermal pedicles are deepithelialized to maintain vascularity to the NAC. The
breast parenchyma is then resected under the medial and lateral skin flaps,
maintaining the NAC on the central breast mound. The NAC is then inset in
its proper position and the medial and lateral skin flaps are sutured together in
midline.
FIGURE 41-1 A: Wise-type pattern. B: Superior and inferior dermal pedicles are
deepithelialized, maintaining the neurovascular supply to the NAC. C: Breast tissue
is removed medially and laterally. D: Central mound of breast tissue beneath NAC is
preserved. E: NAC is inset into position. F: Skin edges are brought together. G:
Final result.
CASES

CASE 1

Figure 41-2 is an intraoperative case in which the MCM secondary


breast reduction technique is utilized.
FIGURE 41-2 A: The initial markings for the modified central mound breast
reduction technique. Care is taken to leave the inferior and superior pedicles
intact. As noted, the nipple areolar complex needs to be lifted in order to
achieve its ideal position on the breast mound. B: The inferior and superior
pedicles are deepithelialized. C: Skin flaps are then elevated both medially
and laterally to the deepithelialized inferior pedicle. D: The breast tissue
underlying the elevated skin flaps is then resected, keeping only the central
mound intact on which the nipple areolar complex is positioned. E: The
medial and lateral skin flaps are then reapproximated and the nipple areolar
complex is inset in its ideal position on the new breast mound.

Figure 41-3 represents before and after photographs of an MCM


secondary breast reduction technique. The before photos are on the left
side and the after are on the right side of the figure.
FIGURE 41-3 Before (left) and after (right) photographs of an MCM
secondary breast reduction.
CASE 2

In Figure 41-4, this patient wanted slightly smaller breasts and her NAC
repositioned. Her initial breast reduction pedicle was unknown so she
also underwent an MCM secondary breast reduction technique. Her
preoperative photographs are on the top of the figure and postoperative
photographs are on the bottom.
As depicted in Case 2 (as well as Case 1), the MCM secondary breast
reduction technique is a powerful tool to help preserve vascularity to the
NAC when the initial pedicle is unknown. It also helps to reposition the
NAC onto the new breast mound, giving the breast a more aesthetically
pleasing appearance.

FIGURE 41-4 Photos on left are preoperative 40 DDD symptomatic


macromastia after previous breast reduction. The photos on right are post
MCM secondary reduction 40 Large C and better symmetry.
OUTCOMES
Historical complication rates from secondary breast reductions are quoted at
37.5% and range from 20% to 60%, a rate exponentially higher than reported
for primary breast reductions (1–5). Within the literature, there are varying
stances on whether the same pedicle should be used, if known, for the
secondary breast reduction. Rohrich et al. recommends the use of a free
nipple graft in all secondary breast reductions in which the primary pedicle is
unknown (5).
Hudson and Skoll reported the outcomes of 16 repeat reductions, in which
2 patients underwent secondary reductions based on different pedicles. Both
of these patients suffered vascular compromise of the NAC. Thus, the authors
concluded that if the NAC is not in good position, a resection with free nipple
grafting is the technique of choice (2). Patel et al. echoed this
recommendation in their study of eight secondary breast reductions (7).
However, in one of the largest studies looking at secondary breast
reductions, Spaniol, Buchanan, and Greco found that an MCM can be
performed safely and effectively in any patient with an unknown NAC
pedicle. In this study of 30 patients (60 breasts), all NACs remained viable
without necrosis or ischemia (8).
With regard to secondary breast reductions using only liposuction
techniques, or an inferior wedge resection, Lejour performed liposuction
alone in 14 patients undergoing secondary reduction and reported zero NAC
complications (3). Likewise, Ahmad et al. performed an inferior wedge
resection on 25 patients undergoing secondary breast reduction with the NAC
remaining viable on a superiorly based pedicle and utilized liposuction on
65% of the patients. They, also, reported no complications (1).
CONCLUSION
The ultimate goal of a secondary breast reduction is to relieve the symptoms
caused by the recurrent macromastia while maintaining vascularity to the
NAC. When the initial breast reduction NAC pedicle is known, care must be
taken to incorporate this vascular pedicle in the secondary breast reduction
design. However, when the initial breast reduction NAC vascular is unknown
the surgeon must assess whether the NAC is in proper position or needs to be
repositioned. When the NAC needs to be repositioned, the MCM procedure is
a technique that has been proven to maintain vascularity to the NAC. The
MCM procedure maintains vascularity to the NAC by preserving the
horizontal septum, as well as the superior and inferior vascular pedicles.
Maintaining these three distinct vascular supplies reduces the risk of NAC
ischemia and reduces the complication rate. Although performing a free
nipple graft is a viable option, the MCM technique is deemed to be superior
as it can maintain NAC sensitivity.

REFERENCES

1. Ahmad J, McIsaac SM, Lista F. Does knowledge of the initial technique


affect outcomes after repeated breast reduction? Plast Reconstr Surg
2012;129(1):11–18.
2. Hudson DA, Skoll PJ. Repeat reduction mammaplasty. Plast Reconstr
Surg 1999;104(2):401–408.
3. Lejour M. Vertical mammaplasty as secondary surgery after other
techniques. Aesthetic Plast Surg 1997;21(6):403–407.
4. Losee JE, Caldwell EH, Serletti JM. Secondary reduction mammaplasty:
is using a different pedicle safe? Plast Reconstr Surg 2000;106(5):1004–
1008; discussion 1009–1010.
5. Rohrich RJ, Thornton JF, Sorokin ES. Recurrent mammary hyperplasia:
current concepts. Plast Reconstr Surg 2003;111(1):387–393; quiz 394.
6. Wuringer E. Secondary reduction mammaplasty. Plast Reconstr Surg
2002;109(2):812–814.
7. Patel SP, Brown DL, Cederna PS. Repeated bilateral reduction
mammaplasty: a 12-year experience. Plast Reconstr Surg
2010;126(5):263e–264e.
8. Spaniol JR, Buchanan PJ, Greco RJ. Secondary reduction mammaplasty:
does initial pedicle design matter? J Plast Surg Hand Surg
2019;53(2):105–110.
CHAPTER 42

Management of Complications in
Breast Reduction: The Displaced NAC
NOLAN S. KARP | ARA A. SALIBIAN | JORDAN D. FREY
HISTORY
Reduction mammoplasty is a frequently performed procedure by plastic
surgeons with a high rate of patient satisfaction (1). The majority of reported
complications relate to “reconstructive” problems such as delayed wound
healing, scarring, fat necrosis, and nipple ischemia (2), with aesthetic
concerns such as asymmetry or nipple malposition less frequently described.
However, upon closer examination, malposition of the nipple areola complex
(NAC) seems to be a more pervasive problem than routinely reported, despite
the wealth of discussions dedicated to the appropriate positioning, movement,
and manipulation of this anatomic subunit. Moreover, it is a problem that is
readily noticed by the patient and can be a source of significant distress for
both the patient and the surgeon.
Rates of postoperative NAC asymmetry, malposition, or both vary with the
presence of preoperative discrepancies, the techniques for reduction utilized,
and the methods of analysis. Nipple overelevation has been reported in nearly
42% of cases in a systematic review of mastopexy and reduction (3). Lewin
et al. reported only 26% of nipples in the optimal mediolateral position and
44% in the optimal craniocaudal direction after reduction mammoplasty (4).
Rates of NAC asymmetry in vertical reductions have also been associated
with preoperative asymmetry, increased NAC translocation, and more
extensive reductions (5). In superomedial pedicle, Wise-pattern reductions,
nipple position has been found to be almost 2 cm higher than initially
positioned (6), and in vertical reductions around 1 cm higher than
preoperative markings after 4 years (7). Regardless of particular values, the
incidence of the ill-positioned nipple, whether symmetric or asymmetric, is
not insignificant, and it behooves the plastic surgeon to know when and how
to correct it.
The vast majority of discussions on correcting nipple malposition after
breast reduction have focused on addressing superior displacement of the
nipple. The “high-riding nipple” has likely received the focus of attention as
it is the most common direction of malposition as well as the most difficult to
correct; an undesirable combination. Strombeck commented on the
significant difficulty of correcting the high-riding nipple in 1976 (8) and later
reflected on the commonality of this error in positioning (9). In 1972, Rees et
al. proposed performing a revision reduction with further resection of lower
pole tissue to resituate the nipple (10). However, we know that parenchymal
resection will help further shape the breast, but do little to reorient nipple
position in true cases of superior nipple malposition. The same year, Millard
et al. described similar inferior crescentic skin resections to shorten the
distance between the nipple and the inframammary fold (IMF), but with the
addition of small implants to further project the nipple and minimize
flattening of the breast (11). In addition, the authors proposed a true
downward repositioning of the nipple, which required incisions placed on the
upper pole of the breast, above the new nipple position.
Elsahy et al. later described a revision Wise-type skin excision below the
NAC to decrease the nipple to IMF distance (12). While this does not
technically move the nipple, it alters the breast mound to have the nipple in a
more favorable orientation relative to the lower pole. The need for additional
skin above the nipple was realized soon thereafter as Raffel et al. proposed
utilizing tissue expansion of the upper pole to allow for an absolute change in
position of the nipple (13). This technique has continued to be utilized for
more severe malposition today (14).
While superior malposition is usually the most frequently encountered
direction of displacement, lateral and medial malposition (often a cause of
asymmetry) and inferior malposition are not without occurrence. Taking
steps to correct nipple malposition requires understanding the error that led to
the initial incorrect placement. More often than not, it is an error in planning,
rather than one that is technical in nature. However, many factors, both in and
out of the surgeon’s control, can influence the positional aesthetics of the
nipple after reduction mammoplasty.
NAC PLACEMENT IN BREAST REDUCTION
The most important step in management of nipple malposition is prevention.
Prevention involves familiarity with the morphometrics of the female breast
and the divergence of these parameters in the individual macromastic patient.
Furthermore, meticulous preoperative planning, precise marking, and
obsessive repeated evaluation and alteration of these measurements are
required both preoperatively and in the operating room.
In 1956, Wise first suggested that the optimal position of the nipple should
be at “the most prominent portion of the breast” (15). Identification of the
appropriate new nipple position in reduction mammoplasty has traditionally
involved anterior translocation of the projected IMF position onto the breast
mound with the surgeon’s nondominant hand as described and popularized
by Arié (16) and Pitanguy (17), respectively. Manual translocation of the
IMF is a subjective process that can be highly variable among different
surgeons. The marked nipple position should therefore be checked with the
IMF position laterally and visualized at the projecting portion of the breast
repeatedly to ensure appropriate placement.
The top of the mosque/future areola is subsequently placed 2 cm above this
marking for an areola that is planned to be around 38 to 45 mm in diameter.
If a patient has severe grade III ptosis with a disproportionately long sternal
notch-to-nipple distance, we prefer to mark the top of the area more
conservatively, at only 1 cm above the planned nipple position. The
contralateral nipple must be marked based on fixed landmarks, and not one
that can further confer asymmetry to the other side. In other words,
transposing the contralateral nipple from the IMF will only translate any
asymmetries in IMF position to the nipples. For this reason, the sternal notch-
to-nipple distance is measured on the initial side, and then used to determine
the position of the nipple on the contralateral side. The medial to lateral
position of the nipple is determined by the breast meridian, drawn through the
midpoint of the breast which does not necessarily bisect the preoperative
NAC.
When marking the nipple, it is important to remember that it is always
easier to raise a nipple that is too low, than to lower a nipple that is too high.
With this in mind, one should always defer to a lower position that offers a
significantly more correctable discrepancy in the case of inappropriate
placement. Similarly, the nipple is most aesthetically pleasing at a slightly
lateral projection (18), and therefore one should err in this direction when
questioning the appropriate placement in a particular direction.
In addition to planning based on the current preoperative measurements of
the breast, one must also consider the evolution of breast shape over times, as
changes in shape postoperatively will inevitably affect nipple position. In this
regard, we place the nipple position at 1 to 2 cm below the level of the IMF
when planning inferior pedicle breast reductions, as the breast has a greater
tendency to bottom out over time under the weight of this pedicle. On the
other hand, when a medial or superomedial pedicle will be utilized,
regardless of the skin excision pattern, the new nipple position remains at the
level of the IMF (19).
While new nipple position has traditionally been determined in relation to
translocation of the IMF, others have suggested it is more appropriately
placed according to the overall footprint of the breast mound. Hall-Findlay et
al. advocate using the upper border of the breast as a landmark, and placing
the new nipple position 10 cm below this border (for a C-cup breast) (18).
This creates a nipple position at the projecting portion of the breast and in the
more aesthetically appropriate lower half of the breast mound. Additional
techniques utilize the patient’s breast width to determine the appropriate
nipple-to-IMF length, and subsequently plan the correct new nipple position
from a “bottom-up” approach based on the existing IMF (20).
Regardless of what techniques are used to determine the appropriate nipple
position, the surgeon must be adamant about visualizing the final result,
ensuring symmetry between both sides and constantly rechecking
measurements prior to making incisions. While minor adjustments in the
operating room can be made, it is best to have the ideal results preoperatively,
and minimize changes to one’s plan in the operating room.
INDICATIONS AND CONTRAINDICATIONS
Indications for repositioning of the malpositioned NAC after breast reduction
are dependent on several factors including the direction of displacement, the
severity of the aesthetic deformity, the presence of asymmetry, the overall
aesthetic outcome of the reduction, and the patient’s satisfaction with the
initial result and desire for correction. Superior malposition is typically
treated more aggressively, as this displacement will usually only
progressively worsen with time as the weight of the residual breast
parenchyma will cause some extent of lower pole expansion, lengthening the
nipple-to-IMF distance. Inferior malposition, or an undercorrection of ptosis,
on the other hand, can be treated more conservatively for similar reasons.
Some degree of “bottoming out” of the breast is to be expected, especially
with inferior pedicle reductions, and can make the slightly inferiorly placed
nipple appear to be in a more favorable position over time. Though not
always ideal, it is better to wait for at least a year and let the position of the
breast settle. While this may help mild discrepancies transition from being
perceived as unacceptable to acceptable, more severe inferior displacement
will require some form of mastopexy.
Symmetric and asymmetric discrepancies are also inherently different
complications in that slight asymmetry is inherently displeasing and more
noticeable to the observer. Therefore, asymmetric malposition of the nipple
tends to warrant correction more than symmetric malposition. For example,
nipples that are positioned slightly too laterally or medially, but are
symmetrically deviated, are often more acceptable than a unilaterally
deviated nipple. These principles apply to mild-to-moderate malposition.
Severely malpositioned nipples, in any direction, and regardless of symmetry,
will require correction.
Importantly, these decisions are arrived upon with consideration of the
patient’s satisfaction with the postoperative result and desire for further
correctional procedures. Different degrees of malposition and asymmetry are
acceptable to different patients. Intervention is pursued if the patient desires
correction (21) and the surgeon believes an improvement in the outcome can
be reasonably obtained. Preoperative consultation in their regard is
paramount.
Contraindications to the correction of nipple malposition are limited.
Revisions of the nipple should not be performed in active smokers to
minimize the chance of NAC necrosis, given the baseline increased risk of
ischemic complications of the nipple with secondary manipulation. Revisions
should also not be planned with any ongoing wound healing problems and
surgery should be delayed until well after complete resolution of these issues.
The surgeon should be weary of demands for correction of negligible
discrepancies that may not necessarily be improved with further surgery.
PREOPERATIVE PLANNING
Preoperative photos prior to the initial reduction should be reviewed and
meticulously compared to the most recent postoperative photographs
displaying the offending malposition. It is important to understand not only
the positional changes needed to remedy the current deformity, but the
sequence of changes that led from the planned preoperative markings to the
current undesirable result. Ideally, preoperative markings for the initial
reduction are also reviewed to identify an error in planning or perception that
will be avoided at the secondary revision.
Regardless of the correctional vector or chosen revision technique, certain
standardized markings are needed for all cases of nipple malposition
correction. These markings are similar to those in primary reductions and
provide topographic landmarks from which alterations in nipple position are
planned. With the patient standing, the sternal midline is marked, as well as
the breast meridians bilaterally and the IMFs. Any discrepancies in IMF
height should be noted as this affects the relative position of the nipple on the
breast mound. The desired new location of the nipple on the breast is marked
and the direction and length of needed movement noted. This measurement is
typically based on the position of the IMF; however, one must be careful to
ensure that fold itself is in the correct position. The desired position of the
nipple should be checked relative to the superior border of the breast and
distance from the sternal notch in order to ensure its appropriate placement
with regard to all important landmarks. Subsequently, changes in the
contralateral nipple are marked, if needed, and symmetry of the two sides is
confirmed and rechecked.
INTRAOPERATIVE CARE

Superiorly Displaced NAC


The high-riding nipple is a formidable challenge. The paucity of excess skin
between the nipple and the clavicle and the poor aesthetic tolerance of
incisions in the upper pole of the breast limits the available revisional
procedures that do not further distort the breast.
These procedures can be classified into indirect and direct methods of
correction. The former attempts to mold the remaining breast skin and
parenchyma in order to shorten the distance between the nipple and the IMF.
The latter involves actual translocation of the NAC, usually based on local
flaps or as a free graft. While direct modifications are inherently more
effective means of repositioning the nipple, certain situations, such as those
with milder or relative malposition, can be amenable to indirect measures.
The critical decision therefore is in the appropriate diagnosis of the deformity
and its etiology, in order to be able to apply the correct revisional technique.
Different models have proposed methods to classify and subdivide types of
superior nipple malposition (14,21). In general, these systems tend to rank the
severity of the positional displacement of the nipple and also determine
whether the nipple has remained in a stable position, but the change in the
shape of the breast parenchyma has conveyed an appearance of malposition,
therefore suggesting a pseudo- or relative deformity. While some argue that
nipple position should be determined by its relation the breast mound
irrespectively (22), the important deductions that one must determine from
physical examination are (1) the severity of the nipple displacement and (2)
the presence of an additional breast deformity, such as bottoming out, that
may improve the perceived nipple position if corrected.

Indirect Correction
Indirect “repositioning” of the nipple refers to different methods of reshaping
the skin and breast parenchyma of the lower pole of the breast in order to
improve the relative position of the nipple to the IMF and projecting portion
of the breast mound. These procedures are usually indicated to correct
superior malposition that is a result of parenchymal descent of the lower pole
of the breast below the IMF (23), otherwise known as pseudoelevation (14)
or relative malposition (21) of the nipple. Such patients have a sternal notch-
to-nipple distance that is relatively normal and a long nipple-to-IMF distance
that is colloquially termed “bottoming out” of the breast.
Lower pole parenchymal remodeling effectively raises the IMF, shortening
the nipple-to-IMF distance and reshaping the breast mound around the nipple
to have the nipple sit closer to the lower pole of the breast. This reshaping
can be performed like a circumvertical reduction without additional elevation
of the nipple. Parenchyma is removed from within the wedge resection below
the areola, as well as below the horizontal scar while preserving skin below
the prior scar to be placed back against the chest wall. Removal of this weight
allows the IMF to be raised while preserving the appropriate shape of the
breast (24). If there is a significant excess of skin, a Wise-pattern skin
excision can be performed instead, limiting the excision of skin to above any
prior horizontal scar. The extent of skin resection can be determined by
measuring the desired nipple-to-IMF length and correcting for vertical skin
excess superior to initial horizontal scar. In this situation, tailor tacking can
be useful to determine if manipulation of the lower pole will provide a
satisfactory change to the appearance of nipple position. These techniques
can also be applied in mild absolute elevation of the NAC, but will otherwise
provide unsatisfactory results in more severe cases.
Additional volume to the upper pole will similarly shift the appearance of
the nipple to a lower position the breast bound, albeit only to a certain extent.
Along these lines, implants can also be utilized to affect indirect changes in
nipple position. Changes in nipple position with breast augmentation have
shown that the nipple is lowered an average of 2 cm with breast
augmentation, with a concomitant elevation in the upper breast border (25). A
small implant can be placed through existing scars behind the breast
parenchyma of the upper pole to affect this change (26).
If greater inferior translation of the nipple is required, tissue expanders can
be utilized to increase the amount of available skin of the upper pole (14).
Expanders are placed through existing scars and biased to under the upper
pole to effectively lengthen the height of skin between the nipple and the
clavicle and increase the sternal notch-to-nipple distance. Though a more
extensive procedure, tissue expansion has been described for more severe
superior displacement of the nipple, with movement of the nipple up to 6 cm
while avoiding scars on the upper breast (14). Tissue expansion is typically
utilized alongside lower pole reshaping to maximize change in the shape of
the breast mound. Small implants can also be utilized after expansion to
maintain the form of the upper pole.

Direct Correction
Direct correction of the high-riding nipple is useful for more severe
malposition of the nipple as well as for cases that have an appropriate nipple-
to-IMF length (5 to 7 cm), but a short sternal notch-to-nipple distance.
Patients must be aware that these techniques often result in more visible
scarring as a trade-off for more tangible NAC translation. These flaps
typically involve various methods of local tissue transfer, most commonly
transpositional flaps.
Double transposition flaps (27) utilize a random-pattern pedicle to move
the NAC to the desired location while a symmetric flap is transposed to fill
the NAC donor site (Fig. 42-1). The areolar margin is marked as well as the
adjacent desired location of the NAC of the same circular size. Pedicles are
designed in opposite directions (either medial/lateral or superior/inferior) for
each flap based on the maximal perfusion as determined by prior scars.
Superficial medial perforators can be incorporated into the medial NAC
pedicle if design is amenable.
FIGURE 42-1 Reciprocal rotation flaps for correction of significant superior NAC
malposition. The high-riding right NAC (red dotted line) is moved inferior as a
transposition flap based on a pedicle roughly the width of its diameter (red solid
line). The donor defect is templated based on the desired new position of the NAC
(blue circle), and transposed superiorly with a similar pedicle (blue solid line) to fill
the donor defect.
FIGURE 42-2 V-Y advancement flap for correction of mild superior NAC
malposition. An upside-down “V” is marked above the nipple (red lines). The NAC is
mobilized (blue dotted line) and the superior triangle advanced inferiorly in a V-Y
fashion (red arrow). This technique only allows for small changes in position and
leaves a scar above the NAC.

Both flaps are incised sharply and elevated at the level of the deep
subcutaneous fat. The use of electrocautery should be minimized and care
should be taken to undermine the transposition flaps only as needed for a
tensionless closure to minimize devascularization of the NAC. Both flaps are
subsequently secured with absorbable suture. Similar varieties of this
procedure include a Z-plasty (28) or a U-plasty (29) design. Advancement
flaps can also be utilized but tend to gain less advancement. A V-Y
advancement can be performed to move the nipple down by designing and
upside “V” at the heightened nipple and subsequently closing superiorly to
inferiorly after mobilizing the NAC (Fig. 42-2). This results in a linear scar
just above the nipple but typically leaves the upper breast pole scar free.
With severe displacement, local tissue transfer may not be adequate to
achieve the desired movement of the NAC. In these cases, the nipple and
areola can be removed and grafted as a full-thickness skin graft to the desired
location, with a reciprocal skin graft from the recipient site used to cover the
donor (30). A circular incision is designed around the existing areola, and a
circle of the same diameter is marked at the new site of the NAC. Both the
NAC and the recipient site skin graft are removed as full-thickness grafts,
transferred to reciprocal sites, and bolstered after suturing in place. Patients
must understand that a visible circular scar will remain at the prior site of the
displaced NAC with this technique.
Inferiorly Displaced NAC
Inferior malposition of the nipple may be secondary to inadequate elevation
at the time of primary reduction mammoplasty, or more commonly with
recurrent ptosis of the breast over time. When an inferiorly displaced nipple
is encountered in secondary breast reductions, it is usually accompanied with
a more common complaint of bottoming out of the breast. Often, glandular
ptosis will actually result in pseudoelevation of the NAC; however recurrent
nipple ptosis can also be seen.
Cases of recurrent ptosis or inferior nipple displacement can be addressed
with a variety of techniques, depending on the severity of displacement. An
overarching principle in these cases is that perfusion to the NAC can usually
be maintained with a random-pattern blood supply by deepithelializing
around the nipple only, rather than attempting to recreate the original pedicle,
especially if the pedicle was unknown (24). The limitations of this technique,
however, must be appreciated, as larger movement of the NAC (greater than
5 to 6 cm) is not recommended. In these cases, conversion to a free nipple
graft may be the best option. Others have advocated using a superior or
superomedial dermoglandular pedicle, again with emphasis on preservation
of the random-pattern, subdermal blood supply (31). Interestingly, the only
reported cases of total NAC necrosis after secondary breast reduction utilized
an inferior pedicle for the revision procedure, regardless of the pedicle
utilized in the initial reduction (32). Inferior pedicles have also been
associated with the highest complication rates after repeat reductions in prior
studies (33).
Minor elevation of the NAC (∼1 cm) can be achieved with a periareolar
mastopexy (Fig. 42-3). The new position of the nipple is marked and the
upper border of the areola is correspondingly translated higher. An ellipsoid
incision is designed starting from the new upper border of the areola and
encircling the inferior border of the areola. The desired cookie cutter size is
used to determine the new areolar diameter and all markings are superficially
incised. The intervening skin is deepithelialized and the areola is tailor tacked
into its new position. If a significant reduction in areolar diameter is
performed, a deep subdermal nonabsorbable purse-string suture may be
needed to prevent areolar widening. The areola is subsequently closed in a
layered fashion with absorbable suture. Modest elevation can be successfully
achieved with this technique; however, more significant elevation will only
result in distortion of the nipple and excess tension.

FIGURE 42-3 An ovoid periareolar mastopexy is designed (red solid line) with the
superior aspect of the template positioned at the new desired position of the superior
areola. The NAC is incised using the desired cookie cutter pattern (red dotted line)
and mobilized superior to the appropriate position.
If further elevation is needed, a vertical mastopexy can be performed. This
is particularly useful if the nipple-to-IMF distance is also increased, as the
vertical skin tightening can reset the IMF to the appropriate position and
reshape the lower pole. Similarly, the new nipple and areola position are
determined and mosque is designed based on the new desired position.
Gentle displacement is used to determine the medial and lateral extents of the
circumvertical incision ensuring that the inferior extent of the vertical skin
excision stops prior to any horizontal scar in the lower pole. The mosque and
vertical excision are meticulously deepithelialized to preserve the underlying
subdermal random-pattern blood supply. The T-point of the inferior areola is
subsequently set with a nylon suture and the remainder of the incisions are
tailor tacked together and subsequently closed. If further elevation is needed,
the dermis can be scored and a partial-thickness superior or superomedial
pedicle is developed.
If additional reduction is required at the time of nipple elevation, breast
parenchyma is resected as a vertically-oriented “V” wedge below the nipple
in combination with lateral liposuction as needed. Finally, if there is
significant excess skin in the horizontal vector of the lower pole, a more
traditional Wise-pattern skin excision can be utilized. Care should be given to
limit skin excision only to above the true IMF to let the remainder of the
lower pole skin redrape over the chest wall and avoid iatrogenically lowering
the fold (24).
Medially and Laterally Displaced NAC
Medial and lateral displacement of the nipple typically results in some degree
of asymmetry after breast reduction. Malposition in either direction is likely a
consequence of poor markings as significant deformational forces do not
typically act in the transverse plane postoperatively. Correctional techniques
are similar to those for superior and inferior malposition, and are based on the
severity of displacement.
For mild deformities (<1 cm), a crescentic skin excision can allow for
some movement without significantly increasing scar burden. A crescent is
marked along the areolar border of the desired change in direction, and the
intervening skin subsequently deepithelialized and closed. V-Y advancement
flaps can also be utilized using a technique similar to correction of high-
riding areolas.
If additional movement is needed, and particularly if there is another
vertical vector of change required, medial or lateral movement can be
incorporated into a mastopexy design. As with reelevation of the inferiorly
displaced nipple, the mosque or Wise pattern can be drawn to also move the
nipple medially or laterally in addition to any necessary vertical vector.
POSTOPERATIVE CARE
Patients undergo standard postoperative care after revision procedures to
correct NAC malposition. They are discharged home on the same day of
surgery with nonnarcotic pain medications and are seen in the office around 1
week after the operation.
Drains are almost never utilized unless a large secondary reduction was
performed with significant dead space. If drains are placed, they are almost
always removed a few days after the procedure. Patients are allowed to
shower 24 to 48 hours after the procedure and will concomitantly remove any
outer nonadherent dressing themselves at this point. Activity restrictions are
typically lifted 2 to 3 weeks after the procedure unless more extensive
secondary parenchymal manipulation was performed.

CASES

CASE 1

A 25-year-old female with bilateral macromastia who had previously


undergone two prior reductions with other providers, with persistent
symptomatic macromastia (Fig. 42-4). The patient had bilateral
pseudoptosis with nipple asymmetry and right superior NAC malposition.
Preoperative bra size was 32G. Patient underwent bilateral Wise-pattern
breast reduction with inferior wedge excision of skin and breast
parenchyma (right: 386 g; left: 484 g) with subsequent improvement in
breast size, nipple-to-inframammary fold length, and symmetry.
FIGURE 42-4 A 25-year-old female with bilateral macromastia who had
previously undergone two prior reductions with other providers with
persistent symptomatic macromastia. (Above) Preoperative photographs
demonstrating bilateral pseudoptosis with nipple asymmetry and right
superior NAC malposition. Preoperative bra size was 32G. Patient underwent
bilateral wise-pattern breast reduction with inferior wedge excision of skin
and breast parenchyma (right: 386 g; left: 484 g). (Below) Postoperative
photographs demonstrating improved size, nipple-to-inframammary fold
length and symmetry.

CASE 2

A 27-year-old female with a prior history of breast augmentation and


subsequent bilateral breast reduction after significant breast growth upon
starting oral contraceptives. The patient presented persistent symptomatic
macromastia as well as areola size mismatch and left superior NAC
malposition (Fig. 42-5). She underwent bilateral Wise-pattern, superior
pedicle breast reduction and concomitant breast implant explantation with
subsequent improvement in breast symmetry and nipple position. Right
and left specimen weights including implants were 450 g and 446 g,
respectively.

FIGURE 42-5 A 27-year-old female with prior history of breast


augmentation and subsequent bilateral breast reduction with an outside
provider after significant breast growth upon starting oral contraceptives.
(Above) Preoperative photographs demonstrate persistent macromastia as
well as areola size mismatch and left superior NAC malposition. Patient
underwent bilateral Wise-pattern, superior pedicle breast reduction and
concomitant breast implant explantation. Right and left specimen weights
including implants were 450 g and 446 g, respectively. (Below) Postoperative
photographs demonstrating improved symmetry and nipple position.

CASE 3

A 47-year-old female with a history of prior breast reduction with another


provider presenting with persistent symptomatic macromastia. The
patient demonstrated severe bilateral pseudoptosis, left partial areola
necrosis, breast size asymmetry, and right superior NAC malposition. She
underwent bilateral revision breast reduction with Wise-pattern skin
excisions with subsequent correction of pseudoptosis as well as improved
symmetry in breast size and NAC position (Fig. 42-6).

FIGURE 42-6 A 47-year-old female with a history of prior breast reduction


with another provider presenting with persistent symptomatic macromastia.
(Above) Preoperative photographs demonstrate severe bilateral pseudoptosis,
left partial areola necrosis, breast size asymmetry, and right superior NAC
malposition. The patient underwent bilateral revision breast reduction with
Wise-pattern skin excisions. (Below) Postoperative photographs demonstrate
correction of pseudoptosis as well as improved symmetry in breast size and
NAC position.
GENERIC RISKS
Major complications with NAC repositioning are relatively rare, as
manipulation of the skin and soft tissues during these procedures are typically
more conservative. The most commonly encountered postoperative issue is
undercorrection of the deformity, particularly if attempting to correct superior
malposition. The difficulty of correcting superior malposition must be
discussed with the patient preoperatively, and the appropriate expectations set
preemptively. Persistent asymmetry (if performing a unilateral correction) or
introduction of asymmetry (if performing a bilateral correction) can also be
encountered, but are generally avoidable if careful preoperative planning and
measurements are performed. Overcorrection of a deformity is less common,
but is more likely if correcting inferior malposition, secondary to similar
errors in measurements made during the primary reduction.
Nipple areola complex ischemia or necrosis is the most feared
complication when manipulating the NAC in secondary revisions, but is
fortunately rare if proper planning and surgical technique are executed.
Meticulous deepithelialization of the skin being excised around the areola
should be performed. If a dermoglandular pedicle is to be utilized, inferior
pedicles should be avoided for secondary procedures given their higher rate
of complications, regardless of the original pedicle choice (33). Importantly,
one must be conscientious of the limits of a specific procedure in moving the
nipple and areola as pushing a technique beyond its capabilities in terms of
the extent of movement may predispose to tissue ischemia.
Larger movements of the areola may result in distortion of the areola
aesthetic subunit, particularly if a type of advancement is being utilized
beyond its capabilities. Reoperation may worsen scarring and scar widening
especially if the NAC is inset under tension. Distortion of the remainder of
breast should also be considered and simulated closure with tailor-tacking
staples utilized to predict the final shape of the breast before final incisions
are made.
If more extensive parenchymal reshaping is being performed, additional
complications such as hematoma, seroma, and fat necrosis, similar to the
risks of primary reductions, become more relevant. Along the same lines,
with significant manipulation of the skin envelope, the increased possibility
of wound dehiscence and wound healing problems should be considered.
OUTCOMES
Outcomes with nipple malposition are dependent on the severity of original
deformity and the results that are being analyzed. Reconstructive outcomes
are good, with low rates of complications. Cosmetic outcomes are inherently
dependent on the degree and direction of malposition. While severe inferior
malposition can be easily corrected, superior malposition is significantly
more challenging. Correction of mild and moderate superior displacement
with both indirect and direct techniques can have excellent outcomes.
However, more severe superior displacement may often have some degree of
residual malposition or a trade-off of scars placed on the upper pole of the
breast.

TABLE 42-1 Techniques for Correction of Superior Malposition


Indirect Correction
Lower pole parenchymal reshaping
Circumvertical reduction
Upper pole implant augmentation
Upper pole tissue expansion
Direct Correction
Reciprocal transposition flap
Z-plasty, U-plasty
V-Y advancement
Reciprocal skin grafts

TABLE 42-2 Techniques for Correction of Inferior Malposition


Crescentic excision
Periareolar mastopexy
Vertical mastopexy
Wise-pattern skin excisions
Most outcomes data are in the setting of secondary reductions, which may
or may not involve correction of nipple malposition. In these cases,
complications are typically similar to those experienced with primary
reductions, including delayed wound healing, seroma, and asymmetry,
though with a higher rate of ischemic complications of the nipple (33–35).
These issues can be minimized by ensuring good subdermal blood supply to
the nipple, limiting skin excision to only what is required, maintaining a
superior/superomedial pedicle (only if needed), as well as measuring and
confirming markings repeatedly preoperatively.
CONCLUSION
The malpositioned nipple is a difficult but treatable complication after
reduction mammoplasty. Techniques for correction of superior malposition
can be divided into indirect and direct procedures that are chosen depending
on the severity of nipple displacement as well as the presence of additional
breast deformities. While indirect techniques place less scars on the visible
upper pole of the breast, direct procedures are more favorable in cases with
absolute increases in nipple height relative to the sternal notch and a normal
nipple-to-fold distance (Table 42-1).
Inferior malposition of the nipple can be treated with various mastopexy
techniques that can be used to successfully elevate the nipple based on the
severity of nipple displacement (Table 42-2).
Medial and lateral malpositions are amenable to direct excisions, local
tissue rearrangements, and mastopexy (Table 42-3).
Successful outcomes in correction of nipple malposition are dependent on
a thorough understanding of the causative etiology, meticulous preoperative
planning, and methodical execution of the appropriate correctional procedure
to optimize restoration of the desired aesthetic result.

TABLE 42-3 Techniques for Correction of Medial and Lateral Malposition


Crescentic excision
V-Y advancement
Mastopexy

REFERENCES

1. Cogliandro A, Barone M, Cassotta G, et al. Patient satisfaction and


clinical outcomes following 414 breast reductions: application of
BREAST-Q. Aesthetic Plast Surg 2017;41:245–249.
2. Cunningham BL, Gear AJ, Kerrigan CL, et al. Analysis of breast
reduction complications derived from the BRAVO study. Plast Reconstr
Surg 2005;115:1597–1604.
3. Swanson E. A retrospective photometric study of 82 published reports of
mastopexy and breast reduction. Plast Reconstr Surg 2011;128:1282–
1301.
4. Lewin R, Widmark-Jensen E, Plate N, et al. Objective evaluation of
nipple position after 336 breast reductions. J Plast Surg Hand Surg
2018;52:198–203.
5. Adham M, Sawan K, Lovelace C, et al. Unfavorable outcomes with
vertical reduction mammaplasty: part II. Aesthet Surg J 2011;31:40–46.
6. Altuntas ZK, Kamburoglu HO, Yavuz N, et al. Long-term changes in
nipple-areolar complex position and inferior pole length in superomedial
pedicle inverted ‘T’ scar reduction mammaplasty. Aesthetic Plast Surg
2015;39:325–330.
7. Ahmad J, Lista F. Vertical scar reduction mammaplasty: the fate of
nipple-areola complex position and inferior pole length. Plast Reconstr
Surg 2008;121:1084–1091.
8. Strombeck JO. Reduction mammaplasty by upper and lower glandular
resections. In: Goldwyn RJ, ed. Plastic and Reconstructive Surgery of
the Breast. Boston, MA: Little, Brown; 1976:165.
9. Strombeck JO. Reduction mammaplasty: some observations and
reflections. Aesthetic Plast Surg 1983;7:249–251.
10. Rees TD, Flag SV. Reduction mammoplasty. In: Goldwyn RM, ed. The
Unfavorable Results in Plastic Surgery: Avoidance and Treatment.
Boston, MA: Little, Brown; 1972:383.
11. Millard DR Jr, Mullin WR, Lesavoy MA. Secondary correction of the
too-high areola and nipple after a mammaplasty. Plast Reconstr Surg
1976;58:568–572.
12. Elsahy NI. Correction of abnormally high nipples after reduction
mammaplasty. Aesthetic Plast Surg 1990;14:21–26.
13. Raffel B. Technique for correction of areola misplacement with no new
scars. Plast Reconstr Surg 1991;88:895–897.
14. Colwell AS, May JW Jr, Slavin SA. Lowering the postoperative high-
riding nipple. Plast Reconstr Surg 2007;120:596–599.
15. Wise RJ. A preliminary report on a method of planning the
mammaplasty. Plast Reconstr Surg (1946) 1956;17:367–375.
16. Arié G. Una nueva técnica de mastoplastia. Rev Latinoam Cir Plast
1957;3:23–31.
17. Pitanguy I. Breast hypertrophy. In: Wallace AB, ed. Transactions of the
Second Congress of the International Society of Plastic Surgeons.
Edinburgh: Livingstone; 1960:509.
18. Hall-Findlay EJ, Shestak KC. Breast reduction. Plast Reconstr Surg
2015;136:531e–544e.
19. Karp NS. Medial pedicle/vertical breast reduction made easy: the
importance of complete inferior glandular resection. Ann Plast Surg
2004;52:458–464.
20. Tebbetts JB. A process for quantifying aesthetic and functional breast
surgery: I. Quantifying optimal nipple position and vertical and
horizontal skin excess for mastopexy and breast reduction. Plast
Reconstr Surg 2013;132:65–73.
21. Spear SL, Albino FP, Al-Attar A. Classification and management of the
postoperative, high-riding nipple. Plast Reconstr Surg 2013;131:1413–
1421.
22. Swanson E. Defining nipple displacement, and the prevention and
treatment of the high-riding nipple. Plast Reconstr Surg 2014;133:64e–
66e.
23. Small KH, Tepper OM, Unger JG, et al. Re-defining pseudoptosis from
a 3D perspective after short scar-medial pedicle reduction
mammaplasty. J Plast Reconstr Aesthet Surg 2010;63:346–353.
24. Mistry RM, MacLennan SE, Hall-Findlay EJ. Principles of breast re-
reduction: a reappraisal. Plast Reconstr Surg 2017;139:1313–1322.
25. Hall-Findlay EJ. The three breast dimensions: analysis and effecting
change. Plast Reconstr Surg 2010;125:1632–1642.
26. Spear SL, Albino FP. Management of the high-riding nipple after breast
reduction. Clin Plast Surg 2016;43:395–401.
27. Spear SL, Albino FP, Al-Attar A. Repairing the high-riding nipple with
reciprocal transposition flaps. Plast Reconstr Surg 2013;131:687–689.
28. Frenkiel BA, Pacifico MD, Ritz M, et al. A solution to the high-riding
nipple-areola complex. Aesthetic Plast Surg 2010;34:525–527.
29. Mohmand H, Naasan A. Double U-plasty for correction of geometric
malposition of the nipple-areola complex. Plast Reconstr Surg
2002;109:2019–2022.
30. Spear SL, Hoffman S. Relocation of the displaced nipple-areola by
reciprocal skin grafts. Plast Reconstr Surg 1998;101:1355–1358.
31. Ahmad J, McIsaac SM, Lista F. Does knowledge of the initial technique
affect outcomes after repeated breast reduction? Plast Reconstr Surg
2012;129:11–18.
32. Austin RE, Lista F, Ahmad J. Management of recurrent or persistent
macromastia. Clin Plast Surg 2016;43:383–393.
33. Patel SP, Brown DL, Cederna PS. Repeated bilateral reduction
mammaplasty: a 12-year experience. Plast Reconstr Surg
2010;126:263e–264e.
34. Hudson DA, Skoll PJ. Repeat reduction mammaplasty. Plast Reconstr
Surg 1999;104:401–408.
35. Sultan MR, Schwartz JA, Smith ML, et al. Revision of Wise pattern
breast reductions with vertical procedures. Ann Plast Surg 2013;71:300–
303.
CHAPTER 43

Male Breast Reduction: Liposuction


Versus Excision
CHARLES M. MALATA | SAMUEL G. COULSON

Male breast reduction is performed for gynecomastia and


pseudogynecomastia. Gynecomastia is benign enlargement of the male breast
due to the proliferation of glandular, fibrous, and fatty tissue.
Pseudogynecomastia or lipomastia is proliferation of breast adipose tissue
without a concomitant increase in the glandular component. Both conditions
may occur with or without skin excess. Male breast enlargement is a common
problem and male breast reduction is one of the commonest male aesthetic
procedures performed being 3rd in the United States (1) and 4th in the UK
(2). In 2018 for instance 24,753 and 285 such cases were performed in the
United States and UK, respectively (1,2). This is not surprising as surgery is
the most effective treatment modality for male breast enlargement. This dates
to the 7th century AD by Paulus Aegineta.
Surgery is indicated if the breast enlargement is persistent, fails to respond
to medical therapy, or is in the fibrous phase. By far the commonest
indication is the psychological effect of the enlarged male breasts with a
female chest wall contour. The goal of any corrective therapy is to restore a
normal masculine contour to the chest with minimal scarring while
maintaining the viability of the nipple areolar complex (NAC) (3).
There are two principal modalities for reducing enlarged male breasts,
namely liposuction and excision, and these may be used alone or in
combination. Indeed, the biggest advance in the treatment of gynecomastia
was the advent of liposuction when combined with open excisional surgery
(3–6). Contemporary surgical options currently focus on initial liposuction
for the removal of excess fatty tissue while several excisional modalities are
used for the removal of any residual glandular tissue and/or excess skin. This
chapter provides a comparative analysis of the roles of liposuction and
excision in the treatment of gynecomastia. It is a distillation of the senior
author’s personal experience over a 20-year period (3,7–13).
INDICATIONS AND DECISION MAKING
Gynecomastia can be physiologic, pathologic, pharmacologic, or most
commonly idiopathic. Diagnosis is made by careful history and clinical
examination. It can present as a unilateral or bilateral condition. Unilateral
gynecomastia should always raise the suspicion of malignancy, especially if
firm, nontender, irregular and not located behind the NAC. Specialized
imaging is only indicated where there is suspicion of breast cancer. Most
patients present to plastic surgeons after work-up by the endocrinologists,
pediatricians, oncologic breast surgeons, urologists, general practitioners
(GPs), radiotherapists, etc.
Indications for surgical intervention in gynecomastia are shown in Table
43-1. Psychological “morbidity” is the most frequent indication for surgery.
A recent systematic review found that surgical management is beneficial in
improving a number of psychological domains in gynecomastia patients (14).
The choice of surgical treatment of gynecomastia and pseudogynecomastia
depends on the grading characteristics of the breast (Table 43-2). Although
Simon et al.’s (15) and Rohrich et al.’s (16) classifications are generally
useful, there is some overlap between the categories leading to interobserver
variability and therefore a lack of reliability in treatment algorithms based on
such grading systems. Additionally, of the many published algorithms none
are universally applicable to all causes of gynecomastia (17). The ideal
classification should guide surgery and be easy to use. At the same time
Waltham et al. recommend that it must ideally include “a comprehensive set
of clinically appropriate patient-related features, such as breast size, breast
ptosis, tissue predominance, and skin redundancy” (17). In our practice we
classify patients into two groups: small to moderate size with minimal skin
excess, and moderate to large size with skin excess (3,10). We also assess the
breast shape and consistency besides the presence or otherwise of well-
developed inframammary folds (IMFs).

TABLE 43-1 Indications for Male Breast Reduction


• Persistent enlargement following puberty >2 yrs and exclusion of medical
causes
• Failure of medical treatment
• Severe breast enlargement
• Unilateral disease or significant asymmetry
• Severe psychosocial effects or morbidity
• Patient wishes
• Gynecomastia in the fibrous phase
• Post massive weight loss
• Specific pharmacologic causes:
• Prostate cancer treatment
• Anabolic steroid or cannabis use (likely to fail medical treatment)

TABLE 43-2 Classification of Gynecomastia


Simon et al.’s Classification of Gynecomastia (1973) (15)
Grade Features
Grade 1 Small enlargement, no skin excess.
Grade 2a Moderate enlargement, no skin excess.
Grade 2b Moderate enlargement, with skin excess.
Grade 3 Marked enlargement, with skin excess.
Rohrich et al.’s Classification of Gynecomastia (2003)a (16)
Grade Features
Grade I Minimal hypertrophy (<250 g) without ptosis.
IA Primarily glandular.
IB Primarily fibrous.
Grade II Moderate hypertrophy (250–500 g) without ptosis.
IIA Primarily glandular.
IIB Primarily fibrous.
Grade III Severe hypertrophy (>500 g) with grade 1 ptosis (glandular
or fibrous).
Grade IV Severe hypertrophy with grade 2 or 3 ptosis (glandular or
fibrous).
aThe problem with this classification is that it does not refer to the fatty glandular tissue with
predominantly fatty tissue, a common occurrence.

As with any aesthetic procedure, another crucial factor in technique


selection is the willingness of the patient to accept the invasiveness of the
surgical modality weighed against its achievable results. There are multiple
surgical treatment options available for reducing male breasts and these have
been eloquently described elsewhere (12). These various techniques fall into
the broad categories of liposuction, minimally invasive excision, and open
excision with the latter including skin excision (Table 43-3). Historically
surgery comprised open excision in the form of subcutaneous mastectomy
with or without skin excision. While this is very effective at removing the
subareolar fibrous discs and firm glandular tissue, it can leave unacceptable
scars, contour irregularities, and/or saucer deformities. Liposuction
revolutionized the treatment of gynecomastia by being less invasive, reducing
the scars, and decreasing the pool of patients who needed open excision. It
also improved the results of or complemented open excisions (principally by
feathering the peripheries and facilitating the excision). Consequently a
number of treatment algorithms were proposed to rationalize the surgical
treatment of gynecomastia/male breast reduction (3,4,15–18).
TREATMENT
Enlargement of the male breast due to benign proliferation of ductal, stromal,
and/or fatty tissue is a common condition which may affect up to 70% of men
at some stage of their lives (12,19). However, not all patients require
treatment. Mild cases of gynecomastia or pseudogynecomastia can
adequately be treated by dietary advice, reassurance, and weight management
(20). Certainly, in pubertal cases there is a high rate of resolution without
intervention and so observation for at least 1 to 2 years should be the first-
line treatment following appropriate investigation (20). However, if
gynecomastia is in its fibrous phase, or present for more than 1 year, it is
unlikely to regress. In these circumstances it is best to resort to surgery to
achieve aesthetic correction and psychological amelioration of the symptoms.
Surgery is the mainstay of treatment and falls into two main categories,
namely liposuction and excisional techniques (Table 43-3).
The focus of the remainder of this chapter will be on the use of liposuction
and surgical excision (including skin reduction). The authors feel that these
two treatment modalities should not be viewed as mutually exclusive, rather
that they are tools to be employed dependent on the surgeon’s assessment and
patient’s wishes and in practice are indeed complementary and carried out
simultaneously.

TABLE 43-3 Surgical Options for Reducing Enlarged Male Breasts


Liposuction/Lipolysis Minimally Invasive Open Excision
Excision Techniques Techniques
Liposuction— Pull-through Webster
conventional (SAL) periareolar
Liposuction—ultrasonic Arthroscopic Circumareolar
(UAL) morselisation/shaver
Liposuction—power Vacuum-assisted biopsy Transareolar
assisted (PAL) (VAB) device
Laser-assisted lipolysis Endoscopic, for example, Circumthelial
(LAL) single incision
Radiofrequency-assisted Microdebrider Subcutaneous
liposuction mastectomy
VASERa assisted Skin reductionb
aVibration amplification of sound energy at resonance.
bSee Table 43-6 for skin reduction types.
OPERATIVE TECHNIQUES
LIPOSUCTION

History
Liposuction, in any of its guises, represents the least invasive technique for
the surgical correction of gynecomastia. Modern liposuction, first described
in 1975 by Fischer and Fischer (21) and popularized by Illouz, has become
the mainstay for gynecomastia treatment (4,10,20,22). As most commonly
performed conventional/traditional liposuction, also known as suction-
assisted lipectomy (SAL), has been used for gynecomastia treatment since the
1980s (6,22).
General Considerations and Conventional Liposuction
The benefits of liposuction are that it is minimally invasive, allows bespoke
contouring with feathering to the peripheries, and leaves minimal scarring
(4,6,23–25). A number of modalities have been employed to augment the
process of liposuction, including power-assisted, ultrasound-assisted, laser-
assisted, and vibration amplification of sound energy at resonance (VASER)
(26).
Liposuction is accepted to be the gold standard treatment for addressing
unwanted lipomatous tissue at any site in the body, and this is no different in
the treatment of diffuse breast enlargement of soft to moderately firm
consistency in gynecomastia patients (3,8,12,22,27,28). There is however a
divide in the literature as to the effectiveness of liposuction alone in
addressing the firmer glandular tissue in gynecomastia correction. Some
studies contend that liposuction alone is an effective treatment in
pseudogynecomastia as well as Simon grade 1 and 2 disease
(3,12,13,23,25,27,29–31). Certainly, there is some evidence that when
addressing the excess skin in grades 2b and 3 disease the use of laser-assisted
and conventional liposuction modalities alone can cause sufficient skin
retraction and reduce the sternal notch-to-nipple distance consistently by 1
cm as well as reduce the NAC surface area by 20%, with positive satisfaction
rates of 92% to 96%, respectively (30,31).
Those wishing to utilize liposuction alone to address the glandular
component of the disease recommend a wide range of cannulae to achieve
satisfactory results, namely barbed, forked, spatulated, sharp, reverse cutting,
to name but a few (23,28,32,33). In our practice we do not employ atypical
sharp cannulas due to the potential risk of intra- and postoperative bleeding.
The liposuction is done via a variety of incisions namely IMF (19,22),
transaxillary (22,23,34), transareolar (22,35), and anterior axillary fold (3)
and often with a combination (Fig. 43-1) (3,19).
The senior author is a proponent of crosstunneling in cases where there is a
large volume of excess tissue, ptosis, and a prominent or well-defined IMF in
order to give more consistent contraction of the skin and to break up/disrupt
the IMF. Some surgeons feel this can be achieved through a single incision,
such as a concealed transaxillary approach (34). We prefer to use two-access
ports away from the areola to allow crisscross treatment (3,10,21). A superior
incision also enables a more efficient undermining and disruption of well-
developed IMFs thus allowing better redraping and contraction of the skin in
this area (Fig. 43-1).
Power-Assisted Conventional Liposuction
Power-assisted liposuction is a common modality for the treatment of
gynecomastia (36,37). It increases the amount of tissue that can be removed
compared to standard, conventional, or traditional liposuction. It also reduces
surgeon fatigue and allows better surgeon control in the contouring of the
chest (36).
Liposuction With New Devices (Nonconventional Liposuction)
Other techniques of liposuction like ultrasound-assisted liposuction (UAL),
VASER, laser-assisted liposuction (LAL), radiofrequency-assisted
liposuction (RFAL), etc. liquefy the fat at the same time as contracting
vessels (to reduce blood loss) and promoting skin tightening (8,19,30,31,38).
These modalities are particularly useful in fibrous fatty tissue as this is not
amenable to correction alone. They have also widened the pool of
gynecomastia patients who can effectively benefit from this minimally
invasive technique. They are also particularly effective in redo cases
(recurrence, recalcitrant, or persistent cases) (8,19,38). Often these methods
are combined with a variety of excisional techniques especially those which
are minimally invasive. Rohrich’s group have, for instance, recently
presented a technique which combines ultrasonic liposuction and a pull-
through removal of residual breast tissue (19). An outline of nontraditional
liposuction methods used for male breast reduction is given below.

Ultrasound-Assisted Liposuction or Ultrasonic Liposuction for


Gynecomastia
UAL, first described by Zocchi, has been found to selectively target adipose
tissue, which is particularly useful in the setting of gynecomastia correction
(8,13,16,39–42) and is now a widely accepted (and indeed preferred)
treatment for gynecomastia (8,13,18,43). UAL breaks up the dense
fibroconnective tissue of gynecomastia more efficiently than conventional
liposuction. It has been established that at higher-energy settings UAL can
remove the dense parenchymal tissue that SAL leaves behind (8,16). In a
direct comparison of UAL and SAL Wong and Malata found that UAL had a
lower intraoperative conversion rate to open excision and lower late revision
rate thus confirming the superiority of UAL for gynecomastia. UAL benefits
include less bruising, improved contour, increased skin retraction, and lower
rates of conversion to open surgical excision and recurrence
(8,13,16,27,39–41). In the authors’ opinion UAL is the preferred modality of
liposuction when available.
FIGURE 43-1 SAL alone: A 59-year-old patient treated with conventional
liposuction alone. This is widely available in most hospitals. Planning A–C:
Concentric circles denote the areas to be liposuctioned. The + sign signifies the larger
left breast. The Xs are the areas not to be suctioned or to be gentle with suction. The
old IMF is marked with dots so as to target it during the suction procedure. The
inferior extent of the liposuction and pretunneling is well below the IMF. This allows
better redraping of the skin. During planning all patients are consented for + or −
open excision. There was no need for open excision during surgery. Pre- and 7-
month postoperative appearances (D–M).
UAL like other liposuction techniques leads to minimal scarring. Other
advantages include superior/improved skin retraction which obviate the need
for skin resection even in patients with grade III and IV gynecomastia (19).
The key feature of UAL is the “efficient removal of both glandular and
fibrotic breast tissue” (19). UAL is an effective treatment and often used as a
sole treatment modality for the correction of gynecomastia (Fig. 43-2)
(8,16,39,40). High energy levels are used and increased especially under the
nipple to help in removing the fibrous glandular tissue. Additionally,
targeting the immediate subdermal layer increases skin contraction but
caution is needed to avoid thermal injury.
The limitations of UAL are that it is technically more demanding and has a
steep learning curve, needs complex and bulky equipment which is more
expensive, is not widely available, has a higher potential for complications
and notably an increased incidence of skin necrosis (when combined with
open excision), and there are a multitude of safety precautions to adhere to
(8,44–46). There are several reports of successful combination of UAL with
subareolar excision techniques (18,47).

Vibration Amplification of Sound Energy at Resonance Liposuction for


Gynecomastia
This is a newer form of UAL, using pulsed and continuous ultrasonic energy
which many consider safer than standard UAL when treating fibrous areas
close to the surface of the skin (26). The process requires similar incisions
and infiltration as with SAL, PAL, and UAL, but requires comparatively
lower amounts of ultrasonic energy than UAL. As with UAL, VASER is a
pretreatment (fat emulsification and liquefaction) prior to evacuation by
standard liposuction with a narrow (2.9- to 3.7-mm diameter) probe and a
grooved tip. The skin puncture incision still requires protection with a port
site and the surrounding skin with a wet towel. The probe is kept moving
with gentle axial movements and should require less force than that with PAL
or SAL. “End-hits” and “punching” of the dermis should be avoided. The
VASER pulsed mode is described for finer more delicate work and the
continuous mode for firmer gland areas. Due to the relatively reduced energy
the safety profile is better compared to earlier generations of UAL (26).

Laser-Assisted Lipolysis in Gynecomastia


Laser-assisted lipolysis has also been used for the correction of gynecomastia
using the Nd:YAG laser at varying wavelengths (25,48). Again, this
technique requires similar incisions and infiltration as for SAL and PAL. The
absorption of the light energy and conversion to thermal energy causes
lipolysis due to expansion and rupture. The 2-mm diameter probe has an
exposed 1 to 2 mm of a fiberoptic tip using ultrashort pulses at high peak
power. Although this technique is promising the experience is limited, and its
usefulness remains to be defined (25,49).

Radiofrequency-Assisted Liposuction in Gynecomastia (38,50)


Radiofrequency energy is transmitted from a small-diameter internal probe to
a large external receiver placed on the skin. The transmission through the
tissues leads to thermal energy thus simultaneously causing lipolysis, vessel
coagulation, and dermal contraction, similar to UAL and VASER. The
benefit in this case is that the fat evacuation and contouring parts of the
procedure (liposuction) can be performed simultaneously. The same incisions
and infiltration as with the other aforementioned techniques is required.
Outcomes in Liposuction for Gynecomastia
Gynecomastia patients are generally a difficult patient group to satisfy
(51,52). Satisfaction rates for liposuction-only treatment range between 83%
and 100% (23,30,31).
The proponents of a combined “liposuction–excision” approach for all
grades of gynecomastia point out that the main complication of liposuction
alone is underresection, ranging from 2% to 19% in Simon grade 1 and 2
disease (3,4,13,18,23,27).
Other complications of liposuction alone include open conversion rates and
seromas. Conversion rates of liposuction to open resection for UAL is 25%
and SAL 39% (13,27). Recurrence or persistence of tissue and need for
revision in UAL is 2% and in SAL 19% (13,27). The seroma rate in SAL is
1% and in UAL is 2% to 15% (27). Burns have also been reported with
liposuction modalities in which thermal energy is generated such as UAL,
VASER, RFA, and laser (38,53).
Because the main drawback of liposuction-only treatment is underresection
or the failure to adequately treat fibrous/glandular tissue it is often combined
with excision techniques. As with all other surgery this is best kept to a
minimum. There are thus several minimally invasive adjuncts to liposuction,
including endoscopically assisted, pull-through technique, arthroscopic
shavers, microdebrider, and mammatome excision techniques
(18,19,24,34,36,54–58).
FIGURE 43-2 UAL alone: Patient treated by ultrasonic liposuction alone—pre- and
postoperative views. A: Infiltration of the breast with liposuction fluid. B: Safety
precautions undertaken during UAL emulsification of the breast tissue. C:
Application of the UAL to the left breast—hollow cannula with a sheath and a port
protector. D, E: Evacuation and contouring after emulsification using standard
cannulae—first palm down then pinch techniques, respectively. This is because UAL
the UAL cannula is inefficient at evacuation of the product/fat. Pre- and
postoperative photos (F–K). A 62-year-old man with mild to moderate gynecomastia
treated by UAL alone without open excision. The skin contraction is satisfactory.
Note the minor skin lines typically seen in patients over the age of 50 undergoing
liposuction only.

The aim is to reduce unsightly scars compared to open excision techniques,


but as yet there has been no widespread acceptance of one particular
noninvasive adjunct to liposuction.
MINIMALLY INVASIVE EXCISIONAL TECHNIQUES (TABLE 43-3)
These techniques have attempted to complement and rival liposuction
techniques in their aim to minimize the amount of scarring, increase patient
acceptance, reduce morbidity, and offer quicker recoveries. They utilize very
limited incisions as used in liposuction but address fibrous or firm glandular
tissue by sharp excision through these incisions. Almost all of them utilize
liposuction to start off with in order to remove the fatty tissue. This is then
followed by cutting up the remaining fibroglandular or fibrous tissue into
smaller pieces via the same small incision. The morselized tissue is then
removed via the small incisions in either the traditional pull-through
techniques or via the endoscope (56). Sharpened and reinforced cannulas
have also been explored for removal of the fibrous component during
liposuction (28,33) with the express aim of avoiding open excision and
minimizing the invasiveness of the surgery.
The indications for minimally invasive techniques include mild to
moderate gynecomastia especially those with firm consistency.
Complications are similar to those of liposuction with which it is often or
invariably combined.
Pull-Through Technique
The pull-through technique deserves special mention as it effectively
complements liposuction. First described by Morselli in 1996 it is now a
widely accepted technique with conventional, power-assisted, and ultrasonic
liposuction (19,36,37,54,59). The pull-through is accomplished via the
liposuction incision or endoscopically. It thus obviates the need for open
periareolar excision.
The pull-through involves blind dissection of the breast parenchymal tissue
from the skin and pectoral fascia through the liposuction incision. The tissue
is then grasped and pulled through the incision and then excised piecemeal. It
has the potential to lead to uncontrollable bleeding as it is blind. An
endoscope can prevent this as an adjunct to the initial technique. More
recently the pull-through technique has been combined with UAL (19,54).
Hammond et al. described the use of ultrasonic liposuction, combined with
the pull-through technique, to effectively remove the fibrofatty tissue of the
male breast and the fibrous glandular tissue through a single 1-cm incision
(54). Rohrich’s group report the use of a Kocher clamp introduced through
the stab incisions used for the liposuction to grasp any residual subareolar
dense tissue, pull it through the incision, and excise it directly (19). Further
liposuction can be carried out as appropriate.
Arthroscopic Shavers
Orthopedic arthroscopic (cartilage) shavers have been increasingly used for
morselization of the residual glandular tissue following liposuction because
of the ready availability of orthopedic instruments in most hospitals
(4,18,19,20,37). Prado et al. utilized 5-mm IMF incisions for both the
liposuction and arthroscopic shavers. Their tips rotate at 4,000 to 6,000 rpm
to mechanically separate fibrous glandular tissue for suctioning. This method
is particularly useful for mild to moderate gynecomastia not requiring skin
excision (37).
Endoscopic Techniques
Subcutaneous endoscopic techniques have been utilized and have the
advantage of visualization of the tissue being resected (20,56–58). They may
use multiple incisions for the camera and instruments. The direct vision
reduces the potential for bleeding associated with blind techniques. More
recently Jarrar et al. described the use of liposuction combined with
piecemeal excision under endoscopic visualization using only one 15-mm
lateral chest wall incision hidden in the axilla. The single incision is made
lateral to the anterior axillary line in line with nipple. Standard infiltration
and liposuction are performed first. An assistant manually elevates the breast
skin to provide a space for the endoscope. The incision can then permit three
instruments at any one time: 10-mm general surgery telescope 0 degree, a
laparotomy pair of scissors, a hook diathermy, and an endoscopic grasper.
The authors describe using the scissors to sharply dissect the parenchyma in a
piecemeal manner under direct vision and removal with the grasper. As with
liposuction the breast is palpated after each step to avoid overresection and an
“antiaesthetic depression” (56). They concluded that this was a more accurate
method of resection of firm parenchyma with a lower incidence of
hematomas and underresection.
VAB Techniques
Ultrasound-guided mammatome excision or vacuum-assisted biopsy device
(55,60) is used for relatively small cases as it takes time to perform. It enables
the tissue to be sent for histology and in one study was less painful than open
excision. However, its limitations include size that can be treated, possible
problems with sterility (as not done in the operating room), and the common
posttreatment occurrence of extensive bruising and oedematous swelling.
Furthermore, troublesome or persistent bleeding might necessitate taking the
patient to the operating room as an emergency as it may require exploration
to drain the hematoma and stop the bleeding. While being an attractive
minimally invasive technique, the recurrence rate remains to be determined
(60).
Microdebrider Excision
This technique has been described by Goh et al. in Singapore for the
treatment of fibrous or glandular gynecomastia in conjunction with
liposuction both power assisted and ultrasonic (61,62). It is particularly
useful in patients with palpable breast discs. It achieved effective clinical
outcomes comparable to other traditional techniques but via a small single
incision (62). It will probably become more used in the future.
Summary: Liposuction and Minimally-Invasive Techniques
Liposuction and the less-invasive techniques, while safe and effective
treatments for gynecomastia, are limited by their inability to address
significant skin excess and ptosis. The largest drawback is potential
undercorrection and leaving residual glandular tissue. The senior author has a
very low threshold for intraoperative conversion to open excision because of
the potential for poor patient satisfaction with the results of surgery when
patients are left with firm subareolar nodules (3). Excision techniques
therefore have a significant role to play in the treatment of gynecomastia.
EXCISION
Worldwide direct excision (via periareolar and transareolar incisions) remains
the mainstay of the treatment for gynecomastia (6,15,20,63) because it is
simple, effective, and avoids specialized/additional instruments. There are
several open excision techniques which go beyond the minimally invasive
incisions discussed above, some combining with skin excision. The common
options for open excision are the periareolar, circumareolar, transareolar, and
circumthelial (6,15,20,32,52,63–66).
These direct excision techniques used to be the mainstay of treatment in
many centers. However, with the advent of liposuction it has been possible to
reduce the invasiveness or magnitude of the direct excisional techniques by
utilizing the liposuction incisions, minimizing the scarring with such options
as pull-through, arthroscopic techniques, etc. Liposuction and the open
excision technique are not mutually exclusive and indeed the latter is more
commonly utilized following liposuction.
Indications
The indications for open excision alone are limited to those cases with small
well-defined breast buds or in an athletic physique with higher gland-to-fat
ratio (67–69). The outcomes of open excision of tissue in these indications
show more stable and satisfactory results (69).
The treatment of asymmetric bilateral gynecomastia is a relative indication,
with the evidence suggesting that open excision bilaterally gives better long-
term outcomes (34,69). Direct excision is also mandatory in patients with an
increased risk of malignancy most notably Klinefelter syndrome where
liposuction is contraindicated as the tissue needs to be sent for
histopathologic examination (4,19).

TABLE 43-4 Indications for Open Excision in Gynecomastia


• Firm consistency or nodular discrete breasts, often unilateral nodules
• Previous liposuction
• Intraoperative residual tissue
• Unilateral cases
• Large breasts +/− ptosis
• Liposuction not deemed to be effective
• Patient dissatisfaction and return
• Patient agreement with comparatively more overt scarring
• Asymmetrical gynecomastia—relative indication

The indications for open excision are summarized in Table 43-4.


Techniques for Excision
There are many methods used for the open excision of glandular
(ductal/stromal) and fatty tissue comprising large male breasts (Table 43-5).
The specific incisions used are given in Table 43-5.

Periareolar Excision
The time-honored direct excision via periareolar incision (63) remains an
invaluable technique in gynecomastia treatment (6,15,20,63) although today
it is almost invariably combined with liposuction (Fig. 43-3). The classical
Webster (inferior semicircular periareolar) incision is the senior author’s
preferred choice and our technique has been illustrated elsewhere (3). The
incision is made in the lower half of the circumference of the areola exactly at
the junction between the areola and the breast skin in order to minimize
visibility of the scar (3). The incision is then used to directly excise any
residual areas of fibrous glandular tissue or to perform a complete
subcutaneous mastectomy. It is important to leave enough subareolar
glandular tissue to avoid a depression or saucer deformity (3,4,70).

TABLE 43-5 Methods Used for Open Glandular Excision in Gynecomastia


• Periareolar (Webster, 1946) (63)
• Inverted omega (Barsky, 1964)
• Radial intra-areolar (Eade, 1974)
• Nipple transposition on a dermal pedicle for moderate cases (Letterman et
al., 1972) (65)
• Nipple transposition on a vertical dermal bipedicle for moderate to large
cases (Pers et al., 1972) (80)
• Nipple advancement on a dermal pedicle for moderate to large cases
(Bretteville-Jensen, 1975)
• Breast amputation and free nipple grafting (Wray et al., 1974) (76)
Note: The first 3 are suitable mainly for mild cases (and some moderate cases).
Adapted from Magdy A. A limited scar approach to massive gynecomastia. Egypt J Plast Reconstr
Surg 2008;32:229–235.
FIGURE 43-3 Liposuction + Webster open excision technique: This is the
commonest procedure-performed. A: Following a variable amount of liposuction, the
breast tissue is dissected out as we have described using Bostwick scissors starting
caudally, then proceeding deeply to resect the breast tissue off the pectoralis fascia
without damaging the muscle, then using a no. 10 blade carefully leaving a 1-cm disc
of tissue underneath the areola to prevent a saucer deformity. This 23-year-old man
with firm discrete discs of breast tissue in the retroareolar area (B–D) was treated by
open excision preceded by minimal conventional liposuction. His nipple areolae are
characteristically tense and full. D–G: The nipple areolae which looked “herniated”
preoperatively no longer protrude and are not under tension. The stab incisions and
the periareolar scars have healed very well (H–K). The herniation of the areolae is
effectively eliminated producing a very acceptable outcome.

TABLE 43-6 Types of Skin-Reduction Techniques Undertaken in Male


Breast Reduction in Conjunction With Gland Excision and/or Liposuction
• Concentric mastopexy
• LeJour (vertical scar)
• Elliptical
• Wise pattern (inverted T-scar)
• Lateral wedge
• Lalonde type (no vertical scar with nipple transposition)
• Breast amputation and free nipple-grafting
Derived from Malata CM, Wong KY. Gynaecomastia surgery. In: Nahabedian MY, Neligan P, eds.
Neligan’s Plastic Surgery. 4th ed. Vol 5. London, UK: Elsevier; 2018:174–195.

Standard glandular excision techniques (Tables 43-5 and 43-6), like


minimally invasive techniques, are not able to correct breasts with significant
skin excess or ptosis or skin redundancy. In such cases skin-reduction
techniques (ranging from concentric skin excision to breast amputation and
free nipple grafts) are needed.

Skin-Reduction Techniques (Part of the Excisional “Family” or Spectrum


of Open Excision Surgery)
On the whole however, patients with large breasts, significant ptosis, and
poor skin quality tolerate large scars well. The relative indications for such
skin excision are Simon grade 2b and 3 disease/Rohrich grade III, ptosis,
poor skin quality, or post bariatric surgery massive weight loss (12,16,67,71).
The options for skin excision are shown in Table 43-6 and can be used in
conjunction with liposuction or following liposuction in a staged manner
(16), but there is no consensus on the timing of such an approach. Proponents
of staged/“delayed” skin resection after the initial liposuction contend that
the 6- to 9-month period of settling down enables maximal skin retraction
and healing and therefore the amount of the final excision is reduced
(4,16,19). Furthermore, staged skin resection can be a good choice in patients
who object to the inevitable scarring and wish to see how things settle down
before subjecting themselves to another surgery in the hope that, with
postoperative skin contraction, they may not need future skin resection. We
do not, however, subscribe to delayed skin resection and gland excision as it
often leads to more difficult and bloodier gland excision due to the fibrosis
caused by the initial liposuction. We favor immediate skin resection as it
subjects the patient to only one operation and is technically easier. A single-
stage operation (72) is our preference (3,12) and this is supported by the
findings of others who have also moved away from a staged approach (with
“delayed” skin resection) and shown that with an immediate combined
procedure they had no immediate complications and a 1.3% chance of
recurrence/underresection (19,36,54).

TABLE 43-7 Disadvantages of “Female” Breast Reduction Techniques for


Gynecomastia
Disadvantages of Standard Breast Reduction Techniques for
Gynecomastia
• Often leaves an excess of glandular tissue
• Scar patterns look like/resemblance of female breast reduction
• Coning of the breast—when male patients want the opposite, that is, flat
breasts
• Unacceptable scarring except in the hirsute

The techniques for the skin (and gland) resection and pedicles to preserve
the nipple mirror those used in female mastopexy and breast reduction
operations. The disadvantages of traditional female breast reduction
techniques in men are summarized in Table 43-7. Of these skin-reduction
techniques, the senior author prefers the periareolar concentric mastopexy-
type reduction method (3) along the lines of the descriptions of others
(64,67,72,73), where possible. The concentric pattern avoids extra-areolar
scars (minimizes the scar burden) and in our opinion is, therefore, preferable
to most other skin-reduction techniques.
Skin Reduction Without Extra-Areolar Scars: The Periareolar
Concentric Mastopexy
The concentric mastopexy pattern places all the scars in the periareolar zone,
avoiding any extra-areolar scarring (Fig. 43-4) (6,64,71,73). Unfortunately, it
does not negate the risk of adverse scarring in susceptible individuals (6,71).
There is also some skin puckering around the circumareolar scars (73).
While Huang et al. described leaving the nipple–areola based on or
perfused by a central mound with an intercostal blood supply through the
pectoral fascia (64), we prefer leaving the NAC on a subdermal plexus using
a superiorly based dermoglandular flap (Fig. 43-4) (72): intraoperative
sequence of concentric skin reducing gynecomastia post–prostate cancer
treatment. We prefer this because it allows a more uniform excision of breast
tissue and flattens while avoiding coning of the breast. The concentric
technique is performed at the first operation (our preference) or later if there
is inadequate skin contraction after the liposuction. Sutures used for the purse
string include: Ethibond, Ethilon/Prolene, on a large-curved needle or Keith
needle.
In very large breasts this technique is, however, associated with excessive
puckering of the periareolar skin, palpable permanent suture, and persistent
discharge/possible infection if the knot is exposed. The concentric mastopexy
technique is, therefore, not applicable to very large breasts with skin excess
(massive gynecomastia Simon grade III) and especially in patients with
darker skin, the senior author resorts to the use of reduction techniques with
extra-areolar scars such as the LeJour, Wise, and Lalonde patterns
(3,9,12,74,75).
FIGURE 43-4 Pre and postoperative appearances of a 64-year old man with large
gynaecomastia secondary to bicalutamide therapy for prostate cancer. In view of the
breast size and skin excess he needed liposuction, open glandular excision +
concentric skin reduction (A–F). The intraoperative steps are also illustrated (G–V).
Doughnut deepithelialisation (I, J), infiltration (K), liposuction by palm down (M)
and pinch (N) techniques. Disruption of the IMF with a liposuction cannula (O),
inferior dermis incised to access the glandular tissue (P), excision of gland from chest
wall with a Bostiwick scissors (Q, R) leaving ~1 cm subareolar disc (R). The resected
specimen (S), followed by insertion of a purse string suture (2/0 Ethibond) (T) which
is tightened to about 2 cm diameter (U). Final on-table appearance after skin closure
with 3/0 monocryl (deep dermal) and 4/0 monocryl (subcuticular) with some
periareolar puckering and drain is situ (V).

Skin Reduction With Extra-Areolar Scars: LeJour, Wise Pattern,


Lalonde, and Elliptical Excisions
In patients with Simon grade III or Rohrich grade IV, that is, severe
gynecomastia with marked ptosis and severe skin excess, techniques with
extra-areolar scars are unavoidable. These include lateral and medial elliptical
excision techniques, use of the Wise-pattern mammaplasty, LeJour pattern,
breast amputation (via an IMF incision) with free nipple grafting (4,76), and
the no-vertical-scar Lalonde technique (9,74,75,77). The last two are
particularly useful for post bariatric massive weight loss and dark-skinned
patients. Potential disadvantages of skin excision techniques with extra-
areolar scars are potential nipple loss (partial or total), hypopigmentation of
the NAC and malposition of the NAC, poor scars, as well as all other risks
associated with gynecomastia correction surgery.

LeJour Pattern
The LeJour vertical (mammaplasty) scar pattern is best suited for patients
with true ptosis and very large breasts (Fig. 43-5). The excess skin and tissue
are resected in the vertical ellipse; however, the final vertical scar is very
noticeable. It can also lead to an unwanted depression along the vertical
excision. This vertical scar does, however, avoid the traditional Wise-pattern
inverted T scar first reported for gynecomastia by Kornstein and Cinelli (Fig.
43-6) (78).

FIGURE 43-5 Asymmetrical gynaecomastia in a young man corrected by


liposuction, open glandular excision and LeJour skin reduction of the right breast
and on the left-hand side conventional liposuction only via inframammary and
anterior axillary fold incisions. A–D: The LeJour technique is indicated when
patients want a very flat chest contour. It can also come in handy when one breast is
affected and the surgeon needs to lift the NAC and flatten the chest to match the
contralateral side as in this patient. The LeJour pattern skin reduction on the right
(after liposuction) flattened the breast area and simultaneously lifted the nipple-
areola albeit at the expense of a noticeable vertical scar.

Wise Pattern
The Wise pattern (78) is used in large ptotic breasts (Fig. 43-6). However, it
tends to cone the breast and should ideally be avoided in men because of the
coning of the breast and the extensive scarring, which is not such a
significant issue in hirsute individuals. This is particularly so in dark-skinned
patients who may develop scar hypertrophy and keloid formation and
possible hypopigmentation.

Lalonde Technique
In an attempt to minimize the scarring and female appearance associated with
the Wise pattern we have adopted the Lalonde no-vertical-scar technique
(9,74,75). The advantages of the Lalonde technique include the fact that the
IMF scar is less conspicuous and therefore better accepted. It avoids a scar
that crosses the midchest passing around the areola. It avoids undercorrection
unlike the Wise pattern or female reduction techniques. Figure 43-7 shows
the intraoperative sequence of the Lalonde technique of superior nipple
transposition.

Mastectomy and Free Nipple Grafting


Elliptical mastectomy combined with free nipple grafting (4,76) or superior
nipple transposition of the Lalonde technique (Fig. 43-7) (9,74) avoid the
traditional female breast reduction scars, but hypopigmentation can be an
issue for the NAC especially in free nipple grafts. In extremely severe cases
of gynecomastia with significant skin redundancy and ptosis, such breast
amputation with free nipple grafting, first described in 1974 (76), remains an
effective option. Breast amputation and free nipple grafting is unacceptable to
most patients because of the loss of nipple sensation, possible NAC
depigmentation. The senior author has found no indication to use this rather
radical technique in his experience of over 20 years, but it might be
applicable in transgender surgery.
Elliptical Excision Techniques
There are a number of elliptical excision techniques with scars medially and
laterally (Fig. 43-8A,B) (4,79). Miscellaneous techniques such as the oblique
Dufourmentel-Mouly procedure based on an elliptical incision with a
bipedicled dermal areolar flap (65) and the vertical bipedicled technique (80)
are largely historical because of the large long oblique extra-areolar scars
(Figs. 43-8 and 43-9); but may be unavoidable in post massive weight loss
(PMWL) patients. For pseudogynaecomastia a number of techniques have
been used including a transverse elliptical incision on a superolateral pedicle
(81), breast amputation, and free nipple grafting, the no-vertical-scar Lalonde
technique (Table 43-8).
FIGURE 43-6 Liposuction + open excision + Wise-pattern skin reduction (A–F).
(From Malata CM, Wong KY. Gynaecomastia surgery. In: Nahabedian MY, Neligan P,
eds. Neligan’s Plastic Surgery. 4th ed. Vol 5. London, UK: Elsevier; 2018:174–195.)

Complications and Limitations of Open Excision


Other complications of open excision include: infection 1.5%, dehiscence
0.3% to 3%, hematoma, loss of NAC 3.7%, adverse scarring 8.8% to 11%,
seroma, retraction of the nipple, and reduced nipple sensitivity (29,35,82).
The use of drains tends to be down to each surgeon’s preference. In
gynecomastia correction the use of drains is viewed as in other areas, they
reduce the rate of seromas from 0.6% to 0% but make no difference to
hematoma rates (83).
FIGURE 43-7 Liposuction + open excision + Lalonde (no-vertical-scar) skin
reduction. A 32-year-old Hispanic man presented with severe gynecomastia with at
least grade 2 ptosis and well-developed inframammary folds. His weight had
fluctuated but he was still obese. The poor skin quality meant that the skin was not
going to shrink postoperatively. He therefore underwent correction by liposuction,
open glandular excision, and skin reduction using the Lalonde no-vertical-scar
nipple transposition technique. The pre- and 6-month postoperative (A–G)
appearances are shown. The nipple transposition was 6 to 8 cm right and left sides,
respectively. The scarring and feminine breast contour were minimized by the lack
of a vertical scar component and the disruption of the inframammary folds
respectively. The long horizontal scar, however, has a potential for hypertrophy and
keloid formation. The circumareolar scar has no tension on it and thus is unlikely to
stretch or undergo hypertrophy. The Lalonde intraoperative sequence. Liposuction
prior to de-epithelialisation of the inferior skin ellipse (H–L). Development of the
inferior pedicle whilst carefully preserving the nipple vascularity followed by
glandular resection (M–P) illustrates the completed resection with a thin superior
flap and the neo-areloar button hole. Images Q and S demonstrate transposition of
the nipple under the superior flap and retrieving it through the button hole followed
by skin closure. It is important to shorten the horizontal suture line as the resultant
puckering settle down satisfactorily (S).
FIGURE 43-8 Elliptical excisions (these are largely historical because of the
excessive scarring). Lateral elliptical excision in a body builder (with no liposuction):
Pre- and postoperative images (A–F). This patient 32-year-old body builder had
significant weight loss. He wanted no skin excess or lateral laxity. He underwent
concentric reduction with resection of the lateral laxity through the marked elliptical
skin excision. This pattern avoids periareolar puckering, achieves a very tight
appearance, and gives a lateral rather than vertical scar—which is less apparent on
the AP view. He happened to have a mild pectus excavatum. At 12 weeks he has a
much flatter tighter contour which he wanted. The NAC shapes and positions have
been maintained. The areolae are smaller because of the concentric periareolar skin
reduction.
FIGURE 43-9 Elliptical excisions (both medial & lateral) with a bipedicled nipple
transposition in a post massive weight loss (PMWL) patient showing preservation of
the nipples but very severe scarring: Pre- and postoperative images (A–G). This 43-
year-old male lost 76 kg (168 lbs = 12 stone). PMWL patients pose extra challenges
because of poor skin quality, asymmetrical skin excess, and risk of delayed and poor
healing. Accurate planning is vital. He required complex gynaecomastia correction
as the breasts were very large and very droopy (grade 3 ptosis), with well-developed
IMFs positioned low on the chest mound. This comprised liposuction, modified
concentric excision with skin and gland resection, and excision of the lateral rolls.
This combination gave his upper trunk a better contour. There are lateral and
medial extensions of lax tissues which needed contiguous excision resulting in very
long and noticeable scars which were, however needed to correct breasts and lateral
folds. A masculine chest contour was achieved. Of note the long scars were more
acceptable to patient than the excess skin folds/rolls. He also underwent a
simultaneous lower body lift (belt lipectomy).

TABLE 43-8 Pros and Cons of the Concentric Skin-Reduction Technique


Pros Cons
• Avoids long extra-areolar scars • Periareolar skin puckering/ripples
• Less scarring versus Wise • Scar stretching—wide scars possible
pattern • Scar hypertrophy/keloid formation
• Flattens the breast • Palpable sutures (± permanent)
• Oval nipples • Resection can sometimes be limited
• No hypopigmentation, unlike • Wide scars and skin puckers but this
free nipple grafts can be revised under local anesthetic
• Avoids the female breast but none needed in our practice
reduction scar pattern • Exposed or infected permanent purse-
string suture
COMPLICATIONS AND OUTCOMES IN MALE BREAST REDUCTION (TABLES
43-9 AND 43-10)
The overall complication rates vary between 14.5% and 53% (18,29,82,84).
Hematoma is the commonest complication being about 9% to 16% with open
excision (29,84) but as low as 1% in liposuction alone or with shavers
(13,18).
The commonest late complication is inadequate resection of the glandular
tissue or skin. Glandular tissue underresection is the commonest aesthetic
complaint in small/moderate breasts especially following liposuction alone.
The treatment is open excision.
In terms of satisfaction it is important to note that this is a difficult group
of patients (14,51). Satisfaction rates, however, are high at over 86% (for
breast shape, scarring, and chest wall contour [3,20,29,52]). The possibility
of redo or second-stage surgery is an important consideration in the consent
process. Undercorrection (due to persistence) should be differentiated from
recurrence. In cases of true recurrence, consider an underlying systemic
disease or even malignancy.

TABLE 43-9 Complications of Male Breast Reduction for Gynecomastia


and Pseudogynecomastia
• Bleeding and hematoma formation
• Seroma
• Infection
• Inadequate correction
• Poor scarring: wide, hypertrophic or keloid scars
• Contour deformity: saucer deformity
• Breast asymmetry: residual or new
• Sensory changes: numbness, paraesthesia
• Pain
• Overcorrection
• Undercorrection
• Nipple inversion/tethering
• Skin necrosis
• Skin redundancy
• Irregularities/lumpiness of breast area
• Recurrence
• Need for a second stage or redo:
• asymmetry
• residual tissue (undercorrection)
• skin excess (redundant skin)
• depressed nipples
POSTOPERATIVE CARE
Our protocol for postoperative care has been detailed elsewhere and a
summary of the recovery period given to patients is given in Table 43-11.
Combining Liposuction and Open Excision
As we have alluded to before, the combination of the aforementioned
techniques is what is most commonly used by the modern plastic surgeon.
The order most purported in the literature is liposuction followed by open
excision and is believed to be effective in all grades of the disease
(4,19,52,69,85,86).
The senior author prefers to sequence such a combination approach. It is
technically simpler to undertake liposuction at the outset of the operation and
not after the open excision. Pretunneling with the liposuction cannulae
specifically reduces bleeding and contours the peripheries in order to prevent
a “dish deformity” (3). Early liposuction will also stimulate skin retraction
and so minimize the amount of skin excision required. Following open
excision of any resistant firm glandular tissue, and or excess skin, further
finer bore liposuction is performed to complete any contouring required.
Combining liposuction and open excision is now the standard of care for
almost all grades of gynecomastia.
Comparing and Contrasting Liposuction and Open Excision
There is an inherent difficulty in contrasting liposuction against open
excision alone, the reason being that the two are nearly always combined, and
the literature reflects this (3,12,19,20).
There is no current panacea to the question of the optimum operation for
gynecomastia correction, more that each of the techniques described in this
chapter has a place in treating the spectrum of disease present. Surgeon
preference, skill, and experience will of course guide which options are
favored, but each will likely retain a combination approach of some form.

TABLE 43-10 Head to Head Comparison of Liposuction and Open


Excision in Male Breast Reduction
Liposuction/Lipolysis Excision
Indications Indications
• Small, moderate, and large breasts • Small, moderate, and large breasts
• Best on fatty or predominantly fatty • Firm consistency discrete
breasts • Glandular tissue
• Patients who do not want noticeable • Firm to hard discs; often rubbery
scars and tender
• Usually unilateral—exclude cancer
• Specialized indications
• Previous steroid use
• Redo cases: previous liposuction
• Post massive weight loss
Effectiveness Effectiveness
• Very effective on fatty breasts but • Highly effective on the gland (firm
VASER/UAL/laser effective on mastectomy)
glandular–fatty tissue
Advantages Advantages
• Very effective on fatty breasts but • Highly effective on the glandular
UAL/VASER/laser also effective tissue or firm discs
on glandular–fatty tissue • Enables resection of redundant skin
• Minimally invasive
• Minimizes the scar burden
• Quicker recovery, usually day case
• Fewer complications
Drawbacks Drawbacks
• Can leave skin redundancy • Scarring—if not positioned
• Can leave residual tissue—this can properly
be excised via minimally invasive • More invasive and hence slower
techniques such a pull-through recovery. Might necessitate a
or endoscope or open excision hospital admission
• Overnight stay more likely
• Relatively longer recovery
Algorithmic approach: The senior author has previously proposed a
unifying approach to gynecomastia surgery (Fig. 43-10) (the first reported
comprehensive algorithm for gynecomastia treatment), which seeks to
combine treatments in order to maximize the strengths of each of the above
techniques modalities while minimizing the drawbacks of each technique
without the limitations of one particular modality (3).

TABLE 43-11 Male Breast Reduction Postoperative Recovery Protocol


Handed to Patients
Procedure time 1–2 hrs
Anesthetic General
Hospital stay 0 (rarely 1 night)
Time off work 10–14 days
Driving 1–2 wks
Back to work 2 wks
Pressure garment support 4–6 wks
Back to normality/sports 6–8 wks

The starting point for all cases of gynecomastia is liposuction even in those
cases with firm subareolar discs because it facilitates subsequent open
excision. It is also technically easier to undertake liposuction at the beginning
of the operation rather than after excision. We only use conventional
liposuction when ultrasonic liposuction is not available.
In patients in whom open excision is not mandated by the appearance and
consistency we always consent them for open excision in case the liposuction
leaves significant residual stromal tissue. Whenever there is skin excess
and/or ptosis we prefer to address the skin excess at the original operation
especially in cases of poor or borderline skin elasticity. The choice of skin-
reduction technique depends to a large extent on the surgeon’s preference.
We favor the periareolar concentric mastopexy-type reduction. Where this is
not applicable another skin-reduction method is employed based on the
degree of ptosis and size of the breasts.
Although many plastic surgeons can obtain excellent results using many
treatment modalities today’s surgeon who is faced with a plethora of
techniques can achieve predictable results with high patient satisfaction by
following a pragmatic approach along the lines that we have proposed.

FIGURE 43-10 Algorithm for a practical approach to gynecomastia surgery.


(Reproduced with permission from Fruhstorfer BH, Malata CM. A systematic approach to
the surgical treatment of gynaecomastia. Br J Plast Surg 2003;56(3):237–246.)

In conclusion, surgical treatment of gynecomastia consists of three basic


steps: liposuction, open excision, and skin reduction. Liposuction should
always be used in diffuse or large breast enlargements. It is optional in the
small breast with a firm, subareolar nodule, but facilitates the subsequent
open excision. Occasionally it achieved complete contour correction in
patients who were clinically assessed to need and consented for open
excision. Following liposuction, the consistency of the breast is again
assessed and open excision or where appropriate a pull-through method, is
performed, if a residual lump/s is/are present. Skin excision is indicated, if
there is still noticeable skin excess. This decision is often and best made
preoperatively but can be modified intraoperatively. The choice between
concentric, LeJour pattern, Wise, and Lalonde techniques depends on the
amount of the skin excess and the surgeon’s preference/experience. Our
results with UAL have led us to conclude that it is preferable to SAL because
it is more efficacious and stimulates better skin contraction. There may also
be less bruising. It should be used preferentially where it is available.
CONCLUSION
Today there is a wide range of treatment options available for male breast
reduction, with increasingly new technologies on offer. As we have shown in
this chapter all modalities have a place on the spectrum of gynecomastia
treatment. Surgeon familiarity, preference, and training will of course play a
role as will the availability of specialized equipment. Although direct
excision via periareolar incisions remains the mainstay of many management
algorithms (on account of its simplicity, ready availability, and high
efficacy), liposuction has become an invaluable and indispensable adjunct in
the surgical treatment of gynecomastia. This can be achieved by
SAL/PAL/UAL/VASER etc. This is then combined with minimally invasive
techniques such as pull-through or arthroscopic shaver and microdebrider
techniques if available. If these are not available or appropriate or no
experience with them then open excision is used. Skin resection is reserved
for severe gynecomastia, ptosis, PMWL, poor skin elasticity, and significant
ptosis/size. Most patients will obtain adequate correction with less-invasive
techniques. We favor minimally invasive and single-stage surgery of
liposuction, direct glandular excision +/− concentric skin excision (if
indicated) to obtain a flat male chest contour (8).
The key message is that not one sole modality is appropriate for the
management of every patient with gynecomastia. To gain the best results a
combination of treatments from the armamentarium is almost always
required. We would suggest that the order such modalities be deployed be as
follows: Liposuction, open excision (± skin excision if indicated), then
further tapering or contouring liposuction. Clearly some patients will require
all three steps and others only one. Following liposuction, the consistency of
the breast is reassessed, and open excision is performed if a residual firm or
discrete lump is present. Skin resection is indicated if there is still noticeable
skin excess—although this is a decision that is largely made preoperatively.
The choice between concentric, vertical scar (LeJour technique) or elliptical
or no-vertical skin reduction depends largely on the amount of the skin
excess to be resected and also the surgeon’s experience.
Gynecomastia surgery should be tailored to the individual patient in order
to achieve the desired cosmetic outcome, while minimizing the morbidity or
scarring and negating risks of complications where possible. The algorithm
(see Fig. 43-10) we have proposed and modified can assist the surgeon in
obtaining predictable results.

REFERENCES

1. ASPS Plastic Surgery Statistics Report—2018 Cosmetic Surgery Gender


Distribution.
https://www.plasticsurgery.org/documents/News/Statistics/2018/cosmetic-
procedures-men-2018.pdf
2. BAAPS Annual Audit 2019.
https://baaps.org.uk/media/press_releases/1708/cosmetic_surgery_stats_number_of_s
3. Fruhstorfer BH, Malata CM. A systematic approach to the surgical
treatment of gynaecomastia. Br J Plast Surg 2003;56(3):237–246.
4. Brown RH, Chang DK, Siy R, et al. Trends in the surgical correction of
gynecomastia. Semin Plast Surg 2015;29(2):122–130.
5. Farag M, Ali A, Safe K, et al. Combination of liposuction and excisional
surgery as a standardized minimal scarring technique for gynaecomastia:
experience with 150 cases. Egypt J Plast Reconstr Surg
2007;31(2):201–205.
6. Teimourian B, Perlman R. Surgery for gynaecomastia. Aesthetic Plast
Surg 1983;7(3):155–157.
7. Adekunle A, Malata CM. Gynecomastia: evolving paradigm of
management and comparison of techniques. Plast Reconstr Surg
2012;129:366e–367e.
8. Hodgson ELB, Fruhstorfer BH, Malata CM. Ultrasonic liposuction in
the treatment of gynecomastia. Plast Reconstr Surg 2005;116(2):646–
653; discussion 654–655.
9. Kazzazi F, Malata CM. Application of the Lalonde (horizontal-only
scar) breast reduction technique for correction of gynaecomastia in dark
skinned patients. Gland Surg 2019;8(3):287–293.
10. Malata CM, Lau CK, Kumiponjera D. Gynaecomastia: an algorithmic
approach to surgical management (with special emphasis on
liposuction). In: Stone C, ed. The Evidence for Plastic Surgery.
Shrewsbury, UK: TFM Publish Ltd; 2008:273–285.
11. Malata CM, Rabey NG. Surgery for Gynaecomastia. London:
Association of Breast Surgery Yearbook; 2011:72–76. RCS; 2011.
ISBN 978095679 3706.
12. Malata CM, Wong KY. Gynaecomastia Surgery. Chapter 11: Breast. In:
Nahabedian MY, Neligan P, eds. Neligan’s Plastic Surgery. Vol 5. 4th
ed. London: Elsevier; 2018:174–195.
13. Wong KY, Malata CM. Conventional versus ultrasound-assisted
liposuction in gynaecomastia surgery: a 13-year review. J Plast
Reconstr Aesthet Surg 2014;67(7):921–926.
14. Sollie M. Management of gynecomastia—changes in psychological
aspects after surgery—a systematic review. Gland Surg 2018;7(Suppl
1):S70–S76.
15. Simon BE, Hoffman S, Kahn S. Classification and surgical correction of
gynaecomastia. Plast Reconstr Surg 1973;51(1):48–52.
16. Rohrich RJ, Ha RY, Kenkel JM, et al. Classification and management of
gynecomastia: defining the role of ultrasound assisted liposuction. Plast
Reconstr Surg 2003;111(2):909–923.
17. Waltham D, Hatchell A, Thoma A. Gynecomastia classification for
surgical management: a systematic review and novel classification
system. Plast Reconstr Surg 2017;139(3):638e–648e.
18. Petty PM, Solomon M, Buchel EW, et al. Gynecomastia: evolving
paradigm of management and comparison of techniques. Plast Reconstr
Surg 2010;125(5):1301–1308.
19. Bailey SH, Guenther D, Constantine F, et al. Gynecomastia
management: an evolution and refinement in technique at UT
Southwestern medical center. Plast Reconstr Surg Glob Open
2016;4(6):e734.
20. Fagerlund A, Lewin R, Rufolo G, et al. Gynecomastia: a systematic
review. J Plast Surg Hand Surg 2015;49(6):311–318.
21. Fischer A, Fischer G. First surgical treatment for molding body’s
cellulite with three 5 mm incisions. Bull Int Acad Cosmet Surg
1976;3:35.
22. Rosenberg GJ. Gynecomastia: suction lipectomy as a contemporary
solution. Plast Reconstr Surg 1987;80(3):379–386.
23. Abdelrahman I, Steinvall I, Mossaad B, et al. Evaluation of glandular
liposculpture as a single treatment for grades I and II gynaecomastia.
Aesth Plast Surg 2018;42(5):1222–1230.
24. Shirol SS. Glandular liposuction in the treatment of gynaecomastia.
Aesthetic Plast Surg 2018;42(6):1436.
25. Yoo KH, Bae JM, Won CY, et al. Laser-assisted liposuction using the
novel 1,444-nm Nd:YAG laser for the treatment of gynecomastia: a pilot
study. Dermatology 2015;231(3):224–230.
26. de Souza Pinto EB, Abdala PC, Maciel CM, et al. Liposuction and
VASER. Clin Plast Surg 2006;33(1):107–115.
27. Collins PS, Moyer KE. Evidence-based practice in liposuction. Ann
Plast Surg 2018;80(6S Suppl 6):S403–S405.
28. Samdal F, Kleppe G, Amland PF, et al. Surgical treatment of
gynaecomastia. Five years’ experience with liposuction. Scand J Plast
Reconstr Surg Hand Surg 1994;28:123–130.
29. Colombo-Benkmann M, Buse B, Stern J, et al. Indications for and
results of surgical therapy for male gynecomastia. Am J Surg
1999;178(1):60–63.
30. Ergun SS, Kayan RB, Gules ME, et al. Effects of laser-assisted lipolysis
on the nipple-areola complex. J Cosmet Laser Ther 2017;19(4):215–
218.
31. Ozlap B, Berkoz O, Aydinol M. Is the transposition of the NAC nipple-
areolar complex necessary in Simon grade 2b gynaecomastia operations
using suction-assisted liposuction? J Plast Surg Hand Surg
2018;52(1):7–13.
32. Becker H. The treatment of gynecomastia without sharp excision. Ann
Plast Surg 1990;24(4):380–383.
33. Rosenberg GJ. A new cannula for suction removal of parenchymal
tissue of gynecomastia. Plast Reconstr Surg 1994;94(3):548–551.
34. Lee YK, Lee JH, Kang SY. Gynaecomastia: Glandular-liposculpture
through a single trans-transaxillary one hole incision. J Plast Surg Hand
Surg 2018;52(2):117–125.
35. Ibrahiem SMS. Severe gynaecomastia. New technique using superior
pedicle NAC flap through a circumareolar approach. Ann Plast Surg
2016;76(6):645–651.
36. Lista F, Ahmad J. Power-assisted liposuction and the pull-through
technique for the treatment of gynecomastia. Plast Reconstr Surg
2008;121(3):740–747.
37. Prado AC, Castillo PF. Minimal surgical access to treat gynecomastia
with the use of a power-assisted arthroscopic-endoscopic cartilage
shaver. Plast Reconstr Surg 2005;115(3):939–942.
38. Ion L, Raveendran SS, Fu B. Body-contouring with radiofrequency-
assisted liposuction. J Plast Surg Hand Surg 2011;45(6):286–293.
39. Gingrass MK, Shermak MA. The treatment of gynecomastia with
ultrasound-assisted lipoplasty. Perspect Plast Surg 1999;12:101.
40. Gingrass MK, Kenkel JM. Comparing ultrasound-assisted lipoplasty
with suction-assisted lipoplasty. Clin Plast Surg 1999;26:283–288; ix.
41. Rohrich RJ, Beran SJ, Kenkel JM, et al. Extending the role of
liposuction in body contouring with ultrasound-assisted liposuction.
Plast Reconstr Surg 1998;101(4):1090–1102; discussion 1117–1119.
42. Zocchi M. Ultrasonic liposculpturing. Aesthetic Plast Surg
1992;16:287–298.
43. Ratnam BV. A new classification and treatment protocol for
gynaecomastia. Aesthet Surg J 2009;29(1):26–31.
44. Gerson RM. Avoiding end hits in ultrasound-assisted lipoplasty. Aesthet
J Surg 1997;17(5):331–333.
45. Grolleau JL, Pienkowski C, Chavoin JP, et al. Morphological anomalies
of breasts in adolescent girls and their surgical correction. Arch Pediatr
1997;4:1182–1191.
46. Rohrich RJ, Beran SJ, Kenkel JM. Chapter 7 Operative Principles and
Basic Procedure. In: Rohrich RJ, Beran SJ, Kenkel JM, eds. Ultrasound-
Assisted Liposuction. St Louis, MO: QMP, Inc; 1999:121–152.
47. Hammond DC. Surgical correction of gynaecomastia. Plast Reconstr
Surg 2009;124:61e–68e.
48. Sönmez Ergün S, Kayan RB, Güle¸s ME, et al. Effects of laser-assisted
lipolysis on nipple-areola complex. J Cosmet Laser Ther
2017;19(4):215–218.
49. Goldman A, Wollina U, de Mundstock EC. Evolution of tissue
tightening by the subdermal Nd:YAG laser assisted liposuction alone. J
Cutan Aesthet Surg 2011;4(2):122–128.
50. Blugerman G, Schavelzon D, Mulholland RS, et al. Gynaecomastia
treatment using radiofrequency assisted liposuction (RFAL). Eur J Plast
Surg 2013;36(4):231–236.
51. Ridha H, Coleville RJ, Vesely MJ. How happy are patients with their
gynaecomastia reduction surgery? J Plast Reconstr Aesthteic Surg
2009;62(11):1473–1478.
52. Taheri AR, Farahvash MR, Fathi HR, et al. The satisfaction rate among
patients and surgeons after peri-areolar surgical approach to
gynaecomastia along with liposuction. World J Plast Surg
2016;5(3):287–292.
53. Levy AS, O’Sullivan G, Parizh DO, et al. 363 full thickness burn
injuries following laser-assisted liposuction. J Burn Care Res
2018;39(Suppl 1):S152.
54. Hammond DC, Arnold JF, Simon AM, et al. Combined use of ultrasonic
liposuction with the pull-through technique for the treatment of
gynecomastia. Plast Reconstr Surg 2003;112(3):891–895; discussion
896–897.
55. Iwuagwu OC, Calvey TA, Ilsley D, et al. Ultrasound guided minimally
invasive breast surgery (UMIBS): a superior technique for
gynecomastia. Ann Plast Surg 2004;52(2):131–133.
56. Jarrar G, Peel A, Fahmy R, et al. Single incision endoscopic surgery for
gynaecomastia. J Plast Reconstr Aesthet Surg 2011;64(9):e231–e236.
57. Liu J, Han Y, Cheung K, et al. Single incision surgery for
gynaecomastia using Tri-Port: a case report. Exp Ther Med
2018;16(2):797–801.
58. Ohyama T, Takada A, Fujikawa M, et al. Endoscope-assisted
transaxillary removal of glandular tissue in gynecomastia. Ann Plast
Surg 1998;40(1):62–64.
59. Morselli PG. “Pull-through”: a new technique for breast reduction in
gynecomastia. Plast Reconstr Surg 1996;97(2):450–454.
60. Wang Y, Wang J, Liu L, et al. Comparison of curative effects between
mammotome-assisted minimally invasive resection (MAMIR) and
traditional open surgery for gynecomastia in Chinese patients: a
prospective clinical study. Breast J 2019;25(6):1084–1089.
61. Goh T, Tan BK, Song C. Use of the microdebrider for treatment of
fibrous gynaecomastia. J Plast Reconstr Aesthet Surg 2010;63(3):506–
510.
62. Sim N, Tan G, Tan BK, et al. Review of the microdebrider excision and
liposuction technique (MELT) for the treatment of gynecomastia. J Plast
Reconstr Aesthet Surg 2020;73(2):303–312.
63. Webster JP. Mastectomy for gynecomastia through a semi-circular
incision. Ann Surg 1946;124:557–575.
64. Huang TT, Hidalgo JE, Lewis SR. A circumareolar approach in surgical
management of gynecomastia. Plast Reconstr Surg 1982;69(1):35–40.
65. Letterman G, Schurter M. Surgical correction of massive gynecomastia.
Plast Reconstr Surg 1972;49(3):259–262.
66. Pitanguy I. Transareolar incision for gynaecomastia. Plast Reconstr
Surg 1966;38(5):414–419.
67. Aiache AE. Surgical treatment of gynecomastia in the body builder.
Plast Reconstr Surg 1989;83(1):61–66.
68. Blau M, Hazani R. Correction of gynecomastia in body builders and
patients with good physique. Plast Reconstr Surg 2015;135(2):425–432.
69. Innocenti A. Discussion: Long term follow up of recurrence and patient
satisfaction after surgical treatment of gynaecomastia. Aesth Plast Surg
2017;41(5):1242–1243.
70. Hosnuter M. An Ameliorated approach for sharp resection in
gynaecomastia surgery. Indian J Surg 2014;76(5):419–424.
71. Wiseman IM, Lehman JA Jr, Parker MG, et al. Gynaecomastia: an
outcome analysis. Ann Plast Surg 2004;53(2):97–101.
72. Smoot EC 3rd. Eccentric skin resection and purse-string closure for skin
reduction with mastectomy for gynecomastia. Ann Plast Surg
1998;41(4):378–383.
73. Mohamad Hasan R. Modified Benelli procedure for subcutaneous
mastectomy in gynecomastia: a randomised controlled trial. Ann Med
Surg (Lond) 2019;47:19–23.
74. Lalonde DH, Lalonde J, French R. The no vertical scar breast reduction:
a minor variation that allows to remove vertical scar portion of the
inferior pedicle wise pattern T scar. Aesthetic Plast Surg
2003;27(5):335–344.
75. Magdy A. A limited scar approach to massive gynecomastia. Egypt J
Plast Reconstr Surg 2008;32:229–235.
76. Wray RC Jr, Hoopes JE, Davis GM. Correction of extreme
gynaecomastia. Br J Plast Surg 1974;27(1):39–41.
77. Thiénot S, Bertheuil N, Carloni R, et al. Postero-inferior pedicle surgical
technique for the treatment of grade III gynecomastia. Aesthetic Plast
Surg 2017;41(3):531–541.
78. Kornstein AN, Cinelli PB. Inferior pedicle reduction technique for larger
forms of gynecomastia. Aesthetic Plast Surg 1992;16(4):331–335.
79. Ward CM, Khalid K. Surgical treatment of grade III gynaecomastia. Ann
R Coll Surg Engl 1989;71(4):226–228.
80. Pers M, Bretteville-Jensen G. Reduction mammaplasty based on vertical
bipedicle and “tennis ball” assembly. A different approach. Scand J
Plast Reconstr Surg 1972;6:61–68.
81. Molina AR, Kokkinos C, Soldin M. Male pseudogynaecomastia
following massive weight loss: introducing the superolateral pedicle. J
Plast Reconstr Aesthet Surg 2014;67(1):e25–e26.
82. Courtiss EH. Gynecomastia: analysis of 159 patients and current
recommendations for treatment. Plast Reconstr Surg 1987;79(5):740–
753.
83. Chao JW, Raveendran JA, Maly C, et al. Closed-suction drains after
subcutaneous mastectomy for gynecomastia: do they reduce
complications? Aesthetic Plast Surg 2017;41(6):1291–1294.
84. Li CC, Fu JP, Chang SC, et al. Surgical treatment of gynecomastia:
complications and outcomes. Ann Plast Surg 2012;69(5):510–515.
85. Innocenti A, Ghezzi S, Melita D, et al. Clinical characteristics of
asymmetric bilateral gynaecomastia: Suggestion of desirable surgical
method based on a single institution experience. Aesth Plast Surg
2018;42(6):1716–1717.
86. Lee SR, Lee SG, Byun GY, et al. Clinical characteristics of asymmetric
bilateral gynaecomastia: suggestion of desirable surgical method based
on a single institution experience. Aesthetic Plast Surg 2018;42(3):708–
715.
SECTION IV

Implant Based Reconstruction


44 Evolution of Breast Surgery and the Bioengineered Concept
45 Overview of Indications and Consideration for Prepectoral Versus
Subpectoral Reconstruction
46 Patient Selection for One-Stage Subpectoral Reconstruction
47 Patient Selection for One-Stage Reconstruction Prepectoral
48 Breast Reconstruction With Form-Stable Implants
49 Management of Ptotic Patient Desiring Nipple-Sparing Mastectomy
With Implant-Based Reconstruction
50 Two-Staged Nipple-Sparing Mastectomy for Preservation of the Nipple
Areolar Complex in the Large or Ptotic Breast: Reconstructive
Algorithm and Approach
51 Can We Identify Risky Patients for NSM?
52 Implant-Based Reconstruction in High-BMI Patients
53 When Is Delayed Breast Reconstruction Indicated?
54 Immediate Two-Stage Breast Reconstruction Using a Tissue Expander
and Implant
55 Delayed Expander/Implant Sequenced Breast Reconstruction
56 Prepectoral Direct-to-Implant Reconstruction: What Is the Role for
Dermal Substitutes?
57 Role of Acellular Dermal Matrix in Breast Reconstruction
58 Use of Meshed Acellular Dermal Matrix in Breast Reconstruction
59 Role of Implant Reconstruction in Previously Radiated Patients
60 Management and Prevention of Nipple and Mastectomy Skin Necrosis
61 Management of the Exposed Implant
62 Management of Animation Deformity in Implant-Based Reconstruction
63 Symmetry Procedures Following Unilateral Implant Breast
Reconstruction
64 Implant-Based Breast Reconstruction After Unilateral Mastectomy
65 Patient Satisfaction in Unilateral Versus Bilateral Mastectomy With
Reconstruction
66 Surgical Treatment of Nipple Malposition in Nipple-Sparing
Mastectomy
67 Salvage of the Contracted Radiated Implant: Radiation Sequelae and
Evolving Strategies in Prevention and Reconstruction
68 Reconstruction of Previously Augmented Patients Undergoing
Mastectomy: Options for Implant-Based Reconstruction
69 Latissimus Dorsi Musculocutaneous Flap Breast Reconstruction
70 Radiating Implants Versus Expanders: Plastic Surgeon’s Perspective
and Experience
71 Perioperative Pain Management: ERAS Protocols, Blocks, and the Role
of Pharmacogenomics
CHAPTER 44

Evolution of Breast Surgery and the


Bioengineered Concept
ALLEN GABRIEL | G. PATRICK MAXWELL | MAURICE Y. NAHABEDIAN
HISTORY
Prosthetic breast reconstruction is currently the most frequently performed
method of breast reconstructive surgery in women undergoing mastectomy
(1). The preference for prosthetic reconstruction over autologous
reconstructive options is attributed to its shorter operative time, hospital stay,
and recovery; absence of donor-site morbidity (2); and lower risk of
postoperative complications (3–5). However, it is generally believed that the
prosthetically reconstructed breast is less natural looking than the
autologously reconstructed breast (2). But, this perception is changing due to
advances in mastectomy and reconstructive techniques and prosthetic
devices, as well as the incorporation of the “bioengineered breast” concept in
recreating the breast. Hence, good-to-excellent long-term aesthetic outcomes
and high overall patient satisfaction are now possible in the majority of
patients who undergo prosthetic reconstruction (6,7). This chapter reviews
the evolution of prosthetic breast reconstruction and the role of the
bioengineered breast concept for achieving predictable and aesthetically
pleasing outcomes.
EVOLUTION OF PROSTHETIC BREAST RECONSTRUCTION

Subcutaneous Reconstruction
The modern era of prosthetic breast reconstruction commenced in 1962 with
the introduction of silicone-filled breast implants (8). The first breast
implants were placed through a delayed insertion in the subcutaneous plane
(beneath the mastectomy skin but over the chest wall muscles) after radical or
modified-radical mastectomy (9,10). This subcutaneous approach was
simple, quick, preserved the integrity of the chest wall muscles, and was
viewed as nothing more than to recreate the breast mound. Soon it became
evident that this was not an ideal approach.
The tightness of the skin after a radical or modified-radical mastectomy
meant that only small implants could be placed. This resulted in size
mismatch with the reconstructed breast often being smaller than the
contralateral breast. Further, the overlying thinned mastectomy skin lacked
soft tissue to cushion and support the prosthesis and led to implant
malposition (bottoming out), visibility, palpability, rippling, and exposure in
the event of skin rupture (11,12). In addition, subcutaneous placement
increased the risk of capsular contracture and reconstructive failure (13). The
subsequent introduction of saline-filled tissue expanders in the early 1980s
(14) allowed larger implants to be placed at a second stage after gradual
stretching of the skin envelope, which ameliorated breast symmetry.
However, the aforementioned complications related to subcutaneous implant
placement persisted. Despite the shortcomings, the breast mound created
from subcutaneous implant placement brought psychological relief to the
women as mastectomies at that time were aggressive and resulted in
significant breast deformities (10).
Submuscular Reconstruction
The soft tissue limitations of subcutaneous implant placement led to the
recruitment of chest wall muscles to provide tissue coverage. This
necessitated moving the implant from the subcutaneous to the submuscular
plane and the genesis of the submuscular approach to breast reconstruction.
The submuscular approach, still performed to this day in selected patients,
has a couple of variations. Initially, it was performed by placing the implant
completely under the pectoralis major muscle. In this variation, also referred
to as the subpectoral approach, the inferior attachment of the pectoralis major
muscle is completely released and the prosthesis is placed in a pocket under
the elevated muscle, with the muscle completely covering the implant. Full
pectoral coverage eliminated some of the limitations of the subcutaneous
approach but resulted in an unnatural appearance of the breast due to size
restriction of the subpectoral pocket and restricted expansion of the lower
breast pole (12,15).
To address the limitations of full subpectoral coverage, various muscle
flaps (serratus anterior, rectus abdominis sheath, obliquus major, and
pectoralis minor) and/or their fasciae are recruited to provide lateral and
inferior muscle coverage of the prosthesis (16). Although coverage with
muscle flaps provides a larger subpectoral pocket, it still restricts lower pole
expansion resulting in poor breast projection and poor definition of the breast
shape (12,15). In addition, recruitment of various muscle flaps introduced an
added set of complications related to muscle-flap viability and muscle donor-
site morbidity (17,18).
Partial-Muscle or Dual Plane Reconstruction
The partial-muscle coverage or dual plane technique was introduced to
address the inferior restriction of full-muscle coverage. In this approach, the
implant is placed partially in the subpectoral plane and partially in the
subcutaneous plane, hence, its designation as the dual plane technique. The
partially released pectoralis muscle covers the superior aspects of the implant
while inferior coverage is provided by the mastectomy skin (11,19,20).
Partial-muscle coverage allows for lower pole expansion and eliminates
donor-site morbidity as various flaps are not recruited, but the pectoralis
major muscle which lacks inferior attachment can migrate superiorly causing
“window-shading.” In addition, because the lower pole of the breast is only
covered by the mastectomy flap, the same risk of complications associated
with subcutaneous implant placement exists with partial-muscle coverage.
Window-shading can be addressed by the use of marionette sutures to anchor
the inferior edge of the partially released pectoralis major muscle to the
overlying skin (19), but complications associated with inadequate
subcutaneous coverage of the lower pole remain.
To address the problem of lower pole coverage, acellular dermal matrices
(ADMs) were introduced in breast reconstruction in 2006. In this widely
utilized modification of the partial-muscle coverage technique, ADM placed
at the lower pole is attached to the partially released pectoralis major muscle
superiorly and to the inframammary fold inferiorly (17,18,21,22). In addition
to providing lower pole coverage of the implant, the ADM also supports and
stabilizers the implant, thus minimizing implant movement; stabilizes the
pectoralis major muscle along its inferolateral margin, thus eliminating
window-shading; and creates a well-defined inframammary fold, without
restricting lower pole expansion (23,24).
The dual plane technique, with or without ADM, is currently the standard
technique for implant-based breast reconstruction. Many of the
disadvantages/complications of subcutaneous implant placement (implant
visibility, palpability, and exposure; and capsular contracture) are mitigated
because of the thicker coverage provided by the muscle and the ADM, if
used. The elevation of the muscle, however, has introduced its own set of
problems. Major concerns are the functional impairment of the muscle,
particularly the adduction, anteversion, and inward rotation of the upper limb,
and animation deformities caused by muscle contraction (Fig. 44-1) (25–27).
All patients experience some degree of animation deformity. The majority of
patients are bothered by it and it can affect the quality of life of patients (27).
Chest tightness, pain, and muscle spasm are other significant concerns
associated with the elevation of the pectoralis muscle. Subpectoral placement
also creates an unnatural state as the natural breast is anterior to the muscle.
Despite the concerns with dual plane reconstruction with ADM, patients
can have aesthetically pleasing results (28); but, with any contraction of the
pectoralis major, animation deformity can be immediately noted. Fat grafting
may be used as a means to establish a natural gliding surface between the thin
mastectomy flap and the pectoralis/ADM interface which decreases the pain
and the visual deformities associated with the scarred mastectomy flap being
pulled by the pectoralis major (6). This ameliorates but does not eliminate
animation deformity and some degree of animation remains.
FIGURE 44-1 Patient with animation deformity years after mastectomy and dual
plane reconstruction with silicone implants. A. Without contraction of the pectoralis
major muscle. B. With contraction of the pectoralis major muscle. (From Gabriel A,
Maxwell GP. The Evolution of prosthetic breast reconstruction: from subpectoral to
prepectoral utilizing the bioengineered concept. In: Gabriel A, Nahabedian MY, Sigalove
SR, et al., eds. Prepectoral Techniques in Reconstructive Breast Surgery. Philadelphia,
PA: Wolters Kluwer; 2019:1–6.)

Prepectoral Reconstruction
Prepectoral reconstruction was conceived to alleviate the muscle-related
issues of the dual plane and submuscular/subpectoral approaches by moving
the implant back to the subcutaneous plane (29–32). This involves placing
the implant under the mastectomy skin envelope and over the pectoralis
major muscle, similar to the subcutaneous approach of the 1960s. However,
the present-day subcutaneous approach differs from the historic approach by
using modern techniques and devices and is specifically referred to as the
prepectoral approach.
Modern techniques and devices are critical to overcoming the limitations
of subcutaneous placement and improving the aesthetic outcome in the
prepectoral technique. In fact, the renewed interest in the prepectoral space
began after a number of technique and device advancements were introduced
over the years in breast reconstructive surgery. Mastectomies became less
aggressive, deviating from radical mastectomies to skin- and nipple-sparing
mastectomies that preserved mastectomy flap perfusion and viability, which
are critical for the prepectoral approach. Tissue perfusion devices became
available that could assess perfusion in real time, providing an objective
means of evaluating flap viability. The use of ADMs for lower pole soft
tissue coverage in the dual plane approach eventually led to the idea that the
matrix could be used to provide total coverage of the prepectorally placed
implant, obviating the need to elevate the pectoralis major muscle.
Improvements in implant designs, such as the highly cohesive gel implants,
which are associated with less rippling and wrinkling, meant that these
complications which are a concern with prepectoral implant placement could
be mitigated. Lastly, advances in autologous fat grafting technique has
permitted the use of autologous fat to provide additional soft tissue coverage
that is often needed in the prepectoral approach to mask implant visibility and
rippling. All of these advancements collectively are credited with making the
prepectoral approach a reality.
The simplicity of the prepectoral procedure makes it an attractive
reconstructive option for both surgeons and patients. It is a less invasive
procedure as it obviates the need to elevate the pectoralis major muscle. With
muscle sparing, surgical time is shortened, the requirement for intravenous
pain control or a pain pump is diminished, and patients can typically be
discharged after one night of hospital stay. For patients, it is a less traumatic
procedure with less pain and a faster recovery. However, the prepectoral
approach is not suitable for all patients. Patient selection is critical and is
discussed in Chapter 46.
BIOENGINEERED BREAST CONCEPT
Integral to prepectoral reconstruction is the bioengineered breast concept
(6,33). Introduced in 2009, bioengineered breast is defined as an enhanced
breast form consisting of a combination of form stable or higher-fill breast
implant, regenerative scaffold, and regenerative cells (Fig. 44-2). The implant
is no longer the sole factor in recreating the female breast form. Recreating
the breast shape and form also requires the replacement of the soft tissue
cover overlying the implant. Enhancing the soft tissue coverage has been
made possible with the use of regenerative scaffolds and physiologically
processed fat. Volume enhancement is critical for aesthetics, such as masking
implant palpability, visibility, and rippling/wrinkling, as well as functionality
of the breast. It also alters how the recipient’s host tissue responds to the
foreign body implant. With the bioengineered breast, the ultimate goal of
breast reconstruction—to recreate a breast that looks and feels like the natural
breast (Fig. 44-3)—is achievable. The utilization of form stable implants and
regenerative constructs and cells can be applied to all aspects of breast
surgery, including primary reconstruction and augmentation and secondary
revisionary reconstruction and augmentation (Fig. 44-4). This concept
combined with prepectoral implant placement allows for aesthetically
pleasing outcomes (Fig. 44-5) (29).
FIGURE 44-2 The advances in the availability of more cohesive and higher-fill
implants, and scaffolds (acellular dermal matrices), and regenerative cells (processed
fat with good quality), have revolutionized modern-day breast reconstruction
utilizing this bioengineered concept to “Aesthetic Breast Reconstruction.” (From
Gabriel A, Maxwell GP. The evolution of prosthetic breast reconstruction: from
subpectoral to prepectoral utilizing the bioengineered concept. In: Gabriel A, Nahabedian
MY, Sigalove SR, et al., eds. Prepectoral Techniques in Reconstructive Breast Surgery.
Philadelphia, PA: Wolters Kluwer; 2019:1–6.)
FIGURE 44-3 All layers of the breast form should be addressed planning the
reconstruction. (From Gabriel A, Maxwell GP. The evolution of prosthetic breast
reconstruction: from subpectoral to prepectoral utilizing the bioengineered concept. In:
Gabriel A, Nahabedian MY, Sigalove SR, et al., eds. Prepectoral Techniques in
Reconstructive Breast Surgery. Philadelphia, PA: Wolters Kluwer; 2019:1–6.)
FIGURE 44-4 The principles described utilizing the bioengineered concept
(implants, ADMs, and cells) are interchangeable between augmentations, revisions,
and reconstructions. ADM, acellular dermal matrix. (From Gabriel A, Maxwell GP.
The evolution of prosthetic breast reconstruction: from subpectoral to prepectoral utilizing
the bioengineered concept. In: Gabriel A, Nahabedian MY, Sigalove SR, et al., eds.
Prepectoral Techniques in Reconstructive Breast Surgery. Philadelphia, PA: Wolters
Kluwer; 2019:1–6.)

FIGURE 44-5 Patient following bilateral nipple-sparing mastectomy and immediate


two-stage reconstruction utilizing the bioengineered approach. All layers were
addressed and results remain stable at 3 years post op. (From Gabriel A, Maxwell GP.
The evolution of prosthetic breast reconstruction: from subpectoral to prepectoral utilizing
the bioengineered concept. In: Gabriel A, Nahabedian MY, Sigalove SR, et al., eds.
Prepectoral Techniques in Reconstructive Breast Surgery. Philadelphia, PA: Wolters
Kluwer; 2019:1–6.)
CONCLUSION
The breast reconstructive process is continuously evolving given the
increasing expectations of both patients and surgeons for stable aesthetic
outcomes with minimal complications and a fast recovery. Prosthetic breast
reconstruction has come a full circle, from implant placement in the
subcutaneous plane to the subpectoral/submuscular plane and back to the
subcutaneous (prepectoral) plane. Advancements in mastectomy technique
and implant designs as well as the introduction of ADMs and autologous fat
have enabled the transition back to the prepectoral space. The success of
prepectoral reconstruction rests on the bioengineered breast concept wherein
highly cohesive, form-stable implants are utilized in combination with
regenerative scaffold and regenerative cells to augment the soft tissue
envelope of the reconstructed breast.

REFERENCES

1. American Society of Plastic Surgeons. 2018 Plastic Surgery Statistics


Report. Available at
https://www.plasticsurgery.org/documents/News/Statistics/2018/plastic-
surgery-statistics-full-report-2018.pdf
2. Howard-McNatt MM. Patients opting for breast reconstruction
following mastectomy: an analysis of uptake rates and benefit. Breast
Cancer (Dove Med Press) 2013;5:9–15.
3. Mioton LM, Smetona JT, Hanwright PJ, et al. Comparing thirty-day
outcomes in prosthetic and autologous breast reconstruction: a
multivariate analysis of 13,082 patients? J Plast Reconstr Aesthet Surg
2013;66(7):917–925.
4. Wilkins EG, Hamill JB, Kim HM, et al. Complications in
postmastectomy breast reconstruction: one-year outcomes of the
Mastectomy Reconstruction Outcomes Consortium (MROC) Study. Ann
Surg 2018;267(1):164–170.
5. Bennett KG, Qi J, Kim HM, et al. Comparison of 2-year complication
rates among common techniques for postmastectomy breast
reconstruction. JAMA Surg 2018;153(10):901–908.
6. Maxwell GP, Gabriel A. Bioengineered breast: concept, technique, and
preliminary results. Plast Reconstr Surg 2016;137(2):415–421.
7. Cordeiro PG, McCarthy CM. A single surgeon’s 12-year experience
with tissue expander/implant breast reconstruction: Part II. An analysis
of long-term complications, aesthetic outcomes, and patient satisfaction.
Plast Reconstr Surg 2006;118(4):832–839.
8. Cronin TD, Gerow FJ. Augmentation mammaplasty: a new “natural
feel” prosthesis. In: Transactions of the Third International Congress of
Plastic and Reconstructive Surgery. Amsterdam: Excerpta Medica;
1963.
9. Freeman BS. Technique of subcutaneous mastectomy with replacement;
immediate and delayed. Br J Plast Surg 1969;22(2):161–166.
10. Snyderman RK, Guthrie RH. Reconstruction of the female breast
following radical mastectomy. Plast Reconstr Surg 1971;47(6):565–567.
11. Hammond DC, Capraro PA, Ozolins EB, et al. Use of a skin-sparing
reduction pattern to create a combination skin-muscle flap pocket in
immediate breast reconstruction. Plast Reconstr Surg 2002;110(1):206–
211.
12. Glasberg SB, Light D. AlloDerm and Strattice in breast reconstruction: a
comparison and techniques for optimizing outcomes. Plast Reconstr
Surg 2012;129(6):1223–1233.
13. Nahai F, Bostwick J 3rd. Aesthetic aspects of breast reconstruction.
Aesthetic Plast Surg 1982;6(2):61–67.
14. Radovan C. Breast reconstruction after mastectomy using the temporary
expander. Plast Reconstr Surg 1982;69(2):195–208.
15. Spear SL, Spittler CJ. Breast reconstruction with implants and
expanders. Plast Reconstr Surg 2001;107(1):177–187.
16. Little JW 3rd, Golembe EV, Fisher JB. The “living bra” in immediate
and delayed reconstruction of the breast following mastectomy for
malignant and nonmalignant disease. Plast Reconstr Surg
1981;68(3):392–403.
17. Breuing KH, Warren SM. Immediate bilateral breast reconstruction with
implants and inferolateral AlloDerm slings. Ann Plast Surg
2005;55(3):232–239.
18. Spear SL, Parikh PM, Reisin E, et al. Acellular dermis-assisted breast
reconstruction. Aesthetic Plast Surg 2008;32(3):418–425.
19. Spear SL, Pelletiere CV. Immediate breast reconstruction in two stages
using textured, integrated-valve tissue expanders and breast implants.
Plast Reconstr Surg 2004;113(7):2098–2103.
20. Serra-Renom JM, Fontdevila J, Monner J, et al. Mammary
reconstruction using tissue expander and partial detachment of the
pectoralis major muscle to expand the lower breast quadrants. Ann Plast
Surg 2004;53(4):317–321.
21. Salzberg CA. Nonexpansive immediate breast reconstruction using
human acellular tissue matrix graft (AlloDerm). Ann Plast Surg
2006;57(1):1–5.
22. Zienowicz RJ, Karacaoglu E. Implant-based breast reconstruction with
allograft. Plast Reconstr Surg 2007;120(2):373–381.
23. Breuing KH, Colwell AS. Inferolateral AlloDerm hammock for implant
coverage in breast reconstruction. Ann Plast Surg 2007;59(3):250–255.
24. Spear SL, Sher SR, Al-Attar A. Focus on technique: supporting the soft-
tissue envelope in breast reconstruction. Plast Reconstr Surg 2012;130(5
Suppl 2):89S–94S.
25. de Haan A, Toor A, Hage JJ, et al. Function of the pectoralis major
muscle after combined skin-sparing mastectomy and immediate
reconstruction by subpectoral implantation of a prosthesis. Ann Plast
Surg 2007;59(6):605–610.
26. Spear SL, Schwartz J, Dayan JH, et al. Outcome assessment of breast
distortion following submuscular breast augmentation. Aesthetic Plast
Surg 2009;33(1):44–48.
27. Becker H, Fregosi N. The impact of animation deformity on quality of
life in post-mastectomy reconstruction patients. Aesthet Surg J
2017;37(5):531–536.
28. Vardanian AJ, Clayton JL, Roostaeian J, et al. Comparison of implant-
based immediate breast reconstruction with and without acellular dermal
matrix. Plast Reconstr Surg 2011;128(5):403e–410e.
29. Sigalove S, Maxwell GP, Sigalove NM, et al. Prepectoral implant-based
breast reconstruction: rationale, indications, and preliminary results.
Plast Reconstr Surg 2017;139(2):287–294.
30. Woo A, Harless C, Jacobson SR. Revisiting an old place: single-surgeon
experience on post-mastectomy subcutaneous implant-based breast
reconstruction. Breast J 2017;23(5):545–553.
31. Vidya R, Masià J, Cawthorn S, et al. Evaluation of the effectiveness of
the prepectoral breast reconstruction with Braxon dermal matrix: first
multicenter European report on 100 cases. Breast J 2017;23(6):670–676.
32. Sbitany H, Piper M, Lentz R. Prepectoral Breast Reconstruction: a safe
alternative to submuscular prosthetic reconstruction following nipple
sparing mastectomy. Plast Reconstr Surg 2017;140(3):432–443.
33. Maxwell GP. Introduction of bio-engineered concept in breast surgery.
Paper presented at American Association of Plastic Surgeons Annual
Meeting; March 22, 2009; Palm Springs, Calif.
CHAPTER 45

Overview of Indications and


Consideration for Prepectoral Versus
Subpectoral Reconstruction
GEORGE KOKOSIS | MAURICE Y. NAHABEDIAN
HISTORY
Implant-based reconstruction remains the most common modality of breast
reconstruction after mastectomy in the United States with more than 86,000
procedures performed in 2017 (1). Implant-based reconstruction can be
performed in a variety of ways, including one stage or two stages and with
device placement in the subpectoral, partial subpectoral, or prepectoral plane.
The majority of the plastic surgeons in the United States perform a two-stage
reconstruction (1). The ideal location for device placement has changed over
the years and more recently has become a matter of discussion. Initially in
1970s and 1980s the trend was to place implants in the prepectoral plane (2).
However that was associated with significant complications mostly related to
the skin envelope (wound complications) and capsular contracture and was
therefore subsequently followed by a shift to the subpectoral plane use with
either complete or partial muscle coverage (3). This technique became the
gold standard for almost 20+ years as it reduced those complications as well
as provided a more natural appearance. However since 2015, there has been a
gradual shift toward prepectoral placement of implants (4). Revisiting the
prepectoral placement of prosthetic devices is based on significant
improvement in technique and technology (5). Advancements in fat grafting,
acellular dermal matrices, intraoperative perfusion techniques, and modern
generation implants have made prepectoral breast reconstruction safe and
feasible. Additionally, refinements in skin-sparing and nipple-sparing
mastectomy have optimized the amount of soft tissue that can be maintained
to cover the device, with the caveat of not compromising the oncologic
outcome (6). The prepectoral placement is gaining in popularity for a variety
of reasons including the prevention of animation deformity, minimizing the
postoperative discomfort associated with subpectoral implants as well as a
optimizing device placement on the chest wall (7).
SUBPECTORAL BREAST RECONSTRUCTION
In submuscular placement, the implant is placed fully under the pectoralis
major muscle providing a layer of well-vascularized tissue between the
implant and the skin flap. The advantages of this technique include enhanced
soft tissue coverage of the device and potentially limiting adverse events such
as rippling, palpation of the implant, and capsular contracture. Full muscle
coverage is achieved by recruiting the serratus anterior laterally and the
rectus abdominis inferiorly (7). The inferior restriction caused by the full
muscle coverage can sometimes limit lower pole expansion and may affect
the final appearance and contour of the breast.
Partial muscle coverage was introduced to overcome some of the
limitations of total muscle coverage. The advantages of partial muscle
coverage include improved lower pole contour with increased projection of
the breast; however, this can lead to retraction of the muscle superiorly,
termed “window-shading” as well as result in less soft tissue coverage of the
implant inferiorly. Thus, rippling and wrinkling were more common resulting
in outcomes that resembled the early years of subcutaneous placement of
devices. With the introduction of acellular dermal matrix (ADM) around
2006, partial muscle coverage could be achieved superiorly with the ADM
providing the lower pole coverage. The advantages of this technique included
optimizing lower pole contour, improving projection, and enhancing soft
tissue support. Other benefits included a more rapid expansion in the setting
of a tissue expander, better control of the inframammary fold (IMF), and a
potentially decreased incidence of capsular contracture. The ADM would
serve as a barrier between the implant and the skin envelope, thus minimizing
the morbidity of an “uncovered” lower pole of the implant. By suturing the
superior edge of the ADM to the inferior divided edge of the pectoralis major
muscle, the position and stability of the pectoralis major could be stabilized
and the incidence of window-shading can be minimized. Disadvantages of
this technique include animation deformity, muscle spasms, and chest
tightness and pain.
PREPECTORAL BREAST RECONSTRUCTION
Prepectoral breast reconstruction has been used more frequently the last few
years and is gaining popularity as the data is justifying its utilization. This
technique involves placing the device above the pectoralis muscle, in the
anatomic location previously occupied by the breast parenchyma, therefore
there is no muscle dissection performed. This minimizes the chances for
animation deformity as well and results in significantly less postoperative
pain that was attributable to the elevation and spasm of the pectoralis major
muscle.
INDICATIONS
The ideal candidate for prepectoral breast reconstruction is based on patient
factors, oncologic considerations, intraoperative characteristics, and patient
preference. Ideal candidates include those with a BMI less than 30 kg/m2,
nonsmoker, mild to moderate breast volume, and minimal ptosis. Larger BMI
patients (<40 kg/m2) can also be considered with close attention being paid to
comorbidities such as uncontrolled diabetes and hypertension. The quality of
the mastectomy skin flaps is the limiting factor and is often dependent on
whether the mastectomy was performed for therapeutic or prophylactic
indications. Confirming adequate perfusion is a critical determinant of
success. Intraoperatively, the plastic surgeon needs to assess the mastectomy
skin flaps for adequate perfusion. This will be further discussed in the
Intraoperative Care section. Extremely important is the patient preference
after a thorough discussion about the risks and benefits of each reconstructive
approach. The benefit of prepectoral placement of devices is not intended to
mitigate the benefits of subpectoral placement of devices as both techniques
have demonstrated success. Given that both modalities are oncologically and
anatomically feasible, patients may choose to have prepectoral reconstruction
to avoid animation deformity and reduce muscle spasm.
CONTRAINDICATIONS
Multiple comorbidities, especially uncontrolled diabetes mellitus (HgbA1c
>7.5) and morbid obesity (BMI >40 kg/m2), immunocompromised state, and
active or recent smoking are relative contraindications to prepectoral
reconstruction. A thin flap intraoperatively with questionable perfusion is an
absolute contraindication to prepectoral reconstruction and should prompt the
plastic surgeon to choose an alternative modality of reconstruction, either
subpectoral or delayed. Prior radiation of the mastectomy flaps can further
compromise the flap perfusion and should be considered a relative
contraindication. Tumor location can also influence the decision-making
process as tumors that are within 5 mm of the pectoralis major muscle or
abutting the skin may compromise oncologic surveillance or pose increased
risk and is considered to be a relative contraindication to prepectoral
reconstruction. In the event of deep recurrence, the prepectoral location of the
device can obscure palpation; whereas a very superficial tumor can lead to a
thin flap with potentially compromised mastectomy flap perfusion and
subsequent wound complications such as skin necrosis, dehiscence, infection,
and ultimately reconstructive failure. Other oncologic considerations for
avoiding prepectoral reconstruction are inflammatory breast cancer and
advanced stage cancer (stage IV) with bulky axillary lymphadenopathy.
PREOPERATIVE PLANNING
A thorough multidisciplinary evaluation as part of the preoperative planning
process is paramount. At the time of the consultation, the patient
characteristics as discussed above (comorbidities, history of radiation, breast
size, grade of ptosis) should be assessed. A multidisciplinary team including
the oncologist, breast surgeon, and plastic surgeon should be involved with
the patients’ decision protocols regarding the oncologic suitability for
specific approaches (nipple-sparing mastectomy, prepectoral reconstruction,
need for postoperative radiation). Provided that the patient is a candidate for
prepectoral reconstruction, the plastic surgeon will discuss the benefits (no
animation deformity, decreased postoperative pain) and risks (rippling,
implant palpability) of this approach. Additionally, a review of the one- or
two-staged approaches for prosthetic breast reconstruction is discussed.
Shared decision making is a critical aspect of the preoperative consultation
and patients need to be aware of the implications of each reconstructive
technique.
OPERATIVE TECHNIQUE
In the preoperative area with the patient standing, the footprint of the
reconstructed breast is marked on the chest wall and the desired incision
placement is delineated. Preoperative intravenous antibiotics are administered
followed by a short course of postoperative antibiotics (3 to 5 days). The
intraoperative irrigation protocol consist of a 50% povidone solution
followed by a triple antibiotic (Cefazolin, gentamycin, and bacitracin)
solution. A single drain is used and placed between the ADM and the
mastectomy skin flap. In cases of obese patients or extensive axillary
dissection a second drain is placed. Two sheets of contour medium perforated
ADM (AlloDerm) are used and sutured together along the short axis with an
absorbable suture (Fig. 45-1). The thickness of the ADM is 2 to 3 mm. A cuff
of ADM is created inferiorly to provide additional support along the IMF.
The exact method by which the ADM is placed on the chest wall varies. U.S.
Food and Drug Administration labeling requires that ADM for breast
reconstruction be used for tissue support and not implant support. With the
on-label technique, the ADM is inserted into the prepectoral space and
sutured to the perimeter of the pocket. The device is then inserted and
optimally positioned. With this technique, an inferior gutter of ADM along
the IMF is created to provide lower pole support (Fig. 45-2).
FIGURE 45-1 Two sheets of contour medium perforated acellular dermal matrix are
sutured together along the short axis with a running absorbable suture, creating a
larger oval contoured sheet.
FIGURE 45-2 The on-label application where a cuff of acellular dermal matrix is
sutured along the inframammary fold followed by device insertion.
FIGURE 45-3 The off-label technique of acellular dermal matrix assembly involves
wrapping the matrix around the device, followed by insertion of the acellular dermal
matrix/device construct insertion in the pocket.

With the off-label technique, the ADM is wrapped around the anterior
surface aspect of the device (tissue expander or implant), creating a
peripheral cuff (Fig. 45-3). The device is then turned upside down and
sutures are placed along the posterior surface (Fig. 45-4). The ADM/device
construct is then placed in the prepectoral space, properly positioned and
oriented. When a tissue expander is used, the tabs are exteriorized from
within the ADM construct and sutured to the anterior chest wall. The tissue
expander is filled with saline or room air. The advantages of filling the
expander with air is to allow for even distribution throughout the expander,
reduce the weight of the filled expander because saline-filled devices may
result in suture pull through at the tab-muscle interface, and finally to off-
load pressure on the inferior skin flap. During postoperative follow-up, the air
is evacuated from the tissue expander usually between 1 and 2 weeks and
replaced with an equal or higher amount of saline. When a permanent implant
is used instead of a tissue expander, it is important to ensure that the device is
adequately compartmentalized within the mastectomy pocket. This can be
accomplished by using sutures to reduce the breast footprint or by suturing
the edges of the ADM at the base of the implant circumferentially around the
perimeter of the pectoralis major muscle. In the event that a direct-to-implant
reconstruction is decided, a highly cohesive, form-stable implant is desirable
to avoid rippling and wrinkling. It is important that the implant fits like a
hand in glove within the mastectomy pocket.
FIGURE 45-4 Posterior view of the off-label assembly of the acellular dermal
matrix/device construct. The acellular dermal matrix is wrapped around the device
and stabilized with posteriorly based spanning sutures.
INTRAOPERATIVE CARE
The most important determining factor for success of the prepectoral breast
reconstruction is the viability of the mastectomy skin flap. Clinical
assessment is the most common method of soft tissue analysis and perfusion
and is an absolute requirement. Bleeding from the edges, skin color,
preservation of the subcutaneous fat, and lack of exposed dermis are
indicators of viable flaps. In case of equivocal clinical signs, fluorescent
angiography with indocyanine green can be used to evaluate the mastectomy
flap perfusion. Other assessment options include hyperspectral imaging to
determine hemoglobin saturation. If there is any concern regarding flap
viability, the reconstruction can be delayed or performed using a subpectoral
coverage technique.
It is important to recognize that several factors can alter early tissue
perfusion immediately following mastectomy including vasospasm,
hypothermia, and hypotension. The thickness of the mastectomy skin flap is
less important than the actual perfusion when it comes to predicting viability.
Thin patients will most likely have thinner flaps, but that does not equate to
poor perfusion. By the same token, thicker flap in larger patients does not
guarantee adequate perfusion.
Another intraoperative decision is whether to perform the prosthetic
reconstruction in one or two stages. In situations where a direct-to-implant
reconstruction was discussed preoperatively and preferred, it is incumbent
upon the plastic surgeon to ensure adequate perfusion and thickness of the
mastectomy skin flaps to ensure adequate implant support. Although there is
no absolute thickness that will guarantee success, a thickness of 1 cm is
preferable in order to continue with direct-to-implant reconstruction.
Fluorescent angiography or hyperspectral imaging is highly recommended to
assess the skin flap before and following implant insertion and it is
recommended that this be performed at least 30 minutes following the
mastectomy to allow enough time for the vasospasm to subside.
POSTOPERATIVE CARE
Following prepectoral breast reconstruction the dressing type varies among
surgeons. Incisional vacuum-assisted closure is gaining popularity as a means
of minimizing fluid production and seroma formation (8). Alternatively
transparent dressing such as Tegaderm can be applied over the breast mound,
especially after nipple-sparing mastectomies to reduce the shear forces
around the nipple areola complex. A soft compression bra is applied to
decrease the rates of seroma. Patients are required to refrain from using
tobacco products 4 weeks before and following prepectoral reconstruction.
They are also advised to minimize strenuous activity for 1 month.
The mastectomy skin flaps are evaluated at various intervals during the
first month. Immediately following the operation, signs of ischemia or
necrosis are assessed. Early signs of necrosis or delayed healing require
surgical debridement because the implant is directly underneath the
mastectomy flaps. Erythema or cellulitis are managed aggressively with
antibiotics to prevent or control infection.
Drain management varies between surgeons. Usually the drain is removed
once the output is less than 30 mL/day for two consecutive days. The drains
should stay for at least 1 week regardless. Serial expansion commences at 2
weeks postoperatively. A seroma requires aspiration with a large-bore needle
with or without drain placement, or surgical evacuation for refractory cases.
Rippling and wrinkling as well as edge visibility can also occur following
prepectoral breast reconstruction. The etiology may be secondary to an overly
expanded pocket, use of a less cohesive silicone gel breast implant, and thin
mastectomy skin flaps. The most common remedy is autologous fat grafting
to increase the thickness of the mastectomy skin flaps to camouflage the
implant surface. Fat grafting is a common modality utilized, usually with 50
to 100 cc of fat injected in each breast. The use of an implant with more
cohesivity as well as capsulorrhaphy can also be helpful.

CASE

CASE 1
A 45-year-old woman with a family history of breast cancer and a BRCA
gene mutation carrier elected to have bilateral nipple-sparing mastectomy
through an inframammary incision (Fig. 45-5). Assessment of the
mastectomy skin flaps and perfusion angiography demonstrated viable
and well-perfused tissue. Immediate prosthetic reconstruction was
performed with a prepectoral smooth round silicone gel implant with full
anterior and partial posterior coverage with an acellular dermal matrix.
Postoperatively, she did well without any adverse events.
FIGURE 45-5 A: Preoperative picture of a woman with a family history of
breast cancer and a BRCA gene mutation carrier elected to have bilateral
nipple-sparing mastectomy. B: Preoperative markings of the same patient
about to undergo bilateral nipple-sparing mastectomy. C: Assessment of
mastectomy flaps ensures good perfusion, adequate thickness, and a
peripheral meniscus of fat. Intraoperative perfusion angiography confirmed
the adequate perfusion of bilateral mastectomy flaps. D: Immediate bilateral
prosthetic reconstruction was performed with a prepectoral smooth round
silicone gel implant with full anterior and partial posterior coverage with an
acellular dermal matrix. The acellular dermal matrix/device construct is
shown in situ. E: Following the bilateral mastectomies and prepectoral
reconstruction a Tegaderm™ splint is placed at the lower breast pole to
stabilize the reconstructed breasts. The mastectomy flaps as well as the nipple
areola complex appears viable. F–H: Postoperative images showing the result
of the bilateral immediate prepectoral implant-based reconstruction at 6-
month follow-up (F—anterior, G—right lateral, H—left lateral). The patient
healed well without any adverse effects.

CASE 2

A 53-year-old woman with a stage I invasive ductal carcinoma of the


right breast elected to have bilateral skin-sparing mastectomy and breast
reconstruction (Fig. 45-6). Assessment of the mastectomy skin flaps
demonstrated good perfusion throughout; therefore, immediate bilateral
tissue expanders were inserted. Acellular dermal matrix was used for soft
tissue support and covered the entire anterior surface of the expander and
partially covered the posterior surface. Following complete expansion,
the tissue expanders were removed and replaced with smooth round
silicone gel implants. Three-dimensional nipple areolar reconstruction
was performed 3 months later.
FIGURE 45-6 A: Preoperative picture of a woman with a stage I invasive
ductal carcinoma of the right breast elected to have bilateral skin-sparing
mastectomy and breast reconstruction. B: Assessment of the mastectomy skin
flaps demonstrated good perfusion throughout. Acellular dermal matrix was
used for soft tissue support and covered the entire anterior surface of the
expander and partially covered the posterior surface. C: A closed suction
surgical drain is placed in the prepectoral pocket. Sterile dressings are
applied over the drain and the surgical incision. D: Preoperative markings
before stage two of breast reconstruction, following full expansion. E:
Intraoperative picture demonstrating complete incorporation and
revascularization of the acellular dermal matrix providing adequate soft
tissue support. F–H: Postoperative images at 6-month follow-up
demonstrating the result of the bilateral immediate prepectoral breast
reconstruction after replacement of tissue expanders with smooth round
silicone gel implants. Incisions are well healed and three-dimensional nipple
areolar reconstruction was performed 3 months later (F—anterior view, G—
left lateral view, H—right lateral view).
OUTCOMES
Prepectoral breast reconstruction is a muscle-sparing procedure that
simplifies reconstruction, yielding significant clinical benefits to patients.
Among many advantages of this approach are the significantly lower
associated pain, subsequently followed by less opioid use (9), decreased
hospital stay (0 to 1 days, compared to 1 to 2 days with prior subpectoral
breast reconstruction), shorter operative time, ease of technique, less
postoperative expansions, quicker return to work, earlier enhanced range of
motion, and overall increased patient satisfaction. However, it is also
associated with postoperative complications. In our practice, the incidence of
hematoma is 4.8%, surgical site infection and seroma is approximately 8%
and 4.8%, respectively, skin necrosis 9.7%, and explantation rates of 6.5%.
The incidence of these adverse events is similar to what was observed in
patients following subpectoral breast reconstruction (10).
CONCLUSION
The resurgence of prepectoral breast reconstruction is now backed up by
sufficient data with significantly lower pain scores and mitigation of
animation deformity when compared with the subpectoral breast
reconstruction. Though this technique is not suitable for all reconstructions,
strict attention to patient selection yields superior results. The revival of this
technique reflects the evolution in dermal tissue matrix production for device
support, breast implant properties that resist rippling, and the refinement of
fat grafting with better dissection of mastectomy flaps by modern, qualified
breast surgeons.

REFERENCES

1. ASPS procedural statistics. Available online at www.plasticsurgery.org.


2. Gruber RP, Kahn RA, Lash H, et al. Breast reconstruction following
mastectomy: a comparison of submuscular and subcutaneous
techniques. Plast Reconstr Surg 1981;67(3):312–317.
3. Cordeiro PG, Jazayeri L. Two-stage implant-based breast
reconstruction: an evolution of the conceptual and technical approach
over a two-decade period. Plast Reconstr Surg 2016;138(1):1–11.
4. Nahabedian MY, Cocilovo C. Two-stage prosthetic breast
reconstruction: a comparison between prepectoral and partial
subpectoral techniques. Plast Reconstr Surg 2017;140(6S Prepectoral
Breast Reconstruction):22S–30S.
5. Glasberg SB. The economics of prepectoral breast reconstruction. Plast
Reconstr Surg 2017;140(6S Prepectoral Breast Reconstruction):49S–
52S.
6. Salibian AA, Frey JD, Karp NS. Strategies and considerations in
selecting between subpectoral and prepectoral breast reconstruction.
Gland Surg 2019;8(1):11–18.
7. Sigalove S, Maxwell GP, Sigalove NM, et al. Prepectoral implant-based
breast reconstruction: rationale, indications, and preliminary results.
Plast Reconstr Surg 2017;139(2):287–294.
8. Gabriel A, Sigalove SR, Maxwell GP. Initial experience using closed
incision negative pressure therapy after immediate postmastectomy
breast reconstruction. Plast Reconstr Surg Glob Open 2016;4(7):e819.
9. Walia GS, Aston J, Bello R, et al. Prepectoral versus subpectoral tissue
expander placement: a clinical and quality of life outcomes study. Plast
Reconstr Surg Glob Open 2018;6(4):e1731.
10. Sbitany H, Piper M, Lentz R. Prepectoral breast reconstruction: a safe
alternative to submuscular prosthetic reconstruction following nipple-
sparing mastectomy. Plast Reconstr Surg 2017;140(3):432–443.
CHAPTER 46

Patient Selection for One-Stage


Subpectoral Reconstruction
AMY S. COLWELL | ERIN M. TAYLOR
HISTORY
Single-stage breast reconstruction was the original type of implant-based
breast reconstruction. Initially performed in a prepectoral plane, this first
implant-based technique was deserted for high rates of skin necrosis and
capsular contracture. Subsequent techniques of total submuscular coverage of
implants reduced rates of capsular contracture but restricted implant size due
to a tight submuscular pocket. The introduction of tissue expander (TE)
placement in the submuscular plane allowed for expansion of the muscular
pocket and increased final implant size through two-stage breast
reconstruction. However, high-riding implants, pain, and poor shape were
common concerns. Partial muscle release allowed improved lower pole
expansion and shape solving some of the issues of total muscle coverage. Yet
pectoralis muscle contraction deformity and TE malposition were sometimes
seen with this technique.
Acellular dermal matrix (ADM) transformed the field of implant-based
breast reconstruction by allowing precise device positioning, increased
pocket size with lower pole coverage, and avoidance of the pectoralis
deformity (1,2). In two-stage implant-based breast reconstruction, aesthetic
outcomes were more predictable (3). Furthermore, the introduction of ADM
allowed for the ability to perform single-stage breast reconstruction in
medium- to large-sized breasts with expansion of the lower pocket.
Patient selection for single-stage breast reconstruction is critical for
successful breast reconstruction outcomes. This chapter will focus on patient
selection, operative decision-making, technique, and postoperative
management to optimize success in subpectoral direct-to-implant (DTI)
single-stage breast reconstruction.
INDICATIONS
Single-stage breast reconstruction indications include immediate breast
reconstruction in patients desiring reconstruction in one stage and who desire
to stay approximately the same size. Patient preferences, oncologic plan, and
tissue quality determine if a patient is a good candidate for single-stage
reconstruction. The most important patient preferences include preferred size
and acceptance for undergoing single- versus multiple-stage reconstruction.
In nipple-sparing mastectomy (NSM), a breast volume comparable to that
preoperatively or slightly larger can be achieved with viable mastectomy
flaps and intact nipple perfusion. In skin-sparing mastectomy with nipple
removal, often the soft tissue envelope volume is decreased and flattened.
This may lead to a size similar or smaller than the preoperative breast. In
general, if a patient desires to be significantly larger in size, the patient is
better suited to undergo two-stage breast reconstruction with TEs. If the
patient desires to be significantly smaller in size, single-stage surgery is
possible with a skin- or areola-sparing procedure.
Single-stage breast reconstruction is particularly well suited for bilateral
NSM and reconstruction. Patients diagnosed with unilateral breast cancer
with a higher stage of disease are more likely to pursue bilateral mastectomy
(4). Younger patients also are more likely to undergo bilateral risk-reducing
mastectomies, particularly with a BRCA mutation, HER2 positivity, positive
node status, increased tumor size, or fear of recurrence (5). Bilateral breast
reconstruction allows for greater ease of symmetry with implant-based
reconstruction versus achieving symmetry to the contralateral natural breast
in unilateral reconstruction. NSM has become more prevalent with increased
number of eligible patients allowing for more natural-appearing breast
reconstruction and preservation of the soft tissue envelope. Oncologic
feasibility of NSM is based on tumor proximity to nipple, tumor size, and
tumor pathology.
Soft tissue quality, based on perfusion of skin flaps after mastectomy and
baseline patient anatomy, determines feasibility of single-stage breast
reconstruction. After mastectomy, skin flaps and nipples should be evaluated
for viability and perfusion. Once confirmed, single-stage reconstruction can
proceed. Patient physiology relating to baseline soft tissue quality is largely
based on age, smoking status, degree of ptosis, history of breastfeeding,
weight loss, and prior radiation. History of previous breast surgery does not
increase the risk of ischemic complications or nipple loss (6).
Compared to prepectoral DTI reconstruction, subpectoral reconstruction is
smoother and has improved elevation of the breast mound. The muscle
coverage of the upper pole is less likely to need fat grafting thus offering a
true single-stage procedure with only one operation. For large breasts and
DTI, there may be an advantage to the subpectoral technique in improved
hold of the implant. The main disadvantages are in potential animation with
pectoralis muscle contraction and more contralateral asymmetry in patients
with ptotic breasts undergoing unilateral reconstruction. In prepectoral
reconstruction, the implant may still move with pectoralis muscle contraction;
however, there is no anterior distortion. Because a prepectoral reconstruction
typically sits lower on the chest wall, it may offer better contralateral
symmetry to a breast with grade 2 to 3 ptosis. Disadvantages of prepectoral
reconstruction include increased need for ADM material leading to increased
cost, more implant visibility and lumpiness, perceived heaviness of large
implants, and risk for a step-off deformity in the upper pole, which may be at
least partially corrected with fat grafting.
CONTRAINDICATIONS
Absolute contraindications to single-stage reconstruction include poor soft
tissue quality, insufficient mastectomy flap perfusion, and inadequate volume
of soft tissue envelope while patient preference for an increased breast cup
size from baseline and discordance between patient goals and achievable
outcomes are relative contraindications assessed on an individual basis. Poor
soft tissue quality can result from poor mastectomy technique, increased age,
smoking, massive weight loss, steroid use, and radiation therapy. Poor skin
flap perfusion after mastectomy would not allow for placement of an implant
immediately as additional pressure on a compromised skin flap would
significantly increase risk of necrosis. Mastectomy skin flaps should always
be evaluated prior to proceeding with single-stage reconstruction. If
mastectomy flaps are not well perfused, then either two-stage reconstruction
with TE or no immediate reconstruction should be performed. The soft tissue
envelope must have not only adequate perfusion but also adequate volume to
allow for an immediate implant placement. Removal of the nipple areola
complex would decrease the volume of the soft tissue envelope, reducing the
size of implant and flattening the breast, thus reducing projection. In patients
with significant ptosis, a vertical incision is preferred for improved
centralization of the nipple; however, this incision places additional stress on
the mastectomy skin flaps making DTI less likely.
Patient preference for an increase in breast size from baseline would
benefit from two-stage reconstruction with TEs to allow for expansion of the
breast soft tissue envelope. Small increases in size are possible in the setting
of optimal soft tissue quality and mastectomy flap perfusion in NSM.
PREOPERATIVE PLANNING
After deciding to proceed with single-stage breast reconstruction,
preoperative planning depends on the oncologic plan, patient preference for
size, and patient breast anatomy with particular attention to ptosis and nipple
position. Incision choice will depend on nipple-sparing versus skin-sparing
mastectomy, ptosis, prior breast surgery, and history of radiation.
Preoperative markings begin with breast landmarks, including
inframammary fold (IMF) position, breast footprint, and lateral border of the
breast in the anterior axillary line. These markings serve as general guidelines
to mastectomy dissection and breast mound reconstruction. Nipple-sparing
mastectomy incisions include inferolateral IMF, vertical, periareolar, lateral,
and extension of a prior scar. The inferolateral IMF incision provides the best
cosmesis with a hidden scar; however, excessive retraction may compromise
the lower pole skin, so particular care must be taken as experience is gained.
Increasing the length of the incision from approximately 6 o’clock to 3 or 9
o’clock on the breast improves the visibility of the upper pole allowing less
retraction and the scar remains hidden along the lateral border of the implant.
The vertical incision allows for narrowing of the breast and centralization of
the NAC in large breasts; however, it is also more ischemic to the
mastectomy skin flaps making DTI less likely. The periarealar incision is
ofern preferred by the mastectomy surgeon as it gives the same access as the
skin sparing mastectomy incision; however, risk of nipple necrosis is
increased (7). The lateral incision preserves nipple perfusion; however, the
scar can be prominent and may pull the nipple laterally. Extension of a prior
scar avoids new scars; however, risks for complications are increased in the
setting of a previously radiated lumpectomy incision (6,8).
Skin-sparing mastectomy incisions may be oriented in a horizontal,
vertical, or oblique orientation. The horizontal incision typically is chosen for
small to medium-sized breasts, providing the least tension on the skin flaps.
The vertical incision may be chosen for larger breasts to narrow and shape
the breasts. Caution must be taken not to chase vertical incision dog-ears into
the superior pole of the breast that may be visible in clothing. Although a
Wise pattern offers the best ability to control the skin envelope in a large
breast, it is also associated with the most skin necrosis. Therefore, a
conservative approach utilizes the vertical incision in the first step and
addition of a horizontal component in a second surgery if needed.
OPERATIVE TECHNIQUE
After mastectomy, intraoperative evaluation of mastectomy skin quality,
pectoralis muscle quality, and soft tissue envelope is performed. Assessment
of the breast skin flaps after mastectomy includes skin flap perfusion,
thickness, and uniformity. In experienced hands with consistent mastectomy
flaps, observation alone suffices for perfusion assessment. However, for
those inexperienced or working with many different oncology surgeons,
intraoperative perfusion devices may help determine overall viability of the
skin and its ability to undergo DTI reconstruction. The pectoralis major size
and thickness determines the degree of superior pole coverage of the implant.
The ADM sling provides support and coverage along the inferior pole of the
implant pocket. Any sign of skin flap compromise should lead to two-stage
TE-implant reconstruction or delayed reconstruction. After initial inspection,
a sizer is placed into the prepectoral space to determine implant volume and
ability of the skin to withstand the additional pressure from the implant. The
implant is chosen based on volume and breast base width for nipple
centralization or breast base diameter for skin-sparing procedures.
After the mastectomy flap is evaluated and determined to be of good
quality, the decision is made to proceed with single-stage implant
reconstruction. The pectoralis muscle is released along its inferior and lateral
borders. A cuff of muscle is typically preserved inferiorly for anchoring the
ADM. Adequate muscle release to the 4 or 8 o’clock position on the chest
wall is key to allow medial implant positioning. The inferior sling is then
sewn in to complete the pocket (Fig. 46-1). ADM comes in rectangular or
contour configurations. The authors prefer contour for ease of use. General
guidelines for size include medium contour for up to 400-cc implant, large
contour ADM for 400- to 600-cc implant, and extra-large contour for 600 to
800 cc implant. The ADM recreates the inferior pole of the breast pocket and
acts as an extension to the pectoralis muscle. A pocket width is measured 1
cm less than the anticipated width of the implant. This accounts for the
inherent stretch of human ADM. Nonabsorbable Ethibond 0-0 sutures are
placed medially to laterally to tack the ADM initially to the breast skin flap
and then to the chest wall. Absorbable Vicryl 2-0 are used between ADM and
pectoralis major, with a central area left open to insert a sizer and subsequent
implant. The sizer is placed with U-stitch to close the pocket and staples to
close the skin temporarily. The patient is sat upright to confirm size and
assess position of the implant pocket.
The sizer volume should approximate the size desired by the patient while
allowing adequate mastectomy skin perfusion. Breast base width, sizer
volume, and nipple position influence the ultimate implant chosen. Implants
may be silicone versus saline, round versus shaped, and smooth versus
textured. Silicone implants are preferred over saline implants due to
decreased rippling and more natural appearance and feel compared to saline
implants. Smooth implants are often preferred over textured implants due to
their improved mobility and decreased risk of biofilm. Anatomic, shaped
implants tend to have less rippling and more natural breast shape compared to
round implants; however anatomic implants have a risk of rotation. Textured
implants are under increased scrutiny due to a rare risk of breast implant–
associated anaplastic large cell lymphoma (BIA-ALCL).
Once the type and volume of implant are determined, the sizer is removed
and hemostasis completed. Two drains are placed, one within the pocket
along the IMF and the other external to the pocket into the axilla and both
exiting at or above the level of the IMF lateral. For prevention of biofilm and
postoperative infection, irrigation with Betadine 1:1 with saline followed by
two irrigation cycles with triple-antibiotic solution (cefazolin, gentamycin,
bacitracin) are performed. Gloves are changed, skin cleaned with an
antibiotic-soaked sponge, and retractors are held by an assistant to open the
pocket. If a textured implant is chosen, a Keller funnel is used to achieve a
no-touch technique. The pocket is closed with absorbable Vicryl 2-0 sutures
between the ADM and pectoralis muscle junction (Fig. 46-2). Skin edge is
deepithelialized with any poorly perfused skin removed, followed by three
layers of closure with Monocryl 3-0. Surgical glue, Tegaderm, and
Microfoam tape along the inferior and lateral borders of the breast mound are
placed (Figs. 46-3 and 46-4). Biopatches are placed around the drains
insertion sites and covered with Tegaderm.
FIGURE 46-1 The pectoralis muscle is released inferiorly and becomes the superior
coverage of the implant. The acellular dermal matrix is sewn to the chest wall and
inframammary fold to act as an extension of the pectoralis muscle for precise
implant positioning.
FIGURE 46-2 The implant pocket is closed under tension with absorbable sutures
following implant placement.
FIGURE 46-3 Incisions are sealed with surgical glue, Steri-Strips, Biopatches, and
Tegaderm.
FIGURE 46-4 Lateral view of implant closure.
POSTOPERATIVE CARE
Postoperative dressings, surgical bra, antibiotic regimen, and duration of
drains vary based on surgeon preference. Our team places surgical bras on
postoperative day 1 to avoid immediate postoperative mastectomy flap
pressure on postoperative day 0 but light compression on postoperative day 1.
Antibiotic prophylaxis evidence is not consistent, leading surgeons to
determine their own antibiotic prophylaxis protocol based on preference. A
comprehensive review on antibiotic prophylaxis in implant-based breast
reconstruction examined two prospective randomized trials, three
retrospective cohort studies, and two systemic reviews (9): a prospective
randomized trial determined a single preoperative dose of antibiotics was
superior to placebo (10); another prospective randomized trial found no
difference between 24 hours of perioperative antibiotics and prolonged
antibiotics until drain removal (11). Among the three retrospective cohort
studies, one demonstrated no significant difference between a single
preoperative dose and prolonged antibiotics (12) versus the two other
retrospective cohort studies that demonstrated significant reduction in
infection rates with prolonged antibiotics (13,14). In review of the two
systemic reviews, one review revealed an increased infection rate with
prolonged antibiotics (15), and the other review demonstrated that antibiotics
<24 hours or >24 hours had no significant difference; however, antibiotic
treatment was superior to no antibiotic treatment (16). Our team prefers to
continue antibiotics until drain removal, correlating to drain output of 30 cc
or less per day. Massage can be initiated 1 month postoperative to prevent
capsular contracture. Vigorous activity should be held until 6 weeks
postoperative.
Mastectomy skin flap perfusion can be improved with placement of
nitropaste cream with Tegaderm dressing to cover. Low-dose nitro paste
dressings have been shown to decrease mastectomy flap necrosis compared
to no nitro paste dressings (3.8% vs. 23.8%) after mastectomy (17).
Pain control starts prior to the surgery. Patients should be enrolled in an
enhanced recovery after surgery protocol to minimize pain and the need for
narcotics. A typical preoperative regimen includes Tylenol and gabapentin.
Our preference then is to proceed with paravertebral blocks performed by
anesthesia using ultrasound guidance. Alternatives include local anesthetic
injection of incision sites and intercostal nerve blocks.

CASES

CASE 1

This 45-year-old female had DCIS of the left breast (Fig. 46-5A–C). She
desired to stay approximately the same size and did not want to have any
additional surgical procedures if possible. She underwent bilateral nipple-
sparing mastectomy and single-stage subpectoral reconstruction with
smooth round moderate-profile silicone implants and an acellular dermal
matrix sling (Fig. 46-5D–F). A higher-profile implant at the same volume
would have given better projection; however, the nipple would have been
lateralized. Prepectoral reconstruction could have been considered;
however, it is more likely she would have had upper pole visibility and
she desired to avoid fat grafting and additional procedures.
FIGURE 46-5 DCIS of the left breast.

CASE 2

This 50-year-old female had multifocal invasive carcinoma of the left


breast (Fig. 46-6A,B). She desired to stay the same overall size.
Unilateral subpectoral reconstruction with ADM allows good
symmetrical results in a single-stage procedure for patients with grade I
breast ptosis as seen in follow-up photos (Fig. 46-6C,D). No additional
procedures have been performed.
FIGURE 46-6 Multifocal invasive carcinoma of the left breast.

CASE 3

This 43-year-old female had a history of bilateral subpectoral breast


augmentation and was diagnosed with left invasive ductal carcinoma with
lymph node involvement (Fig. 46-7A,B). She was happy with her breasts
and desired to stay the same size. She required postmastectomy
radiotherapy. In the setting of postmastectomy radiotherapy, the authors
prefer DTI reconstruction. Because of her current subpectoral position
and her large implant size, submuscular DTI reconstruction was chosen.
Although radiation to the pectoralis muscle may contribute to capsular
contracture and fold elevation, the authors have found less significant
contributions in large breasts. Furthermore, given the large size of the
breasts, prepectoral reconstruction would have given her less predictable
implant positioning and possibly more feelings of implant heaviness. She
is shown preoperative and postoperative following bilateral NSM and
subpectoral DTI reconstruction using smooth round silicone implants and
left postmastectomy radiotherapy (Fig. 46-7C,D). No additional
procedures have been performed.
FIGURE 46-7 Left invasive ductal carcinoma with lymph node involvement.
COMPLICATIONS
Risks to single-stage breast implant reconstruction include mastectomy skin
flap necrosis, nipple necrosis, infection, seroma, hematoma, implant rupture,
and capsular contracture. Patients should be educated about the small but
present risk of ALCL, or anaplastic large cell lymphoma, which has been
associated primarily with use of textured implants. Animation deformity may
occur with subpectoral placement of implants given the inferior edge of the
pectoralis muscle is detached.
OUTCOMES
Single-stage reconstruction has no significant difference in complication rates
compared to two-stage reconstruction with TEs (18,19). Single-stage breast
reconstruction complications include skin necrosis (0.9%), infection (3%),
seroma (1.5%), and explantation (1.5%) (20). Neoadjuvant radiation prior to
mastectomy is associated with an increased risk of overall complications,
implant loss, need for secondary procedures for capsular contracture, and fat
grafting (8). Skin necrosis can be treated with sharp debridement in the office
or operating room with primary closure. If the area of skin excision is large,
then implant downsizing or TE placement may be required. Implant infection
should be treated with oral or intravenous antibiotics depending on severity
of clinical symptoms. If antibiotic therapy does not resolve the infection or if
the patient presents with significant systemic symptoms, explantation, breast
pocket irrigation and debridement, and placement of drains is required.
Seroma can be treated with repeated aspiration with or without ultrasound
guidance. If seroma is recurrent and not resolving with conservative
measures, then operative irrigation and debridement of seroma cavity should
be performed. Late seromas should always be sent for culture and cytology to
diagnose infection or ALCL. Cytology testing of fluid evaluates for CD-30, a
marker for ALCL.
Revision rates are not significantly different between single-stage and two-
stage TE reconstruction in experienced centers, with total revision rates
20.9% versus 20.3% × p = 0.861, respectively (21) at 5 years. Implant
malposition (3.4% vs. 5.5%, p = 0.200), size change (6.7% vs. 5.5%, p =
0.569), fat grafting (8.6% vs. 9.7%, p = 0.647), and capsular contracture
(4.5% vs. 3.2%, p = 0.429), were also found to not be significantly different
between single-stage and two-stage implant reconstruction. Revisions most
commonly attempt to correct implant malposition, size discrepancy, contour
deformity, step-off between implant and chest wall, and capsular contracture.
Implant malposition commonly requires capsulotomy and capsulorrhaphy to
correct the implant position by modifying the pocket. Size discrepancy
between the implant and pocket necessitates either capsulorrhaphy to tighten
the pocket or implant exchange with change in size. Contour deformity can
be corrected with fat grafting, often performed superior and medial to soften
the transition from the chest wall to implant. Mild capsular contracture may
be treated with gentle massage in an attempt to loosen the pocket with a trial
of Singulair. If there is a concern for implant rupture, MRI is beneficial to
evaluate. If capsular contracture is severe or if the implant is ruptured, total
capsulectomy and implant exchange is required.
Patient-reported outcomes between single-stage and two-stage implant-
based reconstruction are similar. Single-stage immediate implant
reconstruction has equivalent BREAST-Q scores with satisfaction of breasts,
satisfaction with outcome, psychosocial well-being, physical well-being, and
satisfaction with nipples and higher BREAST-Q scores for sexual well-being
as compared to two-stage implant reconstruction (18).
CONCLUSION
Immediate single-stage breast reconstruction provides breast reconstruction
in one stage with similar complication profiles, revision rates, and patient-
reported outcome measures compared to two-stage implant reconstruction.
Patients must be appropriately selected based on patient preferences
including size and desire for single-stage procedure, well-perfused
mastectomy flap, adequate soft tissue envelope, and good soft tissue quality.

REFERENCES

1. Breuing KH, Warren SM. Immediate bilateral breast reconstruction with


implants and inferolateral AlloDerm slings. Ann Plast Surg
2005;55(3):232–239.
2. Breuing KH, Colwell AS. Inferolateral AlloDerm hammock for implant
coverage in breast reconstruction. Ann Plast Surg 2007;59(3):250–255.
3. Vardanian AJ, Clayton JL, Roostaeian J, et al. Comparison of implant-
based immediate breast reconstruction with and without acellular dermal
matrix. Plast Reconstr Surg 2011;128(5):403e–410e.
4. Freedman RA, Kouri EM, West DW, et al. Higher stage of disease is
associated with bilateral mastectomy among patients with breast cancer:
a population-based survey. Clin Breast Cancer 2016;16(2):105–112.
5. Rosenberg SM, Sepucha K, Ruddy KJ, et al. Local therapy decision-
making and contralateral prophylactic mastectomy in young women
with early-stage breast cancer. Ann Surg Oncol 2015;22(12):3809–3815.
6. Frederick MJ, Lin AM, Neuman R, et al. Nipple-sparing mastectomy in
patients with previous breast surgery: comparative analysis of 775
immediate breast reconstructions. Plast Reconstr Surg
2015;135(6):954e–962e.
7. Colwell AS, Tessler O, Lin AM, et al. Breast reconstruction following
nipple-sparing mastectomy: predictors of complications, reconstruction
outcomes, and 5-year trends. Plast Reconstr Surg 2014;133(3):496–506.
8. Reish RG, Lin A, Phillips NA, et al. Breast reconstruction outcomes
after nipple-sparing mastectomy and radiation therapy. Plast Reconstr
Surg 2015;135(4):959–966.
9. Phillips BT, Halvorson EG. Antibiotic prophylaxis following implant-
based breast reconstruction: what is the evidence? Plast Reconstr Surg
2016;138(4):751–757.
10. Amland PF, Andenaes K, Samdal F, et al. A prospective, double-blind,
placebo-controlled trial of a single dose of azithromycin on
postoperative wound infections in plastic surgery. Plast Reconstr Surg
1995;96(6):1378–1383.
11. Phillips BT, Fourman MS, Bishawi M, et al. Are prophylactic
postoperative antibiotics necessary for immediate breast reconstruction?
Results of a prospective randomized clinical trial. J Am Coll Surg
2016;222(6):1116–1124.
12. McCullough MC, Chu CK, Duggal CS, et al. Antibiotic prophylaxis and
resistance in surgical site infection after immediate tissue expander
reconstruction of the breast. Ann Plast Surg 2016;77(5):501–505.
13. Avashia YJ, Mohan R, Berhane C, et al. Postoperative antibiotic
prophylaxis for implant-based breast reconstruction with acellular
dermal matrix. Plast Reconstr Surg 2013;131(3):453–461.
14. Clayton JL, Bazakas A, Lee CN, et al. Once is not enough: withholding
postoperative prophylactic antibiotics in prosthetic breast reconstruction
is associated with an increased risk of infection. Plast Reconstr Surg
2012;130(3):495–502.
15. Phillips BT, Bishawi M, Dagum AB, et al. A systematic review of
infection rates and associated antibiotic duration in acellular dermal
matrix breast reconstruction. Eplasty 2014;14:e42.
16. Phillips BT, Bishawi M, Dagum AB, et al. A systematic review of
antibiotic use and infection in breast reconstruction: what is the
evidence? Plast Reconstr Surg 2013;131(1):1–13.
17. Yun MH, Yoon ES, Lee BI, et al. The effect of low-dose nitroglycerin
ointment on skin flap necrosis in breast reconstruction after skin-sparing
or nipple-sparing mastectomy. Arch Plast Surg 2017;44(6):509–515.
18. Susarla SM, Ganske I, Helliwell L, et al. Comparison of clinical
outcomes and patient satisfaction in immediate single-stage versus two-
stage implant-based breast reconstruction. Plast Reconstr Surg
2015;135(1):1e–8e.
19. Salzberg CA, Ashikari AY, Koch RM, et al. An 8-year experience of
direct-to-implant immediate breast reconstruction using human acellular
dermal matrix (AlloDerm). Plast Reconstr Surg 2011;127(2):514–524.
20. Colwell AS, Damjanovic B, Zahedi B, et al. Retrospective review of 331
consecutive immediate single-stage implant reconstructions with
acellular dermal matrix: indications, complications, trends, and costs.
Plast Reconstr Surg 2011;128(6):1170–1178.
21. Clarke-Pearson EM, Lin AM, Hertl C, et al. Revisions in implant-based
breast reconstruction: how does direct-to-implant measure up? Plast
Reconstr Surg 2016;137(6):1690–1699.
CHAPTER 47

Patient Selection for One-Stage


Reconstruction Prepectoral
ROY DE VITA | ERNESTO MARIA BUCCHERI
HISTORY
Prepectoral implant-based reconstruction (IBR) was first described in the
1970s by Snyderman and Guthrie; it was an easy and fast approach
preserving the pectoralis muscle (1). A number of complications were
described for prepectoral IBR including skin flap necrosis and reconstruction
failure, capsular contracture, implant visibility, and wrinkling/rippling (2).
Since high rates of complications, prepectoral approach of IBR has been
improved with a submuscular two-stage breast reconstruction using a tissue
expander followed by definitive implant, reducing the complication rates.
The introduction of modern oncoplastic surgery such as subcutaneous
mastectomies and the acellular dermal matrices (ADMs) and synthetic
meshes era changed IBR radically; surgeons started to perform immediate
direct-to-implant (DTI) breast reconstruction with a dual plane coverage:
pectoralis major muscle and meshes/matrices, without the use of tissue
expanders (1,3,4).
However, breast animation deformity, implant displacement, function
impairment, and chronic pain, were estimated as major complications due to
pectoralis major muscle involvement (5).
Recently, prepectoral one-stage implant-based breast reconstruction has
gained a new interest: trying to solve muscle-related complications. In 2015
an implant-based prepectoral breast reconstruction with a total ADM
coverage was reported which was followed by numerous scientific reports
with different kind of matrices and ADMs (6–8). On April 2019 we have first
reported in literature our experience with nipple-sparing mastectomies
(NSMs) and DTI breast reconstructions using a prepectoral approach and
micropolyurethane sponge-coated implants. We have termed it Breast
Reconstruction Actualized in NSM and DTI with PrePectoral Polyurethane
Positioning (BRAND4P) (1). The aim of this chapter is to describe our
experience in patient selection for subcutaneous mastectomy and DTI
prepectoral approach, focusing on BRAND4P procedure and to correct
animation deformity, to reduce chronic pain and capsular contracture with a
subpectoral to prepectoral implant exchange.
PATIENT SELECTION
The aim of this chapter is to report our experience in one-stage prepectoral
breast reconstruction using micropolyurethane implant in primary nipple
sparing mastectomy both prophylactic and therapeutic and in revision surgery
due to animation deformity, chronic pain and capsular contracture.
BRAND4P PROCEDURE
Several patient characteristics, such as body mass index (BMI), oncologic
preop therapies, or smoking habit, portend high risk of complications related
to NSM with prepectoral reconstruction. Moreover, as well reported in
literature, the most critical factor in the success of prepectoral reconstruction
is the quality and viability of mastectomy flaps (9,10). So we advocate the
oncoplastic surgeon as “one-man band,” a central role to manage breast
cancer from the oncologic procedure to the breast reconstruction and follow-
up (11).
We report encouraging results without any kind of major complications
from our previous studies allowing us to declare how to conduct a safe
BRAND4P reducing the flap/nipple areolar complex (NAC) necrosis,
suffering, and subsequent reconstruction failure; we have used always a
selected incision, scissors solely for mastectomy, a mastectomy flap thickness
between 5 and 8 mm, and proper patient selection (1,10,12). Our indications
for revision to prepectoral reconstruction include animation deformity, pain,
and capsular contracture. (13).
The skin incision is the first and a crucial step in NSM because the blood
supply to the NAC and flap viability must be preserved. The surgical incision
has a considerable impact on complication rates. Lazy-S, vertical incisions,
and periareolar or laterally extended incisions are reported in literature such
as lateral inframammary fold incision with different rates of skin suffering
and flap necrosis (11,12). Considering our previous experiences described in
literature (1,10,12,21), we always use lateral inframammary fold incisions for
small to medium breasts to achieve the best contouring, with a well-hidden
scar with a correct NAC and skin flap perfusion.
We always perform subcutaneous dissection by scissors solely instead of
electrocautery uses. It is well investigated that diathermal use increase
complications’ risk. Previous reports confirm that electrocautery dissection,
in subcutaneous mastectomy, increases the possibility of subdermal plexus
thrombosis and consequent skin flap suffering up to 25% (14).
From our previous experience in NSM and DTI (10), we suggest a 5- to 8-
mm flap and NAC thickness for oncologic safety and blood supply. As stated
in literature, skin flaps less than 5 mm thick could be a cause of major skin
suffering and partial/total necrosis. In contrast, flaps thicker than 8 mm allow
a difficult lymphatic drainage and cellulitis. Stated for a safe BRAND4P we
advocate for a strict patient selection, according to our experience and
literature review. Patients with a preoperative history of neoadjuvant
chemotherapies and/or radiation therapy are not eligible for a safe procedure.
A known risk factor is preoperative oncology therapies which lead to poor
heeling and more stress on the breast skin viability after NSM (2,15,16).
Smoking patients are also excluded from our patient selection; smoking is a
risk factor for NAC necrosis and flap viability, literature reports a high rate of
flap necrosis up to 40% after subcutaneous mastectomy (17).
Body Mass Index (BMI) is an important parameter in patient selection
when we perform BRAND4P. BMI greater than 30 kg/m2 presents a higher
risk of skin suffering. Previous researches also showed a high rate of major
complication related to ischemia for patients with a first grade of obesity
(higher than 30 kg/m2) (18,19). Regardless of BMI, breast volume is another
parameter to selection for the best BRAND4P patient. Large and voluminous
breasts determine an increase in flap length between the thoracic wall and the
NAC which reduces blood supply to the breasts edges (20). So, the large
volume of the breast is considered as a risk factor of necrosis of the NAC
area in NSM. So we include in our patient selection BMI range between 18
and 30 kg/m2 and large-size breasts are definitively excluded for a safe
BRAND4P; we treat large breast by preoperative planned skin-reducing
pattern incision, such as skin-reducing mastectomy and NAC free graft
followed by DTI breast reconstruction with prepectoral polyurethane implant
positioning (12,21).
Statistical analysis reported in literature showed a lower risk of flap failure
in patient with age below 45 years; nevertheless authors report NSM and
implant-based breast reconstruction with a lower complication rate in older
women than in younger women (22,23). So the last exclusion criterion
considered was age. We always select patients younger than 65 years old.
OPERATIVE TECHNIQUE
BRAND4P
BRAND4P procedures need to be performed under general anesthesia by the
oncoplastic surgeon. The preoperative markings is performed with the patient
in a stand-up position starting to include the middle and parasternal lines,
inframammary creases, upper pole parenchyma limits, and the incision site.
Incision place is located at the inframammary crease laterally, or skin-
reducing pattern is followed for large breasts; we perform subcutaneous
mastectomy with scissors solely to achieve the best control of skin flap
thickness where the average was between 5 and 8 mm minimizing tissue
trauma and suffering; skin flap thickness is measured by means of calipers at
upper outer, lower outer, upper inner, lower inner, and beneath the NAC. At
the end of the oncologic procedure, the skin flap vasculature is assessed by
checking the clinical flap perfusion and bleeding from the wound edges and
intraoperative laser-assisted indocyanine green (ICG) fluorescent
angiography (LA-ICGA) is performed in order to provide a real-time
visualization of postmastectomy skin flap perfusion. The fluorescent agent
ICG important features are in terms of short half-life, strong binding to
plasma proteins, excellent safety profile, and rapid clearance (10,24). Implant
pocket conversion and polyurethane uses is offered to patients that require
surgical plane changing from retropectoral to prepectoral positioning. The
prior incision is reused to perform the secondary procedure. Dissection is
carried down through the skin and subcutaneous tissue until the pectoralis
major muscle is showed at its anterior surface. Once the superior flap is
raised, the pectoralis major muscle is opened and the implant is removed, the
muscle is now transferred back to its anatomical position on the chest wall,
and the muscle incision site is secured using Vicryl 3-0 running sutures.
When the subcutaneous pocket is performed the micropolyurethane
sponge-coated implant is placed directly using a sterile bag to prevent
contamination during passage through the incision site. We always use the
micropolyurethane foam-coated anatomic implant from the Microthane
Sublime Line (Polytech, Dieburg, Germany).
Particular care was taken in the correct positioning of the implant. A
suction drainage was routinely placed into the pocket.
POSTOPERATIVE CARE
All the procedures are followed by pharmacologic therapy consisting of
cephalosporin administered at anesthesia induction and continued until drains
is removed. Moderate compression dressing with impregnated gauze is
applied for 2 days after surgery. The patient (shown preoperatively in Fig.
47-1) is discharged on second/third postoperative day after dressing removal
and sport bra placement, with the drainage in place. The drainage is removed
after a range of 7 days (4 to 10 days) postoperatively, when the fluid
collection is less than 50 cc. The bra is usually removed after postoperative
day 30 to 45. No sport activity is recommended for 6 months postoperatively.
FIGURE 47-1 A–E: Preoperative patient views.

Follow-up consists of 3 weeks of postoperative visits conducted on Days


3–6–14–21 followed by a 2–6 (Fig. 47-2), and 12 months period thereafter
(Fig. 47-3).
FIGURE 47-2 A–E: Postoperative patient views at 6 months.
CONCLUSION
Any oncologic breast surgery and breast reconstruction needs a very good
planning and standardized execution. Regardless of the surgical oncology and
reconstructive procedure, the approach is based on these principles and
should be performed in every patient by the same surgeon, the oncoplastic
surgeon. NSM and IBR is nowadays a safe procedure (9). On the other side,
patients submitted to retropectoral implant positioning report breast
animation deformity and chronic pain; previous studies found up to 80%
prevalence rate of animation deformity in a cohort of patients who had
undergone submuscular prosthetic breast reconstruction (8).
Investigators have considered NSM and prepectoral IBR a less-invasive
option to subpectoral approach (7,8,10). The benefits include a low rate of
animation deformity and reduced pain. The authors first reported early
experience with NSMs and DTI breast reconstructions using a prepectoral
approach and micropolyurethane sponge-coated implants. The authors termed
it Breast Reconstruction Actualized in NSM and DTI with PrePectoral
Polyurethane Positioning (BRAND4P) (1).
FIGURE 47-3 A–E: Postoperative patient views at 1 year.

The polyurethane foam-coated breast implant is a well-known device in the


breast prosthetic panorama, both for augmentation and for reconstruction
(26). Since its introduction, a very low capsular contracture rate has been
reported by the authors (<1%) (1,25,26). We report our experience using
Polytech Microthane implants that are made of a 1.4-mm micropolyurethane
sponge layer that covers the whole implant, forming an integrated ready-to-
use surgical device for a safe IBR. Thus, no further coverage is needed for
the breast implant such as ADM or a synthetic mesh in a DTI; the implant is
then safely placed in the prepectoral pocket, resulting in a simple, reliable and
cost-effective procedure. Because the surgery does not require implant
manipulation and preparation, polyurethane implant uses also decreases the
time of the surgery. Our experience, started in December 2017 (1) with
BRAND4P, has shown encouraging results. No major complications, chronic
pain, capsular contracture and animation deformity have been reported until
now with satisfactory cosmetic outcomes.
In September 2018 the authors started to extend indication from primary
procedures both prophylactic and therapeutic to secondary procedures to
correct complications. After their initial retropectoral IBR, patients often
complain breast animation deformities, chronic pain and capsular contracture.
These sequelae are uncomfortable and aesthetically displeasing. Our
preferred approach to solve existing animation deformity and solving
patients’ pain needs a secondary surgery with implant pocket conversion to
the prepectoral plane and implant substitution with the anatomic profile
micropolyurethane sponge-coated implants.
The authors believe that outcomes resulted mainly from accurate patient
selection, a proper operative technique, and the implant features. Longer-term
follow-up will demonstrates maintenance of the integrity and quality of the
reconstructions over time with low rates of capsular contracture and absence
of animation deformity and chronic pain. The prepectoral approach presented
as a fast, reliable and reproducible method, is the authors’ primary choice for
immediate IBR following sub-cutaneous mastectomies and for muscle related
complications solution with secondary procedures.

REFERENCES

1. Snyderman RK, Guthrie RH. Reconstruction of the female breast


following radical mastectomy. Plast Reconstr Surg 1971;47(6):565–567.
2. Schlenker JD, Bueno RA, Ricketson G, et al. Loss of silicone implants
after subcutaneous mastectomy and reconstruction. Plast Reconstr Surg
1978;62:853–861.
3. Breuing KH, Warren SM. Immediate bilateral breast reconstruction with
implants and inferolateral AlloDerm slings. Ann Plast Surg
2005;55:232–239.
4. Dieterich M, Dieterich H, Timme S, et al. Using a titanium coated
polypropylene mesh (TiLOOP bra) for implant-based breast
reconstruction: case report and histological analysis. Arch Gynecol
Obstet 2012;286:273–276.
5. Becker H, Fregosi N. The impact of animation deformity on quality of
life in postmastectomy reconstruction patients. Aesthet Surg J
2017;37:531–536.
6. Vidya R, Masià J, Cawthorn S, et al. Evaluation of the effectiveness of
the prepectoral breast reconstruction with Braxon dermal matrix: first
multicenter European report on 100 cases. Breast J 2017;23:670–676.
7. Casella D, Di Taranto G, Marcasciano M, et al. Nipple-sparing bilateral
prophylactic mastectomy and immediate reconstruction with TiLoop bra
mesh in BRCA1/2 mutation carriers: a prospective study of long-term
and patient reported outcomes using the BREAST-Q. Breast 2018;39:8–
13.
8. Sbitany H, Piper M, Lentz R. Prepectoral breast reconstruction: a safe
alternative to submuscular prosthetic reconstruction following nipple-
sparing mastectomy. Plast Reconstr Surg 2017;140:432–443.
9. Salibian AA, Frey JD, Karp NS. Strategies and considerations in
selecting between subpectoral and prepectoral breast reconstruction.
Gland Surg 2019;8:11–18.
10. de Vita R, Buccheri EM. Nipple sparing mastectomy and direct to
implant breast reconstruction, validation of the safe procedure through
the use of laser assisted indocyanine green fluorescent angiography.
Gland Surg 2018;7:258–266.
11. Baxter RA. Update on the split-muscle technique for breast
augmentation: prevention and correction of animation distortion and
double-bubble deformity. Aesthetic Plast Surg 2011;35:426–429.
12. De Vita R, Zoccali G, Buccheri EM, et al. Outcome evaluation after
2023 nipple-sparing mastectomies: our experience. Plast Reconstr Surg
2017;139:335e–347e.
13. Lentz R, Alcon A, Sbitany H. Correction of animation deformity with
subpectoral to prepectoral implant exchange. Gland Surg 2019;8:75–81.
14. Féron JG, Leduey A, Mallon P, et al. The role of nipple-sparing
mastectomy in breast cancer: a comprehensive review of the literature.
Ann Chir Plast Esthet 2014;59:333–343.
15. Alperovich M, Choi M, Frey JD, et al. Nipple-sparing mastectomy in
patients with prior breast irradiation: are patients at higher risk for
reconstructive complications? Plast Reconstr Surg 2014;134:202e–206e.
16. Dolen UC, Schmidt AC, Um GT, et al. Impact of neoadjuvant and
adjuvant chemotherapy on immediate tissue expander breast
reconstruction. Ann Surg Oncol 2016;23:2357–2366.
17. Komorowski AL, Zanini V, Regolo L, et al. Necrotic complications
after nipple- and areola-sparing mastectomy. World J Surg
2006;30:1410–1413.
18. Davies K, Allan L, Roblin P, et al. Factors affecting post-operative
complications following skin sparing mastectomy with immediate breast
reconstruction. Breast 2011;20:21–25.
19. Platt AJ, Mohan D, Baguley P. The effect of body mass index and
wound irrigation on outcome after bilateral breast reduction. Ann Plast
Surg 2003;51:552–555.
20. Chirappapha P, Petit JY, Rietjens M, et al. Nipple sparing mastectomy:
does breast morphological factor related to necrotic complications? Plast
Reconstr Surg Glob Open 2014;2:e99.
21. De Vita R, Pozzi M, Zoccali G, et al. Skin-reducing mastectomy and
immediate breast reconstruction in patients with macromastia. J Exp
Clin Cancer Res 2015;34:120.
22. Garwood ER, Moore D, Ewing C, et al. Total skin-sparing mastectomy:
complications and local recurrence rates in 2 cohorts of patients. Ann
Surg 2009;249:26–32.
23. August DA, Wilkins E, Rea T. Breast reconstruction in older women.
Surgery 1994;115:663–668.
24. Sood M, Glat P. Potential of the SPY intraoperative perfusion
assessment system to reduce ischemic complications in immediate
postmastectomy breast reconstruction. Ann Surg Innov Res 2013;7:9.
25. Schatten WE. Reconstruction of breasts following mastectomy with
polyurethane covered, gel-filled prostheses. Ann Plast Surg
1984;12:147–156.
26. Capozzi A, Pennisi VR. Clinical experience with polyurethane-covered
gel-filled mammary prostheses. Plast Reconstr Surg 1981;68:512–520.
CHAPTER 48

Breast Reconstruction With Form-


Stable Implants
MAURIZIO BRUNO NAVA | GIUSEPPE CATANUTO | NICOLA ROCCO
HISTORY
Breast reconstructive surgery evolution keeps step with the evolution of
breast oncologic surgery. The reconstructive choice should always balance
the optimal local control of disease and the best cosmetic result, achieving an
informed and shared decision with the patient, the woman always
representing the center of the decision-making process.
Implant-based breast reconstruction with form-stable implants following
mastectomy represents a complex choice. In order to obtain the better results,
it is mandatory to to thorough plan the surgery preoperatively, having a
complete knowledge of the devices we are using, to perform accurate
surgery, and scheduling a correct follow-up.
THE EVOLUTION OF BREAST RECONSTRUCTIVE SURGERY
Breast reconstructive surgery evolution keeps step with the evolution of
breast oncologic surgery.
In the late 90s and early 2000s, the two separate worlds of mastectomy and
lumpectomy (1–4) started to mingle with the development of oncoplastic
breast surgery: breast reconstruction became a standard and a huge range of
surgical techniques with a progressive reduction of the degree of
aggressiveness have been offered to women having a diagnosis of breast
cancer, achieving optimal oncologic and reconstructive results, no more
related to the level of breast conservation.
In 2000s breast cancer surgery did not represent a dichotomous choice
anymore (5).
Higher sensitivity of diagnostic imaging, new genetics’ investigations, and
opportunity for risk-reducing procedures led to a renewed increase of
mastectomy rates during the first decade of 2000s (6,7). A higher percentage
of women well-informed about the equivalence in terms of survival between
breast-conserving surgery (BCS) and mastectomy started to prefer
undergoing a mastectomy thanks to the optimal aesthetic results obtained
with reconstruction (8). Even if well-informed, many women still consider
mastectomy a safer approach for oncologic reasons and choose this surgical
option for reasons of peace of mind.
The years from the 80s to the first decade of the 21st century saw an
amazing evolution of biomaterials and devices available for the breast
surgeon: the round implants, with smooth surface and filled with low
cohesive gel have given way to anatomical shaped form-stable implants, with
a textured surface and filled with a high cohesive gel.
The evolution of biomaterials led to a decreased rate of capsular
contracture around the implants, with a significant improvement of
reconstructed breast shape, paving the way for new reconstructive paradigms
(9).
Evidences from literature definitively demonstrated how immediate breast
reconstruction following mastectomy does not affect oncologic outcomes,
even in patients with advanced disease, without significantly delaying
adjuvant therapies (10,11).
Moreover, as we demonstrated more than 25 years ago, immediate breast
reconstruction presents great advantages from a psychological point of view,
delayed breast reconstruction possibly triggering anxiety and distress during
the period of mastectomy in the women and their partners (12).
In 2008 we presented an alternative surgical model for breast
reconstruction using extra-projected form-stable anatomical implants,
achieving a well-shaped breast and a contralateral reshaping with less
surgical trauma, reserving autologous flap reconstruction only for patients
treated with radiotherapy (13). The 90s paradigm of a large breast to be
reconstructed with an autologous flap, a medium/small breast with an
implant, and to possibly doing nothing to the contralateral breast was
subverted by the extraprojected form-stable anatomical implants’ surgical
model.
We also demonstrated how contralateral breast symmetrization with pexy
reduction techniques does not significantly impact on oncologic follow-up in
breast cancer patients, without leading to a significantly higher need for
second-level imaging examinations and diagnostic biopsies, thus not delaying
contralateral breast cancer diagnosis (14).
We also investigated the timing of radiotherapy in implant-based breast
reconstruction, presenting our decisional algorithms, a very useful tool for the
breast surgeon planning together with his/her patient the best reconstructive
option after radiotherapy or in view of a postmastectomy radiotherapy (15).
The first decade of the new century also saw the possibility of radiotherapy
damages’ treatment with autologous fat cell transplantation, a fast and safe
procedure that further extended the indications to form stable anatomical
implant–based reconstruction (16).
Moreover the introduction of acellular dermal matrices (ADM) and
synthetic meshes further extended the possibility of one-stage direct-to-
implant (DTI) breast reconstructions. ADM and meshes allow improved
implant positioning, creating a larger pocket, helping to rebuild the
inframammary fold, and to achieve a better lower pole projection.
We rationalized and systematically organized our reconstructive
algorithms, giving a new different light to mastectomies, the so-called
“conservative mastectomies” (17–19) and expanding the breast reconstructive
opportunities and choices with the introduction of the skin-reducing
mastectomy for patients with large and ptotic breast (20–22).
BREAST RECONSTRUCTION: A SHARED DECISION
Nowadays breast surgical oncology and breast reconstructive surgery
represent a shared decision with the patient with the duty of tailoring the
surgical treatment on each woman, never forgetting the patient’s own desires
and wishes.
The oncoplastic decision-making process should consider three steps:
balancing the optimal local control of disease, the best reconstructive result,
and giving all the necessary information to the patient in order to achieve a
shared decision, the woman always representing the center of the decision-
making process (23,24).
In order to achieve this purpose, each surgeon involved in the oncoplastic
decision-making process should be aware of all possible breast reconstructive
options and even though not able to perform each surgical technique (the
auspicable so-called “vertical surgeon”), he/she must at least be aware of the
indications to all techniques to offer the patient the best-informed choice for
her breast reconstruction.
FORM-STABLE IMPLANT-BASED BREAST RECONSTRUCTION: A COMPLEX
CHOICE
Implant-based breast reconstruction with form-stable anatomical implants
following mastectomy represents a complex choice. In order to obtain the
better results it is mandatory a thorough preoperative planning, a complete
knowledge of the devices we are using, an accurate surgery and a correct
follow-up.
Moreover the reported evidence about the role of bacterial biofilm in
implant-associated infection, capsular contracture, late seromas, and BIA-
ALCL stresses the importance of applying accurate preoperative and
intraoperative strategies to reduce the risk of breast implants’ bacterial
contamination and biofilm formation. Our experience leads to several
recommendations in order to minimize contamination and reducing bacterial
access during implant-based breast surgery, in accordance with the strategies
for prevention of device-associated infection in breast prostheses proposed by
Deva et al. (25). This is particularly relevant in relation to the recent proposed
association (actually not demonstrated by evidence-based data) between
texturization and BIA-ALCL development.
We must always remember that a good cosmetic result in breast
reconstructive surgery starts with a good mastectomy. Nowadays we know
that a total preservation of the breast envelope can be performed in patients
with early-stage breast cancer without clinical involvement of the nipple
areolar complex. The preservation of the whole breast envelope can be
considered a technical challenge more than an oncologic issue, long
mastectomy skin flaps only receiving blood supply from the subdermal
plexus. Risk factors for ischemic complications (previous radiotherapy,
smoking, etc.) should be preoperatively thoroughly estimated and patients at
high risk should be discouraged to undergo nipple preservation (26–28). The
larger the breast the higher is the ischemic complication rate: large breast
envelopes cannot be easily preserved either for the risk of necrosis and for the
possibility of dislocation of the NAC (28).
Women with early-stage breast cancer for whom a mastectomy is planned
can reach good outcomes with either a two- or a one-stage implant-based
reconstruction if an accurate planning is performed (Fig. 48-1).
A rigorous approach toward breast reconstruction with form-stable
implants starts with an accurate first consultation with the patient, taking into
account patient’s wishes, analyzing the characteristics of the skin and soft
tissues, measuring the chest wall and breast width, the cleavage, assessing the
breast shape, always remembering that if you fail to plan, you plan to fail.
Accurate measurements together with a thorough assessment of the
patient’s wishes are mandatory in order to obtain good outcomes, long-lasting
results, low complication rates, and high patient satisfaction levels, exactly
like in aesthetic breast surgery.
Obviously we always have to balance the wishes of the patient with her
anatomical measurements and soft tissue characteristics. The more clearly the
patient’s expectations are defined and the achievable results are
communicated, the higher the patient’s satisfaction level with her breast
reconstruction can be obtained.

FIGURE 48-1 Algorithm for selection of mastectomy and contralateral technique.

Today form-stable implants offer the opportunity to the breast


reconstructive surgeon of using a wide portfolio of breast implants with
combinations of three different heights and four different projections for each
implant width, thus making it possible to tailor the best implant on the single
woman, according to her anatomical characteristics and wishes. Moreover we
could offer an extraprojected Dual Gel Implant to women wishing a more
sloping upper pole, without a contralateral adjustment.
Everything must be exactly planned together with the patient that always
remains the center of our decision making, before going to the operating
theatre.
We developed a planning method to guide the decision-making process in
breast reconstruction based on the characteristics of the skin and soft tissues,
the breast and chest wall size, breast ptosis, and patient’s wishes (Fig. 48-2).
In order to achieve predictable outcomes, we must make decisions based
on objective data.
According to our reconstructive algorithm, we usually consider autologous
flaps for previously radiotreated patients, even though good results could be
achieved with the use of fat grafting.
AN EVOLUTION OF OUR DECISIONAL ALGORITHM
When evaluating our reconstructive outcomes, we assessed some suboptimal
results even accurately following our algorithm. In order to define risk factors
for suboptimal results, we retrospectively evaluated our patients and found a
significant association with the breast characteristics at preoperative imaging
(digital mammography). In this way, in 2017 we added a new variable in our
reconstructive choice: the selection of patients according to preoperative
digital mammogram characteristics (29).
Preoperative digital mammography imaging could represent a very useful
tool for the breast surgeon to plan the best reconstructive option following
mastectomy, to be considered together the morphovolumetric breast
assessment.
Digital mammography could clearly determine the thickness of the breast
tissue coverage overlying the gland, corresponding to the superficial tissues
between the skin and the Cooper ligaments (i.e., dermis and subcutaneous
fat), thus facilitating the planning of the most adequate reconstructive
technique.
We recently proposed a breast tissue coverage classification (BTCC)
according to the thickness of the superficial tissues covering the mammary
gland measured in centimeters: 1) type 1, poor coverage, <1 cm; 2) type 2,
medium coverage, 1 to 2 cm; 3) type 3, good coverage, >2 cm (Fig. 48-3)
(29).
According to the BTCC, we now suggest an evolution of our decisional
algorithm, balancing the morphovolumetric characteristics of the breast with
digital mammogram breast assessment, always considering the central role of
patient wish (Table 48-1).
We may consider three categories of patients according to women’s
morphology:

1. Patients with small breast


2. Patients with medium-sized breast
3. Patients with large and ptotic breast

Pooling together women’s morphology and breast characteristics according


to the BTCC we propose an evolution of our reconstructive algorithm, to
optimize reconstructive results.

FIGURE 48-2 Algorithm for implant-based breast reconstruction choice according


to morphovolumetric breast characteristics.
FIGURE 48-3 Breast tissue coverage classification. A: Digital mammograms showing
tissue coverage that could be maintained during the mastectomy. B: Type 1: tissue
coverage up to 1 cm (poor coverage); type 2: between 1 and 2 cm (medium
coverage); type 3: more than 2 cm (good coverage).

Type 1 Breasts
Patients With Small Breast
Patients with small breast can be offered a two-stage breast reconstruction. In
these patients we always consider fat grafting before the second
reconstructive time. Afterward we consider an implant positioning with
ADM.
According to patient’s wish, a contralateral augmentation could be
considered. In this case a two-stage breast reconstruction represents the best
option, to achieve the desired volume for the contralateral breast. All these
choices must be done when planning the surgery in order to accurately
evaluate measurements and implant/expander choice. If considering a two-
stage approach with contralateral augmentation, the expander width will be
selected according to the anatomical characteristics of the patients and the
desired contralateral volume that will be chosen according to the chest wall
width and anatomical characteristics of the patient (Fig. 48-4).

Patients With Medium-Sized Breast


Patients with medium-sized breasts should be evaluated according to the
ptosis degree.

TABLE 48-1 Breast Reconstruction Choice According to Breast


Morphovolumetric Characteristics and Breast Tissue Coverage
Classification
FIGURE 48-4 Two-stage breast reconstruction. When considering a two-stage
approach with contralateral augmentation, always choose the expander according to
the anatomical characteristics of the patients, taking in consideration the desired
final contralateral volume. A–C: Preoperative view with the expander on the left side
(Allergan MV 400); D: Accurate preoperative measurement. E: 1-year postoperative
follow-up following right augmentation (Allergan Style 410 MM 250 cc) and left
second reconstructive stage (Allergan Style 410 MX 410 cc). ADM, acellular dermal
matrix; DTI, direct to implant; C/L, contralateral.
FIGURE 48-5 Skin-reducing mastectomy. A 45-year-old BRCA1-mutated patient
undergoing bilateral risk-reducing mastectomy. Preoperative mammogram and
preoperative views.

Patient without significant breast ptosis or presenting moderate ptosis


could undergo a two-stage reconstruction, always considering fat grafting
before the second stage that will be ADM assisted. If presenting a moderate
ptosis, we could consider a contralateral mastopexy with autoprosthesis
technique.
If showing a severe ptosis, the best option could be a skin-reducing
mastectomy with two-stage breast reconstruction and a contralateral
mastopexy with autoprosthesis. Also in this case, we suggest performing fat
grafting before the second reconstructive stage that will be ADM-assisted. In
a type 1 breast, we do not suggest to preserve the NAC (considering a NAC
grafting) if it has to be lifted up more than 3 cm.

FIGURE 48-6 Skin-reducing mastectomy. Same patient as in Figure 48-5. Skin-


reducing mastectomy and bilateral positioning of Allergan MV600 expanders. Six-
month follow-up before the substitution of the expanders with the permanent
implants.

Patients With Large and Ptotic Breast


In these cases we may recommend a skin-reducing mastectomy and two-
stage breast reconstruction and contralateral breast reduction (Figs. 48-5 to
48-7). We suggest fat grafting before the second reconstructive stage that will
be ADM assisted. In a type 1 breast, we do not suggest to preserve the NAC
(considering a NAC grafting) if it has to be lifted up more than 3 cm.
Type 2 Breasts
Patients With Small Breast
Patients with small breast can be offered a DTI breast reconstruction with
ADM. According to patient’s wish, a contralateral augmentation could be
considered. In this case a two-stage breast reconstruction could be the best
option, to achieve the desired volume for the contralateral breast. All these
choices must be done when planning the surgery in order to accurately
evaluate measurements and implant/expander choice. Small contralateral
augmentations could be also planned without a two-stage approach (Fig. 48-
8). When considering a DTI, on the mastectomy side the implant width
should be selected according to the existing breast width, subtracting the
thickness of the skin flaps medially and laterally spliced by two. The height
of the implant will be calculated according to the height of the contralateral
breast when gently pressing it toward the chest wall. In these conditions we
suggest to use extraprojected or full-projected form-stable implants when the
NAC is preserved. The contralateral implant will present the same width of
the mastectomy-side implant approximately reduced by the thickness of the
skin-glandular flap (Fig. 48-9).
FIGURE 48-7 Skin-reducing mastectomy. Same patient as in Figures 48-5 and 48-6.
One-month postoperative view after the substitution of the expanders with Allergan
Style 410 MX 550-cc permanent implants.
FIGURE 48-8 Right NAC-sparing mastectomy. Direct-to-implant reconstruction
with ADM and Allergan Style 410 MX implant (370 cc). Contralateral breast
augmentation (Allergan Style 410 MF implant 225 cc). A: Preoperative digital
mammography showing a type 2 breast; B: Postoperative view at 2-year follow-up.

FIGURE 48-9 Implant selection guide. Direct-to-implant breast reconstruction in


women with small breast.
FIGURE 48-10 Implant selection guide. Direct-to-implant breast reconstruction in
women with medium-sized and/or moderately ptotic breast.

If considering a two-stage approach with contralateral augmentation, the


expander width will be selected according to the anatomical characteristics of
the patients and the desired contralateral volume, that will be chosen
according to the chest wall width and anatomical characteristics of the
patient.
In these patients we could also consider a prepectoral approach, according
to patient’s wish, informing the patient about the possibility of poorer
cosmetic results.

Patients With Medium-Sized Breast


Patients with medium-sized breasts should be evaluated according to the
ptosis degree.
Patient without significant breast ptosis or presenting moderate ptosis
could undergo a DTI dual plane ADM-assisted breast reconstruction (Figs.
48-10 to 48-12) or, if wishing a contralateral augmentation, a two-stage
reconstruction. If presenting a moderate ptosis, we could consider a
contralateral mastopexy with autoprosthesis technique.
If showing a severe ptosis, the best option could be a skin-reducing
mastectomy with DTI breast reconstruction covered inferiorly by the dermal
flap and a contralateral mastopexy with autoprosthesis. In a type 2 breast, we
do not suggest to preserve the NAC (considering a NAC grafting) if it has to
be lifted up more than 4 cm.

Patients With Large and Ptotic Breast


In these cases we may recommend a skin-reducing mastectomy and DTI
breast reconstruction covered inferiorly by the autologous dermal flap and a
contralateral breast reduction.
In a type 2 breast, we do not suggest to preserve the NAC (considering a
NAC grafting) if it has to be lifted up more than 4 cm.
The implant choice will follow the same rules already considered for the
other subgroups. In the assessment of the breast width we advise to avoid
implants exceeding the anterior axillary line even if the breast boundaries
would overcome this border (Fig. 48-13).
FIGURE 48-11 Left NAC-sparing mastectomy. Direct-to-implant reconstruction
with synthetic mesh and Allergan Style 510 MX implant (width 13.5 cm, height 12.5
cm, projection 5.9 cm, 385 cc). A: Preoperative digital mammography showing a
type 2 breast; B: Preoperative view; C: Postoperative view at 2-year follow-up. We
opted for a Style 510 Dual Gel implant according to the patient’s wishes of not
performing any contralateral adjustment.
FIGURE 48-12 Bilateral NAC-sparing mastectomy. Direct-to-implant reconstruction
with Allergan Style 410 MF implants (295 cc) and ADM (ARTIA, LifeCell Corp,
Branchburg, NJ). A: Preoperative digital mammography showing a type 2 breast; B:
Preoperative markings; C: Postoperative results at 6-month follow-up.
FIGURE 48-13 Implant selection guide. Direct-to-implant breast reconstruction in
women with large and ptotic breast.

Type 3 Breasts
Patients With Small Breast
For type 3 breasts we could propose a prepectoral DTI breast reconstructive
approach with synthetic meshes/ADMs.
According to patient’s wish, a contralateral augmentation could be
considered. In this case a two-stage breast reconstruction could be the best
option, to achieve the desired volume for the contralateral breast. All these
choices must be done when planning the surgery in order to accurately
evaluate measurements and implant/expander choice. If considering a DTI,
on the mastectomy side the implant width should be selected according to the
breast width, subtracting the thickness of the skin flaps medially and laterally
spliced by two. The height of the implant will be calculated according to the
height of the contralateral breast when gently pushing to toward the chest
wall. In these conditions we suggest to use extraprojected or full-projected
form-stable implants when the NAC is preserved. The contralateral implant
will present the same width of the mastectomy-side implant approximately
reduced by the thickness of the skin-glandular flap (see Fig. 48-2).
If considering a two-stage approach with contralateral augmentation, the
expander width will be selected according to the anatomical characteristics of
the patients and the desired contralateral volume, that will be chosen
according to the chest wall width and anatomical characteristics of the patient
(Fig. 48-4).

Patients With Medium-Sized Breast


Patients with medium-sized breasts should be evaluated according to the
ptosis degree.
Patient without significant breast ptosis or presenting a moderate ptosis
could undergo a prepectoral DTI breast reconstructive approach with
synthetic meshes/ADMs (Fig. 48-14). If presenting a moderate ptosis, we
could consider a contralateral mastopexy with autoprosthesis technique.
FIGURE 48-14 Prepectoral breast reconstruction. A: Preoperative mammogram
showing a type 3 breast; B: Preoperative view; C: Preoperative markings; D:
Prepectoral breast reconstruction with TiLOOP Pocket, Style 410 MF 375-cc
implant and fat grafting.

If showing a severe ptosis, the best option could be a skin-reducing


mastectomy with prepectoral DTI breast reconstruction (covering the inferior
pole of the implant with the dermoadipose autologous flap and the upper pole
with an ADM/synthetic mesh) and a contralateral mastopexy with
autoprosthesis. The implant could be also completely covered with an
ADM/synthetic mesh further covering the inferior pole with the dermal flap.
In a type 3 breast, we do not suggest to preserve the NAC (considering a
NAC grafting) if it has to be lifted up more than 5 to 6 cm.
Patients With Large and Ptotic Breast
In these cases we may recommend a skin-reducing mastectomy and DTI
prepectoral breast reconstruction (covering the inferior pole of the implant
with the dermoadipose autologous flap and the upper pole with an
ADM/synthetic mesh) and contralateral breast reduction (Figs. 48-5–48-7).
The implant could be also completely covered with an ADM/synthetic mesh
further covering the inferior pole with the dermal flap. In a type 3 breast, we
do not suggest to preserve the NAC (considering a NAC grafting) if it has to
be lifted up more than 5 to 6 cm.
The implant choice will follow the same rules already considered for the
other subgroups. In the assessment of the breast width we advise to avoid
implants exceeding the anterior axillary line even if the breast boundaries
would overcome this border.
FUTURE DIRECTIONS

Hybrid Breast Reconstruction


Our target and main aim for the next years to 2030 is to further reduce
surgical aggressiveness, improving cosmetic and reconstructive outcomes.
Our pathway of research and development will move through advancements
in biomaterials, with new and safer ADMs and synthetic meshes together
with enhanced fat grafting, achieving the next step: the “hybrid
reconstruction” that will allow an immediate breast reconstruction combining
the use of fat, implants, and meshes (30).
The so-called “hybrid” model will represent a sort of evolution of the
form-stable anatomical implants’ surgical model, allowing higher stability of
the results (in ptotic breasts too), more aesthetic impact (we add a body
recontouring to the traditional reconstructive model, transferring fat cells
from other anatomical areas to the breast), and better feeling and perception
of the implant (also reducing capsular contracture). The development of fat
injection techniques to refine the results of implant-based breast
reconstructions is changing the outcome of breast surgery (31).
We are firmly convinced the future of breast reconstruction will be based
on refined applications of autologous fat grafting (AFG), in particular in the
light of the growing, even though not definitive, evidence about the safety of
AFG use in breast reconstruction following mastectomy for breast cancer
(32). This is the reason why we are currently developing and validating an
innovative surgical model, we called “hybrid breast reconstruction.” This
new reconstructive system encompasses prostheses, fat grafting, and meshes
as integrated tools to improve the final reconstructive outcome. Fat grafting
in our view is not only employed for breast reconstruction refinements or to
treat radio-induced tissue damages but is a preoperatively planned part of the
reconstruction. The final volume we want to achieve will be made up of fat
and implants in a variable percentage according to patient’s body contour and
breast morphology. Hybrid breast reconstruction will represent the best
option for patients with medium–large breasts with moderate–high ptosis:
they will benefit from the positioning of an expander (as an immediate or
delayed reconstruction) together with a first fat grafting to the reconstructed
breast, followed by at least two other lipotransfers (the number of procedures
will be tailored on the single patient according to body contour and desired
final breast size), while progressively deflating the expander. At the end of
the fat-/expander-mediated tissue expansion, the patient will undergo a
standard expander to permanent implant replacement, following a different
time protocol, being the second reconstruction time planned in a shorter
period compared with a usual two-stage reconstruction. Hybrid reconstructive
pathway must derive from a shared decision with the patient, who should
have good motivation in pursuing the entire planned reconstructive protocol
consisting in multiple, even if minimally invasive, procedures. The “hybrid-
reconstructed women” will benefit from the positioning of a smaller
permanent implant compared with a standard two-stage reconstruction, with
better outcomes both related to surgical technical aspects (fewer immediate
and long-term complications) and to their quality of life (more natural feeling
of the implant). We schematized the “hybrid reconstructive approach” in
three algorithms according to the body mass index of the patient to treat (see
Figs. 48-9 to 48-11). Patients with small or very large breasts with high ptosis
will be good candidates for a one-stage DTI reconstruction, following a
conservative mastectomy, respectively a skin/NAC-sparing and a skin-
reducing mastectomy. These patients will also benefit from a planned fat
grafting, after the main (permanent implant positioning) procedure, in order
to achieve the better cosmetic result. This is another option for a planned
hybrid reconstruction program, with the positioning of a permanent implant
smaller than the one usually considered for a one-stage reconstruction, being
the final breast volume and shape reached with a planned lipotransfer.
Following this way, a breast reconstruction will more and more closely
reproduce the results and outcomes of a cosmetic breast augmentation. We
used the “Hybrid Breast Reconstruction” technique in more than 350
reconstructions, both immediate and delayed, two stage and DTI, without
experiencing higher locoregional recurrence and complication rates when
compared with conventional two-stage reconstructions, obtaining excellent
aesthetic results and high patients’ satisfaction levels (Fig. 48-15). We think
that a total replacement of prostheses with fat would be auspicable but not
realistic at the moment. The use of implants will be required unless new
technologies will be discovered to stabilize the shape of a full-fat
reconstructed breast, achieving a better fat survival through fat enhancement
techniques (33) or through dedicated scaffolds to drive cell regeneration and
shape definition. We are also exploring this field in a preclinical setting, as
presented in a recent paper (34). We presented an innovative breast
reconstructive technique, with the use of a reverse engineering approach and
additive manufacturing methods (3D image capture, 3D modelling, and rapid
prototyping with 3D printers) combined with AFG: a 3D-structure with
autologous adipose-derived stem cells will be used as a construct for tissue
regeneration. The 3D-printed scaffold will be generated from computed
tomography or magnetic resonance imaging data of the breast to reconstruct
through image capture and analysis techniques and will be placed in the
subcutaneous position at the level of the mastectomy side. The scaffold will
be colonized with autologous fat tissue in some sessions. The biodegradable
customized structure will help to maintain the breast shape and the natural
consistency will be obtained with the fat grafting, also considering adequate
enhancement techniques.
FIGURE 48-15 Hybrid breast reconstruction. Postoperative results at 5-year follow-
up. The patient underwent a right modified radical mastectomy and two-stage
reconstruction. Three bilateral fat transfer sessions have been performed between
the first stage and the second stage (Allergan Style 410 MF 335 cc implant), while
progressively deflating the expander with a definitive fat transferred volume of 250
cc for each breast. Left symmetrization augmentation mastopexy (Allergan Style 410
MM 215-cc implant).
Future clinical studies will validate the use of these innovative breast
reconstructive techniques that will probably become standard options for the
next-generation breast surgeon.

REFERENCES

1. Halsted WS. The results of operations for the cure of cancer of the
breast performed at the Johns Hopkins Hospital from June, 1889 to
January, 1894. Ann Surg 1894;20(5):497–555.
2. Fisher B, Bauer M, Margolese R, et al. Five-year results of a
randomized clinical trial comparing total mastectomy and segmental
mastectomy with or without radiation in the treatment of breast cancer.
N Engl J Med 1985;312:665–673.
3. Fisher B, Redmond C, Poisson R, et al. Eight-year results of a
randomized clinical trial comparing total mastectomy and lumpectomy
with or without irradiation in the treatment of breast cancer. N Engl J
Med 1989;320:822–828.
4. Veronesi U, Saccozzi R, Del Vecchio M, et al. Comparing radical
mastectomy with quadrantectomy, axillary dissection, and radiotherapy
in patients with small cancers of the breast. N Engl J Med 1981;305:6–
11.
5. della Rovere GQ, Benson JR, Breach N, et al., eds. Oncoplastic and
Reconstructive Surgery of the Breast. London: Taylor & Francis; 2004.
6. Katipamula R, Degnim AC, Hoskin T, et al. Trends in mastectomy rates
at the Mayo Clinic Rochester: effect of surgical year and preoperative
magnetic resonance imaging. J Clin Oncol 2009;27(25):4082–4088.
7. McGuire KP, Santillan AA, Kaur P, et al. Are mastectomies on the rise?
A 13-year trend analysis of the selection of mastectomy versus breast
conservation therapy in 5865 patients. Ann Surg Oncol
2009;16(10):2682–2690.
8. Bhat S, Orucevic A, Woody C, et al. Evolving trends and influencing
factors in mastectomy decisions. Am Surg 2017;83(3):233–238.
9. Rocco N, Rispoli C, Moja L, et al. Different types of implants for
reconstructive breast surgery. Cochrane Database Syst Rev
2016;5:CD010895.
10. Zhang P, Li CZ, Wu CT, et al. Comparison of immediate breast
reconstruction after mastectomy and mastectomy alone for breast
cancer: a meta-analysis. Eur J Surg Oncol 2017;43(2):285–293.
11. Park SH, Han W, Yoo TK, et al. Oncologic safety of immediate breast
reconstruction for invasive breast cancer patients: a matched case
control study. J Breast Cancer 2016;19(1):68–75.
12. Filiberti A, Rimoldi A, Callegari M, et al. Immediate versus delayed
breast reconstruction. A psychological answer. Eur J Plast Surg
1990;13:55–58.
13. Nava MB, Spano A, Cadenelli P, et al. Extra-projected implants as an
alternative surgical model for breast reconstruction. Implantation
strategy and early results. Breast 2008;17(4):361–366.
14. Nava MB, Rocco N, Catanuto G, et al. Impact of contra-lateral breast
reshaping on mammographic surveillance in women undergoing breast
reconstruction following mastectomy for breast cancer. Breast
2015;24(4):434–439.
15. Nava MB, Pennati AE, Lozza L, et al. Outcome of different timings of
radiotherapy in implant-based breast reconstructions. Plast Reconstr
Surg 2011;128(2):353–359.
16. Nava MB, Catanuto G, Pennati AE, et al. Lack of activation of telomere
maintenance mechanisms in human adipose stromal cells derived from
fatty portion of lipospirates. Plast Reconstr Surg 2015;135(1):114e–
123e.
17. Nava MB, Catanuto G, Pennati A, et al. Conservative mastectomies.
Aesthetic Plast Surg 2009;33(5):681–686.
18. Nava MB, Rocco N, Catanuto G. Conservative mastectomies: an
overview. Gland Surg 2015;4(6):463–466.
19. Rocco N, Catanuto G, Nava MB. What is the evidence behind
conservative mastectomies? Gland Surg 2015;4(6):506–518.
20. Nava MB, Cortinovis U, Ottolenghi J, et al. Skin-reducing mastectomy.
Plast Reconstr Surg 2006;118(3):603–610; discussion 611–613.
21. della Rovere GQ, Nava M, Bonomi R, et al. Skin-reducing mastectomy
with breast reconstruction and sub-pectoral implants. J Plast Reconstr
Aesthet Surg 2008;61(11):1303–1308.
22. Nava MB, Ottolenghi J, Pennati A, et al. Skin/nipple sparing
mastectomies and implant-based breast reconstruction in patients with
large and ptotic breast: oncological and reconstructive results. Breast
2012;21(3):267–271.
23. Catanuto G, Rocco N, Nava MB. Surgical decision making in
conservative mastectomies. Gland Surg 2016;5(1):69–74.
24. Catanuto G, Pappalardo F, Rocco N, et al. Formal analysis of the
surgical pathway and development of a new software tool to assist
surgeons in the decision making in primary breast surgery. Breast
2016;29:74–81.
25. Deva AK, Adams WP Jr, Vickery K. The role of bacterial biofilms in
device-associated infection. Plast Reconstr Surg 2013;132:1319–1328.
26. Griffiths M, Chae MP, Rozen WM. Indocyanine green-based fluorescent
angiography in breast reconstruction. Gland Surg 2016;5(2):133–149.
27. Nahabedian MY. Implant-based breast reconstruction: strategies to
achieve optimal outcomes and minimize complications. J Surg Oncol
2016;113:895–905.
28. Dent BL, Small K, Swistel A, et al. Nipple-areolar complex ischemia
after nipple-sparing mastectomy with immediate implant-based
reconstruction: risk factors and the success of conservative treatment.
Aesthet Surg J 2014;34(4):560–570.
29. Rancati A, Angrigiani C, Hammond D, et al. Preoperative digital
mammography imaging in conservative mastectomy and immediate
reconstruction. Gland Surg 2016;5(1):9–14.
30. Nava MB, Catanuto G, Rocco N. Hybrid breast reconstruction. Minerva
Chir 2018;73(3):329–333.
31. Zhou Y, Wang J, Li H, et al. Efficacy and safety of cell-assisted
lipotransfer: a systematic review and meta-analysis. Plast Reconstr Surg
2016;137(1):44e–57e.
32. Kronowitz SJ, Mandujano CC, Liu J, et al. Lipofilling of the breast does
not increase the risk of recurrence of breast cancer: a matched controlled
study. Plast Reconstr Surg 2016;137:385–393.
33. Tissiani LA, Alonso N. A prospective and controlled clinical trial on
stromal vascular fraction enriched fat grafts in secondary breast
reconstruction. Stem Cells Int 2016;2016:2636454.
34. Rocco N, Gloria A, De Santis R, et al. Improving outcomes in breast
reconstruction: from implant-based techniques towards tissue
regeneration. Procedia CIRP 2016;49:23–27.
CHAPTER 49

Management of Ptotic Patient Desiring


Nipple-Sparing Mastectomy With
Implant-Based Reconstruction
ANNE M. NICKODEM
HISTORY
Nipple-sparing mastectomy (NSM) has evolved from a technique for
reconstruction in prophylactic cases to therapeutic indications (1–7). This
allows for a better aesthetic outcome than skin-sparing mastectomy.
Oncologic safety concerns are widely debated but the literature supports no
increased risk of local or regional recurrence or impact on patient survival
rates (8–11).
In the prophylactic patient population, they are at increased risk for breast
cancer due to a genetic mutation (BRCA l/BRCA 2), personal history of
unilateral breast cancer, or extensive family history of cancer. Prophylactic
mastectomy in high-risk patients has already been shown to reduce the
incidence of breast cancer (12–18).
The procedure was originally described by Freeman (19) in the 1960s and
others (20–23) followed in the 70s and 80s. This technique was abandoned
due to oncologic safety concerns and poor aesthetic outcomes. The
improvement in oncologic resection technique, perforator flap surgery,
implant devices, and biologic materials has made it possible for the technique
of prepectoral reconstruction to be considered as an alternative to breast
conservation and skin-sparing mastectomy.
Oncologic Parameters
In the therapeutic patient population, a multidisciplinary team approach must
be taken. The following oncologic parameters must be evaluated:

Tumor distance from nipple


Tumor size
Tumor invasion of chest wall or muscle
Inflammatory cancer component
Clinical node status
Stage of cancer
Radiation therapy
Adjuvant or neoadjuvant chemotherapy
Preoperative MRI assessment when indicated

The absolute and relative contraindications have changed as assessment


modalities, treatment therapies, and techniques have evolved (24–26). Tumor
eradication and patient safety remain the surgeons’ primary concern in
evaluating reconstruction options.
PATIENT CONSULTATION
The patient is evaluated thoroughly. Overall patient health including prior
medical and surgical history, comorbidities, and smoking history are
investigated and proper treatment confirmed or initiated.
A complete physical examination assesses the body habitus, breast
dimensions and anatomy, skin quality and quantity, scar locations and
quality, and prior radiation effects on skin envelope of the breast.
Cardiopulmonary assessment must be performed for withstanding general
anesthesia for any length of time. Referral for clearance is prescribed as
needed.
If the oncologic parameters previously discussed are determined to be
favorable for the patient being a candidate for NSM with reconstruction, the
surgeon may proceed. However, if criteria are unfavorable, this will result in
a delayed reconstruction until adequate treatment obtained, autologous
reconstruction as an alternative procedure, or no reconstruction at all.
Obesity was a contraindication for NSM and/or prepectoral reconstruction
in the early years; it is no longer absolute. Obesity is an epidemic in the
United States. Assessment of the comorbidities associated with obesity and
insuring proper medical treatment is instituted is paramount before
proceeding with reconstruction. All obese patients should be counseled by a
nutritionist throughout the pre- and postoperative recovery to establish proper
dietary intake.

TABLE 49-1 Renault Breast Ptosis Classification


Grade Severity Description
Grade 1 Mild Nipple at or above IMS
ptosis
Grade 2 Moderate Nipple within 2 cm below
ptosis inframammary fold
Grade 3 Severe Nipple position greater than 2-cm
ptosis inferior breast position
Pseudoptosis Bottom of breast Nipple position remains at or above if
dropped/lengthened level and gland drop below

Smoking has also been identified as being detrimental to the nipple areolar
complex (NAC) and mastectomy flap in reconstruction (27). Patient
reconstruction may be delayed until smoking cessation occurs. The surgeon
must provide information to the patient on preferred technique as well as
alternatives to have a fully informed consent.
The breast reconstruction consultation should include a lengthy discussion
of the patient’s desired breast volume, projection, and shape. This will help in
selecting the implant device and in managing patient expectations.
The challenge for the plastic surgeon is the patient with severe breast
ptosis that desires NSM.
The classification of ptosis is best described by Regnault (Table 49-1).
The ideal candidate is a small breast and little to no ptosis (Figs. 49-1–49-3).
Patients with moderate ptosis and wishing to increase their breast volume
are good candidates (Figs. 49-4).
The larger the breast volume and degree of ptosis, prior radiation, along
with increased body mass index and smoking, were found to be the greatest
predictors of increased complications (28–31). The complications were
increased NAC necrosis, partial and full, malposition of the NAC, necrotic
skin flaps, and implant exposure. The current and desired breast volume and
level of ptosis will determine the incisions used for the procedure.
INDICATIONS
NSM is indicated in patients at high risk for breast cancer due to genetic
mutation, and personal or family history of cancers.
In the therapeutic group the indications are the tumor may not be within 2
cm of the NAC and it should not be an inflammatory carcinoma.
Both groups must have excellent perfusion in the breast skin flaps and this
often precludes smokers.
CONTRAINDICATIONS
NSM is contraindicated in patients with poorly controlled locoregional
disease, muscle or chest wall involvement, tumor proximity to NAC, and
poorly perfused skin flaps.
Relative contraindications are morbid obesity, smoking, and prior radiation
therapy.

FIGURE 49-1 Ideal candidate with little ptosis for two-stage reconstruction. A–C:
Preop, BMI: 20.2, grade 1 ptosis, LIDC/DCIS/BRCA2+. D–F: Postop, second-stage
NSM, prepectoral, IMF approach, 500-cc TE/dermal matrix, 560-cc smooth round
cohesive gel implants, extra projection, 321 g R/337 g L 1/3 SLN+.

FIGURE 49-2 Ideal candidate with no ptosis for direct-to-implant reconstruction. A–


C: Preop, BMI: 27.3, family history of breast cancer, PALB2 carrier, IDC, left DCIS.
D–F: Postop, NSM, prepectoral, DTI, direct lateral incision, cadaver matrix, 445-cc
smooth round gel, Alloderm 304 cm2 per side.

Morbid obesity is generally associated with increased comorbidities which


are associated with high complication and failure rates (28).
Patients with a prior history of radiation therapy having NSM are restricted
in breast volume and may not increase in size. If a greater volume is desired,
a soft tissue flap, pedicle, or perforator microsurgical flap reconstruct ion is
warranted (32–34).
INCISION LOCATION

IMF
Patients with small to moderate volume with little to no ptosis have several
options for incision location. The inframammary fold is the least noticeable
and with the appropriate length, the patients’ breast can be entirely resected
and provide access to reconstruction (Figs. 49-3 and 49-4).

FIGURE 49-3 Inframammary fold (IMF) approach. A–C: Preop, BMI: 25, grade 1
ptosis, LIDC neoadjuvant chemotherapy. D–F: Postop, three-stage NSM,
prepectoral, IMF, 500-cc TE dermal matrix, 650-cc smooth round cohesive gel
implants and 160-cc fat graft per side.
FIGURE 49-4 Inframammary fold incision. A–C: Preop, BMI: 26.9, right breast
cancer, grade 1 ptosis, RIDC/BRCA2+, neoadjuvant chemotherapy. D–F: Postop,
three-stage NSM, prepectoral, IMF approach, 600-cc TE/dermal matrix, 750-cc
smooth round cohesive gel implants, extra projection, 200-cc fat graft per side.

Lateral Incision
An alternative incision is a lateral placement. This allows the breast surgeon
to perform the sentinel node biopsy through the same approach and provides
easier access to the entire breast for surgeons not comfortable with the IMF.
This also allows easier access to the internal mammary artery in patients
undergoing immediate or immediate delayed autologous reconstruction (Fig.
49-5).
Vertical Incision
A vertical incision is useful in patients with the need for some reduction of
the skin envelope and little or no NAC repositioning superiorly (Fig. 49-6).
Reduction Pattern Incision
The larger and longer breast will require skin envelope reduction. This is
performed by deepithelialization of the inferior mastectomy flap with the
NAC attached and the inferior flap is tucked under the superior portion of the
mastectomy flap (Fig. 49-7B).
FIGURE 49-5 Lateral incision. A: Left breast cancer, BL two-stage reconstruction.
B: BMI 19.9, SSF 295-cc implants.

FIGURE 49-6 Vertical incision approach. A, B: Preop, second stage, BMI: 37, grade
2 ptosis, LIDC, neoadjuvant chemotherapy. C, D: Postop, second-stage NSM,
prepectoral, vertical approach, 750-cc TE/dermal matrix, 650-cc smooth round
cohesive gel implants.
FIGURE 49-7 A: Depicts key anatomical points. B: Demonstrates the area of the
inferior mastectomy flap to be deepithelialized in reduction pattern NSM.

TABLE 49-2 Surgical Techniques

Variations exist to eliminate the vertical scar or to increase the surface area
of inferior skin flap (35).
An NAC delay may be performed with reduction of breast volume in
conjunction with wide excision of the tumor and the sentinel lymph node
biopsy. Patient returns to operating room for completion of mastectomy and
implant-based reconstruction at a later date that does not interfere with
adjuvant therapy (Fig. 49-8) (28,36–38).
The incision choices are well summarized by Maxwell et al. in Table 49-2.
MARKING THE PATIENT
The patient should be marked in the upright position. The following
anatomical points must be marked:

The level of the IMF


The mid sternum
The base diameter from the sternal costal margin to the anterior axillary
line
Breast gland perimeter
Inferior mastectomy flap area to be deepithelialized
Central clavicle-/notch-to-nipple distance

Landmarks are shown in Figure 49-7A.


DEVICE SELECTION
The device selected is based upon the desired breast volume, projection, and
anatomical base diameter. The more cohesive the prefilled implant device the
less rippling is evident in the prepectoral reconstruction patient. This device
will also have the most projection and provide greater fullness at the upper
pole of the reconstructed breast.
The less cohesive implants are useful for patients desiring a more natural
slope or matching the opposite breast in a unilateral reconstruction.
The appropriate dimension of the biologic matrix is selected to support the
overlying soft tissue mastectomy flap or as an extension of the pectoralis
major muscle in a dual plane reconstruction.

FIGURE 49-8 Reduction pattern incision approach. A–C: Top photos: Preop, BMI:
28, left IDC, grade 3 ptosis. D–F: Postop, BL NSM, 716 g on left 778 g on right, two-
stage reconstruction, prepectoral reconstruction with dermal matrix and anatomical
gel 740-cc implants.
OPERATIVE TECHNIQUE
Through the appropriate incision chosen in consultation with the oncologic
breast surgeon, and based on patient anatomy and planned reconstruction, the
pocket is inspected, hemostasis obtained, and antibiotic irrigation performed.
Flap perfusion is assessed with ICG angiography, spectral imaging, near-
infrared spectroscopy, or clinical observation of bleeding at wound edges and
capillary refill. The method used is dependent upon the modalities available
in surgeon’s surgical facility. Excellent perfusion of the mastectomy flap and
NAC may allow for direct-to-implant reconstruction (39–42) versus a multi-
staged procedure.
DUAL PLANE
The biologic dermal matrix shaped in a semicircle or small rectangle is
placed for inferior pole soft tissue support from the pectoralis major
inferolateral margin to the level of the IMF.
The matrix is placed dermal side up in the pocket.
PREPECTORAL PLANE
Prepectoral plane reconstruction requires larger rectangular shape matrix or
two semicircle shapes are sewn together to provide mastectomy flap soft
tissue support (Fig. 49-9).
This is sutured to the perimeter of the pocket no greater than the dimension
of the selected implant device (Fig. 49-10). The material should be folded
posterior along the distal half of the lateral dimension and continued across
the IMF. This prevents the device from drifting laterally and defines the IMF
level. Any excess matrix may be excised and reapproximated once the
expanded device or prefilled implant is placed in the space between the
matrix and anterior surface of the pectoralis muscle. The lateral gutter soft
tissue is approximated to the lateral chest wall with mattress sutures after
drain placement.
FIGURE 49-9 Soft tissue matrix.
REDUCTION PATTERN
The patient is marked in the upright position. The inferior mastectomy flap is
deepithelialized with a broad base extending medially to the margin of skin to
meet the IMF (Fig. 49-7B). The mastectomy approach is through the lateral
mound. This may be customized by identifying preoperatively the perfusion
of the NAC on MRI.
The matrix is placed as described above or off label, wrapping the implant.
It is placed in the pocket at the appropriate height and the IMF and lateral
anterior axillary defined (35,43,44).
Reduction for NAC Perfusion Delay
Performing a reduction in the high-risk level 3 ptosis patient to preserve NAC
viability in conjunction with tumor resection and sentinel lymph node biopsy
has reduced NAC complications. The patient is returned to the operating
room in minimum of 3 weeks to complete the mastectomy and perform the
implant-based reconstruction as previously described (38,45–54).
FIGURE 49-10 Matrix and implant in prepectoral position.
CONCLUSION
Patients are seeking risk-reducing mastectomy and aesthetic reconstructions
that have little impact on them psychologically (24,25). Genetic mutation
detection and early screening continue to facilitate detection of high-risk
patients and stage 0 lesions.
As the number of NSM procedures increase in therapeutic population, the
goal is to reconstruct the patient with no delay in cancer treatment and
minimize the number of procedures to obtain the best aesthetic result
(55–59).
A multidisciplinary approach is the only safe way to accomplish this goal.
As surgeons, we must be aware of the timelines for adjuvant therapy and
emphasize to the patient that cancer treatment takes precedence over
reconstruction (18).
We are challenged to achieve aesthetic reconstruction results in the
severely ptotic patient whether due to massive weight loss or morbid obesity.
The need for reduction of the excess skin envelope while maintaining nipple
perfusion and proper positioning of the NAC can be accomplished with
proper patient and surgical technique selection.
The search for procedures to adequately address these challenges will
continue to evolve. There is no one correct way to reconstruct the breast.

REFERENCES

1. Spear SL, Willey SC, Feldman ED, et al. Nipple-sparing mastectomy for
prophylactic and therapeutic indications. Plast Reconstr Surg
2011;128:1005–1014.
2. Sacchini V, Pinotti JA, Barros AC, et al. Nipple-sparing mastectomy for
breast cancer and risk reduction: oncologic or technical problem?. J Am
Coll Surg 2006;203(5):704–714.
3. Dent BL, Miller JA, Eden DJ, et al. Tumor-to-nipple distance as a
predictor of nipple involvement: expanding the inclusion criteria safe for
nipple-sparing mastectomy. Plast Reconstr Surg 2017;140:1–8.
4. Jensen JA. When can the nipple-areola complex safely be spared during
mastectomy?. Plast Reconstr Surg 2002;109:805–807.
5. Jensen JA. Nipple-sparing mastectomy: what is the best evidence for
safety?. Plast Reconstr Surg 2009;124:2195–2197.
6. Rushy JE, Gui GP. Nipple-sparing mastectomy in women with large or
ptotic breasts. J Plast Reconstr Aesthet Surg 2010;125:818–829.
7. Al-Mufarrej FM, Woods JE, Jacobson SR. Simultaneous mastopexy in
patients undergoing prophylactic nipple-sparing mastectomies and
immediate reconstruction. J Plast Reconstr Aesthet Surg.
2009;124(6):1772–1780.
8. Yao K, Liederbach E, Tang R, et al. Nipple-sparing mastectomy in
BRCAl/2 mutation carriers: an interim analysis and review of the
literature. Ann Surg Oncol 2015;22:370–376.
9. Rebbeck TR, Friebel T, Lynch HT, et al. Bilateral prophylactic
mastectomy reduces breast cancer risk in BRCAl and BRCA2 mutation
carriers: The PROSE Study Group. J Clin Oncol 2004;322:1055–1062.
10. Cemal Y, Albornoz CR, Disa JJ, et al. A paradigm shift in U.S. breast
reconstruction: part 2. The influence of changing mastectomy patterns
on reconstructive rate and method. Plast Reconstr Surg 2013;131:320–
326.
11. Tuttle TM, Habermann EB, Grund EH, et al. Increasing use of
contralateral prophylactic mastectomy for breast cancer patients: a trend
toward more aggressive surgical treatment. J Clin Oncol 2007;25:5203–
5209.
12. Hartmann LC, Sellers TA, Schaid DJ, et al. Efficacy of bilateral
prophylactic mastectomy in BRCAl and BRCA2 gene mutation carriers.
J Natl Cancer Inst 2001;93:1633–1637.
13. Hartmann LC, Schaid DJ, Woods JE, et al. Efficacy of bilateral
prophylactic mastectomy in women with a family history of breast
cancer. N Engl J Med 1999;320(2):77–84.
14. Maxwell P, Whitworth P, Gabriel A. Nipple sparing mastectomy. In:
Spear S, ed. Surgery of the Breast: Principles and Art. 3rd ed. Vol.I.
Wolters Kluwer/Lippincott Williams & Wilkins; 2011:298–307.
15. Spear SL, Schwarz KA, Venturi ML, et al. Prophylactic mastectomy and
reconstruction; Clinical outcomes and patient satisfaction. Plast
Reconstr Surg 2008;122:1–9.
16. Spear SL, Hannan CM, Willey SC, et al. Nipple-sparing mastectomy.
Plast Reconstr Surg 2009;123(6):1665–1673.
17. Spear SL, Carter ME, Schwarz K. Prophylactic mastectomy: indications,
options, and reconstructive alternatives. Plast Reconstr Surg
2005;15(3):891–909.
18. Frey JD, Salibian AA, Karp NS, et al. Comparing Therapeutic versus
prophylactic nipple-sparing mastectomy: Does indication inform
oncologic and reconstructive outcomes? Plast Reconstr Surg
2018;142(2):306–314.
19. Freeman BS. Subcutaneous mastectomy. Plast Reconstr Surg
1962;30:676.
20. Woods JE. Detailed technique of subcutaneous mastectomy with and
without mastopexy. Ann Plast Surg 1987;18(1):51–61.
21. Goulian D, McDivitt RW. Subcutaneous mastectomy with immediate
reconstruction of the breasts, using the dermal mastopexy technique.
Plast Reconstr Surg 1972;50(3):211–215.
22. Jarrett JR, Cutler RG, Teal DF. Subcutaneous mastectomy in small,
large, or ptotic breasts with immediate submuscular placement of
implants. Plast Reconstr Surg 1978;62(5):702–705.
23. Georgiade NG, Hyland W. Technique for subcutaneous mastectomy and
immediate reconstruction in the ptotic breast. Plast Reconstr Surg
1975;56(2):121–128.
24. Frey JD, Choi M, Salibian AA, et al. Comparison of outcomes with
tissue expander, immediate implant, and autologous breast
reconstruction in greater than 1,000 nipple sparing mastectomies. Plast
Reconstr Surg 2017;139(6):1300–1310.
25. Bailey CR, Ogbuagu O, Baltodano PA, et al. Quality-of-life outcomes
improve with nipple-sparing mastectomy and breast reconstruction.
Plast Reconstr Surg 2017;140(2):219–226.
26. Salibian AA, Frey JD, Choi M, et al. BRCA mutations in the young,
high risk female population: genetic testing, management of
prophylactic therapies, and implications for plastic surgeons. Plast
Reconstr Surg 2018;141(6):1341–1347.
27. Frey JD, Alperovich M, Levine JP, et al. Does smoking history confer a
higher risk for reconstructive complications in nipple-sparing
mastectomy?. Breast J 2017;23(4):415–420.
28. Colwell AS, Tessler O, Lin AM, et al. Breast reconstruction following
nipple-sparing mastectomy: predictors of complications, reconstruction
outcomes, and 5-year trends. Plast Reconstr Surg 2014;133(3):496–506.
29. Mallon P, Feron JG, Couturaud B, et al. The role of nipple-sparing
mastectomy in breast cancer: a comprehensive review of the literature.
Plast Reconstr Surg 2013;131(5):969–984.
30. Galimberti V, Vicini E, Corso G, et al. Nipple-sparing and skin-sparing
mastectomy: review of aims, oncological safety and contraindications.
Breast 2017;34 Suppl 1:S82–S84.
31. Tang R, Coopey SB, Colwell AS, et al. Nipple-sparing mastectomy in
irradiated breasts: selecting patients to minimize complications. Ann
Surg Oncol 2015;22(10):3331–3337.
32. Reish RG, Lin A, Phillips NA, et al. Breast reconstruction outcomes
after nipple sparing mastectomy and radiation therapy. Plast Reconstr
Surg 2015;135(4):959–966.
33. Frederick MJ, Lin AM, Neuman R, et al. Nipple-sparing mastectomy in
patients with previous breast surgery: Comparative analysis of 775
immediate breast reconstructions. Plast Reconstr Surg 2015;135(6):954–
962.
34. Alperovich M, Choi M, Frey JD, et al. Nipple-sparing mastectomy in
patients with prior breast irradiation: Are patients at higher risk for
reconstructive complications? Plast Reconstr Surg 2014;134:202e–206e.
35. Salibian AH, Harness JK, Mowlds DS. Primary buttonhole mastopexy
and nipple sparing mastectomy: a preliminary report. Ann Plast Surg
2016;77(4):388–395.
36. Schneider LF, Chen CM, Stolier AJ, et al. Nipple -sparing Mastectomy
and immediate free flap reconstruction in the large ptotic breast. Ann
Plast Surg 2012;69(4):425–428.
37. Schwartz JD, Skowronski PP. Surgical delay facilitates pedicled nipple-
sparing mastectomy and reconstruction in the ptotic patient. Plast
Reconstr Surg Glob Open 2016;4:e735.
38. Jensen JA, Lin JH, Kapoor N, et al. Surgical delay of the nipple-areolar
complex: a powerful technique to maximize nipple viability following
nipple-sparing mastectomy. Ann Surg Oncol 2012;19(10):3171–3176.
39. Colwell AS, Christensen JM. Nipple-sparing mastectomy and direct-to-
implant breast reconstruction. Plast Reconstr Surg 2017;140(5S
Advances in Breast Reconstruction):44S–50S.
40. Van Deventer PV. The blood supply to the nipple-areola complex of the
human mammary gland. Aesthet Plast Surg 2004;28(6):393–398.
41. Nakajima H, Imanishi N, Aiso S. Arterial anatomy of the nippleareola
complex. Plast Reconstr Surg 1995;96(4):843–845.
42. Gunnarsson GL, Bille C, Reitsma LC, et al. Prophylactic nipple-sparing
mastectomy and direct-to-implant reconstruction of the large and ptotic
breast: Is shaping of the challenging breast a key to success? Plast
Reconstr Surg 2017;140(3):449–454.
43. Pontell ME, Saad N, Brown A, et al. Single stage nipple-sparing
mastectomy and reduction mastopexy in the ptotic breast. Plast Surg Int
2018;2018:9205805.
44. Colwell AS, Taylor E, Specht M, et al. Optimizing nipple position
following nipple sparing mastectomy. Plast Reconstr Surg Glob Open
2017;5(9):1490.
45. Spear SL, Rottman SJ, Seiboth LA, et al. Breast reconstruction using a
staged nipple-sparing mastectomy following mastopexy or reduction.
Plast Reconstr Surg 2012;129(3):572–581.
46. Nava MB, Ottolenghi J, Pennati A, et al. Skin/nipple sparing
mastectomies and implant-based breast reconstruction in patients with
large and ptotic breast: oncological and reconstructive results. Breast
2012;21(3):267–271.
47. Schwartz JD, Skowronksi PP. Improved outcomes with pedicled nipple-
sparing mastectomies using a new surgical delay: mastectomy through
wise incisions. Plast Reconstr Surg Global Open 2017;5:e1259.
48. Karian LS, Therattil PJ, Wey PD, et al. Delay techniques for nipple-
sparing mastectomy: a systematic review. J Plast Reconstr Aesthet Surg
2017;70:236–242.
49. Martin E. Schwartz JC. Patient satisfaction and experience with a four-
stage procedure to facilitate extreme nipple sparing mastectomy and
reconstruction. Proceedings of the American Society for Breast
Surgeons 19th Annual Meeting Abstract; May 2–6. Orlando, FL; 2018.
50. Alperovich M, Tanna N, Samra F, et al. Nipple-sparing mastectomy in
patients with a history of reduction mammoplasty or mastopexy: how
safe is it? Plast Reconstr Surg 2013;131(5):962–967.
51. Schwartz JC. A new approach to nipple-sparing mastectomy and
reconstruction in the high risk ptotic patient. Plast Reconstr Surg Glob
Open 2018;6(5):e1779.
52. Kronowitz SJ, Hunt KK, Kuerer HM, et al. Delayed-immediate breast
reconstruction. Plast Reconstr Surg 2004;113(6):1617–1628.
53. Bertoni DM, Nguyen D, Rochlin D, et al. Protecting nipple perfusion by
devascularization and surgical delay in patients at risk for ischemic
complications during nipple-sparing mastectomies. Ann Surg Oncol
2016;23(8):2665–2672.
54. Rochlin DH, Nguyen DH. Deepithelialized skin reduction preserves skin
and nipple perfusion in immediate reconstruction of large and ptotic
breast. Ann Plast Surg 2018;81(1):22–27.
55. Choi M, Frey JD, Alperovich M, et al. Breast in a day: examining
single-staged immediate, permanent implant reconstruction in nipple-
sparing mastectomy. Plast Reconstr Surg 2016;138(2):184–191.
56. Frey JD, Choi M, Karp NS. The effect of neoadjuvant chemotherapy
compared to adjuvant chemotherapy in healing after nipple-sparing
mastectomy. Plast Reconstr Surg 2017;139(1):10e–19e.
57. Cohen O, Lam G, Choi M, et al. Risk factors for delays in adjuvant
chemotherapy following immediate breast reconstruction. Plast
Reconstr Surg 2018;142(2):299–304.
58. Blondeel PN, Hijjawi J, Depypere H, et al. Shaping the breast in
aesthetic and reconstructive breast surgery:An easy three-step principle.
Plast Reconstr Surg 2009;123(2):455–462.
59. Blondeel PN, Hijjawi J, Depypere H, et al. Shaping the breast in
aesthetic and reconstructive breast surgery: An easy three-step principle.
Part II-Breast reconstruction after total mastectomy. Plast Reconstr Surg
2009;123(3):794–805.
CHAPTER 50

Two-Staged Nipple-Sparing
Mastectomy for Preservation of the
Nipple Areolar Complex in the Large
or Ptotic Breast: Reconstructive
Algorithm and Approach
TROY A. PITTMAN | JAMES M. ECONOMIDES
HISTORY
The earliest accounts of nipple-sparing mastectomy (NSM) date to the 1960s
when Freeman performed subcutaneous mastectomies for benign lesions of
the breast (1,2). While not initially offered for oncologic indications, early
work in the prophylactic population established the safety and technical
feasibility of NSM (3). With advances in systemic cancer therapies and
surgical techniques, NSM has become more widespread for patients with
breast cancer (4–7). Together with the rise in genetic testing and the resulting
increase in indications for bilateral mastectomies, many women now demand
the superior aesthetics of the NSM.
As the viability of the nipple areolar complex (NAC) relies on random
pattern perfusion from the surrounding mastectomy skin, NSM has
historically been offered only to patients with small nonptotic breasts (8–11).
Several techniques with an aim toward allowing nipple preservation in the
large or ptotic breast have been developed through the years. In 1987, Woods
first reported on a technique for a “subcutaneous” mastectomy combined
with a mastopexy in a single stage (12). This technique, however, required
the elevation of thick mastectomy flaps to maintain tissue perfusion, resulting
in residual breast tissue. To achieve an adequate breast resection while
maintaining NAC perfusion, others have described preserving the NAC on an
inferiorly based pedicle at the time of NSM together with skin resection
through a Wise-pattern incision in a single stage (13).
More commonly a two-stage approach is used to employ the delay
phenomenon to preserve perfusion to the NAC (14). Techniques vary from a
“hemi-batwing” design to traditional vertical or Wise-pattern reductions
(15–17). Our favored approach toward NSM in the large or ptotic breast is
performed in two stages using a Wise pattern. The first stage involves a
nipple repositioning procedure (oncoplasty, reduction mammoplasty, or
mastopexy) at time of tumor extirpation and lymph node sampling followed
by a second-stage definitive NSM and reconstruction at 10 to 12 weeks.
INDICATIONS AND CONTRAINDICATIONS
In 2009, Spear et al. reported guidelines for the ideal candidate for NSM by
introducing the “Georgetown criteria” which included oncologic and
anatomic parameters (18). Oncologically, NSM was limited to patients with
small, peripheral tumors (>2 cm from the nipple) and clinically negative
nodes. These guidelines were based on early studies demonstrating histologic
evidence of cancer in the nipple of a significant proportion of non-NSM
specimens. The likelihood of cancer in the nipple increased when tumors
were closer to the nipple and larger in size, or had evidence of nodal
involvement (19–21).
While current National Comprehensive Cancer Network (NCCN)
guidelines remain conservative and recommend that the NAC be removed for
most breast cancers, they do suggest that NSM may be in considered in early-
stage, biologically favorable, node-negative, and peripheral tumors (22).
Various centers have begun to liberalize their indications in certain
circumstances to allow for NSM that don’t meet these criteria (11,23–25). In
particular, NSM may be offered to this subset of patients when demonstrating
an appropriate response to neoadjuvant chemotherapy (26). While oncologic
safety must always take precedence to aesthetics, currently there are only two
absolute contraindications to NSM (27):

Inflammatory breast cancer


Known nipple involvement
FIGURE 50-1 NSM/BCT approach algorithm.

From an anatomic perspective, NSM has traditionally only been offered to


patients with small (A to B cup), nonptotic (grade I) breasts. As NAC
survival is dependent on random pattern perfusion from the mastectomy
flaps, NSM was not offered to patients with larger and/or ptotic breasts who
would be at higher risk for NAC ischemia and necrosis. Similarly, it was
thought that patients with a history of prior surgery to the breast (i.e.,
reduction mammoplasty or mastopexy) would be at an unacceptable risk for
NAC ischemia. More recently this notion has been disproven and NSM
following prior breast surgery is no longer a contraindication (28).
Ideal candidates for staged NSM include young, healthy, nonsmoking
patients without prior history of radiation. Obesity, multiple medical
comorbidities, and prior chest wall irradiation are relative contraindications.
However, in certain circumstances these patients may still be offered staged
NSM. Our practice is to offer NSM in a staged approach to the following
patients (Fig. 50-1):

Patient desires NSM


Breast oncologist recommends NSM
Grade II/III breast ptosis
Macromastia
Patient previously underwent lumpectomy with oncoplasty and now
desires avoidance of radiation
PREOPERATIVE PLANNING
Preoperative planning for a two-stage NSM in the larger or ptotic breast
begins with a thorough assessment of the patient’s prior and current breast
history including prior breast surgeries and biopsies as well as the current
oncologic status of the breast. A history of prior surgeries and an examination
of autologous donor sites are also performed at this time. If NSM is offered
by the breast oncologist, a discussion with the patient is undertaken to review
the two-stage approach involving a first-stage lumpectomy, sentinel lymph
node biopsy, and oncoplasty and a second-stage completion NSM with
reconstruction. Prior to the initial stage, standard breast measurements are
taken to aid in reduction mammoplasty/mastopexy planning and breast
imaging films are reviewed to locate and identify the anticipated lumpectomy
defect. Breast measurements are again taken prior to the second stage to aid
in appropriate reconstructive planning (either implant based or autologous).
OPERATIVE TECHNIQUE
STAGE ONE: MAKING THE BREAST ENVELOPE SMALLER: LUMPECTOMY,
LYMPH NODE SAMPLING, AND ONCOPLASTY AND/OR
MASTOPEXY/REDUCTION
Surgical markings are made in the preoperative holding area together with the
breast oncologist and the aid of mammographic images to locate the
anticipated resection defect. Once this area is identified, a Wise-pattern skin
resection pattern is marked on the breast with standard reduction
mammoplasty technique and a suitable pedicle for NAC is chosen to allow
for perfusion directed away from the planned lumpectomy defect. We
preferentially chose broad-based pedicles that maintain as much superior
vascularity to the NAC as possible to ensure that the blood supply is not
further compromised during the second-stage NSM which we approach
inferiorly through an inframammary fold (IMF) incision.
Prior to skin incision, the NAC is marked with an appropriately sized
cookie cutter and the previously marked pedicle is deepithelialized. This is
for mere practical purposes only, as it is difficult to safely deepithelialize the
pedicle without the countertension that comes with the breast intact. The
breast oncologist then proceeds with the lumpectomy and sentinel lymph
node biopsies employing incisions within the marked Wise pattern. Once
oncologic resection is adequately completed, we proceed with oncoplasty or
completion mastopexy/reduction of the involved breast. Our primary
objective is ideal NAC placement in an anatomically pleasing location and
reduction of the skin envelope to allow for a successful reconstruction
following second-stage NSM. It is our experience that excessive parenchymal
reshaping and repositioning is inconsequential, as this tissue will be removed
at the second stage. A symmetry procedure such as a contralateral reduction
mammoplasty or mastopexy is performed at this time.
STAGE TWO: NSM AND RECONSTRUCTION
Completion NSM occurs at a minimum of 10 to 12 weeks following the first
stage. This time period is similar to the timing of radiation therapy for
patients who would have otherwise undergone breast-conservation therapy
(BCT), and is intended to reduce wound healing complications noted with
more accelerated protocols. In our experience, a minimum period of 10 to 12
weeks is preferred to allow adequate delay at the NAC pedicle. Alternatively,
if possible, we try to avoid delaying the second stage beyond 6 months due to
increased scarring of the tissue planes, making the mastectomy more difficult
for the breast oncologist. If required, adjuvant chemotherapy is performed
between the first and second stages once successful wound healing has been
achieved. Chemotherapy should commence within 8 weeks of the ablative
surgery (29).
Again, markings are made in the preoperative holding area together with
the breast oncologist. An IMF incision is preferred. Past experience with
periareolar and lateral incisions have shown an increase in complications
involving nipple necrosis and lateralization of the NAC (30). The
mastectomy is then performed by the breast oncologist including separate
pathologic evaluation of retroareolar tissues (18,31). Mastectomy flap
perfusion is assessed with indocyanine green (ICG) fluoroscopy to guide
decision making for either direct-to-implant (DTI) reconstruction or staged
tissue-expander reconstruction. For patients undergoing autologous
reconstruction, it is our preference to delay the definitive flap reconstruction
as we have found a trend toward increased complications in the immediate
setting likely attributable to postoperative flap edema compressing the
mastectomy flaps (32). In this instance, a temporary tissue expander is placed
until flap reconstruction. Once the reconstruction has been completed, the
incisions are dressed and a surgical bra is placed.
POSTOPERATIVE CARE
Following the first stage, the patient may be treated as any other
lumpectomy/oncoplasty patient and is generally discharged home the same
day. We do not regularly use surgical drains at this stage. The patient is seen
regularly in follow-up during the intervening 12 weeks to assess for
satisfactory wound healing and to review final permanent pathology to guide
any adjuvant therapy. During this time, the patient may undergo
chemotherapy if necessary. Following the second stage, the patient is
admitted overnight for pain control and is generally discharged home on the
first postoperative day. Regular follow-up is necessary to monitor drain
output and assess wound healing.

CASES

CASE 1

A 37-year-old female with right breast DCIS and BRCA-1 gene mutation
(Fig. 50-2A). The patient did not want an increase in breast size after
reconstruction. The decision was made to perform mastopexy at the time
of her lumpectomy (Fig. 50-2B). Twelve weeks after her initial surgery,
given her genetic predisposition to breast cancer, she opted for bilateral
prophylactic mastectomy with direct-to-implant breast reconstruction
(Fig. 50-2C,D).
FIGURE 50-2 A: Preop. B: Preoperative marking. Note the broad-based
superior pedicle. This allows ample access for tumor extirpation while
providing excellent blood supply to the NAC. C: Postop lumpectomy and
mastopexy. D: Postop prophylactic completion mastectomy with direct-to-
implant reconstruction.

CASE 2

A 47-year-old female with macromastia and infiltrating ductal carcinoma


of the left breast (Fig. 50-3A). Patient wanted to avoid radiation therapy
and opted to undergo completion mastectomy at the second stage (Fig.
50-3B). Second-stage operation was performed 13 weeks following
tumor extirpation and breast reduction (Fig. 50-3C).
FIGURE 50-3 A: Preop. B: Postop lumpectomy and breast reduction. C:
Postop completion mastectomy with direct-to-implant reconstruction.

CASE 3

A 38-year-old female with breast ptosis and infiltrating ductal carcinoma


of her right breast (Fig. 50-4A). After lumpectomy and mastopexy, the
patient was found to have a positive sentinel lymph node. She underwent
treatment with chemotherapy following her initial operation. The patient
wanted to avoid radiation therapy and opted for bilateral mastectomy.
The mastectomy and direct-to-implant reconstruction were performed 9
months following the initial operation (Fig. 50-4B).
FIGURE 50-4 A: Preop. B: Postop following mastectomy.
OUTCOMES
The safety and efficacy of two-stage NSM for large or ptotic breasts has been
demonstrated throughout the literature. In 2011, Spear et al. published a small
series of patients undergoing NSM 3 to 4 weeks following reduction
mammoplasty or mastopexy (28). Of 24 breasts, 17% required reoperation
for NAC necrosis, flap ischemia, or implant removal. This high rate of
reoperation ultimately resulted in delays in oncologic treatment, as initiation
of chemotherapy and/or radiation required complete soft tissue healing. A
later study of 13 breasts which had previously undergone reduction
mammoplasty or mastopexy prior to diagnosis of breast cancer and
mastectomy noted an improved safety profile attributed to the increased
interval of time between stages (33).
In 2019, we published an updated algorithm which incorporated an
increased interval between stages to allow for sufficient tissue healing in
patients without prior history of reduction or mastopexy (32). Increasing the
length of time between stages from 4 weeks to 12 weeks resulted in a
decrease in overall complications with wound healing complications and
explantation seen in only 4% of patients. The key change during this time
was the inclusion of oncologic ablation at time of the initial nipple-
repositioning surgery. By employing BCT techniques (lumpectomy plus node
sampling) and keeping within an appropriate time constraint of 10 to 12
weeks before leading to definitive mastectomy, we demonstrated increased
tissue healing and decreased complications.
As our comfort with this staged approach has increased, we have noticed a
concomitant increase in patients with larger breasts who had intended on
pursuing BCT now considering conversion to NSM to avoid radiation
therapy. This is especially true for those patients whose lumpectomy margins
return positive for disease. Given the safety profile of the staged approach,
we are now comfortable offering these women a NSM following lumpectomy
and oncoplasty when not originally intending on this treatment protocol.
Notably, we have seen a higher rate of mastectomy flap complications in
patients undergoing immediate autologous reconstruction despite the
assistance of ICG angiography to assess mastectomy flap perfusion
intraoperatively. We attribute these findings to the influence of postoperative
flap swelling and the prolonged ischemic insult caused during prolonged
mastectomy flap retraction necessary for vessel exposure during
microsurgery. As such, we now delay autologous reconstruction to allow for
further mastectomy flap revascularization.
CONCLUSION
Traditionally, NSM is offered to women with small, nonptotic breasts to
maintain perfusion to the NAC. Originally believed to interfere with NAC
perfusion, reduction mammoplasty/mastopexy can be combined with tumor
resection to open an avenue toward NSM in larger and ptotic breasts when
optimal timing for tissue healing is allowed. The indications for NSM,
therefore, may be extended to this population with careful planning and
considerations of tissue perfusion principles.

REFERENCES

1. Freeman BS. Subcutaneous mastectomy for benign breast lesion with


immediate or delayed prosthetic replacement. Plast Reconstr Surg
Transplant Bull 1962;30:676–682.
2. Freeman BS. Complications of subcutaneous mastectomy with
prosthetic replacement, immediate or delayed. South Med J
1967;60(12):1277–1280.
3. Hartmann LC, Schaid DJ, Woods JE, et al. Efficacy of bilateral
prophylactic mastectomy in women with a family history of breast
cancer. N Engl J Med 1999;340:77–84.
4. Agarwal JP, Mendenhall SD, Anderson LA, et al. The breast
reconstruction evaluation of acellular dermal matrix as a sling trial
(BREASTrial): design and methods of a prospective randomized trial.
Plast Reconstr Surg 2015;135:20e–28e.
5. Petit JY, Veronesi U, Orecchia R, et al. Risk factors associated with
recurrence after nipple-sparing mastectomy for invasive and
intraepithelial neoplasia. Ann Oncol 2012;23:2053–2058.
6. Gabos Z, Thoms J, Ghosh S, et al. The association between biological
subtype and locoregional recurrence in newly diagnosed breast cancer.
Breast Cancer Res Treat 2010;124:187–194.
7. Lin NU, Vanderplas A, Hughes ME, et al. Clinicopathologic features,
patterns of recurrence, and survival among women with triple negative
breast cancer in the National Comprehensive Cancer Network. Cancer
2012;118:5463–5472.
8. de Alcantara Filho P, Capko D, Barry JM, et al. Nipple-sparing
mastectomy for breast cancer and risk-reducing surgery: the Memorial
Sloan-Kettering Cancer Center experience. Ann Surg Oncol
2011;18:3117–3122.
9. Coopey SB, Tang R, Lei L, et al. Increasing eligibility for nipple sparing
mastectomy. Ann Surg Oncol 2013;20:3218–3222.
10. Wang F, Peled AW, Garwood E, et al. Total skin-sparing mastectomy
and immediate breast reconstruction: an evolution of technique and
assessment of outcomes. Ann Surg Oncol 2014;21:3223–3230.
11. Krajewski AC, Boughey JC, Degnim AC, et al. Expanded indications
and improved outcomes for nipple-sparing mastectomy over time. Ann
Surg Oncol 2015;22:3317–3323.
12. Woods JE. Detailed technique of subcutaneous mastectomy with and
without mastopexy. Ann Plast Surg 1987;18(1):51–61.
13. Broer N, Narayan D, Lannin D, et al. A novel technique for nipple-
sparing mastectomy and immediate reconstruction in patients with
macromastia. Plast Reconstr Surg 2010;126(2):89e–92e.
14. Jensen JA, Lin JH, Kapoor N, et al. Surgical delay of the nipple-areolar
complex: a powerful technique to maximize nipple viability following
nipple-sparing mastectomy. Ann Surg Oncol 2012;19(10):3171–3176.
15. Bertoni DM, Nguyen D, Rochlin D, et al. Protecting nipple perfusion by
devascularization and surgical delay in patients at risk for ischemic
complications during nipple-sparing mastectomies. Ann Surg Oncol
2016;23:2665–2672.
16. Palmieri B, Baitchev G, Grappolini S, et al. Delayed nipples paring
modified subcutaneous mastectomy: rationale and technique. Breast J
2005;11:173–178.
17. Martinez CA, Reis SM, Sato EA, et al. The nipple-areola preserving
mastectomy: a multistage procedure aiming to improve reconstructive
outcomes following mastectomy. Plast Reconstr Surg Glob Open
2015;3:e538.
18. Spear SL, Hannan CM, Willey SC, et al. Nipple-sparing mastectomy.
Plast Reconstr Surg 2009;123:1665–1673.
19. Brachtel EF, Rusby JE, Michaelson JS, et al. Occult nipple involvement
in breast cancer: clinicopathologic findings in 316 consecutive
mastectomy specimens. J Clin Oncol 2009;27:4948–4954.
20. Cense HA, Rutgers EJ, Lopes Cardozo M, et al. Nipple sparing
mastectomy in breast cancer: a viable option? Eur J Surg Oncol
2001;27:521–526.
21. Laronga C, Kemp B, Johnston D, et al. The incidence of occult nipple-
areola complex involvement in breast cancer patients receiving a skin-
sparing mastectomy. Ann Surg Oncol 1999;6:609–613.
22. NCCN Clinical Practice Guidelines: Breast Cancer Risk Reduction
v1.2016. Available online at
http://www.nccn.org/professionals/physician_gls/pdf/breast.pdf.
23. Burdge EC, Yuen J, Hardee M, et al. Nipple skin-sparing mastectomy is
feasible for advanced disease. Ann Surg Oncol 2013;20:3294–3302.
24. Peled AW, Wang F, Foster RD, et al. Expanding the indications for total
skin-sparing mastectomy: is it safe for patients with locally advanced
disease? Ann Surg Oncol 2016;23:87–91.
25. Fortunato L, Loreti A, Andrich R, et al. When mastectomy is needed: is
the nipple-sparing procedure a new standard with very few
contraindications? J Surg Oncol 2013;108:207–212.
26. Santoro S, Loreti A, Cavaliere F, et al. Neoadjuvant chemotherapy is not
a contraindication for nipple sparing mastectomy. Breast 2015;24:661–
666.
27. Tousimis E, Haslinger M. Overview of indications for nipple sparing
mastectomy. Gland Surg 2018;7(3):288–300.
28. Spear SL, Rottman SJ, Seiboth LA, et al. Breast reconstruction using a
staged nipple-sparing mastectomy following mastopexy or reduction.
Plast Reconstr Surg 2012;129(3):572–581.
29. Chavez-MacGregor M, Clarke CA, Lichtensztajn DY, et al. Delayed
initiation of adjuvant chemotherapy among patients with breast cancer.
JAMA Oncol 2016;2(3):322–329.
30. Rawlani V, Fiuk J, Johnson SA, et al. The effect of incision choice on
outcomes of nipple-sparing mastectomy reconstruction. Can J Plast
Surg 2011;19(4):129–133.
31. Spear SL, Hannan C, Seiboth L, et al. Nipple-sparing mastectomy: a
review of indications, techniques and safety. Plast Reconstr Surg
2010;126:25.
32. Economides JM, Graziano F, Tousimis E, et al. Expanded algorithm and
updated experience with breast reconstruction using a staged nipple-
sparing mastectomy following mastopexy or reduction mammaplasty in
the large or ptotic breast. Plast Reconstr Surg 2019;143(4):688e–697e.
33. Alperovich M, Tanna N, Samra F, et al. Nipple-sparing mastectomy in
patients with a history of reduction mammaplasty or mastopexy: how
safe is it? Plast Reconstr Surg 2013;131(5):962–967.
CHAPTER 51

Can We Identify Risky Patients for


NSM?
ALBERTO O. RANCATI | AGUSTIN RANCATI
HISTORY
The evolution of breast surgery during the past 50 years moved from the
maximum tolerable treatment with aggressive and mutilating interventions,
like radical mastectomy, to the minimum effective treatment, and from an
anatomical concept of cancer spread to a biologic concept.
Conservative mastectomies incorporate the advantage of tumor and total
glandular excision (offered by the traditional total mastectomy) with
improvement in the aesthetic result, by the conservation of the skin envelope
and the nipple areolar complex (NAC). The use of anatomical expanders and
highly cohesive silicone implants ensures a high-quality immediate
reconstruction for these patients, but autologous tissue can be also used to fill
the empty skin pocket after glandular resection is made.
NAC ischemia and necrosis are feared complications, and the possibility of
identifying risky patients for NSM preoperatively, by breast imaging, can
help us in the selection of the correct breast reconstruction techniques for
these patients.
Digital mammography clearly distinguishes gland tissue density from the
overlying nonglandular breast tissue coverage, which corresponds to the
existing tissue between the skin and the Cooper ligaments surrounding the
gland (i.e., dermis and subcutaneous fat). Preoperative digital imaging can
determine the thickness of this breast tissue coverage, thus facilitating the
planning of the most adequate surgical technique and reducing the rate of
necrotic complications after direct-to-implant (DTI) reconstruction in nipple-
sparing mastectomy (NSM).
ONCOPLASTIC SURGERY
Oncoplastic surgery, which combines oncologic and reconstructive surgery,
has become increasingly popular (1–3). Conservative mastectomy, including
skin-sparing mastectomy (SSM), NSM, and skin-reducing mastectomy
(SRM) (1), is a well-established, validated (4), and widely used procedure for
breast cancer treatment; in such cases, immediate breast reconstruction is the
current standard (1,4).
Ideally, oncoplastic surgery will provide aesthetically pleasing results
while achieving appropriate oncologic safety (5). However, a potential pitfall
of these oncoplastic techniques is uncertainty regarding the blood supply to
the remaining flaps and the NAC (2,3). Postprocedural nipple and skin
necrosis rates as high as 38% have been reported (5). Patients with a large
cup size or a previous history of surgery or radiation are considered high risk
for NSMs because these factors are associated with even higher rates of
complications (2).
Several recommendations have been proposed to avoid necrosis of the
mastectomy flaps and/or the NAC (7,8). Preservation of adequate flap
thickness during mastectomy significantly reduces skin necrosis. However,
this is not always possible, depending on the breast characteristics of each
patient (9). Performing an oncologically safe mastectomy requires dissection
below the superficial layer of the fascia superficialis (10). The distance
between the skin and the gland determines the subcutaneous tissue or “gland
envelope” thickness.
Currently, standard film mammograms do not allow the clear identification
and measurement of nonglandular breast tissue coverage. In contrast, digital
mammography clearly distinguishes gland tissue density from tegument and
fat coverage; accordingly, this preoperative imaging modality can determine
the coverage thickness (6,7) (i.e., the distance between the breast skin and
Cooper ligaments surrounding the gland; Figs. 51-1 to 51-3A,B). As incision
planning, treatment selection, surgical technique, and reconstructive
procedures are usually related to the breast volume, tumor characteristics, and
surgeons’ and patients’ preferences, preoperative information regarding the
breast tissue coverage thickness might highlight the likelihood of
postmastectomy flap issues and assist with the planning process, rather than
relying on breast volume alone as a guideline (2).
Adequate fat tissue coverage thickness is one of the most important
independent factors in immediate breast reconstruction and flap survival
(11–13,17,18). Anatomically, the vascular network that ensures flap and
NAC survival runs between Cooper ligaments and the skin (14).
Compression of this vascular network by implant insertion, surgical damage,
tissue tension at closure, or extremely thin flaps might endanger
vascularization, and such events have been shown to cause tissue damage in
the distal parts of flaps (8–21). Consideration must therefore be given to
preoperative breast tissue coverage measure as an important factor in
immediate reconstruction.

FIGURE 51-1 Difference of density between digital (A) and standard (B, film)
mammograms of a same patient.

Preoperative evaluation of gland coverage can help predict the viability of


the remaining flaps after conservative mastectomies, and to select the optimal
immediate reconstructive procedure to diminish postoperative coverage
complications.
FIGURE 51-2 Preoperative digital mammograms, showing different thickness in
breast tissue coverage on two C cup, breast patients (A, B).
FIGURE 51-3 Digital mammograms showing tissue coverage to be maintained
during mastectomy (A) and different types of tissue coverage in different patients
with the same breast volume (B).

One of the most important factors for vascularization of the remaining


postmastectomy flaps is the preservation of the skin perforators and flap
thickness (11,12,17,18). The remaining skin flap thickness after gland
resection during conservative mastectomy plays an important role in flap
integrity and NAC vitality. Cooper ligaments separate the mammary gland
from the superficial fat and skin tissue layers that contain the vascular plexus,
of which the mastectomy flaps are composed (13). Preoperative information
regarding this tissue coverage is therefore of the utmost importance to avoid
complications associated with immediate reconstruction procedures
(11,16,17).
Larson et al. (28) reported differences in the thickness of the subcutaneous
breast tissue not related to breast volume. Therefore, it could be advantageous
to know the thickness of the subcutaneous breast tissue before considering a
DTI reconstruction following an NSM.
A more comprehensive indication for a reconstructive method could be
evaluated considering this preoperative information over the possible
resulting flap thickness after mastectomy. We propose a breast tissue
coverage classification (BTCC) (Table 51-1) according to the digital
mammogram evidence (29).
Based on the obtained range of coverage values, a three-type BTCC is as
follows:

Type 1: <1 cm (poor coverage)


Type 2: between 1 and 2 cm (medium coverage)
Type 3: >2 cm (good coverage)

This classification may also allow a rational use of materials for individual
patients.

TABLE 51-1 Breast Tissue Coverage Classification (BTCC)


Classification Size (cm) Coverage
Type 1 <1 Poor
Type 2 1–2 Medium
Type 3 >2 Good
FIGURE 51-4 A 42-year-old patient with DCIS on her left breast, with previous
biopsy (BRCA+). Bilateral NSM; immediate bilateral DTI reconstruction was
performed with Mentor CPG shaped 323 345 cc. A: Preoperative digital
mammogram showing a type 3 breast. B–D: Frontal and oblique preoperative views.
E, F: Frontal and oblique 10-month postoperative views. The scar running through
the NAC was due to a surgical accident by excessive tension with the retractors
during surgery.

We confirmed that the selection of patients with breast subcutaneous tissue


coverage above 2 cm, as an evidence at preoperative digital mammogram
evaluation, determines an adequate flap for NSM, directly representing the
distance between the Cooper ligaments (the “safe” mastectomy surgical
plane), and the skin (29).
In this kind of patients, an immediate DTI reconstruction could be safely
performed.
The selection of mastectomy and reconstruction procedures should be
made jointly by the oncologic and plastic surgeon based on objective
preoperative information (12,18,19). We observed that breast tissue coverage
and breast volume are independent factors in large breasts with poor coverage
and small ones with good coverage; this suggests that preoperative
measurement of the breast tissue coverage thickness is important for surgical
decisions independently of breast volume. Regardless of breast volume,
however, preoperative evaluation of tissue coverage is crucial for surgical
planning by both the oncologic and plastic surgeon as this factor is directly
related to the risk of flap and NAC ischemia/necrosis (22–24). Thin flaps can
lead to ischemic complications following mastectomies and reconstructive
procedures (11,17). Preoperative digital mammography or MRI is therefore
potentially useful not only for tumor detection but as an objective tool to
predict the resulting flap thickness, thus improving patient safety
(13,14,20,25–27).
As a result, preoperative communication between the reconstructive and
oncologic surgeons regarding the incision choice and integumentary
preservation according to digital mammogram findings might lead to
improved outcomes with a decreased rate of complications (Figs. 51-4 and
51-5).
CONCLUSION
Preoperative planning should not depend only on breast volume. Flap
evaluations based on preoperative imaging measurements might be helpful
when planning a conservative mastectomy. Accordingly, we propose a
BTCC. DTI immediate reconstruction with silicone implants following NSM
appears to be a safe option in selected cases with enough tissue coverage,
also providing a high level of patient satisfaction. The possibility of selecting
cases for this procedure according to the preoperative digital mammogram
showing more than 2 cm of superficial tissue thickness may help reduce the
risk of immediate ischemic complications. Additionally, the use of surgical
materials may be evaluated according to this coverage measure. According to
our classification, for patients in the poor coverage group (type 1), it would
be helpful to add supplementary coverage for the reconstruction, such as
ADM, meshes, retropectoral implant placement, and delayed fat grafting. In
the medium coverage group (type 2), a two-stage expander-implant
reconstruction should be suggested to avoid tension at the flap closure,
whereas, in the good coverage group (type 3), single-stage, DTI prepectoral
reconstruction with implants could be performed.

FIGURE 51-5 A 42-year-old patient with DCIS on her right breast (BRCA+). NSM
and immediate DTI reconstruction were performed with Mentor CPG shaped
implants 323 345 cc. A: Preoperative digital mammogram showing a type 3 breast.
B–D: Frontal and oblique preoperative views, showing planned incision and special
interest in keeping fat and perforators in the lower inner quadrant. E, F: Frontal
and oblique postoperative views after 1 year.
REFERENCES

1. Nava MB, Cortinovis U, Ottolenghi J, et al. Skin-reducing mastectomy.


Plast Reconstr Surg 2006;118:603–610; discussion 611–613.
2. Zenn MR. Staged immediate breast reconstruction. Plast Reconstr Surg
2015;135:976–979.
3. Staub G, Fitoussi A, Falcou MC, et al. Breast cancer surgery: use of
mammaplasty. Results. Series of 298 cases. Ann Chir Plast Esthet
2008;53:124–134.
4. della Rovere GQ, Nava M, Bonomi R, et al. Skin-reducing mastectomy
with breast reconstruction and sub-pectoral implants. J Plast Reconstr
Aesthet Surg 2008;61:1303–1308.
5. Longo B, Farcomeni A, Ferri G, et al. The BREAST-V: a unifying
predictive formula for volume assessment in small, medium, and large
breasts. Plast Reconstr Surg 2013;132:1e–7e.
6. Kuhl C. The current status of breast MR imaging. Part I. Choice of
technique, image interpretation, diagnostic accuracy, and transfer to
clinical practice. Radiology 2007;244:356–378.
7. Kuhl CK. Current status of breast MR imaging. Part 2. Clinical
applications. Radiology 2007;244:672–691.
8. Lalardie JP, Jouglard P. Chirurgie plastique du Sein. Paris: Masson;
1974.
9. van Dongen JA, Voogd AC, Fentiman IS, et al. Long-term results of a
randomized trial comparing breast-conserving therapy with mastectomy:
European Organization for Research and Treatment of Cancer 10801
trial. J Natl Cancer Inst 2000;92:1143–1150.
10. R Development Core Team. R: a language and environment for
statistical computing. Vienna, Austria: R Foundation for Statistical
Computing. Available online at http://www.R-project.org/
11. Nahabedian MY. Overview of perforator imaging and flap perfusion
technologies. Clin Plast Surg 2011;38:165–174.
12. Seitz IA, Nixon AT, Friedewald SM, et al. “NACsomes”: A new
classification system of the blood supply to the nipple areola complex
(NAC) based on diagnostic breast MRI exams. J Plast Reconstr Aesthet
Surg 2015;68:792–799.
13. Spear SL, Rottman SJ, Seiboth LA, et al. Breast reconstruction using a
staged nipple-sparing mastectomy following mastopexy or reduction.
Plast Reconstr Surg 2012;129:572–581.
14. Nahabedian MY, Tsangaris TN. Breast reconstruction following
subcutaneous mastectomy for cancer: a critical appraisal of the nipple-
areola complex. Plast Reconstr Surg 2006;117:1083–1090.
15. Wapnir I, Dua M, Kieryn A, et al. Intraoperative imaging of nipple
perfusion patterns and ischemic complications in nipple-sparing
mastectomies. Ann Surg Oncol 2014;21:100–106.
16. Colwell AS, Tessler O, Lin AM, et al. Breast reconstruction following
nipple-sparing mastectomy: predictors of complications, reconstruction
outcomes, and 5-year trends. Plast Reconstr Surg 2014;133:496–506.
17. Heywang-Köbrunner SH, Hacker A, Sedlacek S. Magnetic resonance
imaging: the evolution of breast imaging. Breast 2013;22 Suppl 2:S77–
S82.
18. Cunningham L. The anatomy of the arteries and veins of the breast. J
Surg Oncol 1977;9:71–85.
19. Longo B, Campanale A, Santanelli di Pompeo F. Nipple-areola complex
cutaneous sensitivity: a systematic approach to classification and breast
volume. J Plast Reconstr Aesthet Surg 2014;67:1630–1636.
20. Murray JD, Jones GE, Elwood ET, et al. Laser angiography as a
predictor of mastectomy flap necrosis after breast reconstruction. Plast
Reconstr Surg 2012;129:1017e–1018e.
21. Phillips BT, Lanier ST, Conkling N, et al. Intraoperative perfusion
techniques can accurately predict mastectomy skin flap necrosis in
breast reconstruction: results of a prospective trial. Plast Reconstr Surg
2012;129:778e–788e.
22. Gerber B, Krause A, Dieterich M, et al. The oncological safety of skin
sparing mastectomy with conservation of the nipple-areola complex and
autologous reconstruction: an extended follow-up study. Ann Surg
2009;249:461–468.
23. Mallon P, Feron JG, Couturaud B, et al. The role of nipple-sparing
mastectomy in breast cancer: a comprehensive review of the literature.
Plast Reconstr Surg 2013;131:969–984.
24. Salgarello M, Visconti G, Barone-Adesi L. Nipple-sparing mastectomy
with immediate implant reconstruction: cosmetic outcomes and
technical refinements. Plast Reconstr Surg 2010;126:1460–1471.
25. Spear SL, Willey SC, Feldman ED, et al. Nipple-sparing mastectomy for
prophylactic and therapeutic indications. Plast Reconstr Surg
2011;128:1005–1014.
26. Cordeiro PG, Pusic AL, Disa JJ, et al. Irradiation after immediate tissue
expander/implant breast reconstruction: outcomes, complications,
aesthetic results, and satisfaction among 156 patients. Plast Reconstr
Surg 2004;113:877–881.
27. Chu CK, Carlson GW. Techniques and outcomes of nipple sparing
mastectomy in the surgical management of breast cancer. Curr Breast
Cancer Rep 2013;5:118–124.
28. Larson DL, Basir Z, Bruce T. Is oncologic safety compatible with a
predictably viable mastectomy skin flap? Plast Reconstr Surg
2011;127:27–33.
29. Rancati A, Angrigiani C, Hammond D, et al. Preoperative digital
mammography imaging in conservative mastectomy and immediate
reconstruction. Gland Surg 2016;5:9–14.
CHAPTER 52

Implant-Based Reconstruction in High-


BMI Patients
ALLEN GABRIEL | MAURICE Y. NAHABEDIAN | G. PATRICK MAXWELL
HISTORY

Key Points
Patients with high body mass index (BMI) have poorer outcomes after
implant-based reconstruction
Postoperative complications are elevated with increasing BMI
Surgical factors, such as overdissection of the pocket, skin redundancy,
and poorly vascularized flaps, are partly responsible for this elevated
risk
Placing the implant under the pectoral muscle and its attendant
complications contributes further to the elevated risk
Proactive management of the surgical factors and moving the implant to
the prepectoral plane can lead to improved outcomes
BMI alone should not be used to estimate risk of complications or
exclude patients for implant-based reconstruction

High body mass index (BMI) or obesity, defined as a BMI of greater than 30
kg/m2, is a major health concern as it increases the risk of medical conditions
(such as heart disease, stroke, type 2 diabetes, and certain types of cancer) as
well as the risk of premature mortality (1). In the United States,
approximately 42% of women are obese (2). With a 12% lifetime risk of
breast cancer (3), and the growing trend of more women opting for
mastectomy and reconstruction as a treatment for breast cancer (4),
reconstructive surgeons are likely to encounter an increasing number of obese
patients.
Reconstructive options in high-BMI patients are similar to normal-weight
patients and include both autologous and prosthetic options (5). The optimal
approach for high-BMI patients, however, remains to be determined. In the
past, immediate prosthetic reconstruction was discouraged in high-BMI
patients due to high complication rates. Autologous options were encouraged
but donor-site morbidity became an additional area of concern and source of
complications. In the current era, autologous options are considered to be less
favorable as they are associated with higher postoperative complications
compared with prosthetic reconstruction (6). The prosthetic option, however,
is not any better in this population for compared with normal-weight patients,
there is nonetheless an increased risk of complications and poorer outcomes
(6–10).
Since the introduction of acellular dermal matrices (ADMs), prosthetic
reconstruction has been performed exclusively via the dual plane subpectoral
approach. In addition, the two-stage expander/implant approach is favored
over the one-stage direct-to-implant approach (4). Recently, the prepectoral
approach, a newer prosthetic approach, is gaining popularity given its
simplicity (11–15). We have been performing prepectoral reconstruction
since 2008, initially in revision cases and then in primary reconstructions
(11). Prepectoral reconstruction, in our experience, appears to be a better
approach for high-BMI patients than subpectoral reconstruction (16).
In this chapter, we highlight the technical challenges of implant-based,
prepectoral reconstruction in high-BMI patients, which are also applicable to
the subpectoral approach. We also provide an insight into the changing
paradigm of postoperative outcomes in this high-risk population.
PREPECTORAL RECONSTRUCTION IN HIGH-BMI PATIENTS

Operative Planning
BMI does not dictate the indications and contraindications for immediate
prepectoral reconstruction, which remain the same across all BMI strata.
Obesity, as an isolated factor, is not a contraindication; but, morbid obesity
(>40 kg/m2) with comorbidities, such as diabetes mellitus and hypertension,
is a contraindication (Table 52-1) (11).
The availability of well-perfused, viable, mastectomy skin flaps is the
single most absolute requirement for immediate prepectoral reconstruction in
all patients. Given the proximity of the prepectorally placed implant to the
overlying skin flaps, flap perfusion is extremely important. Underperfused
flaps increase the risk of skin necrosis and associated complications of
infection, implant extrusion, and reconstructive failure. For this reason, any
patient characteristic or factor that compromises flap perfusion or quality is a
contraindication for immediate prepectoral reconstruction. Thus, patient
comorbidities such as uncontrolled diabetes (HbA1c >7.5%) and active
smoking are contraindications for immediate reconstruction. In patients with
HbA1c >7.5%, reconstruction is delayed until after blood glucose is
controlled with treatment. In patients who use tobacco products, cessation of
smoking for at least 2 months is required before reconstruction can be
considered.

TABLE 52-1 Contraindications to Immediate Prepectoral Reconstruction


Reconstructive Contraindications Oncologic Contraindications
Poorly vascularized mastectomy flaps Large tumors (>5 cm)
Prior radiation Late-stage cancer
BMI >40 kg/m2a Deep tumors
Immunocompromised Chest wall involvement
HbA1c >7.5% Axillary involvement
Active smokers High risk of recurrence
Lack of fat depots
aWith other associated comorbidities (e.g., diabetes mellitus, hypertension); body mass index alone is
not a contraindication.
BMI, body mass index; HbA1c, hemoglobin A1c.
Derived from Sigalove S, Maxwell GP, Sigalove NM, et al. Prepectoral implant-based breast
reconstruction: rationale, indications, and preliminary results. Plast Reconstr Surg 2017;139:287–
294.

In the absence of contraindications, patient eligibility for immediate


prepectoral reconstruction is ascertained provisionally preoperatively and
confirmed intraoperatively after mastectomy following assessment of flap
vascularity and viability. Assessment of flap vascularity is performed
objectively with a tissue perfusion device or clinically in its absence in all
cases prior to proceeding with immediate reconstruction. Flap thickness is not
an indication of flap vascularity. This is of particular importance in obese
patients who often have thick mastectomy flaps.
Reconstructive Considerations
The basic principles of preoperative reconstruction remain the same
irrespective of BMI status. The challenge in obese patients involves
managing skin redundancy as well as the excessive dead space in the
postmastectomy pocket. These same challenges are also encountered in the
subpectoral approach. Obese patients have an oversized pocket with a
generous amount of subcutaneous tissue (Fig. 52-1) that is displaced when
breast tissue is removed. The challenge involves repositioning the
subcutaneous tissue so as to collapse and minimize the pocket size for a snug
fit of the future implant. Repositioning of subcutaneous tissue also reinforces
the pocket providing additional support to the future implant, eliminates dead
space, and minimizes the risk of seroma formation.
With the removal of breast tissue, the lateral anterior subcutaneous tissue
naturally descends to the posterior axillary line. This tissue is repositioned
and anchored to the anterior axillary line with cloture sutures (0-Vicryl on
CT-1) (Fig. 52-2A). Removal of breast tissue also retracts the cephalad-
subcutaneous tissue, which is repositioned more caudally (Fig. 52-2B).
Repositioning of the cephalad-subcutaneous tissue further collapses the
pocket and renders a smoother transition of the mastectomy pocket to the
implant, which is an additional benefit of prepectoral reconstruction. With a
smoother transition zone, fat grafting may not be needed at the upper pole in
some instances, depending on the final outcome of the breast form following
the second-stage reconstruction. In dual plane reconstruction, the cephalad
area is ignored since all pocket work is limited to under the pectoralis major
muscle.
Prepectoral reconstruction is typically performed as a two-staged,
expander/implant procedure. Although obese patients have adequate
subcutaneous tissue, direct-to-implant reconstruction is rarely performed
because complication and revision rates increase with increasing BMI
following direct-to-implant reconstruction (17). Poor breast projection and
contour irregularities are common in patients with high BMI and the second
stage provides an opportunity to address these problems and improve the
overall appearance of the breast. The expander is inflated with air
intraoperatively to 50% to 70% of maximum capacity. Underfilling alleviates
the pressure on the overlying flap and reduces the risk of ischemia while the
use of air alleviates the pressure on the inferior mastectomy flap and
minimizes suture pull-through. Use of ADM for expander coverage is an
essential component of prepectoral reconstruction, irrespective of the
thickness of the flap or the amount of subcutaneous tissue present.

FIGURE 52-1 Oversized mastectomy pocket and excess subcutaneous tissue.

FIGURE 52-2 Repositioning of subcutaneous tissue. A: Repositioning of the lateral


anterior subcutaneous tissue from the posterior axillary line to the anterior axillary
line. B: Caudal repositioning of the cephalad-subcutaneous tissue.
Management of skin redundancy is a critical aspect of breast
reconstruction in obese patients. Redundant skin flap is utilized as much as
possible in reconstructing the new breast; but, only adequately vascularized
tissue is utilized. Poorly vascularized flap tissue is excised. Excess skin flap
can be reduced by closing the central mastectomy incision horizontally by
extending laterally to the anterior and at times to the posterior axillary line
(Fig. 52-3). Although the excess skin can be addressed in this fashion, the
result is a long scar in an unnatural location that is inconsistent with aesthetic
principles of breast surgery. In addition, the central flattening and the
extenuation of the lateral chest-wall tissue make this an unpreferred
approach. Alternatively, given the large size of the breasts, excessive skin
envelope can be managed similarly to an aesthetic, skin-reducing procedure
similar to a mastopexy, which is detailed below.

FIGURE 52-3 Skin-reduction closure utilizing the horizontal central mastectomy


incision.

Preoperatively, the breast meridian and the highest point of the vertical
incision on the breasts that matches the contralateral side are marked on the
patient (Fig. 52-4). These are the only two preoperative markings, which are
done in collaboration with the breast surgeon. The mastectomy approach is
discussed with the breast surgeon, which involves a circumareolar approach
with nipple areolar complex (NAC) removal in all cases. The circumareolar
approach allows the reconstructive surgeon maximum flexibility to manage
the skin envelope. As in aesthetic breast surgery when mastopexy
augmentation is performed, the implant is first placed and the skin envelope
is addressed by tailor tacking that leads to removal of the excess skin. In the
reconstructive approach, following completion of mastectomy through the
circumareolar incision with NAC removal, the expander/ADM construct is
placed and filled with air so the skin envelope can be addressed
appropriately. The breast meridian is remarked as well as the position of the
cephalad vertical tip while matching it to the contralateral side (Fig. 52-5A).
Then the inframammary fold on the skin flap is marked (Fig. 52-5B). The
central flap is tailor tacked vertically to help assess the extent of skin
reduction that will be needed (Fig. 52-6). At this point, there is the option to
proceed with definitive vertical closure, depending on the extent of lower
pole excess skin that remains, or to proceed with converting the vertical
closure to an inverted T. In both cases, there is excess skin under the tailor-
tacked portion and this leads to the creation of the dermal flap at the lower
pole. If the length of the vertical closure is more than 9 to 10 cm and there is
too much excess lower pole tissue that cannot be addressed with only the
vertical approach, an inverted T is added. The area of the lower dermal flap is
marked (Fig. 52-7A) and the skin over the dermal flap surface is
deepithelialized (Fig. 52-7B). The deepithelialized flap is arranged over the
ADM and is tacked down with 3-0 Monocryl (Fig. 52-7C). The flap provides
an additional layer of soft tissue coverage, supports the incision, and prevents
expander exposure in the event of incisional dehiscence. It also adds
additional projection, which may be needed in some cases. Skin closure over
the dermal flap begins with securing the medial and lateral flaps to the
inframammary fold (Fig. 52-8A), followed by vertical closure over the breast
mound (Fig. 52-8B), and then horizontal closure at the inframammary fold.
FIGURE 52-4 Preoperative markings.

FIGURE 52-5 Skin reduction markings for mastopexy-like procedure. A: Position of


breast meridian and cephalad vertical tip. B: Position of inframammary fold.

Fat grafting is an important adjunct to prepectoral reconstruction. Some


patients will require fat grafting to enhance breast aesthetics in spite of
having a thick subcutaneous layer. Obese patients typically require fat
grafting at the upper pole to improve the step-off that is present at the
transition zone between the upper pole and the implant unless the rotation of
tissue from the cephalad portion of the pocket was successful to blunt the
transition zone. If needed, fat grafting is performed as a third stage after
allowing sufficient time for the reconstructed breast to recover from surgery.
FIGURE 52-6 Tailor tacking the central flap. A: Grasping the excess skin edges with
forceps. B: Using the skin stapler to achieve the desired skin contour. C: The staples
skin edges create a template for optimal skin excision.

FIGURE 52-7 Lower dermal flap creation. A: Marking of flap. B: Deepithelialized


flap. C: Deepithelialized flap tacked down over the acellular dermal matrix.
BENEFITS OF PREPECTORAL RECONSTRUCTION IN HIGH-BMI PATIENTS
Obese individuals lack core body strength and rely on their upper body
strength using their arms to help them to rise from a seated position (18).
Chest wall muscles, including the pectoralis major muscles, are enlisted for
this maneuver. In a patient who has undergone subpectoral breast
reconstruction, in the immediate postoperative period, repeated use of the
pectoralis major muscle could potentially have a shearing effect on the
overlying skin flap and the underlying ADM. The shearing effect on the
dermal matrix could potentially compromise the incorporation of the matrix
and lead to seroma formation (Fig. 52-9). The prepectoral approach
eliminates this shearing effect and may be a particularly beneficial approach
in obese patients. In addition, the majority of these patients require a higher-
projecting implant given the depth of the chest. With a higher-projecting
implant, generally only less than a third of the implant is covered by the
muscle in dual plane plus ADM reconstructions (Fig. 52-10). This is only in
the upper pole and in this population, fat grafting can be performed to
camouflage any implant visibility, if any. In addition, subpectoral
reconstruction generally minimizes the projection of the implant. Placing the
implant over the muscle provides the surgeon the opportunity to create a
maximally projecting breast without any compression from the pectoralis
major (Fig. 52-11). Further, by preserving the integrity of the pectoralis
major muscle, prepectoral implant placement eliminates the problems of
muscle elevation, including pain, muscle spasm, animation deformity, and
functional impairment of the muscle (11).

FIGURE 52-8 Skin closure. A: First stitch securing the medial and lateral skin flap
to the inframammary fold. B: Vertical closure over the central breast.
FIGURE 52-9 Seroma formation.
FIGURE 52-10 ADM reconstructions.
FIGURE 52-11 Pectoralis major.
IMPROVING OUTCOMES IN OBESE PATIENTS
It is well documented in the published literature that high-BMI patients
generally have poorer outcomes after breast reconstructive surgery compared
with normal-weight patients (6–10). In implant-based,
subpectoral/submuscular reconstructions, BMI has been shown to be an
independent, continuous predictor of outcomes. Every unit increase in BMI
increased the odds of complications by 6% and reconstructive failure by 8%
(19). Rates of impaired wound healing, incision dehiscence, skin necrosis,
infections, and seroma increased with progressive increases in BMI.
The elevated risk of postoperative complications in high-BMI patients may
be partly explained by impairment of normal physiologic processes by
obesity itself. Collagen deposition and maturation and myofibroblast activity
are required for normal wound healing (10). Impaired collagen deposition
also weakens the mechanical strength of the skin. Further, the chronic, low-
grade systemic inflammation present in obese individuals decreases
mastectomy skin flap survival. Flap survival is also linked to malperfusion
that is usually due to the increased tissue volume and a limited vascular
supply in these patients. Hypoxia resulting from inadequate perfusion of flap
edges furthest from the vascular source can lead to skin necrosis and
infection. Hypoxia also impedes collagen synthesis and contributes to
impaired wound healing.
In addition to obesity itself, the presence of comorbid conditions and
surgery-related factors may also in part play a contributory role to the
elevated risk of postoperative complications in obese patients. Type 2
diabetes and hypertension are very common among obese patients (20). In
fact, both comorbidities increase with increasing BMI. Diabetes is a well-
established predictor of complications after implant-based breast
reconstruction (19,21,22). In some studies, hypertension has also been shown
to be a predictor of postoperative complications (21). Smoking is another
well-established predictor of complications after implant-based
reconstructions. Using multivariate logistic regression analyses, we have
found that diabetes and smoking likely pose a far greater risk of
complications than BMI per se in obese patients (20). Even temporary
smoking cessation or reducing HbA1c to within normal levels prior to
reconstruction, may not be adequate to completely eliminate the risk of
complications associated with these factors. With respect to surgery-related
factors, overdissection of the pocket and poorly vascularized flaps are
important risk factors for seroma and skin necrosis, respectively, in high-BMI
patients.

TABLE 52-2 Strategies to Improve Outcomes in High-BMI Patients


Surgical Considerations
Maximize flap viability
Assess flap perfusion objectively
Avoid overdissection of the mastectomy pocket
Reduce pocket size with meticulous pocket work
Appropriately manage skin redundancy
Postoperative Care
Apply negative-pressure wound therapy over incision
Recommend compression bra in the immediate postoperative period
Aggressively manage seroma and infection should they arise

Although losing weight, smoking cessation, and controlling blood glucose


level before surgery are encouraged, these alone may not be sufficient to
reduce the elevated risk of complications in high-BMI patients (20). Our data
suggest that the physiologic damage caused by these factors is likely to
persist and negatively influence outcomes even after the factors are
controlled. But, controlling for surgical factors, together with diligent
postoperative care and follow-up (Table 52-2), can lead to improved
outcomes in these patients (see Case 1 and Case 2). In fact, when surgical
factors are controlled and the implant is moved to the prepectoral space, BMI
appears to be no longer an independent, continuous predictor of
complications. BMI alone should, thus, not be used to estimate risk of
complications or exclude patients for implant-based reconstruction.

CASES
CASE 1

Forty-five-year-old female with left breast invasive ductal carcinoma, a


body mass index of 43 kg/m2, and no other comorbidities. Her HbA1c
was 5.8%. Figure 52-12A–E shows preoperative views. Figure 52-12F–
J shows patient 6 weeks after bilateral skin-reducing mastectomy and
prepectoral reconstruction with 133MV 500-cc expanders and AlloDerm.
Figure 52-12K–O shows patient 4 years after bilateral breast
reconstruction with style 20 800-cc implants, one session of fat grafting,
areolar tattooing, and nipple reconstruction.
FIGURE 52-12 Forty-five-year-old female with left breast invasive ductal
carcinoma, a body mass index of 43 kg/m2, and no other comorbidities. See
case description for additional details.
CASE 2

Fifty-nine-year-old female with left breast invasive ductal carcinoma, a


body mass index of 35 kg/m2, and no other comorbidities. Her HbA1c
was 5.5%. Figure 52-13A–E shows preoperative views. Figure 52-13F–
H shows bilateral skin-reducing mastectomy and prepectoral
reconstruction with 133 FV 550-cc expanders and AlloDerm. Patient is
shown at postoperative day 7 following removal of negative-pressure
incision management device. Figure 52-13I–M shows patient 3 years
after bilateral breast reconstruction with SRX 800-cc implants, one
session of fat grafting, and 3D nipple tattooing.
FIGURE 52-13 Fifty-nine-year-old female with left breast invasive ductal
carcinoma, a body mass index of 35 kg/m2, and no other comorbidities. See
case description for additional details.
CONCLUSION
High-BMI patients are generally believed to have poorer outcomes after
implant-based breast reconstructive surgery compared with normal-weight
patients. The prepectoral approach in these patients may offer some benefits
and may be a better reconstructive approach. Managing mastectomy flap
redundancy and minimizing pocket size are important reconstructive
challenges in this population that when properly addressed can lead to
acceptable and consistent outcomes.

REFERENCES

1. Centers for Disease Control and Prevention (CDC). Adult obesity facts.
Page last reviewed August 13, 2018. Available at
https://www.cdc.gov/obesity/data/adult.html. Accessed September 3,
2019.
2. Hales CM, Carroll MD, Fryar CD, et al. Prevalence of Obesity Among
Adults and Youth: United States, 2015–2016. NCHS Data Brief, No.
288. Hyattsville, MD: National Center for Health Statistics; 2017.
3. BREASTCANCER.ORG. U.S. Breast cancer statistics. Last modified
on February 13, 2019. Available at
https://www.breastcancer.org/symptoms/understand_bc/statistics
Accessed September 3, 2019.
4. American Society of Plastic Surgeons. 2018 Plastic surgery statistics
report. Available at
https://www.plasticsurgery.org/documents/News/Statistics/2018/plastic-
surgery-statistics-full-report-2018.pdf. Accessed September 3, 2019.
5. Rolph R, Mehta S, Farhadi J. Breast reconstruction: options post-
mastectomy. Br J Hosp Med (Lond) 2016;77:334–342.
6. Hanwright PJ, Davila AA, Hirsch EM, et al. The differential effect of
BMI on prosthetic versus autogenous breast reconstruction: a
multivariate analysis of 12,986 patients. Breast 2013;22:938–945.
7. Fischer JP, Nelson JA, Kovach SJ, et al. Impact of obesity on outcomes
in breast reconstruction: analysis of 15,937 patients from the ACS-
NSQIP datasets. J Am Coll Surg 2013;217:656–664.
8. Fischer JP, Nelson JA, Serletti JM, et al. Peri-operative risk factors
associated with early tissue expander (TE) loss following immediate
breast reconstruction (IBR): a review of 9305 patients from the 2005–
2010 ACS-NSQIP datasets. J Plast Reconstr Aesthet Surg
2013;66:1504–1512.
9. Fischer JP, Wes AM, Tuggle CT 3rd, et al. Risk analysis of early
implant loss after immediate breast reconstruction: a review of 14,585
patients. J Am Coll Surg 2013;217:983–990.
10. Panayi AC, Agha RA, Sieber BA, et al. Impact of obesity on outcomes
in breast reconstruction: a systematic review and meta-analysis. J
Reconstr Microsurg 2018;34:363–375.
11. Sigalove S, Maxwell GP, Sigalove NM, et al. Prepectoral implant-based
breast reconstruction: rationale, indications, and preliminary results.
Plast Reconstr Surg 2017;139:287–294.
12. Sbitany H, Piper M, Lentz R. Prepectoral breast reconstruction: a safe
alternative to submuscular prosthetic reconstruction following nipple-
sparing mastectomy. Plast Reconstr Surg 2017;140:432–443.
13. Onesti MG, Maruccia M, Di Taranto G, et al. Clinical, histological, and
ultrasound follow-up of breast reconstruction with one-stage muscle-
sparing “wrap” technique: a single-center experience. J Plast Reconstr
Aesthet Surg 2017;70:1527–1536.
14. Highton L, Johnson R, Kirwan C, et al. Prepectoral implant-based breast
reconstruction. Plast Reconstr Surg Glob Open 2017;5:e1488.
15. Vidya R, Berna G, Sbitany H, et al. Prepectoral implant-based breast
reconstruction: a joint consensus guide from UK, European and USA
breast and plastic reconstructive surgeons. Ecancermedicalscience
2019;13:927.
16. Gabriel A, Sigalove S, Sigalove NM, et al. Dual-plane versus
prepectoral breast reconstruction in high BMI patients. Plast Reconstr
Surg 2019 (In Press).
17. Gdalevitch P, Ho A, Genoway K, et al. Direct-to-implant single-stage
immediate breast reconstruction with acellular dermal matrix: predictors
of failure. Plast Reconstr Surg 2014;133:738e–747e.
18. Gabriel A, Maxwell GP. Prepectoral breast reconstruction in challenging
patients. Plast Reconstr Surg 2017;140:14S–21S.
19. Nguyen KT, Hanwright PJ, Smetona JT, et al. Body mass index as a
continuous predictor of outcomes after expander-implant breast
reconstruction. Ann Plast Surg 2014;73:19–24.
20. Gabriel A, Sigalove S, Sigalove NM, et al. Effect of body mass index on
outcomes after prepectoral breast reconstruction. Plast Reconstr Surg
2019;144:550–558.
21. McCarthy CM, Mehrara BJ, Riedel E, et al. Predicting complications
following expander/implant breast reconstruction: an outcomes analysis
based on preoperative clinical risk. Plast Reconstr Surg 2008;121:1886–
1892.
22. Abedi N, Ho AL, Knox A, et al. Predictors of mastectomy flap necrosis
in patients undergoing immediate breast reconstruction: a review of 718
patients. Ann Plast Surg 2016;76:629–634.
CHAPTER 53

When Is Delayed Breast


Reconstruction Indicated?
CHRISTOPHER A. BOBBITT | HAHNS Y. KIM
HISTORY
Breast cancer has a lifetime risk of up to 10% in women, making it the most
common cancer in females. Approximately one-third of women with breast
cancer receive a mastectomy of some kind (1). The increased knowledge and
identification of genetic susceptibility to breast cancer has led to more
bilateral prophylactic mastectomies and contralateral prophylactic
mastectomies than in past decades. It has been clearly demonstrated that
patients with BRCA mutations who undergo prophylactic mastectomy benefit
from a significantly lower risk of breast cancer (2,3). Because of this data,
BRCA-positive patients are frequently undergoing bilateral prophylactic
mastectomies at a young age. Additionally, patients with early-stage breast
cancer, who would be candidates for breast conserving therapy, can choose a
mastectomy as their surgical therapy (4). Furthermore, patients with
unilateral breast cancer can elect to undergo a contralateral prophylactic
mastectomy. This is especially true in the United States. In fact, in 1998,
1.9% of women who were eligible for breast-conserving surgery elected to
undergo bilateral mastectomy. In 2011, this percentage jumped to 11.2% (5).
In patients recommended to undergo unilateral mastectomy, 5.4% elected for
bilateral mastectomy in 1998 compared to 29.7% in 2011 (5). Not only have
the number of mastectomies being performed increased, but the rates of
breast reconstruction have increased as well. There has been an increase in
the proportion of women undergoing reconstruction over the last decades,
with a sharp rise especially noted in the mid-2000s (5). These statistics help
quantify the commonness of this problem and highlight the critical position
of the plastic surgeon in breast cancer treatment.
Paramount to any reconstruction is the proper multidisciplinary care of a
patient, ensuring appropriate surgical and neoadjuvant or adjuvant therapies
as recommended by national guidelines. Nevertheless, the plastic surgeon
should be involved early in this process. The pathology, stage, and plans for
neoadjuvant or adjuvant therapies, especially radiation therapy will play a
critical role in decision making.
Many women elect to undergo breast reconstruction following
mastectomy, especially younger women undergoing prophylactic
mastectomy. Breast reconstruction after mastectomy has been shown to lead
to improved self-esteem and quality of life (6,7). However, the timing and
type of breast reconstruction that a patient receives varies greatly upon a
multitude of factors, including surgeon, pathology, staging, neoadjuvant or
adjuvant therapies, and patient preference. Current thinking regarding
reconstruction type and timing continues to evolve to this day and varies
between countries and institutions.
Breast reconstruction can be divided based upon two major clinical
determinations: the timing of reconstruction (immediate versus delayed) and
the type of reconstruction (implant based versus autologous). In this chapter,
we will focus on delayed breast reconstruction (DBR): when to perform
delayed reconstruction and considerations for the type of DBR.
IMMEDIATE VERSUS DELAYED BREAST RECONSTRUCTION
Immediate breast reconstruction (IBR) has become increasingly popular and
has many advantages. The first obvious advantage is combined oncologic
resection and reconstruction during one anesthetic exposure, and possible
elimination of a separate operation. For these primary reasons, patients are
the main driving factor for IBR. A recent large survey of surgical oncologists
and plastic surgeons demonstrated that “patient-driven desire to have
immediate reconstruction” was the primary motivator for pursuing IBR (8).
Some studies have shown that women undergoing IBR have improved
quality of life, lower surgical costs, shorter recovery times, and improved
aesthetic results (9,10). Some literature suggests that IBR positively affects
the psychological well-being of patients, although other authors have
concluded that, in the long-term, psychological outcomes are similar in IBR
and DBR (11). Surprisingly, a relatively small number of patients who are
candidates for IBR elect for this. In fact, one study showed that only 33% of
IBR candidates choose to proceed with immediate reconstruction.
Importantly, IBR has been shown to be safe, have acceptable complication
rates, and not interfere with oncologic treatment (12,13).
IBR does have drawbacks. It has been associated with delays in adjuvant
therapies secondary to post-operative complications (14). Risk factors that
have been shown to place a patient at higher risk of delays in initiation of
adjuvant chemotherapy include age over 51.7, diabetes, and autologous
reconstruction (15). In a recent, large, multicenter, prospective study that
controlled for clinical covariates, immediate reconstruction was found to have
equivalent patient satisfaction and quality of life when compared to DBR, but
higher rates of complications and failure (16). Complication rates become
amplified when post-mastectomy radiation therapy (PMRT) is at play. PMRT
following alloplastic IBR leads to higher rates of capsular contracture, wound
issues, rates of explant, and reoperation rates (17). PMRT also causes inferior
outcomes and lower satisfaction scores in patients who undergo autologous
IBR (18,19). Autologous IBR followed by PMRT leads to increased late
complications including fat necrosis and skin contracture when compared to
autologous DBR (20). Nevertheless, with proper patient selection, IBR is
oncologically safe and can offer excellent results with lower costs and shorter
recovery time. However, some patients are not candidates for IBR and would
perhaps be better suited for delayed reconstruction, or simply present delayed
to the plastic surgeon.
The decision to perform DBR has absolute and relative indications.
Overall, it has been shown that there are lower complication rates and
improved cosmetic outcomes with DBR (16,21). The most common clinical
scenario for DBR is a patient that presents as a new patient after not being
offered or not pursuing breast reconstruction after her mastectomy or after a
prior failed attempt at reconstruction. Patients choose not to undergo IBR for
a variety of reasons. Some women are too preoccupied with or overwhelmed
by their cancer diagnosis that they are unable to process reconstruction. It has
been shown that patients with higher levels of anxiety and stress are much
more likely to elect for DBR (22). Patients who initially were not candidates
for IBR also present in a delayed fashion, including those with advanced
breast cancer or in whom complete tumor extirpation is not possible.
Concern for skin flap viability can also be a determining factor in deciding
to delay breast reconstruction. If there is obvious skin flap ischemia or
necrosis, reconstruction should be delayed as additional volume in the form
of an expander or implant will only worsen the skin flap ischemia.
Intraoperative fluorescence angiography with indocyanine green can be a
helpful tool in making this determination. Figure 53-1 is an excellent
example of intraoperative findings of poor skin flap perfusion prompting a
decision to forego IBR. While intraoperative clinical exam is the most
important and final determinant, intraoperative fluorescence angiography
provides useful data to aide decision making.
FIGURE 53-1 A 48-year-old female patient with a history of elective bilateral breast
augmentation who was diagnosed with left breast invasive ductal carcinoma. She
underwent left nipple-sparing mastectomy via an inframammary fold incision and
left sentinel lymph node dissection along with removal of the left breast implant.
Intraoperative fluorescence angiography following mastectomy clearly demonstrates
skin flap ischemia with a deflated sizer in place. Due to these findings, immediate
reconstruction was aborted. The patient did go on to develop necrosis of the inferior
aspect of the skin flap. (Image courtesy of Hahns Kim, MD.)

Apart from these few clinical scenarios, there are no absolute indications
for DBR. There are, however, relative indications for DBR, which vary from
practice to practice. The most controversial of these relative indications is the
choice to delay reconstruction in those with plans for PMRT. While IBR has
been shown to be safe and have acceptable complication rates (10,12,23),
more caution should be taken if the patient is to undergo PMRT, as there are
higher complication rates in this patient population. How plastic surgeons
deal with this issue depends on surgeon preference and varies from patient to
patient.
Billig et al. concluded that immediate autologous breast reconstruction
with PMRT did not affect breast aesthetics or quality of life (24). Another
recent article of a retrospective, multicenter study found that acceptable rates
of surgeon and patient satisfaction can be achieved in patients undergoing
PMRT with IBR or DBR, and propose that both options should be open to
patients regardless of radiation status (25). Despite some conflict in the
literature, the overall trend suggests that patients that undergo PMRT have
higher rates of complications and revisions in both implant-based
reconstruction as well as immediate autologous reconstruction. Certainly,
placing an implant immediately after mastectomy in patients set to undergo
PMRT has increased risks; however, placing the implant or expander
immediately is better than delayed in this population (26). At our institution,
in select patients who are resolute on having immediate reconstruction and
have reasonable goals, we will perform implant-based IBR in patients who
will be receiving PMRT. In these cases, we place a tissue expander at the
time of the mastectomy and replace the expander for a permanent implant
after radiation therapy is completed. If the patient’s goals and tissues allow,
we will place the permanent implant in an immediate fashion. Some patients
can achieve good results, but inevitably, we see the ill effects of PMRT in
these patients (Fig. 53-2). These ill effects have led to many authors to
recommend DBR, usually with autologous reconstruction, in patients set to
undergo PMRT (18,27–29). PMRT has been shown to be an independent risk
factor for poor aesthetic results, volume loss, and fat necrosis (30). Some
studies have even concluded that autologous IBR can compromise PMRT by
affecting the field overlap, heterogenicity, and underdosing of radiation (31).
Although this study showed that radiation delivery can be altered by
autologous IBR, no studies have shown that it affects outcomes or recurrence
(32). The complication rates associated with IBR subjected to PMRT have
led some authors to perform delayed-immediate reconstruction in an attempt
to capture the benefits of both immediate and delayed reconstruction (33–35).
IMPLANT-BASED VERSUS AUTOLOGOUS DELAYED BREAST
RECONSTRUCTION
One of the first determinations that must be made in a patient set to undergo
DBR is whether to perform implant-based or autologous reconstruction.
Obviously, this is a decision that is made in conjunction with the patient.
However, there are several considerations when offering patients
reconstructive options.

FIGURE 53-2 A 71-year-old female with a history of left breast cancer who
underwent bilateral mastectomy and left sentinel lymph node dissection with
immediate breast reconstruction with tissue expanders at an outside facility. She
subsequently underwent adjuvant chemotherapy and radiation followed by
replacement of the expanders with silicone implants. The patient presented to us
with concerns of contour irregularity and asymmetry. The ill effects of radiation
therapy are evident. The patient has skin damage, capsular contracture, significant
contour deformity and unstable soft tissue coverage. She subsequently underwent
delayed breast reconstruction with a latissimus myocutaneous flap and silicone
implant placement. (Courtesy of Hahns Kim, MD.)

Delayed autologous reconstruction is indicated in several patient


populations. First and foremost is the patient who desires autologous-only
reconstruction and can safely undergo the operation. Many patients do not
desire implant-based reconstruction and request autologous-only
reconstruction. This is a reasonable option for many people and has excellent
aesthetic outcomes, whether it be from a latissimus dorsi flap, transverse
rectus abdominis myocutaneous (TRAM) flap, deep inferior epigastric
perforator (DIEP) flap, or other free flap breast reconstruction. Another
category of patient who is preferentially an autologous reconstruction
candidate is one who has failed prior implant-based reconstruction.
Attempting implant reconstruction in this patient again is likely to yield the
same result, and most surgeons would elect for flap-assisted reconstruction in
this patient population (36–38).
The other obvious category of patient who should undergo autologous
reconstruction is the patient with significant PMRT damage. These patients
frequently present with poor skin envelopes that are inelastic, hardened, and
discolored. A lack of skin envelope is also a common finding if the patient
did not undergo breast-conserving therapy. When there is a lack of skin
envelope, and that envelope is contracted, irradiated skin, these are signs
predictive of failure of implant-based reconstruction; these patients would be
better suited to undergo autologous reconstruction. The type of autologous
breast reconstruction (latissimus dorsi +/− implant, TRAM, DIEP, or other
free flap) and how to select between these options for each patient is
discussed further in other chapters.
The ideal delayed implant-based reconstruction patient is one who has not
undergone PMRT, is a normal BMI, and has a soft and supple skin envelope.
While the ideal patient for implant-based DBR is a patient with a lower BMI,
obesity is not a strict contraindication for implant-based DBR. While we
agree that the aesthetic outcome may be superior in those with normal or
near-normal BMIs, we have found that excellent aesthetic outcomes can be
achieved in the obese population as well (Fig. 53-3). Additionally, with the
anticipated approval of breast implants with sizes greater than 800 cc in the
near future, we expect outcomes to be improving for the obese population.
While delayed implant-based reconstruction in the PMRT patient is
challenging, it is not impossible. Of course, a pre-requisite of a soft, pliable,
and healthy-appearing skin envelope is critical to accepting an expansion. A
patient who had previous breast-conserving therapy and subsequent radiation
will be a better candidate for implant-based DBR than a patient who had a
mastectomy, PMRT, and no reconstruction. The latter patient has much less
of an available skin envelope, and the radiated skin is less likely to tolerate
expansion. Nevertheless, implant-based DBR in the radiated patient has come
a long way in recent years. While aesthetic results of prosthetic
reconstruction in radiated patients is inferior to that of autologous
reconstruction, patient satisfaction is still quite high (39). There are
modifications that can be made that assist in performing safe expansion in the
radiated breast. Total submuscular expander placement gives muscle
coverage over the entire expander. Additionally, the introduction of acellular
dermal matrix (ADM) has facilitated safer and more effective expansion in
the radiated breast. ADM is used to provide complete coverage of the
expander in conjunction with the pectoralis muscle. This provides an
additional layer of coverage between the expander and the skin. Once it
incorporates, it makes the irradiated inferior skin flap more robust. Although
use of ADM is associated with a higher seroma and infection rate, it has a
valuable and increasing role in immediate and DBR (40).
Another modification that has influenced expansion in the radiated breast
is autologous fat transfer (AFT). Studies have shown that AFT in irradiated
prosthetic reconstruction improves aesthetic outcomes (41). But AFT may
play an even more important role than that. Serra-Renom et al. showed that
AFT at the time of expander placement improved the skin quality of patients,
improved outcomes, had no capsular contracture, and no complications
associated with the fat injections (42). We have also found that AFT at the
time of expander placement or serial fat grafting prior to expander placement
leads to a more robust and supple skin flap and improves outcomes in
patients who have undergone PMRT (Figs. 53-4 and 53-5). In the future,
AFT will likely have an expanding role in implant-based DBR in the radiated
breast.
DELAYED-IMMEDIATE BREAST RECONSTRUCTION
Delayed-immediate breast reconstruction is the protocol in which a tissue
expander is placed immediately after the mastectomy. The expander is then
inflated to maintain the soft tissue envelope. The patient then undergoes
radiation therapy, typically deflating the expander prior to radiation. Delayed-
autologous reconstruction follows after radiation therapy has completed. The
most well-known protocols are those described by Kronowitz (33,34) and
Otte M, et al., Immediate-DElayed AutoLogous (IDEAL) breast
reconstruction protocol (32,35). The main difference between these two
protocols is in the location of placement of the tissue expander: Kronowitz
favors a subpectoral expander placement, whereas the IDEAL protocol favors
a prepectoral expander placement. These protocols were developed out of the
desire to improve aesthetic outcomes and decrease complications and
reoperations in patients receiving PMRT. Interestingly, a recent publication
concluded that patient and surgeon panel satisfaction with DIEP breast
reconstruction was significantly higher in the delayed group when compared
to the immediate and delayed-immediate groups; they found no difference
between the immediate and delayed-immediate groups (19). Nevertheless,
these reconstructive protocols show promise in minimizing complications
and maximizing aesthetic outcomes in a complex patient population.
Obviously, the decision to perform delayed-immediate breast reconstruction
must be in discussion with the patient, as it can subject a patient who has
already been through a significant amount of stress and exhaustion to an
additional operation. Further studies are needed to further analyze and
compare outcomes, but it certainly shows promise.
FIGURE 53-3 A 46-year-old obese female with a BRCA mutation who underwent
bilateral prophylactic mastectomies and immediate breast reconstruction with
batwing mastopexies and prepectoral placement of silicone implants with acellular
dermal matrix. She unfortunately failed her immediate breast reconstruction on the
left and required explanation. She subsequently underwent left delayed breast
reconstruction with tissue expansion followed by silicone implant placement. Her
implants are Natrelle Inspira 750 cc, round, smooth, SRX-profile bilaterally. A–E
are premastectomy photos and F–J are final reconstruction photos. Excellent results
were achieved. The patient’s BMI is 35.61 kg/m2. (Courtesy of Hahns Kim, MD.)
FIGURE 53-4 A 50-year-old female with a history of right breast cancer who
underwent bilateral mastectomies followed by adjuvant chemotherapy and
radiation. She then underwent bilateral implant-based delayed breast
reconstruction. The patient developed right breast cellulitis and required removal of
the right breast implant. She then underwent two rounds of serial autologous fat
transfer to the right breast (64 cc + 56 cc = 120 cc total) prior to tissue expansion.
She tolerated expansion well and without complication. The expander was then
replaced with a Mentor 350 cc, smooth, rough, high-profile silicone implant.
Excellent results were achieved. A–D are preoperative photographs. E–H are
postoperative photographs. (Courtesy of Hahns Kim, MD.)

FIGURE 53-5 Intraoperative photograph of an irradiated mastectomy skin flap


following serial fat grafting. This photograph was taken at the time of tissue
expander placement. The skin flap is healthy and robust. This is the same patient as
Figure 53-4, who underwent delayed implant-based breast reconstruction in an
irradiated breast following serial fat grafting. (Courtesy of Hahns Kim, MD.)
CONCLUSION
The decision to delay breast reconstruction is sometimes easy but is
frequently immensely challenging. A multitude of factors contribute to this
decision, one that varies between countries, regions, and practitioners, the
most controversial of which is PMRT. One must weigh the risks and benefits
with the patient of the timing and type of breast reconstruction, all in the
scope of the overall cancer treatment. Much literature has been published,
although without obvious conclusion. Certainly, the decision to pursue
delayed DBR is one that varies from patient-to-patient.
IBR is oncologically safe and has good outcomes in properly-selected
patients. PMRT increases complications and leads to worse aesthetic
outcomes in implant-based and autologous IBR. Delayed-immediate breast
reconstruction offers a promising compromise between immediate and DBR
in those set to undergo PMRT, although further comparative clinical studies
are needed. DBR after post-mastectomy radiation therapy leads to improved
outcomes and lower complication rates. ADM and AFT have improved
outcomes and safety of delayed prosthetic breast reconstruction in the
radiated breast. However, autologous breast reconstruction remains the
workhorse for DBR in patients who have received radiation therapy.

REFERENCES

1. Cordeiro PG. Breast reconstruction after surgery for breast cancer. N


Engl J Med 2008;359(15):1590–1601.
2. Domchek SM, Friebel TM, Singer CF, et al. Association of risk-
reducing surgery in BRCA1 or BRCA2 mutation carriers with cancer
risk and mortality. JAMA 2010;304(9):967–975.
3. Rebbeck TR, Friebel T, Lynch HT, et al. Bilateral prophylactic
mastectomy reduces breast cancer risk in BRCA1 and BRCA2 mutation
carriers: the PROSE Study Group. J Clin Oncol 2004;22(6):1055–1062.
4. Albornoz CR, Matros E, Lee CN, et al. Bilateral mastectomy versus
breast-conserving surgery for early-stage breast cancer: the role of breast
reconstruction. Plast Reconstr Surg 2015;135(6):1518–1526.
5. Kummerow KL, Du L, Penson DF, et al. Nationwide trends in
mastectomy for early-stage breast cancer. JAMA Surg 2015;150(1):9–
16.
6. Razdan SN, Patel V, Jewell S, et al. Quality of life among patients after
bilateral prophylactic mastectomy: a systematic review of patient-
reported outcomes. Qual Life Res 2016;25(6):1409–1421.
7. Neto MS, De Aguiar Menezes MV, Moreira JR, et al. Sexuality after
breast reconstruction post mastectomy. Aesthetic Plast Surg
2013;37(3):643–647.
8. Lee M, Reinertsen E, McClure E, et al. Surgeon motivations behind the
timing of breast reconstruction in patients requiring postmastectomy
radiation therapy. J Plast Reconstr Aesthetic Surg 2015;68(11):1536–
1542.
9. Neyt MJ, Blondeel PN, Morrison CM, et al. Comparing the cost of
delayed and immediate autologous breast reconstruction in Belgium. Br
J Plast Surg 2005;58(4):493–497.
10. Yang X, Zhu C, Gu Y. The prognosis of breast cancer patients after
mastectomy and immediate breast reconstruction: a meta-analysis. PLoS
One 2015;10(5):e0125655.
11. Heimes AS, Stewen K, Hasenburg A. Psychosocial aspects of
immediate versus delayed breast reconstruction. Breast Care (Basel)
2017;12(6):374–377.
12. Zhang P, Li CZ, Wu CT, et al. Comparison of immediate breast
reconstruction after mastectomy and mastectomy alone for breast
cancer: a meta-analysis. Eur J Surg Oncol 2017;43(2):285–293.
13. Munhoz AM, Montag E, Filassi JR, et al. Immediate nipple-areola-
sparing mastectomy reconstruction: an update on oncological and
reconstruction techniques. World J Clin Oncol 2014;5(3):478–494.
14. Henry LR, Morris LL, Downs R, et al. The impact of immediate breast
reconstruction after mastectomy on time to first adjuvant treatment in
women with breast cancer in a community setting. Am J Surg
2017;213(3):534–538.
15. Cohen O, Lam G, Choi M, et al. Risk factors for delays in adjuvant
chemotherapy following immediate breast reconstruction. Plast
Reconstr Surg 2018;142(2):299–305.
16. Yoon AP, Qi J, Brown DL, et al. Outcomes of immediate versus delayed
breast reconstruction: results of a multicenter prospective study. Breast
2018;37:72–79.
17. Reish RG, Lin A, Phillips NA, et al. Breast reconstruction outcomes
after nipple-sparing mastectomy and radiation therapy. Plast Reconstr
Surg 2015;135(4):959–966.
18. Rogers NE, Allen RJ. Radiation effects on breast reconstruction with the
deep inferior epigastric perforator flap. Plast Reconstr Surg
2002;109(6):1919–1924; discussion 1925–1926.
19. O’Connell RL, Di Micco R, Khabra K, et al. Comparison of immediate
versus delayed DIEP flap reconstruction in women who require
postmastectomy radiotherapy. Plast Reconstr Surg 2018;142(3):594–
605.
20. Dewael S, Vandevoort M, Fabré G, et al. Immediate versus delayed
autologous breast reconstruction: a retrospective matched cohort study
of irradiated patients. J Plast Reconstr Aesthetic Surg
2019;72(11):1769–1775.
21. Sullivan SR, Fletcher DRD, Isom CD, et al. True incidence of all
complications following immediate and delayed breast reconstruction.
Plast Reconstr Surg 2008;122(1):19–28.
22. Metcalfe KA, Semple J, Quan ML, et al. Why some mastectomy
patients opt to undergo delayed breast reconstruction: results of a long-
term prospective study. Plast Reconstr Surg 2017;139(2):267–275.
23. Malata CM, McIntosh SA, Purushotham AD. Immediate breast
reconstruction after mastectomy for cancer. Br J Surg
2000;87(11):1455–1472.
24. Billig J, Jagsi R, Qi J, et al. Should immediate autologous breast
reconstruction be considered in women who require postmastectomy
radiation therapy? A prospective analysis of outcomes. Plast Reconstr
Surg 2017;139(6):1279–1288.
25. Steele KH, Macmillan RD, Ball GR, et al. Multicentre study of patient-
reported and clinical outcomes following immediate and delayed
Autologous Breast Reconstruction And Radiotherapy (ABRAR study). J
Plast Reconstr Aesthetic Surg 2018;71(2):185–193.
26. Berbers J, van Baardwijk A, Houben R, et al. “Reconstruction: before or
after postmastectomy radiotherapy?” A systematic review of the
literature. Eur J Cancer 2014;50(16):2752–2762.
27. Tran NV, Chang DW, Gupta A, et al. Comparison of immediate and
delayed free TRAM flap breast reconstruction in patients receiving
postmastectomy radiation therapy. Plast Reconstr Surg 2001;108(1):78–
82.
28. Chevray PM. Timing of breast reconstruction: immediate versus
delayed. Cancer J 2008;14(4):223–229.
29. Ananthakrishnan P, Lucas A. Options and considerations in the timing
of breast reconstruction after mastectomy. Cleve Clin J Med
2008;75(SUPPL1):30–33.
30. Carlson GW, Page AL, Peters K, et al. Effects of radiation therapy on
pedicled transverse rectus abdominis myocutaneous flap breast
reconstruction. Ann Plast Surg 2008;60(5):568–572.
31. Kronowitz SJ, Robb GL. Radiation therapy and breast reconstruction: a
critical review of the literature. Plast Reconstr Surg 2009;124(2):395–
408.
32. Thamm OC, Andree C. Immediate versus delayed breast reconstruction:
evolving concepts and evidence base. Clin Plast Surg 2018;45(1):119–
127.
33. Kronowitz SJ, Hunt KK, Kuerer HM, et al. Delayed-immediate breast
reconstruction. Plast Reconstr Surg 2004;113(6):1617–1628.
34. Kronowitz SJ. Delayed-immediate breast reconstruction: technical and
timing considerations. Plast Reconstr Surg 2010;125(2):463–474.
35. Otte M, Nestle-Krämling C, Fertsch S, et al. Conservative mastectomies
and Immediate-DElayed AutoLogous (IDEAL) breast reconstruction:
the DIEP flap. Gland Surg 2016;5(1):24–31.
36. Kroll SS, Freeman P. Striving for excellence in breast reconstruction:
the salvage of poor results. Ann Plast Surg 1989;22(1):58–64.
37. Hamdi M, Casaer B, Andrades P, et al. Salvage (tertiary) breast
reconstruction after implant failure. J Plast Reconstr Aesthet Surg
2011;64(3):353–359.
38. Mohan AT, Al-Ajam Y, Mosahebi A. Trends in tertiary breast
reconstruction: literature review and single centre experience. Breast
2013;22(2):173–178.
39. Spear SL, Boehmler JH, Bogue DP, et al. Options in reconstructing the
irradiated breast. Plast Reconstr Surg 2008;122(2):379–388.
40. Draper LB, Disa JJ. Do acellularized dermal matrices change the
rationale for immediate versus delayed breast reconstruction? Clin Plast
Surg 2012;39(2):113–118.
41. Panettiere P, Marchetti L, Accorsi D. The serial free fat transfer in
irradiated prosthetic breast reconstructions. Aesthetic Plast Surg
2009;33(5):695–700.
42. Serra-Renom JM, Muñoz-Olmo JL, Serra-Mestre JM. Fat grafting in
postmastectomy breast reconstruction with expanders and prostheses in
patients who have received radiotherapy: Formation of new
subcutaneous tissue. Plast Reconstr Surg 2010;125(1):12–18.
CHAPTER 54

Immediate Two-Stage Breast


Reconstruction Using a Tissue
Expander and Implant
MARK L. VENTURI
HISTORY
Over the past two decades, the United States has seen an increase in both
immediate and delayed breast reconstructions following mastectomy (1). In
2018, an estimated 101,657 women underwent breast reconstruction, which
represents a significant 29% increase from the year 2000 (2). The majority of
these breast reconstructions are device-based reconstructions. The most
common approach to device-based breast reconstruction remains the two-
stage tissue expander and implant technique. This approach involves placing
the tissue expander either at the time of mastectomy (immediate) or after
(delayed). Following the completion of expansion, the tissue expander is
exchanged for a breast implant in a second surgical procedure.
The tissue expander was originally described by Radovan in 1975 (3). He
published his first clinical series with two-staged prosthetic breast
reconstruction following mastectomy in 1982 (4). Since that time, expanders
have evolved to include both smooth and textured surfaces, integrated valves,
suture tabs, and a variety of shapes and projections. Today, the majority of
tissue expanders available have integrated valves and are filled with saline.
INDICATIONS
Breast reconstruction is typically divided into two general types: prosthetic
and autologous. Prosthetic breast reconstruction, also known as device-based
breast reconstruction, refers to breast reconstruction that uses a device: either
a tissue expander or an implant to perform the breast reconstruction. On the
other hand, autologous breast reconstruction refers to flap surgery where the
patient’s own tissue is used to perform the reconstruction. Typically, these
flaps come from the abdominal region (5).
The timing of prosthetic breast reconstruction is divided into immediate or
delayed. Immediate breast reconstruction describes reconstruction that is
performed at the time of mastectomy. Whereas, delayed breast reconstruction
is performed after the mastectomy has already been completed.
The vast majority of patients are candidates for prosthetic breast
reconstruction. Tissue expanders and implants come in a variety of shapes,
sizes, surfaces, and projections (6). This wide range of devices can fit almost
any body type successfully.
Two-stage prosthetic breast reconstruction begins with the placement of a
tissue expander, which is later exchanged to an implant. The tissue expander
can be placed in either an immediate or delayed setting (7).
There are a variety of reasons to begin the reconstruction with a tissue
expander. First, the surgeon must evaluate the goals of the patient. If the
patient wants to increase the size of her breasts significantly, then a tissue
expander is indicated to increase the size of the reconstructive breast pocket
(Figs. 54-1 and 54-2) (8). This is accomplished postoperatively by adding
saline to the tissue expander on a weekly basis until the desired size is
achieved. Secondly, tissue expanders are used when the mastectomy flap
quality cannot support direct-to-implant breast reconstruction (9). The quality
of the mastectomy flaps must be evaluated at the time of mastectomy in an
immediate reconstruction to determine if an implant or tissue expander is
indicated. If there is significant compromise to the profusion of the
mastectomy flaps then it is safer to proceed with a tissue expander, which can
be completely deflated to minimize pressure on the mastectomy flaps. If the
mastectomy flaps are well profused, then direct-to-implant reconstruction can
be considered. Perfusion imaging technologies are helpful to evaluate blood
flow in the mastectomy flaps, especially in the setting of nipple-sparing
mastectomies (10).
CONTRAINDICATIONS
The contraindications for two-stage prosthetic breast reconstruction are
typically dictated by the condition of the mastectomy flaps and the health of
the patient. In the setting of severe radiation, damage to the tissues may
preclude the patient from a prosthetic breast reconstruction. In such patients,
autologous breast reconstruction is preferred as it allows the surgeon to
replace any tissues damaged by radiation with healthy flap tissue. Similarly,
patients who have a compromised immunity or wound healing deficiencies
are poor candidates for device-based two-stage breast reconstruction.

FIGURE 54-1 A–C: Anterior views of a breast cancer patient preoperatively,


following nipple-sparing mastectomy and completion of prepectoral tissue
expansion, and 6 months after exchange of tissue expanders to implants. The
patient’s goals were to increase her reconstructed breast volume, which necessitated
the two-stage approach.
FIGURE 54-2 A–C: Anterior views of a breast cancer patient preoperatively,
following nipple-sparing mastectomy and completion of dual plane tissue expansion,
and 6 months after exchange of tissue expanders to implants.
FIGURE 54-3 There are a large number of possible skin excision patterns. Some of
the more common excision plans are shown here.
PREOPERATIVE PLANNING
Once the decision has been made to proceed with two-stage prosthetic breast
reconstruction, careful preoperative planning is essential to achieving an
acceptable result. It is the author’s preference to pursue a nipple-sparing
mastectomy approach whenever possible assuming that it is oncologically
favorable. Careful coordination with the surgical oncologist is required to
verify the option for nipple-sparing mastectomy.
For smaller breasts in the A to C cup range with grade 0 or 1 ptosis, an
inframammary fold incision approach is preferred. For larger breasts with
grade 2 ptosis, a vertical or oblique pattern is indicated. It should be noted
that when using these patterns, the incision should never extend around the
areola. Such an extension does not facilitate the mastectomy and dramatically
compromises the blood supply to the nipple areolar complex. For extremely
large–breasted patients, a breast reduction prior to mastectomy is preferred. If
this is not possible, then the author will perform an IMF flap with nipple
preservation to save the nipple in the setting of a grossly enlarged breast with
grade 3 ptosis (Fig. 54-3).
Once the breast has been assessed for volume and degree of ptosis then
measurements are taken to determine which tissue expander will best fit the
reconstructive breast pocket. The measurements taken include base width,
sternal notch to nipple, nipple to inframammary fold, and nipple to midline.
The most important of these measurements is the base width of the breast.
The author will typically select a tissue expander that is 1 cm less than the
base width of the breast pocket. This will allow for safe expansion without
violating the anatomic boundaries of the breast (Fig. 54-4).

FIGURE 54-4 The selection of the proper implant is facilitated by measuring the
width, height, and projection of the opposite breast. This is easily done with calipers.
OPERATIVE TECHNIQUE
There are three main options for placing a tissue expander: subpectoral, dual
plane, and prepectoral. The choice of technique is determined by the
preference of surgeon. The different techniques represent an evolution in the
degree of invasiveness that was required previously to protect the tissue
expander during the expansion process.
SUBPECTORAL
Following the completion of the mastectomy, the field is redraped with new
towels. The pocket is irrigated copiously with triple-antibiotic–impregnated
sterile saline and hemostasis is obtained. Next, Exparel (Bupivacaine) is
injected into pocket diffusely under the pectoralis and serratus fascia and into
the fat for postoperative pain control. The lateral border of the pectoralis
major is identified and elevated with an Allis clamp. The anesthesiologist,
prior to the subpectoral dissection, administers muscle relaxation. The
subpectoral dissection is performed with an electric cautery and the inferior
attachments of the pectoralis major are released from the chest wall. Care is
taken to not elevate the pectoralis minor or the serratus anterior. Next, the
tissue expander is deflated of any air in it and placed into the subpectoral
pocket. The expander is secured to the chest wall by suturing the tabs to the
chest wall. It is important to line up the lower edge of the expander with the
inframammary fold. If the fold was elevated during the mastectomy then it
should be sutured back down to the chest wall with 2-0 PDS suture (Fig. 54-
5).
Placing marionette sutures from the lower border of the pectoralis major
through the lower mastectomy flap then holds down the lower edge of the
pectoralis major. This maneuver keeps the pectoralis major from migrating
superiorly during expansion and keeps it attached to the overlying
mastectomy flap. Another round of irrigation and hemostasis is performed
and the expander is expanded with sterile saline in a closed system. Two 15
Blake drains with trocars are placed and brought out laterally. Closure is then
performed in the skin layer and waterproof dressings are placed.
Although technical details may vary, subpectoral two-stage breast
reconstruction is an extremely safe and reliable technique. Cordiero and
McCarthy published a large series of 1,522 reconstructions in 1,221 patients.
In this series of subpectoral two-stage reconstructions, they reported an
infection rate of 3.1% and a seroma rate of 0.2% (11).
DUAL PLANE
The dual plane technique is a modification of the subpectoral technique
requiring an additional piece of tissue to bridge the gap between the released
lower border of the pectoralis major and the chest wall. Typically, human
acellular dermal matrix (ADM) is used but a variety of tissue types including
porcine and bovine tissues have also been described.
Originally described by Breuing in 2005, ADM-assisted two-stage breast
reconstruction has gained enormous acceptance over the last decade (12).
Popularized by Nahabedian, ADM-assisted dual plane breast reconstruction
allows the surgeon to shape the breast pocket and restore the anatomic
boundaries that are often violated during the mastectomy. Suturing the lower
border of the pectoralis major to the ADM prevents superior migration of the
muscle and adds an extra layer of tissue in the lower pole of the mastectomy
pocket to protect the tissue expander and ultimately the permanent implant
(13).
FIGURE 54-5 Operative sequence for tissue expander placement in a partial
subpectoral pocket, right mastectomy site. A: The lateral border of the pectoralis
major muscle is separated to begin dissection. B: A fiberoptic retractor is used to
dissect medial and inferior tissue pocket. C: The medial dissection is completed, and
an optical field is created for main pectoral release at the inframammary fold. D:
The release to the subcutaneous plane seen just below the edge of the fiberoptic
retractor. E: Tissue attachments maintained in subcutaneous plane, creating a “dual
plane” effect, shown following the mastectomy technique of H. Jane Bussey, MD. F:
Handling of the tissue expander, and evacuation of air to allow the device to be
infolded prior to placement. This allows the base of the device to conform to the
curve of the inframammary fold. G: A tissue expander in place with base along the
curve of the inframammary fold. This allows the device to unfold downward as fluid
is added. H: Muscle layers closed over the tissue expander.

The initial steps of the surgical technique mirror those of the subpectoral
approach. Following completion of the mastectomy, the field is redraped with
new towels and irrigated with triple-antibiotic sterile saline. Next hemostasis
is obtained and Exparel (Bupivacaine) is injected into pocket diffusely under
the pectoralis and serratus fascia and into the fat for postoperative pain
control. The inframammary fold is then identified by pulling on it internally
with forceps and observing that it correlates with the external location of the
fold. The lateral border of the pectoralis major is identified and elevated with
an Allis clamp. The anesthesiologist, prior to the subpectoral dissection
administers muscle relaxation. The subpectoral dissection is performed with
an electric cautery and the inferior attachments of the pectoralis major are
released from the chest wall. Care is taken to not elevate the pectoralis minor
or the serratus anterior.
The ADM is then rinsed off with triple-antibiotic–impregnated sterile
saline and brought into the field. Minimal handling of the ADM is performed
and the lower border is sutured to the inframammary fold and chest wall
inferiorly and the serratus fascia laterally (14). Next, the tissue expander is
deflated of any air in it and placed into the subpectoral pocket superiorly and
under the ADM inferiorly. The superior border of the ADM is then sutured to
the inferior border of the pectoralis major with a running 3-0 PDS suture.
Another round of irrigation and hemostasis is performed and the expander is
expanded with sterile saline in a closed system. Two 15 Blake drains with
trocars are placed and brought out laterally (15). Closure is then performed in
the skin layer and waterproof dressings are placed (Fig. 54-6A–D).
PREPECTORAL
The prepectoral approach for two-stage prosthetic breast reconstruction is the
most recent advancement in an effort to minimize recovery and operative
morbidity. Ironically, prosthetic breast reconstruction began with the
prepectoral approach but at the time mastectomies were extremely aggressive
often removing large quantities of skin resulting in a tight, poorly perfused
reconstructive pocket. This exact scenario is what necessitated the need for
muscle coverage in order to protect the tissue expander during the expansion
process.
Fortunately, mastectomy surgery has improved dramatically so that now
most mastectomies are skin sparing or even nipple sparing. The improvement
in the quality of the mastectomy flaps and the utilization of ADM has created
a clinical scenario where prepectoral prosthetic breast reconstruction is not
only possible but also highly successful.
The prepectoral approach for prosthetic breast reconstruction was
rediscovered and popularized by Jacobson who at the time was caring for
severely ill patients that required mastectomies and desperately wanted
reconstructions. He wanted to be minimally invasive in these high-risk
patients yet achieve aesthetically acceptable results. He published his early
series in 2017 (16). The technique is now widely accepted and has been
shown by Venturi and Mesbahi to have a lower postoperative requirement for
narcotic pain medications, decrease recovery time, and eliminate animation
deformity while still having a similar complication profile to dual plane (17).
There are several ways to place the ADM when creating the prepectoral
pocket. Some surgeons will completely wrap the tissue expander with ADM
and place the wrapped tissue expander in the pocket, then suture the tabs of
the tissue expander in place. It is the author’s preference to define the
boundaries of the breast pocket with one or two pieces of ADM. This
provides anterior-only coverage of the tissue expander but defines the
superior, medial, lateral, and inferior borders precisely.
The operative technique demonstrated in the photographs shows the
prepectoral approach for a patient having Wise-pattern mastectomy and
nipple preservation with an IMF flap (Fig. 54-7A–F). The initial steps of the
surgical technique mirror those of the subpectoral and dual plane approach.
Following completion of the mastectomy, the field is redraped with new
towels and irrigated with triple-antibiotic sterile saline. Next hemostasis is
obtained and Exparel (Bupivacaine) is injected into pocket diffusely under
the pectoralis and serratus fascia and into the fat for postoperative pain
control. A single piece of nonperforated ADM is placed in the upper pole and
sutured to the pectoralis major with 3-0 PDS. Next a perforated piece of
ADM is placed in the lower pole and sutured to the inframammary fold and
chest wall with 3-0 PDS. Next, the tissue expander is deflated of any air in it
and placed into the prepectoral pocket with nonperforated ADM superiorly
and perforated ADM inferiorly. The sutures tabs are sutured down to the
chest wall and the two pieces of ADM are sutured together to cover the
expander. Another round of irrigation and hemostasis is performed and the
expander is expanded with sterile saline in a closed system. Two 15 Blake
drains with trocars are placed and brought out laterally. One drain is placed
superiorly in the upper gutter and the second inferiorly along the
inframammary fold. Closure is then performed in the skin layer and
waterproof dressings are placed (Fig. 54-8A–C).
POSTOPERATIVE CARE
The introduction of long-acting numbing medications and the popularization
of the prepectoral technique have transformed mastectomy with immediate
tissue expander reconstruction surgery into an outpatient procedure. The vast
majority of patients at our institution with early surgery times are able to
leave the hospital on the day of their operation. Waterproof dressings allow
for patients to shower the following day and routine drain care instructions
are given. The upper drains are removed at the first postoperative visit, which
occurs at approximately 1 week. The lower drains are removed at the second
visit, which occurs the following week. The first postoperative expansion is
done at the same visit as the removal of the lower drains. This allows for the
expander to fill and obliterate the space being drained. If the bottom drain is
putting out more than 30 cc over a 24-hour period at the time of the second
postoperative visit, then an expansion is performed without removing the
lower drain. Expansion typically takes 3 to 4 weeks to complete and the
second-stage surgery is scheduled approximately 3 months after the first
stage assuming there is no need for chemotherapy or radiation.
FIGURE 54-6 A: The internal mammary fold location is confirmed by pulling on the
tissues internally and observing that the pull correctly correlates with the marking of
the fold on the skin. B: The lateral border of the pectoralis major is identified,
elevated with an Allis clap, and then the subpectoral dissection is performed with an
electric cautery. C: At the lower border of the breast pocket, the ADM is sutured to
the inframammary fold and the chest wall. D: After the tissue expander is deflated it
is placed under the pectoralis major superiorly and under the ADM inferiorly. The
suture tabs are secured and the superior border of the ADM is sutured to the
inferior border of the pectoralis major. E: The tissue expander is expanded with
sterile saline in a closed system. The goal is to expand enough to remove any folds of
redundant ADM tissue but not too much which would stress the mastectomy flaps
following closure. F: Two 15 Blake drains are placed with one drain in the superior
pole and one in the lower pole. The lower pole drain will remain for approximately 2
weeks and be removed simultaneously with the first postoperative expansion.

FIGURE 54-7 A: The IMF flap has been raised and deepithelialized. B: The IMF
flap has been draped inferiorly to exposed the prepectoral pocket. C: A
nonperforated piece of ADM is sutured to the pectoralis muscle in the superior pole
of the pocket. D: A perforated piece of ADM is sutured to the inframammary fold
and chest wall in the inferior pole of the pocket and the tissue expander is deflated
and placed in the prepectoral space under the nonperforated ADM superiorly and
the perforated ADM inferiorly. E: The superior border of the perforated ADM is
sutured to the inferior border of the nonperforated ADM creating complete anterior
coverage of the tissue expander. F: Minimal intraoperative tissue expansion is
performed due to the tenuous blood supply to IMF flap. Closure is then performed
after two 15 Blake drains are placed.
SECOND STAGE
The second stage of two-stage prosthetic breast reconstruction consists of the
exchange to the tissue expander to an implant. This surgery is typically
performed 3 months after the immediate reconstruction. The time frame
allows for maturation and relaxation of the expanded tissues. If chemotherapy
is indicated then the second stage is delayed until after the completion of
chemotherapy. It is important to confirm the WBC count has normalized
before proceeding with the exchange. If radiation is indicated then exchange
is further delayed for approximately 4 to 6 months after the completion of
radiation. The decision to proceed with exchange depends largely on the
condition of the radiated mastectomy flaps. If the radiation changes are
minimal then it is possible to proceed with an exchange to an implant. If the
changes are more significant then autologous reconstruction should be
considered.
Once the decision has been made to proceed with the exchange to an
implant, then implants need to be selected for the procedure. Typically the
base width of the tissue expander guides the selection of the implant to a
similar base width. The projection of the implant correlates to the amount of
fill in the tissue expander. For example, a fully expanded tissue expander will
often necessitate a full or high-profile implant to match its projection. There
are a variety of implant sizes and dimensions available. The author prefers
smooth round silicone implants with fill ratios that favor projection and
minimize visible rippling.
This second-stage surgery is not only necessary, but gives the surgeon an
opportunity to improve the overall aesthetics of the result. Often there are
contour irregularities from the mastectomy, which will benefit from
autologous fat grafting. Similarly, any areas of excess adipose deposits on the
lateral aspect of the reconstructed breasts can also be addressed during the
second stage with liposuction contouring. Capsulorrhaphy and capsulotomy
are occasionally required to adjust the pocket symmetry. These maneuvers
allow the surgeon to maximize the aesthetic result during the second-stage
procedure.
FIGURE 54-8 Anterior views of a breast cancer patient preoperatively (A) following
Wise pattern nipple-sparing mastectomy with IMF flap and completion of tissue
expansion (B) and 6 months after exchange of tissue expanders to implants (C). The
degree of ptosis in the patient’s breasts and her desire to preserve her nipples
necessitated the two-stage approach.
EMERGING TECHNOLOGIES
Tissue expanders have evolved significantly since Radovan first described
them in 1975. Their shape, surface, and anchoring mechanisms have all
changed to provide a variety of devices with a multitude of profiles. One
feature that has not changed until recently has been the way tissue expanders
are filled. The standard tissue expander is filled with a percutaneous injection
of saline intermittently during postoperative office visits. In 2017, the FDA
approved the first carbon dioxide–filled tissue expander: the AeroForm
Tissue Expander (AirXpanders, Inc., Palo Alto, Calif.) (18). This novel
device is comprised of a tissue expander containing a reservoir of compressed
carbon dioxide that is activated by a remote control (19). The system
eliminates the need for serial saline injections and allows for expansions to be
self-administered by the patient. One significant drawback to this system is
that gas cannot be partially removed from the expander to decrease its size.
Despite this drawback, this technology remains an exciting innovation in the
continuing evolution of tissue expanders.
CONCLUSION
Two-stage breast reconstruction has evolved significantly since Radovan first
described it in 1975. Improvements in the quality and variety of tissue
expanders and breast implants have greatly facilitated the development of the
procedure. The introduction of enhanced recovery after surgery (ERAS)
protocols and the popularization of the prepectoral technique have
transformed this procedure into an outpatient surgery with a speedy and
predictable recover. It remains the most popular form of breast reconstruction
performed today and undoubtedly will continue to improve with the advent of
new technologies.

REFERENCES

1. Albornoz CR, Bach PB, Mehara BJ, et al. A paradigm shift in U.S.
breast reconstruction: increasing implant rates. Plast Reconstr Surg
2013;131:15–23.
2. American Society of Plastic Surgeons. 2018 Plastic Surgery statistics
report. Available online at www.plasticsurgery.org.
3. Radovan C. Breast reconstruction after mastectomy using the temporary
expander. Plast Reconstr Surg 1982;69:195–208.
4. Radovan C. Tissue expansion in soft-tissue reconstruction. Plast
Reconstr Surg 1984;74:482–492.
5. Nahabedian MY, Momen B, Galdino G, et al. Breast reconstruction with
free TRAM or DIEP flap: patient selection, choice of flap, and outcome.
Plast Reconstr Surg 2002;110(2):466–475.
6. Spear SL, Onyewu C. Staged breast reconstruction with saline filled
implants in the irradiated breast: recent trends and therapeutic
implications. Plast Reconstr Surg 2000;105:930–942.
7. Spear SL, Pelletiere CV. Immediate breast reconstruction in two stages
using textured, integrated-valve tissue expanders and breast implants.
Plast Reconstr Surg 2004;113:2098–2103.
8. Strock LL. Two-stage expander implant reconstruction: recent
experience. Plast Reconstr Surg 2009;124:1429–1436.
9. Salzberg AC. Nonexpansive immediate breast reconstruction using
human acellular tissue matrix graft (AlloDerm). Ann Plast Surg
2006;57:1–5.
10. Venturi ML, Mesbahi AN, Copeland-Halperin LR, et al. SPY Elite’s
ability to predict nipple necrosis in nipple-sparing mastectomy and
immediate tissue expander reconstruction. Plast Reconstr Surg Glob
Open 2017;5(5):e1334.
11. Cordeiro P, McCarthy C. A single surgeon’s 12-year experience with
tissue expander/implant breast reconstruction: Part 1. A prospective
analysis of early complications. Plast Reconstr Surg 2006;118:825–831.
12. Brueing KH, Warren SM. Immediate bilateral breast reconstruction with
implants and inferolateral AlloDerm slings. Ann Plast Surg
2005;55:232–239.
13. Nahabedian MY. AlloDerm performance in the setting of prosthetic
breast surgery, infection, and irradiation. Plast Reconstr Surg
2009;124:1743–1753.
14. Nahabedian MY. Prosthetic breast reconstruction with acellular dermal
matrices: achieving predictability and reproducibility. Plast Reconstr
Surg Glob Open 2016;4:e698.
15. Nahabedian MY. Implant–based breast reconstruction: strategies to
achieve optimal outcomes and minimize complications. J Surg Oncol
2016;113:895–905.
16. Woo A, Harless C, Jacobson SR. Revisiting an old place: single-surgeon
experience on post-mastectomy subcutaneous implant-based breast
reconstruction. Breast J 2017;23:545–553.
17. Copeland-Halperin LR, Yemc L, Emery E, et al. Evaluating
postoperative narcotic use in prepectoral versus dual-plane breast
reconstruction following mastectomy. Plast Reconstr Surg Glob Open
2019;7:e2082.
18. Ascherman JA, Castle J, Colwell A, et al. XPAND patient-activated
controlled tissue expander systems for breast reconstruction: a multi-
centered randomized controlled clinical trial. Plast Reconstr Surg
2014;134(4S-1).
19. Zeidler K, Berkowitz L, Johnson D, et al. Patient activated controlled
tissue expander system for breast reconstruction: a prospective,
multicentered, randomized, controlled, open label clinical study-
preliminary results. Ann Plast Surg 2014;72:S51–S55.
CHAPTER 55

Delayed Expander/Implant Sequenced


Breast Reconstruction
DREW WELK
HISTORY
Many prospective patients are attracted to the perceived simplicity and
minimal invasiveness of implant-based breast reconstruction following
mastectomy. Skilled oncologic and plastic surgeons regularly achieve results
that may equal or even surpass original breast appearance. The prospect of
exiting mastectomy with restoration of breast appearance well under way is
compelling, so immediate reconstruction is often requested by patients and
recommended by surgeons. It is challenging to elevate “delay” as a principled
option in the timing of expander (or implant) insertion following mastectomy
when immediate reconstruction might otherwise be desired and advised, but
delay can have merit. Patient habitus and health history, preoperative breast
size and ptosis, and more advanced cancer stage with corresponding impact
on conduct of mastectomy and subsequent adjuvant therapy requirements
may all significantly affect conduct and results of reconstruction, yet often
little can be done to mitigate any correlated risks between the date of first
consultation and that of mastectomy with immediate reconstruction.
However, timing of reconstruction is always subject to consideration.
Attaining excellent results with implant-based reconstruction is greatly
facilitated by a complication-free first-stage procedure, but suboptimal timing
can compound risk at the outset. Complication rates of 20% or more
associated with immediate reconstruction have been documented (1–4).
Mastectomies vary: although the safety of retaining an anatomic layer of
subcutaneous fat has been demonstrated (5), some surgeons regularly dissect
thin flaps with broad areas of uncertain viability. Delay should be preferred in
such cases—if you need the SPY, don’t even try! Reconstruction following
on a delayed-immediate or delayed basis can substantially diminish risk in
higher-risk circumstances by optimizing the biologic environment in which
reconstruction is initiated, thereby lowering initial complication rates and
improving final results.
Two primary goals apply to breast reconstruction performed by any
technique on any timeline: first, the creation of convincing reconstructed
breasts; and second, a consistent means of doing so. This chapter is based on
the author’s 30-year experience performing more than 2,000
expander/implant sequenced breast reconstructions, with emphasis on ways
in which delay may facilitate these goals by better controlling entry into the
first stage of reconstruction and diminishing complications thereafter.
INDICATIONS AND TIMING
The most obvious indication for delayed expander/implant sequenced breast
reconstruction is the presentation of a qualified patient fully recovered from
mastectomy who desires implant-based reconstruction but who has not yet
undergone any reconstruction. The most important consideration preceding
first-stage expander insertion is mastectomy site status. The ideal mastectomy
site presents pliant skin, favorable flap thickness, a well-placed mastectomy
scar, no history of prior radiation, centered nipple areolar complex (NAC)
position (if retained), and ordinary pectoralis muscle anatomy if a
conventional dual plane pocket will be developed (Fig. 55-1). Acceptable
final results are possible despite substantial flap thinning, but preparatory
structural fat grafting before expander insertion may facilitate subsequent
reconstruction (Fig. 55-2). When tissue losses are severe, hybrid
reconstruction with a supplementary latissimus flap may be necessary if other
autologous options are not available, or are declined (Fig. 55-3). Obesity is
not a contraindication to delayed expander/implant sequenced reconstruction
if skin retention has been sufficient following mastectomy. Many such
patients may not wish to proceed with more complex autogenous
reconstructive options if implants succeed. Bilateral implant-based
reconstruction can prove straightforward, but unilateral reconstruction is
more challenging when trying to match the much larger native breast
common in obese patients, even after substantial contralateral reduction (Fig.
55-4).
The mastectomy site may be so impaired, especially by prior irradiation or
severe skin loss, that autologous alternatives must be considered instead.
Following therapeutic mastectomy with radiation and prophylactic
contralateral mastectomy on thinner patients, unilateral implant-based
reconstruction of the nonirradiated prophylactic mastectomy site may
facilitate autologous reconstruction of the radiated site to desired final size
when donor tissue is insufficient for bilateral reconstructive deployment (Fig.
55-5).
FIGURE 55-1 A: Preoperative appearance. B: Ideal post-mastectomy site. C: Dual
plane reconstructioncompleted with Mentor Style 1600 saline 325-cc implants. D:
Preoperative appearance. E: Ideal post-mastectomy site. F: Dual plane
reconstruction completed with Allergan Style 15 silicone 265-cc implants.

Although this chapter is devoted to delayed reconstruction, it is clarifying


to consider when best to recommend immediate rather than delayed
reconstruction: ideal patient, ideal anatomy, and ideal surgeons. A healthy
woman with moderately sized breasts with little or no ptosis who will
undergo NAC-sparing mastectomy via optimal incisions by a technically
facilitative oncologic surgeon working with an experienced plastic surgeon is
certainly well advised to consider immediate reconstruction. When other
factors are favorable, I also consider immediate reconstruction in patients
with preoperative grade 1 to 2 ptosis following NAC-sparing mastectomy. In
these cases, Wise-pattern–based deepithelialized infolded mastopexy can
shorten the redundant cutaneous sleeve with optimum scar position to
centralize the retained NAC; optimum associated mastectomy incision
placement is from the 6 o’clock edge of the areola to the mid-inframammary
fold (IMF). Direct-to-implant reconstruction is feasible in this circumstance,
but an expander is often placed for the latitude to further refine breast shape
and size before committing to an implant (Fig. 55-6). Immediate implant or
expander insertion can of course be performed under less ideal anatomic or
technical circumstances, but risks and complication rates then rise.

FIGURE 55-2 A: Very thin flaps. B: Marked for expander insertion following
preparatory fat grafting. C: Expansion completed. D: Dual plane reconstruction
completed with Allergan SRM silicone 485-cc implants.
FIGURE 55-3 A: Mastectomy site following excision of parasternal fibromatosis. B:
Hybrid reconstruction completed with latissimus myocutaneous flap/Mentor Style
1600 saline 325-cc implant.
FIGURE 55-4 A: Preoperative appearance. B: One week following bilateral NAC-
sparing mastectomy. C: Prepectoral reconstruction completed with Mentor Style
1000 silicone 800–cc implants. D: Two months following skin-sparing right
mastectomy. E: Two stage reconstruction and left completed with Mentor Style 1600
saline 700-cc implants, with left reduction.
FIGURE 55-5 A: Postmastectomy and left radiation therapy. B: Reconstruction
completed with left TRAM/right dual plane Mentor Style 1600 saline 625-cc implant.
C: Postmastectomy and left radiation therapy. D: Reconstruction completed with left
TRAM/right prepectoral Mentor Style 2000 saline 350-cc implant.

Delayed-immediate or delayed reconstruction may accrue significant


biologic and technical advantages, with lower complication rates. Heightened
control results from delay: pathology results and oncologic ramifications are
certain; patient response to mastectomy is established (while uncommon, the
occurrence of acute severe refractory postmastectomy pain is a
contraindication to expander or implant insertion until pain resolves); flap
vascularity is assured; and any complications intrinsic to mastectomy have
been identified and resolved or at least avoided. Outpatient surgery for first-
stage expander insertion is almost always possible.
Delayed-immediate expander (or implant) insertion, performed 6 to 14
days following mastectomy, allows flap transition into proliferation phase
healing (6): flaps are lined with granulocytes, lymphocytes, macrophages,
and fibroblasts; drainage has subsided; and flap vascularity is certain and
often much improved from the day of mastectomy by the “delay
phenomenon.” Pockets are typically drained with one lateral 15-Fr Blake
drain when performing delayed-immediate reconstruction (or the mastectomy
drain retained if still present and originally exited well away from the field).
Prolonged postoperative drainage is uncommon, so prompt drain
discontinuation is routine. Intraoperative expander fill is performed to a soft
subjective endpoint following skin-sparing/nipple-sparing mastectomy, with
significant restoration of form commonly obtained. With as little as a 1-week
delay, the prepectoral plane is already healing to the overlying flap and
acellular dermal matrix (ADM) is often unnecessary to secure pectoralis
position following costal origin release of the pectoralis muscle during
conventional dual plane pocket dissection. If flap thickness favors prepectoral
reconstruction then the prepectoral pocket is carefully opened to boundaries
delineated by preoperative markings and the expander positioned
subcutaneously. If expander position cannot be precisely secured due to the
extent of mastectomy dissection then ADM may be of benefit in this regard,
but I find that the use of tabbed expanders with careful anchoring of tabs will
generally secure the expander without the need for ADM.
FIGURE 55-6 A: Preoperative markings. B: Prepectoral expansion completed with
133 LV expanders. C: Prepectoral reconstruction completed with Mentor Style 2000
saline 350-cc implants.

Full-delayed expander insertion occurs 8 weeks or more after mastectomy.


The patient is usually fully recovered, with soft mastectomy flaps.
Postoperative tissue contraction in the weeks following mastectomy may
elevate the NAC sufficiently in pseudoptotic or grade I ptotic breasts to
center the NAC without further modification during reconstruction (Fig. 55-
7). With full delay the plane of mastectomy is healed, so pocket dimensions
specific to the expander can be precisely marked preoperatively and dissected
intraoperatively. Accurate expander position is assured even when the
mastectomy dissection extended well beyond that ideal to circumscribe the
expander. The prepectoral plane is healed, but can easily be reopened for
prepectoral reconstructions. Dual plane dissection is straightforward.
Full delay following skin or NAC-sparing mastectomy on large breasts can
result in significant infolding and fibrosis of the retained skin envelope. The
retained skin will usually drape smoothly over a larger low-height expander
within a month postoperatively if carefully released when the expander
pocket is developed, but the associated dissection is more tedious and
concurrent tailoring of the skin sleeve less certain than if the expander is
inserted prior to established fibrosis, so immediate or delayed-immediate
expander insertion is preferable if possible in such cases (Fig. 55-8).

FIGURE 55-7 A: Preoperative breast ptosis. B: Marked for 133 LV expanders with
NAC elevation following full delay. C: Expansion completed. D: Dual plane
reconstruction completed with Mentor Style 4000 silicone 600-cc implants.
CONTRAINDICATIONS
Severely impaired tissues at the mastectomy site are an absolute
contraindication to delayed expander insertion. Thin tight skin flaps
following aggressive mastectomy are unlikely to allow expander/implant
sequenced progression to a durable natural result, no matter how the
expansion phase is managed, and will never allow it if previously radiated. If
such a patient is unsuited to or declines fully autogenous reconstruction
options, then latissimus myocutaneous flaps may enable successful hybrid
delayed expander/implant sequenced reconstruction, but the latissimus flap
should transpose a substantial cutaneous segment in that event (Fig. 55-9).
Relentless postmastectomy pain and associated disability obviously
contraindicate expander insertion, which may severely exacerbate such pain.

FIGURE 55-8 A: Preoperative marking for 133 LV insertion. B: Two weeks


following expander insertion.

FIGURE 55-9 A: Very thin left mastectomy flap. B: Reconstruction completed with
hybrid latissimus myocutaneous flap/Mentor Style 4000 silicone 450-cc implant.
Prior radiation is not an absolute contraindication to delayed
expander/implant sequenced reconstruction if flaps are mobile with good skin
preservation, but preparatory fat grafting of the radiated tissues prior to first-
stage expander insertion and fat grafting at each subsequent stage of
reconstruction may substantially improve ultimate outcome, understanding
that complication rates are higher and enduring excellent final results less
likely (7).
Secondary implant-based reconstruction following failed primary implant-
based reconstruction may succeed if soft tissue status remains favorable, but
careful review of conduct and consequences of prior surgery is in order. It is
common in such cases for the pectoralis muscle to be “window-shaded”
superiorly despite prior use of ADM, with ADM detached and disarrayed,
and the implant malpositioned. Staged explantation of encapsulated primary
implants, capsulectomy, and ADM removal, and mastectomy site
“restoration” (perhaps including pectoralis origin reinsertion and structural fat
grafting) prior to secondary placement of tissue expanders may dispose to
best final results in challenging cases that present a history of refractory
encapsulation and associated deformity (Fig. 55-10).
PREOPERATIVE PLANNING
Once flap status is acceptable and the patient cleared to proceed, the initial
variables most subject to control by the surgeon are expander selection and
pocket plane. Expansion phase biomechanics vary substantially among the
many possible expander choices. Lower quadrant contour and symmetry
obtained upon completion of expansion entirely dispose the breast to the final
form it will have following implant insertion. Allergan 133 LV crescent “low
height” (or similar PMT crescent) expanders are preferred in all delayed
reconstructions, whether placed in prepectoral or conventional dual plane
pockets. Crescent expanders optimize expansion phase breast polarity,
distinguished by anatomic lower quadrant projection and contour with little
upper quadrant fullness, greatly predisposing to desired final breast form
(Fig. 55-11). Lower quadrant–focused expansion is not assured with “full
height” or even “mid height” expanders. An expansion phase endpoint of
inadequate asymmetric lower quadrant projection compounded by
overprojected upper quadrants (Fig. 55-12) is unlikely to render an anatomic
result no matter what implant follows. In that event, the expansion phase
should be continued but substantially revised, perhaps by exchange for a
crescent expander with associated upper quadrant pocket closure and lower
quadrant capsular/tissue release, in order to achieve requisite expansion phase
lower quadrant contour and projection before committing to an implant.
FIGURE 55-10 A: Deformed primary right reconstruction with longstanding
capsular contracture. B: Explanted with mastectomy site “restored”. C: Right
expansion completed. D: Right dual plane reconstruction completed with Allergan
Style 15 silicone 457 implants and balancing left mastopexy and augmentation.
FIGURE 55-11 A: Marked for bilateral delayed 133 LV insertion. B: Expansion
completed. C, D: Dual plane reconstruction completed with Mentor Style 1600
smooth 425-cc implants.

FIGURE 55-12 A: Nonanatomic full height expansion. B: Nonanatomic mid height


expansion.
OPERATIVE TECHNIQUE
FIRST STAGE: DELAYED EXPANDER INSERTION
The patient is marked in the preoperative admitting room. The vertical
midline is marked with a Sharpie pen. A perpendicular transverse line is then
marked on a tangent from the lowest point of each IMF. In a unilateral
reconstruction this line simply originates at the lowest point of the IMF on
the remaining breast and crosses over to define the same contralateral point
for the breast to be reconstructed. Expander width is key and matches the
opposite breast if present, or approximates the original anatomic width
following bilateral mastectomy. A 133 LV acetate template corresponding to
the desired width is positioned and outlined. Expanders will expand in vivo
as if they are about 1 cm wider than their stipulated width. For example, a 13-
cm wide 133 LV 300-cc expander will be inserted in a pocket with a marked
14-cm preoperative base width. The inferior expander pocket marking aligns
to the exact desired final position of the IMF, with the lowest point of this
mark centered on the mid-IMF. The most medial pocket marking, at the
medial apex of the template, is typically about 1 cm lateral to the vertical
midline marking. The superior marking follows the upper curve of the
template, and the lateral curve also simply follows the template (Fig. 55-13).
The patient is positioned supine and conventionally prepped and draped. A
single intravenous antibiotic dose is administered preoperatively. Antibiotics
are not usually continued postoperatively. Expander insertion can readily be
performed under local anesthesia with an attending anesthetist or
anesthesiologist administering and monitoring an intravenous sedative.
Incisional and field block injections performed with about 50 cc of mixed
0.25% Marcaine and 0.5% Lidocaine with epinephrine secure anesthesia, and
when ribs are readily palpable lateral intercostal nerve blocks are performed
at 5 to 6 interspaces with 3 cc of this mix at each interspace. This routine
assures good postoperative analgesia and rapid postoperative recovery and
discharge, especially if patients have a prior history of reactive nausea
following inhalation-based anesthesia, but of course conventional general
anesthesia may also be performed.
A 6-cm incision within the existing mastectomy scar allows pocket
dissection and expander insertion. Avoid incising mature periareolar scars
except when revision of an established scar is desired, since reentry may
result in fixed scar depression and areolar distortion. If the original
mastectomy incision is periareolar or was placed well above the mastectomy
fold, but has since healed to an inconspicuous mature status, initial and
subsequent incisions may be positioned in the mid-IMF (as with cosmetic
breast augmentation). Pocket dissection progresses under direct visualization
by fine cautery, inserting narrow Deaver retractors for exposure. Absolute
hemostasis is maintained and dissection is typically rapid, with almost no
blood loss.
The plane of expander insertion is dependent on flap thickness, pectoralis
anatomy, and sometimes patient preference. Prepectoral pocket dissection is
routine when flap thickness is 1 cm or greater, or when pectoralis
musculature is unusually hypertrophic. When flaps are thinner, or when in
doubt, a conventional dual plane pocket is created. If pocket position is
subsequently altered, it is technically easier to transition from a subpectoral
plane to a prepectoral plane than the converse. ADM is not necessary to
secure pectoralis position in delayed reconstruction. Pocket boundaries can
be precisely delineated, since the original mastectomy plane has healed, and
for this same reason the pectoralis muscle will remain at full anatomic length
following lateral margin and costal origin release.
FIGURE 55-13 Core technique. A: Preoperative. B: Marked for delayed 133 LV 300-
cc expander insertion. C: Expansion completed, marked for implants. D, E:
Reconstruction completed with Mentor Style 2000 saline 300-cc implants.

Subpectoral dissection is identical to dual plane pocket development as


performed in cosmetic breast augmentation, with complete release of the low
costal origin of the pectoralis muscle and preservation of the sternal origin,
although division of parasternal slips of muscle just lateral to the primary
sternal origin is routine. All remnant subcutaneous fat is preserved on the
undersurface of the overlying skin flap lateral to the pectoralis muscle edge.
Dissection always remains superficial to the pectoralis minor muscle, which
must remain anatomically situated. The serratus muscle is never elevated or
incorporated in the lateral pocket. Pocket dissection continues precisely to the
boundaries marked preoperatively. The superior pocket is developed to the
upper preoperative template marking.

FIGURE 55-14 A: Preoperative. B: Following right mastectomy. C: Right


prepectoral reconstruction completed with Mentor Style 2000 saline 425-cc implant
and balancing left augmentation with Mentor Style 1600 saline 150-cc implant.

Prepectoral pocket development is simpler: dissection is on the surface of


the chest laterally and the superficial aspect of the pectoralis major muscle
medially within boundaries delineated by preoperative markings, again
carefully preserving all remnant subcutaneous fat on the undersurface of the
elevated breast skin. ADM is seldom used in prepectoral reconstructions with
full-delayed expander insertion following weeks after mastectomy. If flaps
are sufficiently thick (about 1 cm) to facilitate aesthetic prepectoral
reconstruction, then ADM is unnecessary (Fig. 55-14). If flaps are too thin to
secure prepectoral coverage, then ADM is insufficient to function as a soft
tissue surrogate (Fig. 55-15).
If a residual seroma bursa extending outside the preoperative markings is
encountered, the lining of the bursa outside the markings is scored or
carefully excised and a few deep absorbable quilting sutures inserted to close
the bursa and define the pocket perimeter.

FIGURE 55-15 A, B: Prepectoral reconstruction in ADM-lined thin flaps with


silicone implants.

The expander is dispensed, handled only by the surgeon, and all air
evacuated through a 21-gauge butterfly needle. It is rinsed in an antibiotic
solution and then carefully inserted and oriented. Initial fill is performed with
saline through a closed fill kit to a relatively soft subjective end point,
typically 100 to 200 cc in smaller breasts and up to 500 cc in large breasts
with mobile overlying skin, avoiding pressure on overlying tissues or tension
perpendicular to the incision. When expanders are inserted bilaterally the
midvalve position is triangulated from the midline to make sure that valve
alignment is exactly symmetric—if not, expander positions are adjusted until
perfect. When nipple-sparing mastectomy has been performed, the expander
valve will commonly fall directly beneath the NAC if the NAC is
anatomically positioned and the expander accurately chosen and inserted.
Layered incision closure is performed with 4-0 absorbable monofilament
sutures. Drains are not necessary. The incision is dressed with a 1-in strip of
hypoallergenic “Cover-Roll” (BSN Medical) tape. No other dressings or bras
are used. Operating time, including local anesthetic injections, is usually less
than 1 hour per breast. Blood loss rarely exceeds 5 cc.
Skin redundancy following nipple-sparing or skin-sparing mastectomy on
large breasts may be such that deepithelialized and infolded tailoring of the
residual sleeve is performed once the expander is seated and initially filled.
Circumareolar, central “batwing,” or even Wise-pattern cutaneous
modifications can be safely done as long as only epithelium is excised and
dermis and underlying subdermal soft tissues are infolded for closure but not
incised in any way that risks focal flap devascularization. If tissue fibrosis
proves restrictive at the time of expander insertion, cutaneous tailoring can be
deferred to a secondary procedure after flaps are fully expanded and desired
revisions can be precisely configured. When such flap revisions are
extensive, expander retention allows further postoperative contour
refinements to assure nearly perfect final expanded breast form and NAC
position before committing to an implant.

FIGURE 55-16 A: Marked for delayed right 133 LV expander insertion and left
mastopexy. B: Expansion completed.

The patient returns about 1 week postoperatively to assess early healing


status. Postoperative incisional complications, infection, hematomas,
substantial seromas, or expander disruption are uncommon, with a combined
personal incidence following delayed expander insertion of less than 4%.
However, any of these can necessitate return to surgery and of course
infection may result in removal of the expander, with replacement when fully
recovered. Postoperative activity is subject to light no-exercise restrictions,
but prompt recovery is typical and patients are allowed to resume light arm
ranging immediately and unrestricted exercise after 2 or 3 weeks.
Expander fill beyond the initial volume begins when postoperative
discomfort has fully resolved, usually after 2 weeks, and are guided by the
patient’s perception of pressure from the fill, which is discontinued when
tissue or chest wall pressure is perceived. Fifty- to 75-cc fills per session are
typical, with a heightened sensation of pressure often resulting from as little
as the final 10-cc increment (which is then withdrawn). Fill can vary over a
wide range with any given expander and need not progress to nor be limited
by the expander nominal volume, so final size is that desired by the patient,
within evident tissue capacity and aesthetic norms. Width of the breast is
predetermined by the width of the expander, so fills alter breast size and
projection, but have little impact on width. Breasts are not overexpanded
relative to desired final size. Final expansion phase lower quadrant contour
and central projection will be maintained by a well-fitted subsequent implant,
and the absence of upper quadrant dilation facilitates anatomic form once the
implant is inserted.
In unilateral reconstructions, balancing mastopexy or breast reduction may
be performed when contributory to final symmetry at the time of expander
insertion, or deferred until expansion is completed in order to more accurately
mirror the dimensions of the completed expansion (Fig. 55-16).
Augmentation of a smaller contralateral breast may similarly be performed at
the time of expander insertion or deferred until expansion is matured,
commonly 2 months after expander insertion, to allow best assessment of the
implant volume that will secure symmetry to the expanded breast. The
expander is retained when modifying the contralateral breast, since expansion
volume can be adjusted thereafter, if necessary, to refine symmetry. Minor
adjustments of expander position are performed in conjunction with
contralateral breast modification if contributory to best final symmetry and
fold position.
Expansion is successful when desired size is obtained, IMFs are accurately
aligned, anatomic lower quadrant form with near-perfect symmetry is
established, and the overlying flap is relatively soft and free of tension. The
expander is generally retained a minimum of 4 months from the date of
insertion to ensure that the derived soft tissue dimensions are fully matured,
but maturation may be observed sooner if tissue status was ideal at the outset.
Implant Selection
In most cases, smooth round implants are used and will render desired final
breast appearance if implant base width and projection closely approximate
dimensions established by the expander. No real aesthetic advantage
generally derives from shaped implants (8), except possibly in very thin
patients with challenging mastectomy sites. The relative advantages and
disadvantages of saline and silicone implants are thoroughly compared and
contrasted, then the patient’s preoperative preference obliged. Patients often
defer to surgeon judgment regarding implant selection. In that event, both
silicone and saline trial implants are inserted and viewed in the operating
room before making a final decision, with the back of the table elevated to
dependently position the breasts. If appearance is similar with both implants
then saline is usually selected, since the future status of a saline implant will
always be obvious and saline implant reconstructed breasts are warmer to the
touch than silicone implanted reconstructed breasts. Mentor Style 2000
“Moderate Plus” saline implants are a personal favorite, often rendering a
result when well fitted beneath flaps of ordinary thickness that is visibly and
palpably excellent with little or even no visible transcutaneous wrinkling.
When flaps are thin, form-stable silicone implants wrinkle less than saline. In
heavier patients, large saline implants may produce more natural ptosis than
similarly sized coherent gel silicone implants (Fig. 55-20). Concurrent or
subsequent fat grafting is routinely performed and may substantially enhance
final results with either type of implant.
In one sense, selecting the final implant is often not difficult—if accurate
IMF position and lower quadrant breast dimensions have been secured during
the expansion phase and overlying tissues are of optimum quality, then any
base width proportionate implant with matched projection is likely to produce
an excellent result. Conversely, if lower quadrant elaboration is grossly
insufficient following expansion (in which case, expansion has not been
adequately performed), then unfortunately there is no implant that will
salvage the reconstruction. Minor IMF, cutaneous adjustments, and/or
capsular modifications are common and can certainly be contributory, but
any need for wholesale revision at the time of implant insertion
fundamentally belies the primal role of expertly performed expansion: breast
symmetry and form should be secured before implant insertion, not at the
time of implant insertion. The reconstruction should be architecturally
perfected during the dynamic expansion phase. Implant insertion
finalizes breast form but should never be tasked to fundamentally
transform it.
STAGE TWO: FINAL IMPLANT PLACEMENT
Expander removal and implant insertion is scheduled on an outpatient basis
in an ASC under local anesthesia with a monitored sedative, as with expander
insertion. Adjunctive fat grafting is often performed. The patient is
conventionally prepped and draped. The established scar from prior expander
insertion is incised, again requiring about 6 cm for unimpaired access. The
expander is partially deflated and atraumatically removed. With low-height
expanders, the upper pocket has to be opened and developed to accommodate
the upper aspect of the implant. The periprosthetic capsule which has
developed around the expander should be thin and nonreactive.
Capsulectomy is unnecessary. With prepectoral implant insertion, superior
prepectoral pocket dissection is simple, maintaining the dissection on the
surface of the pectoralis muscle. In dual plane pockets, subpectoral pocket
dissection is also straightforward, initiated by entry into the upper subpectoral
plane by focal capsulotomy at the mid subpectoral aspect of the superior
expander capsule. A long narrow Deaver retractor is inserted and gently
swept medially and laterally, lifting the pectoralis somewhat to separate it
cleanly from the superficial aspect of the pectoralis minor muscle. The
remaining superior medial and lateral subpectoral capsule is then cleanly
divided, without entering muscle. Avoid lateral capsulotomy, since the lateral
pocket perimeter and capsule established during the expansion phase will
secure final inferior and lateral implant position. Minor IMF modifications
are performed, if necessary. The sternal origin of the pectoralis is never
detached. This is typically a rapid bloodless dissection.
Trial implants are dispensed, viewing breast appearance within a relatively
narrow range of base width/projection ratios aligned to preoperative
expanded dimensions. The selected implant should precisely span the
established pocket, without peripheral buckling or infolding. The degree to
which the implant volumizes the upper quadrants varies with implant
projection, but because low-height expanders do not dilate the upper
quadrants during the expansion phase, a sort of “compression fit” is obtained
over the upper implant quadrants if it is not too aggressively projected,
disposing to pleasing final breast polarity. Saline implants are filled within
the designated volume range - final volume is that which appears best
intraoperatively. Drains are not inserted. Layered incision closure is
performed with 4-0 absorbable monofilament suture.
In unilateral breast reconstructions, modifications to the native breast are
performed during the expansion phase, so that excellent symmetry is
established prior to implant insertion. Of course, minor “adjustments” may
still factor in, but any necessary modifications should indeed be minor. Major
unilateral or bilateral soft tissue revisions performed at the time of implant
insertion complicate implant selection and placement, often compromising
final form and symmetry. The desired result of expander/implant sequenced
reconstruction is usually realized if expansion phase symmetry is perfected
before an implant is chosen and inserted.

CASES

Natural results can be obtained with the described techniques of delayed


expander/implant sequenced breast reconstruction across a broad
spectrum of breast sizes and patient circumstances.

CASE 1

Unilateral mastectomy, small breast (Fig. 55-17).


FIGURE 55-17 A: Marked for delayed 133 LV expander insertion. B:
Expansion completed, balancing right augmentation. C: Dual plane
reconstruction completed with Mentor Style 1600 saline 325-cc implant.

CASE 2

Unilateral mastectomy, larger breast (Fig. 55-18).


FIGURE 55-18 A: Marked for delayed 133 LV expander insertion. B:
Expansion completed with balancing left augmentation. C: Dual plane
reconstruction completed with Mentor Style 1600 saline 425-cc implant.

CASE 3

Bilateral mastectomy, small breasts (Fig. 55-19).


FIGURE 55-19 A: Marked for delayed 133 LV expander insertion. B:
Expansion completed. C: Dual plane reconstruction completed with Mentor
Style 2000 saline 375-cc implants.

CASE 4

Bilateral mastectomy, larger breasts (Fig. 55-20).


FIGURE 55-20 A: Marked for delayed 133 LV expander insertion. B:
Expansion completed. C, D: Prepectoral reconstruction completed with
Mentor Style 2000 saline 750-cc implants at 900-cc fill.

CASE 5

Unilateral nipple-sparing mastectomy, small breast (Fig. 55-21).


FIGURE 55-21 A: Marked for delayed 133 LV expander insertion. B:
Expansion completed with balancing right augmentation. C: Dual plane
reconstruction completed with Mentor Style 4000 silicone 325-cc implant.

CASE 6

Unilateral nipple-sparing mastectomy, larger breast (Fig. 55-22).


FIGURE 55-22 A: Marked for delayed 133 LV expander insertion. B:
Expansion completed with balancing left augmentation and mastopexy. C:
Dual plane reconstruction completed with Mentor Style 1600 saline 450-cc
implant.

CASE 7

Bilateral nipple-sparing mastectomy, small breasts (Fig. 55-23).


FIGURE 55-23 A: Marked for delayed 133 LV expander insertion. B:
Expansion completed. C: Dual plane reconstruction completed with Mentor
Style 2000 smooth 275-cc implants.

CASE 8

Bilateral nipple-sparing mastectomy, larger breasts (Fig. 55-24).


FIGURE 55-24 A: Marked for delayed 133 LV expander insertion. B:
Expansion completed. C: Dual plane reconstruction completed with Allergan
Style 20 silicone 800-cc implants.

Reconstruction following nipple conservation in larger and more ptotic


breasts presents specific challenges and disposes to aesthetic complications
from NAC malposition. Immediate or delayed-immediate expander insertion
is preferred in such cases under otherwise favorable circumstances, especially
with prepectoral expander insertion, so that retained tissues can be tailored to
centralize the NAC before flaps contract (Fig. 55-25). With delayed-
immediate timing flaps are typically as mobile as on the day of mastectomy.
When healed to mature status after full delay these adjustments can
sometimes still be done at the time of expander insertion but are then more
complex (see Fig. 55-8) or may be deferred until the expansion has been
more fully developed.
Delayed-immediate expander insertion is also preferred when the patient
will require adjuvant radiation following NAC-sparing mastectomy but is
otherwise a favorable surgical candidate. Prospective consultation in such
cases involves the radiation oncologist to assure that expander (or implant)
insertion will not interfere with radiation therapy. When flap status is
excellent following NAC-sparing mastectomy, desired breast form can
usually be established almost immediately after expander insertion, since the
expander is biologically tasked only to “stent” the overlying mastectomy flap,
not to actually expand it. Any further reconstruction is deferred until all
oncologic therapy is completed and the patient fully recovered. Following
full recovery from radiation, the expander may be exchanged for an implant
in the absence of significant periprosthetic fibrosis. Alternatively, an
autogenous flap may finalize reconstruction (Fig. 55-26), particularly if
periprosthetic fibrosis is severe following recovery from radiation.
If the NAC cannot be spared, especially in smaller breasts, expander
insertion is usually deferred until the patient has fully recovered from
radiation (and may not subsequently be performed at all). The role of
expansion in these cases is to induce sufficient skin growth to replace central
skin loss incurred from mastectomy. The available timeline between
mastectomy and desired onset of therapeutic radiation commonly does not
allow the greater time necessary to secure and mature such expansions before
radiation begins, and no technical advantage is gained when a suboptimal
expansion is radiated. Iatrogenic worsening of mastectomy site status occurs,
and salvage is more complicated (9). Upon full recovery from radiation
therapy, all reconstructive options are then revisited.
FIGURE 55-25 A: Marked for immediate 133 LV expander insertion with infolded
mastopexy. B: 9 days postoperatively. C: Dual plane reconstruction completed with
Mentor Style 2000 saline 500-cc implants.
SURGICAL RISKS
There are multiple categories of risk with any timing and modality of breast
reconstruction. Medical risks common to all surgery (postoperative bleeding,
infection, wound disruption, prolonged pain/disability, etc.) need not be
enumerated here, but risks and risk mitigation specific to the preceding
operations bear consideration.
Acute postoperative medical risks principal to expander insertion are
diminished by delayed timing of first-stage reconstruction, since several
prospective risk variables are better controlled than can be the case with
immediate reconstruction. Mastectomy itself, independent of immediate
reconstruction, is not risk free, so immediate reconstruction may be adversely
affected by any complication intrinsic to the mastectomy. When expander
insertion is delayed, such risk is avoided. Flaps status is certain and robust
vascularity is usually assured by the delay phenomenon. Delayed expander
insertion is a nearly bloodless operation performed in a dry field. Significant
hematomas are rare and may require drainage but do not result in expander
removal or flap necrosis. Outpatient surgery is routine. My infection rate
following delayed expander or second-stage implant insertion in a specialized
ASC is less than 1%, comparing favorably to studies which depict much
higher rates (10,11). Use of ADM is largely unnecessary with delayed and
even delayed-immediate reconstruction, so substantial associated expense
and at least modest additional ADM-specific risk is also eliminated.
Complications of the expansion phase of reconstruction are often
iatrogenic. Flap status is evident when evaluating the mastectomy site on a
delayed basis, but sometimes much less so immediately following
mastectomy, even with use of intraoperative vascular imaging modalities.
Cutaneous flaps are acutely devascularized to some degree by mastectomy.
Thin flaps are especially vulnerable to venous outflow obstruction, which
may be exacerbated by immediate implant or expander insertion. When major
flap loss or dehiscence occurs reconstruction becomes far more complex,
with much additional expense and heartache for all involved (Fig. 55-27).
Delay allows tenuous flaps to fully recover prior to first stage reconstruction.
Excellent results are often as likely (and perhaps more so) with delayed-
immediate or delayed first stage reconstruction as with immediate
reconstruction. When in doubt, delay is an uncompromised option.
FIGURE 55-26 A: Preoperative appearance. B: Marked for delayed-immediate 133
LV expander insertion 8 days after mastectomy. C: Expansion completed 2 weeks
later. D: 3 months following completion of right breast radiation. E, F: Dual plane
reconstruction completed with Allergan SSF silicone 365-cc implants.
FIGURE 55-27 A, B, C: Failed immediate expansion.

Any application of a breast implant may be complicated by capsular


contracture. Choice of implant may impact the long-term incidence and
degree of encapsulation, and is subject to many other considerations, with no
consensus regarding the “best” choice (12,13). Irrespective of the selected
implant, acute encapsulation following expander removal and implant
insertion is rare if the expander capsule is soft and nonreactive, as it should
be. If the expander is densely encapsulated, then the expansion stage has not
yet been successful and revisions should be considered with retention of the
expander until expansion is entirely satisfactory. This includes capsulectomy
with selective insertion of ADM to mitigate recurrent encapsulation, fat
grafting, and sometimes just simple capsulotomy with expander
repositioning, particularly if focal capsular tethering rather than extensive
periprosthetic fibrosis has displaced the expander from the intended position.
The need for this is uncommon, but associated revisions are straightforward
and the results are usually durable (Fig. 55-28).
We have all dissembled by asserting that a misshapen breast “looks good
in clothing” but we know this isn’t what the patient really wanted, nor what
we truly find acceptable. An egregiously nonanatomic result isn’t necessarily
indexed as a complication, but it ought to be.
CONCLUSION
No timeline nor device is a technique in and of itself, but delayed
expander/implant sequenced breast reconstruction implemented with accurate
expansion phase endpoints as presented in this chapter can result in
consistently excellent breast appearance across a broad range of
circumstances, with associated outpatient surgery, low complication rates,
and expeditious recovery, and merits consideration under an array of
circumstances. Patients have many options when contemplating implant-
based reconstruction, but a central consideration applies to all: when her
reconstruction is completed, every patient will assign much greater value to
how well each phase of the process went and how her reconstruction looks
and feels than she will to the date on which it all began.

FIGURE 55-28 A: Marked for 133 LV insertion. B: Marked for left expander
repositioning. C: Expansion completed. D: Dual plane reconstruction completed with
Allergan SRF silicone 345 cc-implants.
DISCLOSURE AND ADDENDUM
A presentation by Dr. Eugene Perrin at the 1993 annual meeting of the
Northwest Society of Plastic Surgeons entitled “Breast Reconstruction Using
the Crescent Tissue Expander” illustrating results obtained through use of
300 and 600 cc McGhan Style 134 expanders (now discontinued) profoundly
influenced me. My subsequent elaborations and NWSPS/ASPS presentations
resulted in a consultancy at McGhan/Inamed from 1997 until 2003, during
which I assisted in design and refinement of clinical applications of the 133
LV series of expanders. I derived no income from sales of these expanders.
In 2006, Allergan acquired McGhan/Inamed-associated expander and
implant lines. On July 24, 2019, Allergan recalled all Biocell textured
implants and expanders, including the 133 LV line cited in this chapter. No
identical Allergan, Mentor, or Sientra expanders are available at the time this
chapter was submitted to the publisher. The PMT Corporation has both
smooth and textured crescent expanders available with volumes and
dimensions almost identical to the Allergan 133 LV expander line. Clinical
characteristics of the PMT expanders are identical to those of 133 LV
expanders (Fig. 55-29) and are now being used by this author and his
associates with results comparable to those obtained with LV expanders.
FIGURE 55-29 A: Allergan 133 LV expander series. B: PMT crescent expander
series.

REFERENCES

1. Alderman AK, Wilkins EG, Kim HM, et al. Complications in


postmastectomy breast reconstruction: two-year results of the Michigan
Breast Reconstruction Outcome Study. Plast Reconstr Surg
2002;109:2265–2274.
2. Sullivan SR, Fletcher DR, Isom CD, et al. True incidence of all
complications following immediate and delayed breast reconstruction.
Plast Reconstr Surg 2008;122:19–28.
3. Santosa KB, Qi J, Kim HM, et al. Long-term patient-reported outcomes
in post-mastectomy breast reconstruction. JAMA Surg 2018;153:891–
899.
4. Potter S, Conroy EJ, Cutress RI, et al. Short-term safety outcomes of
mastectomy and immediate implant-based breast reconstruction with
and without mesh (iBRA): a multicenter prospective cohort study.
Lancet Oncol 2019;20:254–266.
5. Larson DL, Basir Z, Bruce T. Is oncologic safety compatible with a
predictably viable mastectomy skin flap? Plast Reconstr Surg
2011;127:27–33.
6. Landen XL, Li D, Stahle M. Transition from inflammation to
proliferation: a critical step during wound healing. Cell Mol Life Sci
2016;73:3861–3885.
7. Salgarello M, Visconti G, Barone-Adesi M. Fat grafting and breast
reconstruction with implant: another option for irradiated breast cancer
patients. Plast Reconstr Surg 2012;129:317–329.
8. Frey JD, Salibian AA, Karp NS, et al. Implant-based breast
reconstruction: hot topics, controversies, and new directions. Plast
Reconstr Surg 2019;143:404e–416e.
9. Chetta MD, Aliu O, Zhong L, et al. Reconstruction of the irradiated
breast: a national claims-based assessment of postoperative morbidity.
Plast Reconstr Surg 2017;139:783–792.
10. Ooi ASH, Song DH. Reducing infection risk in implant-based breast-
reconstruction surgery: challenges and solutions. Breast Cancer (Dove
Med Press) 2016;8:161–172.
11. Phillips BT, Bishawi M, Dagum AB. A systematic review of antibiotic
use and infection in breast reconstruction: what is the evidence? Plast
Reconstr Surg 2013;131:1–13.
12. Siotos C, Sarmiento S, McColl M, et al. Cost-effectiveness analysis of
silicone versus saline implant-based breast reconstruction using the
BREAST-Q. Plast Reconstr Surg 2019;143:276e–284e.
13. Macadam SA, Ho AL, Cook EF, et al. Patient satisfaction and health-
related quality of life following breast reconstruction: patient-reported
outcomes among saline and silicone implant recipients. Plast Reconstr
Surg 2010;125:761–771.
CHAPTER 56

Prepectoral Direct-to-Implant
Reconstruction: What Is the Role for
Dermal Substitutes?
TYLER SAFRAN | TASSOS DIONISOPOULOS
HISTORY
Is it possible to perform a prepectoral immediate postmastectomy
reconstruction without the use of dermal substitutes? Has the role of dermal
substitutes been overstated in the setting of prepectoral breast reconstruction?
This chapter aims to review the reported uses of dermal substitutes in
prepectoral reconstruction and its supporting evidence. We will also offer our
approach to a direct-to-implant (DTI) prepectoral method without the use of
any dermal substitutes. Finally, we will report the evidence and our outcomes
in nondermal substitute, DTI immediate breast reconstruction.
MODERN-DAY PREPECTORAL RECONSTRUCTION
The resurgence of muscle-sparing, prepectoral reconstruction has been the
result of innovations in both surgical technique and technology (1,2).
Minimally disruptive skin sparing mastectomy (SSM) and nipple sparing
mastectomy (NSM) have helped the plastic surgeon achieve more aesthetic
reconstructions by leveraging the increased availability of the native breast
envelope and the aesthetic unit of the nipple areolar complex (NAC) (1,2).
Prior, complete submuscular or partial submuscular (dual plane)
reconstructions, provided surgeons with the ability to place vascularized
muscle over the implant, decreasing the high complication rate that plagued
the historic prepectoral reconstruction era (3–5). These complications
included implant rippling, capsular contracture, implant exposure, and skin
flap necrosis (3,4). The initial reports of the modern prepectoral technique
showed a complication rate similar to the subpectoral technique, but with less
pain, no animation deformity, and a minimal impact of postmastectomy
radiotherapy (PMRT) on the construct. Furthermore, performing these
reconstructions as a single-staged procedure has been shown to yield
significant cost-benefit and decreased patient length of stays (6).
The primary reason for the successful reintroduction of the prepectoral
reconstruction is the evolution of the mastectomy procedure itself. SSM and
NSM maintain larger skin surfaces compared to traditional modified radical
mastectomies, thereby enhancing breast aesthetics. However, this increases
vulnerability to skin flap ischemia. The minimally disruptive, anatomic
mastectomy allows for reliable vascularized skin flap coverage of the
prosthetic device (7). Leveraging recent understandings of the superficial
fascial layers of the breast, the modern mastectomy removes the breast tissue,
leaving behind the subcutaneous layer and vasculature (8). Mastectomy flaps
have therefore moved from the almost transparent skin flaps of old to ones
that are better vascularized, thicker, and more robust. Better vascularized
flaps decrease complications while thicker flaps improve the aesthetics of the
reconstruction (9).
Besides surgical technique, innovations in the area of implants, perfusion
imaging, and dermal matrices have also been credited with renewed interest
and success in prepectoral breast reconstruction (10,11). The predictive
advantage of skin flap assessment with perfusion devices is credited with
decreasing complications by offering the surgeon the ability to promptly
intervene. It has also served as a learning tool by providing real-time
feedback and thereby improving mastectomy performance by the oncologic
surgeons. Breast implant technology has evolved both as expanders and
permanent devices. Decreased rupture rates and improved cohesivity have
helped decrease capsular contracture and reconstruction failures (11).
The purpose of dermal substitutes has been defined and promoted in the
dual plane literature. Table 56-1 summarizes the dermal substitutes available
for use, as well as their composition (12). Their introduction allowed for a
transition from complete submuscular coverage of the implant toward a dual
plane technique with an inferiorly based sling. The dermal substitute
extended from the free edge of the pectoralis major to the newly defined
inframammary and lateral mammary folds, effectively confining the device.
Varying the dimensions of the dermal substitute accommodated different
sizes of devices.

TABLE 56-1 List of Available ADMs for Use


AlloDerm Ready to Use Human dermal extracellular matrix
AlloDerm Human dermal extracellular matrix
AlloMax (Neoform) Human dermal extracellular matrix
DermACELL Human dermal extracellular matrix
DermaMatrix Human dermal extracellular matrix
Flex HD Human dermal extracellular matrix
Permacol Porcine dermal extracellular matrix
Seri Scaffold Purified silk
Strattice Porcine dermal extracellular matrix
SurgiMend PRS Fetal bovine extracellular matrix
Veritas Fetal bovine pericardium
Vicryl Mesh Synthetic polyglactin 910
TiLOOP Titanized Type 1a polypropylene mesh
Braxon Porcine dermal extracellular matrix
BellaDerm Human dermal extracellular matrix

The indications for using dermal substitutes in prepectoral breast


reconstruction have been carried over from the subpectoral literature. Given
the fundamental change in technique, these indications warrant further
review. It is important to note, the majority of studies describe the use of a
regenerative tissue matrix (acellular dermal matrix—ADM, Alloderm—
Allergan, Dublin, Ireland) as a primary dermal substitute.
INDICATIONS

Usage of Dermal Matrices in Prepectoral Reconstruction


Capsular contracture, definition of the prepectoral pocket, reinforcement of
anatomic landmarks, increased flap thickness, decreased skin flap
compliance, and resistance to the negative effects of PMRT have been cited
as indications for the use of a dermal substitute (13).

1. Capsular contracture:
Regenerative ADMs have been described to mitigate the rates of
capsular contracture. This has been described mainly in the
submuscular literature and has been carried forward to modern-day
prepectoral reconstruction (10,13).
The definition of capsular contracture for breast reconstruction must
be different than that of aesthetic breast surgery. Spear and Baker
attempted to reconcile this with their modified scale (14). The firmness
of the construct may be acceptable and nonpathologic in many cases.
The lack of consistency of reporting and evaluating capsular
contracture has made comparisons between series difficult, including
between dual plane and prepectoral methods.
The hypothesis is that a regenerative matrix prevents significant
capsular contracture through its anti-inflammatory effects on the
biology of capsular formation (15). Reconciling the reported low rates
of capsular contracture when nonregenerative matrices are used in dual
plane and more recently prepectoral reconstruction is challenging.
The described capsular contracture rates in the prepectoral
reconstruction literature are inconsistent because the prepectoral
reconstruction varies between a DTI and a two-staged approach. The
largest studies have employed a two-staged technique, which includes
either capsulotomies and/or fat grafting at the second stage (16,17).
These interventions impact the incidence of capsular contracture,
especially given that the incidence of recurrent capsular contracture
after capsulotomy is sparsely reported (18).
To date, lacking are prospective comparison studies published in
humans showing a difference in capsular contracture rates in the
prepectoral literature between the use of regenerative, nonregenerative,
or no matrices.
2. Define prepectoral pocket:
Dermal substitutes are used by many authors in their techniques to
define and secure the implant pocket. This is often required when the
mastectomy has exceeded the anatomic boundaries of the breast. This
is performed by suturing the dermal substitute to the chest wall,
keeping the implant within the defined aesthetic boundaries, while
maintaining anatomic landmarks.
Pocket-defining sutures and maintenance of the anatomic landmarks of
the breast during the mastectomy may be sufficient in defining the
prepectoral pocket without the need of a dermal substitute. There is no
evidence-based comparison between suture pocketplasty and dermal
substitute pocket contour. Furthermore, if the ADM is only wrapped
around the implant (anterior vs. complete), it does not affect pocket
control. The anterior coverage/wrap of the ADM is a technique
commonly employed in the literature (6).
3. Reinforce anatomic landmarks:
Dermal substitutes have been described to help reinforce anatomic
landmarks and prevent subsequent displacement and migration of the
implant. These landmarks include the inframammary crease, the lateral
mammary fold, and the medial border of the breast preventing
synmastia. In the subpectoral era, dermal substitute–based approaches
were claimed to provide superior control of inframammary fold (IMF)
positioning compared with alternative techniques.
However, as reported by Vardanian et al., ADM-assisted immediate
breast reconstruction (dual plane) had a trend toward fewer IMF-
related postoperative concerns and mechanical shift of the implant, but
the noted difference was not statistically significant (19,20).
4. Increase flap thickness:
Some authors have described adding a sheet of ADM to help increase
flap thickness and thus decrease implant visibility in a thinner
mastectomy flap. A sheet of ADM provides an insignificant addition
to the overall thickness of the mastectomy flap and it has been shown
that thicker dermal matrices have an increased risk of complications
(21). Within the prepectoral technique, much emphasis is placed on the
“thickness” of the mastectomy flaps. It is not the actual thickness of
the mastectomy flap, but the vascularity that is important. The
superficial fascial system of the breast describes the dissection plane
that maintains the superficial subcutaneous tissue (9). It is in this plane
where the important breast perforators are found and if kept, ensure a
well-vascularized flap. In fact, in thinner flaps where vascularity may
be compromised, there is a higher chance of nontake of the ADM,
which can lead to subsequent infection and seroma (12).
5. Decrease skin flap compliance:
Many authors have suggested that a prepectoral placement of an
implant may have a gravitational downward force on an already thin
mastectomy flap. This stretching may cause further ptosis, rippling,
and a “ball in sock” phenomenon. Once integrated, dermal substitutes
have been hypothesized to decrease the compliance of the skin flaps
by adding a further lamella to the flap. However, currently, no peer-
reviewed evidence exists to support this claim (22).
6. Postmastectomy radiation therapy:
The use of regenerative tissue matrices has been hypothesized to help
mitigate the negative effects of PMRT. In a large retrospective study in
the subpectoral literature, ADM-assisted reconstructions when
compared to total submuscular coverage were shown to have fewer
failures post-PMRT, although with a higher overall complication rate
(23).
The negative effects of PMRT in subpectoral reconstruction have been
its impact on the pectoralis major muscle. The scarred and fibrotic
tissues cause an increase in pain, implant displacement, and capsule
formation. When compared to the muscle-sparing prepectoral plane,
patients undergoing subpectoral breast reconstruction who received
PMRT had a capsular contracture rate three times greater with more
severe contractures (Baker grade 3 or 4) than the patients receiving
PMRT who underwent prepectoral breast reconstruction (24).
There is currently no literature comparing capsular contracture rates
between prepectoral reconstructions with and without ADM.
OPERATIVE TECHNIQUE
PREPECTORAL IMPLANT-BASED RECONSTRUCTION WITHOUT DERMAL
SUBSTITUTES: OUR TECHNIQUE
The author’s current preference is to perform DTI prepectoral reconstruction
with smooth-walled cohesive gel implants, without dermal substitute, for all
patients who are candidates for a device-based reconstruction. The tissue
expander stage is removed, expansion visits are avoided, and the obligatory
second stage is traded for a possible revisional procedure.
Early on, all prepectoral reconstructions were performed with a fenestrated
coverage of the anterior surface of the implant using Alloderm ADM with
spanning sutures on the posterior surface. ADM was not required in a
structural context, because of careful mastectomy technique minimizing
disruption of the anatomic boundaries of the breast. If breached, the
landmarks were reconstructed using internal sutures to provide a snug pocket
for the device.
The ADM was viewed as akin to an internal skin graft (Mitch Brown,
personal communication, 2018,25). As such, the fenestrations allowed for
drainage of blood/serum from beneath the ADM and increased take and
revascularization. Later, we noticed postoperative seromas and pocket
infections requiring operative intervention. Intraoperative findings were
nonadherence of the ADM with granulation tissue formation. Non-ADM take
can be followed by seroma and infection +/− dehiscence of the wounds (12).
As such, we began more stringent in ADM use, excluding its use unless the
pocket was an ideal environment for integration (Table 56-2). We quickly
realized that the “ideal” circumstances were few and less ADM was being
used, especially in patients requiring skin-reducing mastectomies. As we saw
similar rates of surgical and aesthetic outcomes in both the ADM and non-
ADM groups, we decided to forgo its use completely.

TABLE 56-2 Poor Pocket Characteristics for Dermal Matrix Use


Patient Factors
• Patient refusal/decline
• Known allergy to preservatives/antibiotics
• History of radiation (relative)
Intraoperative Factors
• Thin compromised mastectomy flaps
• Friable adipose tissue
• Oily subcutaneous tissue (with necrotic fat)
• Large areas of exposed dermis/thermal injury
Reconstructive Factors
• Unable to achieve a hand-in-glove pocket
• Presence of large dead space

Clinical Scenarios
Patients fell into either one of two groups: those with nonptotic breasts (65%)
and those with breast ptosis requiring skin-reducing techniques (35%). The
following techniques describe our prepectoral reconstructions without any
dermal substitutes.

Nonptotic Breasts
In nonptotic breasts a midlateral incision is designed from the breast–chest
wall junction, extending medially up to 1 cm from the edge of the NAC at the
equator of the breast (Fig. 56-1). This leaves a cuff of skin away from the
NAC to protect periareolar circulation and possible distortions. The
midlateral incision allows facilitated exposure and reach during the
mastectomy, affording the surgical oncologist equal access to all quadrants of
the breast. This is especially important given that the most common
recurrences are found in the upper quadrants where resection may be difficult
from an inframammary crease incision (26). More importantly, by using the
midlateral incision, the lateral mammary boundary can be more easily
reconstructed to yield the natural “OGEE” curve of the breast, the axial
circulation to the NAC is preserved, and neither the IMF nor its perforating
vasculature is breached.
After completion of the mastectomy a “pocketplasty” is performed, as
needed, to rebuild the boundaries of the breast and yield a hand-in-glove fit
for the implant. The aim is to rebuild the breast footprint, repair the breached
anatomic boundaries such as the lateral mammary fold/inframammary crease,
and close the dead space created from pocket overdissection. It is performed
using heavy absorbable sutures in an internal tailor-tack fashion to the
periosteum of the rib. The often-detached lateral chest wall is advanced
medially. This pillar keeps the implant from displacing while enhancing the
cleavage. Sizers are used to confirm the size and shape of the reconstruction.
Drains are inserted and after placement of the implant, the incision is closed
in a layered fashion often with closed incision negative pressure therapy
(CINPT).

FIGURE 56-1 Midlateral incision markings.


Ptotic Breast
Patients with breast ptosis often require NAC relocation and skin reduction.
In a ptotic patient presenting for a prophylactic mastectomy, our preference
is to perform a staging mastopexy or reduction before undergoing a
subsequent NSM. The mastectomy is then performed at least 8 weeks later.
This yields the benefit of a more reliable NAC circulation, reduction in the
excess skin envelope, and allows for an easier mastectomy via the IMF
incision. In our center the first stage is completed as a traditional inferior
pedicle breast reduction. At the time of the subsequent NSM, if any pocket
work modification is required, it is performed as described above.
In a patient with active cancer, our preference is a Wise-pattern
mastectomy. It is essential to control the dead-space and ensure proper hand-
in-glove fit of the implant. This pocket-controlling technique obviates the
need for a dermal substitute sling.

FIGURE 56-2 Vascular supply IMF-anterior intercostal artery perforator flap.

The planned pedicle is marked as an inferior pedicle breast reduction,


except that the entire inferior width is used and deepithelialized before
starting the mastectomy. Once deepithelialization is finished, the mastectomy
is begun leaving the NAC on the inferior pedicle. The mastectomy is
performed according to the superficial fascial system (9). This mastectomy
plane preserves the preglandular subcutaneous tissue and associated
cutaneous perforators. The final result following the mastectomy is medial
and lateral superior skin flaps and a widely based, IMF “anterior intercostal
artery perforator–based adipocutaneous flap” that supplies the NAC.
Additionally, this flap acts as an autologous, vascularized dermal-substitute
(Figs. 56-2 and 56-3). This IMF “anterior intercostal perforator flap” carrying
the NAC, can confine the implant and removes the need for further implant
support. The mastectomy pocket itself needs to be modified laterally as
mentioned prior, with larger absorbable sutures to the rib periosteum to
advance the chest wall. Once the implant is inserted, the IMF adipodermal
flap can be additionally secured to rib periosteum, both laterally and
medially, in a similar fashion.

FIGURE 56-3 Vascular supply prepectoral pocket.


FIGURE 56-4 Markings of Wise-pattern mastectomy.

If the vascularity to the NAC is deemed adequate, the NAC is left attached
to the IMF adipodermal flap, then exteriorized, and inset in the ideal NAC
location. If the NAC vascularity is unfavorable, found to be compromised, or
unable to be assessed, the NAC was harvested as a thick split-thickness graft
and placed thereafter as a free nipple graft (FNG) over a deepithelialized
patch of skin at the ideal NAC location. Currently CINPT is showing promise
to improve outcomes and decrease complications (Figs. 56-4 to 56-9) (27).

FIGURE 56-5 Steps to complete Wise-pattern mastectomy reconstruction: de


epthilialized flap to protect t-junciton.
FIGURE 56-6 Steps to complete Wise-pattern mastectomy reconstruction.

Adjunctive Procedures
Given the inflammatory nature of any residual blood in the pocket,
meticulous hemostasis cannot be overstated given the hypothesized increase
in capsular contracture. After meticulous hemostasis and pectoral nerve
blocks (28) with long-acting local anesthesia, topical tranexamic acid (3 g in
100-cc ns) is irrigated and left to soak in the pocket for 5 minutes before
insertion of the implant. Finally, prior to the insertion of the implant, a triple-
antibiotic solution (10% povidone-iodine solution mixed with 750 mg of
cefuroxime and 80 mg of gentamicin diluted in 15 mL of 0.9% sodium
chloride solution) is irrigated into the pocket and implant. The implant is
placed using a “no-touch” technique with Keller funnel.
REVISION PROCEDURES
In our experience, the four most common revision procedures required were
to address capsular contracture, implant rippling, malrotation, and lateral
displacement of the implant. Capsular contractures are addressed in the
standard fashion with capsulotomies and implant exchange allowing for any
correction of implant displacement. Lateral displacement is corrected with
pocket adjustment via capsulorraphy either with suture, popcorn technique, or
both.
FIGURE 56-7 Steps to complete Wise-pattern mastectomy reconstruction: secure t
junction and start closure.

In the case of rippling or malrotation, our preference is to address either the


pocket and/or the implant without the use of a dermal substitute. In midlateral
patients, the old incision is included with an ellipse, whose edges are tailor
tacked to see if adequate tightening and correction of the rippling occurs. The
skin is incised and deepened just enough to allow for access to the device or
imbrication of the incision. In the case of a skin-reducing mastectomy, a skin
mastopexy can be performed (29). Alternatively, the implant can be removed
and replaced with a larger size for the given pocket. Both techniques have
been very effective at eliminating rippling in our population.
Results and Literature
It has been 5 years since our adoption of DTI prepectoral reconstructions. In
over 300 patients, half of which are without dermal matrices, our experience
showed no significant difference in surgical outcomes, aesthetic outcomes
including capsular contracture, and patient satisfaction through Breast-Q
analysis.

FIGURE 56-8 Steps to complete Wise-pattern mastectomy reconstruction: secure


full thickness NAC graft.
Our surgical complication rate was similar to that found in the literature
through a recent meta-analysis. Flap necrosis (7.8%) and seroma (6.7%) (30)
are the two most frequent complications described, while infection,
hematoma, and dehiscence are described as occurring in 4.2%, 3.4%, and
3.2% of reconstructions, respectively (30). In our experience, there was no
significant difference between surgical complications and the use of dermal
matrices. There was, however, a nonsignificant positive crude and adjusted
odds ratio for major complications (seroma, hematoma, pocket infection)
requiring main operating room (OR). This is similar to what is described in
the literature, with an increased risk of repeat OR when using dermal
substitutes, especially when placed in an unfavorable mastectomy pocket
(12).
The most commonly cited aesthetic complications in prepectoral
reconstruction are implant rippling, implant rotation, and capsular contracture
(31). We have used smooth-walled round implants exclusively for our
reconstructions. Form-stable and/or textured implants are not currently
available. Implant rippling and malrotation (anterior–posterior flipping) are
aesthetic complications that are more apparent in prepectoral reconstruction.
This can be due to an excessively large pocket for the size of the implant and
a lack of stable attachment of the prothesis to the pocket. The degree of
cohesivity of the implant also plays a role, with less inherent rippling in the
highly cohesive gel implants. Dermal matrices have not shown a significant
role in preventing these complications and we have not noticed any
differences in rippling or malrotation rates when comparing our ADM and
non-ADM reconstructions.
FIGURE 56-9 Preoperative (A,B) and postoperative (C,D) results for Wise pattern.

In our series, we had few significant capsular contractures in both the


ADM and non-ADM groups, but of the major contractures, a large majority
had undergone PMRT. However, the impact of PMRT in prepectoral
reconstruction is significantly less than in the dual plane submuscular groups,
where fibrosis and contracture of the overlying muscle cause severe changes,
displacement of the implant, and pain (24). The current published evidence
demonstrates a low capsular contracture rate for both ADM and non-ADM
prepectoral reconstructions (16).
The two-staged method allows for capsulotomies to be performed at the
time of final implant placement. A recent review showed that in the decades
between 1970 and 2009, the reported severe capsular contracture rate was
between 0.0% and 40.0% (16). These patients were primarily reconstructed
immediately without ADM (16). Between 2010 and 2019, two studies
described immediate prepectoral reconstruction without ADM (16), one of
which did not describe capsular contracture and the other described a
population of 19 breasts that underwent a plane change with a mean follow-
up of 13.8 months (32,33). In that small study, 4 of the 19 breasts developed
Baker III/IV contractures requiring capsulotomy, which was ultimately
curative.
Another interesting point was that authors described placing the dermal
substitute in the first stage of the surgery. When they took the patient back to
perform capsulotomies and implant exchange, the role of the previously
placed dermal matrix was questioned. The capsule had been formed by the
time of implant exchange and was modified through the use of
capsulotomies. Lastly, the effect of PMRT was compared between implants
and expanders. A study of 257 patients demonstrated that radiotherapy during
tissue expansion may compromise the outcome of the reconstruction. They
found that there were significantly more complications associated with
expanders and radiotherapy (34). This is just another reason why we choose
to employ a DTI reconstruction.
CONCLUSION
In conclusion, dermal matrices may play a role in prepectoral reconstruction,
however further evidence needs to be published with evidence-based benefit.
There needs to be an extremely stringent patient/pocket selection when opting
to utilize a dermal matrix. As shown, through the use of proper anatomical
mastectomies and pocket optimization, dermal substitute–free reconstructions
may be employed with comparable results.

REFERENCES

1. Safran T, Al-Halabi B, Dionisopoulos T. Prepectoral breast


reconstruction: a growth story. Plast Reconstr Surg 2019;144(3):525e–
527e.
2. Gabriel A, Maxwell P. Chapter 1; The evolution of prosthetic breast
reconstruction: from subpectoral to prepectoral utilizing the
bioengineered concept. In: Gabriel A, Maxwell P, Nahabedian M,
Sigalove S, eds. Prepectoral Techniques in Reconstructive Breast
Surgery. Wolters Kluwer; 2019.
3. Nahabedian MY. Innovations and advancements with prosthetic breast
reconstruction. Breast J 2018;24(4):586–591.
4. Nahabedian MY, Glasberg SB, Maxwell GP. Introduction to
“prepectoral breast reconstruction.” Plast Reconstr Surg
2017;140(6S):4S–5S.
5. Schlenker JD, Bueno RA, Ricketson G, et al. Loss of silicone implants
after subcutaneous mastectomy and reconstruction. Plast Reconstr Surg
1978;62(6):853–861.
6. Viezel-Mathieu A, Alnaif N, Aljerian A, et al. Acellular dermal matrix-
sparing direct-to-implant prepectoral breast reconstruction: a
comparative study including cost analysis. Ann Plast Surg
2020;84(2):139–143.
7. Storm-Dickerson T, Sigalove NM. The breast surgeons’ approach to
mastectomy and prepectoral breast reconstruction. Gland Surg
2019;8(1):27–35.
8. Frey JD, Salibian AA, Choi M, et al. Mastectomy flap thickness and
complications in nipple-sparing mastectomy: objective evaluation using
magnetic resonance imaging. Plast Reconstr Surg Glob Open
2017;5(8):e1439.
9. Rehnke RD, Groening RM, Van Buskirk ER, et al. Anatomy of the
superficial fascia system of the breast: a comprehensive theory of breast
fascial anatomy. Plast Reconstr Surg 2018;142(5):1135–1144.
10. Gabriel A. Chapter 5. In: Gabriel A, Maxwell P, Nahabedian M,
Sigalove S, eds. Prepectoral Techniques in Reconstructive Breast
Surgery. Wolters Kluwer; 2019.
11. Gabriel A, Maxwell GP. Implant selection in the setting of prepectoral
breast reconstruction. Gland Surg 2019;8(1):36–42.
12. Gravina PR, Pettit RW, Davis MJ, et al. Evidence for the use of acellular
dermal matrix in implant-based breast reconstruction. In: Seminars in
Plastic Surgery. 33(04). New york: Thieme Medical Publishers;
2019:229–235.
13. Nguyen TJ, Carey JN, Wong AK. Use of human acellular dermal matrix
in implant-based breast reconstruction: evaluating the evidence. J Plast
Reconstr Aesthet Surg 2011;64(12):1553–1561.
14. Spear SL, Baker JJ. Classification of capsular contracture after
prosthetic breast reconstruction. Plast Reconstr Surg 1995;96(5):1119–
1123; discussion 1124.
15. Tevlin R, Borrelli MR, Irizarry D, et al. Acellular dermal matrix reduces
myofibroblast presence in the breast capsule. Plast Reconstr Surg Glob
Open 2019;7(5):e2213.
16. Wagner RD, Braun TL, Zhu H, et al. A systematic review of
complications in prepectoral breast reconstruction. J Plast Reconstr
Aesthet Surg 2019;72(7):1051–1059.
17. Sigalove S, Maxwell GP, Sigalove NM, et al. Prepectoral implant-based
breast reconstruction: rationale, indications, and preliminary results.
Plast Reconstr Surg 2017;139(2):287–294.
18. Hidalgo DA, Spector JA. Breast augmentation. Plast Reconstr Surg
2014;133:567e–583e.
19. Vardanian AJ, Clayton JL, Roostaeian J, et al. Comparison of implant-
based immediate breast reconstruction with and without acellular dermal
matrix. Plast Reconstr Surg 2011;128(5):403e–410e.
20. Ivey JS, Abdollahi H, Herrera FA, et al. Total muscle coverage versus
AlloDerm human dermal matrix for implant-based breast reconstruction.
Plast Reconstr Surg 2019;143(1):1–6.
21. Rose JF, Zafar SN, Ellsworth IV WA. Does acellular dermal matrix
thickness affect complication rate in tissue expander based breast
reconstruction? Plast Surg Int 2016;2016:2867097.
22. Maxwell GP, Gabriel A. Revisionary breast surgery with acellular
dermal matrices. Aesthet Surg J 2011;31(6):700–710.
23. Craig ES, Clemens MW, Koshy JC, et al. Outcomes of acellular dermal
matrix for immediate tissue expander reconstruction with radiotherapy: a
retrospective cohort study. Aesthet Surg J 2018;39(3):279–288.
24. Sinnott CJ, Persing SM, Pronovost M, et al. Impact of postmastectomy
radiation therapy in prepectoral versus subpectoral implant-based breast
reconstruction. Ann Surg Oncol 2018;25(10):2899–2908.
25. Vu MM, Kim JY. Current opinions on indications and algorithms for
acellular dermal matrix use in primary prosthetic breast reconstruction.
Gland Surg 2015;4(3):195–203.
26. Moo TA, Pinchinat T, Mays S, et al. Oncologic outcomes after nipple-
sparing mastectomy. Ann Surg Oncol 2016;23(10):3221–3225.
27. Gabriel A, Sigalove S, Sigalove N, et al. The impact of closed incision
negative pressure therapy on postoperative breast reconstruction
outcomes. Plast Reconstr Surg Glob Open 2018;6(8):e1880.
28. Moon EJ, Kim SB, Chung JY, et al. Pectoral nerve block (Pecs block)
with sedation for breast conserving surgery without general anesthesia.
Ann Surg Treat Res 2017;93(3):166–169.
29. Salibian AH, Harness JK, Mowlds DS. Primary buttonhole mastopexy
and nipple-sparing mastectomy: a preliminary report. Ann Plast Surg
2016;77(4):388–395.
30. Chatterjee A, Nahabedian MY, Gabriel A, et al. Early assessment of
post-surgical outcomes with pre-pectoral breast reconstruction: a
literature review and meta-analysis. J Surg Oncol 2018;117(6):1119–
1130.
31. Gabriel A. Chapter 20. In: Gabriel A, Maxwell P, Nahabedian M,
Sigalove S, eds. Prepectoral Techniques in Reconstructive Breast
Surgery. Wolters Kluwer; 2019.
32. Bayram Y, Kulahci Y, Irgil C, et al. Skin-reducing subcutaneous
mastectomy using a dermal barrier flap and immediate breast
reconstruction with an implant: a new surgical design for reconstruction
of early-stage breast cancer. Aesthet Plast Surg 2010;34(1):71–77.
33. Hammond DC, Schmitt WP, O’Connor EA. Treatment of breast
animation deformity in implant-based reconstruction with pocket change
to the subcutaneous position. Plast Reconstr Surg 2015;135(6):1540–
1544.
34. Nava MB, Pennati AE, Lozza L, et al. Outcome of different timings of
radiotherapy in implant-based breast reconstructions. Plast Reconstr
Surg 2011;128(2):353–359.
CHAPTER 57

Role of Acellular Dermal Matrix


in Breast Reconstruction
MAURICE Y. NAHABEDIAN
HISTORY
The use of acellular dermal matrix (ADM) in the setting of prosthetic breast
reconstruction has become common clinical practice (1,2). The indications
are extensive and include prepectoral and partial subpectoral reconstruction,
one- and two-stage reconstruction, as well as revision reconstruction. The
primary reasons to use ADM are to compartmentalize the implant or tissue
expander, reduce the incidence of capsular contracture, and to facilitate
direct-to-implant reconstruction. The first description of ADM use for
revision breast surgery was in 2001 (3) and the first description of ADM use
for prosthetic breast reconstruction was in 2005 (4). Although the Food and
Drug Administration considers ADM use off-label for breast surgery, it is
considered on-label as a means of providing support to compromised tissue;
thus, many plastic surgeons have used ADM on a regular basis for prosthetic
and revision breast reconstruction. The routine use of ADM has been based
on its track record of safety and efficacy, facilitated techniques, and improved
surgical outcomes. This chapter will review the role of ADM in all of these
scenarios and provide tips for improving outcomes.
FIGURE 57-1 The elasticity of human ADM is demonstrated.
WHAT IS ADM
ADM is cadaveric skin that has been processed to remove all cellular
components. The resultant extracellular matrix is composed of various
components that include collagen, elastin, and hyaluronin. In general, sterile
ADM is preferred to nonsterile ADM despite some reviews that demonstrate
no difference in the infection rates between the two (5,6). Human ADM (Fig.
57-1) is preferred to nonhuman because of the inherent elasticity of human
skin relative to other animal skin. Perforated ADM (Fig. 57-2) is preferred to
nonperforated ADM (Fig. 57-3) to minimize the risk of seroma formation
and to promote zones of adherence that can promote better incorporation
(Fig. 57-4) (7,8). ADM is available in various thicknesses ranging from 1 to
4 mm. Thin ADM (1 to 2 mm) is associated with a more rapid
revascularization compared to the thicker sheets (2 to 3 mm) and may
facilitate more rapid incorporation and adherence (7).

FIGURE 57-2 Acellular dermal matrix is available in a variety of contoured shapes


and sizes and may be perforated.
FIGURE 57-3 Nonperforated and rectangular ADM can be considered.
HANDLING OF ADM
When the ADM is removed from the packaging, recommendations include
minimal handling and manipulation because there are sterile devices and
should be treated as such. Most ADMs require some degree of soaking in a
sterile bath when removed from the package. Freeze-dried materials typically
require 20 to 30 minutes whereas the prehydrated materials are usually
soaked for 2 to 5 minutes. The benefit of soaking is to remove any preserving
materials or antibiotics that are included in the packaging. It has been
postulated that these additives may be responsible for the development of
“red breast syndrome” that represents an inflammatory reaction to the ADM
manifesting as a localized erythematous hypersensitivity reaction located
along the cutaneous distribution overlying the ADM (9).

FIGURE 57-4 The ability of ADM to incorporate into the mastectomy skin flaps and
revascularize is demonstrated.
ADM TECHNIQUE
The technical aspects of ADM use are an important determinant of a good to
excellent outcome. Most ADMs are available in a rectangular or a
contoured/crescent form (see Figs. 57-2 and 57-3). The utility of ADM is
noteworthy for one- and two-stage reconstruction as well as prepectoral and
dual plane reconstruction. The important point is that the ADM is used
primarily for soft tissue support following the mastectomy; however, added
benefits include compartmentalization of the prosthetic device, maintaining
the position of the pectoralis major muscle to prevent window-shading, and
to increase the thickness of the mastectomy and potentially minimize rippling
and wrinkling of the implant. Human ADMs are usually polarized and have a
dermal and basement membrane surface. It is recommended that the dermal
surface be in contact with the mastectomy skin flap to enhance soft tissue
incorporation.
Dual Plane Reconstruction and ADM
Dual plane reconstruction is characterized by elevation of the pectoralis
major muscle with placement of the prosthetic device under the muscle such
that the upper two-thirds of the device is covered with muscle and the lower
one-third is covered by ADM (Fig. 57-5) (10). The superior edge of the
ADM is positioned and sutured to the inferior edge of the pectoralis major
muscle, pulled inferiorly, and then sutured to the inframammary fold. The
length of the ADM should be sufficient to span the width of the device and
the height should be sufficient to stabilize and extend the inferior edge of the
pectoralis major such that it is pulled down to at least the midheight of the
device. A high-riding pectoralis major muscle functions poorly and may
create more distortion and animation. The preferred suture is a 2-0 or 3-0
absorbable that can be running or interrupted. When using a tissue expander,
it is important not to suture the ADM so that it is too tight because the
position of the implant or expander may be elevated, thus creating a footprint
of the reconstructed breast that is suboptimal. Therefore, during the initial
inset and suturing, the ADM should be sutured in place with a mild degree of
laxity to permit optimal expansion of the device without compression or
superior displacement. As the tissue expander is expanded, the folds and
laxity of the ADM will be eliminated. The initial expansion in the operating
room is typically limited to 40% to 60% of the tissue expander capacity in
order to minimize compression of the subdermal plexus of vessels that may
lead to delayed healing or tissue necrosis.

FIGURE 57-5 With the dual plane technique, ADM is used to extend the incised and
elevated inferior edge of the pectoralis major muscle to the inframammary fold.

When performing a direct-to-implant reconstruction with ADM, the


desired footprint of the new breast must be determined and the ADM sutured
to it to maintain its position (11). With robust skin flaps, direct-to-implant
reconstruction can be considered. In cases where the patient desires an
increase in breast volume beyond baseline, then tissue expansion is
considered. Following the placement of a tissue expander or implant, the
surface of the ADM should have minimal to no folds or pleats in order to
ensure 100% contact with the mastectomy skin flap and minimize dead
space. This will tend to reduce the likelihood of a fluid collection or poor
adherence of the ADM to the surrounding mastectomy skin flaps. During
final skin closure, the mastectomy incision and nipple areolar complex should
ideally be over muscle and not ADM. Closed suction drains are used in all
patients.
Prepectoral Reconstruction and ADM
With prepectoral placement of prosthetic devices following mastectomy, the
use of an ADM can be beneficial (12,13). There are two general techniques
for placement of the ADM. The first technique is based on fitting and
suturing the ADM into the mastectomy space to provide soft tissue support to
the mastectomy skin flaps. The ADM is sutured to the pectoralis major
muscle or fascia superiorly, medially and laterally according to the base
diameter of the implant and the desired footprint of the new breast using
absorbable sutures. Once complete, the prosthetic device is inserted and the
remaining edge of the ADM is sutured to close off the pocket.
The second technique is based on wrapping the ADM around the anterior
and sometimes posterior surface of the prosthetic device while outside the
mastectomy space (Fig. 57-6). The ADM–implant construct is stabilized
using absorbable sutures to prevent the ADM from sliding off the device.
Once complete, the construct is placed into the mastectomy space in the
desired location and secured. With tissue expanders, the tabs are sutured to
the pectoral muscle or fascia; whereas with permanent implants, the ADM
edge at the base of the implant is grasped and sutured to the muscle or fascia.
FIGURE 57-6 With prepectoral prosthetic reconstruction, ADM can be used to
cover the anterior surface of the prosthetic device to provide additional tissue
support.
ADM AND CAPSULAR CONTRACTURE
The prevention and management of capsular contracture has been as
challenge for plastic surgeons. Grade 3 and 4 capsular contractures rates have
varied between 10% and 30% in the core studies (14–17). The etiology of
capsular contracture is multifactorial and related to inflammation from
bacteria, blood products, radiation, and tissue trauma (18). ADMs have been
postulated to reduce the inflammatory reaction associated with prosthetic
breast reconstruction and reduce the incidence of capsular contracture to 0%
to 4% (19).
Several experimental and clinical studies have attempted to explain the
mechanism of action related to the observation that the use of ADM can
reduce the incidence of capsular contracture. In an experimental study,
Uzunismail implanted silicone sheets into the dorsum of 20 rabbits (20). The
sheets were wrapped in ADM in 10 rabbits and without ADM in 10 rabbits.
All periprosthetic tissues were analyzed at 13 weeks. In the ADM group, the
capsule was thin with minimal cellularity or inflammatory infiltrates;
whereas, in the non-ADM group, the capsule was thick with increased
cellularity. In another experimental study in monkeys, Stump observed that
implanted devices that were partially wrapped in ADM demonstrated less
capsule formation than those devices that were not wrapped in ADM (21).
The authors postulated that the ADM is able to isolate the implant from the
macrophages of the neighboring tissues resulting in a partial or total block of
the signaling associated with tissue repair and thus preventing the effector
cells from reaching the peri-implant tissues.
In a clinical study, Basu studied the histology of implanted ADM and
native capsule in 23 women following prosthetic reconstruction (22). ADM
histology demonstrated a lack of granulation tissue and vascular proliferation
as well as a mild increase in collagen and inflammatory infiltrates. Capsule
histology demonstrated abundant granulation with mild vascular proliferation
as well as a moderate increase in collagen and inflammatory infiltrates. This
clinical study demonstrates that the presence of ADM seems to attenuate the
process of fibrosis in humans. In another clinical study comparing prosthetic
reconstruction with and without ADM, Vardanian et al. demonstrated a
capsular contracture rate of 3.8% (208 breasts) in the setting of ADM and in
19.4% (129 breasts) in the setting of no ADM (23). Salzberg reported 13-year
follow-up on 1,584 breast reconstructions in 863 patients and demonstrated a
cumulative incidence of capsular contracture rate of 1.8% (19).
Several theories have emerged to explain how ADM may reduce the
incidence of capsular contracture. These include cell-signaling pathways
between the ADM and the surrounding soft tissue that minimize the
inflammatory response. The fact that ADM is usually human in origin and
that human skin has elastic properties may also explain why elasticity rather
than contracture occurs more frequently. By limiting the amount of scar
formation, the ADM can impede the spherical fibrosis–associated capsular
contracture. Finally, although ADM is not a full-thickness graft, in some
ways it mimics the properties of a full-thickness graft by inhibiting wound
contraction and minimizing capsular contracture.
Traditional options for the management of capsular contracture include
capsulectomy, capsulotomy, implant exchange, pocket conversion,
mechanical manipulation, and ADM (18,24–26). The technique of ADM for
capsular contracture can be completed using three different methods. The
first method is the “reconstructive technique” that can be performed
following a total or posterior capsulectomy in a patient with a dual plane
device. The ADM is positioned and sutured between the inferior edge of the
pectoralis major muscle and the inframammary fold. The second method is
the “patch technique” that can be performed after a large capsulectomy. The
ADM is essentially placed over the territory of the old capsule to provide
elasticity and soft tissue support. The third method is considered in the setting
of a subpectoral capsular contracture in which a capsulectomy or
capsulectomy has been performed. This is followed by a prepectoral
conversion in which the pectoralis major muscle is repositioned to the chest
wall followed by anterior soft tissue support using an ADM and placement of
a new breast implant in the prepectoral position. Cheng et al. have used ADM
to treat capsular contracture in 15 patients with Baker grade 3 and 4 capsular
contracture (27). The ADM was wrapped around the anterior surface of the
implant with resolution of the contracture in 9 patients. One patient
developed a postoperative grade 2 capsular contracture at 9-month follow-up.
ADM AND RADIATION THERAPY
It is known that standard prosthetic reconstruction following mastectomy in
the setting of radiation therapy is more prone to failure compared to the
setting of no radiation (28). The reasons for this are multifactorial and include
infection, fibrosis, fat atrophy, delayed healing, and capsular contracture.
Given that ADM has been demonstrated to reduce the incidence of capsular
contracture, the question becomes whether or not ADM can minimize the
incidence of untoward events in the setting of radiation therapy. The ability
of ADM to recellularize and revascularize in the setting of radiation has been
demonstrated in several experimental and clinical studies. In two separate
experimental studies in rats, ADM was demonstrated to recellularize and
revascularize following preoperative or postoperative radiation (29,30). The
main difference, when compared to the nonradiated setting, was that
fibroblast ingrowth and revascularization occurred more slowly in the setting
of previous radiation. In a study using rats, Komorowska-Timek placed two
dorsal 5-cc implants, one wrapped in ADM and the other bare (31). Both
devices were radiated. The implant wrapped in ADM demonstrated less
capsular tensile strength, less inflammatory cell infiltration, less thinning of
the ADM, and less pseudoepithelium formation. These results have suggested
that certain ADMs may decrease radiation-related inflammation and may
slow the progression to capsular formation, fibrosis, and contraction.
In a clinical study to evaluate the feasibility of using ADM in the setting of
radiation Nahabedian reviewed 100 women following prosthetic
reconstruction with ADM of which 23 had received radiation therapy and 77
had not (32). Nine were radiated premastectomy, 13 were radiated
postmastectomy, and 1 was radiated before and after ADM placement. Total
to partial ADM adherence was noted in all 23 (100%). Complications
occurred with greater frequency in the failed breast conservation therapy
cohort (4/9, 44%), compared to the radiation post ADM cohort (3/13, 23%)
and to the nonradiated cohort (6/77, 7.8%). Thus, despite the ability of ADM
to adhere, revascularize, and recellularize in the setting of radiation therapy,
the incidence of complications remains higher than in nonradiated patients.
The timing of radiation therapy relative to prosthetic reconstruction with
ADM has been considered and evaluated (28,33,34). In most studies,
morbidities are increased when radiation therapy precedes the reconstruction.
Colwell has demonstrated that complication rates in women following one-
and two-stage reconstruction without radiation therapy was 13.6% and
14.7%, respectively; however, in the setting of preoperative radiation therapy,
the complication rate for one- and two-stage reconstruction was 24.2% and
41.1%, respectively whereas with postoperative radiation therapy, the
complication rate for one- and two-stage reconstruction was 16.7% and 23%,
respectively (33). Other morbidities included incisional dehiscence, seroma,
lack of ADM adherence, and infection.
Spear et al. evaluated 289 patients and 428 two-stage prosthetic breast
reconstructions for clinically significant capsular contracture (34). Following
complete expansion, clinically significant capsular contracture (grade III/IV)
was higher when radiation therapy was delivered during the expansion phase
and also when radiation therapy was delivered before mastectomy (failed
breast conservation therapy) compared to that in the nonradiated cohort.
Following device exchange in 353 breasts, clinically significant capsular
contracture (grade III/IV) was highest in the cohort that received radiation
therapy during expansion.
FIGURE 57-7 A preoperative photograph demonstrating severe capsular
contracture of the right breast implant following mastectomy and radiation therapy.
FIGURE 57-8 The use of ADM following capsulectomy can provide additional
elasticity and reduce the inflammatory response resulting in periprosthetic fibrosis.

In summary, current evidence suggests that certain ADMs can adhere,


revascularize, and recellularize in the setting of radiation therapy. Morbidities
however, can still occur and occur in higher frequency compared to the
nonradiated cohorts. The adverse effects of radiation therapy do not appear to
be reversed by ADM. Revascularized ADM that is secondarily radiated may
be subject to the same untoward effects that normal human dermis is when
radiated. Figures 57-7 to 57-9 illustrate a patient following bilateral
prosthetic reconstruction that developed right capsular contracture following
radiation therapy.
FIGURE 57-9 A 1-year follow-up demonstrating minimal asymmetry following
revision of the right breast with ADM and mastopexy of the left reconstruction.
ADM AND REVISION OF BREAST RECONSTRUCTION
The use of ADM for breast revision has facilitated our ability to manage
complex breast deformities following mastectomy and prosthetic
reconstruction. ADM can be used in a variety of circumstances that include
implant malposition, rippling and wrinkling, and capsular contracture. Spear
et al. have demonstrated success in 96% of patients when ADM was used for
malposition, rippling, capsular contracture, and skin deficiency in the setting
of reconstructive breast surgery (26).
Rippling and Wrinkling
Rippling and wrinkling following prosthetic breast reconstruction following
total mastectomy is relatively common. Traditional methods for correction of
rippling have included converting from a saline implant to a silicone gel
implant, use of smooth surface devices, autologous fat grafting, and
conversion to a flap. The use of ADM for rippling and wrinkling has been
previously evaluated (35). ADM can be used as a capsular onlay graft or by
the lower pole suspension technique. When used as an onlay graft, the area of
rippling and wrinkling is marked preoperatively with the patient standing. In
the operating room, the dermal side is placed in direct contact with the
capsule and anchored to the periphery of the capsule with an absorbable
suture. The capsule may have to be excised prior to ADM placement if thick
or radiated. An alternative technique for ADM use in this setting is as a lower
pole suspension graft also known as the “reconstructive technique.” As with
the onlay technique, the area of rippling is delineated. The technique of ADM
use is very similar to that used for primary prosthetic reconstruction in which
the ADM is sutured to the inframammary fold and to the inferior edge of the
pectoralis major muscle. The goal of this operation is to support the lower
pole of the breast and to elevate the device to fill the upper pole.
Postoperative results have generally demonstrated improved outcomes with
less rippling. Figures 57-10 to 57-14 illustrate a patient with rippling and
wrinkling following prosthetic reconstruction managed with ADM alone.
FIGURE 57-10 A preoperative photograph demonstrating rippling and wrinkling
following left mastectomy and implant reconstruction.
FIGURE 57-11 ADM is used to line the upper capsular surface and provide
additional tissue support.

Implant Displacement/Malposition
Device malposition is defined as inferior, medial or lateral displacement of an
implant. The etiology of malposition is multifactorial and includes
overdissection of the mastectomy pocket, contraction of the pectoralis major
muscle causing inferior or lateral displacement of the implant, excessive
external pressure applied to the anterior chest wall, and placement of an
implant that is too large for the defined footprint of the breast. Inferior
displacement may result from undermining below the level of the
inframammary fold during the mastectomy. Traditional management of
displacement has included capsulorrhaphy of the inferior or lateral breast
pocket (36,37). The technique of using ADM for implant displacement first
requires performing a capsulorrhaphy or a neopocket dissection in the
standard fashion. The second maneuver is to reinforce this repair using ADM.
The ADM is positioned in the breast pocket lengthwise such that half of the
ADM is resting on the posterior chest wall and the other half is over the
mastectomy skin flap or capsule. The device or temporary sizer is inserted
and the ADM is redraped over that device and sutured to the inferior, medial
or lateral mastectomy skin flap or capsule. Figures 57-15 to 57-18 illustrate a
patient following nipple-sparing mastectomy and smooth implant
reconstruction with severe malposition and rippling managed with shaped
silicone gel implants and ADM.

FIGURE 57-12 Postoperative image demonstrating improved contour with less


rippling.
FIGURE 57-13 Intraoperative photograph demonstrating adherence of the ADM to
the upper pole of the mastectomy pocket. The purpose of the operation was to
change the size of the left implant.
FIGURE 57-14 Final postoperative photograph demonstrating no rippling and
improved symmetry.
FIGURE 57-15 Preoperative photograph demonstrating severe asymmetry,
malposition, and rippling following bilateral mastectomy and smooth round implant
reconstruction.
FIGURE 57-16 Revision reconstruction using shaped implants and ADM to provide
additional soft tissue support to the periprosthetic space following capsulorrhaphy.
FIGURE 57-17 The ADM is positioned along the inferior aspect of the implant space.
CONCLUSION
The use of ADM in the setting of prosthetic and revisionary breast
reconstruction has arguably been one of the major advancements to facilitate
surgical techniques and improve surgical outcomes. It can facilitate
compartmentalization of the device, lessen the inflammatory response
associated with prosthetic devices, and provide tissue support to the
mastectomy skin flaps. The use of ADM for the prevention and management
of capsular contracture has been demonstrated in many level 3 and 4 studies.
Its use in the setting of radiation therapy has also been demonstrated to lessen
the inflammatory response in the short term but may not ameliorate soft
tissue–related morbidities in the long term.

FIGURE 57-18 Postoperative photograph demonstrating improved symmetry, no


rippling, and acceptable positioning of the breast implant at 1-year follow-up.

REFERENCES
1. Nahabedian MY. Acellular dermal matrices in primary breast
reconstruction: principles, concepts, and indications. Plast Reconstr
Surg 2012;130(5 Suppl 2):44S–53S.
2. Nahabedian MY. Prosthetic breast reconstruction with acellular dermal
matrices: achieving predictability and reproducibility. Plast Reconstr
Surg Global Open 2016;4(5):e698.
3. Duncan D. Correction of implant rippling using allograft dermis. Aesthet
Surg J 2001;21:81–84.
4. Breuing KH, Warren SM. Immediate bilateral breast reconstruction with
implants and inferolateral AlloDerm slings. Ann Plast Surg
2005;55:232–239.
5. Lyons DA, Mendenhall SD, Neumeister MW, et al. Aseptic versus
sterile acellular dermal matrices in breast reconstruction: an updated
review. Plast Reconstr Surg Glob Open 2016;4:e823.
6. Macarios D, Griffin L, Chatterjee A, et al. A meta-analysis assessing
post-surgical outcomes between aseptic and sterile AlloDerm
regenerative tissue matrix. Plast Reconstr Surg Global Open
2015;3(6):409–417.
7. Cottler PS, Olenczak JB, Ning B, et al. Fenestration improves acellular
dermal matrix biointegration: an investigation of revascularization with
photoacoustic microscopy. Plast Reconstr Surg 2019;143:971–981.
8. Frey JD, Alperovich M, Weichman KE, et al. Breast reconstruction
using contour fenestrated AlloDerm: does improvement in design
translate to improved outcomes? Plast Reconstr Surg Glob Open
2015;3:e505.
9. Wu PS, Winocour S, Jacobson SR. Red breast syndrome: a review of
available literature. Aesth Plast Surg 2015;39:227–230.
10. Nahabedian MY, Mesbahi AN. Breast reconstruction with tissue
expanders and implants. In: Maurice Y, Nahabedian MD. Cosmetic and
Reconstructive Breast Surgery. London: Elsevier Publishers; 2009:1–19.
11. Salzberg CA. Focus on technique: one-stage implant-based breast
reconstruction. Plast Reconstr Surg 2012;130(5 Suppl 2):95S–103S.
12. Nahabedian MY, Cocilovo C. Two-stage prosthetic breast
reconstruction: a comparison between prepectoral and partial
subpectoral techniques. Plast Reconstr Surg 2017;140(6S Prepectoral
Breast Reconstruction):22S–30S.
13. Nahabedian MY. Current approaches to prepectoral breast
reconstruction. Plast Reconstr Surg 2018;142(4):871–880.
14. Spear SL, Murphy DK. Natrelle round silicone breast implants: Core
Study results at 10 years. Plast Reconstr Surg 2014;133:1354–1361.
15. Maxwell GP, Van Natta BW, Bengston B, et al. Ten-year results from
the Natrelle 410 anatomical form-stable silicone breast implant core
study. Aesthet Surg J 2015;35(2):145–155.
16. Stevens WG, Harrington J, Alizadeh K, et al. Eight-year follow-up data
from the U.S. clinical trial for Sientra’s FDA-approved round and
shaped implants with high-strength cohesive silicone gel. Aesthet Surg J
2015;35(Suppl 1):S3–S10.
17. Hammond DC, Migliori MM, Caplin DA, et al. Mentor contour profile
gel implants: clinical outcomes at 6 years. Plast Reconstr Surg
2012;129:1381–1391.
18. Adams WP. Capsular contracture: what is it? What causes it? How can it
be prevented and managed. Clin Plast Surg 2009;36:119–126.
19. Salzberg CA, Ashikari AY, Berry C, et al. Acellular dermal matrix-
assisted direct-to-implant breast reconstruction and capsular contracture:
a 13-year experience. Plast Reconstr Surg 2016;138(2):329–337.
20. Uzunismail A, Duman A, Perk C, et al. The effects of acellular dermal
allograft (AlloDerm®) interface on silicone-related capsule formation:
an experimental study. Eur J Plast Surg 2008;31:179–185.
21. Stump A, Holton LH, Connor J, et al. The use of acellular dermal matrix
to prevent capsule formation around implants in a primate model. Plast
Reconstr Surg 2009;124:82–91.
22. Basu CB, Leong M, Hicks MJ. Acellular cadaveric dermis decreases the
inflammatory response in capsule formation in reconstructive breast
surgery. Plast Reconstr Surg 2010;126:1842–1847.
23. Vardanian AJ, Clayton JL, Roostaeian J, et al. Comparison of implant-
based immediate breast reconstruction with and without acellular dermal
matrix. Plast Reconstr Surg 2011;128(5):403e–410e.
24. Spear SL, Carter ME, Ganz JC. The correction of capsular contracture
by conversion to “dual-plane” positioning: technique and outcomes.
Plast Reconstr Surg 2006;118(Suppl 7):103S–113S; discussion 114S.
25. Araco A, Caruso R, Araco F, et al. Capsular contracture: a systematic
overview. Plast Reconstr Surg 2009;124:1808–1819.
26. Spear SL, Seruya M, Clemens MW, et al. Acellular dermal matrix for
the treatment and prevention of implant-associated breast deformities.
Plast Reconstr Surg 2011;127(3):1047–1058.
27. Cheng A, Lakhiani C, Saint-Cyr M. Treatment of capsular contracture
using complete implant coverage by acellular dermal matrix: a novel
technique. Plast Reconstr Surg 2013;132:519–529.
28. Nava MB, Pennati AE, Lozza L, et al. Outcome of different timings of
radiotherapy in implant based breast reconstructions. Plast Reconstr
Surg 2011;128:353–359.
29. Dubin MG, Feldman M, Ibraham HZ, et al. Allograft dermal implant
(AlloDerm) in a previously irradiated field. Laryngoscope
2000;110:934–937.
30. Ibraham HZ, Kwiatkowski TJ, Montone KT, et al. Effects of external
beam radiation on the allograft dermal implant. Otolaryngol Head Neck
Surg 2000;122:189–194.
31. Komorowska-Timek E, Oberg KC, Timek TA, et al. The effect of
AlloDerm envelopes on periprosthetic capsule formation with and
without radiation. Plast Reconstr Surg 2009;123:807–816.
32. Nahabedian MY. AlloDerm performance in the setting of breast
implants, infection, and radiation. Plast Reconstr Surg 2009;124:1743–
1753.
33. Colwell AS, Damjanovic B, Zahedi B, et al. Retrospective review of 331
consecutive immediate single-stage implant reconstructions with
acellular dermal matrix: indications, complications, trends, and costs.
Plast Reconstr Surg 2011;128:1170–1178.
34. Spear SL, Seruya M, Rao S, et al. Two-stage prosthetic breast
reconstruction using AlloDerm including outcomes of different timings
of radiotherapy. Plast Reconstr Surg 2012;130(1):1–9.
35. Maxwell GP, Gabriel A. Revisionary breast surgery with acellular
dermal matrices. Aesthet Surg J 2011;31(6):700–710.
36. Spear SL, Dayan JH, Bogue D, et al. The “neosubpectoral” pocket for
the correction of symmastia. Plast Reconstr Surg 2009;124(3):695–703.
37. Chasan PE. Breast capsulorrhaphy revisited: a simple technique for
complex problems. Plast Reconstr Surg 2005;115(1):296–301;
discussion 302–303.
CHAPTER 58

Use of Meshed Acellular Dermal


Matrix in Breast Reconstruction
MICHAEL SCHEFLAN | ADI MAISEL LOTAN
HISTORY
Breast cancer is the most common cancer affecting women worldwide (1).
Mastectomy has damaging physical and emotional consequences. Many
women are offered an immediate breast reconstruction to mitigate these
effects, resulting in improvements in self-image, quality of life, and overall
well-being (2–4).
The most commonly employed method of breast reconstruction worldwide
is implant based (5). More than half of breast reconstructions now use
acellular dermal matrix (ADM) for tissue reinforcement (5). ADMs have
been in use for soft tissue reinforcement since 1995, initially for the treatment
of burns (6). Salzberg et al. performed the first ADM-assisted breast
reconstruction in 2001 (7). Since then, the use of ADMs in breast
reconstruction has increased exponentially (7–15). ADM enables surgeons to
stabilize and shape the implant pocket, increase initial expander inflation
volume, and reduce the invasiveness of the surgical procedure (16). The
ADM also acts like a hammock for the lower pole and lateral aspect of the
implant, offloading implant weight off the soft tissue envelope. In addition, it
functions as a regenerative scaffold, facilitating new tissue formation through
angiogenesis, cell infiltration, and collagen production. Hence, when an
ADM is used, aesthetic outcomes, patient satisfaction, and physical and
sexual well-being are improved (17).
ADM-assisted direct-to-implant (DTI) breast reconstruction may reduce
overall costs compared with two-stage non–ADM-assisted implant or
autologous reconstruction (12,18,19).
ADM can significantly reduce the risk of capsular contracture and implant
malposition compared with total muscle coverage techniques (20). However,
concerns remain regarding possible increases in the rates of seroma,
infection, and skin flap necrosis (8,9,21).
One possible method of reducing postoperative complications is to
enhance matrix adherence by meshing the ADM. The underlying logic is the
same as with the meshing of skin grafts: that blood and serum can diffuse
freely through the graft and do not accumulate on either side. Also, physical
sheet expansion facilitates pliability and draping over the implant or tissue
expander (TE), forms a better fit, and promotes early incorporation by
speeding the inflammatory process, as well as neovascularization and
remodeling (Fig. 58-1). Using a preclinical in vivo porcine model, our studies
support this hypothesis showing that meshing of the ADM may allow cells to
populate the matrix more rapidly, promoting faster vascularization and
production of neocollagen. This leads to more rapid incorporation of the
matrix (22).
Meshing may also reduce ADM cost in breast reconstruction by allowing
smaller expanded sheet to be utilized for a given implant volume. This may
be particularly important with the advent of prepectoral breast reconstruction,
which requires larger pieces of ADM for implant coverage and stabilization.
In this scenario, meshing may allow larger implants to be covered with
smaller pieces of ADM, with potentially greater cost effectiveness.

FIGURE 58-1 Meshed ADM 4 years after implantation. Notice complete integration
of the mesh to the mastectomy flap, and tissue ingrowth into the gaps.

Meshing makes matrices more pliable and adaptable to any implant/TE


curvature, but also weakens the matrix, depending on the meshing ratio.
However, in kinematic models, meshing ADM at a 2:1 ratio yielded a safety
factor of >10 fold over the maximum force needed to tear the mesh,
demonstrating that it is safe for plastic surgery applications (C.B. Jessee,
Ph.D., June 2017) (23). Practically, with meshed matrices, there seems to be
a better “hand-in-glove” fit between the sheet and the implant or expander on
one side and the overlying soft tissues on the other.
ADMs may be in solid sheet, fenestrated, or meshed forms. There are
important biophysical differences between them; in particular, finely
fenestrated sheets tend to behave like solid ones (although wider slits may
indeed change the behavior of the matrix). They do not expand and have the
same surface area and similar permeability as solid sheets. These different
physical properties may affect integration of the matrices, and hence outcome
and complication rates (24).
Clinical studies have demonstrated a number of potential benefits of
physically modifying solid ADMs. ADMs in general improve intraoperative
fill volume of TE, increase expansion rate, decrease the time to full
expansion, improve drapability, and reduce postoperative pain (25). Studies
have also evaluated the effect of fenestration on complications—and
particularly on seroma formation—and there is a growing evidence base that
these physical alterations of the matrix can significantly reduce seroma rates,
infection, and drain time without negatively affecting aesthetic outcomes
(10,26–28).
After having used all forms of ADM in our practice (i.e., solid, fenestrated,
perforated, and meshed) and comparing clinical outcomes (11,28), since
January 2015 we have meshed all ADMs used in immediate breast
reconstructions at a 2:1 ratio.
In this chapter the rationale, indications, and surgical technique of using
meshed ADM in immediate, implant-based breast reconstruction are
presented. Ways to minimize complications and maximize patient outcomes
are discussed along with selected patient examples.
FIGURE 58-2 A, B: A 10 × 20 cm sheet meshed at 1:2 ratio (A) expands to 18 × 23
cm area (B).
INDICATIONS

Partial submuscular or prepectoral immediate implant-based (DTI) one-


stage breast reconstruction.
Partial submuscular or prepectoral immediate implant-based (TE) two-
stage breast reconstruction.
Partial submuscular or prepectoral delayed TE two-stage breast
reconstruction.
Revision reconstructive and aesthetic breast surgery: Tissue
reinforcement for implant displacement, bottoming out, synmastia,
pocket exchange, capsular contracture, rippling, and implant visibility
and palpability.
PREOPERATIVE CONSIDERATIONS
Breast volume should be estimated preoperatively, using Vectra 3D
photography (Canfield Scientific, Parsippany, NJ) and volumetric plastic
bowls (Plastikmott, Gothenburg, Sweden) or other methods.
ADMs come in several sizes and shapes. We order the ADM for each
patient according to prior assessment of breast volume and estimating the
range of implant or TE to be used. Bigger sheets are usually required for
larger implant. A meshed matrix expands significantly. For example, a 10 ×
20 cm (0.75 to 1.5 mm thick) ADM sheet (Fig. 58-2A) expands to an 18 × 23
cm area (Fig. 58-2B). This may allow surgeons to order smaller sheets and
lower operative costs.
Mostly, for implants ≤400 g and for partial retropectoral implant placement
we use a 10 × 15 cm piece of ADM; for implants >400 g and for prepectoral
reconstructions, a rectangular, 10 × 20 cm piece of ADM is used.
Our preferred incisions are inframammary for nipple-sparing mastectomy
(6 to 9 o’clock), radial oblique in the upper outer quadrant for skin-sparing
mastectomy, and combined trans-vertical ellipses for skin-reducing
mastectomy (29). The decision on whether to place the implant in a
prepectoral pocket is based on the thickness of the subcutaneous fat in
mammography and clinically assessed flap viability.
OPERATIVE TECHNIQUE
The operative technique for breast reconstruction procedures has been
defined and presented in other chapters of this book. The focus here is to go
through a series of surgical techniques and strategies for surgeons in order to
maximize patient outcomes and minimize complications when using meshed
ADM.
CAVEAT 1: TREAT MATRICES LIKE AN IMPLANT
Use no-touch technique. Do not place the ADM on the skin. Soak the ADM
in a triple-antibiotic solution (Cefamezin 1 g, Garamycin 80 mg, and
Bacitracin 50,000 IU in 500-cc Saline 0.9%; Bacitracin may be replaced with
50 cc of Betadine).
CAVEAT 2: ADM MAY BE PREMESHED BY MANUFACTURER OR MESHED
WITH A MESHER
We use a ∼0.75- to 1.5-mm thick premeshed at 2:1 ratio ADM (SurgiMend®
1.0, Integra Life Science, Plainsboro, NJ, USA) in all reconstructed breasts.
However, all matrices may be meshed with a mesher that fits the matrix,
which is usually thicker and larger in diameter than a skin graft. We have
found the Rosenberg mesher (4MED, Sderot, Israel) at 2:1 ratio the best fit
for the job.
Caveat 3: Use Gaps Within the ADM to Suture the Mesh to the Pocket
Vicryl Plus sutures (Ethicon, Inc., Somerville, NJ) are used to suture the
matrix to the surrounding envelope by putting the sutures through the open
spaces created by meshing. In partial submuscular reconstructions we place a
running suture between the cut end of the pectoralis major and the ADM, and
three to four sutures to fix the ADM to the IMF. In prepectoral
reconstructions, depending on implant volume, the mesh either covers most
or all the implant circumferentially (a wrap-around technique, Fig. 58-3) or
only the anterior dome of the implant.

FIGURE 58-3 A, B: Anterior (A) and posterior (B) surfaces of TE with meshed
ADM-wrap around technique, for prepectoral breast reconstruction.

In the wrap-around technique, ADMs are sutured around the implant using
2/0 Vicryl Plus sutures (Ethicon, Inc., Somerville, NJ) on a sterile back table
in the operating room. The matrix surrounding the implant is then sutured
directly to the confines of the pocket to secure implant positioning.
Alternatively, three to four tabs are created and sutured to the pectoralis
major fascia with parachute sutures once the device is placed inside the
pocket. In cases in where the meshed ADM is too small to cover the implant
all around, only the anterior surface of the implant is draped over with the
matrix by first securing it to the pectoralis major muscle in the superior and
medial margins of the pocket. The implant/expander is then inserted
underneath the matrix and tailored laterally and inferiorly.
Gaps created by meshing facilitate ADM suturing around the implant and
reduces the risk of inadvertent puncture of the implant. The needle may be
more easily passed through the large mesh openings rather than the smaller
mesh strands with equal suture retention.
POSTOPERATIVE CARE
It is important to keep breasts immobilized following reconstruction when
ADMs are used. In the DTI approach it is important to obtain a “hand-in-
glove” fit between the implant, the matrix, and the overlying soft tissue
envelope. Note that when using a TE covered with a meshed ADM, meshing
affords full conformability of the ADM to the TE, whether fully or partially
filled (Fig. 58-4). In breast reconstruction with expanders, the expansion
effect will “push” the ADM into the soft tissues to help facilitate integration
and revascularization.
Postoperatively, patients can move and stretch and resume normal day-to-
day activity but the breasts should remain “quiet” for 4 weeks with no impact
or chest-focused activities.

CASES

CASE 1

A 36-year-old patient, BRCA carrier, following mastectomy and


immediate reconstruction using a 10 × 20 cm meshed SurgiMend. Pre-
(Fig. 58-4A,B) and 12-month post-NSM and prepectoral two-stage breast
reconstruction (Fig. 58-4C,D).
FIGURE 58-4 A–D: A 36-year-old patient, BRCA carrier, following
mastectomy and immediate reconstruction using a 10 × 20 cm meshed
SurgiMend. Pre- (A,B) and 12 months post-NSM and prepectoral two-stage
breast reconstruction (C, D).
CASE 2

A 42-year-old patient 3 years following right lumpectomy and radiation


therapy (Fig. 58-5A–C). Patient underwent bilateral NSM and
prepectoral tissue expanders (Mentor 250 cc style 6100) and 10 × 20 cm
meshed ADM reconstruction. Mastectomy weight was 132 g on the right
and 168 g on the left.
At 2.5 years following TE replacement with Allergan 410 MF 295 g
and 140-cc fat grafting on each side (Fig. 58-5D–F).

FIGURE 58-5 A–F: A 42-year-old patient 3 years following right lumpectomy


and radiation therapy (A–C). Patient underwent bilateral NSM and
prepectoral tissue expanders (Mentor 250 cc style 6100) and meshed ADM
reconstruction. Two and a half years following TE replacement with Allergan
410 MF 295 gr and 140-cc fat grafting on each side (D–F).
CASE 3

A 41-year-old patient before (Fig. 58-6A–C) and 16 months following


right unilateral NSM and immediate DTI prepectoral reconstruction with
455-cc round, smooth, moderate plus implant, and a 10 × 20 cm meshed
ADM wrapped around the implant (Fig. 58-6D–F).
FIGURE 58-6 A–F: A 41-year-old patient before (A–C) and 16 months
following right unilateral NSM and immediate DTI prepectoral
reconstruction with 455-cc round, smooth, moderate plus implant, and a 10 ×
20 cm meshed ADM wrapped around the implant (D–F).
RISKS AND COMPLICATIONS
Seroma formation is the main complication associated with ADMs reported
in the literature (8,9,21). In our recent comparative study between solid and
meshed matrices, we found ADM meshing to reduce postoperative seroma
and infection rates and shorten drain time in patients undergoing immediate
implant-based breast reconstruction (28). These data are supported by our
previous preclinical study that shows reduced bioburden (the mass of added
ADM at the implantation site), and increased surface area of the matrix. The
latter means that more host connective tissue and vasculature are in direct
contact with matrix margins, potentially leading to faster incorporation
processes, such as inflammation, fibroplasia, and new tissue formation. Thus,
the expanded surface area of meshed ADMs promotes better cellular
penetration and faster integration and replacement by the host (22).
While theoretically meshing increases explantation risk in cases of skin
flap necrosis and implant exposure it has not been the case in our experience.
Using meshed ADM in over 200 breasts with a 5-year follow-up, the
incidence of reconstructive failure has not increased when compared to solid
sheet ADM (28,30).
CONCLUSION
ADM in implant-based breast reconstruction has been the standard of care in
our practice for the past decade. ADM meshing has been shown to reduce
postoperative infection and seroma rates and shorten drain time. By
expanding the sheet, meshing may also reduce surgical costs in patients
undergoing implant-based breast reconstruction.

REFERENCES

1. World Health Organization. International Agency for Research on


Cancer. GLOBOCAN 2012: estimated cancer incidence, mortality and
prevalence worldwide in 2012. Available online at
http://globocan.iarc.fr/Pages/fact_sheets_population.aspx. Accessed
June 18, 2018.
2. Oh DD, Flitcroft K, Brennan ME, et al. Patterns and outcomes of breast
reconstruction in older women—A systematic review of the literature.
Eur J Surg Oncol 2016;42:604–615.
3. Bertozzi N, Pesce M, Santi P, et al. One-stage immediate breast
reconstruction: a concise review. Biomed Res Int 2017;2017:6486859.
4. Serletti J, Fosnot J, Nelson JA, et al. Breast reconstruction after breast
cancer. Plast Reconstr Surg 2011;127:124e–135e.
5. American Society of Plastic Surgeons. Plastic surgery statistics report
2016. Available online at
www.plasticsurgery.org/documents/News/Statistics/2016/plastic-
surgery-statistics-full-report-2016.pdf. Accessed June 18, 2018.
6. Wainwright DJ. Use of an acellular allograft dermal matrix (AlloDerm)
in the management of full-thickness burns. Burns 1995;21:243–248.
7. Salzberg CA, Ashikari AY, Koch RM, et al. An 8-year experience of
direct-to-implant immediate breast reconstruction using human acellular
dermal matrix (AlloDerm). Plast Reconstr Surg 2011;127:514–524.
8. Skovsted Yde S, Brunbjerg ME, Damsgaard TE. Acellular dermal
matrices in breast reconstructions—a literature review. J Plast Surg
Hand Surg 2016;50:187–196.
9. Lee KT, Mun GH. Updated evidence of acellular dermal matrix use for
implant-based breast reconstruction: a meta-analysis. Ann Surg Oncol
2016;23:600–610.
10. Palaia DA, Arthur KS, Cahan AC, et al. Incidence of seromas and
infections using fenestrated versus nonfenestrated acellular dermal
matrix in breast reconstructions. Plast Reconstr Surg Glob Open
2015;3:e569.
11. Scheflan M, Grinberg-Rashi H, Hod K. Bovine acellular dermal matrix
in immediate breast reconstruction: a retrospective, observational study
with SurgiMend. Plast Reconstr Surg 2018;141:1e–10e.
12. Colwell AS, Damjanovic B, Zahedi B, et al. Retrospective review of 331
consecutive immediate single-stage implant reconstructions with
acellular dermal matrix: indications, complications, trends, and costs.
Plast Reconstr Surg 2011;128:1170–1178.
13. Butterfield JL. 440 Consecutive immediate, implant-based, single-
surgeon breast reconstructions in 281 patients: a comparison of early
outcomes and costs between SurgiMend fetal bovine and AlloDerm
human cadaveric acellular dermal matrices. Plast Reconstr Surg
2013;131:940–951.
14. Headon H, Kasem A, Manson A, et al. Clinical outcome and patient
satisfaction with the use of bovine-derived acellular dermal matrix
(SurgiMend™) in implant based immediate reconstruction following
skin sparing mastectomy: a prospective observational study in a single
centre. Surg Oncol 2016;25:104–110.
15. Zhao X, Wu X, Dong J, et al. A meta-analysis of postoperative
complications of tissue expander/implant breast reconstruction using
acellular dermal matrix. Aesthetic Plast Surg 2015;39:892–901.
16. Scheflan M, Colwell AS. Tissue reinforcement in implant-based breast
reconstruction. Plast Reconstr Surg Glob Open 2014;2:e192.
17. Barone M, Cogliandro A, Persichetti P. Use of acellular dermal matrix
in breast surgery: our experience and analysis of satisfaction using
BREAST-Q. Plast Reconstr Surg 2017;139:1014e–1015e.
18. Ibrahim AM, Ayeni OA, Hughes KB, et al. Acellular dermal matrices in
breast surgery: comprehensive review. Ann Plast Surg 2013;70:732–
738.
19. Jansen LA, Macadam SA. The use of AlloDerm in postmastectomy
alloplastic breast reconstruction: part II. A cost analysis. Plast Reconstr
Surg 2011;127:2245–2254.
20. Salzberg CA, Ashikari AY, Berry C, et al. Acellular dermal matrix-
assisted direct-to-implant breast reconstruction and capsular contracture:
a 13-year experience. Plast Reconstr Surg 2016;138:329–337.
21. Ibrahim AM, Shuster M, Koolen PG, et al. Analysis of the National
Surgical Quality Improvement Program database in 19,100 patients
undergoing implant-based breast reconstruction: Complication rates
with acellular dermal matrix. Plast Reconstr Surg 2013;132:1057–1066.
22. Lotan AM, Cohen D, Nahmany G, et al. Histopathological study of
meshed versus solid sheath acellular dermal matrices in a porcine model.
Ann Plast Surg 2018;81(5):609–614.
23. Wood LE, White J, Milligan A, et al. Predictors of three-dimensional
breast kinematics during bare-breasted running. Med Sci Sports Exerc
2012;44:1351–1357.
24. Wirth GA, Mowlds DS, Guidotti P, et al. Acellular dermal matrix
fenestrations and their effect on breast shape. Eur J Plast Surg
2015;38:267–272.
25. Martin JB, Moore R, Paydar KZ, et al. Use of fenestrations in acellular
dermal allograft in two-stage tissue expander/implant breast
reconstruction. Plast Reconstr Surg 2014;134:901–904.
26. Mowlds DS, Salibian AA, Scholz T, et al. Capsular contracture in
implant-based breast reconstruction: examining the role of acellular
dermal matrix fenestrations. Plast Reconstr Surg 2015;136:629–635.
27. Paydar KZ, Wirth GA, Mowlds DS. Prepectoral breast reconstruction
with fenestrated acellular dermal matrix: a novel design. Plast Reconstr
Surg Glob Open 2018;6:e1712.
28. Maisel Lotan A, Ben Yehuda D, Allwies T, et al. Comparative study of
meshed and non-meshed acellular dermal matrix in immediate breast
reconstruction. Plast Reconstr Surg 2019;144(5):1045–1053.
29. Scheflan M, Maisel Lotan A, Allweis TM. Trans-vertical mastectomy
with immediate implant-based reconstruction: a retrospective,
observational study. Aesthet Surg J 2019;39(7):733–742.
30. Scheflan M, Allweis T, Ben Yehuda D, et al. Meshed ADM in Pre
pectoral immediate breast reconstruction (Pending publication).
CHAPTER 59

Role of Implant Reconstruction in


Previously Radiated Patients
ANGELA CHENG | ALBERT LOSKEN
HISTORY
Breast-conservation therapy (BCT) is a popular option for patients with early-
stage breast cancer that preserves nipple sensation and avoids the need for
additional reconstructive procedures. Advances with oncoplastic surgery
techniques have allowed more expanded indications for BCT with larger
tumors (1). These patients typically complete postsurgical radiation therapy
as part of their cancer treatment. The radiation therapy can be administered
using various techniques which can result in different exposure and soft
tissue effects. External beam radiotherapy is most common but alternative
techniques including brachytherapy and intraoperative therapy are also
available at some institutions and may have more focal and local soft tissue
damage. Variation in radiation delivery also must be reviewed as some
patients receive whole-breast, partial-breast, or boost radiation therapy.
The resulting breast mound may demonstrate a variety of effects due to the
radiation ranging from minimal scarring or volume loss, to severe deformity
with skin changes and nipple malposition. The ideal BCT result should have
minimal deformity and no further intervention is required or contralateral
symmetrizing procedure. However, a subset of patients present with recurrent
disease, new malignancies, positive genetic testing, or personal choice for
subsequent completion mastectomy. After prior oncoplastic reduction
mammaplasty, approximately 10% of patients require completion
mastectomy for positive margins and 5.2% of patients present with
recurrence (2). Reconstruction in this setting following BCT with
radiotherapy can be challenging. While implants are often not the first option,
there are patients who can achieve reasonable results with this technique.
This chapter will focus on the use of implants following mastectomy in
patients with recurrent breast cancer who undergo skin-sparing mastectomy
(SSM), and the use of implants to correct BCT deformities.
USE OF IMPLANTS FOLLOWING MASTECTOMY
INDICATIONS
With the growing popularity of BCT we are now seeing previously irradiated
patients with recurrent breast cancer who need a mastectomy and present for
reconstruction. Patients with mild stigmata of radiation therapy may still be
excellent candidates for implant-based reconstruction. The skin should be
supple with minimal radiation fibrosis on examination. The nipple areolar
complex and inframammary fold should be in good position. Patients with
smaller breasts tend to have less fibrosis and are often better candidates for
implant-based reconstruction compared to those with larger breasts.
CONTRAINDICATIONS
Patient with severe damage due to radiation side effects such as soft tissue
contracture, hypo-/hyperpigmentation of the skin, fibrosis, nipple areolar
complex or inframammary fold malposition, and nonhealing wounds, and
unfavorable scar locations are poor candidates for an implant-based
reconstruction. These patients benefit from autologous tissue transfer such as
deep inferior epigastric artery perforator (DIEP) or transverse rectus
abdominis muscle (TRAM) flaps. Nonabdominal-based autologous flaps
such as transverse upper gracilis (TUG), profunda artery perforator (PAP),
superior/inferior gluteal artery perforator (SGAP/IGAP), lumbar artery
perforator (LAP), and lateral thigh perforator (LTP) can also be considered.
For patients with inadequate donor-site volume, a latissimus flap with
expander/implant is a solid option for breast reconstruction.
PREOPERATIVE PLANNING
A thorough evaluation of a previous BCT patient should include a complete
breast history of all prior disease and treatments. A realistic discussion of the
patient’s current breast size versus goals and review of all reconstructive
options with outcomes is necessary to select the appropriate treatment option.
Comorbidities such as smoking and/or obesity also may lead a surgeon to
caution against implants and consider autologous reconstruction or even
delayed reconstruction until medical optimization.
Careful physical examination should be performed to note prior biopsy
and/or lumpectomy scar locations, nipple position, soft tissue quality,
inframammary fold position, extent of radiation damage, breast size and
asymmetries, and location of new mass (if applicable). The breast surgeon
may plan to reexcise the prior scar if the disease is recurrent. In these
situations, careful discussion and planning of skin excision pattern should be
performed in conjunction with your breast surgeon. Patients should
understand that they have a reasonable chance of requiring autologous
reconstruction later if results are unfavorable.
OPERATIVE TECHNIQUE
The usual techniques for two-stage versus single-stage implant reconstruction
apply in this situation and are covered in other chapters. Healthy and
preferably thicker mastectomy flaps are desired and radiated flaps won’t
tolerate tension as well as nonirradiated flaps. Liberal use of acellular dermal
matrix (ADM) will provide a healthier environment for radiated skin flaps
and are preferred to having direct contact of the prosthesis with the skin flaps.
The dual plane technique provides vascularized tissue coverage of the
prosthesis in the upper pole and has been the preferred technique in the past.
More recently the prepectoral approach eliminates the elevation of a radiated
and often fibrosed pectoralis muscle and provides a softer, more natural
appearance in the previously irradiated breast.
INTRAOPERATIVE CARE
Careful handling of radiated skin flaps by the extirpative surgeon is crucial
for successful implant-based reconstruction. Inexperienced surgeons may
have more technical difficulty performing a mastectomy on patients with
prior radiation and scarring. Mastectomy skin flaps should be carefully
examined for signs of compromise and technology such as indocyanine green
angiography can be useful. While immediate breast reconstruction is
desirable, delaying reconstruction in the setting of compromised skin flaps
may be most prudent, however this make the patient a poor candidate for
implant reconstruction. In cases of threatened ischemia, we may consider
placing a tissue expander filled with air to minimize weight on the skin flaps.
The air can easily be exchanged for saline in clinic or simply allowed to
diffuse and reabsorb. All efforts should be made to minimize risks of
contamination or infection including but not limited to appropriate
perioperative antibiotic administration and redosing, Tegaderm nipple
coverage, limited incisions, pocket irrigation, change of gloves, and/or no-
touch technique for implant introduction with devices such as the Keller
funnel.
POSTOPERATIVE CARE
Our routine postoperative care of patients with prior BCT and radiotherapy is
the same as that of normal mastectomy patients. Most patients are placed in
observation and discharged the following day after appropriate drain care
teaching and pain control. We do not routine prescribe postoperative
antibiotics as there is no data to suggest efficacy.

CASES

CASE 1

This is a 57-year-old woman with prior history of left breast triple-


negative intraductal carcinoma treated with chemotherapy, lumpectomy 5
years prior. In the interim, genetic testing was positive for PALB2
mutation and now she presents with a newly diagnosed right breast triple-
negative tumor and elects for bilateral mastectomy and requests
reconstruction. The left breast was notably smaller with a scar in the
lower outer quadrant and otherwise minimal radiation skin changes (Fig.
59-1A–C). Her medical history was significant for coronary artery
disease on anticoagulation, diabetes mellitus, hypertension, and recent
smoking cessation (30 pack-year history). Examination also demonstrated
right upper quadrant scar from open cholecystectomy and midline
laparotomy scar from hysterectomy and bilateral salpingo-oopherectomy.
Collaborating with the extirpative surgeon, we designed the
mastectomy markings to remove the previous lumpectomy scar. A skin-
reducing Wise pattern incorporating the prior scar minimizes the scarring
and permits correction of her ptosis and asymmetry (Fig. 59-1D,E). The
significant volume difference of the breasts is clearly seen in the different
mastectomy specimens (Fig. 59-1F). The mastectomy skin flaps were
evaluated using laser-assisted indocyanine green angiography to confirm
viability and additional poorly perfused skin was marked and excised
(Fig. 59-1G). The expander is secured to the chest wall in a standard
fashion with tabs (Fig. 59-1H). The lower mastectomy skin flap is de-
epithelialized to function as an autoderm and provide vascularized
coverage of the expander with the upper pole of the expander covered by
acellular dermal matrix (Fig. 59-1I). Then the expander filled with
minimal volume (200-mL saline) to avoid tension on the skin closure,
and a drain is placed. The superior mastectomy skin flap is redraped over
the construct (Fig. 59-1J) and the small dart is de-epithelialized to
complete the Wise pattern closure (Fig. 59-1K,L).
FIGURE 59-1 Figure 59-1 A–C: Anterior, lateral, and oblique views of a
patient during initial consultation. The previous lumpectomy scar is visible in
the left lower outer quadrant. She has minimal radiation damage to her skin
but significant volume discrepancy compared to the contralateral native
breast. D, E: Anterior and lateral views of Wise-pattern markings. The
lumpectomy scar is incorporated into the area for removal. The right and left
mastectomy specimens were significantly different in size and volume/weight.
G: The area of poor perfusion observed on laser-assisted indocyanine green
angiography of the left mastectomy skin flap is marked for excision. H: The
deflated expander is secured to the chest wall. I: The inferior mastectomy
skin flap is deepithelialized and draped over the lower half of the expander.
The upper pole is covered with acellular dermal matrix secured to the chest
wall and the lower mastectomy skin flap. J: The superior mastectomy skin
flap is repositioned for a second layer of soft tissue coverage over the
expander and a drain is placed. K, L: Final on-table result with the expander
is partially filled and the skin closed.
CASE 2

This is a 35-year-old with a history of prior left breast lumpectomy and


radiation therapy 4 years ago. She now presented with recurrence on the
left and was scheduled for a left mastectomy. Her breasts are soft and
despite being irradiated her skin envelope on the left is soft with only
very minimal radiation fibrosis (Fig. 59-2A). She underwent a left skin
sparing mastectomy encorporating the old scar in the resection and left
prepectoral direct to implant reconstruction with ADM anterior coverage.
This resulted in a soft, symmetric left breast at 1 year post operatively
without any capsular contracture of or breast fibrosis (Fig. 59-2B).

FIGURE 59-2
CASE 3

This is a 42-year-old with moderate breast size and minimal ptosis with a
history of right lumpectomy and irradiation therapy (Fig. 59-3A). She
underwent a bilateral skin sparing mastectomy with tissue expander
reconstruction using the dual plane approach with ADM (Fig. 59-3B). At
the time of tissue expander removal and implant placement she had
wound dehiscence and subsequent implant exposure on the right (Fig. 59-
3C). This then required implant exchange to a smaller implant and a right
latissimus dorsi flap reconstruction (Fig. 59-3D).
FIGURE 59-3
GENERIC RISKS
Patient with prior radiation to the breast are at higher risk for complications
following mastectomy with implant-based reconstruction. The patient should
be counseled on risks of skin necrosis, wound complications, infection,
dehiscence, capsular contracture, implant loss, and the increased need for
additional procedures. As per usual, we advise the patients to seek medical
attention for any early signs of infection or complication such as erythema,
worsening pain, fever, increased drainage, increased swelling, etc. Patients
with prior radiation therapy who also smoke are at significant risk of wound
healing complications and need to be approached very cautiously.
OUTCOMES
It can be difficult to accurately predict which patient with prior BCT and
radiotherapy will experience complications with mastectomy and
expander/implant reconstruction. Many surgeons consider preoperative
radiotherapy to be a relative contraindication to tissue expander/implant
reconstruction and we often advise patients to consider autologous
reconstruction. Even with healthy-appearing radiated skin, the outcomes with
implant reconstruction can be relatively unpredictable. The downside of
attempting implant reconstruction in these patients is limited since it is not
difficult to convert down the road to an autologous reconstruction if
necessary.
Early publications by Evans (3) and Spear (4) suggested implants should
be avoided in patient with previous radiotherapy or anticipated postoperative
radiotherapy. Evans noted higher rates of implant loss and unfavorable
outcomes such as capsular contracture with both preoperative and
postoperative radiation. Both authors suggested autologous reconstruction
should be favored for these patients. While this paradigm has remained
relatively unchallenged, preoperative radiotherapy for breast cancer has
become uncommon and advances in breast reconstruction using ADMs and
nipple-sparing mastectomies have pushed the frontiers.
In one of the largest series, Cordeiro reported his 12-year experience with
breast reconstruction using tissue expanders/implants and noted a higher rate
of complications with previously irradiated breasts. He compared 136
previously irradiated patients to 2,140 control patients and concluded that
higher rates of complications were noted but the absolute rate remained low
(5). Expander/implant reconstruction remains an acceptable option for
patients who are not candidates for autologous reconstruction. However, the
nature of the previous radiation was not clarified and it should be noted that
there are other indications for chest wall or thoracic irradiation such as
Mantle cell radiation for lymphoma or chest wall radiation for other soft
tissue malignancies with different dosage and penetration which may have
been included.
Other authors have also noted significantly higher complication rates,
especially infection, in patients with prior radiation therapy. In a 10-year,
single-surgeon retrospective study by Lin et al. with 267 breasts, 32 with
prior radiation exposure suffered a 43.8% complication rate versus 13.8%
without prior radiation. Patients with device loss either completed implant
reconstruction after resolution of infection or were offered autologous
reconstruction (6).
Sbitany et al. also compared patients with prior history of radiation before
SSM and reconstruction to patients with no radiation or postoperative
radiation. The authors found patients with any radiation delivery resulted in
increased risk of infection requiring antibiotics (21.6%) and increased risk of
device loss (18.75%). Prior radiation therapy also increased risks of wound
breakdown (7).
In a small case control study, Weichman et al. compared prior unilateral
radiation therapy for bilateral mastectomy reconstruction with
expander/implants using ADM. A total of 23 patients had no significant
difference in mastectomy skin flap necrosis, explantation, hematoma, or
seroma. Notably, capsular contracture was one grade more severe in the
radiated breast in 60% of patients. The authors concluded that previous
irradiation did not increase the risk of early postoperative complications with
use of ADM (8).
Despite these studies demonstrating increased complications, many
surgeons (including ourselves) will still offer these patients implant-based
reconstruction either out of necessity (lack of donor-site availability) or
patient preference. Complications such as wound infection can be salvaged
with delayed reconstruction or autologous reconstruction. In a study by
Alperovich et al. of 26 nipple-sparing mastectomy patients with prior
radiation therapy and an average of 12 years between treatment and
mastectomy, 16 patients received either an expander or implant and the
overall mastectomy flap necrosis requiring surgical intervention was only 3
of 26 or 11.5%. The authors noted the irradiated group was older but found
no statistically significant difference with regard to complications such as
mastectomy flap necrosis, partial/complete nipple areolar complex necrosis,
implant loss, hematoma, seroma, or capsular contracture (9). This suggests
that implant-based reconstruction can be safely and successfully completed
for properly selected and counseled patients.
With nipple-sparing mastectomy popularity increasing, viability of the
nipple areolar complex following preoperative radiation therapy is a serious
concern. Colwell et al. reported their series of 500 nipple-sparing
mastectomies and upon reviewing their 42 patients with prior radiation
therapy, noted a 4.8 odds ratio for nipple areolar complex necrosis (10). In
another publication with 982 nipple-sparing mastectomies, 67 had prior
radiotherapy and overall increased complication rates but nipple areolar
complex necrosis was infrequent. Therefore, prior radiation alone is not a
contraindication to nipple-sparing mastectomy (11).
CONCLUSION
Patients with prior radiation therapy due to other indications or previous BCT
may present for mastectomy subsequently and desire implant-based
reconstruction. The history of radiation therapy is not an absolute
contraindication to successful implant-based reconstruction but should be
approached with caution and careful patient selection. Careful evaluation of
the remaining breast tissue envelope, scars, nipple position, volume,
inframammary fold, and asymmetry to the contralateral breast combined with
extensive counseling with regard to risks of infection, capsular contracture,
and implant loss are strongly advised. Cooperation with the breast surgeon
during mastectomy to incorporate previous scars, preserve the nipple areolar
complex, and create healthy skin flaps is imperative. Autologous
reconstruction options including latissimus flap with expander/implant or
abdominal-based tissue transfer should be strongly considered for patients
with severe radiation damage or deformity and/or remain solid options for
salvage of failed implant-based reconstruction.
USE OF IMPLANTS TO CORRECT THE BCT
DEFORMITY
Although the general impression is that implants are not good options for
correcting BCT deformities in women with irradiated breasts, there may be
exceptions. However, available literature on this topic is very limited.
PREOPERATIVE PLANNING
When evaluating a patient who has a poor cosmetic result after BCT, it is
important that (1) at least 1 year has passed since the completion of
radiotherapy, (2) she has been adequately screened for any potential
recurrence, and (3) a mammogram of the contralateral breast is obtained.
Although the incidence of unfavorable cosmetic results after BCT is lower
in women with smaller breasts than in women with large breasts, a certain
percentage of patients opt for delayed reconstruction to have the deformity
corrected. Their wishes and goals might include (1) correction of their
asymmetry, (2) correction of the actual deformity, (3) shape improvement,
and (4) breast enlargement. These patients are potential candidates for
reconstruction of their BCT deformity with implants. However, the patient’s
wishes are not enough to determine her eligibility; the breast evaluation is the
main factor.
The physical examination should include a classification of the deformity,
with close attention paid to the size of the breasts, breast symmetry, the
location of the deformity, and the amount of skin retraction and volume loss.
In addition, the quality of the skin envelope should be determined; this is
likely the most important factor for correction with implants. If breast skin
has edema, tightness, or hyperpigmentation with a leathery feel—all evidence
of significant radiation damage—then that patient is not a good candidate for
implants.
If a contour deformity is present, the breast mound needs to be soft for the
implant to correct or improve the deformity. If the mound is firm or
significantly fibrosed, an implant will not allow the remaining breast tissue to
fill out or improve the deformity. The result will be a larger breast with a
persistent contour irregularity, which may be even more pronounced because
of the size enhancement. It is probably preferable to correct the deformity as
long as possible after radiotherapy, because its effects persist.
Although it is often easier to achieve symmetry by placing implants
bilaterally, some patients have a fairly significant size discrepancy and
require only an ipsilateral implant. Generally, however, if a patient has
extensive radiation fibrosis, she will not be an ideal candidate for using
implant placement to correct a BCT defect.
The use of implants to correct BCT deformities in well-selected patients
allows the correction of (1) parenchymal loss by replacing volume and (2)
minor skin deficiencies and contour irregularities by stretching skin.
OPERATIVE TECHNIQUE
The actual surgical technique does differ slightly from regular breast
augmentation surgery. The general principles are the same and are covered
extensively in other reference books. The patient is marked preoperatively,
with close attention given to the level of the inframammary fold, the nipple
position, and the location of the deformity. Any variation in the level of the
inframammary fold can be changed intraoperatively. When the asymmetry is
mainly one of size, and the shape is preserved, then a simple augmentation
with different volumes should suffice. Minor contour irregularities are often
filled and improved with an implant placement. It is important to address any
significant contour irregularity, because it might be even more noticeable
with larger breasts. These irregularities might require contracture or scar
release and/or fat injections in addition to the implant placement. It is also
important to adequately counsel the patient preoperatively and inform her that
the contour irregularity might not be completely corrected with the implant.
Instead, it may become less prominent and subsequently less noticeable.
It is preferable to use an access incision in an area off the breast, one with
good exposure (for e.g., the inframammary fold or axilla). Periareolar
incisions require dissection through the breast mound with skin undermining
and should be avoided if possible. The periareolar approach could be used if
that is where the deformity is located and if contracture release is required in
that location to recreate the deformity.
It makes intuitive sense that submuscular implant placement would be
preferable, especially in upper pole defects, because it provides another layer
of vascularity above the implant. The only potential disadvantage of
submuscular implant placement (especially with upper pole defects) is that
the release of a scar contracture band is occasionally required at the time of
implant placement to improve contour. Subglandular placement might be
more beneficial for these patients and eliminates the muscular variable which
is often fibrosed and tight.
Silicone gel implants often result in a more natural-appearing and natural-
feeling breast mound; however, saline does have one advantage in this
situation. It is easier to make minor volume adjustments with saline, which
may be necessary if small implant volume asymmetries are expected. Smaller
implants are probably safer in the setting of previous breast irradiation. If
tissue expanders are felt to be required to stretch the skin, then these patients
are usually not ideal candidates for placing implants in the first place, and
alternative options should be explored.
Fat grafting is now often used as an adjunct to further correct any
irregularity with the implant providing the needed additional volume.

CASES

CASE 4

This 46-year-old woman presented with an unfavorable result 4 years


after a left lumpectomy and radiotherapy (Fig. 59-4A–C). She was
concerned with the size and shape of her breast, and she expressed an
interest in having larger breasts, if possible. Her left breast had some
volume loss, a fairly significant contour distortion, and scarring on the
lateral aspect (Clough type 2 cosmetic sequelae). Apart from the scarring,
her skin was otherwise soft and appeared healthy, and her nipples were
fairly symmetrical.
After discussing her options, she elected to undergo bilateral implant
augmentation. A subpectoral pocket was created through an
inframammary fold incision, and 250-cc smooth, round saline implants
were inserted into each breast. Her implants were filled to 250 cc on the
left and 260 cc on the right. A small amount of scar release was
performed on the left side. She is shown 3 years postoperatively with
good symmetry, improved contour, and soft breasts (Fig. 59-4D–F).
There is no evidence of capsular contracture.
FIGURE 59-4 See case text.

CASE 5

This is a 50 year old female who has had numerous biopsies from her left
breast and presents with deformities about 3 years after having undergone
breast conservation therapy. She has minor volume differences, and some
fairly prominent contour irregularities beneath and medial to her nipple
on the left side (Clough Type 2). Her skin envelope is otherwise
relatively healthy appearing without evidence of unfavorable radiation
changes (Fig. 59-5A–D). She too was not opposed to being larger on both
sides and elected to undergo bilateral implant augmentation. It is
important that the patient be adequately counseled pre-operatively and
informed that the contour irregularity might not be completely corrected
with the implant, however, rather that it may less prominent, and less
noticeable. She underwent bilateral subglandular implant placement (225-
cc smooth round saline implants) through an IMF incision. Her left
implant was inflated to 215 cc, and 200 cc on the right. Multiple radial
scoring incisions were made in the lower pole parenchyma to release
some of the tethering of her scars to the skin for contour improvement.
This decision was made intra-operatively one the implant was placed and
the deformity was assessed. She is shown 1 year following implant
placement with decent shape and symmetry (Fig. 59-5E, F). Note a
modest improvement, but not complete resolution of her medial contour
irregularity.
FIGURE 59-5
OUTCOMES
The obvious concern in these patients is the higher risk of capsular
contracture and skin envelope retraction with time. In well-selected patients,
results are very favorable and patient satisfaction is high. Given the
unpredictable nature of the irradiated skin envelope, not all patients are going
to do well and if complications arise or if results are unfavorable, it is always
possible to remove the implants without any significant downside. Additional
autologous options are always available in those situations.
CONCLUSION
The use of implants to correct a BCT deformity is always risky, given the
long-term effects of breast irradiation. Theoretically, there is a higher chance
of capsular contraction and breast fibrosis in these patients; however, good
results can be obtained. The key to success using this approach is appropriate
patient selection. Few patients with BCT deformities are good candidates for
implants. The ideal patient has relatively small, nonptotic breasts, with good
nipple position, a soft breast mound, and a normal-appearing skin envelope.
Asymmetries in shape and volume can be corrected using standard
augmentation techniques with some minor variations. Because the effects of
radiation persist, aesthetic results require a long-term, critical evaluation, and
patients need to be aware of the possibility for further shape compromise.

REFERENCES

1. Losken A, Hart AM, Dutton JW, et al. The expanded use of


autoaugmentation techniques in oncoplastic breast surgery. Plast
Reconstr Surg 2018;141(1):10–19.
2. Losken A, Hart AM, Broecker JS, et al. Oncoplastic breast reduction
technique and outcomes: an evolution over 20 years. Plast Reconstr
Surg 2017;139(4):824e–833e.
3. Evans GR, Schustermann MA, Kroll SS, et al. Reconstruction and the
radiated breast: is there a role for implants? Plast Reconstr Surg
1995;96:1111–1115; discussion 1116–1118.
4. Spear SL, Onyewu C. Staged breast reconstruction with saline-filled
implants in the irradiated breast: recent trends and therapeutic
implications. Plast Reconstr Surg 2000;105:930–942.
5. Cordeiro PG, McCarthy CM. A single surgeon’s 12-year experience
with tissue expander/implant breast reconstruction: part I. A prospective
analysis of early complications. Plast Reconstr Surg 2006;118:825–831.
6. Lin KY, Blechman AB, Brenin DR. Implant-based, two-stage breast
reconstruction in the setting of radiation injury: an outcome study. Plast
Reconstr Surg 2012;129:817–823.
7. Sbitany H, Wang F, Peled AW, et al. Immediate implant-based breast
reconstruction following total skin-sparing mastectomy: defining the
risk of preoperative and postoperative radiation therapy for surgical
outcomes. Plast Reconstr Surg 2014;134(3):396–404.
8. Weichman KE, Cemal Y, Albornoz CR, et al. Unilateral preoperative
chest wall irradiation in bilateral tissue expander breast reconstruction
with acellular dermal matrix: a prospective outcomes analysis. Plast
Reconstr Surg 2013;131:921–927.
9. Alperovich M, Choi F, Frey JD, et al. Nipple-sparing mastectomy in
patient with prior breast irradiation: are patients at higher risk for
reconstructive complications? Plast Recontr Surg 2014;134(2):202e–
206e.
10. Colwell AS, Tessler O, Lin AM, et al. Breast reconstruction following
nipple-sparing mastectomy: predictors of complications, reconstruction
outcomes, and 5-year trends. Plast Reconstr Surg 2014;133(3):496–506.
11. Tang R, Coopey SB, Colwell AS, et al. Nipple-sparing mastectomy in
irradiated breasts: selecting patients to minimize complications. Ann
Surg Oncol 2015;22(10):3331–3337.
CHAPTER 60

Management and Prevention of Nipple


and Mastectomy Skin Necrosis
BRIAN P. THORNTON | ELIZABETH TURNER | TIFFANY BERRY
HISTORY
Preservation of the entire native breast skin envelope following mastectomy
allows plastic surgeons to provide an enhanced outcome. It is critical to
maximize the aesthetic results by minimizing vascular embarrassment to the
nipple and skin flaps.
The reported rates of mastectomy flap necrosis (MFN) range from 2% to
40% (1–4) and for nipple areolar complex (NAC) necrosis of 3.8% to 37.5%
(5,6). MFN and NAC necrosis begins when the blood supply to the skin flaps
is insufficient to meet the recovering skin flap’s or nipples’ metabolic needs.
Both patient and surgical variables are contributing factors to the incidence of
these two complications.
Patient factors such as smoking (1,7,8), obesity (3,8–10), history of breast
radiation therapy (1,11–13), breast cup size/breast weight (3,14), age (15,16),
and hypertension (16–18) increase the risk of mastectomy skin flap and/or
nipple necrosis. Operative risk factors include nipple-sparing mastectomy
(NSM) (3), incision pattern (1–3,17,19–21), flap thickness (22,23), use of
tumescent technique (24), immediate versus delayed reconstruction, and type
of breast reconstruction (15,18,25–27). Technology can be utilized to provide
operative assessment of jeopardized skin. Currently, no technology exists that
is perfect in the prediction of skin necrosis for every patient application. In
the management of the postoperative injured skin flap, the needs and
understanding of the patient must also be considered in the treatment
strategy. Both nonoperative and operative measures are effective and often
used in combination.
This chapter will review patient inherent and operative risk factors that are
predictors of MFN and/or NAC necrosis, intraoperative skin/tissue
assessment, and postoperative management strategies.
SKIN ISCHEMIA AND NECROSIS SCORE
Management of superficial epidermal sloughing is different than full-
thickness flap necrosis (Fig. 60-1). The skin ischemia and necrosis (SKIN)
score assigns a composite value to each operated breast (28). The depth of
necrosis is scored using a letter score from A to D while the surface injury
percentage is numerically scored on a scale from 1 to 4. The categories for
depth of MFN include (A) no skin flap injury, (B) skin color change
indicating ischemia (either cyanosis or erythema) without necrosis, (C)
partial-thickness necrosis with at least epidermal sloughing, and (D) full-
thickness necrosis. To assess the surface area involved, four categories were
created starting with (1) 0%, (2) 1% to 10%, (3) 11% to 30%, and (4) greater
than 30% of the breast surface area or NAC. In cases of NSM, the breast skin
envelope and NAC are scored separately. The SKIN score system is an easy
to use, well-validated model that standardizes the description of MFN and
NAC necrosis.
PATIENT RISK FACTORS
An important opportunity to discuss complications with patients is prior to
surgery. Often the newly diagnosed patient with breast cancer struggles with
the diagnosis and is distracted during the reconstructive consultation. There
are known inherent patient risk factors that can contribute to MFN and NAC
necrosis postoperatively. The reconstructive surgeon must set realistic patient
expectations and document risk factors in the medical record.
Smoking
Smoking has a well-documented history of impairing perfusion and oxygen
delivery leading to flap and nipple necrosis (7). Padubidri reported that
smokers undergoing breast reconstruction had a significantly higher rate of
mastectomy skin flap necrosis regardless of reconstruction modality than
nonsmokers (7). Other studies have found similar results (1,8).
Increasingly, patients are replacing standard cigarettes with electronic
cigarettes (e-cigs). No human studies have examined e-cigs’ effect on MFN
and NAC necrosis rates leaving plastic surgeons confused on the effect of e-
cigs compared to the data on cigarettes. Animal models have demonstrated
similar results of skin necrosis and hypoxia between e-cigs and traditional
cigarette smoking (29). Thus, plastic surgeons should consider e-cigs’ impact
on MFN and NAC necrosis no different than cigarettes.
FIGURE 60-1 A: A 50-year-old patient with a history of circumareolar mastopexy,
submuscular augmentation, and recurrent stage IIA right breast cancer. One week
after bilateral NSM and prepectoral air-filled expander with left superficial NAC
necrosis (SKIN Score C2). B: A 49-year-old patient with stage IA right breast
cancer. One week after bilateral NSM and prepectoral air-filled expander-based
reconstruction with right skin and NAC color change suggesting impaired perfusion
(SKIN Score B4 for skin envelope and NAC). C: A 42-year-old patient with stage I
left breast cancer patient 6 weeks after bilateral NSM and prepectoral air-filled
expander with full-thickness right skin flap and NAC necrosis (SKIN Score D3 and
D2, respectively).

To minimize necrosis, patients should cease nicotine consumption for 3


(30) to 4 weeks (31) before surgery. Postoperatively, nicotine consumption
should stop for up to 4 weeks (30) to minimize skin flap necrosis. Cessation
compliance can be monitored by performing a urine, blood, or saliva nicotine
test prior to surgery. Nicotine is metabolized by the liver into multiple
metabolites; the most common being cotinine (32). Cotinine has a longer
half-life than nicotine and is concentrated in the urine at four to six times
higher levels than in blood or saliva. Urine cotinine and its byproducts make
quantitative analysis possible to evaluate active and passive nicotine exposure
over 7 days or more (33). The limitations of urine cotinine testing are that it
requires 4 to 7 days of processing time (32). Therefore, patients must provide
a urine sample 1 week before surgery. Qualitative testing will report results
within a shorter interval, but at the disadvantage of nicotine exposure
measured in hours compared to days for quantitative analysis (33). Smoking
should be considered a modifiable patient variable that contributes to one of
the highest risks of necrosis.
Obesity
When evaluating the vascular architecture of adipose tissue in nonobese
patients, the ratio of capillary beds to fat cells is similar to that of the highly
vascular skeletal muscle (34).
However, obesity is not met with a proportional increase in capillary
density, resulting in a fat vascular insufficiency (34). While the strain on the
obese adipose vascular system exists in the presurgery state, any capillary
damage from surgical injury further exacerbates the hypoxic environment
resulting in necrosis. Therefore, understanding the impacts of obesity on the
complications of potential reconstructive options is critical.
Fischer’s review of the NSQIP database revealed that an increase in the
BMI was associated with higher rates of complications including flap
necrosis (9). Further analysis of the same database revealed that patients with
a BMI greater than 30 had fewer complications when undergoing expander-
based and latissimus reconstructions compared to free and pedicled TRAM
flap reconstruction (10). Similar results have been reported in other studies
(3,8).
The increased rates of MFN must be discussed and appropriate
reconstruction pathways recommended.
Prior Breast Radiotherapy
The predicted recurrence of breast cancer following breast conservation has
been well established at 14% (4). As a result of recurrence, an increasing
number of patients with failed breast conservation will undergo mastectomy
and contemplate reconstruction. Reviewing with the patient the potential
impact of historic breast radiotherapy is vital.
Radiation-induced changes include epidermal atrophy, effacement of the
rete pegs, fibrotic dermis, sclerotic vessels, and reduction of pilosebaceous
glands (35). Impaired healing results from progressive vascular fibrosis and
loss of stem cells (35). Thus, the radiated skin envelope is prone to ischemic
insult.
A review of a single surgeon’s extensive breast reconstruction experience
showed a significant difference in MFN in patients undergoing reconstruction
with a prior history of breast radiation (3.7%) versus nonradiated patients
(1.9%, p = 0.006) (11). Multiple other studies have demonstrated higher risk
of MFN in the previously irradiated breast patient (1,12,13). By contrast,
McCarthy reported no difference in patients undergoing reconstruction with a
history of radiation (5%) versus no radiation (2%, p = 0.13) (16). Berry found
similar results in their publication (8).
Understanding the discrepancy between the reported outcomes—of no risk
to significantly increased risk of MFN in the previously irradiated patient—is
difficult to comprehend. This may be explained by shorter or longer time
intervals between completion of breast radiation and the mastectomy. Thus,
when evaluating individuals with a history of radiation, patients with a
remote history are a distinctly different subset compared to patients who have
recently completed treatment. Although no guidelines have been described to
preoperatively counsel patients regarding the possibility of increased MFN
risk as correlated to their historic radiation completion date, preparing the
patient for this possibility is prudent.
Radiation has been considered a relative contraindication in NSM.
In a review of patients undergoing NSM, Alperovich demonstrated that
implant-based and autologous reconstruction can be performed with NAC
necrosis rates comparable to the nonirradiated NSM control group (6).
Therefore, patients who have a history of breast irradiation may be candidates
for NSM.
Specimen Weight/Breast Cup Size/Ptosis
Women with macromastia undergoing breast cancer extirpation have
decreased perfusion due to larger skin envelopes. When analyzing flap
necrosis risks associated with larger breasts, patients having breast specimen
weights greater than 400 g had a significantly higher rate of MFN and NAC
necrosis (14). Not surprisingly, patients with breast sizes greater than self-
reported C cups also had a significantly higher rate of NAC necrosis (3,14).
Breast ptosis has not been shown to be a significant independent predictor of
necrosis, but patients with grade 1 ptosis have demonstrated less necrosis
than patients with grade 2 or 3 ptosis (17). This is a common phenomenon
that as breast size increases, the breast becomes more ptotic.
Patient Age
Advancing age affects healing through both local and systemic effects (36).
The age-related thinning of the skin confers additional risk on mastectomy
flap and nipple necrosis (22). Patients undergoing expander/implant-based
reconstruction at ages greater than 50 (15) or 65 (16) have an increased risk.
The same age-related increase in necrosis has not been observed in
autologous reconstruction (1,37).
Hypertension
The breast is susceptible to the same atherosclerotic disease process as the
rest of the vascular system. Hypertension affects the arteries by narrowing
and thickening the lumen of the walls. McCarthy showed that hypertensive
patients undergoing expander-based reconstruction were four times more
likely to have failed reconstruction compared to normotensive patients (16).
A similar effect was observed when evaluating hypertension effect on the rate
of nipple necrosis (17). Hypertension was also found to synergistically
increase MFN when combined with high intraoperative expander fill volumes
(18).
Previous Breast Surgery
In 2017, over 400,000 patients underwent elective breast surgery for
reduction, mastopexy, or augmentation (33). Unfortunately, one in eight of
women will be diagnosed with breast cancer, with some electing or required
to have a mastectomy. Previous breast scars are believed to impair vascular
perfusion to the skin and increase the risk of nipple or mastectomy skin flap
necrosis. Frederick performed an analysis of 160 patients undergoing breast
reconstruction after a history of lumpectomy, augmentation, or reduction
(38). Upon multivariate analysis, previous breast surgery was not found to
increase the risk of MFN or nipple necrosis. By contrast, Matsen performed a
multivariate analysis of over 600 consecutive breast reconstruction
procedures demonstrating a significantly higher risk of necrosis in patients
with a history of prior reduction mammaplasty (3). When reviewing a
patient’s surgical breast history who is contemplating reconstruction after
mastectomy, accounting for previous incisions is important. In our working
group, patients with a history of previous breast surgery are not immediately
excluded from having NSM and/or reconstruction.
OPERATIVE RISK FACTORS
There are many operative factors that impact the delicate vascular network
during mastectomy and reconstruction. Some operative factors defy
quantification but may include proximity of tumor to dermis, careful tissue
handling by the surgeon, and gentle retraction by assistants. It is paramount
in minimizing MFN and NAC necrosis to treat the mastectomy flaps gently
and with the same respect one would during a rhytidectomy procedure.
Breast Vascular Anatomy
Understanding the breasts vascular anatomy aids in the prevention of
necrosis. The dominant arterial supply to the skin flaps are perforators from
the internal mammary artery, followed by lateral thoracic, the 2nd through
5th anterior intercostal, thoracoacromial, and superficial thoracic artery (39).
Perforating cutaneous arteries supply blood to the overlying skin of the breast
and combine to form a continuous subdermal and subcutaneous plexus.
The blood supply to NAC is considered segmental and can be
unpredictable. A cadaveric review by Van Deventer noted that the NAC
consistently received perforating branches from the dominant internal
mammary artery (39). Therefore, it is vital to maintaining adequate perfusion
to both the skin and the nipple by sparing the perforators of the internal
mammary artery during mastectomy.
Mastectomy Types and Skin Incision Patterns
Nipple-Sparing Mastectomy
NSM represents the pinnacle of mastectomy skin-sparing surgery. NSM is a
technically demanding surgery and places higher stress on the surgical team
and skin flaps. In a 2014 prospective review of 95 patients undergoing a
mastectomy, NSM had a significant risk of MFN and NAC necrosis
compared to skin-sparing mastectomy (3). In a more recent review of a larger
series of patients undergoing NSM, it revealed a rate of MFN or NAC
necrosis consistent with skin-sparing mastectomy (40). The discrepancy
between these two publications may represent how breast surgeons with
limited experience in advanced techniques, such as NSM, would expect to
suffer higher necrosis complication rates until surgical proficiency is
achieved.
When offering patients NSM, the skin incisions utilized to perform the
surgery can have significant deleterious effects on vascular disruption and
NAC viability. Periareolar incisions generally experience a greater rate of
NAC necrosis and should be avoided when possible (1,2). For some breast
surgeons, a lateral radial incision offers a way to preserve the nipple while
still maintaining easier access to the whole breast for dissection compared to
the inframammary fold incision (19). Overall, the inframammary fold
incision has demonstrated the lowest rate of necrosis when compared to all
NSM incisions (19).

Wise Pattern
For larger breasts, differing incision patterns are utilized to correct the excess
skin. Abedi demonstrated that the use of a Wise-pattern incision had almost
three times the odds of MFN compared to skin-sparing mastectomy
regardless of type of breast reconstruction chosen (1).
Multiple studies have been mirrored the findings (14,19,20). A Wise-
pattern skin reduction is often required to address horizontal and vertical skin
excess, but the higher risk of MFN and NAC necrosis is compounded by
effect of breast weight as described earlier. Some authors have advocated the
use of a staged Wise-pattern skin reduction for the large ptotic patient
undergoing mastectomy (21). Patients in this study underwent a mastectomy
and expander-based reconstruction through the vertical scar to tighten the
horizontal skin excess. At the time of expander exchange to implant, the
vertical skin excess is removed through a horizontal scar completing the Wise
pattern. The authors reported no skin necrosis with the limited number of
patients undergoing this staged Wise-pattern procedure.
Mastectomy Flap Thickness
The balance of local recurrence versus flap necrosis lives between a line that
runs at a variable distance between the skin and the superficial breast fascia.
This thin wispy layer may be difficult to localize and has been reported to be
absent in 44% of patients (41). Studies have shown a distance between 0.8
and 1 cm from the dermis is a safe subcutaneous plane to minimize vascular
injury, but the assigned plane may not uniformly meet the needs of the breast
surgeon to maximize breast tissue extirpation (22,23). All forms of
mastectomy are incomplete in the total extirpation of the breast gland with
retention of residual breast tissue being variable, but prevalent. Estimating
how much residual breast tissue remains after mastectomy is debatable, but
has been reported as high as 5% to 15% of the total weight of breast tissue
(42).
Recommendations to achieve oncologic resection and flap viability balance
include uniform flap thickness and a dissection plane within 1 cm of dermis.
There is no correlation to thickness of skin flaps with BMI or weight (22).
Generally, the balance of minimizing residual breast tissue and maximize
perfusion leads to a mastectomy dissection plane that should be closer to the
dermis in the central portion of the breast and proceed to a thicker distance as
the chest wall is approached (43).
Tumescent Technique Mastectomy
The use of a tumescent solution to minimize blood loss and facilitate
dissection is well documented. Tumescent solutions routinely contain the
potent vasoconstrictor of epinephrine. The concern when using tumescent for
mastectomy is the impact of vasoconstriction on skin flaps that might
normally be at risk for hypoperfusion and the potential to overestimate the
dissection distance from the dermis resulting in skin necrosis. A meta-
analysis on the use of tumescent technique revealed significantly higher rates
of major and minor skin necrosis (24). The authors concluded that the use of
tumescent technique does have described benefits, but its use in patients with
higher inherent risk factors for MFN should be approached with caution (24).
Reconstruction Timing and Type
Patients undergoing immediate reconstruction regardless of reconstruction
type, have higher rates of flap necrosis than patients undergoing delayed
reconstruction (12). When evaluating the impact of reconstruction type on
nipple or flap necrosis, both direct-to-implant and autologous-based
reconstructions had significantly higher rates of necrosis compared to staged
reconstruction (25).
Mastectomy stresses the vascular supply to skin and nipple when spared.
The weight of the reconstruction modality could result in skin flaps with
struggling perfusion being pushed to the point of vascular embarrassment and
flap necrosis. Breast reconstruction with an adjustable tissue expander allows
the plastic surgeon to mitigate the additional stress placed on the
hypovascular mastectomy skin flaps. Autologous reconstruction places a
greater initial stress on the skin flaps given larger flap volumes and has been
shown to increase the risk of MFN when compared to expander-based
reconstruction (25). Increasing implant volumes in direct-to-implant
reconstruction have also been shown to be a positive predictor of skin
necrosis (26); while the same increase risk of flap necrosis is observed with
larger operative tissue expander fill volumes (15,18,27).
Miscellaneous
Methylene blue dye is utilized as a tracer for sentinel node biopsy and has
been shown to increase the risk of MFN or NAC necrosis (44). The dye has
vasoconstrictive effects by inhibiting smooth muscle relaxation and
vasodilation (45). Excessive use or intradermal injection of methylene blue
dye has toxic effects on local tissue and can encourage necrosis.
The use of electrocautery versus scalpel dissection has been postulated to
increase thrombosis of the subdermal plexus and contribute to the ischemic
skin flap. A meta-analysis demonstrated that there was no difference between
the use of a scalpel versus electrocautery (46). In the same analysis, the use
of a harmonic scalpel was shown to decrease the risk of MFN. It makes
cutting and coagulation occur simultaneously at low temperatures resulting in
less thermal injuries compared to electrocautery. The use of harmonic scalpel
was shown to decrease other complications, without increasing operative
time (46).
OPERATIVE ASSESSMENT
The clinical assessment of skin flaps relies on parameters such as skin color,
capillary refill, temperature, and dermal bleeding. While the subjective
evaluation of skin flap viability is a great adjunct in minimizing flap necrosis,
the specificity has been reported at 10% to 30% (47). The continued high
reported rates of MFN and NAC necrosis reflects the limitations of subjective
clinical assessment and highlights the needs for technology to provide
additional intraoperative assessment. The potential use of technology to
evaluate and guide treatment of skin flap viability would yield an increased
benefit in patient experience, decreasing morbidity, and healthcare
expenditures. Technology that appraises skin flap viability include Wood
lamp fluorescein dye angiography (FA) and laser-assisted indocyanine green
angiography (ICG).
Fluorescein Angiography
FA has been utilized as a tool for assessing skin flap perfusion since the
1970s (48). The technique utilizes a one-time dose of 10 mg/kg intravenous
fluorescein and a Wood lamp to visualize the dye through the skin
vasculature (48). Advantages of FA is the technology is readily available and
affordable. Disadvantages include slow rate of the dye to intravascularly
distribute and clinical assessment that is subject to analysis variability. In
particular, fluorescein’s long half-life makes repeat injection for ongoing
analysis impractical.
FA has a high predictive value for flap survival, but underpredicts skin flap
necrosis (49). The use of FA has a reported sensitivity of 75% to 90% and
specificity of 30% to 71% (49).
Indocyanine Green Angiography
Indocyanine green is an intravenous dye that fluoresces and emits infrared
light when excited by an energy source (49). The use of ICG in evaluation of
perfusion has increased over time (50). One advantage of ICG is a short dye
half-life which allows for repeated injections and ongoing assessment of skin
flaps. Other advantages include deeper tissue depth vascular evaluation by
the laser light source to excite the ICG and evaluate flap viability (50).
Ongoing improvement in the software used to analyze perfusion will provide
better guidance for tissue resection (49). Disadvantages of this technology
include cost of machine and the injectable dye (50). The sensitivity and
specificity of ICG range from 38% to 100% and 68% to 91%, respectively
(49).
Currently, intraoperative evaluation of mastectomy flaps using ICG
provides better predictive accuracy than FA and clinical judgment, leading to
reduced rates of MFN (1). However, the use of ICG tends to overpredict
necrosis (49). Further complicating the matter, the published use of ICG
reveals heterogeneity regarding the hardware used for exciting the dye and
the software utilized for reporting skin perfusion. There is disagreement on
whether absolute or relative perfusion units should be the standard to guide
surgeons in skin flap resection (49). For the user of this technology, it is
important to understand that both ICG and FA have been shown to
overpredict potential areas of necrosis although ICG has higher specificity
and positive and negative predictive values (51). Clinically, FA overpredicted
actual and potential areas of necrosis by three times the amount of ICG
resulting in excision of large areas of viable skin (51).
Kanuri performed a retrospective review of over 700 patients who
underwent a mastectomy with prosthesis-based reconstruction and
intraoperative ICG skin flap assessment (52). The results demonstrated that
the routine use of ICG is not cost-effective as a preventive measure for all
patients. However, when ICG is selectively used on high-risk patients
(smokers, obesity, prior breast radiotherapy, macromastia), the cost savings
compared to returning the patient to the operating room for debridement can
be significant (52).
POSTOPERATIVE MANAGEMENT
The postoperative management of mastectomy or nipple necrosis should be
thought of as a continuum along a line anchored on one end by nonoperative
management and surgical treatment on the other end. Postoperative
management may travel along the continuum from one end to the other as the
wound is evaluated at a frequency dictated by changing needs of the injury.
The goal in the management of skin or nipple necrosis is to minimize domain
loss, reduce impact on timing of any adjuvant therapy, and communication
strategy to understand the patient’s expectations while providing reassurance
without blame.
Nonoperative Management
Nonoperative management remains the first action for MFN and NAC
necrosis following mastectomy for all patients. The majority of nonoperative
management involves frequent office visits for wound evaluation and patient
reassurance (Fig. 60-2). In expander-based reconstruction, removing saline,
holding off on expansion, and removal of seroma may minimize tension on
the compromised blood supply.
FIGURE 60-2 A: A 38-year-old female with stage IA right breast cancer, two weeks
after bilateral NSM and prepectoral air-filled expander placement (SKIN Score B3
and C3). B: Three-week postoperative follow-up managed nonoperatively. C: Four
weeks postoperatively with continued nonoperative management and healing
progression.
FIGURE 60-3 A: A 42-year-old patient with stage I left breast cancer patient 2 weeks
after bilateral NSM and air-filled prepectoral expander with full-thickness right skin
flap and NAC necrosis (SKIN Score D3 and C3, respectively) and partial-thickness
left skin flap and NAC necrosis (both with a SKIN score of C3). B: Four weeks
postoperatively with left breast improvement of partial-thickness injury and eschar
of right breast requiring surgical debridement, removal of expander, and skin
closure. C: Three weeks after replacement of right expander, expansion and
exchange to silicone implants bilaterally.

Incisional negative pressure wound therapy minimizes complications by


increasing tissue oxygenation through angiogenesis and decreases tension on
the wound closure (53). The routine use of negative pressure therapy on
patients undergoing immediate expander-based reconstruction demonstrated
a significant decrease in MFN (53). Recently, Gabriel showed that the routine
use of negative pressure therapy was not only associated with decrease in
MFN, but compared to patients in the control group, there was a cost savings
when compared to the surgical treatment of necrosis (54).
Nitroglycerin ointment is a potent topical vasodilator that increases local
blood flow to the skin (2). In a randomized controlled trial, the use of 45 mg
of topical nitroglycerin ointment applied to the skin flap decreased the rate of
MFN by half (1). According to the authors, a benefit was seen in 1 of every
5.4 patients treated. Nitroglycerin ointment is a simple, affordable, and
readily available opportunity to minimize MFN/NAC necrosis.
Although published case reports exist on the successful use of hyperbaric
oxygen as a treatment for necrosis (55), a retrospective review found no
significant differences between treatment groups (56).
Operative Management
The management of necrosis remains controversial. Some surgeons might
advocate an aggressive approach with an early return to the operating room
and excision of necrotic skin with direct closure or adjacent tissue
rearrangement to obtain closure (Fig. 60-3). Proponents of early surgical
revision like the merits of an earlier closed wound, removal of unappealing
necrotic tissue, decreased concerns for infection due to devitalized skin, and
better coordination with adjuvant therapy initiation based on institutional
preferences. Early intervention can be difficult since the extent of MFN is
difficult to assess in the early postoperative period. In addition, often the
surrounding mastectomy skin is partially ischemic and intolerant of
additional surgery or closure under tension. Early unplanned return to the
operating room is often psychologically difficult for some patients and can
lead to patient dissatisfaction.
A benefit of autologous reconstruction over implant-based reconstruction
allows the plastic surgeon to bank donor-site skin when confronted with
concerns of MFN. Donor-site skin banking requires return to the operating
room to either debride necrotic native skin flap and/or deepithelialize the
buried skin. Another advantage of autologous reconstruction is the capacity
to skin graft the flap when there is necrosis.
CONCLUSION
MFN and NAC necrosis can cause significant morbidity: poor wound
healing, infection, unsightly cicatrix, adjuvant therapy delays, and
reoperation. The overall sequela is poor reconstructive result, decreased
patient satisfaction, increased patient anxiety, and greater expenditure of
healthcare dollars (57).
Necrosis may be partial or full thickness in nature. The application of the
SKIN score creates a reproducible metric to follow necrosis rates. Inherent
patient risk factors include a history of smoking, obesity, prior breast
radiation, breast cup size, specimen weight, patient age, hypertension, and
previous breast surgery. Many patient preoperative risk factors are not
modifiable in the time frame between diagnosis and surgery. When patients
are assessed as having a high risk of MFN, performing a mastectomy with
delayed reconstruction may minimize MFN and/or NAC necrosis, but also
deliver timely administration of adjuvant therapy.
Operative risk factors play an important role in avoiding necrosis.
Understanding the vascular anatomy of the breast and nipple is the first step
in maintaining adequate perfusion. During mastectomy dissection,
maintaining the perforators of the internal mammary artery and vein to
supply the segmental vasculature of the skin and the nipple is vital.
Other operative risk factors include balance of mastectomy skin flap
thickness for improved vascularity with oncologic plane, immediate versus
delayed reconstruction, and choice of reconstruction.
Operative assessment continues to be a field of great interest as devices
improve in detecting areas of skin at risk for postoperative MFN and NAC
necrosis. When used in high-risk patients, perfusion imagery can be a cost-
effective method to minimize necrosis. The evaluation of mastectomy flap
perfusion by any method can be affected by vasoconstriction secondary to
patient or operative factors.
Management between operative versus nonoperative treatment modalities
should be decided on each individual case. Treatment should consider
surgeon preferences, requirement for adjuvant treatment, and type of
reconstruction chosen. The balance between an operation to facilitate wound
healing must be weighed against a long course of patient wound care.
Throughout all of this process, it is paramount that the patient remains
informed, their wishes are taken into consideration, blame is avoided and
timing limitations are respected due to adjuvant treatment deadlines.

REFERENCES

1. Abedi N, Ho AL, Knox A, et al. Predictors of mastectomy flap necrosis


in patients undergoing immediate breast reconstruction: a review of 718
patients. Ann Plast Surg 2016;76(6):629–634.
2. Gdalevitch P, Van Laeken N, Bahng S, et al. Effects of nitroglycerin
ointment on mastectomy flap necrosis in immediate breast
reconstruction: a randomized controlled trial. Plast Reconstr Surg
2015;135(6):1530–1539.
3. Matsen CB, Mehrara B, Eaton A, et al. Skin flap necrosis after
mastectomy with reconstruction: a prospective study. Ann Surg Oncol
2016;23(1):257–264.
4. Fisher B, Anderson S, Bryant J, et al. Twenty-year follow-up of a
randomized trial comparing total mastectomy, lumpectomy, and
lumpectomy plus irradiation for the treatment of invasive breast cancer.
N Engl J Med 2002;347(16):1233–1241.
5. Colwell AS, Tessler O, Lin AM, et al. Breast reconstruction following
nipple-sparing mastectomy: predictors of complications, reconstruction
outcomes, and 5-year trends. Plast Reconstr Surg 2014;133(3):496–506.
6. Alperovich M, Choi M, Frey JD, et al. Nipple-sparing mastectomy in
patients with prior breast irradiation: are patients at higher risk for
reconstructive complications? Plast Reconstr Surg 2014;134(2):202e–
206e.
7. Padubidri AN, Yetman R, Browne E, et al. Complications of
postmastectomy breast reconstructions in smokers, ex-smokers, and
nonsmokers. Plast Reconstr Surg 2001;107(2):342–349; discussion
350–351.
8. Berry T, Brooks S, Sydow N, et al. Complication rates of radiation on
tissue expander and autologous tissue breast reconstruction. Ann Surg
Oncol 2010;17 Suppl 3:202–210.
9. Fischer JP, Nelson JA, Kovach SJ, et al. Impact of obesity on outcomes
in breast reconstruction: analysis of 15,937 patients from the ACS-
NSQIP datasets. J Am Coll Surg 2013;217(4):656–664.
10. Hanwright PJ, Davila AA, Hirsch EM, et al. The differential effect of
BMI on prosthetic versus autogenous breast reconstruction: a
multivariate analysis of 12,986 patients. Breast Edinb Scotl
2013;22(5):938–945.
11. Cordeiro PG, McCarthy CM. A single surgeon’s 12-year experience
with tissue expander/implant breast reconstruction: part I. A prospective
analysis of early complications. Plast Reconstr Surg 2006;118(4):825–
831.
12. Alderman AK, Wilkins EG, Kim HM, et al. Complications in
postmastectomy breast reconstruction: two-year results of the Michigan
Breast Reconstruction Outcome Study. Plast Reconstr Surg
2002;109(7):2265–2274.
13. Hultman CS, Daiza S. Skin-sparing mastectomy flap complications after
breast reconstruction: review of incidence, management, and outcome.
Ann Plast Surg 2003;50(3):249–255; discussion 255.
14. Frey JD, Salibian AA, Karp NS, et al. The impact of mastectomy weight
on reconstructive trends and outcomes in nipple-sparing mastectomy:
progressively greater complications with larger breast size. Plast
Reconstr Surg 2018;141(6):795e–804e.
15. Mlodinow AS, Fine NA, Khavanin N, et al. Risk factors for mastectomy
flap necrosis following immediate tissue expander breast reconstruction.
J Plast Surg Hand Surg 2014;48(5):322–326.
16. McCarthy CM, Mehrara BJ, Riedel E, et al. Predicting complications
following expander/implant breast reconstruction: an outcomes analysis
based on preoperative clinical risk. Plast Reconstr Surg
2008;121(6):1886–1892.
17. Gould DJ, Hunt KK, Liu J, et al. Impact of surgical techniques,
biomaterials, and patient variables on rate of nipple necrosis after
nipple-sparing mastectomy. Plast Reconstr Surg 2013;132(3):330e–
338e.
18. Khavanin N, Jordan S, Lovecchio F, et al. Synergistic interactions with a
high intraoperative expander fill volume increase the risk for
mastectomy flap necrosis. J Breast Cancer 2013;16(4):426–431.
19. Frey JD, Salibian AA, Levine JP, et al. Incision choices in nipple-
sparing mastectomy: a comparative analysis of outcomes and evolution
of a clinical algorithm. Plast Reconstr Surg 2018;142(6):826e–835e.
20. Davies K, Allan L, Roblin P, et al. Factors affecting post-operative
complications following skin sparing mastectomy with immediate breast
reconstruction. Breast 2011;20(1):21–25.
21. Liu TS, Crisera CA, Festekjian JH, et al. Staged Wise-pattern skin
excision for reconstruction of the large and ptotic breast. Plast Reconstr
Surg 2010;126(6):1831–1839.
22. Larson DL, Basir Z, Bruce T. Is oncologic safety compatible with a
predictably viable mastectomy skin flap? Plast Reconstr Surg
2011;127(1):27–33.
23. Frey JD, Salibian AA, Choi M, et al. Mastectomy flap thickness and
complications in nipple-sparing mastectomy: objective evaluation using
magnetic resonance imaging. Plast Reconstr Surg Glob Open
2017;5(8):e1439.
24. Siotos C, Aston JW, Euhus DM, et al. The use of tumescent technique in
mastectomy and related complications: a meta-analysis. Plast Reconstr
Surg 2019;143(1):39–48.
25. Frey JD, Choi M, Salibian AA, et al. Comparison of outcomes with
tissue expander, immediate implant, and autologous breast
reconstruction in greater than 1000 nipple-sparing mastectomies. Plast
Reconstr Surg 2017;139(6):1300–1310.
26. Choi M, Frey JD, Alperovich M, et al. “Breast in a day”: examining
single-stage immediate, permanent implant reconstruction in nipple-
sparing mastectomy. Plast Reconstr Surg 2016;138(2):184e–191e.
27. Sue GR, Long C, Lee GK. Management of mastectomy skin necrosis in
implant based breast reconstruction. Ann Plast Surg 2017;78(5 Suppl
4):S208–S211.
28. Lemaine V, Hoskin TL, Farley DR, et al. Introducing the SKIN score: a
validated scoring system to assess severity of mastectomy skin flap
necrosis. Ann Surg Oncol 2015;22(9):2925–2932.
29. Rau AS, Reinikovaite V, Schmidt EP, et al. Electronic cigarettes are as
toxic to skin flap survival as tobacco cigarettes. Ann Plast Surg
2017;79(1):86–91.
30. Riefkohl R, Wolfe JA, Cox EB, et al. Association between cutaneous
occlusive vascular disease, cigarette smoking, and skin slough after
rhytidectomy. Plast Reconstr Surg 1986;77(4):592–595.
31. Sørensen LT. Wound healing and infection in surgery: the
pathophysiological impact of smoking, smoking cessation, and nicotine
replacement therapy: a systematic review. Ann Surg 2012;255(6):1069–
1079.
32. Raja M, Garg A, Yadav P, et al. Diagnostic methods for detection of
cotinine level in tobacco users: a review. J Clin Diagn Res JCDR
2016;10(3):ZE04–ZE06.
33. Benowitz NL, Hukkanen J, Jacob P. Nicotine chemistry, metabolism,
kinetics and biomarkers. Handb Exp Pharmacol 2009;(192):29–60.
34. Markman B. Anatomy and physiology of adipose tissue. Clin Plast Surg
1989;16(2):235–244.
35. Iwahira Y, Nagase T, Nakagami G, et al. Histopathological comparisons
of irradiated and non-irradiated breast skin from the same individuals. J
Plast Reconstr Aesthetic Surg 2012;65(11):1496–1505.
36. Gerstein AD, Phillips TJ, Rogers GS, et al. Wound healing and aging.
Dermatol Clin 1993;11(4):749–757.
37. Chang EI, Vaca L, DaLio AL, et al. Assessment of advanced age as a
risk factor in microvascular breast reconstruction. Ann Plast Surg
2011;67(3):255–259.
38. Frederick MJ, Lin AM, Neuman R, et al. Nipple-sparing mastectomy in
patients with previous breast surgery: comparative analysis of 775
immediate breast reconstructions. Plast Reconstr Surg
2015;135(6):954e–962e.
39. van Deventer PV, Graewe FR. The blood supply of the breast revisited.
Plast Reconstr Surg 2016;137(5):1388–1397.
40. Radovanovic Z, Ranisavljevic M, Radovanovic D, et al. Nipple-sparing
mastectomy with primary implant reconstruction: surgical and
oncological outcome of 435 breast cancer patients. Breast Care Basel
Switz 2018;13(5):373–378.
41. Beer GM, Varga Z, Budi S, et al. Incidence of the superficial fascia and
its relevance in skin-sparing mastectomy. Cancer 2002;94(6):1619–
1625.
42. Griepsma M, de Roy van Zuidewijn DBW, Grond AJK, et al. Residual
breast tissue after mastectomy: how often and where is it located? Ann
Surg Oncol 2014;21(4):1260–1266.
43. Giannotti DG, Hanna SA, Cerri GG, et al. Analysis of skin flap
thickness and residual breast tissue after mastectomy. Int J Radiat Oncol
Biol Phys 2018;102(1):82–91.
44. Lee JH, Chang CH, Park CH, et al. Methylene blue dye-induced skin
necrosis in immediate breast reconstruction: evaluation and
management. Arch Plast Surg 2014;41(3):258–263.
45. Stradling B, Aranha G, Gabram S. Adverse skin lesions after methylene
blue injections for sentinel lymph node localization. Am J Surg
2002;184(4):350–352.
46. Huang J, Yu Y, Wei C, et al. Harmonic scalpel versus electrocautery
dissection in modified radical mastectomy for breast cancer: a meta-
analysis. PloS One 2015;10(11):e0142271.
47. Moyer HR, Losken A. Predicting mastectomy skin flap necrosis with
indocyanine green angiography: the gray area defined. Plast Reconstr
Surg 2012;129(5):1043–1048.
48. Singer R, Lewis CM, Franklin JD, et al. Fluorescein test for prediction
of flap viability during breast reconstructions. Plast Reconstr Surg
1978;61(3):371–375.
49. Jeon FHK, Varghese J, Griffin M, et al. Systematic review of
methodologies used to assess mastectomy flap viability. BJS Open
2018;2(4):175–184.
50. Chattha A, Bucknor A, Chen AD, et al. Indocyanine green angiography
use in breast reconstruction: a national analysis of outcomes and cost in
110,320 patients. Plast Reconstr Surg 2018;141(4):825–832.
51. Phillips BT, Lanier ST, Conkling N, et al. Intraoperative perfusion
techniques can accurately predict mastectomy skin flap necrosis in
breast reconstruction: results of a prospective trial. Plast Reconstr Surg
2012;129(5):778e–788e.
52. Kanuri A, Liu AS, Guo L. Whom should we SPY? A cost analysis of
laser-assisted indocyanine green angiography in prevention of
mastectomy skin flap necrosis during prosthesis-based breast
reconstruction. Plast Reconstr Surg 2014;133(4):448e–454e.
53. Kim DY, Park SJ, Bang SI, et al. Does the use of incisional negative-
pressure wound therapy prevent mastectomy flap necrosis in immediate
expander-based breast reconstruction? Plast Reconstr Surg
2016;138(3):558–566.
54. Gabriel A, Maxwell GP. Economic analysis based on the use of closed-
incision negative-pressure therapy after postoperative breast
reconstruction. Plast Reconstr Surg 2019;143(1S Management of
Surgical Incisions Utilizing Closed-Incision Negative-Pressure
Therapy):36S–40S.
55. Fredman R, Wise I, Friedman T, et al. Skin-sparing mastectomy flap
ischemia salvage using urgent hyperbaric chamber oxygen therapy: a
case report. Undersea Hyperb Med 2014;41(2):145–147.
56. Shuck J, O’Kelly N, Endara M, et al. A critical look at the effect of
hyperbaric oxygen on the ischemic nipple following nipple sparing
mastectomy and implant based reconstruction: a case series. Gland Surg
2017;6(6):659–665.
57. Yalanis GC, Nag S, Georgek JR, et al. Mastectomy weight and tissue
expander volume predict necrosis and increased costs associated with
breast reconstruction. Plast Reconstr Surg Glob Open 2015;3(7):e450.
CHAPTER 61

Management of the Exposed Implant


MEGAN FRACOL | JOHN Y. S. KIM
HISTORY
This chapter covers the exposed implant in breast reconstruction. Specific
attention to the incidence, associated risk factors, radiation as a contributor,
prediction modeling for reconstructive failure, management algorithms, and
case examples which further delve into reconstructive options will be
highlighted.
IMPLANT EXPOSURE: INCIDENCE AND RISK FACTORS
Implant exposure after breast reconstruction has been reported to occur
anywhere from 0.25% to 8.3% of the time (1–3). Looking at the timeline of
implant exposure, less than 20% occur within the first 30 days after surgery
while over half occur 6 months or more after surgery. In fact, over 40% occur
greater than 1 year out from surgery (4). It is important to note that little
literature exists on the mechanisms and etiology of implant exposure, with
reports mostly focused on management of the infected and/or exposed
implant. Implant exposure, in reality, often occurs in conjunction with other
complications such as wound dehiscence, mastectomy skin flap necrosis, and
infection. Thus this section reviews these mitigating factors that contribute to
and complicate the exposed implant.
Wound dehiscence, in particular, contributes directly to implant exposure
and was found to occur 6% of the time in the Tracking Operations and
Outcomes for Plastic Surgeons (TOPS) database and 7.1% of the time in our
own intrainstitutional prospectively maintained database; however, wound
dehiscence is a multifactorial problem and incidence can vary greatly based
on patient characteristics (4,5). Utilizing the Breast Reconstruction Risk
Assessment Score calculator (www.brascore.org), the risk of wound
dehiscence in the first year after tissue expander reconstruction can range
from 2.6% for the healthiest of patients to 58.3% for the sickest of patients.
Thus, much of the risk for wound dehiscence and subsequent implant
exposure largely falls on patient-specific risk factors that are out of the
surgeon’s control.
Mastectomy flap necrosis is one of the most common complications in
breast reconstruction and this, too, directly contributes to wound dehiscence
and implant exposure, occurring 12.4% of the time in our own
intrainstitutional prospectively maintained database (4). This is consistent
with reports in the literature which indicate flap necrosis occurs anywhere
from 5% to 30% of the time (6). The range in reported rates may be due to
variations in how mastectomy skin flap is defined— particularly partial
versus full thickness (6). Thus, partial-thickness skin flap necrosis may not
always lead to implant exposure and the rate of mastectomy skin flap
necrosis may overestimate the rate of implant exposure. Mastectomy flap
necrosis is more common in direct-to-implant reconstructions, reported in a
recent meta-analysis by Basta et al. (7). Based on several retrospective
reviews, risk factors for skin flap necrosis include obesity (BMI >30),
smoking, preoperative radiation, increasing age, use of surgical tumescence,
large expander fill volumes, larger mastectomy weight, and diabetes (8–10).
A prospective series measuring mastectomy skin flap necrosis rates found 8%
of patients experienced mild necrosis, 1% moderate, and 5% severe, with the
majority of the severe cases still not healed by 8 weeks postoperatively (11).
Risk factors for necrosis in this series included nipple-sparing mastectomy,
time from incision to specimen removal, the use of sharp dissection, and prior
breast reduction surgery. At our own institution, we have found tissue
expander fill volume alone does not increase risk of mastectomy skin flap
necrosis; however, it does act synergistically with other factors to increase
flap necrosis: tumescence, hypertension, obesity, and older age (12).
Infection is a separate entity that nevertheless frequently occurs in
conjunction with implant exposure and affects the rate of implant salvage.
Infection rates in implant-based breast reconstruction have been reported
anywhere from 1% to 35% of the time (13). In a report by Spear et al., 94%
of implants with only mild infection were salvaged compared to 28% of
implants with severe infection. In this same group, over 90% of implants with
threatened or actual exposure were able to be salvaged when not associated
with severe infection (14). Thus, the presence of infection is an important
factor to consider in determining subsequent management strategies. The
type of implant may impact whether infection develops when exposed to the
atmosphere. In a pig study by Jacombs et al., textured implants had 11-, 43-,
and 72-fold higher bacterial counts at 2, 6, and 24 hours after exposure to
Staphylococcus epidermidis, respectively, than their smooth implant
counterparts (15).
RADIATION THERAPY: AN ETIOLOGIC CONTRIBUTOR TO
IMPLANT EXPOSURE
Radiation damage impairs wound healing on both a micro- and macroscopic
level. Microscopically, reactive oxygen species (ROS) are primarily
responsible for cell damage—both in tumor cells and healthy tissue (16).
Because tumor cells often live in a hypoxic environment, these ROS can
cause greater damage to healthy cells. ROS contribute to DNA damage and
activate DNA repair mechanisms. Cells most susceptible to this DNA
radiation-induced damage are those in the M-phase, which is why radiation
tends to target rapidly dividing cancer cells; however as stated, healthy cells
are not immune to this damage. In addition to ROS, radiation also activates a
prothrombotic response via gene activation of plasminogen activator
inhibitor-1 (PAI-1) and a proinflammatory state via activation of nuclear
factor kappa beta (NF-KB), contributing to small vessel disease and poor
blood flow to irradiated tissues (17). On a more macroscopic level, studies
have shown irradiated vessels demonstrate increased intimal–medial
thickness and increased arterial stiffness (18,19). Thus, a convergence of
factors both microscopic and macroscopic results in impaired blood flow to
radiated tissues. Poor blood flow in turn contributes to higher rates of wound
dehiscence, infection, flap necrosis, and scarring.
Since radiotherapy reduces skin flap blood flow and increases tissue
fibrosis with enhanced inflammation, the radiation factor in turn increases
risk for any complication in breast reconstruction, with rates over 40%
(16,20,21). Implant extrusion rates in radiated patients approach 15% (21).
Ultimately, patients can be divided into two groups: those with prior radiation
history in the setting of lumpectomy now requiring salvage mastectomy and
reconstruction, and those without prior radiation who will now need
postmastectomy radiation therapy (PMRT). Radiation delivered in the distant
past versus PMRT can have varying effects on the reconstructive outcome.
Several studies have looked at how the timing of radiation therapy impacts
outcomes. Sbitany et al. found patients with premastectomy radiation therapy
had higher rates of wound breakdown than those with PMRT. However, they
found no difference in nipple areolar necrosis rates between timing of
radiation, or even between radiated and nonirradiated breasts (22). Peled et al.
found that increasing the time between PMRT and second-stage expander to
implant exchange to 6 months or greater significantly reduced the failure rate
from 22.4% to 7.7% (23). However, in a systematic review by Momoh et al.,
no difference in minor or major complication rates was found between
breasts with prereconstruction versus postreconstruction irradiation.
Similarly, the reconstruction failure rates were nearly identical at 19% and
20%, respectively (24).
For patients receiving PMRT, most undergo radiation therapy while the
tissue expander is in place, prior to final implant placement. For patients who
received PMRT, Ascherman et al. reported an 18.5% rate of complications
requiring implant removal or replacement compared to 4.2% in breasts
without PMRT (25). By changing the timing of reconstruction, such that
tissue expansion was complete and second-stage expander-to-implant
exchange was performed prior to administration of PMRT, Cordeiro et al.
reported a lower rate of complications requiring implant removal or
replacement at 11.1% (26). In a single study, Nava et al. found patients
irradiated with the tissue expander in place had significantly higher rates of
reconstructive failure (40%) compared to patients irradiated with the implant
in place (6.4%) (27). Thus, it may be possible to reduce acute wound healing
complications in radiated patients by completing the reconstruction prior to
radiation delivery, although this has been associated with worse aesthetic
outcomes.
PREDICTION MODELING FOR EXPOSURE: PROGRESSION TO
RECONSTRUCTIVE FAILURE
We have performed an intrainstitutional analysis of the timing and sequence
of complications that leads to reconstructive failure after implant-based breast
reconstruction. Our cohort included 1,860 reconstructed breasts and we
focused on four common postoperative complications: impaired wound
healing/exposure, seroma, infection, and reconstructive failure. A total of
35.4% of breasts experienced more than one complication and all
complications increased the risk for reconstructive failure. Looking at the
relationship between complications, seroma increased the risk for subsequent
infection (RR = 6.52, p < 0.001) and necrosis (RR = 1.97, p < 0.001), while
necrosis increased the risk of subsequent exposure (RR = 3.56, p < 0.001).
Four common pathways to reconstructive failure were identified, two of
which included exposure as part of the pathway (Fig. 61-1). These were
exposure followed directly by reconstructive failure and exposure followed
by infection followed by reconstructive failure. Notably, exposure
complicated by subsequent infection significantly shortened the time to
reconstructive failure, with an average 6.5 days between exposure and
explantation, compared to exposure alone which had an average 22 days until
explantation or infection alone which had an average 18.5 days until
explantation.

FIGURE 61-1 Four major pathways to reconstructive failure identified at our


institution.
MANAGEMENT OF THE EXPOSED IMPLANT
In a case series presented by Bennett et al., the success rate of attempted
implant salvage (45%) was roughly equivalent to the rate that explanted
patients went on to pursue delayed reconstruction (43%) (13). It should also
be noted that the majority of patients who undergo explantation do not go on
to delayed reconstruction of any kind, which unfortunately is considered a
reconstructive failure.
Because of the high risk for complications in patients who have previously
received radiation therapy, most surgeons now advocate for prospective flap-
based reconstruction in this cohort. For patients in whom postmastectomy
radiation may be necessary but is dependent on pathology results, Kronowitz
et al. and Fine et al. have advocated for immediate-delayed reconstruction,
which involves insertion of a temporary expander with the knowledge that
the patient may have to convert to flap-based reconstruction if radiation is
deemed necessary (28–31). While these maneuvers may mitigate some cases
of implant exposure, this complication nevertheless occurs in a subset of
patients and the following section provides clinical case examples with
management strategies.
When determining the management strategy for an exposed implant, there
should be three considerations: (1) Is the breast irradiated? (2) Is the exposure
associated with a frank and severe infection? (3) Is the tissue healthy with
minimal tension (Fig. 61-2)? These three questions will determine whether
attempted implant salvage is reasonable or not. Looking at the algorithm in
Figure 61-2, the first step is determining whether the exposed implant has
been radiated. If the answer is yes, then the location of the exposure and the
quality of the tissue should be evaluated. In instances where the exposure is
at the periphery of the radiated field (for instance in an IMF incision that has
dehisced) and there is healthy, pliable tissue available outside the field of
radiation, a local flap such as a thoracoepigastric flap can be entertained.
Most of the time, however, dehiscences occur in the central portion of
irradiated tissue where compliance is low and healthy local tissue is
unavailable. In these cases, healthy distant tissue is necessary, often from
either a pedicled latissimus flap or a free abdominal-based flap.
FIGURE 61-2 Algorithm for management of the exposed implant.

If the breast is not irradiated, then the next consideration is whether there is
severe infection present. Severe infection includes the presence of purulent
drainage or systemic signs of infection such as fever or elevated white blood
cell count. In such cases, the patient should be taken to the operating room
for a formal washout, implant removal, and delayed reinsertion. Due to skin
contracture that occurs with temporary removal of the implant, the majority
of these cases require a flap reconstruction to augment the soft tissue
envelope for later implant coverage.
Sometimes there will be evidence of mild infection, such as a mild
overlying cellulitis, but no purulent drainage and no systemic signs of
infection. Other authors have shown that cases of mild infection can
sometimes be salvaged (14). In these instances, multiple options exist for
potential implant salvage. The implant can be downsized, which takes tension
off the closure and improves likelihood of salvage, with primary closure (13).
Alternatively, additional healthy tissue can be brought in, such as from a
latissimus flap, with reinsertion of a clean implant. Because the infection is
mild and does not involve intrapocket evidence of infection with drainage,
the delayed reconstruction can be avoided, allowing the patient to retain their
breast mound.
In the most ideal situation, the breast will not be irradiated and there will
be no signs of infection, either mild or severe. In these cases, the skin and
tissue quality simply needs to be evaluated. If tissue quality is high, primary
closure can be done in the office or the implant can be downsized in the
operating room with primary closure, again to increase the likelihood of
successful salvage. If tissue quality is poor, significant tension exists, or the
patient does not want to downsize, then additional healthy tissue in the form
of a flap can be brought in to augment the soft tissue envelope with
reinsertion of a clean implant. Importantly, the implant does not always have
to be explanted; in instances of healthy tissue with isolated exposure, the
implant can often be salvaged.

CASES

CASE 1

Isolated implant exposure without radiation and without infection.


This patient is a 33-year-old female who was diagnosed with left breast
DCIS for which she underwent bilateral mastectomy with tissue expander
reconstruction. Genetic work-up was negative. Prior to second-stage
breast reconstruction, she developed erosion with extrusion of one of the
expander tabs in the lower outer quadrant of the left breast (Fig. 61-3A).
There was no redness, purulence, or infectious symptoms. Because she
had no history of radiation and no signs of infection, it was decided to
manage this conservatively by proceeding directly from expander to
implant exchange with coverage of the defect utilizing an internal
capsular flap and primary closure of the external defect. A superiorly
based capsular flap was designed and elevated off the chest wall (Fig. 61-
3B, Video 61-1). This was rotated and inset into the internal defect. After
this, the skin surrounding the external defect was trimmed and repaired
primarily. A new implant was placed and the remaining incisions were
closed.
While Gargano et al. first described capsular flaps as a technique for
masking implant contour deformities, they subsequently added
descriptions of capsular flap use in cases of implant exposure to
supplement the soft tissue envelope (32,33). They used these flaps in both
irradiated and nonirradiated tissues. The benefit in capsular flaps lies in
their versatility and ability to be designed from virtually any direction,
including off the chest wall or from the posterior side of the mastectomy
skin flap. They have been deemed viable as random pattern and axial
pattern flaps in animal models and this seems to hold true in the clinical
case series presented by this group (34,35).

FIGURE 61-3 A: This patient had extrusion of one of the tissue expander
tabs through the lower outer breast pocket without evidence of infection. B:
A capsular flap was designed, superiorly based, to rotate over the fistula tract
and provide durable soft tissue coverage.

CASE 2

Radiated, exposed implant without infection.


This patient is a 48-year-old female diagnosed with left breast invasive
ductal carcinoma for which she underwent bilateral skin-sparing
mastectomy followed by adjuvant chemotherapy and left-sided radiation.
After completing radiation therapy, she developed wound dehiscence of
the left breast mastectomy scar with implant exposure (Fig. 61-4A).
There were no signs of frank infection (no erythema, purulent drainage,
or systemic symptoms). After evaluation of local tissues which
demonstrated reasonable mobility with minimal fibrosis, and upon further
discussion with the patient, it was decided to attempt local flap closure of
the wound. Accordingly, a medial-based thoracoepigastric flap was
planned. After implant removal, washout of the breast pocket, and
multiple releasing capsulotomies, the radiated mastectomy incision was
trimmed back to healthier tissue. The medial-based thoracoepigastric flap
was then incised, elevated, and rotated into the defect. Given concern for
chronic biofilm formation on the textured implant, a smooth implant was
used instead for replacement. At her 1-month follow-up, the patient
demonstrated healing of the incision (Fig. 61-4B).
While most radiated exposed implants require pedicled or free flaps for
coverage to promote healing, occasionally local tissues that are outside
the zone of radiation can be used if assessment of these local tissues
demonstrates minimal fibrosis and healthy vascularity, such as was the
case for this patient. In addition, some patients may request options that
do not involve sacrifice of a muscular donor site. The thoracoepigastric
flap is one such described option. It can be based medially or laterally,
depending on what design works best for the defect. Medial-based flaps
are supplied by the superior epigastric vessels while laterally based flaps
are supplied by intercostal perforators and both are segmentally perfused
(36–38). In general, thoracoepigastric flaps are designed as transposition
flaps and perfusion can be enhanced by widening the base medially or
including multiple intercostal levels laterally. When medially based,
perfusion is tenuous beyond the midaxillary line. When laterally based,
perfusion is tenuous beyond the midline (39).
A similar local option is the lateral chest skin, which can oftentimes be
redundant particularly after mastectomy. While this flap can require
tedious microdissection and was originally described for
autoaugmentation in the massive weight loss patient, Hakakian et al. have
described a simplified approach to this flap that is adequate for the breast
reconstruction patient (40–44). In their simplified version, the flap
pedicle is designed with a width of 6 to 8 cm extending from the
midaxillary line to the anterior border of the latissimus dorsi and lying at
the level of the inframammary crease. This pedicle ensures you have
intercostal perforators to your lateral skin fold flap, provided that the
superior extent of the flap does not go above the level of the mastectomy
incision (44).
The reverse abdominoplasty flap is a third local, but rarely described,
option for breast reconstruction. This flap was originally described by
Grazer, but like the lateral chest flap, has also previously been described
for use in the massive weight loss patient (45–47). Like the
thoracoepigastric flap, the blood supply to this flap comes from three
main sources—the intercostals, and inferior and superior epigastrics (48).
The utility in this flap comes from its robust blood supply and ability to
advance the upper abdominal skin onto the breast, thereby taking tension
off the closure.

FIGURE 61-4 A: This patient had an exposed textured implant at the site of
mastectomy incision dehiscence in a radiated field. A thoracoepigastric flap
was designed to bring healthy tissue into the wound bed after extensive
excision of the radiated scar tissue. B: The patient at her 1-month
postoperative visit demonstrating healing of the incision.

CASE 3
Bilateral implant exposure, left side failed implant salvage.
This patient is a 36-year-old female who was diagnosed with
multicentric right breast ductal carcinoma in situ (DCIS). She elected for
bilateral mastectomy with tissue expander reconstruction. In the first
month postoperatively she developed wound dehiscence at the bilateral
mastectomy scars with tissue expander exposure (Fig. 61-5A). Given
lack of radiation and no infectious signs, these were irrigated and closed
primarily. The right side went on to heal but the left side had a
reexposure 1 month later (Fig. 61-5B). Thus, given contraction of local
tissues and excess tension, the patient elected latissimus flap
reconstruction with tissue expander reinsertion (Fig. 61-5C).
The latissimus flap was first described in 1906 by Tansini, but did not
become popularized until the 1970s (49–51). In present day, it is often
used prophylactically in irradiated beds to prevent radiation-related
complications in prosthetic breast reconstruction (52). It also remains an
important bailout option for patients who have failed prosthetic breast
reconstruction and can be performed alone, in conjunction with fat
injection or in conjunction with an implant (53). Variations on the
latissimus have been described, including vertical inset of the skin paddle
to expand both the lower pole and central projection (54).

FIGURE 61-5 A: Preoperative photo of 36-year-old patient prior to bilateral


mastectomy for multicentric DCIS. B: Bilateral tissue expander exposure due
to mastectomy scar wound dehiscence. C: The right tissue expander was
salvaged by irrigation and primary closure, however the left side went on to
reexposure and thus latissimus flap reconstruction with tissue expander
reinsertion was performed.
CONCLUSION
Implant exposure is a complication in prosthetic breast reconstruction that
often occurs in conjunction with other complications (namely, mastectomy
skin flap necrosis and infection). Over half of patients who undergo
explantation will ultimately never complete reconstruction, thus identifying
at-risk patients can help to prevent reconstructive failures. In managing the
exposed implant, certain factors such as radiation history and presence of
infection will impact the likelihood of successful salvage. Fortunately, there
are a multitude of techniques available to promote successful healing and
maintain a reasonable aesthetic outcome even in cases of delayed reinsertion.

REFERENCES

1. Pusic AL, Cordeiro PG. An accelerated approach to tissue expansion for


breast reconstruction: experience with intraoperative and rapid
postoperative expansion in 370 reconstructions. Plast Reconstr Surg
2003;111(6):1871–1875.
2. Disa JJ, Ad-El DD, Cohen SM, et al. The premature removal of tissue
expanders in breast reconstruction. Plast Reconstr Surg
1999;104(6):1662–1665.
3. Slavin SA, Colen SR. Sixty consecutive breast reconstructions with the
inflatable expander: a critical appraisal. Plast Reconstr Surg
1990;86(5):910–919.
4. Hansen N, Espino S, Blough JT, et al. Evaluating mastectomy skin flap
necrosis in the extended breast reconstruction risk assessment score for
1-year prediction of prosthetic reconstruction outcomes. J Am Coll Surg
2018;227(1):96–104.
5. Kim JY, Mlodinow AS, Khavanin N. Individualized risk of surgical
complications: an application of the breast reconstruction risk
assessment (BRA) score. Plast Reconstr Surg Glob Open
2015;3(5):e405.
6. Robertson SA, Jeevaratnam JA, Agrawal A, et al. Mastectomy skin flap
necrosis: challenges and solutions. Breast Cancer (Dove Med Press)
2017;9:141–152.
7. Basta MN, Gerety PA, Serletti JM, et al. A systematic review and head-
to-head meta-analysis of outcomes following direct-to-implant versus
conventional two-stage implant reconstruction. Plast Reconstr Surg
2015;136(6):1135–1144.
8. Mlodinow AS, Fine NA, Khavanin N, et al. Risk factors for mastectomy
flap necrosis following immediate tissue expander breast reconstruction.
J Plast Surg Hand Surg 2014;48(5):322–326.
9. Vargas CR, Koolen PG, Anderson KE, et al. Mastectomy skin necrosis
after microsurgical breast reconstruction. J Surg Res 2015;198(2):530–
534.
10. Abedi N, Ho AL, Knox A, et al. Predictors of mastectomy flap necrosis
in patients undergoing immediate breast reconstruction: a review of 718
patients. Ann Plast Surg 2016;76(6):629–634.
11. Matsen CB, Mehrara B, Eaton A, et al. Skin flap necrosis after
mastectomy with reconstruction: a prospective study. Ann Surg Oncol
2016;23(1):257–264.
12. Khavanin N, Jordan S, Lovecchio F, et al. Synergistic interactions with a
high intraoperative expander fill volume increase the risk for
mastectomy flap necrosis. J Breast Cancer 2013;16(4):426–431.
13. Bennett SP, Fitoussi AD, Berry MG, et al. Management of exposed,
infected implant-based breast reconstruction and strategies for salvage. J
Plast Reconstr Aesthet Surg 2011;64(10):1270–1277.
14. Spear SL, Howard MA, Boehmler JH, et al. The infected or exposed
breast implant: management and treatment strategies. Plast Reconstr
Surg 2004;113(6):1634–1644.
15. Jacombs A, Tahir S, Hu H, et al. In vitro and in vivo investigation of the
influence of implant surface on the formation of bacterial biofilm in
mammary implants. Plast Reconstr Surg 2014;133(4):471e–480e.
16. Hubenak JR, Zhang Q, Branch CD, et al. Mechanisms of injury to
normal tissue after radiotherapy: a review. Plast Reconstr Surg
2014;133(1):49e–56e.
17. Halle M, Ekstrom M, Farnebo F, et al. Endothelial activation with
prothrombotic response in irradiated microvascular recipient veins. J
Plast Reconstr Aesthet Surg 2010;63(11):1910–1916.
18. Faruolo M, Fiorentino A, Gallucci G, et al. Intimal-medial thickness and
carotid arteries lumen in irradiated patients for head and neck cancer:
preliminary data of an observational study. Clin Transl Oncol
2013;15(10):861–864.
19. Van Leeuwen-Segarceanu EM, Dorresteijn LD, Vogels OJ, et al.
Arterial stiffness is increased in Hodgkin lymphoma survivors treated
with radiotherapy. Leuk Lymphoma 2013;8(54):1734–1741.
20. Chen TA, Momeni A, Lee GK. Clinical outcomes in breast cancer
expander-implant reconstructive patients with radiation therapy. J Plast
Reconstr Aesthet Surg 2016;69(1):14–22.
21. Kronowitz SJ, Robb GL. Radiation therapy and breast reconstruction: a
critical review of the literature. Plast Reconstr Surg 2009;124(2):395–
408.
22. Sbitany H, Wang F, Saeed L, et al. Immediate implant-based breast
reconstruction following total skin-sparing mastectomy in women with a
history of augmentation mammaplasty: assessing the safety profile.
Plast Reconstr Surg 2014;134(1):1–9.
23. Peled AW, Foster RD, Esserman LJ, et al. Increasing the time to
expander-implant exchange after postmastectomy radiation therapy
reduces expander-implant failure. Plast Reconstr Surg 2012;130(3):503–
509.
24. Momoh AO, Ahmed R, Kelley BP, et al. A systematic review of
complications of implant-based breast reconstruction with
prereconstruction and postreconstruction radiotherapy. Ann Surg Oncol
2014;21:118–124.
25. Ascherman JA, Hanasono MM, Newman MI, et al. Implant
reconstruction in breast cancer patients treated with radiation therapy.
Plast Reconstr Surg 2006;117(2):359–365.
26. Cordeiro PG, Pusic AL, Disa JJ, et al. Irradiation after immediate tissue
expander/implant breast reconstruction: outcomes, complications,
aesthetic results, and satisfaction among 156 patients. Plast Reconstr
Surg 2004;113(3):877–881.
27. Nava MB, Pennati AE, Lozza L, et al. Outcome of different timings of
radiotherapy in implant-based breast reconstructions. Plast Reconstr
Surg 2011;128(2):353–359.
28. Kronowitz SJ, Robb GL. Breast reconstruction with postmastectomy
radiation therapy: current issues. Plast Reconstr Surg 2004;114(4):950–
960.
29. Kronowitz SJ, Robb GL. Breast reconstruction and adjuvant therapies.
Semin Plast Surg 2004;18(2):105–115.
30. Kronowitz SJ, Hunt KK, Kuerer HM, et al. Delayed-immediate breast
reconstruction. Plast Reconstr Surg 2004;113(6):1617–1628.
31. Fine NA, Hirsch EM. Keeping options open for patients with anticipated
postmastectomy chest wall irradiation: immediate tissue expansion
followed by reconstruction of choice. Plast Reconstr Surg
2009;123(1):25–29.
32. Gargano F, Moloney DM, Arnstein PM. Use of a capsular flap to
prevent palpable wrinkling of implants. Br J Plast Surg 2002;55(3):269.
33. Gargano F, Ciminello F, Podda S, et al. Salvage of exposed breast
implant using capsular flaps. Eplasty 2009;9:e41.
34. Bergtson BP, Ringler SL, George ER, et al. Capsular tissue: a new local
flap. Plast Reconstr Surg 1993;91(6):1073–1079.
35. Cariou JL, Hilligot P, Arrouvel C, et al. Experimental concept of
periprosthetic membrane neo-flap with axial vascular pedicle. Ann Chir
Plast Esthet 1991;36(6):471–479.
36. Baroudi R, Pinotti JA, Keppke EM. A transverse thoracoabdominal skin
flap for closure after radical mastectomy. Plast Reconstr Surg
1978;61(4):547–554.
37. Schneider WF, Frerichs O, Fansa H. A medially based abdominal
transposition flap for large soft tissue defects of the anterior chest wall.
Eur J Plast Surg 2002;24(8):384–386.
38. Brown RG, Vasconez LO, Jurkiewicz MJ. Transverse abdominal flaps
and the deep epigastric arcade. Plast Reconstr Surg 1975;55(4):416–
421.
39. Matros E, Disa JJ. Uncommon flaps for chest wall reconstruction. Semin
Plast Surg 2011;25(1):55–59.
40. Calvert JW, Dickinson BP, Patel A, et al. Lateral breast flap with
superomedial pedicle breast lift. Aesthet Surg J 2011;31(6):658–666.
41. Jiang Z, Li S, Kretlow JD, et al. Closure of large defects after
microcystic lymphatic malformations using lateral intercostal artery
perforator flap. J Plast Reconstr Aesthet Surg 2014;67(9):1230–1236.
42. White A, Kalimuthu R. Salvaging difficult chest and epigastric defects
with the intercostal artery perforator flap. Plast Reconstr Surg
2010;125(3):124e–125e.
43. Persichetti P, Tenna S, Brunetti B, et al. Anterior intercostal artery
perforator flap autologous augmentation in bariatric mastopexy. Plast
Reconstr Surg 2012;130(4):917–925.
44. Hakakian CS, Lockhart RA, Kulber DA, et al. Lateral intercostal artery
perforator flap in breast reconstruction: a simplified pedicle permits an
expanded role. Ann Plast Surg 2016;76 Suppl 3:S184–S190.
45. Grazer FM. Abdominoplasty. Plast Reconstr Surg 1973;51(6):617–623.
46. Akbas H, Guneren E, Eroglu L, et al. The combined use of classic and
reverse abdominoplasty on the same patient. Plast Reconstr Surg
2002;109:2595–2596.
47. Dagregorio G, Darsonval V. Aesthetic surgery techniques after excision
of dermatofibrosarcoma protuberans: a case report. Br J Plast Surg
2005;58(4):556–560.
48. Moon HK, Taylor GI. The vascular anatomy of rectus abdominis
musculocutaneous flaps based on the deep superior epigastric system.
Plast Reconstr Surg 1988;82(5):815–832.
49. Tansini I. Sopra il mio nuovo processo di amputazione della mamella [in
Italian]. Riforma Med 1906;12:757.
50. Schneider WJ, Hill HL Jr, Brown RG. Latissimus dorsi myocutaneous
flap for breast reconstruction. Br J Plast Surg 1977;30:277–281.
51. Olivari N. The latissimus flap. Br J Plast Surg 1976;29:126–128.
52. Durkan B, Amersi F, Phillips EH, et al. Postmastectomy radiation of
latissimus dorsi myocutaneous flap reconstruction is well tolerated in
women with breast cancer. Am Surg 2012;78(10):1122–1127.
53. Demiri EC, Dionyssiou DD, Tsimponis A, et al. Outcomes of Fat-
Augmented Latissimus Dorsi (FALD) flap versus implant-based
latissimus dorsi flap for delayed post-radiation breast reconstruction.
Aesthetic Plast Surg 2018;42(3):692–701.
54. Fracol M, Grim M, Lanier ST, et al. Vertical skin paddle orientation for
the latissimus dorsi flap in breast reconstruction: a modification to
simultaneously correct inferior pole constriction and improve projection.
Plast Reconstr Surg 2018;141(3):598–601.
CHAPTER 62

Management of Animation Deformity


in Implant-Based Reconstruction
ALLEN GABRIEL | STEVEN R. SIGALOVE | G. PATRICK MAXWELL
HISTORY
Implant-based breast reconstruction is currently the most frequently
performed breast reconstructive procedure in the United States, constituting
about 80% of all breast reconstructions in 2018 (1). For the past 2 decades,
this reconstructive procedure has been performed primarily with subpectoral
implant placement by means of the dual-plane approach. Subpectoral implant
placement has been credited with minimizing implant-related complications,
including the risk of capsular contracture, and producing a more natural-
appearing breast (2). However, a concern with this approach is the risk of
animation deformity and associated breast discomfort, which is a direct
consequence of muscle elevation (3–6).
Animation deformity can be eliminated by placing the implant above the
pectoralis muscle; that is, in the prepectoral plane. But, until recently, there
has been less enthusiasm for the prepectoral approach in postreconstruction
patients because these patients often have thinned skin flaps with lack of
subcutaneous tissue following mastectomy. This lack of soft tissue increases
the risk of implant malposition, loss, visibility, and wrinkling. Moreover,
prepectoral implant placement increases the risk of capsular contracture (3,7).
The advent of skin- and nipple-sparing mastectomy techniques coupled with
improvements in fat grafting techniques, improvements in implant designs,
and the availability of a wide range of acellular dermal matrices (ADMs)
have created an era where inadequate soft tissue coverage is no longer
perceived as a barrier to prepectoral implant placement. Rather, prepectoral
implant placement is gaining popularity as a feasible option in select patients
undergoing primary breast reconstruction postmastectomy (8–10). Beyond
primary reconstruction, prepectoral implant placement (i.e., subpectoral to
prepectoral conversion) is now emerging as an option in patients undergoing
revision breast reconstruction, especially in patients presenting with
animation deformity (11–14).
RATIONALE FOR PREPECTORAL CONVERSION
Revision breast surgery is highly prevalent among women who undergo
breast reconstruction following mastectomy. Within 5 to 6 years of their
primary procedure, between a third to half of women undergo revision breast
surgery, most frequently due to capsular contracture, asymmetry, and/or
implant malposition (15–19). Revision surgery for implant-related complaints
has typically involved a site change with creation of a neopectoral pocket in
conjunction with capsulectomy followed by implant exchange and the
adjunctive use of supportive matrices (ADM or bioabsorbable mesh) (20).
Site change is critical to eliminating the distorting forces in the previous
subpectoral pocket, which likely contributed to the asymmetry, malposition,
and/or contracture. However, if the presenting complaints include animation
deformity and associated symptoms, creation of a neopectoral pocket is
unlikely to resolve these problems.
Animation deformity is a recognized complication of subpectoral implant-
based breast reconstruction (3–6). Symptoms arise with contraction of the
pectoralis major muscle and include visible lateral, superior, or inferior
displacement of the implant; implant distortion; pain; chest
tightness/discomfort; and implant wrinkling/rippling. Until recently, the
prevalence and the severity of animation deformity and its impact on
patients’ quality of life had received little attention. A study by Becker and
Fregosi found that all patients with subpectoral implant placement experience
some degree of animation deformity. Moreover, 80% of patients who had
animation deformity were bothered by it, half of whom were bothered to a
significant degree by it. In addition, half of patients who had animation
deformity felt that it interfered with their daily life (4).
Treatment of animation deformity in postreconstruction patients has
typically involved a combination of interventions including pectoralis muscle
release/division, wcapsulotomy, capsulorrhaphy, implant size change, and fat
grafting and/or use of ADM to mask wrinkling/rippling (14,21–23). These
interventions help ameliorate but do not completely eliminate animation
deformity. In postaugmentation patients, an additional treatment approach
involves moving the implant from the subpectoral to the subglandular or
prepectoral plane (24). The prepectoral approach virtually eliminates
animation deformity as the implant lies anterior to the pectoralis muscle and
is minimally impacted by muscle flexion.
OPERATIVE TECHNIQUE
PREPECTORAL CONVERSION

Incision
Typically, site change is executed via an inframammary incision. If the
previous scar is at the inframammary fold (IMF), this scar is reopened and if
the previous scar is centrally located, a new IMF incision is made. In general,
the central scar is not utilized. As the majority of breast projection is in the
central area, repeated access to the pocket via the central mastectomy scar is
avoided to prevent additional thinning in this region. The central incision is
retained only if primary breast reconstruction involved utilization of a
latissimus dorsi (LAD) flap.
Prepectoral Plane Change
After removal of the existing implant, a complete capsulectomy is performed.
If an ADM is present at the lower pole, it is also removed at this time or it
can be retained, if desired. A facelift scissor is utilized to remove the capsule
instead of electrocautery if the overlying skin flap is tenuous to minimize
tissue damage. Lower-pole ADM, if not retained, is removed as much as
possible to redrape the pectoralis major back to the chest wall. In patients
who had a LAD flap placed at the lower pole during primary reconstruction,
the pectoralis muscle is detached from the flap and the flap is retained at the
lower pole. In all cases, the pectoralis muscle is detached from the overlying
subcutaneous tissue and tacked down to the chest wall with 0-Vicryl sutures.
This creates a new pocket—the prepectoral pocket—between the pectoralis
muscle and the overlying skin flap.
Implant Exchange
The old implant is exchanged for a new implant or a tissue expander
depending on the thickness and tightness of the skin flap. In both cases, the
prosthesis can be covered with an ADM after placement (anterior coverage
technique) or it can be wrapped with the ADM prior to placement (wrap
technique) (Fig. 62-1) (11). In the anterior coverage technique, only the
anterior surface of the prosthesis is covered with the ADM. In the wrap
technique, both the anterior and posterior surfaces of the prosthesis are
covered with the ADM. If the original lower-pole ADM is retained, a third
option is to add an ADM to the anterior upper pole only. If an expander is
placed, it is fully inflated at this time. In all three ADM placement scenarios,
the ADM is secured by suturing to subcutaneous tissue. In the anterior
coverage technique, a 3-cm posterior gutter is created, anterior to the tacked
down pectoralis major, when securing the ADM at the IMF. Prior to skin
closure, one or two drains is/are placed between the ADM and the prosthesis.
The use of perforated ADM eliminates the need for a second drain.
Postoperatively, the drain(s) is(are) removed when there are less than 30 mL
of output over 24 hours. If using an expander, it is exchanged for an implant
after an average of 3 months of tissue expansion. In patients who require
additional soft tissue coverage to enhance breast volume and shape,
autologous fat grafting is performed as a secondary surgery.
CLINICAL EXPERIENCE
Several authors have reported on their experience with subpectoral to
prepectoral conversion for the treatment of animation deformity (11–13,25).
Across 4 published studies, a total of 161 patients underwent this procedure
and a total of 299 conversions were performed. In all cases, complete
resolution of the animation deformity was achieved, demonstrating the
effectiveness of prepectoral conversion for the correction of animation
deformity. In general, the procedure was found to be safe, although
complications varied between the studies.
Hammond et al. reported a 26.3% complication rate, including a capsular
contracture rate of 21.1% and a seroma rate of 5.3% in 19 revision
reconstructions in 10 patients (25). No visible implant deformities, infections,
or implant removals were reported. As ADM was not used for implant
coverage in this study, this may partly explain the high rate of complications.
Lentz et al. reported a 14.5% infection rate requiring intravenous
antibiotics, a 10.9% revision operation rate (subsequent to prepectoral
conversion), a 7.3% capsular contracture rate, and a 1.8% implant loss rate in
55 revision reconstructions in 31 patients (13). The authors included two
cohort of patients in this study, one which received ADM for implant
coverage and the other which did not receive ADM. Four of the 9 breasts that
were reconstructed without ADM had capsular contracture while none of the
46 breasts reconstructed with ADM had capsular contracture. In addition, the
authors noted no subsequent revision operations in breasts that had prior fat
grafting (i.e., before revision surgery). In comparison, among breasts that did
not have prior fat grafting, 21.4% had further revision surgeries.
FIGURE 62-1 Revision options from dual plane to prepectoral space. The first
option includes complete capsulectomy and removal of prior acellular dermal matrix
(ADM) and complete anterior ADM coverage with 3-cm posterior gutter coverage.
The second option includes complete capsulectomy and removal of prior ADM and
complete anterior and posterior ADM coverage. The third option includes complete
capsulectomy, and keeping the original lower-pole ADM and adding upper-pole
ADM only. (From Gabriel A, Sigalove S, Sigalove NM, et al. Prepectoral revision breast
reconstruction for treatment of implant-associated animation deformity: a review of 102
reconstructions. Aesthet Surg J 2018;38(5):519–526.)

In 102 revision reconstructions (57 patients), Gabriel et al. observed


complications in 4 breasts for an overall complication rate of 3.9% that
included seroma (2 breasts), skin necrosis (3 breasts), and wound dehiscence
(1 breast) (11). All 4 breasts with complications had their implants removed
and replaced. There were no incidences of infection or clinically significant
capsular contracture.
In another study by Sigalove et al., of 124 breasts (63 patients) that had
prepectoral conversion, complications occurred in 4 breasts (3.2%) and
included implant loss (1.6%), seroma (1.6%), hematoma (0.8%), surgical site
infection (0.8%), and skin necrosis (0.8%). There was no incidence of
capsular contracture (12). This study also demonstrated that prepectoral
conversion is also effective in resolving other presenting complaints, such as
implant malposition, asymmetry, and capsular contracture besides animation
deformity. In this study, implant malposition was a presenting complaint in
79% of breasts, capsular contracture in 17% of breasts, and asymmetry in
96% of breasts; all of which were resolved with prepectoral conversion.
There were no recurrences during a mean follow-up period of 18.9 months.
Aesthetically pleasing soft breasts were achieved in all patients.
Representative Case examples are shown in Figures 62-2 and 62-3.
ELEMENTS OF SUCCESSFUL OUTCOMES

The Appropriate Patient


Careful patient selection is essential for the success of prepectoral revision
reconstruction. The reconstructive contraindications for primary prepectoral
breast reconstruction have been previously reported and now with years of
experience and availability of data the original table has been modified
(Table 62-1) (8), and these are also applicable to prepectoral revision
reconstruction. In general, patients who have thick, adequately vascularized
skin flap and have fat donor sites for autologous fat grafting are good
candidates. Poorly vascularized flaps increase the risk of skin breakdown and
its attendant complications of necrosis and implant exposure/extrusion.
Previous radiotherapy, current tobacco use, and uncontrolled diabetes
(HbA1c >7.5%) are additional contraindications for they can compromise
skin perfusion. However, irradiated breasts that were reconstructed with LAD
muscle recruitment during primary reconstruction can be considered for
prepectoral revision reconstruction, since the pectoralis muscle is eliminated
from this pocket without altering the lower pole where the vascularized flap
is in place. Nonetheless, the irradiated pectoralis major continues to be a
source of pain due to radiation-induced severe fibrosis and cephalad
retraction. Elevated body mass index (BMI) alone (i.e., in the absence of
other contraindications) is not a contraindication for prepectoral revision
reconstruction.
FIGURE 62-2 A 40-year-old female after bilateral mastectomy and two-stage
reconstruction (dual plane and acellular dermal matrix) with 650 cc style 20
implants (A, B, C). Patient presented with concerns of pain and animation. Patient at
1 year following site change to prepectoral plane and reconstruction with acellular
dermal matrix and SCF (Truform 3) 650 cc implants (D, E, F).

FIGURE 62-3 Patient with animation deformity following two-stage dual plane
reconstruction with style 20 650 cc implants (A). Patient at 6 months following site
change to prepectoral plane with no animation deformity with SCF (Truform 3) 650
cc implants (B).

TABLE 62-1 Contraindications to Immediate Prepectoral Reconstruction


Reconstructive Contraindications
Poorly vascularized or ischemic flaps
HbA1c >7.5%
Active smokers
Questionable Contraindications
Prior breast irradiation (unless Latissimus flap is utilized for reconstruction)
Immunocompromised
Body mass index >40 kg/m2a
aWith other associated comorbidities (i.e., diabetes mellitus, hypertension, etc.); body mass index alone
is not a contraindication.
HbA1c, Hemoglobin A1c.
From Sigalove S, Maxwell GP, Sigalove NM, et al. Prepectoral implant-based breast reconstruction:
rationale, indications, and preliminary results. Plast Reconstr Surg 2017;139(2):287–294.

The Appropriate Implant


A wide variety of silicone implants are currently available on the market,
which provides the surgeon and the patient with a range of choices but
selecting an optimal implant for the patient can be challenging. In the
authors’ opinion, implants with a higher fill ratio are particularly suited for
prepectoral placement. As the degree of upper-pole soft tissue coverage in
reconstructive patients varies depending on the extent of the mastectomy,
implants with higher fill ratio and varying gel cohesivity provide a range of
options for augmenting upper-pole fullness. For example, a less cohesive gel
implant may be more appropriate in a patient with relatively thicker soft
tissue at the upper pole, while a more cohesive gel implant may be more
appropriate in a patient with thinner soft tissue at the upper pole (Fig. 62-4)
(26). Soft tissue thickness can be assessed using the pinch test. BMI should
not be used as a surrogate measure of soft tissue thickness because BMI does
not necessarily correlate with tissue thickness (12).

FIGURE 62-4 Round cohesive implant (left) versus round highly cohesive implant
(right). Both implants have the same implant volume, height, and projection but
different gel cohesivities. When held upright, compared with the highly cohesive
implant with the firmer gel, the cohesive implant with a softer gel exhibits shell and
implant collapse at the upper pole. This leads to different implant projections
between the two implant types and different degrees of upper-pole fullness. (From
Gabriel A, Maxwell GP. The science of cohesivity and elements of form stability. Plast
Reconstr Surg 2019;144(1S):7S–12S.)

The Use of ADM


ADM use in the prepectoral space is considered to be essential as it serves to
reinforce the anterior skin flap and cushion the implant from direct contact
with the flap. Placing the implant under the flap without tissue reinforcement
can lead to implant malposition (bottoming out), visibility, and palpability;
rippling/wrinkling; implant exposure subsequent to skin breakdown; and
importantly capsular contracture—complications that were reported with the
subcutaneous approach to breast reconstruction after the introduction of
silicone implants (27,28). Risk of capsular contracture is significantly
reduced with the use of ADM (11–13).
Autologous Fat Grafting
Fat grafting is integral to optimizing outcomes and is required in most
reconstructive patients after prepectoral implant placement, both in the
primary and in the revision setting (8,29). Fat grafting helps to enhance breast
volume and shape as well as mask implant rippling/wrinkling and palpability.
Implant rippling is a frequent complication after prepectoral implant
placement and is due to a combination of subcutaneous tissue deficit and the
use of less cohesive implants. The use of highly cohesive implants helps in
reducing rippling to some extent as these implants are firmer than less
cohesive implants.
Fat grafting is typically performed as an additional surgery and not at the
same time as the prepectoral conversion. Autologous fat is injected into the
subcutaneous space between the skin flap and the ADM. In addition, in some
cases, fat grafting may be performed prior to the revision procedure to ensure
adequate flap thickness and ease the dissection and separation of the
pectoralis major from the overlying skin envelope. This is especially
important if the mastectomy was performed through a central scar and the
scar is completely adherent to the pectoralis major. Similarly, prior fat
grafting is also necessary if the patient had wound healing issues following
mastectomy and the central aspect of the skin envelope is completely adhered
to the pectoralis major/ADM junction. Prior fat grafting appears to reduce the
risk of subsequent revisions after revision surgery, as demonstrated by Lentz
et al. (13).
CONCLUSION
Subpectoral to prepectoral plane conversion is an effective strategy for the
treatment of animation deformity and associated symptoms. It also appears to
be effective for the correction of asymmetry, implant malposition, and
capsular contracture and provides surgeons an additional option for revision
reconstruction. Appropriate patient and implant selection, fat grafting to
enhance breast shape and volume, and the use of ADM for implant coverage
and support are important elements that contribute to achieving successful
outcomes with prepectoral conversion in revision reconstruction patients.

REFERENCES

1. American Society of Plastic Surgeons. 2018 Plastic Surgery Statistics


Report. Available online at
https://www.plasticsurgery.org/documents/News/Statistics/2018/plastic-
surgery-statistics-full-report-2018.pdf Accessed November 27, 2019.
2. Gruber RP, Kahn RA, Lash H, et al. Breast reconstruction following
mastectomy: A comparison of submuscular and subcutaneous
techniques. Plast Reconstr Surg 1981;67:312–317.
3. Spear SL, Schwartz J, Dayan JH, et al. Outcome assessment of breast
distortion following submuscular breast augmentation. Aesthetic Plast
Surg 2009;33(1):44–48.
4. Becker H, Fregosi N. The impact of animation deformity on quality of
life in post-mastectomy reconstruction patients. Aesthet Surg J
2017;37(5):531–536.
5. Nigro LC, Blanchet NP. Animation deformity in postmastectomy
implant-based reconstruction. Plast Reconstr Surg Glob Open
2017;5(7):e1407.
6. Dyrberg DL, Bille C, Gunnarsson GL, et al. Breast animation deformity.
Arch Plast Surg 2019;46(1):7–15.
7. Salibian AH, Harness JK, Mowlds DS. Staged suprapectoral
expander/implant reconstruction without acellular dermal matrix
following nipple-sparing mastectomy. Plast Reconstr Surg
2017;139(1):30–39.
8. Sigalove S, Maxwell GP, Sigalove NM, et al. Prepectoral implant-based
breast reconstruction: rationale, indications, and preliminary results.
Plast Reconstr Surg 2017;139(2):287–294.
9. Reitsamer R, Peintinger F, Klaassen-Federspiel F, et al. Prepectoral
direct-to-implant breast reconstruction with complete ADM or synthetic
mesh coverage—36-Months follow-up in 200 reconstructed breasts.
Breast 2019;48:32–37.
10. Vidya R, Berna G, Sbitany H, et al. Prepectoral implant-based breast
reconstruction: a joint consensus guide from UK, European and USA
breast and plastic reconstructive surgeons. Ecancermedicalscience
2019;13:927.
11. Gabriel A, Sigalove S, Sigalove NM, et al. Prepectoral revision breast
reconstruction for treatment of implant-associated animation deformity:
a review of 102 reconstructions. Aesthet Surg J 2018;38(5):519–526.
12. Sigalove S, Maxwell GP, Gabriel A. Outcomes utilizing Inspira
implants in revisionary reconstructive surgery. Plast Reconstr Surg
2019;144(1S):66S–72S.
13. Lentz R, Alcon A, Sbitany H. Correction of animation deformity with
subpectoral to prepectoral implant exchange. Gland Surg 2019;8(1):75–
81.
14. Alnaif N, Safran T, Viezel-Mathieu A, et al. Treatment of breast
animation deformity: a systematic review. J Plast Reconstr Aesthet Surg
2019;72(5):781–788.
15. Spear SL, Murphy DK, Slicton A, et al. Inamed Silicone Breast Implant
U.S. Study Group. Inamed silicone breast implant core study results at 6
years. Plast Reconstr Surg 2007;120(7 Suppl 1):8S–16S; discussion
17S–18S.
16. Cunningham B, McCue J. Safety and effectiveness of Mentor’s
MemoryGel implants at 6 years. Aesthetic Plast Surg 2009;33:440–444.
17. Stevens WG, Harrington J, Alizadeh K, et al. Five-year follow-up data
from the U.S. clinical trial for Sientra’s U.S. Food and Drug
Administration-approved Silimed® brand round and shaped implants
with high-strength silicone gel. Plast Reconstr Surg 2012;130:973–981.
18. Maxwell GP, Van Natta BW, Murphy DK, et al. Natrelle style 410
form-stable silicone breast implants: core study results at 6 years.
Aesthet Surg J 2012;32:709–717.
19. Hammond DC, Migliori MM, Caplin DA, et al. Mentor contour profile
gel implants: clinical outcomes at 6 years. Plast Reconstr Surg
2012;129:1381–1391.
20. Maxwell GP, Gabriel A. Non-cross-linked porcine acellular dermal
matrix in revision breast surgery: long-term outcomes and safety with
neopectoral pockets. Aesthet Surg J 2014;34:551–559.
21. Baxter RA. Update on the split-muscle technique for breast
augmentation: prevention and correction of animation distortion and
double-bubble deformity. Aesthetic Plast Surg 2011;35(3):426–429.
22. Baxter RA. Acellular dermal matrices in breast implant surgery:
defining the problem and proof of concept. Clin Plast Surg
2012;39(2):103–112.
23. Spear SL, Sher SR, Al-Attar A, et al. Applications of acellular dermal
matrix in revision breast reconstruction surgery. Plast Reconstr Surg
2014;133(1):1–10.
24. Lesavoy MA, Trussler AP, Dickinson BP. Difficulties with subpectoral
augmentation mammaplasty and its correction: the role of subglandular
site change in revision aesthetic breast surgery. Plast Reconstr Surg
2010;125(1):363–371.
25. Hammond DC, Schmitt WP, O’Connor EA. Treatment of breast
animation deformity in implant-based reconstruction with pocket change
to the subcutaneous position. Plast Reconstr Surg 2015;135(6):1540–
1544.
26. Gabriel A, Maxwell GP. The science of cohesivity and elements of form
stability. Plast Reconstr Surg 2019;144(1S):7S–12S.
27. Prpic I. Reconstruction of the breast after mastectomy for carcinoma.
Acta Chir Belg 1980;79(2):103–104.
28. Radovan C. Breast reconstruction after mastectomy using the temporary
expander. Plast Reconstr Surg 1982;69(2):195–208.
29. Darrach H, Kraenzlin F, Khavanin N, et al. The role of fat grafting in
prepectoral breast reconstruction. Gland Surg 2019;8(1):61–66.
CHAPTER 63

Symmetry Procedures Following


Unilateral Implant Breast
Reconstruction
MICHAEL SCHEFLAN | YOAV GRONOVICH
HISTORY
Implant-based breast reconstruction is the most common type of
reconstruction, and is the preferred immediate type of reconstruction around
the world (1–6).
The main reasons for its popularity are:

Relatively simple and fast operation and a short hospitalization.


Excellent aesthetic outcomes using acellular dermal matrices (ADMs)
and fat grafting.
Flexible one or two stages. Direct to implant (DTI) or tissue expander
adaptable to patients, breasts, and risk factors.
Optional delayed autologous reconstruction in a second stage when
indicated due to complications, radiation therapy sequel or patient
request.
Patient preference.

While bilateral nipple-sparing mastectomy (NSM) and immediate implant-


based breast reconstruction is on the rise, unilateral breast reconstruction is
more frequent than bilateral reconstruction (2–4), and hence in order to
achieve symmetry it becomes necessary in many patients to deal with the
contralateral breast. Patients who may not require a symmetry procedure are
those with moderate-sized breasts, good skin tone, and no ptosis and
frequently had a NSM on the affected side (Fig. 63-1). In very small breasts,
it is common practice to augment the other breast for symmetry. On the other
hand, patients with large and ptotic breasts, or those with empty saggy breasts
commonly desire and require a symmetry operation on the healthy
contralateral breast (Fig. 63-2).
TIMING OF THE SYMMETRY PROCEDURE
The main factors influencing timing are: the extent and type of the cancer,
and a relative certainty that there will be no need for further tissue removal
after permanent pathology results, or when postmastectomy radiation therapy
(PMRT) is indicated. The surgical/incisional approach of the mastectomy is
another factor: is it a NSM, skin-sparing mastectomy (SSM), or a skin-
reducing mastectomy (SRM). Other important factors are the plane of
reconstruction, the breast characteristics (size, shape, and degree of ptosis),
and the patient’s desire. There are patients who refuse to have their healthy
breast operated on just for aesthetic purposes, or who are satisfied as long as
they appear symmetric in the bra. In contrary, there are women who are
particular about achieving optimal symmetry in the initial operation. These
factors are summarized in Table 63-1. There is no single factor that
determines the timing of a symmetry procedure. A comprehensive
consideration of all factors contributes to this decision. For example, a
woman who is requesting symmetry may achieve that goal in the first stage if
she undergoes a NSM, with clear margins and a low probability of PMRT. In
such patients a prepectoral or partial subpectoral (depending on the tissue
quality and thickness) direct to implant and ADM may be carried out with a
simultaneous breast augmentation on the contralateral side when indicated.
On the other hand, in women who wish for a volumetric symmetry in a bra
only, or may likely require adjuvant PMRT, with large and ptotic breast,
while it may be still possible to use a definitive implant on the affected side
in selected patients, the final shape and volume may be altered by radiation
sequelae and therefore a symmetry procedure may be preferably deferred to a
second stage. Conversely, in a similar situation in a patient who undergoes
SRM, it may be advisable to proceed with a simultaneous contralateral
reduction thereby improving patient’s comfort, posture, and quality of life.
While the first author (MS) prefers whenever possible, to perform a
simultaneous contralateral symmetry procedure in patients where
reconstruction alone may result in a significant asymmetry, the second author
(YG) prefers to delay the symmetry procedure to a second stage in order to
let the operated breast heal and settle down before operating on the
contralateral breast. Exceptions are very large and ptotic breasts,
unwillingness of the woman to undergo more than one operation or medical
contraindications, and risk factors against future elective surgeries. In these
patients, symmetry procedures are done simultaneously (Fig. 63-3). Women
should be informed that there is often a need for further surgical refinements
and corrections on either breast. The reconstructed breast is influenced by
several factors among them: PMRT, capsular contracture, displacement, and
malposition of the implant and nipple areola and scar deformities. The
contralateral breast also ages with time and at a different pace from the
reconstructed breast and may require further future corrections to maintain
symmetry.
FIGURE 63-1 Patient with cup B size, no ptosis, good skin tonus, with left breast
carcinoma. No need for symmetry. Augmentation is possible if the patient wish to
upsize her breast. Before operation (above) and 3 months after immediate
reconstruction with Mentor CPG 322 225cc and Alloderm (below).
FIGURE 63-2 Patient with cup G size, ptosis grade 3, with right breast carcinoma.
Need for symmetry in the first stage.
SYMMETRY FACTORS
In healthy unoperated breasts, perfect symmetry is the exception, mild
asymmetry is the rule. In a delayed setting, the first question concerning
symmetry procedure is which breast shape and size the patient likes best: is it
the reconstructed breast or the contralateral one? A flow chart can help in
making the right decisions (Fig. 63-4).

TABLE 63-1 Factors Influencing the Symmetry Procedure


Patient’s Choice
• Not willing to have an operation on the contralateral healthy breast
• Accepting volumetric symmetry in the bra
• Expecting shape and size symmetry in and out of a bra
Oncologic Needs
• Contralateral mastectomy after permanent pathology
• PMRT after permanent pathology
• Need for completion extension of the mastectomy after permanent
pathology
Reconstruction Approach
• Type of mastectomy (nipple-sparing, skin-sparing, skin-reducing
mastectomy)
• Plane of implant insertion (partial subpectoral, prepectoral)
• Type of implant
Breast Characteristics
• Size
• Shape
• Volume
• Skin envelope quality
FIGURE 63-3 Patient with cup F size, with right breast carcinoma. Before
reconstruction (left) and 4 weeks after immediate reconstruction with 410 Allergan
560 g and Alloderm in a partial sub-pectoral plane and free nipple graft, and left
breast reduction for symmetry on the same procedure (right).

The surgeon should consider the inherent differences between a breast


reconstructed with an implant and a native breast. In the reconstructed breast,
the implant accounts for the shape, the volume, and the dimensions while in
the native breast shape, volume and weight depend on intrinsic factors and
tissues characteristics. It contains no foreign body (implant) and the fat and
parenchymal tissue have a different consistency. These two, apparently
similar structures move and age differently. If the patient is satisfied with her
natural breast shape and size, the surgeon should attempt to obtain symmetry
by minimally modifying the skin envelope on the affected side and choosing
an implant with dimensions, shape, volume, and feel as close as possible to
the contralateral healthy breast. Symmetry improvement begins with the
tissues of the reconstructed side which dictate what implant volume may be
safely inserted into the mastectomy pocket. Following a unilateral
mastectomy and reconstruction, the main factor affecting symmetry is related
to the implant and the capsule around it. Improvement of the affected side
may include fat grafting, capsulotomy or capsulectomy, remembering that
complete capsulectomy and fat grafting do not belong together. The capsule
helps to contain the lipograft in place. Without it fat may seep into the space
surrounding the implant. Fat injection is a useful addition to mostly any
correction of the reconstructed breast and its importance cannot be
overstated. If the implant is in a partial subpectoral plane then fat is injected
into the pectoralis muscle, between the muscle and the anterior capsule and
the subdermal plane. If it is located in a prepectoral plane, then the fat is
placed in the muscle, the posterior subcapsular plane, and anterior
precapsular and subdermal planes (Fig. 63-5). If the general shape and size of
the reconstructed breast is adequate, and the patient is happy with it then
symmetry procedure is focused on the contralateral side.

FIGURE 63-4 Determination of asymmetry.

Generally, it is preferable to have implants in both breasts in an attempt to


influence long-term symmetry. Ultimately, the main problem is that the
reconstructed breast is made mostly of an implant while the contralateral
breast, even with an implant, contains also fat and fibroglandular tissue. This
is one of the reasons why it is often useful to inject fat into the reconstructed
breast, in the interest of increasing soft tissue coverage and improving long-
term symmetry (Fig. 63-6).
BREAST CHARACTERISTICS

Size
The shape and size of the breast is a fundamental factor influencing short-
and long-term symmetry. The heavier the contralateral breast, the more
challenge to achieve symmetry.
Therefore, it is advisable to perform a breast reduction on the healthy side
with or without an implant at the initial stage. Following completion of
PMRT on the reconstructed side, when indicated, a second stage of fat
grafting is often warranted.

FIGURE 63-5 Planes for fat injection.

Shape
We may never find the exact type, size, and shape of implant to imitate the
contralateral breast. For instance, a breast of width 16 cm that weighs 500 g
may never be exactly reconstructed with an implant of the same dimensions.
Implants of that width usually weigh more than 700 g. Furthermore, implants,
either round or anatomical, are designed for a specific width, height, and
projection, and do not fill the tail of the breast or its lateral aspect. Choosing
the right shape and size of implant is important for the success of breast
reconstruction, but for larger breasts it is often necessary to shape the pocket
to accommodate the implant. When a symmetry procedure is required on the
contralateral breast, the reconstructed side usually serves as the template and
will facilitate the decision as to the nature of the symmetry procedure (7–9).
IMPLANT

Type
The ongoing debate concerning the shape and texture of implants in aesthetic
breast augmentation is far from over and relates to reconstructive breast
surgery as well. With increasing popularity of prepectoral reconstruction with
the use of ADM, the argument is even more relevant (10–15). The breast
implant associated-anaplastic large cell lymphoma (BIA-ALCL) issue and the
moratorium issued by some countries preventing the use of macrotextured
implants make this issue yet more complexed (16–21). The use of a smooth,
round implant in primary reconstruction could theoretically result in a less
natural result compared to the anatomical implant option. This may be even
more pronounced with implants in the prepectoral position. If a two-stage
reconstruction has been carried out with an anatomical tissue expander, then
the replacement of the shaped expander with a round, smooth implant is often
satisfactory because the pocket has already been created and the smooth, soft
gel implant simply fits itself to the existing pocket, acting as a soft filler. In
the subpectoral reconstruction, it may be less obvious whether the implant is
round or anatomical, so the use of a round, smooth implant may be the option
of choice (22–25). A recent study showed equal patients’ and surgeon’s
satisfaction with both round and shaped implants (8).
Plane
Two planes are common: partial subpectoral and prepectoral.
The partial subpectoral plane, which was most common before the era of
the ADM, is thought to be reliable because the pectoralis major covers the
upper pole of the implant providing more soft tissue coverage (26,27).
Nevertheless, some drawbacks such as, animation deformity, unnatural upper
pole, and capsule contracture following PMRT may be common (28–34). On
the other hand, prepectoral reconstruction partially overcomes these
drawbacks by annulling animation, and with complete coverage of the
implant with an ADM creating a more natural result even after PMRT
(33–35).
FIGURE 63-6 Differences in content between native and reconstructed breast.

Stages
One-stage reconstruction (direct to implant—DTI) is somewhat more
challenging and less forgiving. DTI determines the near-final dimensions of
the reconstructed breast immediately. The patient should be informed that
while most steps of the reconstruction are done initially, there is often a need
for refinements at a later stage, such as fat injection, implant exchange, scar
revision, nipple areola complex (NAC) reconstruction, etc. In DTI it is
common to operate on the contralateral breast as well in order to achieve
most of the reconstructive goals in one stage.
Two-stage reconstruction is a safer procedure in patients with poor tissue
perfusion and risk factors (smoking, obesity, and prior radiation therapy) and
the most common type of implant-based reconstruction in the United States
(36,37). It enables the surgeon to control the timing and amount of expander
fill, thus reducing potential complications as well as controlling of the final
size of the reconstructed breast. It allows for all refinements to be carried out
at the second stage, including fat grafting, decision of size, type and shape of
the permanent implant, and plane of its insertion which may be changed from
the original pocket as indicated. In a two-stage reconstruction the surgeon is
committed to a second stage and therefore it is common to attend to the
symmetry at that time.
SECONDARY OPERATIONS ON THE RECONSTRUCTED BREAST
The reconstructed breast may change during the months and years following
the initial procedure. PMRT influences the tissue surrounding the implant. It
may cause pigmentation, induration, telangiectasias and atrophy (PITA)
resulting in a stiffer, harder, painful, and displaced breast. Capsular
contracture and displacement may also happen without PMRT although this
has been dramatically reduced with the advent of ADMs (28–31,38).
Diagnosing the cause of asymmetry helps apply the appropriate solution to
the problem. Treatment options are: capsular release (capsulotomy), total
capsule resection (capsulectomy), change of plane, change of implant, and fat
injection.
Capsule Management
Ways of treating capsular contracture have been described in the literature.
The first important issue is if the tissues have undergone radiation therapy.
For radiated tissue less is more as it relates to manipulating partially
devascularized and damaged tissue. Selected capsulotomies and fat grafting
are preferred in these instances. The patient should be informed that capsular
contracture release may not resolve in one procedure. Recurrent contracture
and inadequate softening may require additional release and fat grafting
procedures (39–43).

FIGURE 63-7 Patient after bilateral immediate reconstruction in a sub-pectoral


plane after radiation to the right breast, with upward displacement of the implant
(A), and after change of plane to a pre-pectoral (B).
Change of Plane
One of the drawbacks of the partial subpectoral (dual plane) reconstruction is
associated with its long-term aesthetic result. The two main issues are:
animation deformity and an upward displacement of the implant. Change of
plane to a prepectoral is the treatment of choice in these patients
(23,33,34,44–46). From the authors’ experience, plane change is technically
easier to dissect with the implant in situ. This facilitates the initial dissection
over the anterior dome of the capsule. After reaching the top projection or
when dissection becomes difficult, the implant is removed, the neo pocket
completed and the pectoralis muscle is sutured to obliterate the previous
pocket (Fig. 63-7). If the reconstructed breast plane is in a prepectoral plane,
and a plane change is necessary due to implant visibility, palpability, contour
deformities, rippling, etc., fat grafting and the addition of a second ADM may
be in order. Two other options are site change to subcapsular, or subpectoral
position. Creation of a subcapsular pocket has the advantage of keeping the
pectoralis intact while using the posterior capsule as reinforcement to anterior
implant coverage. Limitation of this approach is the restricted ability of the
raised posterior capsule to expand anteriorly and provide adequate projection
with the implant in place. Another alternative is creating a new dual plane,
partial subpectoral pocket. It is simple and eliminates the need for releasing
the capsule, and, in many cases, the new pocket is more clearly defined
(41,42).
Change of Implant
Changing the implant as part of the above described solutions or as a sole
procedure, is necessary in many patients. Insertion of an implant to an
already existing pocket is different from placing it in the immediate stage. In
the second stage, there is already a mature capsule, a well-defined pocket,
and the variability of implants to choose from is wider. Whether the implant
is shaped or round, it may look more natural when placed in an existing
pocket. While not a clear cut or absolute indication, changing the implant in
these instances is recommended.
Fat Injection
Fat injection is essential in every secondary operation of breast
reconstruction. Fat, along with its adipose-derived stem cells, is one of the
most important regenerative tools of improving the shape, size, and feel of
the reconstructed breast (47,48). The bigger the size of the contralateral
breast, the more the discrepancy between implant to parenchyma ratios. In
order to overcome this discrepancy fat grafting is indicated.
PRIMARY SYMMETRY PROCEDURES ON THE CONTRALATERAL BREAST

Breast Reduction
In larger breasts with cancer, there is often a need to perform a SRM. Breast
reconstruction in these patients often result in a smaller breast which in return
requires a breast reduction on the contralateral side.
Reduction and Augmentation
It is always better to have both breasts composed of the same “ingredients” in
our quest for long-term symmetry. For that reason, using an implant in the
contralateral breast is often useful. The concept of reduction with
simultaneous augmentation was first proposed by French plastic surgeons
some 28 years ago in order to stabilize results and reduce drawbacks of breast
reduction such as bottoming out. The same logic works in breast
reconstruction. From the authors’ experience it is advisable to insert the
implant on the contralateral breast in the same plane as in the reconstructed
breast. Obviously, the size, shape, and weight of the implants are different in
both breasts (Fig. 63-8).

FIGURE 63-8 Patient with cup E size, with right breast carcinoma: Before operation
(above) and 6 months after immediate reconstruction with 410 Allergan 475 g and
Alloderm in a pre-pectoral plane and reduction of the left breast for symmetry, and
3 months after second stage of fat injection to right breast (250 cc) and insertion of
round textured implant in a subglandular plane to the left breast for equalization
(below).

FIGURE 63-9 Unilateral left skin-reducing mastectomy and immediate direct-to-


implant breast reconstruction with acellular dermal matrix and simultaneous right
augmentation/mastopexy. A 54-year-old woman with left breast cancer before
surgery (above) and 25 months postoperatively (below).

Mastopexy With or Without Augmentation


In cases where the reconstructed breast is of the same size as the contralateral
side and the main challenge is ptosis, it is recommended to add an implant to
the mastopexy along with volume reduction as described above (Fig. 63-9).
Fat Injection
The need for fat injection in the contralateral breast is mainly for contour
refinements. It is the upper pole that may assume a different slope and require
lipografting on either side. Another example is, if the implant on the
contralateral breast is visible, palpable with rippling and irregularities or with
a superior pole step-off deformity. Fat injection to the subdermal plane will
improve the overall result.
TIMING OF THE SYMMETRY PROCEDURE
The two main factors influencing timing of the symmetry procedure are: the
size and shape of the reconstructed breast and the possible need for PMRT.
Size and Shape
In patients with large and ptotic breasts with the reconstructed side ending up
being smaller in size and different in shape, the discrepancy between the
breasts is expected to be significant, and therefore a simultaneous symmetry
procedure on the contralateral breast is recommended.
Postmastectomy Radiation Therapy
It is often advisable to wait 3 months for the inflammatory phase to cool
down after PMRT is completed before initiating a symmetry procedure on the
contralateral breast. PMRT can downgrade the feel, reduce the volume, and
deform the shape of the breast as well as cause complications such as capsule
contracture or even reconstructive failure. In real practice, the decision for
PMRT may happen a few weeks after the mastectomy, when the permanent
pathology report and the analysis of the lymph nodes status become
available. Women who have a significant discrepancy between the breasts at
the initial surgery and undergo a simultaneous symmetry procedure should be
informed that they may require further surgical intervention following
radiation therapy. Some patients may therefore choose to go through a
symmetry surgery at a second stage.
CONCLUSION
Immediate breast reconstruction with implants is the commonest form of
breast reconstruction. In the last few years the pre-pectoral reconstruction
with ADM has become more popular. A reasonable symmetry with the
contralateral breast is paramount in every breast reconstruction and should be
taken into account in the first stage, depending on the original breast size and
shape and the expected discrepancy after reconstruction, along with other
parameters such as risk factors, planned PMRT, and patient’s desires and
expectations.

REFERENCES

1. Tuttle TM, Rueth NM, Abbott A, et al. Trends in the local treatment of
breast cancer: should we be worried? J Surg Oncol 2011;103:313–316.
2. Habermarm EB, Abbott A, Parsons HM, et al. Are mastectomy rates
really increasing in the United States? J Clin Oncol 2010;28:3437–3441.
3. Alderman AK, McMahon L Jr, Wilkins EG. The national utilization of
immediate and early delayed breast reconstruction and the effect of
sociodemographic factors. Plast Reconstr Surg 2003;111:695–703;
discussion 704–705.
4. Albornoz CR, Bach PB, Mehrara BJ, et al. A paradigm shift in U.S.
breast reconstruction: increasing implant rates. Plast Reconstr Surg
2013;131:15–23.
5. Lennox PA, Bovill ES, Macadam SA. Evidence-based medicine:
alloplastic breast reconstruction. Plast Reconstr Surg 2017;140:94e–
108e.
6. Frey JD, Salibian AA, Karp NS, et al. Implant based reconstruction: hot
topics, controversies and new directions. Plast Reconstr Surg
2019;143:404e–416e.
7. Macadam SA, Ho AL, Lennox PA, et al. Patient-reported satisfaction
and health-related quality of life following breast. reconstruction: a
comparison of shaped cohesive gel and round cohesive gel implant
recipients. Plast Reconstr Surg 2013;131:431–441.
8. Khavanin N, Clemens MW, Pusic AL, et al. Shaped versus round
implants in breast reconstruction: a multi-institutional comparison of
surgical and patient-reported outcomes. Plast Reconstr Surg
2017;139:1063–1070.
9. Cordeiro PG, Albomoz CR, McCormick B, et al. The impact of
postmastectomy radiotherapy on two-stage implant breast
reconstruction: an analysis of long-term surgical outcomes, aesthetic
results, and satisfaction over 13 years. Plast Reconstr Surg
2014;134:588–595.
10. Imahiycrobo TA Jr, Small KH, Sackeyfio R, et al. Transition from round
to shaped implants in immediate breast reconstruction: our preferred
approach and clinical outcomes. Aesthetic Plast Surg 2017;41:284–292.
11. McGuire P, Reisman NR, Murphy DK. Risk factor analysis for capsular
contracture, malposition, and late seroma in subjects receiving Natrelle
410 form-stable silicone breast implants. Plast Reconstr Surg
2017;139:1–9.
12. Mallucci P, Branford OA. Concepts in aesthetic breast dimensions:
analysis of the ideal breast. J Plast Reconstr Aesthet Surg 2012;65:8–16.
13. Spear SL, Murphy DK; Allergan Silicone Breast Implant U.S. Core
Clinical Study Group. Natrelle round silicone breast implants: core
study results at 10 years. Plast Reconstr Surg 2014;133:1354–1361.
14. Maxwell GP, Van Natta BW, Bengtson BP, et al. Ten-year results from
the Natrelle 410 anatomical form-stable silicone breast implant core
study. Aesthet Surg J 2015;35:145–155.
15. Spear SL, Seruya M, Clemens MW, et al. Acellular dermal matrix for
the treatment and prevention of implant-associated breast deformities.
Plast Reconstr Surg 2011;127:1047–1058.
16. Clemens MW, Nava MB, Rocco N, et al. Understanding rare adverse
sequelae of breast implants: anaplastic large-cell lymphoma, late
seromas, and double capsules. Gland Surg 2017;6:169–184.
17. Leberfinger AN, Behar BJ, Williams NC, et al. Breast implant-
associated anaplastic large cell lymphoma: a systematic review. JAMA
Surg 2017;152:1161–1168.
18. de Boer M, van Leeuwen FE, Hauptmann M, et al. Breast implants and
die risk of anaplastic large-cell lymphoma in the breast. JAMA Oncol
2018;4:335–341.
19. Brody GS, Deapen D, Taylor CR, et al. Anaplastic large cell lymphoma
occurring in women with breast implants: analysis of 173 cases. Plast
Reconstr Surg 2015;135:695–705.
20. Campanale A, Boldrini R, Marietta M. 22 cases of BIA-ALCL:
awareness and outcome tracking from the Italian Ministry of Health.
Plast Reconstr Surg 2018; 141(1):11e-19e.
21. Doren EL, Miranda RN, Selber JC, et al. U.S. epidemiology of breast
implant-associated anaplastic large cell lymphoma. Plast Reconstr Surg
2017;139:1042–1050.
22. Jones G, Yoo A, King V, et al. Prepectoral immediate direct-to-implant
breast reconstruction with anterior AlloDerm coverage. Plast Reconstr
Surg 2017;140(6S Prepectoral Breast Reconstruction):31S–38S.
23. Pittman TA, Abbate OA, Economides JM. The PI method: prepectoral
breast reconstruction to minimize the palpable implant edge and upper
pole rippling. Ann Plast Surg 2018;80:487–492.
24. Cattelani L, Polotto S, Arcuri MF, et al. One-step prepectoral breast
reconstruction with dermal matrix-covered implant compared to
submuscular implantation. Functional and cost evaluation. Clin Breast
Cancer 2018;18:e703–e711.
25. Downs RK, Hedges K. An alternative technique for immediate direct-to-
implant breast reconstruction: a case series. Plast Reconstr Surg Glob
Open 2016;4:e821.
26. Vardanian AJ, Clayton JL, Roostaeian J, et al. Comparison of implant-
based immediate breast reconstruction with and without acellular dermal
matrix. Plast Reconstr Surg 2011;128:403e–410e.
27. Sbitany H. Management of the post-breast reconstruction
“hyperanimation deformity.” Plast Reconstr Surg 2014;133:897e–898e.
28. Ursino S, Fiorica F, Mazzotti V, et al. The role of clinicopathologic and
molecular prognostic factors in the post-mastectomy radiotherapy
(PMRT): a retrospective analysis of 912 patients. Eur Rev Med
Pharmacol Sci 2017;21:2157–2166.
29. Jassem J. Post-mastectomy radiation therapy after breast reconstruction:
indications, timing and results. Breast 2017;34(Suppl 1):S95–S98.
30. Magill LJ, Robertson FP, Jell G, et al. Determining die outcomes of
post-mastectomy radiation therapy delivered to the definitive implant in,
patients undergoing one and two-stage implant-based breast
reconstruction: a systematic review and meta-analysis. J Plast Reconstr
Aesthet Surg 2017;70:1329–1335.
31. Santosa KB, Chen X, Qi J, et al. Postmastectomy radiation therapy and
two-stage implant-based breast reconstruction: is there a better time to
irradiate? Plast Reconstr Surg 2016;138:761–769.
32. Sigalove S, Maxwell GP, Sigalove NM, et al. Prepectoral implant-based
breast reconstruction: rationale, indications and preliminary results.
Plast Reconstr Surg 2017;139:287–294.
33. Maxwell GP, Gabriel A. Bioengineered breast: concept, technique, and
preliminary results. Plast Reconstr Surg 2016;137:415–421.
34. Hammond DC, Schmitt WP, O’Connor EA. Treatment of breast
animation deformity in implant-based reconstruction with pocket change
to the subcutaneous position. Plast Reconstr Surg 2015;135:1540–1544.
35. Serra-Mestre JM, Muñoz-Olmo JL, Serra-Mestre JM. Fat grafting in
post-mastectomy breast reconstruction with expanders and prostheses in
patients who have received radiotherapy: formation of new
subcutaneous tissue. Plast Reconstr Surg 2010;125:12–18.
36. Kalus R, Dixon Swartz J, Metzger SC. Optimizing safety, predictability
and aesthetics in direct to implant immediate breast reconstruction:
evolution of surgical technique. Ann Plast Surg 2016;76(Suppl 4):S320–
S327.
37. Cordeiro PC, Jazayeri L. Two-stage implant-based breast reconstruction:
an evolution of the conceptual and technical approach over a two-decade
period. Plast Reconstr Surg 2016;138:1–11.
38. El-Sabawi B, Sosin M, Carey JN, et al. Breast reconstruction and
adjuvant therapy: a systematic review of surgical outcomes. J Surg
Oncol 2015;112:458–464.
39. Lee HK, Jin US, Lee YH. Subpectoral and precapsular implant
repositioning technique: correction of capsular contracture and implant
malposition. Aesthetic Plast Surg 2011;35:1126–1132.
40. Melmed EP. Treatment of breast contractures with open capsulotomy
and replacement of gel prostheses with polyurethane-covered implants.
Plast Reconstr Surg 1990;86:270–274
41. Xue H, Lee SY. Correction of capsular contracture by insertion of a
breast prosthesis anterior to the original capsule and preservation of the
contracted capsule: technique and outcomes. Aesthetic Plast Surg
2011;35:1056–1060.
42. Baran CN, Peker F, Ortak T, et al. A different strategy in the surgical
treatment of capsular contracture: leave capsule intact. Aesthetic Plast
Surg 2001;25:427–431.
43. Barbosa MV, Nabas FX, Ferreira LM. Capsulectomy: a mandatory
procedure in the presence of capsular calcification. Plast Reconstr Surg
2006;17:1654–1655.
44. Sbitany H, Piper M, Lentz R. Prepectoral breast reconstruction: a safe
alternative to submuscular prosthetic reconstruction following nipple-
sparing mastectomy. Plast Reconstr Surg 2017;140:432–443.
45. Nahabedian MY, Cocilovo G. Two-stage prosthetic breast
reconstruction: a comparison between prepectoral and partial
subpectoral techniques. Plast Reconstr Surg 2017;140 (6S Prepectoral
Breast Reconstruction):22S–30S.
46. Gabriel A, Sigalove S, Sigalove NM, et al. Prepectoral revision breast
reconstruction for treatment of implant-associated animation deformity:
a review of 102 reconstructions. Aesthet Surg J 2018;38:519–526.
47. de Blacam C, Momoh AO, Colakoglu S, et al. Evaluation of clinical
outcomes and aesthetic results after 5 autologous fat grafting for contour
deformities of the reconstructed breast. Plast Reconstr Surg
2011;128:411e–418e.
48. Khouri R, Rigotti G, Cardoso E, et al. Mega volume autologous fat
transfer: part II. Practices and techniques. Plast Reconstr Surg
2014;133:1369–1377.
CHAPTER 64

Implant-Based Breast Reconstruction


After Unilateral Mastectomy
CHAD M. TEVEN | BHARAT RANGANATH | JOSEPH J. DISA
HISTORY
Breast cancer is the most common nonskin malignancy in women in the
United States. Nearly one in eight women will be affected during their
lifetime. Standard of care for locoregional control includes surgical
extirpation in the form of total mastectomy or partial mastectomy (i.e.,
lumpectomy). Additional treatments may include radiotherapy as well as
systemic forms of therapy such as chemotherapy, hormonal agents, and
targeted therapy. The surgical removal of the breast is a highly morbid
procedure that can result in functional, aesthetic, and psychological sequelae.
To mitigate these effects, patients should consult with plastic surgeons to
discuss options to restore their breast.
The benefits of breast reconstruction are myriad and include improved
symmetry of the chest, a superior breast shape, and the avoidance of having
to use an external breast prosthesis. Importantly, breast reconstruction has
been associated with improved body image, quality of life (QoL), self-
confidence, and self-esteem (1). The initial question one must consider in the
treatment of a breast cancer patient is whether she is in fact a candidate for
breast reconstruction. Assuming one is an appropriate candidate, several
factors must be considered including the timing of reconstruction, whether
autologous tissue or prosthetic implants will be used, and if the procedure is
unilateral or bilateral. Furthermore, if a patient is to undergo implant-based
reconstruction, an appropriate implant type and material must be chosen from
numerous options. In cases of unilateral reconstruction, it is important to also
thoughtfully consider whether the patient would benefit from a symmetrizing
procedure to the contralateral breast. As the amount of information regarding
breast reconstruction continues to increase exponentially, a crucial aspect of a
successful outcome is proper patient education (2). Plastic surgeons offering
breast reconstruction must have a clear understanding of the options available
and their attendant advantages and disadvantages.
The number of women undergoing mastectomy has increased in recent
years. This is due to both an increase in the incidence of breast cancer in the
United States as well as a concomitant rise in the number of prophylactic
mastectomies performed for risk reduction (3). As a result, the number of
reconstructive procedures has also risen. Prior to 2002, autologous tissue was
the more frequently used option for breast reconstruction. More recently,
rates of implant-based reconstruction have increased and now may
outnumber autologous reconstruction by a ratio of 2:1 (4). Several factors
may account for this trend including increased difficulty and operative time
associated with autologous reconstruction, changing reimbursement patterns,
and increased acceptance of implants by patients and the public (5).
Modern thought processes regarding the use of implants in breast
reconstruction took hold in the 1960s when silicone implants were
introduced. Since then, the materials and technology used to produce
implants have progressed significantly, leading to improved clinical
outcomes. Presently, implants used for breast reconstruction are filled with
either silicone or saline. The decision of which material to use is an
individual one, often made by the patient and her surgeon after weighing the
relative risks and benefits of each. Additional decisions that must be made for
implant-based reconstruction include reconstruction timing, whether the
reconstruction is performed in one or two stages, and the plane into which the
implant will be placed. This chapter will detail unilateral implant-based
reconstruction after mastectomy and examine the decisions that must be
considered when performing this procedure.
INDICATIONS
When deciding whether a patient is an appropriate candidate for implant-
based reconstruction, important considerations include surgical history,
comorbidities, previous and planned radiation, body habitus, patient wishes,
and surgeon preference (6). Some evidence suggests that long-term outcomes
may be improved after autologous reconstruction compared to implant-based
reconstruction (7). However, this is not universally true and there are distinct
situations in which implant-based reconstruction is preferred. Advantages of
implant-based reconstruction compared to autologous options include
decreased operative time and recovery, technical ease, absence of donor site
morbidity, and a potentially improved cosmetic outcome by using adjacent
tissue to cover the implant (8). Additional reasons to avoid autologous-based
reconstructive options include significant medical and social factors as well
as limited donor tissue. Ideal candidates for prosthetic reconstruction have
small or moderate native breast volume, adequate skin and soft tissue for
coverage, and a mild degree of breast ptosis. Patients who will not require
adjuvant radiotherapy are also superior candidates.
Prosthetic reconstruction is generally performed as a one- or two-stage
procedure. Single-stage or primary reconstruction involves placement of an
implant at the time of mastectomy and may be referred to as direct-to-implant
(DTI) reconstruction. Two-stage reconstruction denotes the placement of a
temporary tissue expander at the time of mastectomy. Using an integrated or
remote port, the expander is gradually inflated over the course of several
weeks or months until the desired volume is reached. Typically, 1 to 4
months after the completion of expansion, the patient is returned to the
operating room for a second stage in which the expander is removed and
replaced by a permanent implant. The majority of prosthetic reconstructions
are performed in two stages (9). A two-stage approach is preferable when
there is insufficient skin or soft tissue after mastectomy as well as when there
is concern about mastectomy flap viability. A further advantage of a two-
stage approach, by allowing for adjustments, revisions, and scar release at the
second surgery, is improved control of the shape, configuration, and outcome
of the reconstruction by the surgeon. Indications for single-stage
reconstruction include nonobese patients with relatively small, nonptotic
breasts; well-vascularized mastectomy flaps; and sufficient skin and soft
tissue coverage (8). Single-stage reconstruction has the advantage of fewer
procedures and should be considered for patients refusing multiple surgeries
(10).
CONTRAINDICATIONS
Although few absolute contraindications to prosthetic breast reconstruction
exist, many factors are linked to postoperative complications and suboptimal
outcomes. Such factors may be related to the patient, extirpative surgery, or
planned adjuvant treatments. With respect to the patient, relative
contraindications to implant-based reconstruction include obesity (BMI ≥30
kg/m2), very large and/or ptotic breasts, and advanced disease. Additionally,
active smoking and a history of diabetes also significantly increases
postoperative complications and are relative contraindications to prosthetic
reconstruction (11). Obesity is associated with an increased risk of surgical
complications such as infection, seroma, hematoma, wound breakdown, and
implant failure, as well as postoperative medical complications (12).
Additionally, the likelihood of an aesthetically acceptable reconstruction with
implants is significantly reduced for obese patients or patients with large,
pendulous breasts. Part of the challenge relates to the fact that mastectomy
flaps are much less predictable the larger they are. In addition, in these cases
it is difficult to obtain adequate symmetry with the contralateral breast.
Indeed, prosthetic reconstruction has been associated with reduced patient
satisfaction compared to autologous reconstruction and should therefore be
reserved for carefully selected cases (13).
Factors related to the extirpative surgery must also be considered prior to
breast reconstruction. For example, if insufficient skin or soft tissue remains
after resection, autologous or combined reconstruction (e.g., latissimus dorsi
flap + tissue expander) may be preferred to prosthetic reconstruction. For
patients insistent on prosthetic reconstruction, a two-stage approach should
be employed if there is insufficient coverage for the implant after
mastectomy. A further strategy to mitigate this issue is the use of acellular
dermal matrices (ADMs). In patients with thin skin and soft tissue envelopes,
the use of ADM can reduce untoward effects of the implant such as rippling,
palpability, and visibility.
While postmastectomy radiation therapy (PMRT) does not preclude
prosthetic reconstruction, caution is advised in these cases. Numerous studies
have demonstrated that PMRT substantially increases the rate of
complications after prosthetic reconstruction (14). PMRT is also associated
with complications after autologous reconstruction, but to a lesser degree
than with prosthetic reconstruction (14). Accordingly, autologous
reconstruction is preferred by the majority of plastic surgeons if PMRT is
planned. In our practice, autologous reconstruction is recommended to
patients in need of PMRT unless they are not suitable candidates for
autologous reconstruction (e.g., insufficient donor tissue).
PREOPERATIVE PLANNING
Optimal planning of breast reconstruction involves close collaboration
between the plastic surgeon, breast surgeon, radiation and medical
oncologists, and patient. A thorough history and physical examination will
aid in guiding the discussion regarding the safety and efficacy of different
reconstructive options. Once the decision to proceed with reconstruction is
made, the timing of reconstruction must be considered. Breast reconstruction
may occur at the time of mastectomy (immediate reconstruction) or at a later
operation after the patient has sufficiently healed from the extirpative surgery
(delayed reconstruction).

TABLE 64-1 Characteristics of Saline and Silicone Breast Implants


Saline Silicone
Advantages Lower cost More natural look/feel
Saline quickly absorbed if Improved aesthetic outcome
ruptures
Disadvantages Hard, uncomfortable Associated with ALCL
Increased ripping (textured)
Increased cost
Rupture may be undetectable
clinically
ALCL, anaplastic large cell lymphoma.

Immediate breast reconstruction has several advantages compared to


delayed reconstruction. It allows for a more efficient process, improves
psychosocial outcomes (15), and reduces overall cost (16). Additionally,
normal anatomic landmarks of the breast are better preserved, thereby
potentially providing for a more natural appearance (17). Delayed
reconstruction should be considered in cases of advanced disease that are
likely to require PMRT as well as for patients with significant medical
comorbidities or social habits (e.g., active smoking) who may be at risk for
increased complications with a longer operation (18). Delayed reconstruction
should be considered in the setting of PMRT because PMRT may be linked
with worse outcomes in immediate reconstruction. Additionally, the delivery
of radiation may be negatively impacted by the presence of expanders or
implants. In addition, mastectomy skin flap necrosis can impair the aesthetic
appearance of breast reconstruction. If there is concern about perfusion to the
mastectomy flaps at the time of mastectomy, the surgeon should consider
delaying reconstruction (19).
Additional considerations during preoperative planning include implant
selection, reconstruction staging (one vs. two stage), incision location, and
the need for a contralateral symmetry procedure. Table 64-1 lists
characteristics of saline and silicone implants. Silicone implants are more
commonly used in the United States due to a perceived improvement of
appearance, comfort, and softness associated with their use. However, no
large-scale study comparing various implant types has demonstrated
improved outcomes associated with specific implants (20). Additional
features of breast implants are noted in Table 64-2. Recent reports have
linked textured implants to anaplastic large cell lymphoma (21). Therefore,
the practice pattern at our institution has shifted such that we no longer offer
textured implants and only offer smooth round implants to patients requesting
implant-based reconstruction.

TABLE 64-2 Features of Breast Implants That Must Be Considered Prior to


Reconstruction
Fill Saline vs. silicone
Surface Smooth vs. textured
Number of Compartments Single lumen vs. double lumen
Shape Round vs. anatomic
Dimensions Height
Width
Projection

For patients undergoing a staged reconstruction, numerous tissue


expanders exist. The majority of expanders used in the United States consist
of a silicone shell that is periodically filled with saline to expand the soft
tissue until the desired breast size and shape is reached. A recent alternative
to saline-filled expanders is a device that is incrementally filled with carbon
dioxide and can be controlled by the patient at home (22). Expansion with
saline typically commences 1 to 3 weeks after surgery and is expanded over
the course of 6 to 8 weeks. Four to 8 weeks after the completion of
expansion, the patient returns to the operating room for replacement of the
expander with a permanent implant. This schedule may vary for patients who
require adjuvant chemotherapy or radiotherapy and is patient specific.
During planning, the plastic surgeon and breast surgeon must also address
the incision and skin excision pattern to be performed. Numerous skin
patterns exist and depend on several factors including native breast size and
shape, body habitus, location and size of the tumor, whether skin or the
nipple areola complex (NAC) will be spared, and the surgical and adjuvant
treatment plan (Fig. 64-1). In risk-reducing and nipple-sparing mastectomies,
the incision is often placed either at the inframammary crease or along the
NAC margin and may include a lateral extension. In skin-sparing, simple,
and modified radical approaches, incision placement and skin excision should
facilitate effective removal of the breast and a negligible chance of
recurrence, while optimizing perfusion to the remaining mastectomy flaps.
The goal is for well-vascularized coverage of the implant or expander. This
can be accomplished with several different approaches including inverted T-
and Y-shaped incisions, elliptical skin excisions (vertical, transverse,
oblique), and mastopexy and reduction techniques.
FIGURE 64-1 A sample of the numerous possible skin excision patterns is shown.

An acceptable cosmetic result requires relative symmetry between breasts.


Indeed, achieving symmetry is inherently difficult in unilateral implant-based
reconstruction. This challenge is further exacerbated in obese patients and
those with severe ptosis. In such patients, a contralateral symmetry procedure
such as breast augmentation, mastopexy, or reduction may be helpful. The
symmetrizing procedure should be performed at the time of permanent
implant placement. Furthermore, patients whose extirpative surgery included
resection of the NAC may desire reconstruction. Numerous reconstructive
techniques exist, including surgical and tattoo options (23). NAC
reconstruction is often the final stage of reconstruction, generally 2 to 4
months after implant placement.
The final aspect of planning requires marking the patient prior to surgery.
This can be done preoperatively or intraoperatively prior to the mastectomy.
Marks include the midline, inframammary fold, and planned incisions.
OPERATIVE TECHNIQUE
Breast reconstruction is typically performed with the patient supine, under
general anesthesia, and after the administration of perioperative antibiotics.
Our preference is for the arms to be at the patient’s side during
reconstruction. If the breast surgeon desires the arms to be positioned away
from the patient, as is often the case during SLNB (sentinel lymph node
biopsy) or ALND (axillary lymph node dissection), the arms are sterilely
draped with a stockinette that can be attached to the patient during
reconstruction. Once the mastectomy is complete, the surgical site is
inspected for adequate hemostasis, perfusion to the mastectomy flaps, and
appropriate position of anatomic landmarks of the breast. The native boarders
may have been violated during resection and would then require
reconstruction. This is common at the inframammary fold and lateral breast
boarder. Vascularity of the mastectomy flaps is evaluated clinically by
appearance, color, and capillary refill. In equivocal cases, intraoperative laser
angiography using a SPY machine may further elucidate blood flow to the
mastectomy flaps. If perfusion is severely reduced, reconstruction should be
delayed.
In immediate two-stage reconstruction, the tissue expander is introduced at
the time of mastectomy. The expander may be placed in a totally
submuscular plane, a partially submuscular plane (Fig. 64-2), or in a plane
above the pectoralis major muscle (i.e., prepectoral; Fig. 64-3). Historically,
expanders were typically placed totally submuscular, beneath the pectoralis
major, pectoralis minor, serratus anterior, and rectus muscles. Submuscular
placement was thought to reduce postoperative complications including
infection, extrusion, and implant loss. However, it also causes flattening of
the expander, particularly at the inferior pole; difficulty in achieving full
expansion and a natural breast shape; and increased pain and discomfort
related to extensive submuscular dissection. To reduce these adverse effects,
surgeons began placing expanders partially submuscular, beneath the
pectoralis major only. In partial muscle coverage, the superior and middle
aspects of the expander are covered by muscle while the inferior portion is
covered by the mastectomy flaps. This results in a more natural and improved
appearance as the lower pole has more room for expansion than in total
muscle coverage. The disadvantage, however, is that only a thin layer of soft
tissue covers the inferior expander. Breakdown of the overlying flaps can
result in implant exposure and infection. Therefore, if partial muscle coverage
is going to be performed, the mastectomy flaps must be healthy and well
vascularized.
One strategy that combines the advantages of both total and partial muscle
coverage is a dual plane technique. With this approach, the superior expander
is covered by pectoralis major muscle just as with partial submuscular
coverage. Coverage of the inferior expander, in addition to the mastectomy
flaps, is provided by ADM. ADM, which is a biologic scaffold consisting of
decellularized human or animal dermis, has distinct advantages. It augments
soft tissue coverage by the mastectomy flaps, it prevents “window shading”
or upward migration of the pectoralis major muscle, and it facilitates
improved control of the mastectomy pocket (8). It may also allow for a larger
initial fill during intraoperative expansion, thereby reducing the time to
permanent implant placement. However, ADM use is costly and may result in
increased seroma formation.
A more recent strategy in prosthetic reconstruction is placement of the
expander and implant in a prepectoral plane (Fig. 64-4). Advantages of this
approach relate to not having to elevate and dissect the pectoralis muscle,
thereby reducing postoperative pain, muscle distortion, and animation
deformity (24). Limitations include the need for extreme caution in patient
selection and a lack of long-term follow-up data. Because there is no muscle
barrier between the implant and mastectomy flaps, wound breakdown and
mastectomy skin flap necrosis result in dire consequences including implant
exposure and explantation. Similar to dual plane reconstruction, ADM may
be used in this setting to provide an additional tissue layer. Several
techniques have been employed; one common approach is to secure the ADM
entirely around the implant in circumferential fashion and fasten the construct
within the mastectomy pocket at various points around the periphery of the
mastectomy pocket. Another consists of placing meshed ADM anterior to an
expander or implant and suturing it in place around the breast prosthesis. The
ADM serves to secure the position of the prosthesis and also to add an extra
layer of soft tissue between the prosthesis and skin. This ADM should
incorporate with the native tissues, which can often be seen at a second
operation (Fig. 64-5).
FIGURE 64-2 Prepectoral breast reconstruction is increasingly common and may
produce excellent results in appropriately selected patients.

FIGURE 64-3 Acellular dermal matrices are used for both prepectoral and
subpectoral breast reconstruction to secure the prosthesis in place and to provide
additional soft tissue coverage.
FIGURE 64-4 Implant sizers are crucial for a successful outcome in subpectoral and
prepectoral breast reconstruction.

FIGURE 64-5 Submuscular implant placement.


FIGURE 64-6 Prepectoral implant placement.

Second Stage
In cases of two-stage reconstruction, the patient returns to the operating room
several weeks after the completion of expansion for implant exchange. It is
important not to rush the second stage as too quick a time frame between the
initial operation and exchange can result in a less developed or tighter skin
envelope than preferred.
The pocket is accessed through the mastectomy scar. This can be excised
and sent for permanent pathology. If the capsule that surrounds the expander
is thick or tight, capsulotomy or capsulectomy can be performed. Similar to
the placement of the expander, the pocket is irrigated with antibiotic solution
and fresh surgical gloves are donned to put in the implant. Although the size
of the implant may be ascertained based on the volume of fluid within the
expander, one can use a sizer for further precision. Sizers are appropriate
whether implants are placed prepectorally or subpectorally (Fig. 64-6). Once
the implant has been positioned, a drain may be used but is not always
required. The incision is closed in layers and a bra and dressings are applied.
POSTOPERATIVE CARE
Good postoperative care and appropriate follow-up after device placement is
paramount. Patients should be regularly and closely monitored for
appropriate wound healing and signs of infection so that these issues can be
addressed quickly if they arise. It is also important to counsel patients early
and often regarding warning signs as well as general expectations for drain
care, expansion timeline, and chemo/XRT considerations.
Postoperatively, patients are placed in a well-padded bra to provide gentle
support, which they are to wear at all times when not showering. Incisions are
dressed with gauze and a clear occlusive dressing and patients are allowed to
shower after 48 hours.
Drains
Patients are educated on appropriate drain care preoperatively and
postoperatively. As a general rule, drains remain in place until output is less
than 30 mL per day for 2 consecutive days. Generally, we find that drains
remain in place for about 1 to 3 weeks after mastectomy and tissue expander
placement (particularly longer if more ADM is used). The use of drains at the
time of expander exchange to a permanent implant is not always necessary
and generally is the preference of the surgeon. Though not necessarily
universal, our practice has generally been to keep patients on postoperative
antibiotics while drains are in place.
Follow-Up
Patients with tissue expanders are seen at 1 and 2 weeks postoperatively and
then expanded regularly, generally at weekly intervals, until they reach the
target size.
Chemotherapy Considerations
Patients are followed closely in the clinic to assess for appropriate wound
healing and signs of infection. As long as wounds are healing appropriately,
we routinely allow patients to begin chemotherapy rather quickly and we
commence and continue expansion through chemotherapy.
Radiation Considerations
If radiation therapy is expected, it has been our practice to rapidly expand and
move to second stage as quickly as possible. Once the expander is replaced
with the permanent implant, we allow radiation therapy to being to the final
implant. Our data has found that this approach decreases postoperative
infections and wound complications, though it does lead to somewhat higher
rates of long-term capsular contracture (25). Another option, particularly in
the setting of neoadjuvant chemotherapy, is to radiate the expander and delay
the exchange until the acute effects of radiation have resolved. This results in
improved aesthetics and reduced capsular contracture; however, the incidence
of reconstructive failure over time may be higher.
OUTCOMES
Achieving good outcomes after unilateral implant-based breast reconstruction
can be difficult due to the inherent difficulty of matching the artificial side to
the naturally soft, ptotic contralateral breast. However, using techniques
described in this chapter we do feel that delivering an acceptable and
aesthetically pleasing outcome is possible with appropriate preoperative
planning and adhering to the principles outlined (Figs. 64-5 and 64-6).
CONCLUSION
Successful unilateral implant-based breast reconstruction requires attention to
anatomic landmarks and principles as well as careful consideration of pre-
and postoperative factors such as radiation therapy. As cancer care evolves
and trends in patient preference and payor mix change, the ability to create an
aesthetically pleasing breast that matches the contralateral side when
autologous reconstruction is either not preferred or possible will continue to
be a necessary and valuable skill for all plastic surgeons.

REFERENCES

1. Wilkins EG, Cederna PS, Lowery JC, et al. Prospective analysis of


psychosocial outcomes in breast reconstruction: one-year postoperative
results from the Michigan Breast Reconstruction Outcome Study. Plast
Reconstr Surg 2000;106(5):1014–1025; discussion 1026–1027.
2. Heller L, Miller MJ. Patient education and decision making in breast
reconstruction. Semin Plast Surg 2004;18(2):139–147.
3. Craft RO, Colakoglu S, Curtis MS, et al. Patient satisfaction in unilateral
and bilateral breast reconstruction [outcomes article]. Plast Reconstr
Surg 2011;127(4):1417–1424.
4. Quinn TT, Miller GS, Rostek M, et al. Prosthetic breast reconstruction:
indications and update. Gland Surg 2016;5(2):174–186.
5. Albornoz CR, Bach PB, Mehrara BJ, et al. A paradigm shift in U.S.
Breast reconstruction: increasing implant rates. Plast Reconstr Surg
2013;131(1):15–23.
6. Djohan R, Gage E, Bernard S. Breast reconstruction options following
mastectomy. Cleve Clin J Med 2008;75 Suppl 1:S17–S23.
7. Alderman AK, Wilkins EG, Lowery JC, et al. Determinants of patient
satisfaction in postmastectomy breast reconstruction. Plast Reconstr
Surg 2000;106(4):769–776.
8. Nahabedian M. Implant-based breast reconstruction and augmentation.
In: Butler C, Collins K, eds. UpToDate. Waltham, MA; 2019.
9. ASPS Procedural Statistics. [Internet]. 2015 [cited 2019 Mar 15].
Available online at
https://www.plasticsurgery.org/documents/News/Statistics/2015/plastic-
surgery-statistics-full-report-2015.pdf
10. Colwell AS, Damjanovic B, Zahedi B, et al. Retrospective review of 331
consecutive immediate single-stage implant reconstructions with
acellular dermal matrix: indications, complications, trends, and costs.
Plast Reconstr Surg 2011;128(6):1170–1178.
11. Yuen JC, Coleman CA, Erickson SW. Obesity-related risk factors in
implant-based breast reconstruction using AlloDerm. Plast Reconstr
Surg Glob Open 2017;5(2):e1231.
12. Panayi AC, Agha RA, Sieber BA, et al. Impact of obesity on outcomes
in breast reconstruction: a systematic review and meta-analysis. J
Reconstr Microsurg 2018;34(5):363–375.
13. Juhl AA, Christensen S, Zachariae R, et al. Unilateral breast
reconstruction after mastectomy—patient satisfaction, aesthetic outcome
and quality of life. Acta Oncol 2017;56(2):225–231.
14. Yun JH, Diaz R, Orman AG. Breast reconstruction and radiation
therapy. Cancer Control 2018;25(1):1073274818795489.
15. Al-Ghazal SK, Sully L, Fallowfield L, et al. The psychological impact
of immediate rather than delayed breast reconstruction. Eur J Surg
Oncol 2000;26(1):17–19.
16. Khoo A, Kroll SS, Reece GP, et al. A comparison of resource costs of
immediate and delayed breast reconstruction. Plast Reconstr Surg
1998;101(4):964–968; discussion 969–970.
17. Chawla AK, Kachnic LA, Taghian AG, et al. Radiotherapy and breast
reconstruction: complications and cosmesis with TRAM versus tissue
expander/implant. Int J Radiat Oncol Biol Phys 2002;54(2):520–526.
18. Nahabedian M. Overview of breast reconstruction. In: Chagper A,
Collins K, eds. UpToDate [Internet]. Waltham, MA; 2018. [cited 2019
Mar 15]. Available online at www.uptodate.com
19. Zenn MR. Staged immediate breast reconstruction. Plast Reconstr Surg
2015;135(4):976–979.
20. Rocco N, Rispoli C, Moja L, et al. Different types of implants for
reconstructive breast surgery. Cochrane Database Syst Rev 2016;
(5):CD010895.
21. Leberfinger AN, Behar BJ, Williams NC, et al. Breast implant-
associated anaplastic large cell lymphoma: a systematic review. JAMA
Surg 2017;152(12):1161–1168.
22. Ascherman JA, Zeidler K, Morrison KA, et al. Carbon dioxide-based
versus saline tissue expansion for breast reconstruction: results of the
XPAND prospective, randomized clinical trial. Plast Reconstr Surg
2016;138(6):1161–1170.
23. Gougoutas AJ, Said HK, Um G, et al. Nipple-areola complex
reconstruction. Plast Reconstr Surg 2018;141(3):404e–416e.
24. Liliav B, Patel P, Jacobson AK. Prepectoral breast reconstruction: a
technical algorithm. Plast Reconstr Surg Glob Open 2019;7(2):e2107.
25. Cordeiro PG, Albornoz CR, McCormick B, et al. What is the optimum
timing of postmastectomy radiotherapy in two-stage prosthetic
reconstruction: radiation to the tissue expander or permanent implant?
Plast Reconstr Surg 2015;135(6):1509–1517.
CHAPTER 65

Patient Satisfaction in Unilateral


Versus Bilateral Mastectomy With
Reconstruction
HANI SBITANY
HISTORY
Implant-based breast reconstruction continues to be the most utilized
technique for postmastectomy reconstruction in the United States, with over
85,000 cases performed in 2015 (1,2). Techniques involving both 2-stage
(expander–implant) reconstruction and single-stage reconstruction, have
advanced significantly in the past decade, with excellent aesthetic outcomes
consistently being achieved due to improved tools such as cohesive anatomic
implants and acellular dermal matrices (ADMs) (3–6).
Simultaneously, the increasing use of nipple-sparing mastectomy (NSM)
techniques has also improved outcomes and patient satisfaction with
postmastectomy breast reconstruction (7). Large series have shown that NSM
is oncologically safe, compared with skin-sparing techniques, and this has led
to greater acceptance and experience (8). Patients now routinely benefit from
the ability to maintain the entire external breast skin envelope for use in their
reconstruction, and this has improved both aesthetic appearance, and patients’
quality of life.
Along the same time period, autologous tissue breast reconstruction
techniques have also improved significantly. Perforator flaps allow for
harvest of excess subcutaneous tissue and skin for reconstruction, without
sacrificing donor site muscle, patient’s strength, or overall function.
Furthermore, the development of new flap techniques have allowed surgeons
to assess multiple anatomic locations on a patient’s body, and in many cases,
harvest tissue from areas the patients prefer, based on blood supply. This can
include the abdomen, thighs, buttock, and back. All this is while offering fat
that is similar in appearance, feel, and form to the excised breast parenchyma
after mastectomy.
When assessing specific patient satisfaction outcomes with breast
reconstruction, there are many variables that must be separately analyzed, as
they play a significant role in overall satisfaction. Most importantly, this
includes whether the patient has undergone a unilateral or bilateral
reconstruction. There has long been the thought that unilateral reconstruction
presents a greater challenge to the surgeon in achieving symmetry, given that
a reconstructed breast and prosthesis must be matched to a native breast.
Alternatively, when bilateral reconstruction is performed, achieving
symmetry is theoretically easier, as the final product on each breast is
identical. These factors thus play a large role in ultimate patient satisfaction.
EFFECT OF RECONSTRUCTION OPTION ON PATIENT SATISFACTION
A number of factors have been found to be instrumental in determining
patient satisfaction with breast reconstruction. When assessing type of breast
reconstruction, data exists showing that overall long-term satisfaction is
higher with autologous reconstruction, relative to prosthetic reconstruction
(9). The ability of autologous reconstruction to provide greater long-term
satisfaction likely is a byproduct of the autologous tissue offering avoidance
of capsular contracture and other implant-related complications, and the more
natural feel and appearance of tissue. However despite this, prosthetic
reconstruction is more commonly performed in cases of bilateral breast
reconstruction, where achieving symmetry is less difficult. Thus, both types
of reconstruction must be carefully assessed when reporting patient
satisfaction.
SCALE FOR ASSESSING PATIENT-REPORTED OUTCOMES
The use of a validated patient-reported outcomes survey scale is critical. The
most commonly used tool is the BREAST-Q survey (10). Use of this tool is
instrumental in obtaining scientifically quantifiable patient-reported outcome
measures that are pertinent and applicable. As such, this tool allows us to
study the impact and effectiveness of breast surgery from the patient’s
perspective.
PATIENT SATISFACTION DATA
Numerous large cohort studies have been done to date, showing higher
patient satisfaction rates with autologous reconstruction, compared to
prosthetic reconstruction.
Alderman et al. reported that over the first 2 years post reconstruction,
those undergoing autologous scored higher for both aesthetic and general
satisfaction (11). While a smaller subset, those patients undergoing longer-
term analysis similarly showed higher satisfaction in the autologous cohort.
However, this study did not separate unilateral and bilateral reconstruction
patients.
Liu et al. used the BREAST-Q to illustrate a similar higher level of patient
satisfaction and quality of life with autologous reconstruction (9). However,
this study assessed only unilateral reconstruction patients.
To date, the most comprehensive study assessing the effects of unilateral
versus bilateral mastectomy and reconstruction on patient-reported
satisfaction was conducted by Taylor et al. (12). This prospective study both
separated patients out into cohorts based on their option to undergo unilateral
versus bilateral mastectomy, and also compared the two cohorts to each
other.
When assessing the unilateral group, the authors of this study found that
autologous reconstruction patients scored higher than those in the implant
group, in the categories of satisfaction with breast, psychosocial well-being,
and sexual well-being. As a byproduct of this, more patients in the unilateral
implant reconstruction cohort (59.5%) were found to have undergone
contralateral symmetry procedures for balancing, relative to a fewer number
(45.1%) in the autologous cohort.
In both cohorts, when assessing unilateral reconstruction patients, the
satisfaction scores were lower in patients treated with postmastectomy
radiation. This included diminished satisfaction with the breast reconstruction
overall, psychosocial well-being, and sexual well-being. Over many studies,
postmastectomy radiation therapy has been found to be the only treatment
factor consistently impacting reconstruction outcomes in a negative manner
in most BREAST-Q categories. This is due to higher rates of capsular
contracture and implant malposition in the implant-based cohorts, and fat
necrosis and flap volume reduction in the autologous cohort.
When assessing bilateral reconstruction patients, Taylor et al. found that
autologous patients similarly reported higher satisfaction rates, but the
difference with implant-based patients was much less; the two groups were
much more closely matched, and both illustrated high rates of satisfaction
(12). Specifically, there was no difference in patient satisfaction between the
two bilateral groups, in the BREAST-Q categories of psychosocial well-
being and physical well-being. Furthermore, the two groups were statistically
well matched in the categories of sexual well-being. Those categories in
which bilateral autologous patients did score significantly higher than
bilateral implant-based patients included only the overall satisfaction with the
breast; while this was a similar finding to the unilateral reconstruction
groups, this difference in satisfaction between the two groups was less in the
bilateral patients.
EFFECTS OF PATIENT SATISFACTION ON CLINICAL CHOICE
The findings of higher patient satisfaction with both unilateral and bilateral
autologous reconstruction, relative to implant-based reconstruction, are
consistently reproducible over many studies. However, these findings must
be weighed against operative complication rates, recovery timelines, etc.,
when advising patients as to surgical options.
All studies show that overall complications rates are higher with
autologous reconstruction. This is due to the addition of a major secondary
donor site, along with the breast surgical site, as well as longer operative
procedures and recovery periods for autologous reconstruction. This is
greater when autologous bilateral reconstruction is performed.
Thus, weighing the greater morbidity rates of bilateral autologous
reconstruction, even against the slightly higher patient satisfaction rates
relative to bilateral implant-based reconstruction, likely explains why
significantly more patients choose implant-based techniques (13). With
increasing rates of contralateral prophylactic mastectomy in younger patients,
these patients are more likely to be younger, active, and eager to return to
work/life faster. All these factors predispose toward implant-based
reconstruction (14). For patients choosing unilateral reconstruction, there is a
greater relative percentage choosing autologous reconstruction. This is aided
by the patient-reported outcomes studies indicating a significantly higher rate
of satisfaction for unilateral autologous reconstruction.
FUTURE TRENDS IN PATIENT SATISFACTION FOLLOWING BREAST
RECONSTRUCTION
While all the available studies assessing patient satisfaction mirror similar
findings, the satisfaction rates with implant-based reconstruction are likely to
increase in the future, for both unilateral and bilateral reconstruction patients.
This is due to the enhancement of technology related to implant-based
reconstruction available since many of these previous study cohorts were
collected and published.
Implants are improving in terms of gel performance, due to the availability
of cohesive gel in different levels of firmness. This, along with greater
options for implant projections/dimensions, allows for much better matching
to the shape and feel of the patient’s native breasts prior to mastectomy. In
addition to this, ADMs and synthetic meshes now used in breast
reconstruction for prosthetic coverage offer advantages of improved implant
support over time, reduction in capsular contracture rates, and better aesthetic
definition of key landmark positions (IMF, medial cleavage line); all this will
likely also result in greater patient satisfaction with implant-based
reconstruction. The more predictable outcomes afforded by this technology
will significantly assist in unilateral reconstruction, and matching the
position, dimensions, and appearance of the contralateral breast.
In addition to this, the wide adoption of fat grafting offers an autologous
addition to implant-based reconstruction. This ability to tailor implant-based
reconstruction outcomes closer to those of autologous, through injection of
fat to areas in need of contouring and additional volume, will likely improve
well-being and overall satisfaction scores reported by these patients.
Finally, the resurgence of prepectoral implant-based reconstruction
techniques will also result in enhanced patient satisfaction scores. The ability
to safely place implants in the same anatomic plane as breast parenchyma,
has resulted in reduced rates of pain, elimination of hyperanimation, and
improved aesthetic outcomes due to elimination of pectoralis muscle
tightness. Thus, with this shift in clinical paradigms, a likely outcome will be
an improvement in patient satisfaction for unilateral and bilateral implant-
based reconstruction outcomes.
At this time, however, patients should be counseled that in both unilateral
and bilateral breast reconstruction, satisfaction scores are higher with
autologous reconstruction. This is secondary to the enhanced appearance and
feel relative to the native breasts. This should be presented, along with
anticipated complication rates of the two procedures, when presenting
patients with their options.

REFERENCES

1. Sbitany H, Amalfi AN, Langstein HN. Preferences in choosing between


breast reconstruction options: a survey of female plastic surgeons. Plast
Reconstr Surg 2009;124(6):1781–1789.
2. American Society of Plastic Surgeons. 2015 Plastic Surgery Procedural
Statistics. Available online at
https://www.plasticsurgery.org/news/plastic-surgery-statistics. Accessed
November 6, 2016.
3. Strock LL. Two-stage expander implant reconstruction: recent
experience. Plast Reconstr Surg 2009;124(5):1429–1436.
4. Roostaeian J, Sanchez I, Vardanian A, et al. Comparison of immediate
implant placement versus the staged tissue expander technique in breast
reconstruction. Plast Reconstr Surg 2012;129(6):909e–918e.
5. Colwell AS, Damjanovic B, Zahedi B, et al. Retrospective review of 331
consecutive immediate single-stage implant reconstructions with
acellular dermal matrix: indications, complications, trends, and costs.
Plast Reconstr Surg 2011;128(6):1170–1178.
6. Serletti JM, Fosnot J, Nelson JA, et al. Breast reconstruction after breast
cancer. Plast Reconstr Surg 2011;127(6):124e–135e.
7. Spear SL, Willey SC, Feldman ED, et al. Nipple-sparing mastectomy for
prophylactic and therapeutic indications. Plast Reconstr Surg
2011;128(5):1005–1014.
8. Peled AW, Duralde E, Foster RD, et al. Patient-reported outcomes and
satisfaction after total skin-sparing mastectomy and immediate
expander-implant reconstruction. Ann Plast Surg 2014;72 Suppl 1:S48–
S52.
9. Liu C, Zhuang Y, Momeni A, et al. Quality of life and patient
satisfaction after microsurgical abdominal flap versus staged
expander/implant breast reconstruction: a critical study of unilateral
immediate breast reconstruction using patient-reported outcomes
instrument BREAST-Q. Breast Cancer Res Treat 2014;146(1):117–126.
10. Pusic AL, Klassen AF, Scott AM, et al. Development of a new patient-
reported outcome measure for breast surgery: the BREAST-Q. Plast
Reconstr Surg 2009;124(2):345–353.
11. Alderman AK, Wilkins EG, Lowery JC, et al. Determinants of patient
satisfaction in postmastectomy breast reconstruction. Plast Reconstr
Surg 2000;106(4):769–776.
12. Taylor EM, Wilkins EG, Pusic AL, et al. Impact of unilateral versus
bilateral breast reconstruction on procedure choices and outcomes. Plast
Reconstr Surg 2019;143(6):1159e–1168e.
13. Panchal H, Matros E. Current trends in postmastectomy breast
reconstruction. Plast Reconstr Surg 2017;140(5S Advances in Breast
Reconstruction):7S–13S.
14. Panchal H, Pilewskie ML, Sheckter CC, et al. National trends in
contralateral prophylactic mastectomy in women with locally advanced
breast cancer. J Surg Oncol 2019;119(1):79–87.
CHAPTER 66

Surgical Treatment of Nipple


Malposition in Nipple-Sparing
Mastectomy
SETH Z. ASCHEN | JARROD T. BOGUE | MIA TALMOR
NIPPLE-SPARING MASTECTOMY MALPOSITION: HISTORY
Multiple studies have determined that nipple-sparing mastectomies (NSMs)
are oncologically safe and do not increase the probability of a local cancer
recurrence when compared to patients that have total mastectomies (1–4).
Additionally, the improved aesthetic reconstructive results of NSMs are
associated with improved body image and psychological adjustment (5–7).
While NSMs, particularly when performed via an inframammary fold
incision can be more technically challenging than a traditional mastectomy
with skin excision, it has been widely adapted, and mastered by many high-
volume surgeons. Complication rates are expected to continue to decrease as
a surgeon acquires experience, skill, and develops new maneuvers,
instrumentation, and techniques. Perhaps most importantly, with experience,
surgeons gain a better understanding of patient selection, thereby choosing
appropriate patients who are suitable candidates for NSMs.
The complication profile associated with device-based reconstruction after
NSM can be quite high in the initial learning period. Specifically, ischemia of
both the nipple areolar complex (NAC) and the greater mastectomy skin flap
can be more common, leading to a higher rate of extrusion, infection, and
reconstructive failure. Fortunately, in time, these complications occur less
frequently and become easier to both predict and avoid. As our group gained
greater insight and experience, we noted significantly decreased rates of
necrosis and failure. It was during this time period that we discovered that
NSMs introduce the potential complication of NAC malposition. This is an
extremely distressing complication that can lead to decreased overall
satisfaction with reconstructive results (4,8).
Malposition is a devastating risk associated with NSM. In a series of 54
NSMs with predominantly lateral incisions, Wagner reported that 69.2% of
patients experienced lateral malposition and 75.0% experienced vertical
malposition (9). Past literature has suggested that preoperative ptosis (10),
implants instead of autologous tissue (11), and a periareolar incision with
lateral extension (9,12) may be associated with subsequent NAC malposition.
In an 8-year satisfaction survey of 78 patients after NSM, Djohan found that
patients with larger volume resections, larger BMI, and larger tissue expander
volumes had significantly lower satisfaction rates, attributed to necrosis-
related complications and malposition (4). Similarly, Kim recently reported
on equivalent satisfaction rates between patients undergoing NSM and skin-
sparing mastectomy (SSM), but a higher reported dissatisfaction with nipple
position in the NSM group. Choi evaluated 1,000 patients who had
undergone either autologous or device-based reconstruction after nipple
paring mastectomy and reported a 7.4% incidence of nipple repositioning
procedures. While the overall incidence of malposition is not reported in this
series, previous radiation, vertical mastectomy incisions and autologous
reconstruction were independent predictors of need for a repositioning
procedure (13).
In 2014, we published our initial experience in treating nipple malposition.
At the time, we reported a 14% incidence of malposition and 5% underwent
surgical treatment for repositioning. Interestingly, of the 44 patients who
were found to have malposition, 19 were satisfied with their result and
decline further surgical intervention. Eight were found to have inadequate
soft tissue coverage and were offered a conversion to autologous tissue.
Seventeen underwent surgical using crescent mastopexy, pocket revision,
free nipple grafting, pedicled nipple transposition, or some combination of
these. While these techniques are similar to those applied to patients with
malposition after cosmetic breast reduction, augmentation, or mastopexy, the
challenge in healing is far greater in the NSM population as the NAC
maintains blood supply from the subdermal plexus alone without contribution
from the deeper axially based blood supply that should still be present after
cosmetic surgery. Despite this challenge, none of the patients who underwent
repositioning in our series suffered either necrosis or recurrence of the
malposition. The avoidance of necrosis may be secondary to a delay
phenomenon in which the subdermal plexus rendered more robust after the
dominant blood supply is eliminated after mastectomy. More importantly
however, the success of our malposition correction is likely due to the
exclusion of patients at high risk for ischemia. Eight of 44 patients with
malposition were not offered surgical intervention because of a poor skin
envelope. Additionally, candidates for malposition correction were required
to wait 1 year after implant placement. This protocol allowed stabilization of
the implant and delay of the flap, providing an ideal vascular wound bed for
nipple grafting or repositioning (14,15). Of note, 2 of 44 patients ultimately
required nipple excision and reconstruction due to recurrence of disease,
similar to local recurrence rates published elsewhere (16–20).
NSM MALPOSITION: RISK FACTORS AND PATIENT SELECTION
As surgeons gain increasing experience with reconstruction after NSM rates
of nipple malposition are expected to decrease in a similar way that rates of
skin flap necrosis are observed to decrease. This is largely due to a greater
understanding of the risk factors related to malposition and avoidance
through better patient selection. In a series of 54 NSMs with predominantly
lateral incisions, Wagner reported that 69.2% of patients experienced lateral
malposition and 75.0% experienced vertical malposition (9). Past literature
has suggested that preoperative ptosis (10), implants instead of autologous
tissue (11), and a periareolar incision with lateral extension (9,12) may be
associated with subsequent NAC malposition. In an 8-year satisfaction
survey of 78 patients after NSM, Djohan found that patients with larger
volume resections, larger BMI, and larger tissue expander volumes had
significantly lower satisfaction rates, attributed to necrosis-related
complications and malposition (4).
Our own study revealed a 14% incidence of malposition. Significant
factors were age (p < 0.0001), diabetes mellitus (p = 0.0025), body mass
index (p = 0.0093), preoperative sternal notch-to-nipple distance (p = 0.015),
preoperative breast base width (p = 0.0001), periareolar mastectomy incision
with lateral extension (p < 0.0001), prior radiation therapy (p = 0.0004), prior
ipsilateral lumpectomy (p = 0.0125), unilateral NSM (p = 0.0004), and
postoperative NAC ischemia (p = 0.0174). Smoking status, breast volume
resected, implant size, ablative surgeon, acellular dermal matrix, and single-
stage reconstruction were not significant. Most recently, Choi et al. found
that in a series of 1,037 NSMs, 7% of patients ultimately underwent
repositioning procedures. In their series, previous radiation therapy, vertical
radical mastectomy incisions, and autologous reconstruction were positive
independent predictors of NAC repositioning, while implant-based
reconstruction was a negative independent predictor of repositioning (13).
While nipple malposition had been the most common adverse outcome that
we saw after NSM, the incidence in our series has dropped and now ranges
from 2% to 5%. This is largely due to a greater understanding of the causes
for nipple displacement after NSM and resultant improvements in patient
selection. Postmastectomy nipple malposition is the expected outcome in
certain circumstances, and the patient should be alerted to the risk factors in
preoperative counseling so as to choose the ideal option for reconstruction.
Predictable risk factors include contracture, asymmetry, and preoperative
malposition.
Contracture that arises after NSM and results in nipple malposition, is not
restricted to the fibrous capsule of the implant. Contracture in this
circumstance refers to a tightening and shortening that can affect the capsule,
the muscle, or the skin envelope. Previous trauma and vascular compromise
of the breast parenchyma can lead to important structural and functional
changes. Histologic studies have found that previous breast trauma and/or
vascular compromise often leads to fibrosis and skin contracture. These
breast parenchymal tissue changes can make displacement of the NAC after
reconstruction more likely (Fig. 66-1) (21,22). In addition, patients with prior
breast radiation therapy, previous lumpectomy, diabetes mellitus, or
postoperative ischemia of the NAC are at significantly increased risk of NAC
malposition (23). Patients who have undergone previous radiation therapy are
3.7 times as likely as patients who have not had radiation therapy to require
NAC repositioning surgery after initial reconstruction. Yet even in patients
who have not been radiated, ischemia of the mastectomy flap, postoperative
infection, and tight submuscular pockets can all be precursors of nipple
malposition.
Most patients who undergo radiotherapy after mastectomy at our
institution will have the tissue expander exchanged to the permanent implant
prior to the radiation. Most patients in this circumstance will have completed
chemotherapy 3 weeks prior to the exchange and anticipate the start of
radiotherapy 3 weeks after the procedure. In those patients in whom radiation
is anticipated, the tissue expander is used to manipulate the skin envelope,
anticipating the upward and outward malposition that will usually occur after
treatment. In this circumstance, the expander is placed lower than the pre-
existing IMF, and the lower pole is overexpanded in order to recruit more
lower pole skin. The patient is exchanged with the nipple position appearing
slightly ptotic in the postoperative period. The resultant radiation change
corrects this ptosis and yields a more symmetric result, particularly after
bilateral mastectomy with unilateral radiation (Fig. 66-2).
FIGURE 66-1 Nipple malposition following radiation therapy. A: Severe malposition
in the vertical direction with radiation causing contracture of the mastectomy flap
and capsule. B: Operative markings for free nipple transfer procedure. C: Nipple
repositioned in a more anatomic position at point of maximum projection of implant.

FIGURE 66-2 In patients undergoing implant based reconstruction where radiation


treatments are planned nipple malposition can be minimized by placing the tissue
expander below the natural IMF and overexpanding the lower pole. A: Slight ptosis
in the immediate postoperative period. B: Reduced ptosis after radiation treatment
with more symmetric nipple position.

FIGURE 66-3 Patients with preoperative breast ptosis are more likely to develop
nipple malposition. A: Preoperative patient with grade II ptosis. B: Postoperative
from nipple-sparing mastectomy and implant-based reconstruction. Elevation of the
nipple areolar complex is appreciated.

Preoperative malposition is a major factor in the development of


postoperative malposition. Patients with grade I–II ptosis preoperatively will
have some malposition postoperatively, but the malposition is often subtle
enough that patients choose to forgo further operative correction. Patients
with grade I–II ptosis preoperatively will have some malposition
postoperatively, but the malposition is often subtle enough that patients
choose to forgo further operative correction. Patients with grade II or III
ptosis can expect minor elevation of the NAC after NSM and implant-based
reconstruction, but the sternal notch-to-nipple distance will still be relatively
long after the procedure (Fig. 66-3). Preoperative reposition of the NAC in
these circumstances is best achieved through mastopexy or reduction
procedures performed approximately 6 weeks prior to the procedure (Fig. 66-
4). Where possible, when the mastectomy is being performed for treatment
rather than prophylaxis, the repositioning procedure is performed using
oncoplastic technique such that the tumor is removed through the vertical or
Wise-pattern incisions and node sampling is performed. This provides
oncologist with greater data to base adjuvant therapy decisions on and allows
adequate time for healing prior to the planned NSMs.
Patients who present preoperatively with breasts that appear wideset are
likely to have some degree of lateral malposition postoperatively. While these
deformities are not amenable to preoperative repositioning, careful discussion
should be had preoperatively, pointing out the features on preoperative
photographs and explaining the likely outcomes (Fig. 66-5). In these
circumstances, patients who are troubled by this wide-set appearance may
find SSM and delayed nipple reconstruction preferable to NSM.
Preoperative asymmetry of nipple position will not only be conserved after
NSM with implants, it is often magnified (Fig. 66-6). Again, careful attention
to preoperative photography and discussion with the patient are tantamount to
an optimal outcome. These cases represent an opportunity to improve pre-
existing aesthetic deficiencies, but require meticulous planning and execution
in the early stages of reconstruction. In cases in which the patient presents
with a disparity in vertical position, the tissue expander can be used to
lengthen the nipple-IMF distance. Patients with preoperative tuberous breast
deformities will often achieve significant improvement after NSM with
implants if careful analysis and modification is performed.
NSM MALPOSITION: INTRAOPERATIVE MANEUVERS TO AVOID
MALPOSITION
Malposition of the NAC may be inevitable in certain high-risk populations of
patients, such as those mentioned above. For the remainder of the patients,
malposition may be the result of a poorly planned or executed reconstruction.
Our detailed analysis of our own outcomes has enabled us to define a number
of interventions that should be avoided, and a number of maneuvers that can
be helpful in ensuring that the nipple remains central on the mastectomy flap.
In the majority of patients who had no predisposing risk factors,
malposition was in the lateral direction, and a result of erroneous implant
choices at the level of both the tissue expander, and the permanent implant.
Often, patients who presented with either a small breast or with involutional
atrophy who desired augmentation of volume and more fullness of the medial
pole were most likely to be affected. Analysis of the pre- and postoperative
photographs revealed that by augmenting volume or enhancing the cleavage,
there was a relative lengthening of the sternal-nipple distance as compared to
the nipple-to-anterior axillary fold distance. This was particularly apparent in
patients with narrow base widths and in patients in whom the breast meridian
rested lateral with respect to the NAC; because the planned lateral endpoint is
the anterior axillary fold (to avoid lateralization of the implant into the
axilla), excessive volume is eccentrically distributed medial to the NAC. The
malposition that results from this type of error is often high grade and
requires free nipple grafting for correction. As such, it is reasonable in the
preoperative counseling session to suggest SSM with delayed nipple
reconstruction as a safer and more precise way of achieving the desired
outcome with a visible scar profile that is similar.
FIGURE 66-4 Preoperative oncoplastic breast reduction can reduce the risk of a
patient developing postoperative nipple malposition. A: Preoperative patient with
macromastia at increased risk for postreconstruction nipple malposition. B: After
oncoplastic breast reduction the patient has decreased breast ptosis and decreased
risk for nipple malposition after reconstruction. C: After reconstruction malposition
is avoided.
FIGURE 66-5 Patients with wideset breasts are likely to have some degree of lateral
nipple malposition after nipple-sparing mastectomy and reconstruction. A: Patient
with preoperative widest breasts. B: After nipple-sparing mastectomy and implant-
based reconstruction lateral malposition of the nipple is observed. C: Markings for
planned free nipple transfer procedure. D: Postoperatively after nipple transplant
the nipple is more medial.

It is our current practice to advise patients who are undergoing device-


based reconstruction after NSM through an inframammary incision that the
final volume will be within 20% of the preoperative volume. This is true for
both augmentation of volume and reduction of volume. In the latter
circumstance, a large-breasted woman requesting a significant reduction in
volume will be left with a skin envelope that is disproportionate to the
implant pocket. The endpoint of this disproportion is often ptosis of both the
NAC and of the skin envelope off the implant pocket. This scenario is also
often complicated by extreme rippling secondary to the relative excess of
skin in relation to the volume of the implant (Fig. 66-7). Patients who are
desirous of nipple preservation and reduction in final volume are therefore
counseled to undergo a staging mastopexy or reduction prior to the
mastectomy. Given our own experience of significantly increased risk of
ischemia and necrosis when a Wise-pattern or vertical mastopexy is
performed concurrent with the mastectomy, we prefer a staged approach.
FIGURE 66-6 Patients with preoperative nipple asymmetry can be magnified with
implant-based reconstruction after nipple-sparing mastectomy. A: Preoperative
vertical asymmetry with the patient’s left nipple positioned more superiorly than
their right nipple. B: Postoperatively vertical malposition of the left nipple is
exaggerated. C: After crescent mastopexy left nipple malposition is reduced.

The most important maneuver that is utilized in order to avoid malposition


is to center the implant (either tissue expander or permanent implant) on the
NAC and not on the breast meridian. In the early stages of our experience,
many patients had implants placed under total submuscular pockets and
acellular dermal matrix use was preserved for patients undergoing direct-to-
implant reconstruction. While submuscular pockets can provide excellent and
durable coverage and thus decrease the risk of extrusion, they are only rarely
concordant with the outer skin envelope in either shape or position. In a tight
submuscular pocket, there is often a disparity of the lower endpoint such that
the implant is trapped superior to the natural IMF. This superior malposition
of the implant in relation to the skin envelope results in a relative inferior
malposition of the NAC in many cases. The addition of acellular dermal
matrix or other synthetic material to augment coverage of the lower pole
beneath the muscular endpoint is an important element in constructing the
implant pocket in order to avoid malposition. These materials allow the
surgeon to place the lowest portion of the implant pocket at the IMF thus
harmonizing the skin envelope with the implant pocket. Lateral inset of the
material further gives the surgeon control of the lateral endpoint thus
minimizing horizontal displacement. While placement of the implant in a
prepectoral pocket puts the pocket in direct contact with the skin envelope,
we have not adapted this practice widely due to our experience with higher
rates of necrosis and reoperation for aesthetic corrections. Some groups have
suggested that the implant could rest subcutaneously in the inferior pole
(similar to the circumstance for dual plane breast augmentation). It is our
experience that the central lower pole of the skin envelope is the thinnest and
the most apt to necrose; we are therefore hesitant to further challenge the
inferior skin flap in this way.

FIGURE 66-7 Large-breasted women undergoing nipple-sparing mastectomy and


requesting a device-based reconstruction with significant volume reduction are at
risk for extreme rippling and ptosis of the nipple and areola. A: Preoperative
imagine of a large-breasted woman requesting reconstruction with significant
volume reduction. B: Rippling and nipple malposition resulting from deconjugate
skin envelope and implant pocket.

In a recent study, Choi describes a practice of securing the NAC in the


desired position by suturing to the underlying tissue or acellular dermal
matrix, or with drains subsequently placed to close suction, providing
negative pressure to maintain NAC position. We have not found either of
these practices to be effective, though we do routinely drain both the implant
pocket and the subdermal plane (13).
NSM MALPOSITION: CORRECTION—INDICATIONS
After patients complete the final stage of reconstruction, they are evaluated
during the course of routine postoperative visits scheduled at 3 months, 6
months, and 1 year. The presence or absence of nipple malposition is noted,
and when present is graded. Malposition is measured as the distance between
current and ideal nipple position and is graded as mild (1-cm), moderate (2-
cm), or severe (3-cm) displacement. Ideal nipple position is defined as the
point of maximal projection of the implant, or the intersection of the
midclavicular line and the inframammary fold if the implant is malpositioned.
Patients with malposition who are good surgical candidates are offered
correction 6 months to 1 year after implant reconstruction. Surgical
intervention is largely determined by the grade of the malposition; options
include crescent mastopexy, pocket revision with and without the addition of
acellular dermal matrix, free nipple grafting, and pedicled transposition
which can be performed similar to a vertical mastopexy, but can also be
performed on a horizontal plane. Decisions regarding revisional surgery are
made only after careful evaluation of the oncologic status of the patient, and
in consultation with the treating oncologist.
NSM MALPOSITION: CORRECTION—CONTRAINDICATIONS
Patients are not offered surgical correction if their skin envelope is deemed to
be inadequate. Examples include those with severe fibrosis after radiation
therapy, though not all radiated patients are excluded. If the patient has
undergone radiation as part of a prior attempt at breast-conservation therapy
that has failed, a malposition procedure may be offered in 6 to 12 months; for
those who underwent adjuvant radiation to the mastectomy flap, a minimum
of 1 year must lapse before the patient is considered for revisional surgery.
Other examples include patients with extremely thin skin envelopes in whom
further skin excision might lead to extrusion and or exposure of the implant.
While pocket revisions might be offered to these patients, conversion to
autologous tissue is a more common scenario.

FIGURE 66-8 A 55-year-old diabetic patient with stage 0 ductal carcinoma in situ of
the left breast treated with lumpectomy and adjuvant radiotherapy and
subsequently a unilateral nipple-sparing mastectomy for local recurrence. A two-
stage left reconstruction was completed 4 months later with a symmetrizing
augmentation, which was complicated by (A) nipple malposition that was corrected
by crescent mastopexy 1 year after implant reconstruction, with (B) improved
cosmesis at follow-up 2 years later.
NSM MALPOSITION: CORRECTION

Crescent Mastopexy
Crescent mastopexy is offered to patients with mild vertical or horizontal
nipple malposition. A crescent mastopexy is marked in the seated position for
a transposition of the nipple to the appropriate height. When this procedure is
combined with implant exchange or pocket modification, the inframammary
fold incision is used for access and this portion of the procedure is performed
before any repositioning incisions are made. The operating table places the
patient in a 90-degree upright position and the position of the NAC is
reevaluated once the pocket modifications have been performed. At this point
the mastopexy is tailor tacked using skin staples and position and symmetry
are assessed. The patient is brought supine and the skin is marked within the
staple lines. The skin within the markings is excised full thickness. The outer
incision is now undermined sharply using a 15 blade scalpel, thus avoiding
thermal injury to the subdermal plexus that may result from high-temp
electrocautery. The nipple is set into position using interrupted 3-0 Vicryl
(Ethicon Inc., Somerville, NJ) in the deep dermal layer and half-buried
mattress 5-0 nylon on the skin (Figs. 66-8 and 66-9).
FIGURE 66-9 Crescent mastopexy. (A) Preoperative, (B) intraoperative, and (C)
postoperative views. The crescent mastopexy is performed to move an inferiorly
displaced nipple superiorly. A crescent-shaped piece of skin is removed and the
nipple is tacked superiorly to establish the new position of the nipple. (From Small K,
Kelly KM, Swistel A, et al. Surgical treatment of nipple malposition in nipple-sparing
mastectomy device-based reconstruction. Plast Reconstr Surg 2014;133[5]:1053–1062.)
FIGURE 66-10 A 48-year-old woman with recurrent grade III invasive ductal
carcinoma of the left breast first treated with lumpectomy and adjuvant
radiotherapy and subsequently a unilateral nipple-sparing mastectomy. A single-
stage left reconstruction with matching right reduction was completed, which was
complicated by (A) severe nipple malposition and high-grade capsular contraction in
the left breast that was corrected by a pocket revision 1 year later and symmetrizing
revision reduction on the right with (B) improved cosmesis at 1-year follow-up.

Pocket Revision
Pocket revision with or without implant exchange is offered to patients with
moderate or severe vertical or horizontal nipple malposition with capsular
contracture, or to those with discordance of the skin envelope with a more
constricted implant pocket. The implant pockets are approached through the
initial mastectomy incision, and the implants are removed. Capsulotomy and
capsulectomy are performed as is necessary. In patients with high-grade
contracture, a strip of acellular derma matrix may be added to expand the
lower pole of the pocket, or to stabilize the pocket medially or laterally.
Capsulorrhaphy may also be required and is performed using 2-0 silk sutures
with tapered needles. This capsulorrhaphy may be performed to redefine or
reposition the IMF or the lateral breast fold. Implants are often replaced by
smaller implants, or by implants with a base width that is adequate to fill the
pocket, but with less projection than the prior implant. The use of shaped
implants in this setting can be more challenging, and associated with a higher
risk for failure if the implant itself rotates after surgery, leading to potential
recurrence of the malposition (Figs. 66-10 and 66-11).
Free Nipple Graft
Free nipple grafting is offered to patients with severe vertical or horizontal
malposition. First, the NAC is excised as a horizontal or vertical ellipse to
avoid dog ears. A cookie cutter is used to inscribe the desired diameter
around the areola. If excess areolar skin is present it is sent for pathologic
diagnosis and discarded. The nipple is thinned as a full-thickness skin graft,
removing any subcutaneous or scar tissue that may be present at its base. The
location for the placement of the nipple is marked in the standing position
prior to surgery. The skin in this region is deepithelialized with care taken not
to enter the capsule of the implant. If this does occur, the defect is repaired
with buried Vicryl sutures to ensure that the nipple graft is in contact with
dermis throughout. The NAC is inset using 5-0 nylon sutures in a half-buried
mattress manner. The donor site is closed primarily (Figs. 66-12 and 66-13).

FIGURE 66-11 Pocket revision. (A) Preoperative, (B) intraoperative bird’s-eye, and
(C) postoperative views. The laterally displaced implant and medially displaced
nipple are corrected through a pocket revision. The pocket revision is approached
through the inframammary fold. After removal of the implant and partial
capsulectomy, sutures are placed along the anterior axillary fold in the breast
pocket. The sutures reestablish the lateral borders of the implant pocket, resulting in
a more medially placed implant and centrally placed nipple. (From Small K, Kelly
KM, Swistel A, et al. Surgical treatment of nipple malposition in nipple-sparing
mastectomy device-based reconstruction. Plast Reconstr Surg 2014;133[5]:1053–1062.)
FIGURE 66-12 Patient undergoing two-stage device-based reconstruction which was
complicated by (A) severe malposition of the right nipple. Malposition was corrected
by right free nipple graft with (B) improved cosmesis at 1 year.

Pedicled Nipple Transposition


Pedicled transposition is offered to severe malposition patients. Malposition
can be in any direction. The patient is marked in the standing position prior to
surgery. The desired position of the nipple after transposition is the most
important preoperative marking. This can be difficult to determine if the
patient is undergoing a simultaneous implant exchange. In this circumstance,
the markings are made but the implant exchange is performed through the
mastectomy incision, and the markings are reestablished in the operating
room. Unlike a standard vertical or Wise-pattern mastopexy, there is no
specific pedicle that is preserved; rather the skin within the markings is
deepithelialized throughout. Undermining is then performed to the extent that
it will allow tension-free closure and no further. Tethering of the NAC by
thick adherent scar can sometimes be a problem. In this circumstance,
discontiguous release of the dermis and/or scar can be performed. The NAC
was inset using interrupted 3-0 Vicryl in the deep dermal layer and
subcuticular 4-0 Biosyn (Covidien, Mansfield, MA) on the skin (Figs. 66-14
and 66-15).
FIGURE 66-13 Free nipple graft. (A) Preoperative, (B) intraoperative, and (C)
postoperative views. An elliptical-shaped piece of skin is removed medially to the
malpositioned nipple. The nipple is removed as a graft and placed medially in its new
position. The lateral nipple graft donor site is undermined and closed linearly. (From
Small K, Kelly KM, Swistel A, et al. Surgical treatment of nipple malposition in nipple-
sparing mastectomy device-based reconstruction. Plast Reconstr Surg 2014;133[5]:1053–
1062.)
FIGURE 66-14 A: A 67-year-old nonsmoker with ductal carcinoma in situ treated
with a bilateral total nipple-sparing mastectomy and two-stage reconstruction
completed in 3 months, which was complicated by severe malposition. B: Severe
malposition was corrected by (above) pedicled transposition and (below) reduction of
implant size 1 year after implant reconstruction. C: Improved cosmesis at 1-year
follow-up.
NSM MALPOSITION: CORRECTION POSTOPERATIVE CARE
Patients who undergo repositioning procedures are typically discharged from
the hospital on the day of the procedure. Those who have had acellular
dermal matrix placed will have closed suction drains. Those patients who
underwent free nipple grafting will have modified bolster dressings. In both
of these circumstances patients are asked to keep the area dry until they are
seen in the office 5 to 7 days later. Patients who undergo mastopexy or
transposition procedures are asked to keep the area dry for 48 hours.
Moistened gauze is applied in all circumstances and is changed daily. A loose
bra is worn. Patients can resume regular activities after the second
postoperative day but are asked to avoid exercise or other extreme exertions.
NSM MALPOSITION: OUTCOMES
FIGURE 66-15 Pedicle nipple transposition. (A) Preoperative, (B) intraoperative,
and (C) postoperative views. Elliptical incisions are created around the displaced
nipples. The laterally displaced nipples are rotated medially on inferior pedicles. The
new medial nipple positions are established by tailor tacking and closure of the
surrounding skin. (From Small K, Kelly KM, Swistel A, et al. Surgical treatment of
nipple malposition in nipple-sparing mastectomy device-based reconstruction. Plast
Reconstr Surg 2014;133[5]:1053–1062.)

NAC malposition that results from NSM and reconstruction can be difficult
to correct. However, multiple studies using the repositioning techniques
discussed in this chapter have demonstrated that the NAC can be safely
repositioned after a NSM. In our previously published series, we performed
repositioning procedures on 44 patients who achieved subjectively excellent
cosmesis. Correction was achieved using a combination of free nipple grafts,
implant exchanges with repocketing, crescent mastopexies, and vertical
mastopexies. None of the patients developed full-thickness necrosis or tissue
loss, and none had recurrence of the malposition (23).
Other corrective techniques have been reported. Zhang et al. describe their
experience using a procedure whereby mastectomy flaps are reelevated and
redraped over the implant and capsule to correct nipple malposition. In their
series of 44 nipple repositioning procedures they were able to reliably move
the NAC up to 3 cm. The average delay between initial reconstruction and
mastectomy flap reelevation was 115 days. None of the patients in their series
had postoperative ischemia or necrosis of the NAC or mastectomy flaps (24).
To correct a severely malpositioned NAC a free nipple graft can be used.
Severe malposition is often seen in the setting of adjuvant breast radiation
therapy. Radiation treatments and previous breast surgery can negatively
affect the dermal vascular supply of the breast, and surgeons are therefore
cautious in performing repositioning procedures in a radiated field. Rietjens
et al. found that free nipple grafts had a relatively low complication rate.
They evaluated the safety and efficacy of free nipple grafts in a series of 16
patients which included patients who had received locoregional radiotherapy.
Partial graft loss occurred in only 18% of patients. Additionally, no total graft
loss or postoperative infections occurred. All instances of partial graft loss
were managed with conservative local wound care and did not require
additional surgical procedures (25).
While options for correction of malposition exist, identifying those patients
at risk preoperatively is a key factor in avoiding this complication.
Prereconstruction breast ptosis is a significant risk factor for developing
nipple malposition after reconstruction. Performing a prereconstruction breast
reduction is an effective way to correct breast ptosis and decrease the rate of
NAC malposition following breast reconstruction. Choi et al. reported that in
their series no patient that underwent prereconstruction breast reduction or
mastopexy subsequently required a NAC repositioning procedure (13).
Flessas et al. present a novel method for counteracting nipple malposition at
the time of breast reconstruction. Their reconstructive method suggests
suturing the posterior border of nipple to anterior border of pectoralis muscle
with absorbable sutures at the time of reconstruction. In a series of 14
patients who underwent NSMs all patients reported satisfactory cosmetic
results with no degree of malposition noted (26). Our own experience with
this technique has not been as satisfactory, though there is little downside to
the attempt.
NSM MALPOSITION: CONCLUSION
NSMs are oncologically safe and do not increase the risk of local recurrence.
In addition, studies have demonstrated improved aesthetic outcomes with
breast reconstruction following NSMs as compared to traditional skin-sparing
procedures. Improved aesthetic outcomes are associated with improved body
image and psychological adjustment for patients. Performing NSMs is
technically more challenging when compared to a traditional mastectomy
with skin excision. However, NSMs have been widely adapted and mastered
by many high-volume surgeons.
Although NSMs have many benefits, NAC malposition is a potential
complication that can be technically challenging to correct. Risk factors for
malposition have been identified and include preoperative ptosis, implant-
based reconstruction instead of autologous tissue, and a periareolar incision
with lateral extension. By understanding these risk factors patients can be
appropriately counseled on the possibility of malposition and can better be
involved in an informed decision-making process as it relates to their
mastectomy and subsequent reconstruction.
Malposition can be managed at multiple points in the reconstructive
process including preoperatively, intraoperatively, and postoperatively. The
incidence in our series has decreased compared to our originally published
series and now ranges from 2% to 5%. This decreased incidence of
malposition is largely due to a greater understanding of the causes for nipple
displacement after NSM and resultant improvements in patient selection.
Practically, malposition is measured as the distance between the current
and ideal nipple positions and is graded as mild, moderate, or severe
displacement. These grades correlate with different repositioning techniques
that can be used to reposition the displaced nipple. Correction is typically
offered at 6 to 12 months postoperatively. Correction of nipple malposition is
challenging and the major risks associated with corrective procedures are
surgical site infections, nipple necrosis, and recurrence of malposition.
Despite these potential risks, none of the patients in our series suffered from
necrosis or recurrence of the malposition. The avoidance of necrosis may be
secondary to either a delayed flap phenomenon with dilation of choke vessels
within the subdermal plexus or patient selection for less ischemic flaps.
Preoperatively and intraoperatively there are techniques which can be
performed in order to prevent or correct for the formation of nipple
malposition. Before formal mastectomy for individuals with large breast skin
envelope, staging a Wise-pattern reduction or mastopexy can be considered.
At the time of reconstruction ensuring the tissue expander is centered under
the NAC and not the breast meridian can avoid medialization of the device
and subsequent lateralization of the NAC.
Not all cases of malposition are treated. Patients are not offered surgical
correction if their skin envelope is deemed to be inadequate. Radiation is a
risk factor that should give pause. Not all radiated patients are excluded,
however, those that have severe fibrosis are not candidates for revision.
Candidates for revision of nipple malposition have several options for
correction. These options include: crescent mastopexy, pocket revision, free
nipple grafting, and pedicled nipple transposition. An informed discussion
with the patient as well as an assessment of their skin quality and degree of
malposition guide procedure selection. The most important phase of nipple
malposition correction occurs in surgical planning as the correct approach
dictates success.

REFERENCES

1. Gerber B, Krause A, Dieterich M, et al. The oncological safety of skin


sparing mastectomy with conservation of the nipple-areola complex and
autologous reconstruction: an extended follow-up study. Ann Surg
2009;249(3):461–468.
2. Voltura AM, Tsangaris TN, Rosson GD, et al. Nipple-sparing
mastectomy: critical assessment of 51 procedures and implications for
selection criteria. Ann Surg Oncol 2008;15(12):3396–3401.
3. Chung AP, Sacchini V. Nipple-sparing mastectomy: where are we now?
Surg Oncol 2008;17(4):261–266.
4. Djohan R, Gage E, Gatherwright J, et al. Patient satisfaction following
nipple-sparing mastectomy and immediate breast reconstruction: an 8-
year outcome study [outcomes article]. Plast Reconstr Surg
2010;125(3):818–829.
5. Petit JY, Veronesi U, Luini A, et al. When mastectomy becomes
inevitable: the nipple-sparing approach. Breast 2005;14(6):527–531.
6. Jabor MA, Shayani P, Collins JD, et al. Nipple-areola reconstruction:
satisfaction and clinical determinants. Plast Reconstr Surg
2002;110(2):457–463.
7. Didier F, Radice D, Gandini S, et al. Does nipple preservation in
mastectomy improve satisfaction with cosmetic results, psychological
adjustment, body image and sexuality?. Breast Cancer Res Treat
2009;118(3):623–633.
8. Kim H, Park SJ, Woo KJ, et al. Comparative study of nipple–areola
complex position and patient satisfaction after unilateral mastectomy
and immediate expander–implant reconstruction nipple-sparing
mastectomy versus skin-sparing mastectomy. Aesthetic Plast Surg
2019;43(2):313–327.
9. Wagner JL, Fearmonti R, Hunt KK, et al. Prospective evaluation of the
nipple–areola complex sparing mastectomy for risk reduction and for
early-stage breast cancer. Ann Surg Oncol 2012;19(4):1137–1144.
10. Chu CK, Carlson GW. Techniques and outcomes of nipple sparing
mastectomy in the surgical management of breast cancer. Curr Breast
Cancer Rep 2013;5(2):118–124.
11. Nahabedian MY, Tsangaris TN. Breast reconstruction following
subcutaneous mastectomy for cancer: a critical appraisal of the nipple-
areola complex. Plast Reconstr Surg 2006;117(4):1083–1090.
12. Salgarello M, Visconti G, Barone-Adesi L. Nipple-sparing mastectomy
with immediate implant reconstruction: cosmetic outcomes and
technical refinements. Plast Reconstr Surg 2010;126(5):1460–1471.
13. Choi M, Frey JD, Salibian AA, et al. Nipple-areola complex malposition
in nipple-sparing mastectomy: a review of risk factors and corrective
techniques from greater than 1000 reconstructions. Plast Reconstr Surg
2017;140(2):247e–257e.
14. Taneda H, Sakai S. Transposition technique for correction of a
malpositioned nipple-areola complex after reconstruction following a
nipple-sparing mastectomy: a case report. Ann Plast Surg
2011;67(6):579–582.
15. Takayanagi S. Transposition of the malpositioned nipple-areola complex
in breast reconstruction with implants. Aesthetic Plast Surg
2010;34(1):52–58.
16. Caruso F, Ferrara M, Castiglione G, et al. Nipple sparing subcutaneous
mastectomy: sixty-six months follow-up. Eur J Surg Oncol
2006;32(9):937–940.
17. Regolo L, Ballardini B, Gallarotti E, et al. Nipple sparing mastectomy:
an innovative skin incision for an alternative approach. Breast
2008;17(1):8–11.
18. Stolier AJ, Sullivan SK, Dellacroce FJ. Technical considerations in
nipple-sparing mastectomy: 82 consecutive cases without necrosis. Ann
Surg Oncol 2008;15(5):1341–1347.
19. Spear SL, Hannan CM, Willey SC, et al. Nipple-sparing mastectomy.
Plast Reconstr Surg 2009;123(6):1665–1673.
20. Sakurai T, Zhang N, Suzuma T, et al. Long-term follow-up of nipple-
sparing mastectomy without radiotherapy: a single center study at a
Japanese institution. Med Oncol 2013;30(1):481.
21. Schuster RH, Kuske RR, Young VL, et al. Breast reconstruction in
women treated with radiation therapy for breast cancer: cosmesis,
complications, and tumor control. Plast Reconstr Surg 1992;90(3):445–
452.
22. Albino FP, Koltz PF, Ling MN, et al. Irradiated autologous breast
reconstructions: effects of patient factors and treatment variables. Plast
Reconstr Surg 2010;126(1):12–16.
23. Small K, Kelly KM, Swistel A, et al. Surgical treatment of nipple
malposition in nipple-sparing mastectomy device-based reconstruction.
Plast Reconstr Surg 2014;133(5):1053–1062.
24. Zhang S, Blanchet NP. Reelevating the mastectomy flap: a safe
technique for improving nipple-areolar complex malposition after
nipple-sparing mastectomy. Plast Reconstr Surg Glob Open
2017;5(7):e1426.
25. Rietjens M, De Lorenzi F, Andrea M, et al. Free nipple graft technique
to correct nipple and areola malposition after breast procedures. Plast
Reconstr Surg Glob Open 2013;1(8):e69.
26. Flessas I, Michalopoulos NV, Papadopulos NA, et al. Nipple
malposition following nipple-sparing mastectomy: how can we prevent
it?. In: Nipple-Areolar Complex Reconstruction. Cham: Springer;
2018:229–232.
CHAPTER 67

Salvage of the Contracted Radiated


Implant: Radiation Sequelae and
Evolving Strategies in Prevention and
Reconstruction
BRANDON ALBA | ANUJA K. ANTONY
HISTORY
Radiation therapy has yielded significant benefit for the breast cancer patient
over the past several decades with a reduction in recurrence and mortality
rates. Several large-scale clinical trials have demonstrated the efficacy of
postmastectomy radiation therapy (PMRT) and shaped radiotherapy
treatment guidelines. The Danish Breast Cancer Cooperative Group Trials
found that among premenopausal women with high-risk breast cancer
(defined as cases with any positive axillary lymph nodes, tumors greater than
5 cm, and/or skin invasion), radiation therapy was associated with a
significant improvement in disease-free overall survival rates (1). More
recently, the Early Breast Cancer Trialists’ Collaborative Group performed a
meta-analysis of 22 randomized trials consisting of more than 8,000 patients
and concluded that among patients with at least four positive lymph nodes,
radiotherapy treatment reduced locoregional recurrence by 19% and overall
mortality by 9% (2). Accordingly, the National Cancer Center Network
currently recommends PMRT for any women with four or more positive
lymph nodes. In clinical practice, radiation is increasingly utilized as an
alternative to completion axillary dissection to reduce the downstream
sequalae and morbidity associated with lymphadenectomy surgery. Certainly,
while radiation therapy has substantial oncologic benefit, it is not without
collateral damage to the surrounding tissues often complicating and thwarting
the plastic surgeon’s reconstructive efforts. This is especially true in the
setting of implant-based reconstruction.
EFFECTS OF RADIATION ON BREAST TISSUE
The mechanism of action of radiotherapy involves cell death through the
disruption of intracellular architecture and replication. Although the purpose
of this treatment is to work synergistically with oncologic ablative surgery to
eradicate occult cancer cells, radiation also has the unintended effect of
damaging the neighboring healthy tissue. In the acute phase, in the first days
to weeks post treatment, radiation interferes with the normal cellular life
cycle and results in cell death and tissue necrosis. The irradiated tissue then
mounts an inflammatory response with capillary leak and edema. In the
chronic phase, the effects of this inflammatory response manifest as increased
collagen deposition within the skin, muscle fibrosis and contracture, atrophy
of subcutaneous tissue, pigmentation changes, and impaired wound healing
(3,4). These adverse effects manifest for the plastic and reconstructive
surgeon in the setting of an irradiated implant as increased incidence of
postoperative surgical site complications, poorer cosmetic outcome, and
capsular contracture. These consequences ultimately have considerable
impact on patients’ overall quality of life, manifesting as chronic pain,
limited arm mobility, and poor aesthetic outcome which weighs heavily on
the plastic surgery patient from a functional and psychological standpoint. In
a study by McCarthy et al. utilizing the BREAST-Q patient-reported outcome
measurement instrument, history of prior radiation and PMRT were both
found to be significantly associated with lower postoperative patient
satisfaction scores (5).
EFFECTS OF RADIATION THERAPY ON IMPLANT-BASED RECONSTRUCTION

Complications Associated With Irradiated Prostheses


Various studies have demonstrated the negative impact of radiation on
implant-based breast reconstruction highlighting a similar increased risk for
postop complications ranging from wound site concerns to total
reconstructive failure. In a retrospective review of 903 patients, Sbitany et al.
determined that both preoperative and PMRT were significantly associated
with increased incidence of postoperative complications in the setting of
prosthetic reconstruction. Patients with any history of radiation delivery had a
significantly higher rate of surgical site infections, wound breakdown, and
tissue expander or implant loss (6). Similarly, in a review of 1,037 patients,
Berry et al. found that among irradiated implants, 29.9% required
explantation, 10.3% of which ultimately required salvage with autologous
free flap–based reconstruction (7). In a study conducted by Ho et al., patients
who had their tissue expander irradiated before implant exchange had a 4.2
increased odds (p = 0.001) of overall major complications requiring surgical
intervention compared to those who did not receive radiation (8).
Perhaps one of the most daunting challenges associated with the irradiated
implant-based breast reconstruction is capsular contracture. Ho et al. found
grade III and IV capsular contracture to be significantly higher in the
irradiated group compared to the control group (21.7% vs. 10%; p = 0.008)
(8). In a 3-year follow-up study, Spear et al. also found capsular contracture
occurred in 40% of patients who underwent PMRT compared to only 7.8% of
those who underwent breast-conservation therapy (BCT) (9). The risk of
capsular contracture persists long after radiation is delivered; in a 6-year
follow-up study, Whitfield et al. found the incidence of severe capsular
contracture in irradiated implants increased from 0% at 1 year to 30% at 6
years (10).
Subpectoral Reconstruction and Radiation
Increasingly, we understand that there may be several factors that place the
irradiated implant at higher risk for capsular contracture. The location of the
prosthesis, either subpectoral (under the muscle) or prepectoral (above the
muscle), likely plays a central role in mitigating the impact that radiotherapy
has on the final surgical outcome. Traditionally, placing the tissue expander
and implant in the subpectoral plane has been the standard technique for
providing vascularized soft tissue coverage for the prosthesis, reducing
potential risk of infection and implant extrusion. However, in the radiated
setting, radiation-induced fibrosis instigates shortening of the pectoralis
muscle which contributes to tightening of the breast pocket. This ultimately
translates to the patient as painful contracture and displacement of the
prosthesis with poor aesthetic outcome.
Oncologic and reconstructive protocols to minimize the impact of radiation
varies by surgeon and institution, with the net goal of achieving a successful
reconstructive outcome. Cordeiro et al. have described their protocol of
timing surgical intervention with radiotherapy, exchanging the (subpectoral)
tissue expander with the final permanent implant prior to initiating radiation.
In their experience with a large cohort of patients undergoing immediate two-
stage implant-based reconstruction and irradiation, the authors describe
enhanced success utilizing the Memorial Sloan-Kettering Cancer Center
algorithm as follows: (1) mastectomy and immediate tissue expander
placement, (2) expansion beginning 10 to 14 days after expander placement,
(3) tissue expansion during postoperative chemotherapy, (4) exchanging the
tissue expander for the final implant 4 weeks after completion of
chemotherapy, and (5) radiotherapy 4 weeks after final implant placement
(11). In this group’s most recent article published in 2014, they found a 9.1%
incidence of implant loss and 6.9% incidence of grade IV capsular
contracture in irradiated patients (12). Although this was significantly higher
than the nonirradiated patients, Cordeiro et al. concluded this was an
acceptable rate of reconstructive success. Ninety-two percent of irradiated
patients also had a “good” or “excellent” aesthetic outcome, with 90.1%
reporting overall satisfaction with their reconstruction and 94.2% reporting
they would choose implant-based reconstruction again. However, with the
increasing utilization of neoadjuvant chemotherapy, this protocol may not be
an option for many patients as the time to postoperative radiation is
abbreviated and alternative surgical strategies have been employed to
minimize the adverse potential effects of radiation therapy.
Prepectoral Reconstruction (With Acellular Dermal Matrix)
and Radiation
In recent years, prepectoral implant-based reconstruction with acellular
dermal matrix (ADM) has emerged as a reliable alternative to submuscular
prothesis placement for both tissue expanders and direct-to-implant (DTI)
placement techniques (13). We have described our algorithm utilizing
prepectoral breast reconstruction employing ADM for DTI reconstruction
highlighting equivalent safety to traditional retropectoral implant positioning
and potential reconstructive advantages including enhanced aesthetic results
(14,15). As prepectoral reconstruction obviates the need for pectoralis muscle
dissection and elevation, several studies describe a reduction in the incidence
of postoperative pain and animation deformity classically associated with
subpectoral implants (16–18).
As our understanding of prepectoral breast reconstruction has advanced,
several authors have found additional benefit in the setting of radiation
therapy as placement of the implant in the prepectoral plane allows it to be
unaffected by fibrosis or contracture of the pectoralis muscle (12). Sinnot et
al. evaluated 374 patients (589 breasts) and found that subpectoral breast
reconstruction patients who underwent PMRT had a capsular contracture rate
that was three times greater with more severe contractures (grade 3 or 4) than
patients receiving PMRT who underwent prepectoral breast reconstruction
(19).
Additionally, use of ADM in prepectoral breast reconstruction may have
protective effects against capsular contracture in radiated patients. Early work
by Stump et al. in an in vivo primate animal model indicated that ADM may
contribute to a softer breast pole. After implanting tissue expanders with and
without ADM in African green monkeys, the Alloderm-covered expanders
demonstrated no capsule and very few myofibroblasts on histologic
evaluation at 10 weeks (20). Park et al. analyzed breast capsules with and
without ADM in the setting of radiation and found alpha-smooth muscle
actin–positive (alpha-SMA+) myofibroblasts to be positively expressed
throughout the breast capsule without ADM compared to postradiation
capsules utilizing ADM with scarce and irregularly scattered alpha-SMA+
myofibroblasts (21). Moyer et al. similarly found decreased similarly
decreased alpha-SMA staining and elastin content in the irradiated capsule
with ADM (22). Kim et al. further elucidated the inhibition mechanism of
ADM on capsule formation in expander/implant breast reconstruction after
PMRT identifying that use of ADM resulted in reduced myofibroblasts,
vascularity, fibroblasts, EndoMT, macrophages, and TGF-B1 and PDGF-B
expression in capsule tissue (23). These evolving basic science studies
conceptually support use of ADM in the radiated setting and further outline
mechanisms behind its protective benefits in minimizing the capsule
formation and unwanted capsular contracture.
Despite these potential advantages, radiation therapy in the prepectoral
breast reconstruction introduces several issues that warrant consideration,
namely, its effect on the integration of ADM, a key component of modern
prepectoral techniques, and the associated potential for healing complications
during second-stage exchange (in two-stage reconstruction) in the absence of
the vascularized soft tissue interface provided by the pectoralis muscle. In a
small retrospective analysis of 33 patients who underwent prepectoral
reconstruction with ADM, Sigalove found that at the final stage of
reconstruction, the ADM was completely integrated in all breasts, including
those patients who had undergone radiation therapy to the tissue expander
(24). Sigalove also found that none of the irradiated breasts developed grade
III or IV capsular contracture. Elswick et al. demonstrated a favorable
complication profile in irradiated versus nonirradiated prepectoral breast
reconstruction though increased in the irradiated group (nonsignificant) and
consistent with retropectoral breast reconstruction outcomes (25). Of note,
surgical site infection was increased in the irradiated group. The authors
postulated proximity of the tissue expander to the external environment
combined with radiation-induced skin changes that alter perfusion to the
mastectomy flap may be causative. Many surgeons now favor changing the
surgical site for re-entry during exchange (e.g., from an anterior incision to a
lateral inframammary incision) to avoid potential for these complications.
Sbitany et al., in a large single-surgeon review of 411 patients evaluating
prepectoral two-stage reconstruction using ADM with PMRT to the tissue
expander compared with classic submuscular or dual plane reconstruction,
found no significant differences in postoperative complications between these
two groups, including incidence of tissue expander explantation (17). They
concluded that in properly selected patients, prepectoral reconstruction with
ADM is a safe and reliable method, even in the setting of radiation therapy.
Direct-to-Implant Reconstruction
In the setting of PMRT, an increasing number of surgeons favor immediate
DTI breast reconstruction as their preferred method (Fig. 67-1). DTI
reconstruction obviates the need to reenter an irradiated pocket to remove the
tissue expander. While this makes the reconstruction more technically
challenging due to the steep learning curve (14,15), it portends a decreased
risk of certain complications, such as reopening an irradiated incision site to
exchange a tissue expander for a permanent implant and the associated higher
rates of dehiscence (26). Although limited studies have been published to
describe this technique both in retropectoral and prepectoral settings, an
increasing number of surgeons are beginning to recognize its advantages in
the radiated setting. A recent 2018 study, Lin et al. compared the effects of
PMRT between those who underwent DTI reconstruction and those
underwent two-stage reconstruction (tissue expander/implant) (27). The
authors found the DTI group to have significantly higher revision rates
(21.1% vs. 7.4%; p = 0.029). However, in multivariate regression analysis,
the tissue expander group had a significantly higher risk of reconstruction
failure (odds ratio 2.004, 95% CI: 0.987 to 4.067; p = 0.05). Although more
studies are needed to fully understand the utility of DTI for patients
undergoing PMRT, there is increasing evidence to support its use in the
patient who will be undergoing radiation.
Nonoperative Adjunct Therapies
Several nonoperative adjunct treatments are available for reducing the risk of
capsular contracture and subsequent reconstructive failure of irradiated
protheses. Systemic drugs such leukotriene antagonists have been shown to
mitigate the severity of capsular contracture in both augmentation and
reconstructive procedures (28–30). It is believed that through their
antagonistic effect on TGF-B1, leukotriene antagonists result in a reduction
of fibroblast proliferation and fibrosis, thereby decreasing the fibroblast-
mediated mechanism of capsular contracture (31). Accordingly, drugs such as
montelukast (Singulair) and zafirlukast (Accolate) have been used
prophylactically and in early treatment of capsular contracture by some
surgeons in the setting of implant-based reconstruction and postmastectomy
radiation. Studies quantifying the magnitude of their effect in this setting are
lacking.
FIGURE 67-1 A and B: Preoperative photographs of a patient prior to bilateral
mastectomy and prepectoral direct-to-implant reconstruction with acellular dermal
matrix. C and D: Three months after reconstruction and immediately prior to
radiation therapy to the right breast. E and F: Sixth months after radiation therapy.

Although their respective mechanisms of action are not as well understood,


many other drugs have been anecdotally noted to be beneficial for irradiated
implants. In a small prospective study, Cook et al. examined effect of
pentoxifylline (Trental) and vitamin E in implant-based reconstruction with
adjuvant radiation (32). Twenty-six subjects received a 180-day course of
prophylactic postoperative pentoxifylline plus vitamin E and were observed
for a total of 12 months. Only two patients (7.7%) developed severe capsular
contracture and there were no instances of implant loss. Although limited
given no control group and relatively short follow-up time, this study
provides useful preliminary evidence to support the prophylactic use of
pentoxifylline and vitamin E. Further studies are necessary to more
definitively evaluate this treatment modality and other burgeoning drug
therapies.
RECONSTRUCTIVE SURGERY STRATEGIES FOR THE RADIATED BREAST
While the irradiated contracted breast implant can be challenging, recent
advances and improved surgical techniques have provided the reconstructive
surgeon with a wide armamentarium for optimizing functional and aesthetic
outcomes, as well as overall patient satisfaction. Reconstructive options most
commonly employed include autologous tissue such as the pedicled
latissimus dorsi (LD) muscle flap (in combination with an implant) and free
abdominal-based tissue transfer as well as evolving strategies incorporating
autologous fat grafting and implant-based maneuvers utilizing ADM.
Latissimus Dorsi Flap
The LD flap is a popular method for salvage in irradiated patients. As a
pedicled flap, it provides reliable vascularized soft tissue coverage when used
in conjunction with an implant reducing the risk of reconstructive failure
when compared with implant alone (Fig. 67-2). A recent query of the
Nationwide Inpatient Sample showed that in the United States, the LD flap is
most commonly used in delayed reconstructions, in previously irradiated
patients, or as a salvage procedure for patients whose original reconstruction
failed (33,34). In a survey comparing patient satisfaction between those who
underwent deep inferior epigastric perforator (DIEP) versus LD flap
reconstruction of a previously irradiated breast, patients were more satisfied
with the size and shape of LD flaps than DIEP flaps (35). This may be related
to the less conspicuous donor-site scar compared to that of the DIEP flap
(35). Lee and Mun performed a systematic review of 20 studies in 2015 and
noted a 72% decreased risk of reconstructive failure when autologous tissue
with a prosthetic device was utilized as compared with prosthetic device
alone. Though rates of capsular contracture did not differ, reconstructive
failure for prosthetic device with autologous tissue was 6.9% compared with
33.7% for prosthetic-only reconstruction (36). A systematic review of 31
studies in 2016 by Fischer et al. demonstrated a significant decrease in
implant loss with use of LD compared with implant alone (15% vs. 5%, p <
0.001) with an odds ratio of 4.3 favoring LD-assisted reconstruction (37).
FIGURE 67-2 A: A patient who underwent postmastectomy radiation to the left
breast with resultant fibrosis and contracture of local tissue and a deficient envelope.
B: Postoperative result of two-stage prosthetic-based reconstruction of the radiated
side with a round implant and a latissimus flap.

Abdominal-Based Free Tissue Transfer Options


Despite the many advancements that have improved aesthetic and functional
outcomes for women who undergo radiation after implant-based
reconstruction, irradiated prostheses are still associated with unfavorably high
rates of implant loss and reconstructive failure. In the setting of radiation
therapy, autologous free flap–based reconstruction is less prone to major
postoperative complications and can result in superior aesthetic outcomes
(38). Lee and Mun demonstrated a 92% decreased risk of reconstructive
failure in the setting of previous radiation when autologous tissue was used
compared with prosthetic-only reconstruction (36). While there are numerous
free flap options available for reconstruction depending on patient preference,
available tissue for harvest, and surgeon experience, abdominal based free
tissue transfer remains a gold standard for salvage of the contracted radiated
breast.
Delayed-Immediate Reconstruction
When it is known that a patient will require postmastectomy radiation, many
patients and surgeons will choose free flap reconstruction as the definitive
method of reconstruction over prosthetic-only type reconstruction. And while
use of autologous tissue confers reduced reconstructive failure risk in the
radiated patient, it is often not known whether a patient will require radiation
until the postmastectomy period, when final intraoperative pathology results
become available. While there is considerable debate in the literature as to the
ramifications of radiating the autologous construct, Kronowitz et al. at the
University of Texas M.D. Anderson Cancer Center in Houston have
popularized the “delayed-immediate” breast reconstruction method in order
to address this concern.
The delayed-immediate method of reconstruction as described involves
two stages (39). First, all patients undergo skin-sparing mastectomy and
submuscular placement of a tissue expander are expanded to 100% of the
suggested fill volume. When the final pathology report is available, patients
who do not require radiation ultimately undergo definitive reconstruction,
either with a permanent implant or free flap. Those patients who do require
radiation keep their expander inflated during adjuvant chemotherapy
delivery, then have the expander completely deflated prior to radiotherapy.
After radiation-induced skin desquamation resolves, the expander is then
serially reinflated, and the patient ultimately undergoes delayed free flap–
based reconstruction, either with a free flap alone or with an LD flap plus an
implant. Placing the inflated expander in the first stage of reconstruction
helps maintain the mastectomy skin flaps and breast shape during
radiotherapy while avoiding the risks associated with delivering radiation to a
permanent implant. In a 10-year follow-up study involving 364 patients, the
cumulative rate of completed reconstructions was 89.6%, of which 100%
were deemed successful (40). Kronowitz et al. concluded the delayed-
immediate method is a safe, reliable strategy for combining breast
reconstruction and radiotherapy (37). More recently, prepectoral tissue
expander placement has being utilized as a first-stage bridging strategy in
order to facilitate second-stage free flap reconstruction, with increased ease
of internal mammary vessel exposure and avoidance of elevation of the
pectoralis muscle as the final free flap reconstruction will be carried out in
the prepectoral space (41).
Delayed Secondary Free Tissue Transfer for Salvage
Oftentimes, women who require breast radiation still may choose to complete
implant-based reconstruction and remain at high risk for radiation-induced
complications that ultimately necessitate implant removal due to painful
contracture or complications with the device. For these patients, autologous
abdominally-based free flap reconstruction is typically the preferred method
of choice for breast salvage, most often the DIEP flap or its predecessor, the
transverse rectus abdominus myocutaneous (TRAM) flap and its variations in
the muscle-sparing TRAM. Free tissue transfer can help promote wound
healing and provide adequate, healthy soft tissue coverage of an area
damaged by irradiation (Fig. 67-3). Zhao et al. recently conducted a study of
180 patients who had failure of their implant-based reconstruction and
subsequently underwent salvage with an abdominally-based free flap (42).
Postmastectomy radiation was significantly associated with severe implant
failure, that is, implants that required immediate salvage procedures. Salvage
with DIEP and TRAM flaps were equally successful, with an overall flap
failure rate of only 2.6%.
Radiation introduces challenges for the reconstructive surgeon that warrant
consideration. Microvasculature changes and fibrotic tissue can add
additional difficulty for operating in the radiated field and successfully
carrying out microvascular anastomoses. Fosnot et al. in 2011 and Franco et
al. in 2016 demonstrated that microvascular arterial complications were
significantly more common in the radiated field but without a change in
individual outcomes including fat necrosis, delayed vascular complications,
or flap loss (3.1% compared with 1.5%, p = 0.13). Additional care in
microvascular anastomoses may be required with need for revision of the
anastomosis or further dissection of recipient vessels for an acceptable target
(43,44).
Mastectomy Reconstruction Outcomes Consortium (MROC)
Study
The ongoing debate as to the best reconstructive option continues. This large
multicenter study involves 11 sites and 2,234 patients who have undergone
LD, pedicled TRAM, Free TRAM, and DIEP flaps as well expander/implant
reconstructions. While early data at 1 year supports a higher risk for
complications in the autologous tissue options, longer-term data specifically
looking at the irradiated patient and incidence of capsular contracture may
further our understanding of risks and benefits of the various options. Of
note, failure rates were low (<6%) across all cohorts (45). One limitation of
this study may stem from inadequate representation of the prepectoral
expander/implant cohorts.

FIGURE 67-3 A: Preoperative photographs of a patient who underwent bilateral


implant-based reconstruction followed by postmastectomy radiation to the right
breast, resulting in capsular contracture. B: Salvage with bilateral deep inferior
epigastric perforator flaps. C: Final result after nipple areolar complex
reconstruction.
AUTOLOGOUS FAT GRAFTING
In recent years, autologous fat grafting has emerged as a new promising
technique for salvaging the irradiated breast implant. Fat grafting is used as a
delivery system for native stem cells and growth factors to a tissue bed
damaged by radiotherapy. In the author’s experience, fat grafting can also be
particularly useful as an adjunct to augment free flap–based salvage
operations in patients with inadequate native tissue or to improve the
irradiated implant-based reconstruction with milder forms of capsular
contracture.
In a study of patients who had undergone radiation therapy after implant-
based reconstruction, Panettiere et al. compared those who had received
postreconstruction lipofilling to those who had not (46). Using the Late
Effects on Normal Tissue—Subjective, Objective, Management, Analytic
(LENT-SOMA) Scale, the aesthetic scores in the treatment group
significantly improved after lipofilling. The aesthetic scores of the lipofilled
group were also significantly better than the control group who had not
received lipofilling. Beyond its ability to help smooth contour deformities
and improve overall aesthetics, fat grafting may also play an important role in
mitigating the more complex sequelae of radiation of pain and fibrosis. In
another study, Serra-Renom et al. performed lipofilling simultaneously with
delayed tissue expander placement after radiotherapy (47). Patients were then
lipofilled again at the time of tissue expander exchange for a permanent
implant. At 1-year follow-up, there were no cases of capsular contracture
greater than Baker grade I in any of the 65 patients included in the study.
This suggests that fat grafting may play a protective role against the fibrotic
effects of radiation. Although the mechanism of this is still poorly
understood, a growing number of basic science studies are beginning to
provide important new insights. Global gene expression analysis using breast
biopsies has shown that autologous fat grafting to previously irradiated tissue
significantly alters gene expression in interferon-gamma and hypoxia-related
pathways (48). This provides molecular-level evidence that autologous fat
influences the inflammatory and hypoxic response of breast tissue to
radiation.
Critics of fat grafting often cite the theoretical oncologic risk of injecting
fat into an area of prior malignancy. Due to the fact that adipose tissue is rich
in mesenchymal stem cells and growth factors (many of which are postulated
to play a role in the protective effects of fat grafting), some fear this may also
increase the risk of cancer recurrence. Several clinical studies, however, have
found no association between autologous fat grafting and an increased risk of
locoregional or distance recurrence (49,50). A recent meta-analysis of fat
grafting after breast reconstruction also found an overall low rate of surgical
complications compared to other breast procedures, and a high rate of both
surgeon (90.1%) and patient satisfaction (93.4%) (51).

FIGURE 67-4 A: A 76-year-old patient with radiation to her implant and resultant
capsular contracture. This patient had minimal abdominal tissue and was a poor
candidate for autologous tissue transfer. B: This patient underwent alternative
management of her radiated and contracted implant with capsulotomy along the
inframammary fold and placement of acellular dermal matrix in the region of
capsulotomy. C and D: Intraoperative views of capsulotomy along the
inframammary fold and acellular dermal matrix placement.

Implant-Based Salvage Techniques


Traditionally the optimal operation for patients who require salvage of an
irradiated implant is conversion to autologous-based reconstruction.
However, the senior author has found that implant-based strategies which
include capsulotomy along the inframammary fold and circumferentially as
needed, use of bridging ADM in the region of capsulotomy, and assertive fat
grafting during the exchange procedure can yield excellent results (Fig. 67-
4). While the effects of radiation cannot be completely undone, for many
patients, avoidance of an additional donor site remains a primary goal and
these implant-based maneuvers can be another strategy to consider for
addressing the radiation-associated capsular contracture.
CONCLUSION
While radiation is an essential strategy for treatment of breast cancer, it can
have a deleterious effect on the reconstructive result negatively impacting
quality of life for the breast cancer survivor. However, in properly selected
patients, implant-based reconstruction can be successful and aesthetically
satisfactory. Traditionally, autologous free flaps have been the preferred
method of reconstruction for salvage of the contracted irradiated implant.
Recent advances in reconstructive techniques, such as the use of ADM and
prepectoral reconstruction, may assist in optimizing implant-based outcomes
in the radiated setting. It is essential for the reconstructive surgeon to
understand the effects of radiation and inherent additional risk conferred for
reconstructive failure and to adopt strategies to mitigate this risk. The
reconstructive strategies outlined in the chapter should further the plastic
surgeon’s understanding on the downstream sequelae of radiation including
capsular contracture and pain which translate to poor aesthetic outcomes and
decreased patient satisfaction as well as elucidate reconstructive methods that
may yield optimal patient outcomes.

REFERENCES

1. Overgaard M, Hansen PS, Overgaard J, et al. Postoperative radiotherapy


in high-risk premenopausal women with breast cancer who receive
adjuvant chemotherapy. Danish Breast Cancer Cooperative Group 82b
Trial. N Engl J Med 1997;337(14):949–955.
2. EBCTCG (Early Breast Cancer Trialists’ Collaborative Group), McGale
P, Taylor C, et al. Effect of radiotherapy after mastectomy and axillary
surgery on 10-year recurrence and 20-year breast cancer mortality:
meta-analysis of individual patient data for 8135 women in 22
randomised trials. Lancet 2014;383(9935):2127–2135.
3. Kronowitz SJ, Robb GL. Breast reconstruction with postmastectomy
radiation therapy: current issues. Plast Reconstr Surg 2004;114(4):950–
960.
4. Spear SL. Surgery of the Breast: Principles and Art. 3rd ed.
Philadelphia, PA: Lippincott Williams & Wilkins; 2011.
5. McCarthy CM, Klassen AF, Cano SJ, et al. Patient satisfaction with
postmastectomy breast reconstruction: a comparison of saline and
silicone implants. Cancer 2010;116(24):5584–5591.
6. Sbitany H, Wang F, Peled AW, et al. Immediate implant-based breast
reconstruction following total skin-sparing mastectomy: defining the
risk of preoperative and postoperative radiation therapy for surgical
outcomes. Plast Reconstr Surg 2014;134(3):396–404.
7. Berry T, Brooks S, Sydow N, et al. Complication rates of radiation on
tissue expander and autologous tissue breast reconstruction. Ann Surg
Oncol 2010;17 Suppl 3:202–210.
8. Ho AL, Bovill ES, Macadam SA, et al. Postmastectomy radiation
therapy after immediate two-stage tissue expander/implant breast
reconstruction: a University of British Columbia perspective. Plast
Reconstr Surg 2014;134(1):1e–10e.
9. Spear SL, Shuck J, Hannan L, et al. Evaluating long-term outcomes
following nipple-sparing mastectomy and reconstruction in the
irradiated breast. Plast Reconstr Surg 2014;133(5):605e–614e.
10. Whitfield GA, Horan G, Irwin MS, et al. Incidence of severe capsular
contracture following implant-based immediate breast reconstruction
with or without postoperative chest wall radiotherapy using 40 Gray in
15 fractions. Radiother Oncol 2009;90(1):141–147.
11. Cordeiro PG, Pusic AL, Disa JJ, et al. Irradiation after immediate tissue
expander/implant breast reconstruction: outcomes, complications,
aesthetic results, and satisfaction among 156 patients. Plast Reconstr
Surg 2004;113(3):877–881.
12. Cordeiro PG, Albornoz CR, McCormick B, et al. The impact of
postmastectomy radiotherapy on two-stage implant breast
reconstruction: an analysis of long-term surgical outcomes, aesthetic
results, and satisfaction over 13 years. Plast Reconstr Surg
2014;134(4):588–595.
13. Sigalove S, Maxwell GP, Sigalove NM, et al. Prepectoral implant-based
breast reconstruction: rationale, indications, and preliminary results.
Plast Reconstr Surg 2017;139(2):287–294.
14. Antony AK, Poirier J, Madrigrano A, et al. Evolution of the surgical
technique for “breast in a day” direct-to-implant breast reconstruction:
transitioning from dual-plane to prepectoral implant placement. Plast
Reconstr Surg 2019;143(6):1547–1556.
15. Antony AK, Robinson EC. An algorithmic approach to prepectoral
direct-to-implant breast reconstruction: version 2.0. Plast Reconstr Surg
2019;143(5):1311–1319.
16. Sbitany H. Important considerations for performing prepectoral breast
reconstruction. Plast Reconstr Surg 2017;140(6S Prepectoral Breast
Reconstruction):7s–13s.
17. Sbitany H, Gomez-Sanchez C, Piper M, et al. Prepectoral breast
reconstruction in the setting of postmastectomy radiation therapy: an
assessment of clinical outcomes and benefits. Plast Reconstr Surg
2019;143(1):10–20.
18. Nahabedian MY, Cocilovo C. Two-stage prosthetic breast
reconstruction: a comparison between prepectoral and partial
subpectoral techniques. Plast Reconstr Surg 2017;140(6S Prepectoral
Breast Reconstruction):22S–30S.
19. Sinnott CJ, Persing SM, Pronovost M, et al. Impact of postmastectomy
radiation therapy in prepectoral versus subpectoral implant-based breast
reconstruction. Ann Surg Oncol 2018;25(10):2899–2908.
20. Stump A, Holton LH 3rd, Connor J, et al. The use of acellular dermal
matrix to prevent capsule formation around implants in a primate model.
Plast Reconstr Surg 2009;124(1):82–91.
21. Park TH, Chung SW, Song SY, et al. The use of acellular dermal matrix
in immediate two-stage prosthetic breast reconstruction provides
protection from postmastectomy radiation therapy: a clinicopathologic
perspective. J Mater Sci Mater Med 2018;29(3):27.
22. Moyer HR, Pinell-White X, Losken A. The effect of radiation on
acellular dermal matrix and capsule formation in breast reconstruction:
clinical outcomes and histologic analysis. Plast Reconstr Surg
2014;133(2):214–221.
23. Kim IK, Park SO, Chang H, et al. Inhibition mechanism of acellular
dermal matrix on capsule formation in expander-implant breast
reconstruction after postmastectomy radiotherapy. Ann Surg Oncol
2018;25(8):2279–2287.
24. Sigalove S. Prepectoral breast reconstruction and radiotherapy—a closer
look. Gland Surg 2019;8(1):67–74.
25. Elswick SM, Harless CA, Bishop SN, et al. Prepectoral implant-based
breast reconstruction with postmastectomy radiation therapy. Plast
Reconstr Surg 2018;142(1):1–12.
26. Nahabedian MY. AlloDerm performance in the setting of prosthetic
breast surgery, infection, and irradiation. Plast Reconstr Surg
2009;124(6):1743–1753.
27. Lin AM, Christensen JM, Liao EC, et al. Abstract 70: the impact of
post-mastectomy radiation therapy on permanent implants in direct-to-
implant breast reconstruction versus tissue expanders in two-stage breast
reconstruction. Plast Reconstr Surg Glob Open 2018;6(4 Suppl):55–56.
28. Huang CK, Handel N. Effects of Singulair (montelukast) treatment for
capsular contracture. Aesthet Surg J 2010;30(3):404–408.
29. Scuderi N, Mazzocchi M, Fioramonti P, et al. The effects of zafirlukast
on capsular contracture: preliminary report. Aesthet Plast Surg
2006;30(5):513–520.
30. Mazzocchi M, Dessy LA, Alfano C, et al. Effects of zafirlukast on
capsular contracture: long-term results. Int J Immunopathol Pharmacol
2012;25(4):935–944.
31. Sapountzis S, Kim JH, Francescato Veiga D, et al. The effect of
Zafirlukast on capsule formation in post-radiation silicone implants.
Med Hypotheses 2012;78(6):787–789.
32. Cook M, Johnson N, Zegzula HD, et al. Prophylactic use of
pentoxifylline (Trental) and vitamin E to prevent capsular contracture
after implant reconstruction in patients requiring adjuvant radiation. Am
J Surg 2016;211(5):854–859.
33. Sood R, Easow JM, Konopka G, et al. Latissimus dorsi flap in breast
reconstruction: recent innovations in the workhorse flap. Cancer Control
2018;25(1):1073274817744638.
34. DeLong MR, Tandon VJ, Rudkin GH, et al. Latissimus dorsi flap breast
reconstruction—a nationwide inpatient sample review. Ann Plast Surg
2017;78(5 Suppl 4):S185–S188.
35. Lindegren A, Halle M, Docherty Skogh AC, et al. Postmastectomy
breast reconstruction in the irradiated breast: a comparative study of
DIEP and latissimus dorsi flap outcome. Plast Reconstr Surg
2012;130(1):10–18.
36. Lee KT, Mun GH. Prosthetic breast reconstruction in previously
irradiated breasts: a meta-analysis. J Surg Oncol 2015;112(5):468–475.
37. Fischer JP, Basta MN, Shubinets V, et al. A systematic meta-analysis of
prosthetic-based breast reconstruction in irradiated fields with or without
autologous muscle flap coverage. Ann Plast Surg 2016;77(1):129–134.
38. Jhaveri JD, Rush SC, Kostroff K, et al. Clinical outcomes of
postmastectomy radiation therapy after immediate breast reconstruction.
Int J Radiat Oncol Biol Phys 2008;72(3):859–865.
39. Kronowitz SJ, Hunt KK, Kuerer HM, et al. Delayed-immediate breast
reconstruction. Plast Reconstr Surg 2004;113(6):1617–1628.
40. Ayoub Z, Strom EA, Ovalle V, et al. A 10-year experience with
mastectomy and tissue expander placement to facilitate subsequent
radiation and reconstruction. Ann Surg Oncol 2017;24(10):2965–2971.
41. Lee KR, Clavin N. Bridging autologous reconstruction with pre-pectoral
tissue expanders. Gland Surg 2019;8(1):90–94.
42. Zhao R, Tran BNN, Doval AF, et al. A multicenter analysis examining
patients undergoing conversion of implant-based breast reconstruction to
abdominally based free tissue transfer. J Reconstr Microsurg
2018;34(9):685–691.
43. Fracol ME, Basta MN, Nelson JA, et al. Bilateral free flap breast
reconstruction after unilateral radiation: comparing intraoperative
vascular complications and postoperative outcomes in radiated versus
nonradiated breasts. Ann Plast Surg 2016;76(3):311–314.
44. Fosnot J, Fischer JP, Smartt JM Jr, et al. Does previous chest wall
irradiation increase vascular complications in free autologous breast
reconstruction? Plast Reconstr Surg 2011;127(2):496–504.
45. Wilkins EG, Hamill JB, Kim HM, et al. Complications in
postmastectomy breast reconstruction: one-year outcomes of the
Mastectomy Reconstruction Outcomes Consortium (MROC) study. Ann
Surg 2018;267(1):164–170.
46. Panettiere P, Marchetti L, Accorsi D. The serial free fat transfer in
irradiated prosthetic breast reconstructions. Aesthet Plast Surg
2009;33(5):695–700.
47. Serra-Renom JM, Munoz-Olmo JL, Serra-Mestre JM. Fat grafting in
postmastectomy breast reconstruction with expanders and prostheses in
patients who have received radiotherapy: formation of new
subcutaneous tissue. Plast Reconstr Surg 2010;125(1):12–18.
48. Lindegren A, Schultz I, Sinha I, et al. Autologous fat transplantation
alters gene expression patterns related to inflammation and hypoxia in
the irradiated human breast. Br J Surg 2019;106(5):563–573.
49. Kronowitz SJ, Mandujano CC, Liu J, et al. Lipofilling of the breast does
not increase the risk of recurrence of breast cancer: a matched controlled
study. Plast Reconstr Surg 2016;137(2):385–393.
50. Myckatyn TM, Wagner IJ, Mehrara BJ, et al. Cancer risk after fat
transfer: a multicenter case-cohort study. Plast Reconstr Surg
2017;139(1):11–18.
51. Groen JW, Negenborn VL, Twisk D, et al. Autologous fat grafting in
onco-plastic breast reconstruction: a systematic review on oncological
and radiological safety, complications, volume retention and
patient/surgeon satisfaction. J Plast Reconstr Aesthet Surg
2016;69(6):742–764.
CHAPTER 68

Reconstruction of Previously
Augmented Patients Undergoing
Mastectomy: Options for Implant-
Based Reconstruction
MICHAEL SCHEFLAN | YOAV GRONOVICH
HISTORY
Breast cancer is estimated to develop in one in eight women (1–3). For years,
one of the main concerns regarding breast implants was the fear of the
implant hiding a cancer. The cause for worry was the theoretic reduced
ability of the woman or her physician to detect a mass by physical
examination or masking of a tumor in formal imaging (ultrasound,
mammography or MRI) thereby delaying diagnosis and treatment. Studies
have shown that there is no significant difference in the rate and timing of
tumor detection between women with breast implants and those without,
regardless if the implant was in a subglandular or a subpectoral plane.
Interestingly, breast cancer in augmented patients tends to be detected earlier
than in other women. Patients with implants may have more regular checkups
by more than one physician, periodic imaging related to implant integrity,
and possibly greater awareness to breast shape and feel (1–14). In patients
with breast implants and breast cancer, no difference has been found in
detection, when either a solid mass tumor or calcifications only were present.
It has been well documented that breast implants do not cause breast cancer,
do not delay breast cancer detection, and do not modify treatment options or
late outcomes. Nevertheless, many women globally are still worried about
safety of silicone breast implants and their relation to cancer and other breast
implants–related illnesses. In recent years, the issue of breast implant–
associated anaplastic large cell lymphoma (BIA-ALCL) has become a center
of discussion and a great deal of research has been initiated to better
understand this rare entity. Currently, there is still much to learn. What is
known is that BIA-ALCL was found only in patients with textured implants.
The prevailing theory is that the combination of textured implants, bacterial
biofilm, time, and patient’s susceptibility, all play a role in this disease. The
treatment of BIA-ALCL is explantation, complete capsulectomy, and
adjuvant chemo and radiation therapy in advanced disease stages. Due to the
small numbers of BIA-ALCL globally, it is still too early to draw final
conclusions of its causes and ways of prevention (15–25).
Another issue concerning safety is known as the breast implant illness
(BII). Important data is gathered as to the potential connection between
silicone implants and a variety of illness related to body systems such as
immune, respiratory, musculoskeletal, genitourinary and gastrointestinal,
central nervous, psychological etc. Investigators are exploring the mechanism
responsible for the possible higher incidence of these illnesses occurring in
patients with breast implants as compared with the general population
(26–35).
Mastectomy in Patients With Breast Implants
The mastectomy in previously augmented patients should be carried out
following the same oncologic and reconstructive principles as when no
implants are present.
It is usually a good practice to replace both implants regardless of when
they were inserted. Size change may also be desired by patients during the
same session. Women who desire to upsize her implants should understand
that only after mastectomy and evaluating the quality and adequacy of the
soft tissue envelope on the reconstructed side, the surgeon may decide if
putting a larger implant is possible. The contralateral breast is then addressed
to match the reconstructed breast with an appropriate implant. A woman’s
decision for larger implants may often necessitate the placement of a tissue
expander in the reconstructed side.

FIGURE 68-1 Mastectomy of previous dual plane augmented patient. A: Dissection


on top of the pectoralis major muscle, leaving the implant intact until after the end of
the mastectomy. B: Then, removing the implant, leaving the capsule intact (except
for a biopsy).

Mastectomy in Patients With Implants Previously Placed in the


Dual Plane Position
During mastectomy, dissection should be carried out with the implant in situ
for as long as it facilitates the procedure. When reaching the upper pole and
the implant becomes a hindrance, it is removed. The capsule need not be
removed and may be left in the neopocket, unless the tumor is adjacent to it
(Fig. 68-1).
Mastectomy in Patients With Implants Previously Placed in the
Subglandular Position
The implant should be extracted first as it often interferes with completeness
of the mastectomy. Partial (anterior) or complete capsulectomy may be
performed separately or en bloc with breast removal. Infrequently, the
implant may be left intact along with the capsule (Fig. 68-2).
THE RECONSTRUCTION IN PATIENTS WITH PREVIOUS BREAST IMPLANTS
In women with subglandular breast augmentation with rippling, poor shape,
and animation deformity, the reconstruction may be an opportunity for
aesthetic improvement by site change and an ADM for tissue reinforcement.
Tissue Quality
An important issue which determines the aesthetics of the reconstruction is
the quality of the soft tissue envelope following mastectomy. When
evaluating the envelope following mastectomy one should differentiate
between tissue quality and thickness as they are not the same. In thin women
with little subcutaneous fat good perfusion is still possible (36–38). Women
who have been previously augmented are different in that often their tissue
has already been expanded, stretched, and thinned out, especially if capsule
contracture took place. In this situation the subdermal blood supply is more
vulnerable to injury during the mastectomy, and a two-stage reconstruction
with a tissue expander may be indicated. The capsule (unless it has to be
removed) in previously augmented patients may serve as additional coverage
for the implant along with the ADM.
Tumor
Tumor location and size determines if the mastectomy must include nipple
areola, skin, and or muscle. A large tumor or one that is located less than 5
mm from the pectoralis major muscle indicates a subpectoral reconstruction
(36,37,39). Otherwise, a prepectoral reconstruction with an ADM is
preferred.
Complete or Partial Capsulectomy
A tumor close to the capsule indicates a partial or complete capsulectomy. In
patients with capsular contracture or a calcified capsule, it is possible to make
a partial capsulotomy instead, which will on one hand, relieve the
contracture, but on the other hand, keep the capsule as a barrier and a strong
layer reinforcing tissues around the implant. In either case the use of an ADM
helps offset the lack of a capsule by adding a regenerative layer to reinforce
the soft tissues supporting a new implant.
Need for Radiation
Radiation has a negative influence on the tissue, the capsule, and on the
pectoralis muscle (36,37,39,40). If there is a high probability of post
mastectomy radiation therapy (PMRT), it is preferable to reconstruct the
breast in a prepectoral plane with an ADM. Data shows that one of the
advantages of prepectoral positioning of an implant covered with ADM is its
relative protection from capsule contracture and masking the radiation
fibrosis of the pectoralis major muscle (36,37,39).
Reconstruction in Patients With Previous Subpectoral
Augmentation
The first question before making a decision regarding reconstruction is: What
does the patient need, what does the patient want, and what can be reasonable
and safely done for her in her specific condition and tissue characteristics.
Patients who are satisfied with their current augmented breast may be
reaugmented in the same plane and a neopocket. A new implant, of the
proper shape and size should be inserted with an ADM coverage. Neopocket
in either prepectoral or dual plane position is often indicated. A fresh pocket
blood supply will better support the adherence and integration of the ADM
which in return reduces capsule contracture. In patients who are pleased with
their current breast size and shape, it is advisable to insert a sizer calculating
the volume of the existing implant and adding the weight of breast that was
removed in the mastectomy.
FIGURE 68-2 Mastectomy of previous subglandular augmentated patient. A:
Removing the implant. B: Dissection on top of the pectoralis major muscle removing
capsule and breast tisuue.

The patient should then be seated for shape and symmetry. Final
refinements are adjusted until the appropriate implant is chosen
approximating dimensions of the other breast. The next stage is to replace the
contralateral implant with a new implant of the similar size and shape as the
old one preferably in a neopocket.
If the patient desires a bigger implant but apart from that is satisfied with
her breast, then the same plane, neopocket is preferable. In the event that the
tumor location necessitates mastectomy with partial or complete removal of
the pectoralis major muscle, a prepectoral pocket has to be created with the
implant completely or partially covered with an ADM (Fig. 68-3).
Following mastectomy, tissues should be examined clinically or
objectively with an imaging tool (SPY®, KENT®, Vision-Sense® etc.)
(41–44). Assessment should be done with the intended implant in site and the
incision temporarily closed and the patient seated. From the authors’
experience, it is always recommended to use an ADM or synthetic mesh for
tissue reinforcement, pocket stabilization, and capsular contracture reduction.
Meshing of the ADM enables more implant coverage, reduces the risk of
infection and seroma, and creates an overall natural aesthetic result. Both
shaped textured and round textured or smooth implants have been used in
breast reconstruction with similar patient’s and surgeon’s satisfaction. While
it seems that an anatomical implant in a prepectoral plane gives more natural
results and is preferable, round smooth implants with fat grafting in the
second stage have proved to achieve similar aesthetic outcomes.

FIGURE 68-3 Patient with previous subpectoral breast augmentation of 300 cc


round silicone implant. Before reconstruction (above) and 3 months after immediate
reconstruction prepectoral with Mentor CPG 323 495cc and Alloderm 8*16 cm plus
6*12 cm (below).

When tissues are insufficiently perfused, a prepectoral reconstruction is not


a reliable option. In this situation the surgeon may select a tissue expander in
a dual plane site instead or opt to delay the reconstruction (delayed immediate
or delayed reconstruction).
Reconstruction in Patients With Previous Subglandular
Augmentation
The two main reconstructive options are in a prepectoral plane with either full
or anterior ADM coverage, or reconstruction in a new partial subpectoral
plane with an ADM cradling the lower pole of the implant. Again, if the
patient is satisfied with her previous augmented breast, then a neo prepectoral
pocket is the site of choice. As discussed earlier, size and shape are calculated
and selected according to the same principles outlined for the partial
subpectoral augmentation (Fig. 68-4). In patients with rippling, folds,
emptiness, or step-off deformity of the upper pole, we recommend a new
partial subpectoral pocket, or prepectoral placement with fat grafting
procedure in a second stage.
THE CONTRALATERAL AUGMENTED BREAST
A good unilateral reconstruction is judged on a good bilateral symmetry. As
discussed earlier in this chapter, you begin with what the patient wants, and if
she is satisfied with her current breast size and shape on the reconstructed
breast, it is recommended that an implant be placed in a similar neopocket on
the contralateral side.
For patients who desire bigger implants, the authors recommend that the
contralateral equalization is performed simultaneously, as detailed above.
This decision regarding implant position on the healthy side can be made
only after completion of the mastectomy and after evaluating the quantity and
quality of the remaining soft tissue envelope. If it is adequate, the authors
prefer a prepectoral pocket using a ADM for full coverage of the implant. In
this situation, the contralateral augmentation should also be in a subglandular
pocket. It is the authors’ bias to use an ADM for the augmented breast in the
subglandular plane too. The ADM helps to minimize capsular contracture and
improves the aesthetic result by obscuring the ripples and folds.
FIGURE 68-4 Patient with previous subglandular breast augmentation of 195-cc
round silicone implant. Before reconstruction (above) and 12 months after
immediate reconstruction prepectoral with 410 Allergan 375 g and AlloDerm 16*20
cm (below).

An exception for prepectoral reconstruction would be in a woman with


current dual plane augmentation with no indication for PMRT. In this
situation, and for patients unsuitable for prepectoral reconstruction, a dual
plane placement is chosen. A chart flow summarizes the paths leading to the
most appropriate decision (Fig. 68-5).
SPECIAL CONSIDERATIONS

Skin-Reducing Mastectomy
Skin-reducing mastectomy (SRM) in patients with previous breast
augmentation is not common. Most women who undergo breast enlargement
in the first place, have small breast and they are unlikely to end up with large
and ptotic breasts. Occasionally, time, pregnancy, breastfeeding, and weight
gain do result in hypertrophy and ptosis. In this infrequent situation, an SRM
and a contralateral breast reduction are called for (Fig. 68-6).
If the nipple areolar complex (NAC) is to be removed as part of the
mastectomy, a transvertical approach or a Wise-pattern mastectomy is
undertaken (Fig. 68-7). It has been the first author’s experience that Wise-
pattern mastectomy carries a high risk of skin necrosis. Apart from the
technical differences and the ease of performance and incidence of
complications, the final scar in a Wise-pattern mastectomy looks like an
inverted T scar, while in the transvertical it resembles a J. For the
contralateral breast a mastopexy with replacement of the current implant
should be done. The preferred plane for implant placement is prepectoral with
ADM (and subglandular for the contralateral breast). In the reconstructed
breast, the preferred implant placement is in the prepectoral plane using an
ADM whenever possible. If the patient is to undergo PMRT, as mentioned
before, then the final aesthetic results will be better when compared to a
subpectoral plane.
FIGURE 68-5 Chart flow for women who are satisfied with their current breast
shape and size.
FIGURE 68-6 Skin-reducing mastectomy in large and ptotic breast.

FIGURE 68-7 Patient with previous subglandular augmentation mastopexy now


diagnosed with left breast cancer stuck to vertical scar on the left and BRCA1 gene
carrier. Before (above) and 2 years after bilateral skin-reducing mastectomy and
symmetrical skin excision (a triangle centered around the vertical scar where tumor
was close to the skin) and immediate DTI dual plane with ADM closure with a
medially based thoracoepigastric flap. Fat grafting in second stage (below).

If the NAC can be spared from an oncologic and perfusion perspective,


then it should be the plastic surgeon’s decision as to how to preserve it. For a
large breast with degree 3 of ptosis, there may be no other way to keep it but
to make a free nipple graft reconstruction. Remembering that the skin
envelope on the reconstructed side invariably contracts, there is also an
option of delaying the mastopexy to a second stage.
CONCLUSION
Reconstruction of the previously augmented breast is often more challenging.
Factors like the oncologic needs, plane, implant, tissue characteristics, breast
shape and size, and the woman’s personal desires, are essential to
determining the correct procedure and proper timing leading to a final long-
lasting aesthetic result.

REFERENCES

1. Sosin M, Devulapalli C, Fehring C, et al. Breast cancer following


augmentation mammaplasty: a case-control study. Plast Reconstr Surg
2018;141:833–840.
2. Cho EH, Shammas RL, Phillips BT, et al. Breast cancer after
augmentation: oncologic and reconstructive considerations among
women undergoing mastectomy. Plast Reconstr Surg 2017;139:1240e–
1249e.
3. Howlader N, Chen VW, Ries LA, et al. Overview of breast cancer
collaborative stage data items—Their definitions, quality, usage, and
clinical implications: a review of SEER data for 2004–2010. Cancer
2014;120 (Suppl 23):3771–3780.
4. Jakub JW, Ebert MD, Cantor A, et al. Breast cancer in patients with
prior augmentation: presentation, stage, and lymphatic mapping. Plast
Reconstr Surg 2004;114:1737–1742.
5. Robbins CM, Long JN, Fix RJ, et al. Mastectomy with breast
reconstruction in previously augmented patients: indications for implant
removal. Ann Plant Surg 2008;61:500–505.
6. Skinner KA, Silberman H, Dougherty W, et al. Breast cancer after
augmentation mammoplasty. Ann Surg Oncol 2001;8:138–144.
7. Tuli R, Flynn RA, Brill KL, et al. Diagnosis, treatment and management
of breast cancer in previously augmented women. Breast J
2006;12:343–348.
8. Lavigne E, Holowaty FJ, Pan SY, et al. Breast cancer detection and
survival among women with cosmetic breast implants: systematic
review and meta-analysis of observational studies. BMJ 2013;346:f2399.
9. Lavigne E, Holowaty EJ, Pan SY, et al. Do breast implants adversely
affect prognosis among those subsequently diagnosed with breast
cancer? Findings from an extended follow-up of a Canadian cohort.
Cancer Epidemiol Biomarkers Prev 2012;21:1868–1876.
10. Xie L, Brisson J, Holowaty EJ, et al. The influence of cosmetic breast
augmentation on the stage distribution and prognosis of women
subsequently diagnosed with breast cancer. Int J Cancer
2010;126:2182–2190.
11. Dcapen D. Breast implants and breast cancer: a review of incidence,
detection, mortality, and survival. Plast Reconstr Surg 2007;120:70S–
80S.
12. Hoshaw SJ, Klein PJ, Clark BD, et al. Breast implants and cancer:
causation, delayed detection, and survival. Plast Reconstr Surg
2001;107:1393–1407.
13. Brisson J, Holowaty FJ, Villeneuve PJ, et al. Cancer incidence in a
cohort of Ontario and Quebec women having bilateral breast
augmentation. Int J Cancer 2006;118:2854–2862.
14. Noels EC, Lapid O, Lindeman JHN, et al. Breast implants and the risk
of breast cancer: a meta-analysis of cohort studies. Aesthet Surg J
2015;35:55–62.
15. Lamaris GA, Butler CE, Deva AK, et al. Breast reconstruction following
breast implant-associated anaplastic large cell lymphoma. Plast Reconstr
Surg 2019;143:51S–58S.
16. Clemens MW, Nava MB, Rocco N, et al. Understanding rare adverse
sequelae of breast implants: anaplastic large-cell lymphoma, late
seromas, and double capsules. Gland Surg 2017;6:169–184.
17. Leberfinger AN, Bchar BJ, Williams NC, et al. Breast implant-
associated anaplastic large cell lymphoma: a systematic review. JAMA
Surg 2017;152:1161–1168.
18. de Boer M, van Leeuwen FE, Hauptmann M, et al. Breast implants and
the risk of anaplastic large-cell lymphoma in the breast. JAMA Oncol
2018;4:335–341.
19. Brody GS, Deapen D, Taylor CR, et al. Anaplastic large cell lymphoma
occurring in women with breast implants: analysts of 173 cases. Plast
Reconstr Surg 2015;135:695–705.
20. Campanale A, Boldrini R, Marietta M. 22 cases of BIA-ALCL:
awareness and outcome tracking from the Italian Ministry of Health.
Plast Reconstr Surg 2018;141:11e–19e.
21. Loch-Wilkinson A, Beath KJ, Knight RJW, et al. Breast implant-
associated anaplastic large cell lymphoma in Australia and New
Zealand: high-surface-area textured implants are associated with
increased risk. Plast Reconstr Surg 2017;140:645–654.
22. Johnson L, O’Donoghue JM, McLean N, et al. Breast implant associated
anaplastic large cell lymphoma: the UK experience. Recommendations
on its management and implications for informed consent. Eur J Surg
Oncol 2017;43:1393–1401.
23. Doren EL, Miranda RN, Selber JC, et al. U.S. epidemiology of breast
implant-associated anaplastic large cell lymphoma. Plast Reconstr Surg
2017;139:1042–1050.
24. Kim B, Roth C, Cluing KC, et al. Anaplastic large cell lymphoma and
breast implants: a systematic review. Plast Reconstr Surg
2011;127:2141–2150.
25. De Silva IM, Teague JA, Blake WE. Breast implant associated
anaplastic large cell lymphoma: a case report and reconstructive option.
J Plast Reconstr Aesthet Surg 2013;06:1773–1776.
26. Magnusson MR, Cooter RD, Rakhorst H, et al. Breast implant illness: a
way forward. Plast Reconstr Surg 2019;143:74S–81S.
27. Shoenfeld Y, Agmon-Levin N. ASIA—autoimmune inflammatory
syndrome induced by adjuvants. J Autoimmun 2011;36:4–8.
28. Cohen Tervaert JW, Kappel RM. Silicone implant incompatibility
syndrome (SITS): a frequent cause of ASIA (Shoenfeld’s syndrome).
Immunol Res 2013;56:293–298.
29. Dush DM. Breast implants and illness: a model of psychological factors.
Ann Rheum Dis 2001;60:653–657.
30. Tugwell P, Wells G, Peterson J, et al. Do silicone breast implants cause
rheumatologic disorders? A systematic review for a court-appointed
national science panel. Arthritis Rheum 2001;44:2477–2484.
31. Janowsky EC, Kupper LL, Hulka BS. Meta-analyses of the relation
between silicone breast implants and die risk of connective-tissue
diseases. N Engl J Med 2000;342:781–790.
32. Colaris MJL, de Boer M, van der Hulst RR, et al. Two-hundreds cases
of ASIA syndrome following silicone implants: a comparative study of
30 years and a review of current literature. Immunol Res 2017;65:120–
128.
33. Watad A, Rosenberg V, Tiosano S, et al. Silicone breast implants and
die risk of autoimmune/rheumatic disorders: a real-world analysis. Int J
Epidemiol 2018;47:1846–1854.
34. Coroneos CJ, Selber JC, Offodile AC 2nd, et al. US FDA breast implant
post approval studies: long-term outcomes in 99,993 patients. Ann Surg
2018;269:30–36.
35. Colwell AS, Mehrara B. Editorial: US FDA breast implant post approval
studies-long-term outcomes in 99,993 patients. Ann Surg 2018;269:39–
40.
36. Sbitany H. Important considerations for performing prepectoral breast
reconstruction. Plast Reconstr Surg 2017;140:7–13.
37. Gabriel A, Maxwell GP. Prepectoral breast reconstruction in challenging
patients. Plast Reconstr Surg 2017;140:14S–21S.
38. Robertson SA, Rusby JE, Cutress RI. Determinants of optimal
mastectomy skin flap thickness. Br J Surg 2014;101:899–911.
39. Nahabedian MY. Current approaches to prepectoral breast
reconstruction. Plast Reconstr Surg 2018;142:871–880.
40. Elswick SM, Harless CA, Bishop SN, et al. Prepectoral implant-based
reconstruction with postmastectomy radiation therapy. Plast Reconstr
Surg 2018;142:1–12.
41. Komorowska-Timek E, Gurtner GC. Intraoperative perfusion mapping
with laser-assisted indocyanine green imaging can predict and prevent
complications in immediate breast reconstruction. Plast Reconstr Surg
2010;125:1065–1073.
42. Newman MI, Samson MC, Tamburrino JF, et al. Intraoperative laser-
assisted indocyanine green angiography for the evaluation of
mastectomy flaps in immediate breast reconstruction. J Reconstr
Microsurg 2010;26:487–492.
43. Phillips BT, Lanier ST, Conkling N, et al. Intraoperative perfusion
techniques can accurately predict mastectomy skin flap necrosis in
breast reconstruction: results of a prospective trial. Plast Reconstr Surg
2012;129:778e–788e.
44. Munabi NC, Olorunnipa OB, Goltsman D, et al. The ability of intra-
operative perfusion mapping with laser-assisted indocyanine green
angiography to predict mastectomy flap necrosis in breast
reconstruction: a prospective trial. J Plast Reconstr Aesthet Surg
2014;67:449–455.
CHAPTER 69

Latissimus Dorsi Musculocutaneous


Flap Breast Reconstruction
DENNIS C. HAMMOND | JAMES D. GOGGIN
HISTORY
The goals of modern breast reconstruction have become more demanding
secondary to improvements in surgical technique and instrumentation. The
simple creation of a shapeless breast mound is no longer sufficient to meet
the high demands of patients. Advances in approach and methodology,
emphasizing natural breast contours and landmarks, have resulted in
tremendous improvements in the aesthetic outcomes of breast reconstruction.
An integral part of this evolution in breast surgery was the description and
use of the latissimus dorsi musculocutaneous flap (LDMF).
Originally described by Tansini in 1906, the LDMF was used as an axial
musculocutaneous flap to cover mastectomy wound defects (1). Its use in the
management of these defects was popularized in Europe but ultimately fell
out of favor. The significance of Tansini’s discovery was lost until Olivari
revisited the flap in 1976 (2). In 1977, Schneider et al. (3) described the
anatomy of the flap and outlined its use for reconstruction of the breast.
Further reports followed which supported the utility of the pedicle-based flap
(4–6). Initial experiences using the LDMF in free tissue transfer were
subsequently described (7–9). Again, despite early enthusiasm, the use of the
LDMF declined after demonstration of the transverse rectus abdominis
musculocutaneous (TRAM) flap by Hartrampf et al. in 1979 (10). The
TRAM flap’s ability to reconstruct the breast with autogenous tissue obviated
complications associated with the use of prosthetic devices, which were often
required when the LDMF was used. As a result, the use of the LDMF
declined, and the technique was relegated to those few cases that could not be
reconstructed with an implant alone or in women who for various reasons
were not candidates for TRAM flap breast reconstruction.
More recently, the LDMF has regained popularity and is providing
consistently high-quality reconstructive and aesthetic results. Improvements
in tissue expander and implant design have contributed to improved surgical
outcomes. In addition, a completely autogenous reconstruction using the
LDMF can be performed in selected patients without the use of an implant.
Use of the latissimus can be an excellent method of reconstruction without
the morbidity associated with harvest of the rectus abdominis muscles that
accompanies traditional TRAM flaps. As a result, the LDMF has again
assumed a prominent role in the armamentarium of the reconstructive breast
surgeon.
ANATOMY
The latissimus dorsi muscle is the largest and most superficial of the posterior
chest wall musculature (Fig. 69-1). It is a broad, flat muscle whose origin
extends along a wide region spanning the posterolateral thorax. Superiorly, it
overlies the inferior tip of the scapula. As it extends superolaterally toward
the axilla, it joins with fibers of the teres major to form the posterior axillary
fold. The superomedial corner of the muscle is overlain by the trapezius
muscle. Medially, the muscle thins into a fascial aponeurosis that joins with
the lumbosacral fascia along the back, which then extends inferolaterally
along the iliac crest. Inferolaterally, the muscle thickens and fuses with fibers
of the external oblique and intercostal muscles of the lower three to four ribs.
The lateral margin of the muscle then extends freely up into the axilla,
forming the posterior border of the axilla.
The latissimus overlies the serratus anterior and a portion of the external
oblique muscles. At the level of the 10th to the 11th rib, there is a firm, thick
aponeurotic attachment between the serratus anterior and the latissimus,
which divides the sublatissimus plane into an inferior and superior portion.
This aponeurosis corresponds to the lower border of the serratus anterior.
Failure to properly divide this aponeurosis results in inadvertent elevation of
the serratus anterior muscle during flap elevation. From this broad origin, the
muscle fibers spiral 180 degrees to insert onto the intertubercular groove of
the humerus via a flat, distinct tendon.
The blood supply to the latissimus dorsi muscle is constant and typically
does not exhibit significant anatomic variation (Fig. 69-2). The subscapular
artery arises from the axillary artery to give two main branches: the
circumflex scapular and thoracodorsal arteries. The thoracodorsal artery and
vein then give off a branch to the serratus muscle shortly before entering the
underside of the latissimus muscle, approximately 9 to 11 cm below the
axillary artery. In cases in which the thoracodorsal pedicle has been divided,
reversal of flow through this serratus branch provides adequate blood flow to
the flap, allowing it to be safely transposed anteriorly (11). Once within the
muscle itself, the vascular pedicle bifurcates into a transverse and lateral
branch, which then arborizes to produce extensive intramuscular
collateralization (12–14). A secondary blood supply enters the underside of
the muscle from paraspinous perforators off the posterior intercostal arteries
located 4 to 5 cm from the midline of the back. These perforators allow the
flap to be elevated as a fold-over flap to cover midline defects (15).

FIGURE 69-1 The latissimus dorsi and related muscles of the back.
FIGURE 69-2 The blood supply of the latissimus dorsi muscle.

Numerous musculocutaneous perforators extend from this rich vascular


plexus into the overlying tissues, forming anastomoses with the circumflex
scapular artery within the dorsal thoracic fascia (16,17). This allows skin
islands to be safely designed anywhere within the margins of the muscle,
although the most reliable location is over the lateral aspect of the muscle
corresponding to the course of the lateral branch of the thoracodorsal artery
(12–14).
The latissimus dorsi muscle is an adductor and medial rotator of the
humerus. It also assists in securing the tip of the scapula against the posterior
chest wall. Transposition of this muscle anteriorly has been shown to be well
tolerated by patients and results in only minimal functional deficit (18,19)
although dynamic weakness in shoulder extension and adduction may occur
(20).
INDICATIONS
The indications for use of the LDMF in breast reconstruction vary and
depend in part on the preferences of both the reconstructive surgeon and the
patient. The LDMF has proven to be useful in patients who might otherwise
be candidates for tissue expander reconstruction alone. The additional soft
tissue provided by the flap can improve the aesthetic quality of the
reconstruction over that obtained with the addition of only the prosthesis
(21). It can be used as a stand-alone reconstructive option when sufficient
skin and fat are available. A completely autogenous reconstruction can be
particularly effective when fat grafting is utilized as an adjunct (22,23). The
LDMF can also be used to reconstruct patients who are not candidates for a
TRAM flap due to illness/comorbidities, insufficient lower abdominal tissue,
or patient preference. Furthermore it can be a valuable reconstructive option
for patients who have failed prior abdominally based reconstruction. The
LDMF is an excellent option in patients who have experienced partial TRAM
flap necrosis, which, after debridement, leaves a distorted reconstructed
breast. Filling in the tissue defect with an autogenous LDMF can salvage the
reconstruction and provide excellent results. Likewise, using the LDMF to
fill in a lumpectomy defect can provide excellent results, even with a history
of previous radiation. The flap has a vigorous and reliable blood supply,
which allows it to be used safely even in heavy smokers. In these patients,
use of the LDMF with an implant may be a better option than the pedicled
TRAM flap procedure due to the increased incidence of complications noted
in smokers.
OPERATIVE TECHNIQUE
Elevation and anterior transposition of the LDMF is straightforward and can
be accomplished easily after surrounding anatomical landmarks have been
identified. Accurate preoperative markings are critical to proper positioning
of the skin island and should always be made with the patient standing
upright. The superior boundary of the flap is identified by locating the tip of
the scapula and drawing a curved line across this landmark up into the axilla
over the top of the posterior axillary fold. The lateral boundary is identified
by drawing a straight line along the anterior margin of the posterior border of
the axilla down to the iliac crest. Between these lines and the midline of the
back lies the latissimus dorsi muscle. The skin island can be oriented in a
variety of directions. One strategy involves placing the long axis of the
ellipse horizontally across the back such that the donor site scar hides in the
bra line. Unfortunately, this often results in bunching of the skin closure at
the anterior end of the scar under the arm. This irregular folding of skin can
detract from the overall result. A better option is to respect the relaxed skin
tension lines as they extend across the back. These lines can be identified by
gently taking traction off the skin of the back by pinching together the
subcutaneous layer with the index finger and thumb. The lines can then be
seen easily. Orienting the long axis of the ellipse along this line results in a
fine line scar with no bunching or “dog ear” formation at either end. The scar
ends up running obliquely across the back from superomedial to inferolateral
and is usually well hidden. The width of the ellipse will vary from patient to
patient, depending on the body habitus and the degree of elasticity of the
skin. In cases of delayed reconstruction, the width of the ellipse is taken as
wide as possible to still allow primary closure of the back donor site. This can
be assessed by simply pinching the skin of the back together along the long
axis of the ellipse to gauge how much can safely be removed. In immediate
reconstruction, usually all that is required is a circular-shaped skin island
designed to fill in the defect created by removing the nipple areola complex
(NAC). In these cases, the ellipse does not have to be as wide, and the skin
island is designed with sufficient width to allow easy closure of the back
donor site. Last, the anterior border of the muscle is marked and the
subcutaneous tunnel for flap transfer is outlined high in the axilla (Fig. 69-3).
FIGURE 69-3 A, B: Preoperative markings in preparation for elevation of a
latissimus dorsi musculocutaneous flap. Laterally, the anterior border of the muscle
and the lateral border of the breast are diagrammed. The space between these two
landmarks is identified with Xs to reinforce the concept that no undermining should
be undertaken in this area so as to preserve the lateral breast contour. Flap passage
takes place high in the axilla as indicated by the arrow.

For both immediate and delayed bilateral breast reconstructions, the


procedure begins with the patient supine. In immediate reconstruction, the
mastectomy is performed generally through a skin-sparing or nipple-sparing
pattern used in conjunction with the general surgeon. In delayed
reconstruction, the mastectomy wound is opened and the mastectomy flaps
are elevated to the margins of the defect. At this point in both situations,
dissection is performed high in the axilla until the lateral margin of the
LDMF is identified. By opening the mastectomy defect initially, eventual
passage of the LDMF anteriorly to the mastectomy wound is facilitated,
which eases closure of the back donor site after the flap is elevated. This is
opposed to starting prone and packing the flap up into the axilla after flap
elevation, which can crowd the closure of the back. In addition, by keeping
most of the lateral margin of the mastectomy defect largely intact and
communicating with the eventual back donor site high in the axilla, this
important breast contour can be effectively controlled. A 4- to 6-cm skin
bridge is preserved between the posterior border of the axilla and the lateral
breast border to maintain these existing anatomical landmarks. Inadvertent
release of the lateral margin of the breast is difficult to reconstruct with
internal sutures; thus, it is far preferable to keep these attachments intact to
smoothly form the lateral breast contour. The mastectomy wound is
temporarily closed with staples and covered with an occlusive dressing.
The drapes are removed, and the patient is repositioned in the prone
position to prepare for harvesting the LDMF. For unilateral reconstructions,
flap elevation can be performed with the patient in the lateral decubitus
position, however it is helpful to use the prone position for both unilateral
and bilateral cases because positioning and appropriately padding the patient
seem to be more easily accomplished. As the skin is incised, the more
compact superficial layer of fat is divided down to the deep thoracic fascia.
This fascia is then released around the periphery of the skin island. As the
fascia is divided, the wound seems to spring open. With upward traction
placed on the skin edges, the looser and less compact deep layer of fat pulls
away from the underside of the fascia. Dissecting in this plane in all
directions then preserves this deep layer of fat as it remains attached to the
muscle. By adding fat to the flap in this manner, the soft tissue volume of the
LDMF is increased (Fig. 69-4). Even if the thickness of the fatty layer is only
5 mm, over a 20- by 30-cm surface area, an additional 300 cc of volume are
provided, which can add significantly to the ability of the flap to soften the
contours of the reconstructed breast. This technique is referred to as the
volume-added LDMF and is the preferred approach in patients of any body
habitus. Even in very thin patients, this approach provides a ready plane of
dissection even if only a modest amount of extra fat is added to the flap. With
the use of this approach, the donor-site back skin flaps are of even thickness,
which prevents contour irregularities from developing postoperatively.
Dissecting below the fascia as described prevents inadvertent
devascularization of the back flaps because they are essentially
fasciocutaneous in design. Dissection proceeds in this plane in all directions
and extends to the margins of the muscle. After the flaps have been
developed, the deep layer of fat is divided by angling through it toward the
periphery in all directions. Superiorly, dissection proceeds beyond the muscle
border to allow the deep fatty layer in this area to be included with the flap.
In the superomedial corner of the dissection space, the obliquely oriented
fibers of the trapezius muscle are identified. After this important landmark is
isolated, the remainder of the dissection proceeds without difficulty. The
value of this maneuver may not be evident in thinner patients because the
margins of the muscle are usually readily identifiable; however, in heavier
patients, it can be difficult to locate with certainty the exact anatomic
relationships required for accurate flap dissection. By locating the fibers of
the trapezius as described, the rest of the muscle dissection can be accurately
performed. Superiorly, the deep layer of fat is divided and then peeled back
to reveal the superior border of the latissimus, which is released all the way
up into the axilla. It should be noted that in some patients, the fibers of the
teres major will fuse with those of the latissimus and sharp dissection will be
required to separate them. The muscle is then undermined and released from
its attachments under the trapezius and then medially along the midline
paraspinous fascia. Large crossing intercostal perforators are present midway
through this elevation, and these vessels are controlled with silk ties or
surgical clips. Inferiorly, the muscle is released from medial to lateral, and
often a small cuff of muscle is left behind because it is not necessary to
dissect completely down to the iliac crest to appropriately harvest the flap. At
this point, the location of the serratus anterior becomes evident as it attaches
to the scapula and crosses obliquely forward. The dense fascial attachment of
the latissimus to the serratus is divided, and the subserratal fat pad is kept
attached to the latissimus muscle to provide added bulk to the flap. Dissection
then proceeds anteriorly between the serratus and the latissimus until the
anterior border of the latissimus is released. Finally, the anterior inferior
corner of the latissimus is released, with care being taken not to injure the
dense attachments with the muscle fibers of the external oblique and the
intercostals (Fig. 69-5). At this point, the muscle/fat flap is essentially
completely elevated. In the axilla, the deep fatty layer is divided, and
dissection proceeds along the muscle fibers until a communication with the
mastectomy wound is created high in the axilla. Under the muscle insertion,
the vascular pedicle is easily identified and preserved. The serratus branch is
identified and preferably left intact because it is not necessary to divide this
vessel to allow adequate anterior transposition of the muscle. The dense
clavipectoral fascia is divided because this attachment can hinder anterior
transposition of the muscle. The latissimus muscle is fully detached from its
attachments to the teres major and the overlying fat, and any remaining soft
tissue attachments that might possibly restrict flap transposition are released
and the flap is transferred to the anterior mastectomy defect. The back wound
is closed in layers over a suction drain brought out through the posterior
axilla. During closure, quilting sutures attaching the underside of the flaps to
the posterior chest wall can be placed to help close down this potential space.
In addition, at the level of the incision, quilting sutures can be used to help
hold the soft tissue envelope of the back in position and prevent it from
sliding over the chest wall. It has been observed that the incidence and
severity of seroma formation is reduced as a result of placing these sutures.

FIGURE 69-4 A: With release of the deep thoracic fascia, the wounds edges “pop”
open to reveal the looser and more areolar deep layer of fat. B: The deep layer of fat
can be easily dissected from the underside of the deep fascia. C: After flap elevation,
the deep layer of fat can be seen because it has been elevated with the muscle. D:
Forceps point to the subserratal fat pad, which has been harvested with the
latissimus dorsi musculocutaneous flap (LDMF).
FIGURE 69-5 Elevation of the latissimus flap begins at the superomedial border of
the muscle with the trapezius retracted medially and then sweeps across the superior
border of the muscle toward the axilla, easily defining the submuscular plane.
Dissection then proceeds inferolaterally, releasing the muscle from the posterior iliac
crest and then anteriorly up into the axilla, taking care not to inadvertently elevate
the serratus anterior.

The patient is then rotated into the supine position, and the chest is prepped
and draped, including the tops of the shoulders. This is an important nuance
because meaningful evaluation of breast shape requires proper positioning of
the shoulders, and the ability to see this position increases the accuracy of the
procedure. The mastectomy wound is opened, and the LDMF is pulled
completely into the mastectomy defect. At this point, the insertion of the
muscle and the pedicle is more easily visualized than when the patient is
prone. It is helpful to divide 90% of the insertion of the muscle because this
allows an additional 10 to 12 cm of flap advancement into the mastectomy
defect. Such advancement allows tension-free insetting and can facilitate
proper orienting of the skin island, particularly in selected cases of delayed
reconstruction. At the same time, keeping the anterior 10% of the insertion
intact can prevent inadvertent traction from being placed on the pedicle, with
resultant vascular compromise of the flap. Finally, to lessen the degree of
undesirable postoperative animation of the reconstructed breast, it is
advisable to divide the thoracodorsal nerve. This maneuver will not result in a
marked loss of volume in the reconstructed breasts over time, which would
be the concern due to the expected atrophy that likely occurs in the muscle.
Adding the deep layer of fat to the flap may assist in preventing this atrophy
from becoming clinically significant. Immediate fat grafting of the flap can
also be performed to optimize flap volume. Of course, the nerve can be kept
intact; however, the degree of movement that is sometimes present in the
reconstructed breast can be disconcerting to some patients. For small- to
moderate-sized breasts, the flap is then inset into the mastectomy defect by
suturing the muscle and/or fat edge of the flap into the margin of the
mastectomy defect superiorly, medially, and laterally. The tissue expander or
implant is then inserted in a submuscular or prepectoral pocket, and the flap
is inset along the inframammary fold (Fig. 69-6). The skin island is inset, and
final closure over a suction drain completes the procedure.
FIGURE 69-6 A: The LDMF is inset into the superior margin of the mastectomy
defect, and the tissue expander is placed under the muscle. B: The remainder of the
flap is sutured around the inferior margin of the defect, completely covering the
expander with the LDMF. C: The redundant wings of the skin ellipse are removed,
and the circular skin island is inset into the nipple areola complex (NAC) defect. D:
Immediate appearance of the reconstructed breast mounds after placement and
appropriate filling of the tissue expanders.

Postoperative recovery is reasonably straightforward. Most patients stay in


the hospital for 1 to 2 days and are back to a normal level of activity within 2
weeks. Breast drains are typically removed at 1 week; however, the back
drain can sometimes remain in place for up to 6 weeks after the procedure. If
seroma fluid accumulates in the back donor site after drain removal, weekly
aspiration is performed until the seroma resolves, usually within 2 to 3
weeks. Postoperatively, the muscle may swell considerably, and the breast
will have a very full appearance for 4 to 6 weeks. Gradually, the swelling
resolves, and the final volume and shape of the breast can be more accurately
estimated at 4 to 6 months. Second-stage procedures are performed 6 months
or more after the initial flap elevation and include removal of the tissue
expander and replacement with the permanent implant, fat grafting,
reconstruction of the NAC, and revision of the breast capsule or soft tissues
as needed. Tattooing of the reconstructed NAC 4 to 6 months later completes
the reconstruction.
Tissue Expander Versus Implant?
The LDMF can provide a limited skin island and a variable amount of fat, as
well as a large, thin, very reliable, and well-vascularized layer of muscle.
Nevertheless, the volume of soft tissue available to reconstruct the
mastectomy defect often falls short of that required to obtain symmetry with
the opposite breast. For this reason, the LDMF is generally used in
conjunction with either a tissue expander or an implant. In cases in which the
latissimus adds sufficient skin to fully reconstruct the skin envelope, it is
possible to use a prosthesis immediately and avoid a second operation for
expander removal and replacement with a breast implant. However, this
technique does not allow for postoperative adjustment in the size of the
reconstructed breast, which is difficult to accurately assess at the initial
setting due to the swelling and settling of the breast that occurs
postoperatively. In addition, a properly filled-out skin envelope at the time of
surgery can become quite tight over the first week postoperatively due to
swelling of the muscle. Sufficient pressure can develop to potentially
compromise the vascular supply to the mastectomy flaps. It is perhaps a
better strategy to underfill a tissue expander initially to provide
accommodation for the expected level of postoperative swelling. Later, when
the edema of the reconstructed breast subsides, saline can be added to the
tissue expander to create a breast of the desired volume. Knowledge of this
volume assists in accurately choosing a subsequent breast implant of the
correct volume, base diameter, and shape, which is then inserted at the
second-stage procedure when the expander is removed. Such an approach
also allows the patient to have input into the size of the breast she wants.
From an administrative standpoint, it is also much easier to preauthorize a
second-stage adjustment procedure with insurance carriers when that
adjustment involves the standard practice of exchanging the tissue expander
for a permanent implant. For these reasons, it is helpful to place a tissue
expander under the LDMF at the initial procedure rather than a permanent
implant. The ability to adjust the volume of the breast postoperatively
improves the accuracy of final breast implant selection and provides for
better symmetry with the opposite breast.
Management of the Opposite Breast
It is preferable to perform any alteration of the opposite breast at the same
time as the initial flap procedure. In this fashion, the recognized postoperative
changes that may occur following an augmentation, mastopexy, or breast
reduction can mature along with the reconstructed breast. Then, at the second
procedure, a more definitive and accurate adjustment of the reconstructed
breast can be made to provide the best symmetry possible with the opposite
side. Any improvements in the appearance of the normal breast can also be
made at that time. If adjustment of the normal breast is delayed until the
second procedure, phenomena such as “bottoming out” of the breast or
disappointments over breast size or position of the NAC can develop after the
final shaping of the reconstructed breast has been performed. This can create
needless asymmetries that detract from the overall result and may require an
additional third procedure to correct.
Delayed Breast Reconstruction
In cases of delayed reconstruction after mastectomy, it is important to assess
what is needed to achieve the reconstruction of an aesthetic breast mound and
to determine how the LDMF can satisfy these requirements. Although each
mastectomy wound is different, there will generally be a skin defect of
varying degrees, a mastectomy scar oriented anywhere from vertically to
horizontally across the chest wall, and a volume loss with only thin
mastectomy flaps left adherent to the underlying pectoralis major muscle.
The LDMF is therefore used to reconstruct the skin defect and provide
additional muscle for coverage of a prosthetic device. The volume loss is
addressed with the addition of a tissue expander or fat grafting.
The procedure is performed as described. Even though the major function
of the LDMF is to provide a skin island of sufficient width to reconstruct the
skin envelope as much as possible, the volume-added approach is still used to
soften the peripheral margins of the mastectomy defect. After it is passed
anteriorly, the skin island can be oriented in many different directions.
Rotation of the skin island is facilitated by partially releasing the insertion of
the latissimus as described. The most advantageous orientation is low and
lateral because this tends to naturally create a ptotic breast shape with
excellent projection (24–27). This often requires that the mastectomy scar be
ignored and that the mastectomy wound be opened with a separate, gently
angled transverse incision across the lower, lateral portion of the chest wall,
insetting the skin island in the lower outer quadrant of the reconstructed
breast. A tissue expander is then inserted into the submuscular or prepectoral
pocket, and the lower margin of the latissimus muscle is sutured to the
inframammary fold. Creating this fold to provide symmetry with the opposite
breast is critical to achieving an aesthetic result, and the placement of this
fold must be assessed with the patient in the sitting position on the operating
table. The lower border of the tissue expander is positioned directly at the
level of the desired inframammary fold. With the newer shaped devices that
are now available (28), an aesthetic breast shape can often be achieved even
at this stage without further manipulation. It is important to suture the
latissimus muscle along the lateral edge of the reconstructed breast down to
the chest wall to completely close off the pocket from the back donor site.
This will prevent the possibility of postoperative expander slippage and
migration to the back. Insetting of the skin island and filling of the expander
to the tolerance of the surrounding soft tissues complete this first-stage
operation. Postoperatively, the tissue expander is inflated beginning 1 to 2
weeks after insertion until the desired volume is achieved. If the expander has
been properly positioned, the inframammary fold and lateral breast contour
will form passively and will be smooth and contoured. Expansion proceeds
until the desired volume has been added. A mild overexpansion strategy can
create a relaxed soft tissue pocket that allows the implant to settle into a
natural-appearing ptotic shape.
The second operation is performed after 4 to 6 months when all soft tissues
have settled and all swelling has subsided. The lateral incision is opened, and
the muscle is divided along the axis of the muscle fibers. The expander is
removed, and the desired prosthesis is inserted. If there is asymmetry in any
breast contour, it is corrected at this time. If the inframammary fold is too
high or the lateral breast contour too medial, the pocket is opened until these
contours are at the desired level. If the fold is too low or the pocket too wide,
a limited capsulectomy is performed in the area of overdissection to create
internal raw surfaces that are then closed off with carefully placed internal
nonabsorbable sutures to effectively control these contours. Care must be
taken when placing these sutures to avoid scalloping of the skin. The
permanent implant is positioned within the pocket, being certain that the
lower border of the device is positioned at the desired level of the
inframammary fold. All manipulations of the pocket and positioning of the
implant must be checked with the patient placed in the beach chair position
on the operating table to ensure accurate creation of breast shape and contour
and symmetry with the opposite breast. The nipple and areola can then be
reconstructed as desired (Fig. 69-7).
Immediate Breast Reconstruction
Immediate reconstruction of the breast with the LDMF offers several
advantages over delayed reconstruction. Working together, the plastic
surgeon and the general surgeon can plan incisions to maximize aesthetics
and avoid vertically oriented or excessively long incisions. More important,
the amount of skin resected can be minimized to only that which is
oncologically necessary rather than the excessive amount that would need to
be removed to obtain a contoured wound closure were no immediate
reconstruction to be performed. Thus, the effect of the flap becomes centered
more on providing muscle and fat for the creation of a tension-free pocket
that allows the shape of the expander or implant to be fully expressed rather
than on replacing skin.
Again, the operation proceeds as described. Typically, all that is required is
a circular skin island that allows almost any flap orientation for insetting to
be used. In immediate reconstruction, the softening effect of the margins of
the flap as they are inset into the mastectomy defect tends to be more
noticeable than in delayed reconstruction. Often, the immediate aesthetics of
the reconstructed breast tend to be remarkably good with this operative
strategy. The second procedure is performed 4 to 6 months after the initial
insetting of the flap, or when the edema from the first operation has subsided.
Any alterations required to create the most aesthetic result possible are
performed at that time, and the NAC is reconstructed as before. Unilateral
and bilateral reconstructions are performed without difficulty using this
technique. Using this strategy, where many variables can be controlled, often
leads to outstanding results in immediate reconstruction (Figs. 69-8 and 69-
9).
FIGURE 69-7 A, B: Preoperative appearance of a 46-year-old woman with a history
of previous left modified radical mastectomy performed as surgical treatment for
invasive ductal carcinoma. She also underwent postoperative chemotherapy and
radiation therapy. C, D: Preoperative marks in preparation for delayed left
latissimus dorsi musculocutaneous flap breast reconstruction, along with placement
of a tissue expander. She will also undergo a left periareolar mastopexy. E, F: First-
stage result after placement of 150 cc in the expander. A pleasing natural contour
has been created with the low and lateral placement of the latissimus skin island. G,
H: Preoperative marks in preparation for placement of the permanent implant,
slight revision of the breast contour and scar, and reconstruction of the nipple areola
complex. A small augmentation of the opposite breast will also be performed. I, J:
Two-year result after placement of smooth, round silicone gel implants with a
volume of 225 cc on the right and 250 cc on the left. K: Appearance of the back
donor site.
FIGURE 69-8 A, B: Preoperative appearance of a 39-year-old woman with ductal
carcinoma in situ of the right breast. C, D: Preoperative marks in preparation for
right simple mastectomy with immediate breast reconstruction using a volume-
added latissimus dorsi musculocutaneous flap with a tissue expander. E: First-stage
result after placement of a tissue expander filled to 350 cc. F: Second-stage marks in
preparation for replacement of the tissue expander with the permanent breast
implant, elevation of the right inframammary fold, and reconstruction of the nipple
areola complex. G, H: Three-year postoperative result after placement of a 350-cc
textured silicone gel implant showing excellent breast projection and symmetry. I:
Appearance of the back donor site. J: With contraction of the chest wall
musculature, there is no distortion of the breast contour.

Autogenous Latissimus Reconstruction


In selected cases, sufficient fat and skin can be harvested with the LDMF to
make a completely autogenous reconstruction possible (29–36). Preoperative
assessment of the size of the opposite breast and the amount of available fat
overlying the latissimus muscle determines whether this technique is
possible. Generally, women with small- to moderate-sized opposite breasts
and a moderately thick and pliable soft tissue layer on the back are candidates
for this procedure. In many instances, an attempt to perform an autogenous
reconstruction can be made, and if absolute symmetry is not obtained, a small
implant can be added after flap insetting. Alternatively, a small
“augmentation” of the reconstructed breast can be performed at the second
procedure if the volume is found to be lacking. Elevation of the flap proceeds
as described previously. The skin ellipse on the back should be wide to
include as much soft tissue with the muscle as possible. An ellipse up to 10 to
12 cm wide can be harvested and still allow primary closure of the back
wound in most patients. If necessary, fat can be safely harvested several
centimeters beyond the margin of the muscle to increase the volume of the
flap (Fig. 69-10). The volume-added LDMF technique helps to preserve the
deep layer of fat within the flap to maximize volume. Immediate fat grafting
of the flap has been described (22,23). Fat injections can be performed into
the muscle fascia and superficial and deep subcutaneous tissues to augment
volume directly without the need for an implant.
FIGURE 69-9 A, B: Preoperative appearance of a 37-year-old woman with high-
grade ductal carcinoma of the left breast. C, D: Preoperative marks in preparation
for bilateral simple mastectomy through a circumvertical skin-sparing pattern, along
with immediate bilateral volume-added latissimus dorsi musculocutaneous flap and
tissue expander breast reconstruction. E: First-stage result after placement of
bilateral tissue expanders filled to 200 cc. F: Second-stage marks in preparation for
removal of the tissue expanders and replacement with permanent implants, minor
breast recontouring with liposuction and scar revision, and reconstruction of the
NAC. G, H: Six-month postoperative result after placement of 300-cc smooth, round
silicone gel implants and tattooing of the reconstructed NAC, showing excellent
symmetry and projection of the reconstructed breasts. I: Appearance of the back
donor site.

FIGURE 69-10 A: An autogenous latissimus flap has been harvested, keeping the
deep layer of fat attached to the muscle for added bulk. The superficial layer can be
seen attached to the flap under the skin island. B: Fat has been harvested beyond the
margin of the muscle to increase the volume of the flap.

With transposition of the flap to the chest wall, tacking of the flap into the
margins of the mastectomy defect defines the borders of the reconstructed
breast. The flap can then be folded and plicated to itself as needed to provide
projection and symmetry with the opposite breast. The reconstructed breast
should be left approximately 10% to 20% larger than the opposite breast to
account for settling and subsequent atrophy of the muscle after transfer.
Although this method of reconstruction avoids the use of an implant, and
therefore implant-related complications, a significant donor-site defect can
result with a scooped-out appearance to the back. Care should be taken to
maintain donor-site back flaps of even, uniform thickness. In appropriately
selected patients, an aesthetic implant-free reconstruction can be obtained
(Fig. 69-11).
Reconstruction of the Partial Mastectomy Defect
After lumpectomy and radiation, significant deformity of the treated breast
can develop that creates a noticeable asymmetry with the contralateral
unaffected side. In these cases, there is typically volume loss coupled with
scarring and contracture of the remaining soft tissue, both as a result of
surgery and as a sequela of radiation therapy. In these cases, an autogenous
volume-added LDMF can be rotated into the defect to accomplish a soft
tissue reconstruction of the breast. At surgery, the lumpectomy defect is
recreated, and all involved scar is removed. If no additional skin is required
to treat a contracted breast skin envelope, simple transposition of the flap
without a skin island can be performed to accomplish a filling out of the
defect. If the skin envelope is deficient, the skin island is inset in a manner
that will release the contracture and create a normal breast contour. Typically,
the results with this technique are outstanding, and preoperative symptoms
such as breast pain or chest tightness are often completely relieved (Fig. 69-
12). The disadvantage of this technique relates to the potential for recurrence
of cancer in the treated breast. If recurrence develops, a major rung in the
reconstructive ladder will have been used, thus necessitating other methods of
reconstruction. For this reason, it may be advisable to offer this operative
strategy only to those patients who have sufficient abdominal tissue to allow
subsequent TRAM flap reconstruction if needed.
Revision Reconstruction
For patients who have already had one or more prior attempts at breast
reconstruction with unsatisfactory results, the volume-added LDMF has
proven to be an excellent option for revision reconstruction. In particular, the
ability of the flap to provide additional soft tissue to soften the contours of
the reconstructed breast is a particular advantage. By then adding a prosthesis
to replace missing volume, difficult reconstructive cases can be effectively
managed in a predictable and straightforward fashion (Fig. 69-13). Fat
grafting is also routinely used in revision reconstruction cases to improve
infraclavicular step-offs, flap irregularities, and other deformities secondary
to radiation and scar (22,23,37). Principles of gentle harvest, minimal
processing, and placement of thin strips of graft material should be followed.
The entire breast skin envelope can be treated, resulting in softened contours
and improved breast aesthetics (Figs. 69-14 and 69-15).
FIGURE 69-11 A, B: Preoperative appearance of a 69-year-old woman with invasive
lobular carcinoma of the left breast. C, D: Preoperative marks on the breast in
preparation for periareolar skin-sparing mastectomy. E, F: Preoperative marks in
preparation for autogenous latissimus dorsi musculocutaneous flap reconstruction.
A wide skin island can be harvested with the flap due to the redundancy of the skin
envelope of the back. In this fashion, along with the volume-added concept, the
volume of the flap can be increased. G, H: Appearance after flap transfer and inset.
I, J: Second-stage marks in preparation for revision of the reconstructed breast and
back scar, along with reconstruction of the NAC. K, L: Two-year postoperative
appearance after tattooing of the reconstructed NAC. M: Appearance of the back
donor site.
COMPLICATIONS
Extensive clinical experience with the LDMF has documented the safety of
the procedure. The flap has a vigorous blood supply and can be used with
minimal risk of flap necrosis even in smokers, diabetics, and patients with
medical illness. Significant flap necrosis is unusual and is nearly always
associated with either recognized or unrecognized injury to the vascular
pedicle, as when the thoracodorsal artery has been ligated during the original
mastectomy (38,39). Partial flap necrosis has been noted in up to 7% of cases
(6,31,36,38–40) but is more common when an extended flap has been
elevated in an attempt to reconstruct the breast with a totally autogenous
LDMF (31).
FIGURE 69-12 A, B: Preoperative appearance of a 51-year-old woman with a
previous history of lumpectomy and radiation as primary surgical treatment of an
infiltrating ductal carcinoma. Significant distortion of the breast is evident. C, D:
The preoperative plan included recreation of the mastectomy defect through the
mastectomy scar with resection of a portion of the radiated and scarred skin
envelope in the lower medial pole of the breast. A periareolar mastopexy will also be
performed on the opposite breast. E, F: Preoperative marks in preparation for
reconstruction with an autogenous volume-added latissimus dorsi musculocutaneous
flap. The skin island on the flap will be used to replace the skin of the lower medial
pole of the breast. G, H: Appearance of the flap after elevation from the back. The
deep layer of fat attached to the muscle below the skin island is evident, as is the
subserratal fat pad. I–K: The flap is passed high through the axilla and under the
breast to reach the lumpectomy defect. With folding and insetting, the flap easily
provides enough volume to reconstruct the defect without the need for an implant. L,
M: One-year postoperative appearance shows symmetric restoration of normal
breast contours. N: Appearance of the back donor site.
FIGURE 69-13 A, B: Preoperative appearance of a 40-year-old woman after
undergoing bilateral prophylactic mastectomy with immediate reconstruction using
shaped silicone gel implants. The contours of the reconstructed breast are sharply
demarcated and irregular, and the skin envelope is incompletely filled out. C: With
contraction of the pectoralis major muscle, significant distortion of the breast is also
evident because the implants are located in the partial subpectoral pocket. D, E: The
preoperative plan included bilateral capsulectomy with implant removal, placement
of the pectoralis major back into an anatomic position, and reconstruction with
bilateral volume-added latissimus dorsi musculocutaneous flaps with tissue
expanders on top of the pectoralis major. Because the skin envelope of the breast was
intact, no skin island was required from the back. F: Postoperative appearance with
the tissue expanders in place showing restoration of smooth breast contours and a
more complete filling out of the breast skin envelope. G, H: Final appearance 2 years
postoperatively after removal of the tissue expanders and replacement with 450-cc
smooth, round silicone gel implants. An aesthetic, smooth appearance has been
restored to each breast. I: With contraction of the chest wall musculature, there is no
longer any distortion to the reconstructed breast because the pectoralis major was
replaced back down against the chest wall, and the thoracodorsal nerve to the
latissimus dorsi muscle was divided. J: Appearance of the back donor site.

By far the most common complication is seroma at the back donor site
(36,39,40). This fluid collection often requires percutaneous postoperative
drainage multiple times before resolution occurs. For persistent nonresolving
seromas, sclerotherapy techniques have been described (41). Rarely, a
persistent bursa cavity forms that requires operative excision along with
prolonged closed suction drainage. Other complications include loss of
shoulder mobility, shoulder stiffness, and shoulder weakness. These
complications can be avoided with the use of postoperative physical therapy
when patients exhibit difficulty in regaining shoulder function by 2 weeks
postoperatively. Infection and hematoma occur with a frequency equal to that
in other plastic surgery procedures. Donor-site complications, including
delayed wound healing at the back donor site and scar widening, lend
themselves well to scar revision at a later date.
Complications related to the use of prosthetic devices in conjunction with
the LDMF merit special attention. Slippage of the expander or implant
through the axilla and into the back has been reported (39) and can be
avoided easily by securely suturing the latissimus muscle to the lateral chest
wall. This closes off the lateral mastectomy space from the back, preventing
implant or expander migration. More troublesome is the development of
significant capsular contracture. Rates as high as 39% have been documented
in large groups of patients undergoing latissimus reconstruction in
conjunction with silicone gel implants (39,40,42,43). However, this data does
not reflect the latest design improvements in expanders and implants made
since the mid-1990s. Baker III/IV capsular contracture rates were 8% or less
in well-controlled studies of patients undergoing augmentation mammaplasty
(44,45).
FIGURE 69-14 A, B: Preoperative appearance of a 54-year old woman who had
previously undergone bilateral latissimus dorsi musculocutaneous flap and implant
reconstruction. She desired improvement of upper pole hollowing. C, D:
Preoperative marks in preparation for bilateral breast capsulotomies, periareolar
scar revision, and fat grafting. E: Immediate postoperative result following fat
grafting—200 cc of fat grafted to the right breast, 230 cc to the left. F, G: Six-month
postoperative appearance following fat grafting showing improved upper pole
fullness and smooth contours filling out the breast skin envelope.
FIGURE 69-15 A, B: Preoperative appearance of a 61-year-old woman who had
undergone bilateral latissimus dorsi musculocutaneous flap and implant
reconstruction. She desired scar revision and removal of implants. C, D:
Preoperative marks in preparation for bilateral capsulectomies, implant removal,
periareolar scar revision, and fat grafting. E: Immediate postoperative result
following implant removal and fat grafting—330 cc of fat grafted to the right breast,
300 cc to the left. F, G: Six-month postoperative appearance showing appropriate
filling out of the breast skin envelope and an aesthetic breast shape.
CONCLUSION
Use of the LDMF provides the reconstructive surgeon with a consistent and
reliable method of breast reconstruction. Whether it is used as an autogenous
flap or in conjunction with tissue expanders or implants, the reliability of the
flap and the straightforward manner in which it is elevated and transferred to
the mastectomy defect make the technique an attractive option for breast
reconstruction. By softening the contours of the reconstructed breast with the
muscle and fat from the flap, a versatile and effective method to create
aesthetic breast contours is provided. Complications are few, and the results
are predictable. It is recommended as an effective and versatile technique for
the reconstructive breast surgeon to consistently achieve superior results in
postmastectomy reconstruction.

REFERENCES

1. Maxwell GP. Iginio Tansini and the origin of the latissimus dorsi
musculocutaneous flap. Plast Reconstr Surg 1980;65:686–692.
2. Olivari N. The latissimus flap. Br J Plast Surg 1976;29:126–128.
3. Schneider WJ, Hill HL, Brown RG. Latissimus dorsi myocutaneous flap
for breast reconstruction. Br J Plast Surg 1977;30:277–281.
4. Muhlbauer W, Olbrisch R. The latissimus dorsi myocutaneous flap for
breast reconstruction. Chir Plast 1977;4:27.
5. Bostwick J, Vasconez LO, Jurkiewicz MJ. Breast reconstruction after a
radical mastectomy. Plast Reconstr Surg 1978;61:682–693.
6. Bostwick J, Nahai F, Wallace JG, et al. Sixty latissimus dorsi flaps.
Plast Reconstr Surg 1979;63:31–41.
7. Mendelson BC. The latissimus dorsi flap for breast reconstruction. Aust
N Z J Surg 1980;50:200–204.
8. Maxwell GP, Steuber K, Hoopes JE. A free latissimus dorsi
myocutaneous flap. Plast Reconstr Surg 1978;62:462–466.
9. Maxwell GP, Manson PN, Hoopes JE. Experience with thirteen free
latissimus dorsi myocutaneous flaps. Plast Reconstr Surg 1979;64:1–8.
10. Hartrampf CR, Scheflan M, Black PW. Breast reconstruction with a
transverse abdominal island flap. Plast Reconstr Surg 1982;69:216–225.
11. Fisher J, Bostwick J 3rd, Powell RW. Latissimus dorsi blood supply
after thoracodorsal vessel division: the serratus collateral. Plast Reconstr
Surg 1983;72:502–511.
12. Bartlett SP, May JW Jr, Yaremchuk MJ. The latissimus dorsi muscle: a
fresh cadaver study of the primary neurovascular pedicle. Plast Reconstr
Surg 1981;67:631–636.
13. Tobin GR, Schusterman M, Peterson GH, et al. The intramuscular
anatomy of the latissimus dorsi muscle: the basis for splitting the flap.
Plast Reconstr Surg 1981;67:637–641.
14. Rowsell AR, Eisenberg N, Davies DM, et al. The anatomy of the
thoracodorsal artery within the latissimus dorsi muscle. Br J Plast Surg
1986;39:206–209.
15. Bostwick J 3rd, Scheflan M, Nahai F, et al. The “reverse” latissimus
dorsi muscle and musculocutaneous flap: anatomical and clinical
considerations. Plast Reconstr Surg 1980;65:395–399.
16. Kim PS, Gotlieb JR, Harris GD, et al. The dorsal thoracic fascia:
anatomic significance with clinical applications in reconstructive
microsurgery. Plast Reconstr Surg 1987;79:72–80.
17. Hayashi A, Maruyama Y. The “reduced” latissimus dorsi
musculocutaneous flap. Plast Reconstr Surg 1989;84:290–295.
18. Laitung JKG, Peck F. Shoulder function following the loss of the
latissimus dorsi muscle. Br J Plast Surg 1985;38:375–379.
19. Russell RC, Pribaz J, Zook EG, et al. Functional evaluation of latissimus
dorsi donor site. Plast Reconstr Surg 1986;78:336–344.
20. Fraulin FOG, Louie G, Zorrilla L, et al. Functional evaluation of the
shoulder following latissimus dorsi muscle transfer. Ann Plast Surg
1995;35:349–355.
21. Luce PA, Hammond DC. Latissimus dorsi musculocutaneous flaps and
tissue expanders/implants in immediate breast reconstruction. Plast Surg
Forum 1995;64:133.
22. Santanelli di Pompeo F, Laporta R, Sorotos M, et al. Latissimus dorsi
flap for total autologous immediate breast reconstruction without
implants. Plast Reconstr Surg 2014;134:871e–879e.
23. Economides J, Song D. Latissimus dorsi and immediate fat transfer
(LIFT) for complete autologous breast reconstruction. Plast Reconstr
Surg Global Open 2018;6(1):e1656.
24. Maxwell GP. Latissimus dorsi breast reconstruction: an aesthetic
assessment. Clin Plast Surg 1981;8:373–387.
25. Millard DR. Breast aesthetics when reconstructing with the latissimus
dorsi musculocutaneous flap. Plast Reconstr Surg 1982;70:161–172.
26. Biggs TM, Cronin ED. Technical aspects of the latissimus dorsi
myocutaneous flap in breast reconstruction. Ann Plast Surg 1981;6:381–
388.
27. Wolf LE, Biggs TM. Aesthetic refinements in the use of the latissimus
dorsi flap in breast reconstruction. Plast Reconstr Surg 1982;69:788–
793.
28. Hammond DC, Perry LC, Maxwell GP, et al. Morphologic analysis of
tissue-expander shape using a biomechanical model. Plast Reconstr
Surg 1993;92:255–259.
29. Song R, Yang P, Yu H, et al. Breast reconstruction without a silicone
implant. Clin Plast Surg 1982;9:85–89.
30. Hokin JAB. Mastectomy reconstruction without a prosthetic implant.
Plast Reconstr Surg 1983;72:810–818.
31. Hokin JAB, Silfverskiold KL. Breast reconstruction without an implant:
results and complications using an extended latissimus dorsi flap. Plast
Reconstr Surg 1987;79:58–66.
32. Marshall DR, Anstee EJ, Stapleton MJ. Soft tissue reconstruction of the
breast using an extended composite latissimus dorsi myocutaneous flap.
Br J Plast Surg 1984;37:361–368.
33. Papp C, Zanon E, McCraw J. Breast volume replacement using the
deepithelialized latissimus dorsi myocutaneous flap. Eur J Plast Surg
1988;11:120–125.
34. Hartrampf CR Jr. Breast Reconstruction With Living Tissue. New York:
Raven Press; 1991.
35. McCraw JB, Papp C, Edwards A, et al. The autogenous latissimus breast
reconstruction. Clin Plast Surg 1994;21:279–288.
36. Barnett GR, Gianoutsos MP. The latissimus dorsi added fat flap for
natural tissue breast reconstruction: report of 15 cases. Plast Reconstr
Surg 1996;97:63–70.
37. Hammond DC, O’Connor EA, Scheer J. Total envelope fat grafting: a
novel approach in breast reconstruction. Plast Reconstr Surg
2015;135:691–694.
38. Mendelson BC. Latissimus dorsi breast reconstruction: refinement and
results. Br J Surg 1983;70:145–149.
39. De Mey A, Lejour M, Declety A, et al. Late results and current
indications of latissimus dorsi breast reconstructions. Br J Plast Surg
1991;44:1–4.
40. Moore TS, Farrell LD. Latissimus dorsi myocutaneous flap for breast
reconstruction: long-term results. Plast Reconstr Surg 1992;89:666–672;
discussion 673–674.
41. Ali-Khan AS, Orlando A, Kenealy J. Erythromycin sclerotherapy in the
management of seroma. J Plast Reconstr Aesthet Surg 2009;62:e55–e58.
42. McCraw JB, Maxwell GP. Early and late capsular “deformation” as a
cause of unsatisfactory results in the latissimus dorsi breast
reconstruction. Clin Plast Surg 1988;15:717–726.
43. Tschopp H. Evaluation of long-term results in breast reconstruction
using the latissimus dorsi flap. Ann Plast Surg 1991;26:328–340.
44. Coleman DJ, Foo ITH, Sharpe DT. Textured or smooth implants for
breast augmentation? A prospective controlled trial. Br J Plast Surg
1991;44:444–448.
45. Pollock H. Breast capsular contracture: a retrospective study of textured
versus smooth silicone implants. Plast Reconstr Surg 1993;91:404–407.
CHAPTER 70

Radiating Implants Versus Expanders:


Plastic Surgeon’s Perspective and
Experience
JAMES M. ECONOMIDES | TROY A. PITTMAN
HISTORY
Post mastectomy radiation therapy (PMRT) was first introduced in 1997 and
its indications have expanded since that time (1–3). Concurrently, the
popularity of prosthetic-based breast reconstruction (IBBR) following
mastectomy has remained high with over 80% of reconstructions performed
being implant based (4). Radiation therapy, unfortunately, brings unique
challenges to implant based breast reconstruction (IBBR), and is known to
have an adverse impact on prosthetic reconstructions. Rates of reconstructive
failure range between 20% and 50%, rates of capsular contracture range
between 17% and 60%, and the need for revision surgery is as high as 40%
(5–14). Central to the reconstruction of the irradiated patient is the debate of
the optimal timing of PMRT: irradiation of the tissue expander versus
permanent implant. When possible, it is our preference to radiate the
permanent implant.
Much progress has been made with regard to both surgical technique and
technology since the early reports of first- and second-generation silicone gel
implants. These early implants were characterized by underfilled silicone
shells with a high degree of malleability and implant distortion as well as a
significant risk of capsular contracture. Later-generation implants benefited
from more cohesive gel which was filled to the implant shell capacity and
demonstrated a lower incidence of capsular contracture. At the same time, the
development of acellular dermal matrices (ADMs) conferred certain
protections against capsular contracture as well as a more predictable and
reproducible reconstruction. Together, with advances in technology allowing
for real-time tissue perfusion assessment, such as indocyanine green (ICG)
angiography and advances in mastectomy technique such as nipple-sparing
mastectomies (NSMs), our practice has evolved to allow us to offer a
significant proportion of women a single-stage direct-to-implant (DTI)
reconstruction, thus eliminating the use of a tissue expander altogether. This
fact has thus obviated the age-old debate between irradiation of tissue
expander versus implant in PMRT in many patients.
INDICATIONS
According to the American Society of Clinical Oncology (ASCO)
Guidelines, in patients with no prior history of breast irradiation, PMRT is
indicated in the following circumstances (15):
Tumor size greater than 4 cm
Tumor close to the resection margins
Four or more positive lymph nodes
In the setting of local recurrence
In addition to the above circumstances, a 2016 update to the ASCO
Guidelines further clarifies the role of PMRT in four clinical scenarios
involving patients with smaller tumors (T1-T2) (16). These scenarios and
recommendations are:
1. In patients with T1-T2 tumors with one to three positive sentinel lymph
nodes (SLNs) who undergo axillary lymph node dissection (ALND),
PMRT is acknowledged to decrease the incidence of locoregional failure
(LRF). The decision to undergo PMRT in this population should be
conducted in a multidisciplinary fashion early in the patient’s course
taking into consideration the risks and benefits specific to each patient
and their tumor characteristics.
2. In patients with T1-T2 tumors and a positive SLN who do not undergo
completion ALND, PMRT is recommended only when there is already
sufficient information to justify its use without needing to know that
additional axillary lymph nodes are involved.
3. In patients with clinical stage I or II cancers who have received
neoadjuvant systemic therapy (NAST) with a less than complete
pathologic response should undergo PMRT.
4. In general, patients with T1-T2 tumors with one to three positive axillary
lymph nodes, regional nodal irradiation (RNI) should include the internal
mammary (IMNs) and supraclavicular-axillary apical nodes in addition to
the chest wall and reconstructed breast.
The amount of radiation received in PMRT is determined by various
factors including the size of the tumor, surgical margins of resection, the
characteristics of the tumor cells, and lymph node involvement. Generally,
patients who have received higher doses of radiation will develop tissues that
feel tight, inelastic, and thickened. The total dose of radiation following
mastectomy in whole breast irradiation (WBI) is generally 4,500 to 5,000
cGy divided into 25 sessions of 180 to 200 cGy administered over 5 weeks.
Sometimes a 1,000 to 2,000 cGy “boost” dose is prescribed over 1 week
following completion of therapy to target the tumor bed. For comparison,
doses of radiation given in breast-conservation therapy (BCT) are roughly
3,400 cGy given over 1 week. More recently, hypofractionated whole breast
irradiation (HF-WBI), whereby fewer sessions of a higher dose of radiation is
given, has been investigated with some centers showing similar oncologic
outcomes with fewer radiation complications (17).
CONTRAINDICATIONS
The adverse effect of radiation on IBBR is well known, including decreased
mastectomy flap perfusion, wound healing complications, and infection
(5,18,19). These effects are more pronounced in the setting of prior
irradiation. Because of the high rate of complications associated with
implants in irradiated fields, IBBR is generally contraindicated in the setting
of prior premastectomy radiotherapy unless vascularized tissue is used
concurrently (20).
PREOPERATIVE PLANNING
Individual preoperative planning and assuring that patient expectations are
managed is probably one of the most important parts of the reconstructive
process. This begins with an assessment of the likelihood of the patient to
receive PMRT and also the likelihood of their ability to achieve a satisfactory
result with IBBR. As such, it is important to understand thoroughly the
patient’s oncologic history and the possible plan for PMRT to discuss the
risks and benefits of pursuing IBBR. Once the patient has decided to pursue
IBBR, implants are selected based on the patient’s individual anatomy and
preference. We prefer a tissue-based approach to surgical planning and favor
highly cohesive gel implants for their superior aesthetic outcomes.
Specifically, in many of our patients we favor the use of textured, anatomic
implants. We know that textured implants are protective against capsular
contracture and also feel that a more natural result can be achieved with a
more cohesive anatomically shaped implant (21,22). We also discuss with the
patient the use of ICG angiography as an intraoperative tool to guide our
decision making for DTI reconstructions. If tissue perfusion is inadequate
following mastectomy, we would abort DTI and proceed with either tissue
expander placement or a delayed-immediate approach (23).
OPERATIVE TECHNIQUE
Preoperative markings are made in the holding area in conjunction with the
breast oncologist. If a candidate for NSM, an inframammary incision is
preferred. Following completion of the mastectomy, the skin flaps are
assessed for adequate tissue perfusion with ICG angiography. If tissue
perfusion is adequate, we will proceed with DTI. If perfusion is inadequate
we will proceed with a two-stage approach by placing a tissue expander
which may be filled as perfusion allows and can be titrated in real-time using
ICG angiography as a guide. In patients with severe mastectomy flap
perfusion issues, or in patients that wish to avoid the tissue expansion
process, a delayed-immediate approach is used.
For all NSMs and a growing number of skin-sparing mastectomies, we
now offer prepectoral reconstruction using the previously published “P1
Method” approach (23). This approach minimizes implant edge visibility and
rippling, particularly in thin patients. The P1 prepectoral plane is created by
elevating a superior slip of pectoralis major muscle 2 cm in width parallel to
its fibers from the sternal edge to the lateral margin of the muscle. A sheet of
ADM (8 × 16 or 8 × 20 cm) is prepared and sewn to the inferior edge of
pectoralis muscle with running 3-0 Vicryl suture, which now serves as the
leading edge of an ADM sling. After attaching the ADM to the pectoralis
muscle slip, the pocket is thoroughly irrigated. A highly cohesive, gel implant
is placed under the ADM and wedged into position deep to the muscle slip
superiorly but anterior to the bulk of pectoralis muscle, which remains in its
anatomic position. Alternatively, a tissue expander may be placed at this time
if the patient is to undergo two-stage reconstruction. The ADM is then
secured to the chest wall with interrupted 3-0 Vicryl suture at the desired
level of the inframammary fold and lateral breast margin. Before skin
closure, a 15F Blake drain is placed between the ADM and the mastectomy
flap exiting through a lateral stab incision. The incision is closed in layers
with 3-0 Monocryl suture. Tissue perfusion is again assessed with ICG to
confirm there is no undue pressure on the mastectomy flaps prior to dressing
and extubation.
OUTCOMES
The effects of radiation on IBBR are well documented with a clear increase
in reconstructive failure and capsular contracture seen in irradiated implants
compared to nonirradiated implants (24). When radiation is unavoidable,
there are generally three options for the timing of PMRT:
1. Following mastectomy but prior to reconstruction
2. Following placement of tissue expander but prior to implant exchange
3. Following permanent implant placement in either two-stage or single-
stage (DTI) reconstruction
Results from the literature regarding the optimal timing of irradiation in
two-stage IBBR are mixed both in terms of its risk of reconstructive failure
and its impact on aesthetic outcomes such as capsular contracture. The
overarching trend, however, shows a higher increase in reconstructive failure
in irradiation of the tissue expander, but a decreased rate of capsular
contracture. Theoretically, reintroducing an inflammatory reaction in an
irradiated field during implant exchange increases the chance of wound
healing complications and eventual explantation. However, the capsule work
performed during this exchange, whether it be through capsulotomy or
capsulectomy of the radiated capsule, may confer a decreased risk of capsular
contracture. In general, therefore, the decision between irradiating the tissue
expander or permanent implant in two-staged IBBR has historically come
down to a trade-off between an increased risk for reconstructive failure seen
in tissue expander irradiation and an increased risk for capsular contracture
seen in implant irradiation.
It is our opinion and our practice, however, that if given the choice, PMRT
should be administered to the final permanent implant when possible. We
believe that the general consensus in the literature and plastic surgery
community is that there is a higher risk of reconstructive failure with PMRT
administered prior to permanent implant placement. This risk of complete
reconstructive failure outweighs any benefit of improved aesthetic outcomes
associated with decreased risk for capsular contracture in PMRT
administered to the tissue expander prior to implant exchange. Furthermore,
with recent advances in surgical techniques including prepectoral breast
reconstruction and the use of new technologies such as ADMs, these
historical aesthetic benefits may become increasingly irrelevant.
Risk of Reconstructive Failure
Arguably the best-known single-center study by Cordeiro et al. investigated
94 reconstructions which underwent irradiation to the tissue expander and
210 reconstructions which underwent irradiation to the final implant (6). In
this series, reconstructive failure was seen in 18.1% of patients who
underwent irradiation to the tissue expander compared to 12.4% for those
who underwent irradiation to the final implant. Although this finding did not
reach statistical significance, the authors went on to perform a Kaplan–Meier
analysis and noted a significant difference in the 6-year rates of
reconstructive failure at 32.0% and 16.4%, respectively.
Two recent systematic reviews have analyzed the body of literature to
determine optimal timing of radiation with regard to minimizing the risk of
reconstructive failure. The first in 2013 by Lam et al. performed a review and
meta-analysis of nine studies and showed a significantly higher rate of
reconstructive failure in patients undergoing irradiation to tissue expanders
compared to implants (22.9% vs. 5.6%, p < 0.0001) (24). A more recent
systematic review and meta-analysis of eight studies in 2017, however,
demonstrated an insignificantly higher rate of reconstructive failure in the
tissue expander group compared to the implant group (16% vs. 10%) with a
relative risk of 1.72 (25). Similarly, the pooled risk of infection was not
significantly different between the groups. General consensus remains that
there is likely a higher risk of total reconstructive failure when the tissue
expander is irradiated compared to the permanent implant.
Aesthetic Outcomes and Capsular Contracture
The published data on aesthetic outcomes such as capsular contracture are
also mixed. Cordeiro et al. saw a significant difference in capsular
contracture rates between radiation to tissue expanders and permanent
implants (6). Grade III capsular contracture was seen in 15.9% and 44.6%
and grade IV capsular contracture was seen in 1.22% and 6.3% of patients,
respectively. Nava et al. also reported a significantly lower rate of grade IV
capsular contracture in the tissue expander group compared to implant group
(10.1% vs. 13.3%) (26). Pooled results from the 2017 systematic review and
meta-analysis demonstrated that radiation delivery to the tissue expander in
two-stage breast reconstruction resulted in a significantly decreased risk for
capsular contracture (25).
In 2016 the results from the Mastectomy Reconstruction Outcomes
Consortium (MROC) study were published (27). This multicenter study
including 150 patients with PMRT with at least 6 months of follow-up
demonstrated no difference in complication rates between irradiation of tissue
expanders or implants in two-stage breast reconstruction. Although the data
were of high quality and prospectively obtained, these results were limited by
small sample size and short follow-up.
Effect of Timing of Surgical Intervention Following Irradiation
When reoperation either through tissue expander to implant exchange or
revision of a prior permanent implant is required in an irradiated field,
increasing the absolute timing of such an intervention following irradiation
improves outcomes (28,29). It is our practice to allow the acute phase of
radiation damage to subside (at least 6 months from completion of PMRT)
prior to inducing an inflammatory state through reoperation. Animal models
have demonstrated a decrease in endoethelial cells, capillary density, and
dermal blood flow following radiation doses similar to those in PMRT that
occur at 2 to 6 months and level off at 6 to 9 months following radiation
(30,31). Imaging studies also demonstrate that breast edema and skin
thickening following PMRT are most pronounced up to 6 to 9 months
following treatment (30,31).
Clinical data support delaying implant exchange for at least 6 months
following PMRT. In a series of 88 patients who underwent two-stage IBBR
with irradiation to the tissue expander, one study found that patients who
underwent permanent implant exchange within 6 months of irradiation were
significantly more likely to experience reconstructive failure compared with
those who were exchanged after at least 6 months (22.4% vs. 7.7%, p =
0.036) (28). Furthermore, when broken down into 3-month intervals, a higher
rate of failure was seen in the group with less than 3 months following PMRT
compared to the group between 3 and 6 months (28.6% vs. 17.9%). The
interval of time between PMRT and implant exchange did not affect rates of
capsular contracture.
Effect of ADM Use
The rise in ADM has correlated to improvements in outcomes including
decreased rates of capsular contracture (32–34). ADM is decellularized and
does not contain fibroblasts or myofibroblasts. It, therefore, does not create
abnormal collagen molecules in response to radiation therapy, nor does it
fibrose, contract, or migrate. In addition, histologic studies have shown that
ADM decreases the inflammatory response of capsule development leading
to thinner capsules compared to those without ADM (35–37).
Although, there is no singular study directly investigating the use of ADM
and its effect in minimizing complications following PMRT, much can be
inferred from the current body of literature. Historical data reveals that there
may be benefit in capsular contracture rates with ADM use in the setting of
PMRT. A widely cited study by Spear et al. investigating outcomes
specifically in ADM-assisted reconstructions demonstrated an overall 21.4%
failure rate in irradiated breast reconstructions compared to an upward of
40% failure rate by other studies in reconstructions which explicitly did not
use ADM (7,8).
Prepectoral Breast Reconstructions
Recently, prepectoral breast reconstruction has become increasingly popular
as it provides many benefits to the patient including decreased pain, lack of
animation deformity, and high patient satisfaction (38–40). Additionally,
prepectoral breast reconstruction may hold an advantage over traditional
submuscular and partial submuscular approaches in the setting of PMRT.
When the pectoralis muscle is irradiated, it becomes fibrotic and shortens. An
implant placed in a submuscular plane, thus migrates cephalad and laterally
as the pectoralis fibers shorten toward their insertion on the humerus. An
implant placed in a prepectoral plane is not subject to these deformational
forces.
Current clinical data support the safety of PMRT in prepectoral
reconstructions (41). In a series of patients undergoing either submuscular or
prepectoral breast reconstructions, no significant difference was observed in
complication rates between either group receiving PMRT (42). In fact, the
prepectoral cohort saw an insignificantly lower rate of reconstructive failure
(15.4% vs. 19.4%). Additionally, there was a significantly lower rate of
elective revision procedures compared to the submuscular cohort (15.9% vs.
27.8%, p = 0.014) attributed to a more predictable and reliable result with the
prepectoral technique.
Single-Stage DTI Reconstructions
It is important to note the increase in single-stage DTI reconstructions. With
improvements in surgical technique and technologies allowing for real-time
evaluation of mastectomy flap tissue perfusion, we are now able to offer DTI
reconstructions more frequently. Consequently, this has allowed us to obviate
the need for irradiation of tissue expanders as the permanent implant is placed
on the day of mastectomy. In the future, as this technique is more widely
available, the debate surrounding the optimal timing of irradiation in two-
stage breast reconstruction will be inconsequential.
CONCLUSION
To summarize, the literature remains mixed regarding the optimal timing of
PMRT in IBBR. As the historical data include series involving older
technologies and techniques, we believe that the true incidence of
reconstructive failure is higher when radiation is administered prior to final
implant exchange. Therefore, our preference for IBBR in the setting of
PMRT is to complete the reconstruction prior to the administration of
radiation. Given the advances in surgical technique and technologies such as
prepectoral, ADM-assisted reconstructions, we believe that a lower rate of
reconstructive failure may be achieved together with an optimal aesthetic
result and acceptable capsular contracture profile. Additionally, practices are
evolving such that a single-stage DTI reconstruction may become the norm,
and therefore may obviate the discussion of when to administer PMRT.

REFERENCES

1. Ragaz J, Jackson SM, Le N, et al. Adjuvant radiotherapy and


chemotherapy in node-positive premenopausal women with breast
cancer. N Engl J Med 1997;337:956–962.
2. Overgaard M, Hansen PS, Overgaard J, et al. Postoperative radiotherapy
in high-risk premenopausal women with breast cancer who receive
adjuvant chemotherapy. Danish Breast Cancer Cooperative Group 82b
Trial. N Engl J Med 1997;337(14):949–955.
3. Overgaard M, Jensen MB, Overgaard J, et al. Postoperative radiotherapy
in high-risk postmenopausal breast-cancer patients given adjuvant
tamoxifen: Danish Breast Cancer Cooperative Group DBCG 82c
randomised trial. Lancet 1999;353:1641–1648.
4. American Society of Plastic surgeons. 2016 Plastic Surgery Statistics
Report. Available online at
https://www.plasticsurgery.org/documents/News/Statistics/2016/plastic-
surgery-statistics-full-report-2016.pdf.
5. Jagsi R, Jiang J, Momoh AO, et al. Complications after mastectomy and
immediate breast reconstruction for breast cancer: a claims-based
analysis. Ann Surg 2016;263:219–227.
6. Cordeiro PG, Albornoz CR, McCormick B, et al. What is the optimum
timing of postmastectomy radiotherapy in two-stage prosthetic
reconstruction: radiation to the tissue expander or permanent implant?
Plast Reconstr Surg 2015;135:1509–1517.
7. Spear SL, Seruya M, Rao SS, et al. Two-stage prosthetic breast
reconstruction using AlloDerm including outcomes of different timings
of radiotherapy. Plast Reconstr Surg 2012;130:1–9.
8. Nava MB, Pennati AE, Lozza L, et al. Outcome of different timings of
radiotherapy in implant-based breast reconstructions. Plast Reconstr
Surg 2011;128:353–359.
9. Kronowitz SJ, Lam C, Terefe W, et al. A multidisciplinary protocol for
planned skin-preserving delayed breast reconstruction for patients with
locally advanced breast cancer requiring postmastectomy radiation
therapy: 3-year follow-up. Plast Reconstr Surg 2011;127:2154–2166.
10. Berry T, Brooks S, Sydow N, et al. Complication rates of radiation on
tissue expander and autologous tissue breast reconstruction. Ann Surg
Oncol 2010;17:202–210.
11. Brennan ME, Flitcroft K, Warrier S, et al. Immediate expander/implant
breast reconstruction followed by post-mastectomy radiotherapy for
breast cancer: aesthetic, surgical, satisfaction and quality of life
outcomes in women with high-risk breast cancer. Breast 2016;30:59–65.
12. Wong JS, Ho AY, Kaelin CM, et al. Incidence of major corrective
surgery after post-mastectomy breast reconstruction and radiation
therapy. Breast J 2008;14:49–54.
13. Magill LJ, Robertson FP, Jell G, et al. Determining the outcomes of
post-mastectomy radiation therapy delivered to the definitive implant in
patients undergoing one and two-stage implant-based breast
reconstruction: a systematic review and meta-analysis. J Plast Reconstr
Aesthet Surg 2017;70:1329–1335.
14. Clemens MW, Kronowitz SJ. Current perspectives on radiation therapy
in autologous and prosthetic breast reconstruction. Gland Surg
2015;4:222–231.
15. Recht A, Edge SB, Solin LJ, et al. Postmastectomy radiotherapy:
guidelines of the American Society of Clinical Oncology. J Clin Oncol
2001;19:1539–1569.
16. Recht A, Comen EA, Fine RE, et al. Postmastectomy radiotherapy: an
American Society of Clinical Oncology, American Society for Radiation
Oncology, and Society of Surgical Oncology Focused guideline update.
J Clin Oncol 2016;34(36):4431–4442.
17. Smith BD, Bellon JR, Blitzblau R, et al. Radiation therapy for the whole
breast: Executive Summary of an American Society for Radiation
Oncology (ASTRO) evidence-based guideline. Pract Radiat Oncol
2018;8(3):145–152.
18. Krueger EA, Wilkins EG, Strawderman M, et al. Complications and
patient satisfaction following expander/implant breast reconstruction
with and without radiotherapy. Int J Radiat Oncol Biol Phys
2001;49:713–721.
19. Cordeiro PG. Breast reconstruction after surgery for breast cancer. N
Engl J Med 2008;359:1590–1601.
20. Sigalove S, Maxwell GP, Sigalove NM, et al. Prepectoral implant-based
breast reconstruction: rationale, indications, and preliminary results.
Plast Reconstr Surg 2017;139:287–294.
21. Stevens WG, Nahabedian MY, Calobrace MB, et al. Risk factor analysis
for capsular contracture: a 5-year Sientra study analysis using round,
smooth, and textured implants for breast augmentation. Plast Reconstr
Surg 2013;132(5):1115–1123.
22. Constantine RS, Constantine FC, Rohrich RJ. The ever-changing role of
biofilms in plastic surgery. Plast Reconstr Surg 2014;133(6):865e–872e.
23. Pittman TA, Abbate OA, Economides JM. The P1 method: prepectoral
breast reconstruction to minimize the palpable implant edge and upper
pole rippling. Ann Plast Surg 2018;80(5):487–492.
24. Lam TC, Hsieh F, Boyages J. The effects of postmastectomy adjuvant
radiotherapy on immediate two-stage prosthetic breast reconstruction: a
systematic review. Plast Reconstr Surg 2013;132:511–518.
25. Lee KT, Mun GH. Optimal sequencing of postmastectomy radiotherapy
and two stages of prosthetic reconstruction: a meta-analysis. Ann Surg
Oncol 2017;24(5):1262–1268.
26. Nava MB, Catanuto G, Rocco N. How to optimize aesthetic outcomes in
implant-based breast reconstruction. Arch Plast Surg 2018;45(1):4–13.
27. Santosa KB, Chen X, Qi J, et al. Postmastectomy radiation therapy and
two-stage implant-based breast reconstruction: is there a better time to
irradiate? Plast Reconstr Surg 2016;138:761–769.
28. Peled AW, Foster RD, Esserman LJ, et al. Increasing the time to
expander-implant exchange after postmastectomy radiation therapy
reduces expander-implant failure. Plast Reconstr Surg 2012;130:503–
509.
29. Lentz R, Ng R, Higgins SA, et al. Radiation therapy and expander-
implant breast reconstruction: an analysis of timing and comparison of
complications. Ann Plast Surg 2013;71:269–273.
30. Archambeau JO, Pezner R, Wasserman T. Pathophysiology of irradiated
skin and breast. Int J Radiat Oncol Biol Phys 1995;31:1171–1185.
31. Hopewell JW, Campling D, Calvo W, et al. Vascular irradiation
damage: its cellular basis and likely consequences. Br J Cancer Suppl
1986;7:181–191.
32. Bernini M, Calabrese C, Cecconi L, et al. Subcutaneous direct-to-
implant breast reconstruction: surgical, functional, and aesthetic results
after long-term follow-up. Plast Reconstr Surg Glob Open 2016;3:e574.
33. Downs RK, Hedges K. An alternative technique for immediate direct-to-
implant breast reconstruction—a case series. Plast Reconstr Surg Glob
Open 2016;4:e821.
34. Kobraei EM, Cauley R, Gadd M, et al. Avoiding breast animation
deformity with pectoralis-sparing subcutaneous direct-to-implant breast
reconstruction. Plast Reconstr Surg Glob Open 2016;4:e708.
35. Basu CB, Leong M, Hicks MJ. Acellular cadaveric dermis decreases the
inflammatory response in capsule formation in reconstructive breast
surgery. Plast Reconstr Surg 2010;126:1842–1847.
36. Leong M, Basu CB, Hicks MJ. Further evidence that human acellular
dermal matrix decreases inflammatory markers of capsule formation in
implant-based breast reconstruction. Aesthet Surg J 2015;35:40–47.
37. Chopra K, Buckingham B, Matthews J, et al. Acellular dermal matrix
reduces capsule formation in two-stage breast reconstruction. Int Wound
J 2017;14:414–419.
38. Sbitany H. Important considerations for performing prepectoral breast
reconstruction. Plast Reconstr Surg 2017;140(6S Prepectoral Breast
Reconstruction):7S–13S.
39. Gabriel A, Maxwell GP. Prepectoral breast reconstruction in challenging
patients. Plast Reconstr Surg 2017;140(6S Prepectoral Breast
Reconstruction):14S–21S.
40. Nahabedian MY, Cocilovo C. Two-stage prosthetic breast
reconstruction: a comparison between prepectoral and partial
subpectoral techniques. Plast Reconstr Surg 2017;140(6S Prepectoral
Breast Reconstruction):22S–30S.
41. Sigalove S. Prepectoral breast reconstruction and radiotherapy—a closer
look. Gland Surg 2019;8(1):67–74.
42. Sbitany H, Gomez-Sanchez C, Piper M, et al. Prepectoral breast
reconstruction in the setting of postmastectomy radiation therapy: an
assessment of clinical outcomes and benefits. Plast Reconstr Surg
2019;143(1):10–20.
CHAPTER 71

Perioperative Pain Management:


ERAS Protocols, Blocks, and the Role
of Pharmacogenomics
KIRSTEN EDMISTON
HISTORY
Breast cancer surgeries (both oncologic and reconstructive) represent some of
the most common surgeries performed in the United States on an annual
basis. Over 100,000 reconstructive procedures are performed each year (1).
Recognizing the large volume of breast cancer surgery and reconstruction,
perioperative management and pain control is critical to optimizing quality of
care, patient experience, and value. The overwhelming majority of breast
cancer patients will be cured of their cancer but continue to deal with the
long-term health sequelae of their disease and treatments. Within the surgical
realm, patients and their surgeons must manage both the need for excellent
pain control while minimizing the risk of opioid and benzodiazepine
addiction, overdose, and other tragic complications both for themselves and
society.
CURRENT UNDERSTANDING OF PERIOPERATIVE PAIN AFTER BREAST
SURGERY
Pain after breast surgery is very common with up to 50% reporting pain after
surgery (2). In a Danish nationwide cross-sectional questionnaire study of
3,253 patients, 47% complained of pain after surgery (regardless of whether
they had breast-conserving surgery or mastectomy). Of the patients
complaining of pain, 48% had light pain which resolved over time, 39% had
moderate pain and, 13% had persistent severe pain. Breast surgery patients
can experience different types of pain including (3) acute pain related to the
inciting event usually lasting less than 3 months; (4) chronic pain lasting
beyond 3 months related to their previous treatment, visceral and
musculoskeletal pain; (5) chronic inflammatory pain; (6) neuropathic pain;
and (7) pain from their underlying cancer. Sensory disturbances (e.g.,
allodynia, hyperpathia, burning, sensory loss, or aftersensations) within the
breast, axilla, and/or arm also occurred in 31% to 85% of patients. In a
retrospective study of 4,113 opioid-naïve women who underwent immediate
breast reconstruction following total mastectomy, 90% filled their opioid
prescription in the perioperative period, and 10% continued to chronically fill
opioid prescriptions greater than 90 days after surgery (1).
Multiple factors influence the magnitude of pain and subsequently the need
for pain medications including the type of reconstruction, the addition of
axillary surgery, chemotherapy, and radiation. Patients undergoing
mastectomy with immediate reconstruction experience significantly greater
postoperative pain, nausea, and vomiting than patients undergoing
mastectomy alone (8). Women undergoing dual plane (subpectoral) tissue
expander or implant-based reconstruction require 33% more days of opioid-
based pain medication and 66% more prescription refills as compared to
those undergoing prepectoral breast reconstruction (9). Similarly, autologous
pedicled reconstruction or free tissue transfer patient required significantly
fewer average daily oral morphine equivalent prescriptions as compared to
those undergoing implant-based reconstructions. It is perhaps the stretch of
the pectoralis muscle that increases the pain associated with subpectoral
implant reconstruction. Adjuvant chemotherapy increases the risk of chronic
pain and persistent opioid use by 2.4 times (2.2 to 2.7 odds ratio [ORs] 95%
CI) after curative-intent breast cancer surgery (10).
Environmental factors play a significant role in an individual’s pain and
response to treatment. Age, race, ethnicity, socioeconomic status, preferred
language, and psychological factors have all been found to impact pain
perception and pain management. Unfortunately, a large percentage of breast
cancer patients can be diagnosed as depressed (38.2%) with anxiety (32%)
(11). This anxiety and depression are also risk factors for prolonged usage of
pain medications include postoperative complications. Fundamentally, poorly
controlled pain leads to prolonged opioid dependency. Each week of opioid
prescription usage and additional refill is associated with increased misuse
(9). Up to 18% of patients undergoing curative-intent breast surgery and
adjuvant chemotherapy will become chronically opioid dependent (10). Once
a patient transitions into chronic opioid use, cessation is rare, with over half
of patients who were on prescription opioids for a least 90 days remained on
opioid analgesics 5 years later (12).
Lastly, an individual’s pharmacogenomics play an essential role in their
response to a particular drug or class of drugs. Pharmacogenomics is the
“study of genetic variants that impact drug effects through changes in a
drug’s pharmacokinetics and pharmacodynamics” (13). Multiple genes are
involved in the metabolism of opioids including CYP2D6, OPRM1, COMT,
CYP3A4/A5, UGT2B7, and ABCB1. The most commonly studied, CYP2D6,
is a cytochrome P450 enzyme involved in the metabolism of 25% of all drugs
used in clinical practice. Over 100 different CYP2D6 gene alleles have been
identified, many of which directly control the metabolism of codeine,
hydrocodone, oxycodone, and tramadol. Individuals with specific gene alleles
can be stratified as ultrarapid metabolizers (UM) with greater than normal
function of the enzyme, extensive metabolizers (EM), normal metabolizers
(NM), and poor metabolizers with little or no enzyme function. Seven percent
to 10% of the Caucasian population may be poor CYP2D6 metabolizers and
3% may be UM (14).
The role of pharmacogenomics in the clinical management of pain is at its
infancy but offers a significant opportunity for personalized pain
management. The impact of pharmacogenomics in the metabolism of codeine
is a prime example. Codeine, the prodrug, is metabolized to morphine by
CYP2D6. The analgesic effect of codeine comes from its morphine
metabolite. Consequently, poor metabolizers produce low plasma
concentrations of morphine from codeine and are potentially less likely to
achieve adequate pain control. Similarly, UM can reach supratherapeutic
levels of morphine with risks of respiratory suppression with “normal” doses
of codeine. In 2017, the U.S. Food and Drug Administration (FDA) restricted
the use of codeine (to treat pain and cough) and tramadol (to treat pain)
medicines in children due to the risks of respiratory suppression and death,
particularly in children under the age of 12 (15). The Clinical
Pharmacogenetics Implementation Consortium (CPIC) offers actionable
guidelines for pharmacogenetics-based recommendations (16).
In order to optimize patient care, the multidisciplinary team must go
beyond the historical mainstay of perioperative pain control–postoperative
opioids. The patient and her team should take all these factors into account to
develop a comprehensive approach to minimize pain and optimize functional
and psychological outcomes.
ENHANCED RECOVERY AFTER SURGERY: HISTORICAL PERSPECTIVE
Enhanced recovery after surgery (ERAS) is a multimodal, interdisciplinary
approach to optimize perioperative care, originally developed by a group of
academic surgeons in Europe in the late 1990s. They recognized that the
surgical patient is taken care of by multiple departments including surgery,
anesthesia, nursing, primary care, physical therapy, and rehabilitation. No
one individual department controlled the patient’s outcome. This group also
recognized that care could be improved with: (1) a multidisciplinary team
working together across the continuum of care, (2) a multimodal approach to
resolving issues that delay recovery and cause complications, (3) evidence-
based care protocols, and (4) continuous auditing and care refinement (17).
Although this approach was first labeled, Fast Track Surgery in a project
to improve coronary artery bypass surgery outcomes in 1994, it was later
changed to ERAS to emphasize the importance of quality over speed (18).
Bardram et al. first described improved outcomes after laparoscopic sigmoid
resections with epidural analgesia, early oral nutrition, and mobilization a
year later in 1995 (19). Dr. Henrik Kehlet, MD, a Danish colorectal surgeon,
and his team further expanded and publicized multimodal enhanced recovery
after colorectal surgery (20). They determined that the key factors that keep
patients in the hospital after surgery were the need for extra hydration, the
need for parenteral analgesia, and decreased mobility. They then developed a
systemic approach to minimize metabolic stress, optimize pain control while
minimizing narcotic usage, and increase mobility with great success and
improved outcomes (21).
Based on the work done by Drs. Kehlet, Ljungqvist, Fearon, Revhaug, von
Meyenfeldt, and others in the ERAS Study Group, the international ERAS
Society was formed in 2010. They have since published ERAS protocols
guidelines and special papers with adapted procedure-specific guidelines for
cardiothoracic surgery, bariatric surgery, gynecology, cystectomy,
hepatobiliary, orthopedics, and head and neck surgery. The success of ERAS
identified by the early work of Kehlet has been reproduced in each of these
disciplines with decreased complications, reduced opioid usage, shortened
lengths of stay, and improved patient-reported outcomes.
BREAST ERAS
ERAS protocols have been primarily implemented for patients undergoing
mastectomies with or without reconstruction. Batdorf et al. first published the
Mayo Clinic experience with ERAS in the setting of microvascular breast
reconstruction that included the free transverse rectus abdominis
musculocutaneous (TRAM), muscle-sparing TRAM, and the deep inferior
epigastric perforator (DIEP) flaps (22). The authors found the total inpatient
postoperative opioid usage for the first 3 days was less for ERAS patients as
compared to those undergoing traditional postoperative surgery care (167.3
vs. 574.3 mg; p < 0.001 of oral morphine equivalents). Similarly, they found
a significant reduction in length of stay (LOS) (3.9 vs. 5.5 days; p < 0.001)
with no significant difference in 30-day major complications. Dumestre et al.
then published the University of Calgary experience with ERAS for women
undergoing implant-based breast reconstruction (23). They found the ERAS
patients had less severe pain and nausea. The ERAS group was more rested
and had high patient satisfaction. The average LOS was 1.6 days for the
traditional surgical care group and 0 days (same-day discharge) for the ERAS
patients. The authors commented that role of perioperative counseling and
setting the patient expectations as part of ERAS, including the expectation for
same-day discharge is an important contributing fact to high patient
satisfaction. Chiu et al. reviewed their experience in implementing an
evidence-based multimodal ERAS pathway for patients undergoing simple
mastectomy with immediate reconstruction at the University of
California/San Francisco. ERAS patients had significantly lower total
perioperative opioid consumption (mean [SD]: 111.4 mg [46.0] vs. 163.8
[73.2] oral morphine equivalents) and postoperative nausea and vomiting
(PONV) compared with pre-ERAS implementation patients (24).
In 2017, the international ERAS Society published their consensus ERAS
guidelines for patients undergoing mastectomy with reconstruction (Table
71-1) (25). These guidelines can be organized around preadmission,
preoperative holding area, and intraoperative and postoperative optimization
(Figs. 71-1 and 71-2).
BREAST ERAS COMPONENTS

Preadmission Interventions
Preoperative Information/Teaching/Counseling
Women preparing to undergo breast surgery often come with questions,
misconceptions, fear, and anxiety. They may have heard and read conflicting
information and have unrealistic expectations. Providing patients with
culturally appropriate surgical, anesthetic, and postoperative instructions
improves recovery by giving them the skills and self-confidence to manage
their care and address potential complications. Patient education should
include information about the planned procedure and hospital course,
risks/benefits, drain care, and pain management. The surgeon and patient
should have a shared mental model about the patient’s goals and
expectations. This discussion between the patient and surgical team is an
opportunity to build trust/ understanding and good communication.

Medical Optimization
Traditionally, surgeons have been singularly responsible for assessing the
patient before surgery and optimizing their medical comorbidities. This was
frequently fragmented and inefficient. With the advent of patient-centered
medical homes and preoperative evaluation clinics, cardiac and pulmonary
medical issues and medication-related questions can be addressed. ERAS
patients are advised on the importance of smoking cessation and avoidance of
alcohol consumption. ERAS protocols further encourage preoperative weight
management and good nutrition. Obesity (body mass index >30 kg/m2)
increases the risk of flap loss, surgical site infection, venous
thromboembolism, pulmonary complications, and other morbidities (25).
Although, important, the challenge to achieving significant preoperative
weight loss is the time required to achieve nutritionally balanced weight loss,
considering the strong pressure to schedule the patient’s oncologic surgery in
a timely manner. Optimal perioperative glycemic control (HbA1c <8.0% and
blood sugar <150 mg/dL) is further stressed to minimize complications in
diabetics.
FIGURE 71-1 ERAS Recommendations.

TABLE 71-1 ERAS Society Enhanced Recovery After Surgery


Recommendations for Perioperative Care in Breast Reconstruction
Item Recommendation Evidence Recommendation
Level Grade
1. Preadmission Patients should Moderate Strong
Information, receive detailed
Education, and preoperative
Counseling counseling.
2. Preadmission For daily smokers, 1 Moderate Strong
Optimization mo of abstinence (smoking) Strong
before surgery is High Strong
beneficial. For (obesity)
patients who are Low
obese, weight (alcohol)
reduction to
achieve a BMI
≤30 kg/m2 before
surgery is
beneficial. For
alcohol abusers, 1
mo of abstinence
before surgery is
beneficial. For
appropriate
groups, referral
should be made to
resources for
these behavior
changes.
3. Perforator Flap If preoperative Moderate Strong
Planning perforator
mapping is
required, CTA is
recommended.
4. Perioperative Preoperative fasting Moderate Strong
Fasting should be
minimized and
patients should be
allowed to drink
clear fluids up to
2 hrs before
surgery.
5. Preoperative Preoperative Low Strong
Carbohydrate maltodextrin-
Loading based drinks
should be given
to patients 2 hrs
before surgery.

6. Venous Patients should be Moderate Strong


Thromboembolism assessed for
Prophylaxis venous
thromboembolism
risk. Unless
contraindicated,
and balanced by
the risk of
bleeding, patients
at a higher risk
should receive
low–molecular-
weight heparin or
unfractionated
heparin until
ambulatory or
discharged.
Mechanical
methods should
he added.
7. Antimicrobial Chlorhexidine skin Moderate Strong
Prophylaxis preparation
should be
performed and
intravenous
antibiotics
covering common
skin organisms
should be given
within 1 hr of
incision.
8. Postoperative Women should Moderate Strong
Nausea and receive
Vomiting preoperative and
Prophylaxis intraoperative
medications to
mitigate
postoperative
nausea and
vomiting.
9. Preoperative and Women should Moderate Strong
Intraoperative receive
Analgesia multimodal
analgesia to
mitigate pain.
10. Standard General anesthesia Moderate Strong
Anesthetic with TIVA is
Protocol recommended.
11. Preventing Preoperative and Moderate Strong
Intraoperative intraoperative
Hypothermia measures, such as
forced air, to
prevent
hypothermia
should be
instituted.
Temperature
monitoring is
required to ensure
the patient’s body
temperature is
maintained above
36°C.
12. Perioperative Overresuscitation or Moderate Strong
Intravenous Fluid underresuscitation
Management of fluids should
be avoided and
water and
electrolyte
balance should be
maintained. Goal-
directed therapy
is a useful method
of achieving these
goals. Balanced
crystalloid
solutions, rather
than saline, are
recommended.
Vasopressors are
recommended to
support fluid
management and
do not negatively
affect free flaps.
13. Postoperative Multimodal High Strong
Analgesia postoperative
pain management
regimens are
opioid sparing
and should be
used.
14. Early Feeding Patients should be Moderate Strong
encouraged to
take fluids and
food orally as
soon as possible,
preferably within
24 hrs after
surgery.
15. Postoperative Flap monitoring Moderate Strong
Flap Monitoring within the first 72
hrs should occur
frequently.
Clinical
evaluation is
sufficient for
monitoring, with
implantable
Doppler devices
recommended in
cases of buried
flaps.
16. Postoperative For incisional High
Wound closure, (sutures) Strong
Management conventional Moderate
sutures are (NPWT)
recommended.
Complex wounds
following skin
necrosis are
treatable with
debridement and
NPWT.
17. Early Patients should be Moderate Strong
Mobilization mobilized within
the first 24 hrs
after surgery.
18. Postdischarge Early physiotherapy, Moderate Strong
Home Support supervised
and exercise
Physiotherapy programs, and
other supportive
care initiatives
should be
instituted after
discharge.

BMI, body mass index; CTA, computed tomographic angiography; TIVA, total intravenous anesthesia;
NPWT, negative-pressure wound therapy.
From Temple-Oberle C, Shea-Budgell M, Tan M, et al; ERAS Society. Consensus review of optimal
perioperative care in breast reconstruction: Enhanced Recovery after Surgery (ERAS) Society
Recommendations. Plast Reconstr Surg 2017;139(5):1056e–1071e, used with permission.
FIGURE 71-2 Protocol for ERAS multimodal postoperative pain control for breast
surgery. *Reduce acetaminophen dosage for patients with liver disease. B/LB,
bupivacaine/liposomal bupivacaine; POD#1, postoperative day one; NSAID,
nonsteroidal anti-inflammatory drugs; TAP, transversus abdominis plane; PVB,
paravertebral block; PEC II,-pectoral nerve II block; IV, intravenous; COX-2,
cyclooxygenase 2. (Derived and expanded from recommendations from Breast
Reconstruction Advisory Group and Afonso A, Oskar S, Tan K, et al. Is enhanced
recovery the new standard of care in microsurgical breast reconstruction? Plast Reconstr
Surg 2017;139(5):1053–1061.)

Preoperative Fasting
A fundamental component of ERAS is to minimize perioperative fasting and
consider preoperative carbohydrate loading. After extensive research, the
American Society of Anesthesiologists (ASA) developed guidelines to allow
otherwise healthy patients to drink clear liquids up to 2 hours prior to surgery
and a light meal up to 6 hours prior to general anesthesia (6). This does not
apply to patients with a history of gastroparesis or who are at increased risk
of delayed gastric emptying. A Cochrane review of 22 randomized controlled
trials reinforced the safety of drinking clear liquids 2 hours preoperatively
and the lack of increased risk of regurgitation and aspiration (26).
Preoperative carbohydrate loading with maltodextrin-based drinks has
been included in ERAS protocols for other types of major surgery, such as
colectomies and gynecologic oncology procedures in an effort to reduce
insulin resistance and reduce protein catabolism with a positive impact on
perioperative glucose control. For patients undergoing breast surgery with or
without reconstruction, additional research needs to be conducted to prove
the utility of preoperative carbohydrate loading.
PREOPERATIVE HOLDING INTERVENTIONS
In the preoperative holding area, it is important to minimize thromboembolic
risk and postoperative nausea and vomiting. The Caprini Risk Assessment
Model provides effective risk stratification for patients undergoing
reconstructive surgery. This is particularly important with symptomatic
postoperative DVT occurring in 2.2% patients having flap-based breast
reconstruction. Patients with a high Caprini risk score (>8) have an 11.3%
risk of a symptomatic potentially life-threatening DVT between postoperative
day (POD) 0 and 60 without DVT prophylaxis (27). Recognizing the
importance of DVT prophylaxis, all ERAS protocols emphasize perioperative
DVT prophylaxis for both implant- and flap-based reconstruction patients.
This is consistent with the recommendations from the Center for Medicare &
Medicaid Services (CMS) and the Agency for Healthcare Research and
Quality (AHRQ).
Breast surgery surgical site infections (SSI) are expensive, costing about
$10,000 per episode. In addition, SSI can cause delays in treatment time for
adjuvant therapies, poor patient satisfaction, removal of implants, and overall
failed reconstructions. As such, antimicrobial prophylaxis is included in all
ERAS protocols for breast reconstruction. Preoperative prophylactic
antibiotics (PPA), given within 60 minutes of the incision, are recommended
by the Centers for Disease Control and Prevention (CDC), the Surgical Care
Improvement Project (SCIP), and AHRQ (33). In 2017, the American Society
of Breast Surgeons (ASBS) released their guidelines for perioperative
prophylactic antibiotics. The ASBS recommends PPA in patients undergoing
mastectomy, with or without any type of axillary dissection or reconstruction.
PPA may be indicated in patients undergoing partial mastectomy for cancer,
with or without sentinel lymph node biopsy or axillary lymph node dissection
(5). Similarly, the Association of Breast Surgery at the Royal College of
Surgeons of England recommends PPA for patients undergoing simple
mastectomy, axillary lymph node dissection, and all-implant or autologous
breast reconstruction (7). Preop chlorhexidine skin preparation is also
encouraged to minimize the skin bacterial load. There is much more
controversy regarding the length of postoperative antibiotic usage for patients
undergoing implant and autologous reconstruction.
INTRAOPERATIVE INTERVENTIONS
Standard intraoperative ERAS interventions include: (1) Prevention of
intraoperative hypothermia (<36°C) through the use of forced warm air
blankets and warmed IV fluids. This is particularly important for longer
tissue-based reconstruction procedures (i.e., DIEP flap reconstructions) and
(2) Optimized goal-directed perioperative intravenous fluid management.
Balanced crystalloid solution (such as lactated Ringers)–based IV fluids are
recommended over normal saline. ERAS protocols caution against
overresuscitation and underresuscitation. (3) Most ERAS protocols promote
general anesthesia with propofol and total IV anesthesia to minimize PONV
(25).
PERIOPERATIVE MULTIMODAL PAIN
Within ERAS, multimodal analgesia for postsurgical pain is critical to
optimizing patient outcomes. Multimodal reduced opioid–use regimens
improve pain control, reduce LOS, decrease hospital cost, and improve
patient satisfaction. Within breast cancer surgery, the preoperative regimen
includes an antiepileptic medication (i.e., gabapentin), acetaminophen, and
consideration for preoperative regional anesthesia. Historically, breast and
plastic surgeons have been reluctant to use NSAIDs preoperatively due to the
risk of bleeding in large soft tissue wounds. More recently, data has
demonstrated no significant increase in rebleeding with COX2 inhibitors or
ketorolac (28). Preoperative regional anesthesia can include transversus
abdominis plan (TAP) blocks for DIEP flap donor abdominal wounds and
paravertebral blocks/pec blocks to decrease postoperative opioid use, pain
scores and LOS (3,4). Intraoperative local infiltration with liposomal
bupivacaine can be used to decrease postoperative opioid usage and
improved pain scores (29).
REGIONAL PAIN CONTROL FOR PATIENTS UNDERGOING BREAST SURGERY
It is well recognized that traditional IV narcotic–based postoperative pain
management is not optimal to achieve perioperative outcomes. Regional
anesthetic techniques (either in the form of local infiltration or regional
neuronal block) have been identified as effective modalities to treat
postmastectomy pain.
Local Infiltration
Infiltration of local anesthetics (LAs), such as lidocaine and bupivacaine, are
integral to achieve local field blocks in breast surgery. Recently, the
sustained-release LA, liposomal bupivacaine, marketed in the United States
by Pacira Pharmaceuticals, Inc. in Parsippany, NJ as Exparel (bupivacaine
liposome injectable suspension) has become available to expand
postoperative pain control within ERAS protocols. Liposomal bupivacaine is
an encapsulated formation of bupivacaine released over time by liposomes
(30). Liposomal bupivacaine is FDA approved for local administration to
provide postsurgical analgesia and interscalene brachial plexus nerve blocks
for shoulder surgery but not other regional nerve blocks (31). This also
includes TAP blocks for DIEP flaps. The liposomes are metabolized through
normal biologic processes, releasing bupivacaine over 48 to 72 hours (see
Table 71-2). For infiltration, liposomal bupivacaine is mixed with 0.25% to
0.50% bupivacaine and normal saline to inject throughout the patient’s
wound (see Table 71-2). Butz et al. reviewed the University of Chicago
experience with liposomal bupivacaine as compared with IV narcotics or
bupivacaine pain pumps and found that liposomal bupivacaine was associated
with decreased pain scores in the immediate postoperative period compared
with IV narcotics or pain pumps and reduced inpatient LOS (32).
Regional Neuronal Blocks
Two types of regional neuronal blocks (preoperative paravertebral block
[PPVB] and pectoral nerve block) are used to reduce intraoperative and
postoperative pain in mastectomy patients with or without reconstruction.

TABLE 71-2 Liposomal Infiltration Protocol Guidelines


Unilateral Bilateral TAP Block for
Mastectomy Mastectomy DIEP
Reconstructions
Mixture 20 mL of 20 mL of 20 mL of
liposomal liposomal liposomal
bupivacaine bupivacaine bupivacaine
30 mL of 0.25% 60 mL of 0.25% 60 mL of 0.25%
bupivacaine bupivacaine bupivacaine
80 mL of 160 mL of NS 120 mL of NS
injectable
normal saline Total volume to Total volume of
(NS) be injected = injection = 200
240 mL mL
Total volume to For slender to
be injected = average
130 mL patients, reduce
For slender to the volume to
average 80 mL of NS
patients, reduce for a total of
the volume to 160 mL
30 mL NS for a
total of 80 mL
Location for Multiple small Multiple small Inject 40 mL of
Injection (2–3 mL) (2–3 mL) the mixture
aliquots aliquots into the TA
infiltrated infiltrated plane, after
throughout the throughout aspiration to
cavity both cavities ensure that the
tip of the
needle is not
intravascular.
For unilateral
DIEPs, inject
the remaining
around the
fascial closure
(within the
rectus sheath
itself) and
along the
inferior
abdominal skin
edge and drain
sites.
For bilateral
DIEPs, inject
40 mL on each
side, then
inject the
remaining 80
mL around the
fascial closure
and 40 mL
along the
inferior
abdominal skin
edge and drain
sites.
Notes 1. ONLY USE ONE VIAL OF LIPOSOMAL
BUPIVACAINE FOR THE ENTIRE CASE.
2. DO NOT ADD ANY OTHER LOCAL
ANESTHETIC, SUCH AS LIDOCAINE.
3. The administration of liposomal bupivacaine may
follow the administration of lidocaine after a delay of
20 min or more.
4. Monitor for any evidence of side effects or local
anesthetic systemic toxicity.
5. Use a 22 gauge or larger diameter needle for injection.
6. Exact doses of medications and saline may need to be
adjusted for body weight and size.
TA, transverse abdominis; DIEP, deep inferior epigastric perforator.

FIGURE 71-3 Injection of local anesthetic between pectoralis major and minor at
the 3rd rib level.

Paravertebral Blocks
PPVBs deliver percutaneous LA agents to multiple spinal nerve roots. In
addition to preventing pain fiber potentiation and decreasing the
intraoperative/postoperative narcotic requirements, PPVBs have been
identified to decrease chronic postmastectomy pain (33) and shown to
decrease metastasis by reducing inflammation (34). From a value perspective,
PPVB has been associated with decreased pain scores, rates of nausea, and
vomiting along with hospital LOS (35). Ultrasound-guided multilevel PPVB
with ropivacaine has also been identified to decrease postmastectomy chronic
pain at 3 and 6 months postoperatively (36). Unfortunately, PPVB is also
associated with procedural risks including pneumothorax, epidural spread of
anesthetic, spinal cord trauma, inadequate pain control, and fail placement
(37).
Pectoral Nerve Blocks
There are two types of pectoral nerve blocks for breast and axillary surgery.
These can be done either preoperatively under ultrasound guidance or
intraoperatively under direct visualization after completion of the surgical
dissection.
PEC I—LA between pectoralis major and minor at the 3rd rib level to
block the lateral and medial pectoral nerves. PEC I blocks are appropriate for
surgery limited to pectoralis major.
PEC II is a PEC 1 block with additional LA injection between pectoralis
minor and the serratus anterior at the 3rd rib level. The additional local
injection blocks the lateral branch of the T2 to T4 spinal nerves and possibly
the anterior branch if sufficient LA penetrated the external intercostal muscle
(Figs. 71-3 and 71-4). PEC II blocks are appropriate for more extensive
surgeries including mastectomy and axillary clearance.
From a technical perspective, bupivacaine (or levobupivacaine) or
ropivacaine were most commonly used for pectoral nerve blocks. A volume
of 10 mL between the pectoralis muscles and 20 mL superficial to the
serratus anterior muscle are generally used to achieve adequate infiltration.
Ropivacaine may be used, having less cardiovascular and central nervous
system toxicity than racemic bupivacaine.
Versyck et al. conducted a systematic review and meta-analysis in order to
compare the analgesic efficacy of PEC II blocks with systemic analgesia
alone and with a thoracic paravertebral block for women undergoing breast
cancer surgery (38). The primary outcome was postoperative opioid
consumption in the first 24 hours after surgery. The secondary outcomes
were postoperative pain scores, intraoperative opioid consumption, time to
first analgesic request, and incidence of PONV. The authors reviewed 13
randomized controlled trials including 815 patients. The PEC II blocks
significantly reduced acute postoperative pain at all intervals in the first 24
hours and postoperative opioid consumption (standardized difference in
means: −13.64 mg oral morphine equivalents; 95% CI; −21.22 to −6.05; p <
0.01) as compared with systemic analgesia alone. The authors then went on
to compare PEC II blocks with thoracic paravertebral blocks. The PEC II
blocks resulted in similar postoperative opioid consumption and
postoperative pain scores after first measurement. There was no significant
difference in PONV in any of the three groups to accompany the reduction in
opioid consumption. The authors caution that this lack of difference may
represent type 2 error related to inadequate sample size.
PEC II blocks have become increasing popular for regional anesthesia in
this patient population. It is technically simpler, less time consuming, and
safer alternative (39).

FIGURE 71-4 Injection of local anesthetic under pectoralis minor on top of serratus
at the 3rd rib level.
Transversus Abdominis Plan Block
For patients undergoing DIEP flap reconstructions, TAP infiltration with
bupivacaine/ropivacaine or liposomal bupivacaine is recommended. In a TAP
block, local anesthetic is infiltrated in the fascial plane between the internal
oblique and transversus muscle. This provides analgesia to the abdominal
wall. TAP blocks can either be done in the preoperative holding area with
ultrasound guidance or with intravenous sedation by anesthesia.
Alternatively, TAP blocks can be performed intraoperatively under direct
vision by the plastic surgeon.
Postoperative Interventions
Postoperative Analgesia
Optimizing pain control while minimizing the use of narcotics is a
cornerstone of ERAS. Postoperative acetaminophen, nonsteroidal anti-
inflammatory drugs (NSAIDs), gabapentin, muscle relaxants (in subpectoral
reconstructions), and rescue narcotics have been included in multimodal pain
control after breast surgery. Scheduled doses of acetaminophen have been
included in ERAS perioperative pain management protocols (40). Although
there has been very little data regarding the specific role of Tylenol in breast
ERAS protocols, a Cochrane review of 51 randomized controlled studies
demonstrated acetaminophen mildly reduced postoperative pain in surgical
patients (41). Acetaminophen, both widely available and inexpensive, is
generally very well tolerated with minimal toxicity except in patients with
underlying liver disease. A subsequent systematic review further
demonstrated that combining acetaminophen and an NSAID may provide
superior pain control as compared with either agent alone (42).
Acetaminophen 1,000 mg scheduled every 8 hours for nine doses and then
transitioned to as needed has been recommended. Patients with normal liver
function are cautioned to monitor their acetaminophen intake—not to take
more than 4,000 mg/24-hr period.
NSAIDs, including nonselective ketorolac and ibuprofen and the more
selective cyclooxygenase-2 (COX-2) inhibitor (celecoxib) are included in
breast ERAS protocols (43). In the large 72-study Cochrane review with
9,186 patients, ibuprofen was found to be an effective analgesic for treating
postoperative pain in multiple surgical settings compared with placebo (44).
Similarly, perioperative oral selective COX-2 inhibitors significantly
decreased IV opioid consumption and reduced hospital stay after open
colorectal surgery (45). For breast patients specifically, Afonso et al. studied
the role of ketorolac in addition to local wound infiltration with liposomal
bupivacaine to reduce opioid consumption and decrease LOS. They identified
that the addition of ketorolac did significantly reduce opioid consumption but
had no further decrease in LOS (3,4). Although ketorolac has been
demonstrated to achieve postoperative pain control, the concern for
postoperative bleeding has limited its use. Gobble et al. conducted a
comprehensive meta-analysis to study the risk of perioperative bleeding in
ketorolac and control groups. The analysis of 27 studies with 2,314 patients
demonstrated postoperative bleeding in 33 of 1,304 patients (2.5%) in the
ketorolac group and 21 of 1,010 (2.1%) in the control group (OR, 1.1; 95%
CI; 0.61 to 2.06; p = 0.72). They concluded that postoperative bleeding was
not significantly increased with ketorolac as compared with controls (28).
In addition to acetaminophen and NSAIDs, gabapentin is often included in
breast surgery ERAS protocols. Gabapentin is thought to work through
inhibition of excitatory neurotransmitter release from the dorsal horn and thus
inhibiting nociception (46). In the 133 randomized control study systematic
review of gabapentin versus placebo in postoperative pain, Doleman et al.
found gabapentin did reduce postoperative pain scores along with PONV but
did increase the level of postoperative sedation. Siddiqui demonstrated that
postoperative sedation as well as respiratory suppression associated with
gabapentin are dose dependent (0 mg vs. 300 mg vs. 600 mg) and can be the
cause of delays in discharge from PACU (47). As such, it is recommended to
start with 100 mg to 300 mg of gabapentin in the preoperative setting. With
the additional risk of mental status changes, the risk/benefit ratio of
gabapentin in the elderly is unclear requiring additional study.

Postoperative Nutrition
Patients undergoing mastectomy and expander/implant reconstruction are
advanced to a regular diet as tolerated immediately after surgery, often with
juice and crackers in the recovery room. Traditionally, patients undergoing
microvascular reconstruction were kept strictly NPO for at least 24 hours in
case of emergent reoperation. With the expanded use of microvascular
reconstruction and enhanced surgeon experience, the risk of immediate take
backs has decreased significantly. Patients can be frequently started on clear
liquids after the surgery on POD #0 if the case has gone smoothly. With the
ASA guidelines regarding the safety of clear liquids up to 2 hours prior to
surgery, the risk of aspiration is very low even if the patient has to go back to
the operating room. On POD #1, patients can be advanced to a regular diet as
tolerated by patient preference and underlying medical conditions (i.e.,
diabetic and renal diets, etc.).
EARLY MOBILIZATION
Early ambulation after breast surgery with or without reconstruction is an
important component of ERAS. The primary benefit of early ambulation is to
minimize potential complications including venous thromboembolism,
aspiration pneumonia, and muscle deconditioning. It is important to set
expectations with the patient/family and staff that the patient will be
encouraged to ambulate after breast surgery with expander/implant
reconstruction on POD #0. Patients undergoing tissue/microvascular
reconstruction are encouraged to mobilize on POD #1/2 while avoiding
significant flexion and extension.
Urinary catheters are inserted in all patients undergoing microvascular
breast reconstruction due to the length of the procedure and the need for
fluid/volume monitoring. Catheters should be removed on POD #1 to
minimize the risk of catheter-associated urinary tract infections while
encouraging early ambulation.
Fundamentally, minimizing the need for narcotics and the accompanying
lethargy/mental status changes while managing pain control enable many
prepectoral expander/implant patients to go home the same day with proper
patient education.
CONCLUSION
Recognizing the large volume of breast cancer surgery and reconstruction,
perioperative management and pain control is critical to optimizing care
quality, patient experience, and containing cost. ERAS provides a
multidisciplinary model to optimize pain control, patient outcomes, and
patient experience. The key components within ERAS include:
Opioid-sparing perioperative medications
Minimal preoperative fasting and early feeding
Use of regional anesthetic techniques to minimize postoperative
nausea/vomiting and sedation
Support of early mobilization after surgery
Fundamentally, ERAS brings together the patient and entire care team in a
longitudinal care pathway to optimize care.

REFERENCES

1. Marcusa D, Mann R, Cron D, et al. Prescription opioid use among


opioid-naive women undergoing immediate breast reconstruction. Plast
Reconstr Surg 2017;140(6):1081–1090.
2. Gartner R, Jensen MB, Nielsen J, et al. Prevalence of and factors
associated with persistent pain following breast cancer surgery. JAMA
2009;302:1985–1992.
3. Afonso A, Newman M, Seeley N, et al. Multimodal analgesia in breast
surgical procedures: technical and pharmacological considerations for
liposomal bupivacaine use. Plast Reconstr Surg Global Open
2017;5(9):e1480.
4. Afonso A, Oskar S, Tan K, et al. Is enhanced recovery the new standard
of care in microsurgical breast reconstruction. Plast Reconstr Surg
2017;139(5):1053–1061.
5. American Society of Breast Surgeons. Consensus Guideline on
Preoperative Antibiotics and Surgical Site Infections in Breast Surgery.
ASBS; 2017.
6. ASA. Practice guidelines for preoperative fasting and the use of
pharmacologic agents to reduce the risk of pulmonary aspiration:
application to healthy patients undergoing elective procedures: an
updated report by the American Society of Anesthesiologists Task Force
on preoperative fasting and the use of pharmacologic agents to reduce
the risk of pulmonary aspiration. Anesthesiology 2017;126:376–393.
7. Association of Breast Surgery. Guidelines on Antibiotic Prophylaxis in
Breast Surgery. Association of Breast Surgery; 2015. Available online at
https://associationofbreastsurgery.org.uk/media/1430/guidelines-on-
antibiotic-prophylaxis-in-breast-surgery.pdf
8. Vadivelu N, Schreck M, Lopez J, et al. Pain after mastectomy and breast
reconstruction. An Surg 2008;74(4):285–296.
9. Copeland-Halperin L, Yemc L, Emery E, et al. Evaluating postoperative
narcotic use in prepectoral versus dual-plane breast reconstruction
following mastectomy. Plast Reconstr Surg Glob Open
2019;7(2):e2082.
10. Lee J, Hu H, Edelman A, et al. New persistent opioid use among
patients with cancer after curative-intent surgery. J Clin Oncol
2017;35(36):4042–4049.
11. Tsaras K, Papthanasiou I, Mitsi D, et al. Assessment of depression and
anxiety in breast cancer patients: prevalence and associated factors.
Asian Pac J Cancer Prev 2018;19(6):1661–1669.
12. Vanderlip E, Sullivan M, Edlund M, et al. National study of
discontinuation of long-term opioid therapy among veterans. Pain
2014;155:2673–2679.
13. Kaye A, Garcia A, Hall O, et al. Update on the pharmacogenomics of
pain management. Pharmacogenomics Pers Med 2019;12:125–143.
14. Sistonen J, Sajantila A, Lao O, et al. CYP2D6 worldwide genetic
variation shows high frequency of altered activity variants and
continental structure. Pharmacogenet Genomics 2007;17(2):93–101.
15. US Food and Drug Administration. 2017.
https://www.fda.gov/drugs/drug-safety-and-availability/fda-drug-safety-
communication-fda-restricts-use-prescription-codeine-pain-and-cough-
medicines-and.
16. CPIC. 2019. CPIC® Guideline for Codeine and CYP2D6. Available
online at https://cpicpgx.org/guidelines/guideline-for-codeine-and-
cyp2d6/
17. Ljungqvist O, Scott M, Fearon K. Enhanced recovery after surgery: a
review. JAMA Surg 2017;152(3):292–298.
18. Engelman R, Rousou J, Flack J, et al. Fast-track recovery of the
coronary bypass patient. Ann Thorac Surg 1994;58(6):1742–1746.
19. Bardram L, Funch-Jensen P, Jensen P, et al. Recovery after laparoscopic
colonic surgery with epidural analgesia, and early oral nutrition and
mobilisation. Lancet 1995;345(8952):763–764.
20. Kehlet H. Multimodal approach to control postoperative
pathophysiology and rehabilitation. Br J Anaesth 1997;78(5):606–617.
21. Kehlet H, Mogensen T. Hospital stay of 2 days after open
sigmoidectomy with a multimodal rehabilitation programme. Br J Surg
1999;86(2):227–230.
22. Batdorf N, Lemaine V, Lovely J, et al. Enhanced recovery after surgery
in microvascular breast reconstruction. J Plast Reconstr Aesthet Surg
2015;68:395–402.
23. Dumestre D, Webb C, Temple-Oberle C. Improved recovery experience
achieved for women undergoing implant based breast reconstruction
using an enhanced recovery after surgery model. Plast Reconstr Surg
2017;139(3):550–559.
24. Chiu C, Aleshi P, Esserman L, et al. Improved analgesia and reduced
post-operative nausea and vomiting after implementation of an enhance
recovery after surgery (ERAS) pathway for total mastectomy. BMC
Anesthesiology 2018;18:41.
25. Temple-Oberle C, Shea-Budgell M, Tan M, et al. Consensus review of
optimal perioperative care in breast reconstruction: Enhanced Recovery
after Surgery (ERAS) Society Recommendations. Plast Reconstr Surg
2017;139(5):1056–1067.
26. Brady M, Kinn S, Stuart P Preoperative fasting for adults to prevent
perioperative complications. Cochrane Database Syst Rev 2003;
(4):CD004423.
27. Pannucci C, Bailey S, Dreszer G, et al. Validation of the Caprini risk
assessment model in plastic and reconstructive surgery patients. J Am
Coll Surg 2011;212(1):105–112.
28. Gobble R, Hoang H, Kachniarz B, et al. Ketorolac does not increase
perioperative bleeding; a meta-analysis of randomized controlled trials.
Plast Reconstr Surg 2014;133(3):741–755.
29. Abdelsattar JM, Boughey JC, Fahy AS, et al. Comparative Study of
Liposomal Bupivacaine Versus Paravertebral Block for Pain Control
Following Mastectomy with Immediate Tissue Expander
Reconstruction. Ann Surg Oncol 2016;23(2):465–470.
30. Pacira Pharmaceuticals, Inc. Exparel (Prescibing Information).
Parsippany, NJ: Pacira Pharmaceuticals, Inci; 2016.
31. FDA. FDA In Brief: FDA approves new use of Exparel for nerve block
pain relief following shoulder surgeries. 2018. Available online at
https://www.fda.gov/news-events/fda-brief/fda-brief-fda-approves-new-
use-exparel-nerve-block-pain-relief-following-shoulder-surgeries
32. Butz D, Shenaq D, Rundell V, et al. Postoperative pain and length of
stay lowered by use of Exparel in immediate, implant-based breast
reconstruction. Plast Reconstr Surg Global Open 2015;3(5):e391.
33. Offodile A, Sheckter C, Tucker A, et al. Preoperative paravertebral
blocks for the management of acute pain following mastectomy: a cost-
effectiveness analysis. Breast Cancer Res Treat 2017;165(3):477–484.
34. Snyder GL, Greenberg S. Effect of anaesthetic technique and other
perioperative factors on cancer recurrence. Br J Aneaesth
2010;105:106–115.
35. Terkawi A, Tsang S, Sessler DI, et al. Improving analgesic efficacy and
safety of thoracic paravertebral block for breast surgery: a mixed-effects
meta-analysis. Pain Physician 2015;18(5):E757–E780.
36. Qian B, Fu S, Yao Y, et al. Preoperative ultrasound-guided multilevel
paravertebral blocks reduce the incidence of post mastectomy chronic
pain: a double-blind, placebo-controlled randomized trial. J Pain Res
2019;12:597–603.
37. Schnabel A, Reichl SU, Kranke P, et al. Efficacy and safety of
paravertebral blocks in breast surgery; a meta-analysis of randomized
controlled trials. Br J Anaesth 2010;105(6):842–852.
38. Versyck B, van Geffen GJ, Chin KJ. Analgesic efficacy of the Pecs II
block: a systematic review and meta-analysis. Anaesthesia
2019;74(5):663–673.
39. Hornsy C, Lindsey JT. Regional anesthetic blocks in plastic surgery
using portable ultrasound: a simplified approach. Ann Plast Surg
2019;82(6S Suppl 5):S374–S379.
40. Wick E, Grant M, Wu C. Postoperative multimodal analgesia pain
management with nonopioid analgesics and techniques: a review. JAMA
Surg 2017;152(7):691–697.
41. Toms L, McQuay H, Derry S, et al. Single dose oral paracetamol
(acetaminophen) for postoperative pain in adults. Cochrane Database
Syst Rev 2008;(4):CD004602.
42. Ong C, Seymour R, Link P, et al. Combining paracetamol
(acetaminophen) with non-steroidal anti-inflammatory drugs: a
qualitative systematic review of analgesic efficacy for acute
postoperative pain. Anesth Analg 2010;110(4):1170–1179.
43. Parikh R, Myckatyn T. Paravertebral blocks and enhanced recovery after
surgery protocols in breast reconstructive surgery: patient selection and
perspectives. J Pain Res 2018;11:1567–1581.
44. Derry C, Derry S, Moore R, et al. Single dose oral ibuprofen for acute
postoperative pain in adults. Cochrane Database Syst Review 2009;
(3):CD001548.
45. Lohsirinwat V. Opioid-sparing effect of selective cyclooxygenase-2
inhibitors on surgical outcomes after open colorectal surgery within an
enhance recovery after surgery protocol. World J Gastrointest Oncol
2016;8(7):543–549.
46. Doleman B, Heinink T, Read D, et al. A systematic review and meta-
regression analysis of prophylactic gabapentin for postoperative pain.
Anaesthesia 2015;70:1186–1204.
47. Siddiqui N, Yousefzadeh A, Yousuf M, et al. The effect of gabapentin
on delayed discharge from the postanesthesia care unit: a retrospective
analysis. Pain Pract 2018;18(1):18–22.
SECTION V

Autologous Based Reconstruction


72 Tips and Tricks to Achieve Best Result in Autologous-Based
Reconstruction: Shaping Flaps in Delayed Versus Immediate
Reconstruction
73 Efficiency in Autologous Breast Reconstruction
74 Management of the Unilateral Reconstruction and Timing of Matching
75 Pedicle TRAM and Free TRAM
76 Superior Gluteal Artery Perforator Flap (SGAP)
77 DIEP Flap Breast Reconstruction With Sensory Neurotization
78 Profunda Artery Perforator Flaps
79 Transverse Upper Gracilis Flaps
80 The Lumbar Artery Perforator Flap: An Alternative to DIEAP Flap for
Breast Reconstruction
81 Goldilocks Mastectomy for Immediate Reconstruction Without
Implants
82 Neurotization of the Autologous Flap
83 Management of the Failed Free Flap
84 Management of Donor-Site Complications
85 Secondary Procedures for the Autologous Reconstructed Breast
86 Radiation and Autologous Breast Reconstruction: The Role of Delayed-
Immediate Reconstruction
87 Abdominal-Based Breast Reconstruction—Optimizing Aesthetic
Results
88 Autologous Tissue Breast Reconstruction in the Thin Patient
89 Enhancing Volume in Autologous Reconstruction
CHAPTER 72

Tips and Tricks to Achieve Best Result


in Autologous-Based Reconstruction:
Shaping Flaps in Delayed Versus
Immediate Reconstruction
REUBEN A. FALOLA | HOPE SHIN | ABIGAIL RODRIGUEZ | MICHEL SAINT-CYR
HISTORY
With the recent advances in microsurgical technique, modern views of breast
reconstruction have shifted considerably. The goals of breast reconstruction
have changed from creating a mound and filling a postmastectomy volume
defect to instead to shaping a natural, aesthetically pleasing breast.
Autologous reconstruction is challenging and requires a skill set that focuses
on molding a flap of tissue into a three-dimensional (3D) shape, while also
accounting for patient expectations, body habitus, and the existing
mastectomy skin envelope.
In addition, breast reconstruction success is now also being measured by
patient-reported outcomes and patient satisfaction with their reconstructive
experience. Patient questionnaires such as the BREAST-Q survey, which was
developed in 2009, has become more popular and is a necessary tool in
today’s patient-centered care (1). The BREAST-Q survey focuses on a wide
range of patient satisfaction domains, but patient satisfaction with their
breasts and the overall outcome of the breast reconstruction account for 33%
of the module.
Within the last several years, more literature has been published regarding
autologous flap inset and the aesthetics of shaping the breast. In his landmark
work, Blondeel et al. described sculpting and shaping autologous tissue in a
breast with his three-step principle: (1) creating a breast footprint, (2) placing
the proper conus on the footprint, and (3) redraping the skin envelope (3).
Razzano et al. also created an algorithm for inset of the unilateral deep
inferior epigastric perforator (DIEP) flap, specifically considering vessel
position, abdomen type, and contralateral breast shape (4).
The inset and shaping of a breast is a unique and artistic exercise particular
to each surgeon, but this chapter will focus on providing a general framework
to create an aesthetically pleasing autologous reconstruction following total
mastectomy. Specifically, we will discuss preoperative planning, flap inset
and shaping, and implications for revision surgery.
PREOPERATIVE PLANNING
Prior to autologous breast reconstruction, certain patient factors should be
considered and addressed. A thorough history, including prior ablative and
reconstructive surgeries, amount of radiation, and the absence of the nipple
areolar complex (NAC), may indicate a need for a more complex
reconstruction (3). Baseline asymmetry between the breasts, characteristics of
the skin envelope, and tissue bulk in potential donor site(s), are important to
note. Measurements of the breast base width, and the location and size of the
NAC should be taken. The quality of the tissue is also important, specifically
the presence of infection, hematoma, scarring, vascularity, or radiation
damage (3,5).
OPERATIVE TECHNIQUE
The technique utilized for autologous breast reconstruction can vary
depending on patient factors, which ultimately influence flap choice and
timing (intermediate vs. delayed) of reconstruction. The basic principles of
autologous breast reconstruction, as described by Blondeel et al., serve as
guidelines to follow. First, it is necessary to recreate the breast footprint on
the chest wall. When present, the contralateral side can be used as a template.
Secondly, breast conus shaping and inset needs to be performed properly.
Finally, an appropriate skin envelope should be redraped over the breast
conus, which may require progressive skin pre-expansion utilizing a tissue
expander (2).
FOOTPRINT
The full extent of the breast footprint encompassing the area from the
clavicle, anterior axillary line, inframammary fold (IMF), and medial border
of the sternum should be defined and marked. Measurement of the height,
width, and position of the footprint on the chest wall should also be
documented, using the contralateral uninvolved breast as a guide if present. If
the breast footprint was violated during mastectomy, sutures can restore the
normal boundaries to the appropriate height and width. The medial mammary
fold, IMF, and lateral mammary fold are critical boundaries that can be
obliterated during mastectomy or distorted after radiation. These folds can be
recreated by suturing the mastectomy flap to the chest wall, erring on the side
of placing it more superiorly, as it is easier to lower in a revision procedure
than to raise it (3,5). Precise footprint creation can minimize the need for
elaborate flap shaping during insetting, as too many flap-shaping sutures can
produce an unnatural result (3).
FLAP SHAPING AND INSETTING
Three aesthetic considerations for shaping of the reconstructed breast,
described by Blondeel et al., include (1) an inferolateral fullness, (2)
maximum anteroposterior projection at the level of the NAC, and (3) some
degree of ptosis (2). To achieve these aesthetic goals, several techniques can
be employed, including projection sutures, recruitment of extra flap volume,
and insetting.
Shaping
The principles of flap shaping for abdominal, gluteal, or other myocutaneous
and perforator flaps are similar. A 3D conus with inferior pole projection, is
formed out of an initially flat flap. Abdominal flaps most commonly used to
construct the breast include the transverse rectus abdominis
musculocutaneous (TRAM), DIEP, and superficial inferior epigastric
perforator (SIEP) flaps. Perforator flaps have the benefit over myocutaneous
flaps, of greater flexibility for shaping of the conus (3). Bipedicled,
abdominally based flaps can be used to recruit more volume with flap. After
harvest, the flap is turned 180 degrees to allow for easy anastomoses and
orientation of the bulk of the abdominal tissue in the lower breast pole. After
the anastomosis is finished, a wedge of skin is excised in the periumbilical
region, which concentrates more volume in the lower pole of the flap, thereby
improving projection (3).
Selective use of projection sutures and use of larger flaps (zone 1 to 3) can
allow for more projection. Using a cutout template of the contralateral breast,
when present, can aid in achieving a symmetric reconstruction. Alternatively,
some surgeons have described the use of a 3D printed mold which can be
created preoperatively by mirroring 3D measurements from the contralateral
breast (6–8). The flap is placed in the 3D mold and customized suture
placement is performed to shape the flap into a breast that closely resembles
the native contralateral breast in projection, contour, and shape (6–8). This
can potentially improve symmetry and minimize the amount of flap
manipulation required after delicate microvascular anastomosis (6–8).
Perforator gluteal flaps (superior gluteal artery perforator [SGAP] and the
inferior gluteal artery perforator [IGAP]) and the musculocutaneous gluteal
flaps are narrow, thicker, and more rigid that abdominally based flaps (3). As
a result, these flaps cannot be shaped as readily, and secondary contouring is
often necessary (5). Obliquely resecting the fat below the tips of the gluteal
flap allows for a more natural superolateral and medial transition into the
chest wall (3). Thin gluteal flaps may be prone to poor filling at the superior
border, a defect that may need to be corrected by redraping or fat grafting at a
later stage (3). Latissimus dorsi (LD) flaps can be optimized with the
placement of a prepectoral or partially subpectoral prosthesis (9). Immediate
fat grafting of the skin paddle and muscle can be used to maximize volume
(Fig. 72-1).
When the abdomen or back are not suitable donor sites, medial (gracilis) or
posterior (profunda artery perforator) thigh-based flaps can be considered.
Medial thigh flaps tend to be longer and shorter than abdominal flaps and can
be used to reconstruct small-to-moderate–sized breasts (9). Both flaps can be
harvested as an ellipse, making these pliable tissues ideal for coning, and
achieving optimal breast projection.
Insetting
Flap insetting, when used appropriately, can optimize breast position,
contour, projection, and symmetry (5). Insetting is best accomplished with
the patient sitting upright at approximately 45 degrees. Care should be taken
to avoid compression, kinking, or twisting of the vascular pedicle as the
patient is sat up and flap repositioned. Flap perfusion should be assessed and
reassessed throughout the procedure, using skin turgor, capillary refill, and
Doppler (5). When insetting the flap, it is important to consider where future
deficiencies may lie, which is often in the upper pole and axillary crease. A
portion of the flap should be inset into the area of the previous tail of Spence
to decrease hollowing in the axillary crease. The flap can also be inset
medially to increase upper pole fullness. Dual plane flap insetting is another
technique that can also help to improve an aesthetic outcome, mainly
increasing upper pole fullness and addressing the visible step-off that can be
present around the flap. After mastectomy, the pectoralis major muscle is
split without release from the costal margin, and the superior mastectomy
skin and underlying pectoralis major muscle are elevated as a
musculocutaneous flap (10). Flap insetting is a powerful tool that can be used
to improve aesthetic outcomes of autologous breast reconstruction. Dual
plane and vertical inset can be used alone or in combination, when indicated,
to achieve optimal results.
FIGURE 72-1 A, B: Fat grafting the muscle and skin paddle and of a latissimus dorsi
(LD) flap. C, D: The pectoralis muscle and surrounding mastectomy skin flap can
also receive fat grafting prior to flap insetting. This multilayered approach to fat
grafting decreases the risk of fat necrosis.

Flap inset and orientation should take into consideration the patient’s body
habitus and premastectomy breast shape. The hemiabdominal flap is triangle
shaped with the apex (point C in Fig. 72-2A) as the lateral segment and a
narrow base defined by the midline incision (points A to B in Fig. 72-2A).
The flap can be inset either vertically (apex superior or apex inferior) or
horizontally. Vertical insetting is ideal for taller, thinner patients who tend to
have smaller breast volumes and that have a narrow breast base diameter.
Much of the breast volume in these patients is in the lower pole, with a long
vertical breast height and less medial and upper pole fullness. In such cases, a
vertically oriented abdominal flap can be position with the apex superior and
base inferior (Fig. 72-2B) to recreate the natural breast volume distribution
(Fig. 72-2C). If additional volume is needed in these areas, secondary
revisions can be undertaken, including flap repositioning, fat grafting, and
placement of a prosthesis or allograft. To aid in lower pole projection, the
flap tissue can be folded under itself. Step-off deformities or visible edges
can be avoided by trimming or tapering the apex and trimming the periphery
of the flap.

FIGURE 72-2 A: Hemiabdominal flap within the donor site, with the apex (point C)
lateral, and a narrow base defined by the midline incision (points A to B). B: Vertical
insetting of a hemiabdominal flap, with the apex (point C) superior, and an inferior
narrow base (points A to B), for greater lower pole fullness. C: Vertical insetting of a
hemiabdominal flap, with the apex (point C) inferior, and an superior narrow base
(points A to B), for greater upper pole fullness. D: Horizontal insetting of a
hemiabdominal flap, with the apex (point C) lateral, and a medial narrow base
(points A to B), for greater medial fullness.

Conversely, some patients with narrow breast base diameter have more
medial and upper pole fullness. These breast dimensions tend to be found in
younger patients with fuller breast and minimal ptosis. Recreating this breast
is best accomplished with a vertical insetting and the flap apex inferior and
base superior (see Fig. 72-2C and Case 1). This positioning, in effect, gives
the desired upper and medial pole fullness on a narrow base diameter, with
natural ptosis occurring over time, as the breast settles. A smooth breast
contour is achieved by tapering the edges of the flap. If greater medial
fullness is desired, the vertical flap can be positioned in a slight oblique
medial direction. This technique can accentuate the cleavage and minimize
the need for secondary revision upper pole hollowness; however, it comes at
the cost of sacrificing fullness in lateral axillary and thoracic region of the
breast. As a result, secondary revisions with fat grafting for lateral
deficiencies may be needed, and can include fat grafting, flap repositioning,
or locoregional flaps such as the thoracodorsal artery perforator, lateral
intercostal artery perforator, thoracoabdominal advancement, or LD
myocutaneous flap. Patients should be informed of and appropriately
counseled on the potential need for revision procedures preoperatively.
Horizontal insetting is ideal for patient with breast that have less vertical
height and a broad base diameter with a large transverse chest width. The flap
can be inset slightly oblique with the apex of the flap toward the axilla, to
best recreate the larger horizontal dimension of the breast (Fig. 72-2D). To
reduce the width of the mastectomy pocket, the lateral breast border can be
redefined more medially and sutured to the chest wall, and the remaining
excess skin excised. The upper pole volume can be insufficient with flaps
oriented in this direction, and fat grafting and/or a prosthesis may be
necessary to recreate an optimal breast contour. It is important to note that the
breasts in obese patients can create an illusion of a long breast vertical height.
The large breast volumes and significant ptosis frequently encountered in this
population can create a long notch-to-nipple distance; however, the goal of
the reconstruction is typically the creation of a smaller breast mound placed
in an anatomic position on the chest wall. A contralateral breast reduction
and/or mastopexy may be required for symmetry and is based on the true
breast footprint.
Key Sutures
Anchoring sutures are also important for positioning, securing, and shaping
of the flap. There are three key sutures that aid in the formation of an
aesthetically pleasing breast conus (Fig. 72-3). The first key suture secures
the flap to the superolateral aspect of the footprint, recreating the anterior
axillary fold. A temporary conus is then formed with staples, which are
exchanged for permanent sutures. Slight tension is then applied to the flap, to
avoid lateral fullness, and a staple used to secure the lateral edge of the flap to
the lateral aspect of the IMF, recreating a natural “lazy-S” shape of the lateral
breast border (3). The lateral edge of the flap can be shifted medially or
laterally to decrease or increase lateral breast fullness, creating the ideal
“lazy-S” contour. The staple is removed, and the flap is secured in optimal
position with the second key suture (lateral key suture). It is important to note
that the flap will tend to be pulled caudally and laterally postoperatively, so
erring on the side minimal lateral fullness is preferred (3). The skin just
medial to the second key suture near the midclavicular line can then be
bunched up to improve projection. The third key suture is used to secure the
flap at the medial end of the IMF and is thus important for ensuring enough
medial cleavage. Volume of the reconstructed breast should generally be 5%
to 10% larger than the contralateral breast, allowing for some shrinkage after
postoperative swelling has subsided (3). Any poorly perfused tissue can be
resected at this time. A fourth suture may be placed in the infraclavicular
region, to secure the flap to the chest wall and improve projection of the
conus and upper pole fullness (Fig. 72-3).

FIGURE 72-3 Three key anchoring sutures placed superolaterally, laterally, and
medially, respectively, help to position and shape the flap. A fourth, infraclavicular
suture can be placed to improve projection and upper pole fullness.

FIGURE 72-4 Excess mastectomy skin is removed by insetting the flap medially,
excising the excess lateral skin, and closing the skin in a stem and loop or “lollipop”
configuration.
SKIN ENVELOPE
Skin envelope availability and quality are the most critical determinants in
autologous breast reconstruction aesthetic outcomes, in the senior author’s
opinion. These are especially important in immediate reconstruction, and, as
always, a collaborative relationship and clear preoperative communication
with the surgical oncology team is essential. Discussion regarding incision
location and preferred thickness of the mastectomy skin flaps should be
performed preoperatively between the two surgical teams.
Reconstruction may require resection of excess mastectomy flap skin to
contour around the flap dimensions. The resection can follow the pattern of
the initial mastectomy incision, or a “lollipop” pattern can be created by
insetting the flap medially and excising the excess lateral skin (Fig. 72-4,
Case 2, Case 3) (4). This allows the skin envelope to redrape underlying flap
in a hand in glove fashion. An excessive ptotic skin envelope may require a
Wise-pattern or keyhole mastopexy (3). Poorly perfused flaps should be
excised to healthy bleeding margins. If the entire mastectomy flap appears to
be poorly perfused or threatened, or if there is a significant skin envelope
deficiency, plans can be made for a delayed reconstruction. If during the
reconstruction there is impending mastectomy skin flap ischemia of
undetermined quantity, then the flap may be inset without skin paddle
deepithelialization until proper demarcation has occurred later. In this
instance, secondary revision and mastectomy skin flap resection of all clearly
nonviable tissue can be matched with the appropriate amount of skin paddle
deepithelialization (Case 4). In the case where the skin envelope is
inadequate, or where radiation damage may lead to contracted tissues (4),
pre-expansion can be considered (Fig. 72-5). Immediately following the
mastectomy, a tissue expander is placed in the subpectoral or prepectoral
plane, depending on the viability of the mastectomy skin flaps
intraoperatively. The expander remains in place during radiation therapy.
Often, a period of 6 to 12 months is required to allow for recovery from
radiation and improvement of vascularity (11). The expander is removed at
the time of autologous reconstruction and the capsule adjusted to optimize
breast pocket shape in advance of flap inset.
IMMEDIATE RECONSTRUCTION
Immediate reconstruction, especially in a skin- or nipple-sparing technique,
retains the breast skin envelope and the flap acts primarily as a volume filler.
Immediate reconstruction has the psychosocial and economic benefits of
minimizing the number of procedures and quicker advancement to desired
breast dimensions, and improvements in one’s sense of self after mastectomy.
A secondary benefit of immediate reconstruction is that the mastectomy
specimen weight, height, and width can act as a guide for flap shape and
volume (Fig. 72-6). In a study by the senior author, mastectomy weights and
dimensions were measured for a total of 74 immediate breast free flap
reconstructions. The weight of the mastectomy was noted to increase as the
BMI increased (Fig. 72-7). There was also a trend in increase of the
horizontal width of the mastectomy specimen as the patient’s BMI increased,
while the vertical height remained relatively constant regardless of the
increase in BMI. In immediate reconstruction, this can be used to help guide
the orientation of inset. If the BMI of the patient and mastectomy weight is
higher, depending on breast dimensions, we recommend a horizontal inset to
better fill the defect.
FIGURE 72-5 After mastectomy and prior to autologous breast reconstruction, the
placement of acellular dermal matrix and a subcutaneous tissue expansion can be
used, in cases where the skin envelope is inadequate.

FIGURE 72-6 Superior and lateral photographs, demonstrating a mastectomy


specimen. In immediate reconstruction, the height, width, and weight of the
mastectomy specimen can be used as guide for the breast reconstruction.
FIGURE 72-7 In a study by the senior author, mastectomy weights and dimensions
were measured for a total of 74 immediate breast free flap reconstructions.
DELAYED RECONSTRUCTION
In delayed reconstruction (Figs. 72-8 to 72-10 and Case 5), the skin envelope
becomes an even more essential aspect of flap aesthetics. It may be necessary
to build up the recipient site with fat grafting prior to flap placement,
especially in the upper pole (Fig. 72-9 and Case 6). Fat grafting can be
employed within the flap muscle and subcutaneously within the skin paddle
prior to insetting (see Figs. 72-1 and 72-9). The pectoralis muscle and
surrounding mastectomy skin flap can also receive fat grafting prior to flap
insetting, for gain of up to 300 cc of additional breast volume. This
multilayered approach to fat grafting decreases the risk of fat necrosis.
Delayed skin envelopes can be categorized into three main types: an excess
of skin, scarred or radiated skin, or a deficiency of skin. If there is an excess
of skin at the time of the delayed reconstruction, substantial scar release of
the mastectomy skin envelope can be performed followed by partially or
completely deepithelializing the skin paddle after flap insetting (Case 7).
Depending on the severity of radiation injury and time between
mastectomy/radiation and reconstruction, a considerable amount of scar
tissue can be encountered. In this case, the mastectomy skin envelope can be
expanded with a tissue expander in either the prepectoral or the subpectoral
plane. If placement of a tissue expander may not be possible or required
during the immediate setting, the skin is usually closed primarily. If delayed
reconstruction is desired, the redundant mastectomy skin envelope can often
be redeveloped by elevating the skin from the pectoralis major muscle to the
breast borders (Case 7). Scar release and scoring of the mastectomy flaps can
also be performed to increase the volume of the pocket (Case 7). This can
allow for a flap to be inset without a deficiency of tissue.
Finally, for cases in which there is a deficiency of tissue, the autologous
flap skin can be used to contribute to additional skin of the chest wall (Case
8). Recruitment of additional skin can be obtained with a thoracoabdominal
advancement flap as needed. In some patients, a bipedicle DIEP flap can be
considered if additional skin and volume requirements are needed (Case 9).
SECONDARY RECONSTRUCTION
Secondary revisions may be necessary, in either the reconstructed or
nonreconstructed breast, to improve upon breast positioning, symmetry,
contour, and volume. The appropriate surgical plan for secondary
reconstruction can be formed, using the three main anatomical features of the
breast reconstruction described by Blondeel et al.—evaluating anatomical
deformations of the breast footprint, conus, and skin envelope (2).
The footprint of the breast may need to be adjusted to create a more
natural-appearing reconstruction. Over time, it is common for the IMF to
migrate down after breast reconstruction because of the mechanical stretching
of the collagenous fibers due to gravity. It may be necessary to revise the
IMF in a secondary procedure. Similarly, raising the upper border of the
breast to create an artificial “pushup” effect in overly ptotic breast breasts can
also be achieved; however, care must be taken to avoid unnatural-appearing
results (12). In other cases, such as a history of radiation therapy, scarring can
alter the position of the IMF, usually producing a “high-riding” position. In
such cases, simple undermining for scar release with the addition of fat
grafting, can have dramatic effects, lowering the IMF to a more anatomical
position (see Case 7 and Case 10).
The size of the conus is determined by the dimensions and position of the
footprint, the size shape and dimensions of the free flap (or implant), and
quality and expandability of the envelope (12). Common secondary revision
of the conus in the reconstructed breast, includes fat grafting in the upper
pole of the breast and implant placement (Case 11). Fat grafting has been
shown to improve breast skin quality, while allowing for remodeling and
shaping (Case 12) of the breasts with (13). Soft tissue recontouring, such as a
thoracoabdominal advancement flap can also be utilized to increase breast
volume (Figs. 72-11 and 72-12), especially in the lower pole. Alternatively,
the flap can be buried in the case of overly ptotic breast. In order to avoid a
“patchy” appearance and to improve color matching in the mastectomy flaps,
the skin paddles can be excised in a delayed periareolar flap reduction (see
Case 13, Figs. 72-8 and 72-10). This procedure has also been shown to
optimize sensation in the reconstructed breast. Scars may also need to be
revised to improve overall breast symmetry and appearance (Case 14). A
template can be used during flap harvest, to improve upon the symmetry of
the skin paddle, and minimize the need for scar revisions (Case 15). Another
common issue, especially in patients with higher BMI, is increases in lateral
breast fullness due to redundant tissues. Much of the lateral fullness can be
improved with the use of selective dermatolipectomy and liposuction (Case
14 and Case 16).
FIGURE 72-8 Fat graft “buildup” of the recipient site prior to planned flap
placement. A–C: Preoperative images of patient prior to fat grafting. D–F: Anterior
and lateral views of breasts after fat graft buildup and subcutaneous tissue expander
(TE) placement for pre-expansion of the mastectomy pocket. G, H: Demonstration of
pre-expanded autologous reconstruction (PEAR) after skin paddle and TE removal.
FIGURE 72-9 Intraoperative images of patient in the supine position with markings
and results of fat graft “buildup” of the recipient site prior to planned flap
placement.

FIGURE 72-10 Diagrammatic representation of delayed periareolar flap reduction


for improvements, minimization of “patchy” breast appearance and improvements
in sensation.
FIGURE 72-11 Lower or upper lateral pole hollowness can be addressed by using a
pedicled lateral intercostal multiperforator flap or a pedicled anterior intercostal
multiperforator flap, which is deepithelialized and rotated 90 to 180 degrees. This
has the added effect of replenishing volume deficiencies in the lower and upper
lateral pole, while decreasing lateral fullness in the form of a dermatolipectomy.
Illustrated below is an example of an intercostal artery perforator (ICAP) flap which
is used to fill in a lower pole soft tissue defect in a reconstructed breast.
FIGURE 72-12 Oblique view of the right breast after an intercostal artery
perforator (ICAP) flap has been used to fill in a lower pole soft tissue defect
remaining from the initial reconstructive surgery.

FIGURE 72-13 A: Intraoperative view of breast reconstruction revision to correct


upper pole hollowness, which was corrected with fat grafting, as well as, skin paddle
reduction to the anticipated future size of the areola, to contain the final areolar scar
within the anticipated future tattoo. B: Note the correction in the lateral outer skin
envelop excess and ptosis, as well as, fullness of the upper pole, bilaterally.

Internal expansion of the skin envelope may be necessary depending on the


size of the breast desired after reconstruction. Overstretching the envelope
can allow for the placement of larger implants or flaps and ensure that the
final reconstruction is not under too much tension. If the breast envelope is
under too much tension, the result will appear to be less natural or can
potentially lead to flap necrosis, requiring salvage measures, including
excision and debridement. A good indicator of breast envelope expandability
is the degree of breast ptosis prior to expansion. Overexpansion in an
irradiated breast field is commonly done in anticipation of future skin
envelop contraction.
To make the areolas more symmetrical, the NAC may require areolar
cinching, where a circumferential ring of tissue is removed from the areola
(Fig. 72-13). Ideally, the surgeon can attempt to reduce the periareolar
envelope margins to match the entire diameter of the areola. This technique
creates a more natural-appearing areola, and in conjunction with pigment
application via tattooing, can improve the final aesthetic result (Case 17).
In the nonreconstructed breast, modifications used to achieve symmetry
within the reconstructed breast include mastopexy, augmentation, or
reduction mammaplasty. The implant is placed in the prepectoral position in a
breast that has received radiation therapy; otherwise, a subpectoral position is
preferred (9).
The senior author (M.S.C.) has developed and utilized a method to assess
postreconstruction breast defects, focusing on four components: volume,
footprint, projection, and NAC (Fig. 72-14). Volume is more specifically
assessed by identifying the pole(s) that are deficient (upper pole, lower pole,
medial pole, lateral pole) (Fig. 72-15). The footprint should be well defined
at three locations: the medial mammary fold, IMF, and lateral mammary fold.
Systematic analysis of the postreconstruction breast(s) can be performed
using the Classification of Postreconstruction Breast Defects checklist, by
summing the number of deficiencies tallied (Table 72-1). The severity is
determined using the Severity of Postreconstruction Breast Defects checklist
and is based on the total number of deficiencies noted (Table 72-2).
In the experience of the senior author (M.S.C.), utilization of this
postreconstruction breast defect analysis has helped to guide decision making
and patient counseling during the reconstruction process. Generally, simple
defects (Case 18) require 1 to 2 revision surgeries, intermediate defects (Case
19) require 2 to 3 revision surgeries, and complex defects (Case 20) require
3+ revision surgeries. In a review of the senior author’s cases that required
revision, flap reshaping was consistently performed during the initial revision
surgery in patients with simple, intermediate, and complex defects. This
underscores the importance of optimizing the breast flap shape during the
initial reconstruction surgery with purposeful flap inset, coning, and shaping.
Obtaining an ideal shape of the flap during the reconstruction can potentially
minimize the postreconstruction breast defect and reduce the number of
revisions required.
FIGURE 72-14 Algorithm of decision-making process for revision surgery. First,
classify the complexity of the defect. Second, count the number and types of
revisions. Third, counsel the patient on the anticipated change, whether good or bad.
Lastly, create a surgical plan and consider, “When do we stop?” Is the next revision
surgery worth it for that patient? (Reprinted with permission from Saint-Cyr et al.)
FIGURE 72-15 A volume assessment guide is used to identify deficiencies in the
anatomical subunits of the reconstructed breast.

TABLE 72-1 Classification of Postreconstruction Breast Defects


Defect Type Assessment
Upper Pole Adequate Deficient
Medial Pole Adequate Deficient
Lower Pole Adequate Deficient
Lateral Pole Adequate Deficient
Medial Mammary Fold (MMF) Adequate Deficient
Inframammary Fold (IMF) Adequate Deficient
Lateral Mammary Fold (LMF) Adequate Deficient
Projection Adequate Deficient
Nipple Areolar Complex Adequate Deficient

TABLE 72-2 Severity of Postreconstruction Breast Defects


Number of Defects Severity
1–2 Simple
3–4 Intermediate
≥5 Complex

CASES

CASE 1

This is a 48-year-old female with history of bilateral skin-sparing


mastectomies for breast cancer, reconstructed with bilateral deep inferior
epigastric perforator (DIEP) flap reconstruction (Fig. 72-16). The left
DIEP flap failed on postoperative day five. She subsequently underwent a
delayed left breast reconstruction with a fat grafted latissimus dorsi (LD)
flap 2 months postoperatively. The skin paddle was inset in a vertical and
oblique fashion to maximize medial and upper pole volume.
FIGURE 72-16

CASE 2

A 47-year-old BRCA(−) patient with a history of severe mastodynia. She


was treated with bilateral nipple-sparing mastectomies and immediate
deep inferior epigastric perforator (DIEP) flap reconstruction (Fig. 72-
17). Intraoperatively, excess periareolar and lateral skin was excised from
the mastectomy envelopes to provide better draping over the bilateral
DIEP flaps. The skin envelopes were closed in a “lollipop” configuration.

FIGURE 72-17
CASE 3

The patient illustrated below underwent bilateral deep inferior epigastric


perforator (DIEP) flaps, with resultant mastectomy skin envelope
asymmetry (Fig. 72-18). Left: The preoperative image shows significant
asymmetry in terms of volume, skin envelope, and nipple areolar
complex position. Right: The patient underwent aggressive rigotomies in
an effort to decrease the “pin-cushioning” effect in the periphery of her
skin paddle, as well as, fat grafting to bilateral upper poles, lipoaspiration
of lateral areas of fullness, excision of lateral skin excess with “lollipop”
closure, left breast dermatolipectomy, and periareolar skin paddle
reduction to provide better symmetry.

FIGURE 72-18

CASE 4

A 46-year-old patient underwent immediate nipple-sparing mastectomy


bilaterally, with deep inferior epigastric perforator (DIEP) flaps. Note
that during flap insetting, the nipple areolar complexes and mastectomy
flaps were significantly bruised and had questionable viability (Fig. 72-
19). The intraoperative view demonstrates banking of the skin paddles
with temporary closure, allowing the flaps to demarcate in anticipation of
potential further necrosis. This patient did suffer significant necrosis of
her nipple areolar complex. The skin paddles were deepithelialized
accordingly to replace the necrotic mastectomy skin, with definitive flap
insetting 2 weeks after surgery. Six months later, a Wise-pattern skin
incision along with skin paddle removal, and bilateral fat grafting (230 cc
each), improved overall symmetry and cosmesis.

FIGURE 72-19

CASE 5
A 41-year-old patient, with a history of bilateral mastectomy, underwent
first-stage delayed reconstruction with bilateral prepectoral tissue
expander (TE) placement and immediate fat grafting to maximize
subcutaneous tissue volume (60 cc each breast) (Fig. 72-20). Three
weeks later she underwent serial expansion to the desired volume. This
was followed 3 months later by TE removal, capsulotomy, and delayed
reconstruction with deep inferior epigastric perforator (DIEP) flaps.
Secondary revisions included additional fat grafting for symmetry (right
120 cc, left 40 cc) and nipple areolar reconstruction. This two-staged
process, termed pre-expanded autologous reconstruction (PEAR), allows
conversion of a traditional delayed reconstruction into an intermediate
reconstruction-like process.

FIGURE 72-20

CASE 6
A 33-year-old female status post nipple-sparing bilateral mastectomy,
and adjuvant radiation therapy to the right breast (Fig. 72-21). She
underwent delayed prepectoral breast reconstruction for expansion of the
skin envelope, in preparation for abdominal-based free tissue transfer.
Immediate fat grafting was done at the time of tissue expander (TE)
placement to maximize upper pole and medial pole fullness. Patient
underwent serial expansion to further maximize volume, and 6 months
later, her TEs were exchanged for a left muscle-sparing transverse rectus
abdominis muscle (ms-TRAM) flap for right breast reconstruction and a
right deep inferior epigastric perforator (DIEP) flap for left breast
reconstruction. Secondary refinements included additional fat grafting to
bilateral breasts (right breast 240 cc, right subaxillary 100 cc, left
breast 120 cc), a left nipple areolar complex (NAC) elevation, and a NAC
size reduction for symmetry.

FIGURE 72-21

CASE 7
A 63-year-old patient underwent bilateral mastectomies with implant
reconstruction to the right breast, and a previous failed left breast
reconstruction at an outside institution, approximately 18 months prior
(Fig. 72-22). She underwent delayed reconstruction with implant removal
on the right side, bilateral extensive capsulectomy and scar release, and
reconstruction with autologous latissimus dorsi (LD) flaps and immediate
fat grafting. Fat grafting (left 240 cc, right 320 cc, total) was performed
within the surrounding mastectomy skin flaps, pectoralis muscle, and
within the LD muscle and skin paddle to maximize volume. Note the
improvement in scarring contracture of the mastectomy skin flaps, most
apparent on the left, following scar release and autologous reconstruction
with fat grafting. This case underscores the possibility of mastectomy
scar release and envelope reexpansion despite long time lapse since the
original.

FIGURE 72-22

CASE 8
A 58-year-old patient with a history of breast cancer and previous
bilateral nipple-sparing mastectomy (Fig. 72-23). She subsequently
developed a left breast infection requiring tissue expander (TE) removal.
Healing of her mastectomy skin flap created significant scaring and
involution of the nipple areola complex (NAC). This was followed by
extensive capsulectomy and reconstruction with latissimus dorsi (LD)
musculocutaneous flaps. Secondary revisions included a right breast
circumareolar mastopexy, bilateral release of scar tissue, and bilateral
subpectoral implant placement (left 250 cc, right 225 cc). Noted below
are improvements in contouring following serial fat grafting, with
minimized skin envelope scaring and contour irregularities.

FIGURE 72-23

CASE 9

A 55-year-old patient with a history of right-sided breast cancer, status


post adjuvant chemotherapy and mastectomy (Fig. 72-24). The patient
underwent a delayed reconstruction with a right and left deep inferior
epigastric perforator (DIEP) flap for right breast reconstruction. A
bipedicled DIEP flap was used to harvest the entire abdominal tissue to
maximize flap volume and skin resurfacing. The caudal and cephalad
portions of the internal mammary (IM) vessels were used as recipient
vessels for both DIEP pedicles.

FIGURE 72-24

CASE 10

A 51-year-old woman with history of breast cancer, status post bilateral


mastectomies and reconstruction with bilateral muscle-sparing transverse
rectus abdominus myocutaneous (ms-TRAM) free flaps (Fig. 72-25). She
developed an ill-defined inframammary fold (IMF) of the left breast,
which was lower than the right side, and required a thoracoabdominal
advancement flap on the left side, with reinsetting of her flap to create a
higher and better-defined IMF. This was combined with fat grafting (275
cc total) to both upper poles as well as scar revision to maximize
symmetry and improve appearance. Note enhanced upper pole volume
with additional fat grafting. There is improved left IMF definition
following reinsetting of the lower skin paddle edge along the
deepithelialized thoracoabdominal advancement flap (60 cm3).
FIGURE 72-25

CASE 11

A 36-year-old patient with history of prophylactic nipple-sparing


mastectomy followed by immediate reconstruction with bilateral deep
inferior epigastric perforator (DIEP) flaps (Fig. 72-26). She presented
with bilateral breast upper pole hollowness, volume depletion, and lack of
projection. She subsequently underwent bilateral breast reconstruction
revision with fat grafting (70 cc left, 90 cc right) and subpectoral breast
augmentation with high-profile, smooth, silicone implants (right 450 cc
left 415 cc left).
FIGURE 72-26

CASE 12

Illustrated below is patient who underwent right breast reconstruction


with a transverse upper gracilis (TUG) flap (Fig. 72-27). There was a
cephalad migration of the inframammary fold (IMF) and the flap, leading
to IMF asymmetry and a lack of volume projection. She underwent serial
fat grafting of the entire flap, including the skin envelope. Aggressive fat
grafting to the lower pole resulted in the lowering of the IMF and
provided improvements in breast volume. She eventually required a
mastopexy augmentation of the contralateral left breast, to match the fat
grafted, augmented TUG flap on the right side.
FIGURE 72-27

CASE 13

Illustrated below is a patient with a history of bilateral mastectomy and


reconstruction with bilateral deep inferior epigastric perforator artery
(DIEP) flaps prior to revision surgery (Fig. 72-28). The skin paddles
were excised to improve breast sensation and cosmesis. Given the history
of radiation therapy, the right breast was overexpanded in anticipation for
future skin envelope contraction.
FIGURE 72-28

CASE 14

This case (Fig. 72-29A) illustrates a delayed reconstruction with bilateral


deep inferior epigastric perforator (DIEP) flap. The patient underwent
bilateral dermatolipectomy of excess skin (Fig. 72-29B,C). Part of this
tissue was used as a pedicle flap based on lateral thoracic perforators, for
upper and upper lateral pole volume augmentation. The effect was
enhanced with fat grafting in these areas. She also underwent bilateral
scar revision for improvements in symmetry. Postoperative results at 2
weeks demonstrate some bruising, which resolved uneventfully (Fig. 72-
29D,E). There is evidence of improved breast contour and symmetry.
FIGURE 72-29

CASE 15

Demonstrated as shown for the patient in Figure 72-30 is the use of


templating of the skin paddle to achieve greater breast symmetry.
FIGURE 72-30

CASE 16

A 54-year-old patient with a BMI of 59 underwent immediate breast


reconstruction using a “Goldilocks” procedure (Fig. 72-31). This was an
inferior dermal flap, deepithelialized and redraped under and overlying
Wise-pattern skin incisions. Volume was maximized by serial fat grafting
(left 400 cc, right 370 cc total). Bilateral dermatolipectomy (left 22 × 5
cm, 25 × 8 cm) and liposuction of axillary excess (left 350 cc of aspirate
250 cc of infiltrate, right 350 cc of aspirate 250 cc of infiltrate) were
utilized for improved symmetry. This case illustrates the ability to
maximize volume with the use of a “Goldilocks” procedure and inferior
dermal flaps with fat grafting, in high-BMI, high-risk patient.
FIGURE 72-31

CASE 17

A 56-year-old female, status post mastectomy and autologous bilateral


breast reconstruction with DIEP flaps (Fig. 72-32). She presented with
asymmetry and contour irregularity of the bilateral NAC, requiring
revision via “cinching” of periareolar skin. The areolar skin paddle can be
further reduced, or a tattoo can cover the circumferential tissue excess,
based on patient preference.

FIGURE 72-32
CASE 18

In Figure 72-33 a postoperative image of a patient who underwent


immediate reconstruction of the left breast with a deep inferior epigastric
perforator (DIEP) flap that was inset in a medial, vertical oblique fashion,
with residual lateral upper pole hollowness is shown. Postoperative image
shown with a circle indicating the defect. Secondary revisions included
fat grafting to the upper lateral pole and within the flap to improve
projection, as well as, nipple areolar complex (NAC) reconstruction and
reduction of the flap skin paddle to reflect the contralateral areolar
diameter.

FIGURE 72-33

CASE 19

This case (Fig. 72-34) illustrates a bilateral deep inferior epigastric


perforator (DIEP) flap with intermediate-level defect complexity. The
patient demonstrates a lack of projection bilaterally, left lateral upper
poles hollowness, nipple areolar complex (NAC) skin paddle asymmetry,
and lack of projection bilaterally. She underwent subsequent fat grafting
to both upper poles and upper lateral quadrants, as well as centrally
within the flaps, for increased projection. Secondary revision also
included skin paddle reduction and NAC reconstruction for better
symmetry, and to aid in camouflaging of areolar scar within the
boundaries of the anticipated tattooing. Intraoperative markings show
areas of fat grafting and location of NAC reconstruction.

FIGURE 72-34

CASE 20

Illustrated in Figure 72-35 a 54-year-old patient with a history of


bilateral breast reconstruction with free muscle-sparing transverse rectus
abdominis myocutaneous (ms-TRAM) flaps, who developed a sarcoma to
the chest wall requiring reconstruction with a latissimus dorsi (LD) flap.
The patient presented to clinic for revisions of her previous
reconstruction. She then underwent serial advancement and primary
closure of the donor site, serial fat grafting to her LD flap, and a
thoracoabdominal perforator (TAP) advancement flap to improve lower
pole fullness. This was subsequently followed by resection of the inferior
portion of the TAP flap, with readvancement and reinsetting of the TAP
flap, and additional fat grafting.
FIGURE 72-35
CONCLUSION
Autologous breast reconstruction, in conjunction with secondary refinement
procedures, can be used to achieve optimal breast aesthetics after
mastectomy. Previous literature by Blondeel et al. has set forth principles on
creating a proper footprint, conus, and skin envelope. This serves as a guide
for the reconstructive surgeon but flap shaping and inset also requires an
aspect of creativity and ingenuity. In addition, optimal outcomes depend on
the ability of the reconstructive surgeons to marry individual flap
characteristics with the unique need of each patient.

REFERENCES

1. Pusic AL, Klassen AF, Scott AM, et al. Development of a new patient-
reported outcome measure for breast surgery: The BREAST-Q. Plast
Reconstr Surg 2009;124(2):345–353.
2. Blondeel PN, Hijjawi J, Depypere H, et al. Shaping the breast in
aesthetic and reconstructive breast surgery: an easy three-step principle.
Plast Reconstr Surg 2009;123:455–462.
3. Blondeel PN, Hijjawi J, Depypere H, et al. Shaping the breast in
aesthetic and reconstructive breast surgery: an easy three-step principle.
Part II—Breast reconstruction after total mastectomy. Plast Reconstr
Surg 2009;123:794–805.
4. Razzano S, Marongiu F, Wade R, et al. Optimizing DIEP flap insetting
for immediate unilateral breast reconstruction: a prospective cohort
study of patient-reported aesthetic outcomes. Plast Reconstr Surg
2019;143(2):261e–270e.
5. Nahabedian M. Achieving ideal breast aesthetics with autologous
reconstruction. Gland Surg 2015;4(2):134–144.
6. Ahcan U, Bracun D, Zivec K, et al. The use of 3D laser imaging and
new breast replica cast as a method to optimize autologous breast
reconstruction after mastectomy. Breast 2012;21:183–189.
7. Hummelink S, Verhulst AC, Maal TJJ, et al. Applications and
limitations of using patient-specific 3D printed molds in autologous
breast reconstruction. Eur J Plast Surg 2018;41:571–576.
8. Tomita K, Yano K, Hata Y, et al. DIEP flap breast reconstruction using
3-dimensional surface imaging and a printed mold. Plast Reconstr Surg
Glob Open 2015;3(3):e316.
9. Blondeel PN, Hijjawi J, Depypere H, et al. Shaping the breast in
aesthetic and reconstructive breast surgery: an easy three-step principle.
Part III—reconstruction following breast conservative treatment. Plast
Reconstr Surg 2009;124:28–38.
10. Gravvanis A, Samouris G, Galani E, et al. Dual plane DIEP flap inset:
optimizing esthetic outcome in delayed autologous breast
reconstruction. Microsurgery 2015;35:432–440.
11. Kronowitz S. Current status of autologous tissue-based breast
reconstruction in patients receiving postmastectomy radiation therapy.
Plast Reconstr Surg 2012;130:282–292.
12. Blondeel PN, Hijjawi J, Depypere H, et al. Shaping the breast in
aesthetic and reconstructive breast surgery: an easy three-step principle.
Part IV—aesthetic breast surgery. Plast Reconstr Surg 2009;124:372–
382.
13. Rigotti G, Marchi A, Galie M, et al. Clinical treatment of radiotherapy
tissue damage by lipoaspirate transplant: a healing process mediated by
adipose-derived adult stem cells. Plast Reconstr Surg 2007;119:1409–
1422; discussion 1423–1424.
CHAPTER 73

Efficiency in Autologous Breast


Reconstruction
EDWARD BUCHEL
INTRODUCTION
Efficiency is defined as achieving maximum productivity with minimum
wasted effort or expense. Effectiveness is defined as the ability to achieve a
desired quality of outcome. In surgery, the goal of efficiency is to limit the
cost per case. For microsurgical reconstruction, the cost per case is defined
by the highest cost driver, namely the time spent in the operating room (OR).
In pursuit of efficiency with reduction in OR time, it is essential not to
compromise the quality of care delivered. Our ultimate goal is to improve the
efficiency and the effectiveness of surgical care delivery, thereby augmenting
the value of health care provided.
CONCEPTS FOR SURGICAL EFFICIENCY
The time required to complete an operation is the summation of multiple
steps that require the coordinated action of multiple individuals. To improve
the efficiency of an operation, it is important to optimize each step in the
process and each individual’s role in the team. There are four principles to
apply for optimizing surgical efficiency: (1) Elimination of steps; (2)
Synchronous completion of steps; (3) Standardization; (4) Reevaluation.
Elimination of steps aims to simplify the task by reducing steps that are
redundant, unnecessary, potentially hazardous, and only add time without
improving the outcome. It is additionally important to complete one task
before moving forward to the next sequential step because this eliminates the
need to return to an incomplete task, reestablish the necessary setup and
instruments, and reframe your concentration once again.
Synchronous completion of steps is essential for maximizing the use of
each team members’ skills and shortening the time required for completion of
the process. When steps are completed synchronously, as opposed to
sequentially, the productivity is inherently increased per unit of time.
Standardization of the process and the team is the foundation upon which
surgical efficiency is built. Standardization implies that the process is
completed in the same fashion, with the same sequence of steps, the same
setup, and with the same roles for each team member. Consistency in the
process and expectations helps to clarify how and when the operation should
be completed, and who is responsible for what tasks. The team includes the
surgeons and assistants, the anesthesiologist, and the nursing staff. With
multiple individual roles, it is critical for each member to understand their
responsibility during each step of the process and know how to best
contribute to the collective effort. Each member must understand how to
efficiently complete their specific responsibility without impeding the ability
of others to complete theirs.
Best Practice Standardization improves patient care and patient safety by
implementing locally tailored guidelines based on best evidence and local
expertise. Implementing a Best Practice Standard is particularly important
when multiple surgeons, anesthesiologists, and nurses are involved in the
process of autologous breast reconstruction. With standardization of the
agenda, the setup, and the expectations of each team member, there is
decreased variability and more repetition. This facilitates learning, reinforces
good practice, and selects the optimal methods for collaborating as a team to
complete the operation. Unique circumstances or unique exceptions should
be avoided to minimize changes in the standard.
Reevaluation of the process is an important concept to achieve successive
improvements and compound proficiency. As the process becomes more
efficient, there is an increase in expectations from the team and hospital
administrators; a new status quo is established. This external pressure
encourages the culture of standardization, critical self-evaluation, and team
collaboration. If the applied principles of standardization and elimination of
steps are not fruitful, the primary surgeon must lead the reevaluation of the
process and encourage all team members to voice opportunities for
improvement.
PROCESS MAPPING
Process mapping is the evaluation of each task chronologically from
initiation to completion of the process. Each task is critically examined and
altered to optimize completion with maximal efficiency. Process mapping is
applied to autologous breast reconstruction to identify areas for improvement,
redundant steps, and maximize efficiency.
For autologous breast reconstruction, the process begins with the initial
consult, preoperative assessment, and optimization of the patient. At the
initial consult, expectations for postoperative care are detailed with the
patient and family. Whether a formal Enhanced Recovery After Surgery
(ERAS) protocol is followed or not, patients are educated regarding their
postoperative inpatient care, length of stay, discharge medications, and
rehabilitation. Patients who understand these standardized care pathways are
less likely to deviate from them without specific surgical complications.
Patients with medical comorbidities require a preanesthetic evaluation to
obtain necessary investigations to optimize their health status prior to
surgery. For immediate breast reconstruction, there is a limited amount of
time prior to surgery for optimization. Even in this setting, chronic systemic
diseases such as diabetes, hypertension, anemia, and cardiac or pulmonary
disease, can be optimized with medical interventions to reduce perioperative
surgical morbidity. For delayed breast reconstruction, there is the luxury of
time to address supplemental risk factors such as obesity.
Preoperative imaging with a CTA or MRA is performed in multiple centers
to shorten the time required for flap elevation. Although this is not part of our
routine practice, a preoperative angiogram of the abdomen may help to
identify potential perforators and select the preferred primary perforator
based on size, location, and intramuscular course. Limited studies have
suggested that preoperative imaging may reduce the time for flap elevation
and may represent a potential adjunct to improve surgical time. Further
analysis is required to establish whether preoperative imaging is warranted
given the associated cost and radiation exposure. For the majority of routine
abdominal flaps, the use of preoperative imaging becomes less valuable as
the experience of the surgeon increases.
On the day of surgery, standardized preoperative orders for a patient with
autologous breast reconstruction are used, with minimal alterations based on
the type of flap planned. All patients have orders for infection prophylaxis,
with the antibiotics sent to the OR for administration 30 minutes pre incision.
All patients have orders for venous thromboembolism prophylaxis, including
compression stockings and 5,000 units of subcutaneous heparin to be given in
the preoperative unit. An abdominal binder is ordered and sent to the OR for
an abdominal-based flap. Each patient has their consent reviewed, their
markings completed, and their postoperative plan reviewed prior to heading
to the OR.

FIGURE 73-1 Operative theater setup for a microsurgical reconstruction case. Each
surgeon should determine the equipment setup that maximizes their OR space
relative to the patient bed. Note that the base of the microscope is positioned relative
to other equipment to optimize space for draping and facilitate movement to and
from the OR table.

Operative Process Mapping and Standardization


In the operative theater, standardization of the setup and team is critical. The
room setup is standardized to optimize use of space in the operative theater.
Relative to the patient on the operating table, the position of the sterile tables,
the base of the microscope, the cautery machines, and the heating Bair-
Hugger machine (3M Canada) should be consistent, regardless of the
laterality of the reconstruction (Fig. 73-1).
Standardizing all surgical instruments, sutures, irrigation, drugs, and
draping, can be implemented for all surgeons, in all units. When standardized
disposables are used by all surgeons, single OR packs can be ordered from
suppliers. OR packs decrease the setup time and reduce the cost of
disposables. Any instrument that is not routinely used in every case should be
eliminated from the setup. This standard setup contains only the essentials
required to complete the operation (Fig. 73-2A–E). Surgeon practice
variability should be avoided. A limited number of special request
instruments can be added to the standard setup for a particular case but this
should be strongly discouraged. Elimination of unnecessary instruments
simplifies the back table setup, reducing the space needed, and setup time for
the nursing team. A microsurgical case setup for the nursing team should take
10 to 15 minutes to complete.
Standardization of the team roles and expectations is an essential
component of surgical efficiency. There should be a defined agenda for the
operation and the process, with a clear understanding of the roles of each
team member and the expectations for the process. The agenda details the
main steps in the operation, the roles of each team member during these
steps, the anticipated duration of each step, and which steps are synchronous
versus those that are sequential (Table 73-1). For a unilateral immediate
autologous breast reconstruction, the team includes a scrub nurse, a
circulating nurse, an anesthesiologist, a general surgeon (with or without an
assist), the primary plastic surgeon, and a plastic surgery trainee (resident or
fellow).
FIGURE 73-2 Surgical instrument setup for a microsurgical reconstruction case.
Surgical sets contain only the instruments required for the microsurgical case, with
no (or minimal) special request instruments (A). A disposable pack contains multiple
disposables to limit the time required to open each item individually and ensure no
items are missed (B). The microsurgical flap table (C) and the mastectomy table (D)
are setup with all necessary and no superfluous instruments, disposables, or sutures.
Mayo stand setup for the surgeon elevating the flap on the abdomen while the
general surgeon completes the mastectomy and nodal surgery (E).

Once the patient enters the OR, the anesthesia and nursing teams have a set
of tasks to complete in a synchronous fashion, ensuring patient safety and
efficient start to the operation. Standardization of the anesthetic is essential
for surgical efficiency. Intraoperative monitoring is limited to radial arterial
line, temperature probe, neuromuscular monitoring, and two larger-bore IVs.
The patient lays on an underbody warming matt and a MEGADYNE Mega
Soft cautery grounding pad (Ethicon, Johnson & Johnson). Euvolemia is
maintained throughout the case with judicious use of crystalloids and limited
vasopressors. Deep neuromuscular blockade is initiated as soon as the general
surgeon is comfortable with a full neuromuscular block. Synchronous with
initiation of general anesthesia, the circulating nurse places sequential
compression devices, a lower body warmer, two additional cautery pads (so
that four potential cautery devices can be used) and Foley catheter.
Simultaneously, the scrub nurses are setting up both the resection and
reconstruction standardized equipment tables. Total time from “in room” to
“skin incision” is benchmarked at 30 minutes. Since both the resection and
reconstruction will begin immediately at the start of the case, two scrub
nurses during the mastectomy allow for efficient synchronous equipment set
up and surgery.

TABLE 73-1 Agenda Outlining Sequential and Synchronous Steps for an


Immediate Autologous Abdominal-Based Reconstruction Where the Plastic
Surgery (PRS) Team Includes the Primary Surgeon and a Plastic Surgery
Trainee (PRS Cosurgeon Is a Resident or Fellow). The General Surgery
(GS) Team May Be a Single Primary General Surgeon With or Without a
Trainee/Assist
Surgical Step Surgical and Nursing Role
Anesthesia Roles
Mastectomy +/− nodal GS requires surgical Scrub nurse focused on
surgery assist mastectomy
synchronous with
Identification of PRS requires no assist Mayo stand setup for
superficial system PRS on abdomen.
and DIEA/V Second scrub nurse
perforator not needed
identification
Preparation of PRS cosurgeon requires Mayo stand setup for
recipient vessels no assistance. If flap PRS on chest. No
already elevated, PRS scrub nurse assistance
primary surgeon
prepares IMA/V
synchronous with
Elevation of flap PRS primary surgeon Scrub nurse focused on
requires no assist perforator dissection
Anesthesiologist
provides muscle
paralysis
Microsurgical PRS primary surgeon Scrub nurse focused on
anastomosis requires no assist microsurgical
anastomosis
synchronous with
Abdominal donor-site PRS cosurgeon requires Mayo stand setup for
closure no assist PRS cosurgeon
abdomen closure

Throughout the case, it is the responsibility of the primary plastic surgeon


to orchestrate the coordinated efforts of each member of the reconstructive
team. A predetermined agenda defines the set expectations for each team
member and facilitates synchronous care delivery. The primary surgeon
should coordinate, but not necessarily complete, each surgical step; a
synchronous completion of tasks is more efficient with the coordinated
efforts of a general surgeon and an additional plastic surgery trainee. The
scrub nurse focuses on one step at a time with the team members involved in
that step in a defined sequential manner (Table 73-1).
Operative Technique
The primary plastic surgeon must follow an established reliable sequence of
steps to ensure each task is completed in the most proficient and predictable
way possible. The primary surgeon must incessantly be self-critical, evaluate
their technique, and optimize or eliminate redundancy in their surgical steps.
During flap elevation, the use of surgical assistants should be minimized.
Surgical assistance can be variable and unpredictable, especially in teaching
centers, and lead to an increased risk of injury or error during pedicle
dissection and flap elevation. Independent flap elevation is accomplished
primarily with the proper use of self-retaining equipment and monopolar
cautery. Instruments used include staples (or stay sutures), dermahooks (or
fish hooks), and Gelpi (or Weitlaner) self-retaining instruments. Stay sutures
or staples are used to position the flap and to provide a clear line of vision
with stable tension on the flap perforators. Perforator dissection is facilitated
by placing dermahooks to retract the edge of the rectus fascia and muscle
allowing continuous controlled tension on the muscle fibers around the
pedicle. Gelpi self-retaining retractors act as an adjunct to the Dermahooks
and tension the pedicle during dissection off the posterior rectus fascia to the
pedicle origin.
Monopolar cautery is exclusively used for flap elevation, pedicle
dissection, and recipient vessel harvest. Monopolar cautery is clinically safe
to use. A blunt, coated, nonstick cautery tip is used, as opposed to a needle
tip, because the nonactivated cautery tip is essentially used as a blunt
dissector for the majority of the flap dissection. Cautery settings are typically
set to 40/40 blend on a standard cautery machine; the lowest power is chosen
to coagulate or cut the specific tissue being dissected. Anatomic tissue planes
around the perforator and pedicle are established primarily with gentle blunt
dissection. Tendinous insertions and small (<0.5-mm) side branches are cut
and/or coagulated. It is important to cauterize tissue only when it is placed
under tension. If tissue is not held under tension, it will not separate along
anatomic planes and risks transmitting a large amount of heat to the
surrounding pedicle. By using a single instrument for blunt dissection of
anatomic planes and coagulation of branches, the elevation of the flap is more
expeditious. With the primary use of a single instrument for flap elevation,
there are fewer instrument changes, resulting in less dependence on the scrub
nurse and no dependence on a surgical assist. Monopolar cautery setting of a
blended 40/40 for flap elevation is increased to 50/50 for shaping of the flap
and hemostasis of the surgical sites.
The primary surgeon should set benchmarks for the time required to
complete each surgical step in the operation. With targeted times for each
task, it is easier to identify which steps are slowing down the process and
require detailed analysis to eliminate repetitive or nonneeded movements.
With improved efficiency at each step, the surgeon becomes more
proficient and strengthens their confidence. This confidence is contagious
and compounds quickly within the team. Team morale is important, as is a
culture of positivity and motivation to complete the tasks in a safe and
efficient manner for improved patient care. Efficient cases are easy, and easy
cases are typically more effective.
Reliable Near-Equivalent Backup
To be safe as an efficient surgeon, every step should have a reliable near-
equivalent backup. A near-equivalent backup for the primary flap is defined
as a second (alternate) perforator or a different pedicle with an overlapping
vascular territory to the primary flap that allows for near equivalence in terms
of the tissue available for harvest. A near-equivalent back up should exist for
every critical component of the case. Near-equivalent backup pedicles for the
deep inferior epigastric perforator (DIEP) flap include the superficial inferior
epigastric artery (SIEA) and the superficial circumflex iliac artery.
At the start of flap dissection, a secondary perforator or pedicle is first
quickly established and then focus is rapidly switched to the primary
dominant perforator. With an established reliable near-equivalent backup, a
surgical error on the dissection of the primary perforator does not result in
complete flap loss. Anxiety associated with dissecting out a single, dominant
perforator is decreased, thus improving the dissection technique. Overall, the
flap harvest time is markedly improved.
For flaps of the anterior abdomen, the SIEA pedicle is assessed first if the
hemiabdomen provides sufficient tissue. The DIEP perforators are not
dissected until the quality of the SIEA/V is determined. Elevation of the
SIEA flap will expedite the harvest time and maintain the integrity of the
abdominal wall. The contralateral SIEA flap is preferentially selected for two
reasons: (1) the location of the pedicle entrance into the flap is best suited for
a 90-degree rotation and anastomosis to the contralateral chest; (2) there is
more space for the primary surgeon to elevate the flap on the abdomen with
the second team working on the chest. If the SIEA is inadequate or injured
during dissection, the DIEA perforators are isolated.
If the DIEP flap is the planned choice, all perforators are identified. One
dominant perforator is selected for dissection and the second best, or near-
equivalent backup, is kept clamped as a backup. The periumbilical medial
row perforator is most commonly selected as the primary choice and the
inferior lateral row perforator as the second option or backup. Other
nondominant and nonequivalent backups can be sacrificed if this helps with
the dissection and elevation of the flap on the select primary perforator. It is
not advisable to keep all the perforators as backups; this impedes movement
of the flap during dissection as each perforator acts as a tether point to the
fascia. Keeping backups that are not equivalent slows down the dissection of
the dominant perforator and may cause traction injuries on the perforating
veins at the level of the flap.
Recipient Vessel and Flap Selection
The internal mammary (IM) vessels are the preferred site for flap
anastomosis. The IM perforator can be used at the 2nd intercostal space when
of adequate size and a non–nipple-sparing mastectomy technique has been
done. The second and third IM perforators should be preserved in all cases of
a nipple-sparing mastectomy to maintain as much perfusion to the nipple and
periareolar skin as possible. The IM perforator is advantageous as it requires
less time for dissection and spares the removal of rib cartilage. Most
importantly, using the IM perforator shortens the required length of the
pedicle since there is a shorter distance from the level of mastectomy flap to
the level of the anastomosis.
If the IM perforators are inadequate, the IM artery and vein proper are
prepared as the recipients. Regardless of the recipient vessels selected, the
flap pedicle length should be kept as short as possible for adequate
microsurgical anastomosis. This minimizes the time required for pedicle
dissection, limits fascial incision length, and decreases the potential for
transection or a neuropraxia of the motor nerves to the rectus abdominus
muscle. The pedicle is always dissected until it lies on the undersurface of
this muscle. Beyond the extent of the muscle, the pedicle length is then
dictated by the thickness of the flap, the depth of the chest cavity, and the
placement of mastectomy incision. The overall effective length of vessel for
the anastomosis is the summation of the pedicle and the recipient vessel
length. By increasing the length of the IM vessel dissection, the effective
length for anastomosis remains adequate with a shorter pedicle length and
less time spent on the abdominal flap dissection. The deeper the plane of the
vessel, the greater effective pedicle length required. Thus, for patients with
deeper chest cavities or thicker flaps, the length of the pedicle is extended to
ensure adequate length is available. Lastly, the pedicle length can be
shortened if the perforator enters the flap toward the flap edge. In this
scenario, the flap can be ultimately inset with the perforator in close
proximity to the IM vessels.
For flaps with shorter pedicle lengths, it is essential that recipient vessels
have their length maximized. A long recipient vessel will compensate for the
short pedicle length inherent in certain flaps, including the flaps supplied by
the lumbar artery perforators and gluteal artery perforators.
The caliber of the flap vessels is smaller when a shorter pedicle is
dissected. Thus, to improve the size match between the smaller flap vessels
and the IM recipient, the 4th intercostal space is usually selected for
anastomosis. The caliber of the IM vessels reduces as the vessels course
inferiorly. At the 4th rib, the IM vessels are smaller than at the 3rd intercostal
space and the caliber match is more appropriate. In a nipple-sparing
mastectomy through an inframammary crease incision, the 5th rib is removed
to facilitate positioning for the anastomosis. In these cases, the length of
pedicle dissected is even shorter to compensate for the smaller caliber of the
recipient vessels, provided the pedicle length still allows for appropriate flap
inset.
Flap selection in autologous breast reconstruction is not solely based on
efficiency of the flap harvest. The flap choice is based on a combination of
patient preferences, body habitus, and flap harvest efficiency. With advances
in microsurgery and our understanding of perforasomes, it is technically
feasible to elevate perforator flaps from the truncal, gluteal, and lower
extremity regions for breast reconstruction. For a specific patient, the ideal
flap will create a breast mound of proportionate size, mitigate donor-site
morbidity, and simultaneously reconfigure the body to enhance aesthetic
contours.
Shaping
Once the flap is elevated and the recipient vessels are prepared, redefining the
breast foot print is done before anastomosis. The shape of the breast is
formed by recreating the footprint of the breast with plication of the lateral
chest wall and inframammary fold. Instead of only shaping the flap, the
footprint is adjusted to shape the breast. After anastomosis, the skin envelope
is adjusted to the flap for coning of the breast.
Anastomosis
For efficiency during the microvascular anastomosis, the primary surgeon
aims to limit the need for assistance. There is a low tolerance for error during
vessel anastomosis and the surgeon can complete this set of tasks without the
need for a surgical assist. It is the variable skill of many surgical assists that
can dramatically increase the technical difficulty.
Setup for the anastomosis requires proper positioning of the surgeon, the
microscope, the table, the scrub nurse, and the flap. The primary surgeon is
positioned sitting on the ipsilateral side of the anastomosis, with the operating
table rotated in the roll axis toward the surgeon. The scrub nurse is positioned
adjacent to the surgeon to provide the instruments as they are requested into
the surgeon’s hand so that the surgeon can continuously look through the
microscope and not need to look away to grasp an instrument or reposition
the instrument in their hand. The base of the microscope is positioned toward
the head of the patient, ipsilateral to the primary surgeon, so that the arm of
the scope is easily mobilized in and out of the field.
Recipient vessels are clamped far proximally and clipped distally, thus
maximizing the usable length of the vessels. The cut vessels are positioned on
top of a lap sponge placed in the base of the rib defect. This elevates the
vessels from the depth of the wound, lightly adheres the vessels to hold them
in position, and absorbs blood and irrigation fluid. Flap vessel preparation is
initiated on the abdomen by blunt separation of the artery and veins prior to
clipping their origin. The flap is secured on the chest, the flap vessels are
placed on a lap sponge, and the vessels are prepared under the microscope.
Vessels are typically prepared with blunt dissection and minimal separation
of the artery and venae comitantes. Vessel dissection is limited to a few
millimeters from the cut end. The arterial anastomosis is facilitated by
placing the double-approximating clamps on the lap sponge and looping the
ends of the clamp in the sponge threads. This stabilizes the clamp/vessel
construct and allows it to be positioned in any orientation.
During microsurgical anastomosis, the abdominal donor-site closure is
synchronously being completed. The scrub nurse is focused solely on
providing the microsurgical instruments to the operating surgeon at the
microscope. The team working on donor-site closure is cognizant not to
disrupt the scrub nurse and not to cause movements of the patient that would
transmit to the chest operative field during anastomosis.
Postoperative Care
Postoperative care is standardized and is part of the agenda communicated to
the patient at initial consultation. Expectations are communicated to the
patient prior to surgery; the information outlines their course in hospital, with
daily expected milestones for diet, fluid balance, ambulation, pain control,
and date of discharge. Preoperative education is essential to ensure the patient
is an informed member of the team during the postoperative progression in
hospital and the transition to home. Preprinted orders facilitate the
standardization of postoperative care and communication with the ward
nursing team.
Reevaluation of the Process
Standardization of the process is essential to improve efficiency. However, it
is an iterative process to achieve a standard protocol that suits the needs of
the team and can be implemented in a routine way. Each member of the team
must reevaluate the efficiency with which they complete their tasks and fill
their role in the process. For the primary surgeon, it is particularly important
to constantly reevaluate their progress, assess their success in reaching
benchmarks, and to be ruthless is eliminating unnecessary movements in each
step to reduce time wasted. One of the easiest methods for reevaluation is
through videotaping the entire room during specific cases. Once done, the
tapes can be examined to optimize room organization, nursing practices, and
operative techniques. The surgeon must appreciate the importance of
simplifying each step down to the essential tasks.
Outcomes
With these applied principles to improve surgical efficiency, it is routine to
complete two microsurgical cases per 8-hour surgical day by a single surgeon
in an academic setting. On average, 300 microsurgical cases are performed
per surgeon per year. The primary plastic surgeon, general surgeon, nursing
team, and the physician assistant are consistent members of the team
throughout the year. The trainees, including the residents and fellows,
fluctuate throughout the year. Overall, the team roles and process are
standardized as outlined above.
With efficiency during the microsurgical case, there is additional time
available for teaching. The vast majority of the microsurgical anastomosis is
completed by a senior resident in all cases. The flap take-back rate is
maintained at less than 5% with a flap failure rate of less than 1.5%. These
outcomes are comparable with the flap failure and take-back rates in the
literature.
CONCLUSION
Surgical efficiency in autologous breast reconstruction requires
standardization of the process and team. Autologous breast reconstruction
should be as routine as an alloplastic breast reconstruction. Without
improving the efficiency of autologous breast reconstruction, the increased
effort needed will limit the number of patients offered this option. Only when
the free autologous breast reconstruction becomes routine practice will
patients truly be given an equitable choice in their options for breast
reconstruction.

SUGGESTED READINGS
Bernell SL. Health Economics: Core Concepts and Essential Tools. Chicago,
IL: Health Administration Press; 2016.
Blondeel PN, Morris SF, Hallock GG, et al., eds. Perforator Flaps: Anatomy,
Technique and Clinical Applications. 2nd ed. Boca Raton, FL: CRC Press;
2013.
Kane RL, Radosevich DM. Conducting Health Outcomes Research. Sudbury,
MA: Jones & Bartlett Learning; 2011.
Levy A, Sobolev B. Comparative Effectiveness Research in Health Services.
New York: Springer; 2016.
Macadam SA, Bovill ES, Buchel EW, et al. Evidence-based medicine:
autologous breast reconstruction. Plast Reconstr Surg 2017;139:204e–
229e.
Ohkuma R, Mohan R, Baltodano PA, et al. Abdominally based free flap
planning in breast reconstruction with computed tomographic angiography:
systematic review and meta-analysis. Plast Reconstr Surg 2014;133:483–
494.
Piorkowski JR, DeRosier LC, Nickerson P, et al. Preoperative computed
tomography angiogram to predict patients with favorable anatomy for
superficial inferior epigastric artery flap breast reconstruction. Ann Plast
Surg 2011;66:534–536.
Rozen WM, Ashton MW, Grinsell D, et al. Establishing the case for CT
angiography in the preoperative imaging of abdominal wall perforators.
Microsurgery 2008;28:306–313.
Taylor G, Daniel R. The anatomy of several free flap donor sites. Plast
Reconstr Surg 1974;56:243–253.
Taylor GI. The angiosomes of the body and their supply to perforator flaps.
Clin Plast Surg 2003;30:331–342.
Temple-Oberle C, Shea-Budgell MA, Tan M, et al. Consensus review of
optimal perioperative care in breast reconstruction: Enhanced Recovery
after Surgery (ERAS) society recommendations. Plast Reconstr Surg
2017;139:1056e–1071e.
CHAPTER 74

Management of the Unilateral


Reconstruction and Timing of
Matching
YOAV BARNEA | NIV GELERMAN
HISTORY
Breast symmetry is key to achieving a good aesthetic outcome in unilateral
autologous breast reconstruction. Symmetry often necessitates contralateral
breast adjustment, which can be done either simultaneously during the
reconstruction, or in a two-stage approach (1–8). There are multiple factors
that come into play when deciding the most suitable approach for altering the
contralateral breast, and they include both oncologic and reconstructive
considerations (1–11). Making no adjustment to the contralateral breast is
also an acceptable choice for selected patients who have a breast outline that
can be designed similarly by the autologous reconstruction, both for shape
and size (Fig. 74-1A–C). Likewise, patients at high risk for contralateral
breast cancer or those with personal preferences and beliefs often decline to
undergo surgery on the healthy breast, symmetry notwithstanding.
ONCOLOGIC CONSIDERATIONS
When discussing a contralateral matching procedure, the patient needs to
understand the risk of developing breast cancer in the contralateral breast.
The reported 10-year cumulative risk for developing a contralateral breast
cancer in women who were initially diagnosed with unilateral disease is 6.5%
(2). In a review of 4,554 women with a diagnosis of carcinoma of the breast,
Singletary et al. (3) demonstrated that the occurrence of bilateral carcinoma
of the breast was 3.1%. It must also be borne in mind that patients with a
family history of breast cancer, BRCA gene mutation, and other genetic and
environmental risk factors have a significantly higher risk for developing
breast cancer in the contralateral breast (3–5). As a result, all cases of
matching procedures undergo preoperative breast imaging and the breast
tissue that is excised is routinely sent for pathologic evaluation in order to
rule out incidental breast cancer (4).
Another important aspect of matching procedures is the postoperative
anatomic changes in that breast and how they affect the findings on breast
imaging. Operative procedures performed on the contralateral breast, such as
breast reduction, mastopexy, or augmentation, may affect radiologic and
physical findings by leaving behind internal scars, calcifications, fat necrosis,
and a partially obscuring of the radiologic field by the implant (5).
TYPE OF RECONSTRUCTION
The type of reconstruction has a direct impact on the need for a contralateral
procedure aimed at achieving breast symmetry (6). In most cases, the natural
breast has some sagging and upper pole emptiness, which would better match
an autologous reconstruction rather than an alloplastic reconstruction. The
former would reduce the need for contralateral symmetrization procedures
compared to implant-based reconstruction. Furthermore, autologous
reconstruction usually changes proportionally to changes in body weight,
similar to a healthy breast, thus reducing the need for future revisions (6).
TIMING OF A MATCHING PROCEDURE
The ideal timing for a matching procedure on the contralateral breast remains
controversial (7). Surgeons had traditionally preferred matching the healthy
breast to the operated one in a second stage, after allowing the reconstructed
breast to settle in its final shape and form, thereby achieving better symmetry
(Fig. 74-2A–C) (6,7). Additionally, simultaneous matching can potentially
prolong the reconstructive surgery and increase the blood loss and recovery
time. Nonetheless, recent studies have shown that simultaneous contralateral
breast reduction or augmentation only minimally increases the total operative
time, and that they do not increase the overall complication rate (1,4,8,9).
Current trends are therefore shifting toward simultaneous matching
procedures (1,4,8).
FIGURE 74-1 A 55-year-old patient with right breast cancer. She underwent right
lumpectomy with involved margins and planned for right mastectomy (A). One
month after right skin-sparing mastectomy and immediate reconstruction with deep
inferior epigastric perforator (DIEP) flap and no contralateral adjustment (B). One
year after right nipple and areolar (NAC) reconstruction (C).
FIGURE 74-2 A 44-year-old patient diagnosed with right breast cancer (A). She
underwent right skin-sparing mastectomy and immediate reconstruction with DIEP
flap and no contralateral adjustment (B). One year after a second stage left implant
augmentation for symmetry and right NAC reconstruction (C).
FIGURE 74-3 A 58-year-old patient after left mastectomy and radiation therapy (A).
Patient’s planning and marking for left breast reconstruction with DIEP flap and
simultaneous right mastopexy (B). One year after surgery and left NAC
reconstruction (C).

There are obvious advantages in performing the matching procedure


during the same operation as the reconstruction. Simultaneous matching
spares the patient from undergoing another operation under general
anesthesia, minimizes hospital costs, reduces overall recovery time, and
accelerates the return to daily activity and work (Fig. 74-3A–C) (4,10).
Recent publications demonstrated that simultaneous matching can result in a
very good symmetric outcome with a low revision rate (1,4,8). Moreover,
women who had simultaneous matching procedures have demonstrated
significantly better psychosocial well-being compared to patients who
underwent a delayed procedure and were evaluated while waiting to undergo
the contralateral matching surgery (1).
LONG-TERM OUTCOME
Breast symmetry is the most prominent factor for patient satisfaction
following breast reconstruction (8,11). As such, it is essential to achieve and
maintain long-lasting breast symmetry. Since changes in the overall shape
and size of the breast are inevitable over time, this goal is not easily
achievable. The long-term behavior of the reconstructed breast depends
mainly on the type of reconstruction. For example, implant-based
reconstruction has a different biology and long-term alterations compared to
tissue-based reconstruction. According to Barone et al., matching the
contralateral breast with the same type of reconstruction increases the
chances of retaining the breast symmetry over a longer period of time. In
principle, tissue-based reconstruction would match better with breast
reduction/mastopexy contralateral adjustment, while implant-based
reconstruction would match better with contralateral breast augmentation
(11).
CONCLUSION
Breast symmetry is the hallmark of breast reconstruction and a key factor for
aesthetic outcome and patient satisfaction. In cases of unilateral breast
reconstruction, the contralateral healthy breast often requires a matching
procedure. This can be done simultaneously during the breast reconstruction
procedure or it can be performed as a two-staged operation after a delay, with
each choice having its advantages and disadvantages. The timing and type of
matching procedure should be decided upon according to the oncologic
status, type of reconstruction, and specific patient’s physical condition and
emotional needs, with special emphasis on patient’s desires and expectations.
Tips and Tricks
Simultaneous contralateral breast adjustment in unilateral DIEP breast
reconstruction is a safe and a worthwhile procedure, with low revision rate
and high patient satisfaction, and should be offered to the patient when
appropriate.

REFERENCES

1. Inbal A, Gur E, Otremski E, et al. Simultaneous contralateral breast


adjustment in unilateral deep inferior epigastric perforator breast
reconstruction. J Reconstr Microsurg 2012;28(5):285–292.
2. Raabe NK, Sauer T, Erichsen A, et al. Breast cancer in the contralateral
breast: incidence and histopathology after unilateral radical treatment of
the first breast cancer. Oncol Rep 1999;6(5):1001–1007.
3. Singletary SE, Taylor SH, Guinee VF, et al. Occurrence and prognosis
of contralateral carcinoma of the breast. J Am Coll Surg
1994;178(4):390–396.
4. Chang EI, Lamaris G, Chang DW. Simultaneous contralateral reduction
mammoplasty or mastopexy during unilateral free flap breast
reconstruction. Ann Plast Surg 2013;71(2):144–148.
5. Mendelson EB. Evaluation of the postoperative breast. Radiol Clin
North Am 1992;30(1):107–138.
6. Nahabedian MY. Managing the opposite breast: contralateral symmetry
procedures. Cancer J 2008;14(4):258–263.
7. Losken A, Carlson GW, Bostwick J 3rd, et al. Trends in unilateral breast
reconstruction and management of the contralateral breast: the Emory
experience. Plast Reconstr Surg 2002;110(1):89–97.
8. Rizki H, Nkonde C, Ching RC, et al. Plastic surgical management of the
contralateral breast in post-mastectomy breast reconstruction. Int J Surg
2013;11(9):767–772.
9. Cooney C M, Sebai ME, Ogbuagu O, et al. Matching procedures at the
time of immediate breast reconstruction: an American College of
Surgeons National Surgical Quality Improvement Program study of
24,191 patients. Plast Reconstr Surg 2016;138(6):959e–968e.
10. Stevenson TR, Goldstein JA. TRAM flap breast reconstruction and
contralateral reduction or mastopexy. Plast Reconstr Surg
1993;92(2):228–233.
11. Barone M, Cogliandro A, Signoretti M, et al. Analysis of symmetry
stability following implant-based breast reconstruction and contralateral
management in 582 patients with long-term outcomes. Aesthetic Plast
Surg 2018;42(4):936–940.
CHAPTER 75

Pedicle TRAM and Free TRAM


DANA EGOZI
HISTORY
The introduction of transverse rectus abdominis musculocutaneous (TRAM)
flaps for breast reconstruction was the most significant milestone in
autologous breast reconstruction evolution. TRAM flaps were the first flaps
to provide a soft, warm, and naturally feeling reconstructive tissue without
the use of a prosthetic devices and also resulted in an acceptable donor scar.
Along with an increase in skin-sparing mastectomy techniques, higher rates
of satisfaction were achieved with naturally looking reconstructed breasts.
In 1979, Robbins et al. (1) published the first paper on the use of a rectus
abdominis skin-muscle flap with vertical orientation for breast reconstruction.
A modified method was published in 1982 by Hartrampf et al. (2). The
modification consisted of a TRAM flap for breast reconstruction, providing
an aesthetically pleasing donor-site closure. The pedicled TRAM flap soon
became the standard autologous breast reconstruction method for almost a
decade or two (3,4).
Scheflan and Dinner found that the inferior epigastric arterial supply is
dominant to the lower abdomen with a robust blood supply directly over the
muscle where the perforators are located (5). In tandem with this finding,
Holmstrom first described in 1979 abdominal tissue use in breast
reconstruction as free flaps, based on the deep inferior epigastric vessels (6).
This finding and advances in microsurgery techniques, made free TRAM the
methods of choice for breast reconstruction, replacing pedicled TRAM
surgery in many cases. This type of free tissue transfer has a more reliable
blood supply, with lower incidents of partial flap necrosis and fat necrosis.
The flap loss rate was as low as 2%, with lower functional abdominal wall
donor-site impairment, and without the “pedicle bulge” when compared with
the pedicled TRAM flap technique. The only drawback was the longer
operative time documented with free TRAM (7–9). The next development
was the deep inferior epigastric perforator (DIEP) flap. This flap technique
quickly replaced the pedicled and free TRAM flaps, since this flap spares the
rectus muscle. Thus, the DIEP flap provides the advantages of autologous
breast reconstruction while using the lower abdominal tissues but avoiding
abdominal wall complications, such as bulging or herniation, seen in pedicled
or free TRAM flaps (10).
Anatomy: The vessels of both epigastric systems penetrate the rectus
muscles in their deep surfaces. The deep inferior vessel provides the lower
abdomen tissue with a more robust circulation (5) due to the larger venae
comitantes of the inferior system. Arterial perforators ascend from the medial
and lateral rows and penetrate through the muscle and the fascia to the
subcutis and skin. Analysis of the TRAM flap’s vascularization showed that
the lower abdominal tissue could be divided into zones based on the relative
perfusion. There are two major vascular classifications for the TRAM flap’s
blood supply. The best known and earliest description was Hartrampf’s, who
divided the supply into four zones:
Zone I overlying the muscle pedicle. Zone II lying across the midline,
immediately adjacent to zone I. Zone III lying lateral to zone I on the
ipsilateral side. Zone IV lying lateral to zone II on the contralateral side from
the pedicle (Fig. 75-1) (11). Zone I is the most reliable part of the flap. The
medial portion of zone III is the next most reliable part of the flap with the
lateral side of zone III being less reliable. The medial part of zone II is
usually reliable. However, the lateral part is less reliable, and zone IV is
rarely useful in most free flaps and should generally be discarded. Holm et al.
(12) published their work on the DIEP flaps and concluded that while zone I
remains the most reliably perfused part of the flap, any contralateral flow
across the midline is more dangerous than the ipsilateral flow. Thus,
Hartrampf ipsilateral zone III should be renamed zone II, while Hartrampf
zone II should be renamed zone III with a less reliable flow due to its cross-
midline location.
FIGURE 75-1 Hartrampf classification of the TRAM flap blood supply zones (I to
IV) based on vascularity of the different areas of the TRAM flap.

The well-known work of Andrades et al. published the classification of the


different abdominal flaps: the classic pedicled TRAM flap, the free TRAM
flap (MS-0), the muscle-sparing free TRAM flaps (MS-1 and MS-2), the
DIEP or MS-3, and the superficial inferior epigastric perforator (SIEP) flap
(13). The free TRAM flap includes between three and six perforators and
variable amounts of muscle, ranging from the muscle’s whole width to a
small (2 × 2 cm) segment of the rectus muscle. In the muscle-sparing free
TRAM the use of a Doppler probe to identify the intramuscular course of the
superior epigastric vessels is recommended.
In the TRAM flap, unlike the DIEP flap, a piece of the rectus sheath is
always taken with the flap. Meticulous closure of the fascia gap with or
without a mesh is needed to prevent hernias or bulges. It is important to
incorporate both the external and internal oblique aponeuroses into the sheath
closure (14). Bucky and May showed excellent results when routinely
incorporating mesh into all TRAM flap abdominal closures (Fig. 75-2) (15).
TRAM FLAP BREAST RECONSTRUCTION INDICATIONS AND
CONTRAINDICATIONS
Initially, the patient must want an autologous breast reconstruction with an
abdominal operation instead of reconstruction with prosthesis. The first
requirement for pedicled or free TRAM is sufficient abdominal tissue upon
physical examination. This method is suitable both for immediate and late
reconstruction.
Medical comorbidities such as uncontrolled hypertension, cardiovascular
risk factors, poorly controlled diabetes, collagen vascular diseases, and a
refusal to immediately begin a smoking cessation program are strong relative
contraindications.
Absolute contraindications to free tissue transfer include known histories
of clotting abnormalities or bleeding diathesis that cannot be medically
corrected.
Prior abdominal operation like abdominoplasty is also a contraindication.
Cholecystectomy scars are contraindication for a TRAM on the abdomen’s
right side. However, Pfannenstiel incision is not contraindication for pedicled
or free TRAMs.
The main risk factors for complication are obesity and smoking. Smoking
does not increase the rates of vessel thrombosis, fat necrosis, or flap loss
compared with nonsmokers. However, there are increases in the risk for
mastectomy skin flap necrosis, abdominal flap necrosis, and hernia in free
TRAM flap breast reconstruction. Interestingly, if there is a cessation of
smoking at least 4 weeks prior to surgery, the complication rates drop and are
similar to nonsmokers (16,17).
The effects of radiation therapy on TRAM flap’s complication rates are the
same whether the patient receives radiation before or after reconstruction
(Fig. 75-3) (18). Following radiation, the reconstructed breast could become
hyperpigmented and firm. Palpable fat necrosis and loss of symmetry are
possibilities, both in free or pedicled TRAM reconstructions. Immediate
reconstruction with TRAM flap has better aesthetic results as compared to
delayed reconstruction and enables surgeons to achieve naturally feeling
reconstructions, even when taking into account radiation injury. However, in
these cases, surgeons must remember that radiation increases fat necrosis
rates and there are some downsides such as unpredictable volume, contour,
and loss of symmetry while doing postoperative irradiation following TRAM
breast reconstruction (19).
Immediate breast reconstruction with muscle-sparing free TRAM flaps has
similar rates of fat necrosis compared to DIEP flap reconstruction (20).
FIGURE 75-2 Pedicled TRAM, whole-muscle technique. A: Final appearance with
the onlay mesh. B: Rotation of the abdominal flap and position on the chest.
FIGURE 75-3 Transverse rectus abdominis myocutaneous flap reconstruction, a
single pedicle. A: Preoperative photo. B: At the time of the mastectomy, the
contralateral reduction for symmetry. C: Following irradiation, the left breast
reconstruction with TRAM flap. D: Final result following nipple reconstruction.
OPERATIVE TECHNIQUE
THE OPERATION
The abdominal scar can be relatively low, but the skin island must include the
umbilicus and its perforators. It is important when making the upper incision
to bevel it so as to include a maximum number of periumbilical perforators
and as much subcutaneous tissue as possible. The superior abdominal wall is
elevated above the fascia to the costal margin’s level. A medial tunnel
connecting this dissection to the mastectomy defect is created while avoiding
the inframammary fold detachment. The flap is then elevated from lateral to
medial, identifying the lateral row of perforators and the rectus abdominis
muscle’s lateral border (21).
By using a small incision in the rectus fascia, the rectus muscle’s lateral
border can be identified. When harvesting the whole rectus muscle, it is
important to leave 1 to 2 cm of the lateral anterior rectus fascia in the donor
site. This preserves the linea semilunaris ligament, thus allowing the securing
of the mesh during abdominal closure.
Abdominal wall closure with synthetic mesh allows for harvesting of most
of the anterior fascia overlying the rectus muscle. This ensures maximal
vascularity while facilitating flap elevation. Rotation of the TRAM flap from
90 to 180 degrees is then performed and delivered to the mastectomy site,
confirming that there is no tension on the pedicle (Fig. 75-4). If the
reconstructed breast had prior radiation, then a contralateral unipedicled flap,
bipedicled, or free TRAM flap should be done (with or without surgical
delay). If the patient is obese, or smokes, or when a large volume of breast is
needed, it is safer to do a bipedicled TRAM, delayed TRAM, or free TRAM
(4,22). A surgical delay performed 5 to 14 days previously improves TRAM
flap blood supply and should be considered for a pedicled procedure for the
previous mentioned reasons (obesity, smoking or large tissue volume).
FIGURE 75-4 Rotation of the abdominal flap and position on the chest.

Bipedicled TRAM flaps and free TRAM flap transfer are indicated for
large-volume reconstruction, smokers, and obese patients, those with midline
abdominal incisions, and with radiation injury to one pedicle. However,
bipedicled flaps are more robust and probably have a better blood supply than
free TRAM flaps. Bipedicled flaps allow the use of larger flaps at the expense
of greater abdominal donor-site muscle loss (Fig. 75-5) (23).
Bilateral reconstruction using two unipedicled TRAM flaps have identical
operative sequences as the bipedicled procedure. The skin is divided in the
midline, creating two equal-sized flaps. They are then transposed to the chest
wall through ipsilateral tunnels. This prevents possible compression and
kinking through a common central tunnel. In these cases, flap rotation on the
chest wall is typically 90 degrees.
Flap shaping: For most patients, the preference is contralateral muscle use
for best breast fullness and ptosis. If the patient wants more lateral fullness or
to avoid an epigastric bulge, the better choice is an ipsilateral muscle pedicle.
The advantages of ipsilateral transfer are reduced intermammary bulging and
better venous drainage. The tip of zone III and the complete zone IV should
be discarded unless they have an unusually good blood supply. Some
surgeons prefer using only the ipsilateral tissue to reduce fat necrosis. The
shape and symmetry are greatly influenced by the flap orientation (24,25).
The most common orientations are an oblique orientation with a 120- or 80-
degree rotation or a transverse lie with a 180-degree rotation. Generally, the
preference is to place as much volume inferiorly to maximize projection and
natural shape (22). Vertical orientation or oblique flap rotation is preferred
for patients with narrower breasts. Contralaterally based flaps undergo a
rotation of 90 to 180 degrees, leaving zone II superior or medial and zone III
mostly inferior or lateral ipsilateral flaps undergo a 90- to 180-degree rotation
through a lateral tunnel, leaving zone III superior or medial and zone II
inferior or lateral.
FIGURE 75-5 A, B: Patient requires right modified radical mastectomy and who will
undergo split-muscle, bipedicled TRAM flap reconstruction and contralateral left
breast reduction. C, E: Preoperative anterior and oblique views. D, F: Postoperative
anterior and oblique views.

The free TRAM flap involves transecting the entire width of rectus
abdominis muscle, encompassing multiple perforating vessels that supply the
overlying soft tissues. This can cause permanent loss of abdominal muscle
function. To minimize abdominal wall morbidity, muscle-sparing free
TRAMs or DIEP flaps should be used. For the muscle-sparing TRAM flap,
inflow to the subcutaneous tissues is based on two to four perforators, taken
from the medial and lateral row. Typically, the DIEP flap is based on fewer
perforators (one or two) and contains no rectus muscle.
The revision stage: Three to 6 months after reconstruction, reconstructed
breast and donor-site revisions along with symmetry procedures of the
contralateral breast are often needed. This should be done when the patient
has completed chemotherapy and radiation therapy if required. The
procedures done in this stage are nipple reconstruction, fat grafting
procedures to address residual small flap and chest wall defects, contralateral
mastopexy or reduction mammoplasty, and abdominal donor-site scar
revisions.
COMPLICATION
Complications can be divided to breast-related or abdomen-related
complications. Breast complications include partial or complete flap loss, and
skin and fat necrosis. Abdominal complications include abdominal bulges
and hernia, and deep venous thrombosis. Hernia incidence ranges between
1% and 9%, with no differences between free TRAM and pedicled TRAM, or
between bilateral and unilateral reconstruction (26,27). Hartrampf (28)
reported a 1.5% hernia rate in 351 unipedicled TRAM flap reconstructions
while the Emory group reported an 8.8% hernia rate (23).
Abdominal hernia complications are greater in TRAM flaps compared to
DIEP, due to the large fascia gap that is usually closed with a synthetic mesh.
Lower abdominal contour defects are far more common following free
TRAM flaps than when using DIEP flaps. Blondeel et al. found better
abdominal strength in free DIEP flaps compared to free TRAM flaps.
However, free DIEP flaps also create abdominal weakness to some extent
(29).
While complete flap loss is a very rare occurrence in pedicled TRAM flap
reconstruction (2 of 350 unipedicled and 0 of 39 bipedicled TRAM flaps in
Hartrampf series), partial flap loss is more common (28). Hartrampf reported
an 8.5% partial flap loss incidence in his series while Kroll and Netscher
reported in slim patients a 15.4% incidence, increasing in obese patients to
41.7% (2,16). In free TRAM the incidence for complete flap loss is higher;
Chang et al. (30) found a total flap loss of 5.1% in over 700 free TRAM flap
breast reconstructions with a 6.2% partial flap loss. Partial flap loss in free
tissue transfer is significantly less.
Obesity was found to be a significant risk factor for free TRAM flap breast
reconstruction complications, such as partial or full flap necrosis, fat necrosis,
seroma formation, and abdominal bulge. Chang et al. found that normal
weight patients had no total flap loss and a 1.6% partial flap necrosis rate,
whereas obese patients had a 3.2% total and partial flap necrosis rate. Fat
necrosis rates were 6.1% in normal weight patients and 7.8% in obese ones.
Abdominal bulges were 3 times more likely in obese patients compared with
normal ones, and seromas were 10 times more common in obese patients
(30).
Watterson et al. demonstrated a significant correlation between smoking
and general complications (P < 0.002), but not with fat necrosis (31).
Hartrampf found that heavy smoking is a moderate risk for TRAM flap
patients (28). Chang et al. found that smoking is a significant risk for both
reconstruction and donor sites. However, former smokers and nonsmokers
have similar complication rates (30).
A certain degree of fat necrosis is common in all TRAM flap
reconstructions, whether free or pedicled. Reports of fat necrosis range from
6% to 62.5% (27). However, comparisons between pedicles, free TRAM, and
DIEP are hard to do because authors differ in judging what is considered fat
necrosis. Additionally, surgeons have different approaches to the flap’s
design. Therefore, there are major differences in the amount and areas of the
flap that are discarded and also whether they cross the midline of the flap or
not.
Risk factors associated with fat necrosis include obesity (P < 0.02), prior
radiation (P < 0.001), and abdominal scarring (P < 0.01) (22). Kroll et al.
found that free TRAM flaps have an 8.2% incidence of detectable fat necrosis
compared with 26.9% in pedicled TRAM flaps (P < 0.01) (32). A study
examining whether free TRAMs have a better blood supply compared to
DIEP flaps (with one or more perforators) found no significant differences
with fat necrosis rates between free TRAM and DIEP flap breast
reconstruction (27).
CONCLUSION
The uprising of the pedicled TRAM flap breast reconstruction was the most
important step in the evolution of breast reconstruction with autologous
tissues; for the first time aesthetic reconstruction could be achieved only with
patient tissue, without prosthesis, which gave a naturally feeling
reconstruction. It was the mainstay of the reconstructive armamentarium in
the nineties and gradually changed from pedicled TRAM to free TRAM flaps
and then to muscle-sparing free TRAM flaps, based on three to four
perforators with a small piece of the rectus muscle. These led to the
development of DIEP flap, based on one to three perforators with no rectus
muscle. Both pedicled and free TRAM flaps can provide excellent contour
and softness, the same as DIEP flaps. However, the benefits of the DIEP flap
in maintaining abdominal wall strength, less abdominal bulges, and more
vascular reliability, make DIEP the preferred method nowadays. Yet, while
free TRAM flaps are inferior to perforator flap breast reconstruction
techniques regarding donor-site morbidity, there might be some superiority
because of better vascularity.

REFERENCES

1. Robbins TH. Rectus abdominis myocutaneous flap for breast


reconstruction. Aust N Z J Surg 1979;49:527–530.
2. Hartrampf CR, Scheflan M, Black PW. Breast reconstruction with a
transverse abdominal island flap. Plast Reconstr Surg 1982;69:216–225.
3. Uroskie TW Jr, Colen LB. History of breast reconstruction. Semin Plast
Surg 2004;18(2):65–69.
4. Jones G. The pedicled TRAM flap in breast reconstruction. Clin Plastic
Surg 2007;34:83–104.
5. Scheflan M, Dinner MI. The transverse abdominal island flap: part I.
Indications, contraindications, results, and complications. Ann Plast
Surg 1983;10(1):24–35.
6. Holmstrom H. The free abdominoplasty flap and its use in breast
reconstruction. An experimental study and clinical case report. Scand J
Plast Reconstr Surg 1979;13:423–427.
7. Schusterman MA, Kroll SS, Miller MJ, et al. The free transverse rectus
abdominis musculocutaneous flap for breast reconstruction: one center’s
experience with 211 consecutive cases. Ann Plast Surg 1994;32:234–
241; discussion 241–242.
8. Grotting JC, Urist MM, Maddos WA, et al. Conventional TRAM flap
versus free microsurgical TRAM flap for immediate breast
reconstruction. Plast Reconstr Surg 1989;83:828–841; discussion 842–
844.
9. Lee JW, Lee YC, Chang TW. Microvascularly augmented transverse
rectus abdominis myocutaneous flap for breast reconstruction—
reappraisal of its value through clinical outcome assessment and
intraoperative blood gas analysis. Microsurgery 2008;28(8):656–662.
10. Blondeel N, Vanderstraeten GG, Monstrey SJ, et al. The donor site
morbidity of free DIEP flaps and free TRAM flaps for breast
reconstruction. Br J Plast Surg 1997;50(5):322–330.
11. Hallock GG. Zones of the lower transverse rectus abdominis
musculocutaneous flap based on laser Doppler flowmetry. Ann Plast
Surg 1992;29(2):117–121.
12. Holm C, Mayr M, Höfter E, et al. Perfusion zones of the DIEP flap
revisited: a clinical study. Plast Reconstr Surg 2006;117:37–43.
13. Andrades P, Fix RJ, Danilla S, et al. Ischemic complications in pedicle,
free, and muscle sparing transverse rectus abdominis myocutaneous
flaps for breast reconstruction. Ann Plast Surg 2008;60(5):562–567.
14. Kroll SS, Schusterman MA, Mistry D. The internal oblique repair of
abdominal bulges secondary to TRAM flap breast reconstruction. Plast
Reconstr Surg 1995;96:100–104.
15. Bucky LP, May JW. Synthetic mesh. Its use in abdominal wall
reconstruction after the TRAM. Clin Plast Surg 1994;21:273–277.
16. Kroll SS, Netscher DT. Complications of TRAM flap breast
reconstruction in obese patients. Plast Reconstr Surg 1989;84(6):886–
892.
17. Chang DW, Reece GP, Wang B, et al. Effect of smoking on
complications in patients undergoing free TRAM flap breast
reconstruction. Plast Reconstr Surg 2000;105(7):2374–2380.
18. Williams JK, Carlson GW, Bostwick JG, et al. The effects of radiation
treatment after TRAM flap breast reconstruction. Plast Reconstr Surg
1997;100(5):1153–1160.
19. Tran NV, Evans GRD, Kroll SS, et al. Postoperative adjuvant
irradiation: effects on tranverse rectus abdominis muscle flap breast
reconstruction. Plast Reconstr Surg 2000;106(2):313–317; discussion
318–320.
20. Garvey PB, Clemens MW, Hoy AE, et al. Muscle-sparing TRAM flap
does not protect breast reconstruction from postmastectomy radiation
damage compared with the DIEP flap. Plast Reconstr Surg 2014
133(2):223–233.
21. Williams JK, Bostwick J 3rd, Bried JT, et al. TRAM flap breast
reconstruction after radiation treatment. Ann Surg 1995;221:756–764;
discussion 764–766.
22. Slavin SA, Goldwyn RM. The midabdominal rectus abdominis
musculocutaneous flap: review of 236 flaps. Plast Reconstr Surg
1988;81:189–197.
23. Paige KT, Bostwick J 3rd, Bried JT, et al. A comparison of morbidity
from bilateral, unipedicled and unilateral, unipedicled TRAM flap breast
reconstructions. Plast Reconstr Surg 1998;101:1819–1827.
24. Kroll SS, Coffey JA Jr, Winn RJ, et al. A comparison of factors
affecting aesthetic outcomes of TRAM flap breast reconstructions. Plast
Reconstr Surg 1995;96:860–864.
25. Carlson GW, Losken A, Moore B, et al. Results of immediate breast
reconstruction after skin-sparing mastectomy. Ann Plast Surg
2001;46:222–228.
26. Kroll SS, Schusterman MA, Reece GP, et al. Abdominal wall strength,
bulging, and hernia after TRAM flap breast reconstruction. Plast
Reconstr Surg 1995;96(3):616–619.
27. Nahabedian MY, Momen B, Galdino P, et al. Breast reconstruction with
the free TRAM or DIEP flap: patient selection, choice of flap, and
outcome. Plast Reconstr Surg 2002;110:466–475; discussion 476–477.
28. Hartrampf CR. The transverse abdominal island flap for breast
reconstruction. A 7-year experience. Clin Plast Surg 1988;15:703–716.
29. Blondeel N, Vanderstraeten GG, Monstrey SJ, et al. The donor site
morbidity of free DIEP flaps and free TRAM flaps for breast
reconstruction. Br J Plast Surg 1997;50:322–330.
30. Chang DW, Wang B, Robb GL, et al. Effect of obesity on flap and
donor-site complications in free transverse rectus abdominis
myocutaneous flap breast reconstruction. Plast Reconstr Surg
2000;105:1640–1648.
31. Watterson PA, Bostwick J 3rd, Hester TR Jr, et al. TRAM flap anatomy
correlated with a 10-year clinical experience with 556 patients. Plast
Reconstr Surg 1995;95:1185–1194.
32. Kroll SS, Gherardini G, Martin JE, et al. Fat necrosis in free and
pedicled TRAM flaps. Plast Reconstr Surg 1998;102:1502–1507.
CHAPTER 76

Superior Gluteal Artery Perforator


Flap (SGAP)
ASEEL SLEIWAH | GIOVANNI ZOCCALI | JIAN FARHADI
HISTORY
The use of the gluteal area as a donor site to reconstruct breast tissue has
tempted surgeons for many years due to its shape and the quality of fatty
substance. In 1973, Orticochea described a technique to reconstruct an
irradiated breast using the buttock area in a five-staged procedure (1).
However, free microvascular transfer has changed our approach of
reconstruction. Fujino et al. reported the use of free myodermal gluteus
maximus flap to correct unilateral chest wall and breast aplasia (2).
Harvesting the gluteus maximus muscle within the flap adds many
disadvantages to both donor-site morbidity and the flap profile. Gluteus
muscle is a powerful hip extensor and sacrificing it may cause functional
problems. From the aesthetic point, it may cause contour deformity. There is
also unjustified risk of damage to the sciatic nerve during the flap harvest.
The vascular pedicle length is compromised by the intramuscular course of
the artery and the bulk of the muscle.
Understanding the concept of perforator-based flaps decreased the
aesthetic and functional morbidities to the donor site and enhanced the flap
usage by sparing the muscle and increasing the pedicle length.
In 1993, Koshima et al. reported using a pedicled fasciocutaneous flap
based on gluteal parasacral perforators to reconstruct a sacral pressure ulcer
(3). Allen and Tucker applied the same principles to harvest a free
fasciocutaneous flap based on the superior gluteal artery in 1995 (4). Further
refinement of the flap was achieved by identifying the dorsal branches of the
lumbar segmental nerves during flap harvest and joining them to the anterior
ramus of the 4th intercostal nerve in order to achieve early sensory recovery
(5).
INDICATIONS
The modalities and choices available to reconstruct breast tissue have
increased dramatically following advances in microsurgical techniques.
Autologous reconstruction of the breast has never been more popular due to
the abundance of available choices and further training to perform such
complex procedures. The deep inferior epigastric artery (DIEP) flap remains
the workhorse flap and the first choice to consider. There are a multitude of
reasons behind its popularity. From the technical point, there is no need to
reposition the patient during the procedure. Hence, simultaneous mastectomy
and recipient site preparation can be done while the flap is raised. Surgeons
are also more familiar with the anatomy of the abdominal wall which is less
complex than that of the gluteal area. Thus, less time is required to harvest
the flap and the overall surgery time is reduced compared to the superior
gluteal artery perforator (SGAP) flap. From the patient’s perspective, losing
extra tissue from the abdomen is an appealing option for a multiparous
woman with saggy abdomen and it comes with a relatively low cost. The scar
is hidden in the bikini line. Additionally, the downtime following DIEP flap
reconstruction is less when comparing patients reconstructed with types of
autologous reconstruction (6–13).
However, the SGAP flap is increasingly chosen as an alternative option
when the use of abdominal tissue is not feasible. The quality of fat available
in the buttock area allows good projection of the reconstructed breast (14). It
has also relatively low donor-site complications and a concealed scar beneath
the underwear.
Flaps based on the superior gluteal artery are more preferred than those
based on the inferior gluteal artery as the latter requires exposure of the
sciatic nerve which adds unnecessary operative risks to the patients (15). It
also obliterates the natural curvature of the buttock which is hard to replicate.
Common indications include:
Limited abdominal donor-site tissue especially for bilateral breast
reconstruction.
Previous abdominal wall surgery, for example, abdominoplasty.
However, this is not an absolute contraindication to DIEP flap
reconstruction (16).
Abdominal scars that preclude flap harvest due to previous injury to the
flap pedicle.
Patient choice.
Loss of a previous abdominal flap.
Patient selection is of prime importance. Classification of patients
according to donor-site availability has proven effective. The donor site can
be classified into four classes:
1. Minimal tissue availability.
2. Tight closure and insufficient tissue to achieve breast symmetry.
3. Sufficient tissue for tension-free closure and contralateral symmetry.
4. Patient experienced massive weight loss (17,18).
Patients with class three donor site are the best candidates for breast
reconstruction using the SGAP flap, as they have better outcomes in terms of
satisfaction from reconstruction and lower rates of donor-site complications.
This is due to the fact that patients with more donor-site tissue have better
size and shape match compared to the contralateral breast with less secondary
procedures and less tension on donor-site closure, hence less donor-site
complications. Patients with class four require more revisional surgery to
symmetrise the breasts.
CONTRAINDICATIONS
The contraindications to breast reconstruction using the SGAP flap include
those related to autologous free tissue transfer and those peculiar to the
SGAP flap. General contraindications include multiple complex medical
comorbidities that render free tissue transfer a risky operation, patient choice
to undergo implant-based reconstruction instead of autologous reconstruction
or choice to undergo reconstruction from other donor sites. Inadequate
surgical expertise is not a reason to deny patients from reconstructive options.
In the United Kingdom, all the patients should be offered autologous
reconstruction regardless of their location. Contraindications peculiar to the
SGAP flap include inadequate tissue to achieve tension-free closure of the
donor site and previous procedures to the buttock area. Liposuction is also
not an absolute contraindication (16). Other reasons for exclusion include
procedures like gluteal implant augmentation and filler injection to the
buttock area.
PREOPERATIVE PLANNING
Anatomical identification of perforators by performing computerized
tomography CT scan can be used as an adjunct to facilitate surgical planning.
This is especially true in patients who had previous surgery or liposuction to
the area. Typically, there are four to five perforators supplying the flap.
However, the flap is reliably raised on a single perforator in the vast majority
of patients (14,18).
Some argue that imaging may also decrease the operative time, though
preoperative mapping of perforators by magnetic resonance imaging (MRI)
has no proven benefit in reducing operative time and in planning for surgery.
A study conducted by the senior author randomized 62 patients to two
groups. One group underwent MRI for mapping of the perforators, the second
group underwent Doppler ultrasonography. The study showed no significant
difference in operative time between the two groups (19).
Preoperative marking of the flap is performed both with the patient
standing and on the operating table. In the standing position, the vectors of
skin laxity are determined, skin paddle is designed, and the area of
perforators is marked considering the aesthetic subunits of the buttock. On
the operating table, Doppler ultrasonography is used to mark the most lateral
perforator and minor adjustments to the skin paddle are performed. This
approach ensures best cosmetic results to the donor site. To locate the
perforators’ area, a line is drawn joining posterior superior iliac spine and the
coccyx. A second line is drawn bisecting the first line and extending to the
greater trochanter. This line represents the direction of piriformis muscle. The
superior gluteal artery emerges above this muscle. The third line is drawn
from the posterior superior iliac spine to the greater trochanter (Fig. 76-1).
The superior gluteal artery enters the buttock at the junction of the proximal
and middle third of this line. Hence, the area lateral to that is the best place to
locate the perforators (14,18). More lateral perforators are preferred to
increase pedicle length which can reach up to 12 cm. It is important to
maximize the length of the pedicle to give the surgeon more freedom to inset
the flap, to obtain more natural ptotic appearance of the reconstructed breast
and for easier anastomosis to the recipient vessels.
It is crucial to plan the number of operative repositioning, the steps of flap
raising, donor-site closure, and microvascular anastomoses before embarking
on the procedure and to clearly delegate duties among team members. This
will depend on whether the reconstruction is immediate or delayed following
the oncologic procedure and whether it is a unilateral or bilateral
reconstruction.

FIGURE 76-1 Diagram showing anatomical landmarks for SGAP flap planning.

The senior author prefers the following sequence of steps during the
procedure.
Immediate unilateral breast reconstruction: The patient is placed in supine
position; the oncologic resection is done first followed by the exposure of
the internal mammary vessels (IMVs). The patient is then turned prone to
harvest the flap. During donor-site closure, the flap is shaped on a
separate table by another surgeon to attain the appearance of a prosthetic
breast implant and further preparation of vessels is performed. The patient
is turned again to supine position to perform the flap inset and
microvascular anastomoses. In selected patients, the procedure can start
on lateral position to enable mastectomy and flap harvest at the same
time, then the donor site is closed, and patient is turned to supine position
to perform the microvascular anastomoses and flap inset.
Delayed unilateral breast reconstruction: To minimize theatre time and
decrease risk from frequent positioning, the flap is raised first with the
patient in prone position, then turned to supine position to prepare the
IMVs and perform flap inset and microvascular anastomoses. During
donor-site closure, the flap is shaped as described above and further
microsurgical preparation of the flap pedicle is performed.
Immediate bilateral breast reconstruction: The procedure starts by
oncologic resection on both sides followed by preparation of recipient
vessels using the microscope assistance. The patient is then turned to
prone position to harvest the flap on both sides followed by donor-site’s
closure. The patient is then turned to supine position and microvascular
anastomosis is completed.
Delayed bilateral reconstruction: The procedure starts on prone position
by harvesting both flaps and the donor sites are closed. The patient is then
turned to supine position and the IMVs are prepared while the flap is
shaped by another surgeon.
OPERATIVE TECHNIQUE
The following represents the senior author’s account for a unilateral delayed
breast reconstruction. The patient is placed in prone position. The lateral
position is equally good, both provide good exposure. Some surgeons prefer
infiltration with local anesthetic and epinephrine (14). However, the senior
author does not prefer using infiltration around the flap to prevent oozing and
obliteration of the surgical field. Initially, the incision is made all around the
flap. The dissection is bevelled both on the cranial and caudal sides to harvest
good quality and volume of adipose tissue which will be the future lower and
upper pole of the reconstructed breast, respectively. The superior margin of
the flap is dissected down to the fascia in a sharper angle whereas the inferior
one follows a 45-degree angle. This allows to recruit more fat with
preservation of the contour of the gluteal area (Fig. 76-2). If more tissue is
required to reconstruct the lower pole, then we prefer harvesting the flap from
the contralateral side. This is especially true in cases of delayed
reconstruction.
Dissection is performed using monopolar diathermy on medium power
setting (40 W). When the fascia covering the gluteus muscle is reached,
incisions are made around the fascia and the flap dissection is performed in a
subfascial layer. Ideally, complete muscle relaxation should be achieved
during this stage to facilitate dissection, identification of the perforators, and
to prevent muscle twitching and injury to the perforator. The flap is dissected
off the gluteus muscle starting from the medial side. When the area of
perforators is encountered, dissection is performed using bipolar diathermy
on a very low setting (20 W). The aim is to dissect the perforators in the
length of the muscle perimysium and visualize the anatomy of the perforator.
At this stage, the main surgeon performs the procedure without assistance to
be able to adjust the tension on the released tissue. When the perforators are
encountered, dissection is interchanged between scissors and bipolar forceps
aiming to release all the fasciae surrounding the perforators (Fig. 76-3). This
approach will eventually isolate the perforators without risking injury to the
pedicle. Once the anatomy of the desired perforator is delineated, the flap is
dissected completely off the gluteus muscle and the rest of perforators are
disconnected to prevent unnecessary traction on the selected one. The
intramuscular course is then followed; to aid dissection, a self-retained
retractor is used to gradually open the space and avoid tension on the flap
pedicle; this dissection is extended below the sacral fascia.

FIGURE 76-2 Diagram showing fat recruitment during flap harvest.


FIGURE 76-3 Photograph showing intramuscular perforator dissection using the
bipolar forceps.

When the sacral fascia is opened, the origin of the superior gluteal artery
and vein is identified as they emerge above the piriformis muscle. Here, the
vessels lie in adipose tissue with many branches and tributaries. Suction
device is used to have better visualization of the pedicle by performing open
liposuction of the surrounding fat. A common mistake is to stop dissection
early due to the technical difficulty encountered in this area. To avoid this
problem, careful dissection is required using microscope assistance to have
better visualization of the side branches and achieve good hemostasis. The
microscope assistance allows not only better magnification but also perfect
illumination of the operating field (Fig. 76-4).
The flap is then disconnected, and the donor site is closed with a suction
drain left in situ. The length of pedicle is usually 6 to 8 cm. However, a
pedicle length of 12 cm can be achieved by following the artery course to the
gluteal fat pad (14,18). The diameter of the artery is between 2 and 4.5 mm.
The diameter of the vein is between 2.5 and 4.5 mm (9,14,18). The use of
grafts is unusual. However, if needed then the inferior epigastric vessels are
our preferred option (18).
Additional shaping and preparation of the flap pedicle is performed under
the microscope assistance while the donor site is closed.
During this stage, the flap edges are softened, deepithelialization is
performed, and excessive tissue is debrided; the flap is shaped mimicking a
prosthetic breast implant. The patient is placed in supine position and the
IMVs are prepared following removal of the 3rd costal cartilage. Due to its
short pedicle, the flap inset in the chest is performed before the anastomoses.
When satisfactory inset has been achieved, the medial edge of the flap is
retracted laterally exposing the pedicle. Here, the pedicle is laid over the
IMVs to allow the microsurgical anastomoses.

FIGURE 76-4 Photograph showing pedicle dissection under microscope assistance.

No further shaping is attempted following the microvascular anastomosis


to prevent avulsion of the pedicle. Fibrin glue is used to secure the pedicle if
there is too much movement that risks avulsion of pedicle. A negative
pressure drain is used, and the skin is closed using absorbable suture material.
INTRAOPERATIVE CARE
Good communication among theatre staff is crucial during the operation. This
is especially important to ensure safe positioning of the patient, facilitation of
the procedure, and to minimize theatre time. The patient receives a standard
care for all free tissue transfer operations. This include a dose of intravenous
antibiotics at induction followed by two postoperative intravenous doses,
regular temperature monitoring and control to avoid hypothermia, blood
pressure monitoring and control and urinary output measurements,
maintenance of a well-balanced intravascular volume, evaluation of lactate
levels, and arterial blood gas analysis. Venous thromboprophylaxis is
provided with antiembolic stockings and inflatable mechanical pump devices.
Further pharmacologic thromboprophylaxis is warranted according to
preoperative assessment and degree of bleeding during the operation. Also,
continuous care and protection for pressure areas is required by the use of
appropriate appliances and pillows. Maintenance of maximum muscle
relaxation is required during flap harvest as described earlier in the chapter.
POSTOPERATIVE CARE
The enhanced recovery programmed is followed in the postoperative period.
This strategy emphasizes multimodal analgesia, early oral intake, early
mobilization, and a well-balanced intravenous fluid management (20,21).
Oral fluids are started as soon as possible aiming to stop intravenous fluids.
The fluid therapy is guided by maintaining a urine output of more than 0.5
mL/kg/hr and a mean arterial pressure of more than 60 to 70 mm Hg.
Adequate analgesia is administered regularly. The patient should be warmed
for the first 24 hours using a warmer blanket. Antiemetics and proton pump
inhibitors are given during the hospital stay. Pharmacologic venous
thromboprophylaxis is given 6 hours following the procedure.
A standard flap monitoring protocol is followed which includes clinical
monitoring of the flap color, temperature, texture, and capillary refill time.
Handheld Doppler device is used to monitor the perforator. Other adjuncts
can be used to monitor the flap, for example, venous coupler flow monitoring
device. Initially, the flap observations are recorded every hour for the first 24
hours. Routine blood tests are performed in the first postoperative day to
check the hemoglobin levels and the renal function. Patients are encouraged
to mobilize in the first postoperative day. No hip flexion is allowed for more
than 30 degrees. The patient can sit in the second postoperative day.

CASE 1

• A 45-year-old woman who underwent bilateral skin-sparing


mastectomies and immediate reconstruction with bilateral SGAP flap
(Fig. 76-5)
FIGURE 76-5 A 45-year-old woman who underwent bilateral mastectomies
and immediate reconstruction with bilateral SGAP flaps.

• A 53-year-old woman underwent bilateral SGAP flap reconstruction of


her breasts. On the right side she had delayed SGAP flap following
mastectomy. After genetic counselling she underwent left prophylactic
mastectomy and immediate reconstruction (Fig. 76-6)
FIGURE 76-6 A 53-year-old woman following bilateral SGAP flap
reconstruction of her breasts. Delayed reconstruction on the right side and
immediate reconstruction on the left side.

• A 47-year-old woman with right breast cancer underwent skin-sparing


mastectomy and immediate reconstruction with SGAP flap (Fig. 76-7)
FIGURE 76-7 A 47-year-old woman with right breast cancer underwent
skin-sparing mastectomy and immediate reconstruction with SGAP flap
(postoperative at 2 months).
GENERIC RISKS
Microsurgical free tissue transfer is a highly demanding procedure with a
prolonged anesthetic time. Hence, both anesthetic and surgical consequences
can be dramatic. Anesthetic complications include the risk of venous
thromboembolism, postoperative nausea and vomiting, allergies to anesthetic
agents, aspiration, and pneumonia. Immediate surgical complications include
bleeding. This is especially serious during flap harvest at the gluteal fat pad.
The vessels here are branching and the operative filed is tight with poor
illumination. One possible solution to avoid this problem is to perform the
dissection using the microscope assistance as explained earlier in this chapter.
This will provide both magnification and illumination of the surgical field.
Other surgical complications include risk of flap failure which can be partial
or total loss. Partial flap loss is defined as partial loss of skin and
subcutaneous fat and is usually very low <2% (18). The reported success rate
of the SGAP flap in most published series is high (see under outcomes).
The risk of fat necrosis is small. This is because the SGAP flap has a good
blood supply network and does not exhibit the preferential zones of perfusion
when compared to the DIEP flap. In our experience of 134 flaps, the risk of
fat necrosis was 3.7% (five patients). Werdin et al. reported fat necrosis in 3
out of 30 patients (10%) (22).
The risk of flap infection is less than 1% and recipient site hematoma is
approximately 2% (18).
DONOR-SITE COMPLICATIONS
In our series of 134 flaps, the risk of seroma in the donor site was 8.9% (12
patients) (18). However, the reported donor-site seroma is variable; Guerra et
al. reported a seroma rate in 2% (3 out of 136) of his patients whereas Werdin
reported donor-site seroma in 8 patients (27%), one of whom required
surgical intervention (15,22). Another problem that can be encountered is
contour deformity. Careful selection of patients is required to avoid such
complication. Approximately one in ten patients will report donor-site
deformity in the postoperative period (18).
Other donor-site complications include superficial surgical site infection
which is estimated to be around 3%, dog-ear deformity 6.7%, wound
breakdown <1%, and scar hypertrophy <1% (18).
OUTCOMES
The SGAP flap, like all perforator-based flaps, requires a steep learning curve
from the technical point. Despite that it is more technically challenging than
the DIEP flap, the results remains comparatively good in experienced hands.
Yaghoubian et al. compared the results of DIEP versus SGAP performed
by a single surgeon. He examined 16 SGAP flaps and 24 DIEP flaps. The
SGAP group required slightly longer operative time. However, take-back and
the survival rates were similar. Success rate was 100% in their series (23).
For bilateral breast reconstruction, Hamdi et al. published results for
reconstruction of 106 breasts. Eight of the reconstructions were performed
using the SGAP flap while the remainders were performed using DIEP flaps.
They reported one flap necrosis in each group. However, the SGAP flap
failure was attributed to poor recipient vessels’ quality rather than choice of
the flap. The authors performed bilateral SGAP simultaneously for one
patient only while the remainder underwent secondary reconstruction 6
months following the first operation due to prolonged theatre time (24).
DellaCroce et al. published a review of 40 SGAP flaps for simultaneous
bilateral breast reconstruction in 20 patients. There was no flap failure in this
study and the authors limited the surgical time by minimizing the number of
repositioning. The average operative time was 7 hours and 47 minutes (25).
Werdin et al. reviewed the outcomes of 30 SGAP for bilateral breast
reconstruction in 15 women. The reported success rate was 97% with 3 flaps
undergoing fat necrosis. The average operative time was 7 hours and 12
minutes. The same group published later the outcomes of 81 SGAP flaps’
reconstruction. Thirty-nine of those flaps were for bilateral breast
reconstruction and the remainder for unilateral reconstruction. The overall
success rate was 93% (6 flaps were lost). The average operating time was 7
hours and 36 minutes. Surgical revision of the donor site was 6% (22,26).
In a critical analysis of 136 cases of SGAP, Guerra et al. reported a success
rate of 98%. Only 3 flaps have failed in this series—one due to avulsion of
the pedicle, a second due to arterial thrombosis, and a third one due to venous
thrombosis. Two further flaps underwent partial necrosis. Their overall
reported take-back rate was 8% with an overall complications’ rate of 18%
(15).
Feller et al. published their series of 52 SGAP flaps with a success rate of
92.3% (27).
In our experience, we have conducted a study examining our outcomes in
119 patients (134 flaps) reconstructed with SGAP flap. Five flaps were lost
(success rate of 96.3%). Vein grafts were used only in 4 patients. One
required both arterial and venous grafts harvested from the deep inferior
epigastric vessels. Partial flap necrosis occurred in 2 patients (1.4%). Our
average flap-raising time was 4.1 hours. The mean ischemia time for a
unilateral case was 76 minutes while the mean ischemia time for bilateral
cases was 141 minutes (18).
Patient with class three donor site had good satisfaction and less donor-site
comorbidities compared to other classes. The complications’ rate for patients
undergoing immediate breast reconstruction following neoadjuvant therapy is
not usually increased and does not lead to delay of adjuvant therapy (28).
CONCLUSION
Autologous breast reconstruction is the gold standard to replace breast tissue
when possible. The SGAP flap emerges as a well-tolerated flap with high
success rate and a reasonable complications’ rate. Patient selection plays a
central role for successful outcome and the technical difficulties can be
overcome by a steep learning curve. For many surgeons, the SGAP flap is the
second choice for autologous reconstruction when the abdominal tissue is
unavailable or fails to achieve the desired results.

REFERENCES

1. Orticochea M. Use of the buttock to reconstruct the breast. Br J Plast


Surg 1973;26(3):304–309.
2. Fujino T, Harasina T, Aoyagi F. Reconstruction for aplasia of the breast
and pectoral region by microvascular transfer of a free flap from the
buttock. Plast Reconstr Surg 1975;56(2):178–181.
3. Koshima I, Moriguchi T, Soeda S, et al. The gluteal perforator-based
flap for repair of sacral pressure sores. Plast Reconstr Surg
1993;91:678–683.
4. Allen RJ, Tucker C Jr. Superior gluteal artery perforator free flap for
breast reconstruction. Plast Reconstr Surg 1995;95(7):1207–1212.
5. Blondeel PN. The sensate free superior gluteal artery perforator (S-
GAP) flap: a valuable alternative in autologous breast reconstruction. Br
J Plast Surg 1999;52(3):185–193.
6. McAllister P, Teo I, Chin K, et al. Bilateral breast reconstruction with
abdominal free flaps: a single centre, single surgeon retrospective review
of 55 consecutive patients. Plast Surg Int 2016;2016:6085624.
7. Keller A. The deep inferior epigastric perforator free flap for breast
reconstruction. Ann Plast Surg 2001;46(5):474–479; discussion 479–
480.
8. Guerra AB, Metzinger SE, Bidros RS, et al. Bilateral breast
reconstruction with the deep inferior epigastric perforator (DIEP) flap:
an experience with 280 flaps. Ann Plast Surg 2004;52(3):246–252.
9. Hamdi M, Weiler-Mithoff EM, Webster MHC. Deep inferior epigastric
perforator flap in breast reconstruction: experience with the first 50
flaps. Plast Reconstr Surg 1999;103:86–95.
10. Blondeel N, Vanderstraeten GG, Monstrey SJ, et al. The donor site
morbidity of free DIEP flaps and free TRAM flaps for breast
reconstruction. Br J Plast Surg 1997;50(5):322–330.
11. Zoccali G, Rais DS, Farhadi J. How does autologous breast
reconstruction impact downtime? J Reconstr Microsurg
2018;34(7):530–536.
12. Rolph R, Mehta S, Farhadi J. Breast reconstruction: options post-
mastectomy. Br J Hosp Med (Lond) 2016;77(6):334–342.
13. Farhadi J, Pierer G. Breast reconstruction with flaps from the abdomen.
European Surgery 2007;39(4):216–226.
14. Gagnon AR, Blondeel PN. Superior gluteal artery perforator flap. Semin
Plast Surg 2006;20(2):79–88.
15. Guerra AB, Metzinger SE, Bidros RS, et al. Breast reconstruction with
gluteal artery perforator (GAP) flaps: a critical analysis of 142 cases.
Ann Plast Surg 2004;52(2):118–125.
16. De Frene B, Van Landuyt K, Hamdi M, et al. Free DIEAP and SGAP
flap breast reconstruction after abdominal/gluteal liposuction. J Plast
Reconstr Aesthet Surg 2006;59(10):1031–1036.
17. Alamouti R, Hachach Haram N, Farhadi J. A novel grading system to
assess donor site suitability in autologous breast reconstruction. J Plast
Reconstr Aesthet Surg 2015;68:e129–e130.
18. Zoccali G, Mughal M, Giwa L, et al. Breast reconstruction with superior
gluteal artery perforator free flap: 8 years of experience. J Plast
Reconstr Aesthet Surg 2019;72(10):1623–1631.
19. Zoccali G, Mughal M, Roblin P, et al. Preoperative perforator mapping
in SGAP flap, does the MRI make the difference? Plast Reconstr Surg
2019;144(4):812–819.
20. Temple-Oberle C, Shea-Budgell MA, Tan M, et al. Consensus review of
optimal perioperative care in breast reconstruction: ENHANCED
Recovery after Surgery (ERAS) Society recommendations. Plast
Reconstr Surg 2017;139(5):1056e–1071e.
21. Arezoo A, Temple-Oberle C, Markus N, et al. An enhanced recovery
after surgery pathway for microvascular breast reconstruction is safe and
effective. Plast Reconstr Surg Glob Open 2018;6(1):e1634.
22. Werdin F, Peek A, Martin NC, et al. Superior gluteal artery perforator
flap in bilateral breast reconstruction. Ann Plast Surg 2010;64(1):17–21.
23. Yaghoubian A, Boyd JB. The SGAP flap in breast reconstruction:
backup or first choice? Plast Reconstr Surg 2011;128(1):29e–31e.
24. Hamdi M, Blondeel P, Van Landuyt K, et al. Bilateral autogenous breast
reconstruction using perforator free flaps: a single center’s experience.
Plast Reconstr Surg 2004;114(1):83–89; discussion 90–92.
25. DellaCroce FJ, Sullivan SK. Application and refinement of the superior
gluteal artery perforator free flap for bilateral simultaneous breast
reconstruction. Plast Reconstr Surg 2005;116(1):97–103; discussion
104–105.
26. Baumeister S, Werdin F, Peek A. The SGAP flap: rare exception or
second choice in autologous breast reconstruction? J Reconstr
Microsurg 2010;26(4):251–258.
27. Feller AM, Richter-Heine I, Rudolf KD. The superior gluteal artery
perforator flap (S-GAP-Flap). Handchir Mikrochir Plast Chir
2002;34(4):257–261.
28. Zweifel-Schlatter M, Darhouse D, Roblin P, et al. Immediate
microvascular breast reconstruction after neoadjuvant chemotherapy:
complication rates and effect on start of adjuvant treatment. Ann Surg
Oncol 2010;17(11):2945–2950.
CHAPTER 77

DIEP Flap Breast Reconstruction With


Sensory Neurotization
MINAS CHRYSOPOULO | OSCAR OCHOA | STEVEN PISANO | PETER LEDOUX | GARY
ARISHITA | RAMON GARZA | CHET NASTALA
HISTORY
Most practices proficient in autologous tissue transfer techniques consider the
deep inferior epigastric perforator (DIEP) flap to be the gold standard for
breast reconstruction. Abdominal-based microsurgical tissue methods are
preferred in general secondary to superior aesthetic results with low
morbidity, even in higher-BMI patients (1). Benefits include a soft, warm,
“natural” result; the ability to achieve optimal symmetry with the opposite
native breast, and a “durable” result that is maintained, or even improves,
over time. Additionally, in striving to adhere with the fundamental plastic
surgery axiom of “replacing like with like,” abdominal-based reconstruction
potentiates sensate recovery with the addition of sensory microneurorrhaphy
upon flap transfer (2–4). Superior vascular perfusion and the avoidance of an
upper epigastric bulge secondary to muscle tunneling are additional benefits
over the traditional pedicled TRAM flap.
The DIEP flap (with or without sensory neurotization) offers flexibility in
breast reconstruction and can be used for primary and secondary
reconstructions (to salvage a failed implant or other nonabdominal flap
procedure), in cases in which the chest wall has been irradiated, and in
circumstances in which the residual native breast skin-chest wall envelope is
exceedingly thin or absent following extensive tissue resection (Figs. 77-1 to
77-3). Use of the DIEP flap allows one to avoid the pitfalls of tissue expander
implant reconstructions: infection, malposition, contracture, deflation, and
infection (5), particularly when breast cancer treatment includes radiation
therapy. Implant reconstruction patients often require multiple procedures
aimed at maintaining the breast mound. Furthermore, long-term resource
costs associated with a tissue expander/implant reconstruction may be higher,
depending on practice location and surgeon experience and preference, than
those associated with a DIEP flap reconstruction (6–8). The DIEP flap also
offers the potential advantage of improvement in the contour of the
abdominal wall: elimination of soft tissue excess, correction of lower
abdominal musculofascial laxity, and repair of epigastric rectus diastasis.
Indeed, higher-BMI patients may preferentially benefit from such
improvements in abdominal wall aesthetics without a relative increase in risk
regarding abdominal morbidity (1). Contour abnormalities, however, may
result; the rate of donor-site complications such as lower abdominal fascial
bulging and even hernia generally speaking increase with the number of
previous abdominal surgeries (9–14).

FIGURE 77-1 Delayed right breast reconstruction following modified radical


mastectomy and chest wall radiation therapy (A: preop; B: postop).

FIGURE 77-2 Failed right breast implant reconstruction with significant breast
asymmetry and attenuation of the right breast skin envelope (A: preop; B: postop).

Neurotization of autologous flaps for restoration of sensory function


represents a significant advancement in breast reconstruction. Indeed,
increased reconstructed breast sensibility following neurotization (15–19) has
been associated with improved quality-of-life measures in recent studies
(20,21). Given the sensory neuronal density of the infraumbilical abdominal
wall (22), restoration of breast sensation may be readily achieved through
coaptation of the anterior branch of the 3rd or 4th intercostal nerves and a
segmental sensory nerve harvested during flap elevation (23). While we have
been performing sensory neurotization of our DIEP flap breast
reconstructions routinely in our practice for many years, direct autologous
sensory nerve coaptation is not possible in some patients due to insufficient
length of the segmental sensory nerve harvested with the abdominal flap, or
rarely, a lack of an identifiable, adequate sensory nerve during perforator
dissection. In the former cases, use of a nerve allograft to bridge the gap
between the recipient and donor sensory nerves has proven efficacious
(23,24).
Minimizing donor-site morbidity and the sequential evolution of technique
to spare muscle sacrifice (from pedicled TRAM to DIEP flap) with the
potential for neurotization has further improved the balance of risk and
benefit in favor of muscle-sparing, free tissue transfer. However, many
factors contribute to implants remaining the preferred reconstructive method
across the country. The need for microsurgical training, the overall
complexity of the operation, the mental and physical demands on the
operative team, the need for a team approach, and declining reimbursement
are all factors which favor the tertiary academic centers or large specialized
niche group private practices, both of which take years to develop. However,
identification of the factors contributing to the underutilization of these and
other flaps allows for design and implementation of surgical and clinical
pathways that increase efficiency and improve clinical outcomes (25).

FIGURE 77-3 Failed left breast implant reconstruction with significant breast
asymmetry and deficit in left breast skin envelope (A: preop; B: postop).
INDICATIONS AND PATIENT SELECTION
In our practice, patients range in age from young to old (21 to 78 years) and
in body types ranging from thin to obese (body mass index 17 to over 40).
Approximately 41% of our patients are obese or morbidly obese (BMI ≥30).
We have performed breast reconstruction in primary, secondary (after
previous failed reconstruction), and tertiary (after multiple failed
reconstructions) settings; in smokers; in patients with significant past medical
histories (typically diabetes and/or hypertension) and significant surgical
histories (multiple previous abdominal procedures); following breast and/or
chest wall radiation; and even following kidney and heart transplant surgery.
While this may read like a laundry list of “who not to operate on” we feel that
microsurgical breast reconstruction offers the best option for these patients as
it typically allows for transfer of a larger volume of well-vascularized,
potentially sensate tissue and is associated with fewer complications than
other reconstructive options in experienced hands. Perforator flap
reconstruction with neurotization is now the preferred method of breast
reconstruction in our practice due to the lower donor-site morbidity, although
tissue expander/implant reconstructions are also performed in patients who
are not candidates for a flap reconstruction, who do not want additional
scarring, wish to avoid the risk of donor-site morbidity, or who simply favor
an “implant look.”
CONTRAINDICATIONS
Absolute contraindications to free tissue transfer include a known history of
hypercoagulability or bleeding diathesis that cannot be corrected medically,
and prior abdominoplasty with prior elevation of the abdominal apron.
Medical comorbidities such as uncontrolled hypertension, poorly controlled
diabetes, and a refusal to begin an immediate smoking cessation program are
also strong relative contraindications. We have performed abdominal flap
procedures on patients who have had multiple abdominal surgeries with
resultant suprapubic, midline, and/or subcostal incisions; however, one must
realize that measures must be taken to mitigate risk, such as
discontinuous/limited undermining, and consideration of the use of
preoperative CT angiography for evaluation of perforator size, location, and
branching patterns.
PREOPERATIVE PLANNING AND OPERATIVE
TECHNIQUE
Successful breast reconstruction depends heavily on planning every step of
the patient’s clinical pathway, starting with setting appropriate expectations
of the reconstructive process at the initial consultation. Promoted by a shared
decision-making process and based on the patient’s individual goals, the
optimal reconstructive modality is selected and thoroughly reviewed with the
patient and their supporting network.
Subsequently, prior to surgery, expectations are reinforced and patient
education is completed by our nursing staff at the corresponding preoperative
appointment. In this setting, preoperative components of our Enhanced
Recovery After Surgery (ERAS) protocol, integrated into our practice several
years ago, are initiated. Based on our experience and previous studies
(26,27), ERAS pathways in breast reconstructive surgery have been shown to
decrease postop pain and opioid use, hasten return to ambulation and normal
diet, decrease hospital length of stay, shorten overall recovery, and improve
patient outcomes in general.
Beginning the morning before surgery, our regimen of celecoxib,
gabapentin, and acetaminophen ensures a strong foundation of pain control is
already in place before surgery begins. During surgery, we perform long-
acting local anesthetic blocks (pectoral nerve blocks in the chest and
transversus abdominis plane [TAP] blocks in the abdomen) with liposomal
bupivacaine. Narcotics are usually only used for breakthrough pain during the
first few postoperative days. We have found since implementing our ERAS
protocol, narcotic medications are rarely necessary beyond the initial
postoperative period.
An operating room consisting of well-trained, motivated personnel and
well-maintained, high-quality equipment is essential. A high priority is
placed on assembling surgical technicians and circulating nurses who can
perform all methods of breast reconstruction and, especially in our practice,
perforator flap procedures. Ideally, as the same relatively few personnel
participate in flap reconstructions, skill and efficiency improve. Similarly,
assembling a small core group of anesthesiologists who are willing and able
to perform special tasks during the procedure is helpful. Key functions
include: establishing and maintaining dense muscle paralysis to permit rapid,
safe flap harvest; maintaining euvolemia to avoid vasospasm; controlling
blood pressure; keeping the patient warm; extubating the patient smoothly
and painlessly; and preventing postoperative nausea and vomiting.
The precise boundaries of the breast are marked preoperatively with the
patient in a sitting position, highlighting the inframammary fold (IMF) and
medial, lateral, and superior extent of the breast parenchyma (Fig. 77-4). A
skin-sparing or nipple-sparing mastectomy pattern is marked for all patients
undergoing reconstruction except in cases when this isn’t possible for
oncologic reasons. Excellent communication preoperatively and a
collaborative approach with the breast surgeon is key in ensuring optimal
planning and results.

FIGURE 77-4 Preoperative markings outlining the boundaries of the breast. A


vertical radial mastectomy incision, incorporating a short periareolar extension if
required, provides very good access to the entire breast parenchyma and axilla while
allowing for a vertical mastopexy at the revision stage without additional scarring.

For skin-sparing patients with grade I to grade II ptosis a periareolar or


vertical mastopexy/reduction pattern (Fig. 77-4) is often used. For grade III
ptosis a Wise pattern is considered. For nipple-sparing patients, IMF or
vertical mastectomy incisions are utilized preferentially. In patients with mild
to moderate ptosis, the vertical incision with a partial periareolar extension (if
needed) provides full access to the entire breast parenchyma and axilla while
setting the stage for a vertical mastopexy at a subsequent surgery. By 3
months following the initial reconstruction, the nipple areolar complex is
fully perfused via neovascularization from the underlying DIEP flap which
allows for a full periareolar incision and mastopexy (28).
In our practice, the plastic surgeon or plastic surgery physician assistant
(PA) usually assists the breast surgeon performing the mastectomy. The
breast surgeon is encouraged to respect the boundaries of the breast,
especially the IMF, and to keep the skin flaps of appropriate thickness to
preserve perfusion. Two microsurgeons are involved in every free flap
procedure. Whenever possible, DIEP flap harvest begins at the same time as
the mastectomy. Following the mastectomy, the remaining portions of the
DIEP flap harvest and exploration and dissection of the recipient vessels
proceed simultaneously.
Chest wall preparation begins with assessment of possible bleeding sites
from the mastectomy site and axilla in cases involving axillary lymph node
sampling. Small perforating vessels from the serratus musculature and upper
rectus musculature at the IMF, and the axilla are often the source of unwanted
postoperative bleeding when it occurs. Recreation of the IMF landmarks and
lateral boundary of the breast will be necessary after the mastectomy if these
have not been respected in order to recreate an aesthetic inferolateral breast
envelope curvature and achieve the best possible cosmetic result. During this
time, as a possible alternative recipient nerve (29), the lateral cutaneous
branch of the 4th intercostal sensory nerve is sought and isolated if not
extensively cauterized during the mastectomy. We encourage our breast
surgeons to spare this nerve whenever possible. A single drain is usually
sufficient to minimize the possibility of postoperative seroma even if nodal
dissection was performed, in which case the drain is draped laterally to
include the axilla.
We prefer to use the internal mammary vessels as recipient vessels. Once
the exposure technique is mastered, these vessels are readily accessible,
provide strong arterial inflow and several options for additional venous
outflow (if required), and permit rapid positioning of the flap with a
comfortable working position under the microscope. A rib-sparing approach
can be utilized in patients with an adequate intercostal space, but vessel
exposure is facilitated by resection of a small segment of cartilage at the
costochondral junction (3rd or 4th). This also allows full exposure and easy
skeletonization of the anterior cutaneous intercostal sensory nerve traveling at
the cranial border of the lower rib if sensory flap neurotization is planned
(Figs. 77-5 and 77-6). We routinely use the 3rd or 4th costochondral junction
with the latter preferred to ensure the rib cartilage harvest site is covered by
the DIEP flap and a potential contour defect is avoided.

FIGURE 77-5 Schematic drawing showing the right internal mammary artery and
vein, as well as the expected anatomical locations of the 2nd and 3rd intercostal
sensory nerves (ICNs).
FIGURE 77-6 Intraoperative dissection showing excision of a 2.5-cm segment of
costochondral junction (3rd) to allow full exposure of the left internal mammary
vessels and 3rd sensory intercostal nerve (marked blue).

A potential disadvantage of using the internal mammary vessels is that the


left internal mammary vein, or veins, can be thin walled and of small caliber
(1 to 1.5 mm), making the venous anastomosis slightly more difficult.
Despite this caveat, in our experience the left internal mammary vein can
routinely and safely be used for venous outflow. The right internal mammary
vein is routinely of larger caliber (2 to 3 mm). We have also used intercostal
perforator vessels, if they have been left intact during the mastectomy and
they are of good caliber. Use of this recipient pedicle obviates the need for
excision of a segment of costochondral cartilage, which saves time and
reduces parasternal soreness postoperatively. Other recipient vessels with
which we have experience but are rarely required include the thoracodorsal,
circumflex scapular, serratus anterior, and descending (pectoral) branch of
the thoracoacromial trunk. The cephalic vein can also be transposed and
utilized for additional venous outflow if required.
The flap is marked prior to prepping and draping of the patient so that the
entire trunk is in full view. Previous abdominal surgery is common in our
patient population; right subcostal, Pfannenstiel, and lower abdominal
midline scars are frequently encountered, singly or in combination. These
incisions do not preclude the surgery. Careful preoperative assessment with
the patient in the standing and sitting position, appropriate placement of the
flap, and intraoperative decision making regarding flap viability are required.
Lower abdominal perforators are also easily evaluated preoperatively in the
office with a pencil Doppler in these situations. CT angiography can be very
helpful for preoperative perforator evaluation and surgical planning,
particularly in patients with complex abdominal surgical histories, though we
do not feel routine use in every patient is necessary.
Pedicled and free TRAM flap procedures involve transection of the entire
width of rectus abdominis muscle encompassing multiple perforating vessels
supplying the overlying soft tissue ellipse. This is associated with permanent
loss of abdominal muscle function which is particularly noticeable to active
patients and those requiring bilateral procedures. The DIEP flap minimizes
abdominal wall morbidity by preserving all the abdominal muscle. Typically,
the flap is based on one or two perforators; in our experience an upper medial
perforator (periumbilical) frequently includes a large draining vein, ranging
from 2.0 to 2.5 mm in diameter. More laterally located perforators are
associated with less fat necrosis (30).
Usually local anesthetic with 1:100,000 epinephrine is used along the
incision lines locally around the flap design, but not in the proximity of the
superficial inferior epigastric artery (SIEA) vessels. After a few minutes, the
upper abdominal incision is made in line with the upper border of the
umbilicus. The incision is deepened to the anterior abdominal fascia,
beveling cephalad to allow for greater flap volume and to ensure
periumbilical perforators in line with the umbilicus are included in the flap if
needed.
Once the anterior abdominal fascia is reached a variable amount of
discontinuous undermining is performed based upon tissue requirements and
patient factors such as previous scars or comorbidities. Perforators to the
upper abdominal apron are preserved. Suprafascial dissection is routinely
continued centrally up to the xiphoid to expose a rectus diastasis and allow
for plication at the time of donor-site closure if required. The patient is flexed
on the operating table to ensure the lower abdominal markings are consistent
with an abdominal closure that will be under appropriate tension, as well as
an aesthetic, low-lying final scar position. The lower incision is then made.
All inferiorly directed veins of significant caliber should be dissected and
included with the flap in the event that additional venous outflow is required.
Occasionally we find that a flap’s inflow and outflow occur via different
systems, that is, inflow via the deep system and outflow via the superficial
system. In these instances, it is crucial to recognize the presence of a large
superficial draining vein and include it with the flap harvest if venous
congestion is to be avoided. This phenomenon, commonly referred to as
“superficial venous dominance” (31), results in cutaneous venous congestion
due to venous insufficiency requiring DIEP flap venous supercharging at the
time of flap transfer. Some flaps have two smaller caliber superficial veins
that coalesce into one larger vein inferiorly that is required for adequate
venous outflow. The temporal relationship of development of venous
congestion to flap dissection may suggest a possible etiology and effective
corrective measures (32).
The SIEA and accompanying vein (SIEV) are also routinely dissected if
they are of significant caliber or if the artery has a palpable pulse at the lower
flap incision. However, SIEA flaps are infrequently used in our practice due
to the large number of patients that have had the vessels transected by
previous surgeries. If these vessels are identified as large enough for
consideration of an SIEA-based flap, then they are dissected to their origin
from the femoral vessels. The flap is then elevated from lateral to medial in
the areolar plane just above the abdominal wall fascia propria under loupe
magnification. Deep perforators are temporarily occluded with
microaneurysm clips to leave the flap perfused only by the superficial system
if an SIEA flap is being considered.
An excellent technique for determining the clinically dominant vessel or
perforators is intraoperative indocyanine green fluorescence angiography.
Indocyanine green dye is administered intravenously by the anesthesiologist.
A fluoroscopic digital camera is then used to image the flap showing arterial
inflow as a bright or colored movie image of the complete flap to its edges.
This system can also be used to determine the boundaries of optimal flap
perfusion which can be used along with clinical evaluation for appropriate
trimming of the flap prior to inset. This can significantly decrease the risk of
fat necrosis at the periphery of the flap (33).
During DIEP flap dissection, clinically relevant perforators and sensory
nerves are sought and identified. Perforators selected for flap elevation are
based on caliber, number, location, and branching pattern. The fascial rent
through which the main deep inferior epigastric perforator passes can be
opened with the tenotomy scissors and the surrounding soft tissues are
dissected away from the perforator. A segmental intercostal sensory nerve
(T10, T11, or T12) is identified entering the substance of the flap along with
the vascular perforator (Fig. 77-7). Under microscopic or loupe
magnification, the nerve is dissected in retrograde fashion to the sensory–
motor nerve junction. This is where the sensory and motor nerve components
separate. The motor nerve component is preserved by either transecting the
sensory nerve at this “Y-junction,” or by performing fascicular dissection to
recruit more sensory nerve length. The mixed motor and sensory nerve
plexus adjacent to the lateral branch of the deep inferior epigastric pedicle
must be avoided in order to prevent inadvertent motor nerve injury (34).
T10, T11, and T12 intercostal sensory nerve (ICN) branches follow the
lateral perforators in 75% of cases (35). In 25% of cases, sensory nerves
pierce the anterior rectus sheath or external oblique fascia at various distances
from the lateral perforators (35). The diameter of these sensory nerves also
varies widely averaging 1.23±0.6 mm (0.5 to 2.4 mm) (35).
Dissection continues in retrograde fashion following the course of the
perforator vessels toward the main pedicle. The pedicle is traced below the
rectus abdominis muscle while minimizing the length of the fascial incision
as much as possible. A lighted breast retractor can be used to facilitate
retrograde dissection under the muscle. The pedicle vessels are encircled with
a vascular loop and teased from their surrounding structures with the nonstick
plated bipolar cautery, using ligaclips to facilitate and speed dissection. A
history of previous abdominal surgery or multiple incisions in the suprapubic
area often means extensive scarring to the deep inferior epigastric pedicle in
the retropubic space and care must be taken to avoid injury during dissection
in such cases. There is no set “optimal pedicle length.” This is potentially
influenced by several factors including flap size and thickness, the anticipated
inset and shaping requirements, whether an ipsilateral or contralateral flap is
used, and perforator location. All these factors should be considered and
balanced with the benefits of minimizing the length of the fascial incision
prior to limiting the length of the pedicle.
The surgeon must also be familiar with the anatomic variations of the
epigastric pedicle and its perforators. For the DIEP flap, a wide range of
perforator size and intramuscular anatomy exists. In the absence of a single
large perforator or two favorably located perforators, the inclusion of a very
small cuff of rectus muscle to permit the inclusion of two to three small
perforators will minimize the incidence of fat necrosis and will have little
impact on abdominal wall strength and overall recovery (36,37).
The infraumbilical segment of rectus muscle is innervated by T9-L1 motor
nerves entering laterally and posteriorly (34). Every effort is made to preserve
these motor nerve branches (Fig. 77-8); however, a motor nerve located
between perforators may require transection to extricate a multiple-perforator
flap from its bed. In this instance the transected motor nerve is repaired via
microneurorrhaphy after completion of the flap dissection whenever possible.
Once the flap has been harvested and the recipient vessels dissected, the
patient is given an intravenous heparin bolus of 1,500 units. After several
minutes the contralateral flap is brought to the chest wall and secured. We
prefer using the contralateral flap as this facilitates performing an additional
venous anastomosis between the superficial inferior epigastric vein (SIEV)
and a recipient vein in the chest if required. Recipient options include a
medial intercostal perforator vein, second internal mammary vein (if present),
or retrograde internal mammary vein.
Under microscopic magnification the epigastric and internal mammary
vessels are prepared for anastomosis: the vessels are cut to the appropriate
length, trimmed of excess adventitia, dilated, and irrigated with a heparin–
saline solution (25,000 units of heparin in 1 L of Ringer lactate). The solution
is delivered by an Infinity Irrigator Set (manufactured by Infinity Surgical
Technology, Inc., Mequon, WI), fitted with a 27-gauge anterior eye chamber
needle. We routinely perform the arterial and venous anastomosis in an end-
to-end fashion using 9-0 nylon suture with a running suture technique. The
epigastric and internal mammary vessels are immobilized in double aneurysm
clips and set on top of a papaverine-soaked cottonoid to permit accurate
suture placement. Use of the double aneurysm clips and running suture
technique result in relatively short flap ischemic times, ranging from 14 to 24
minutes. Coupling devices may be used though we have not found that they
reduce flap ischemia time. Furthermore, couplers have been associated with
an increased risk of thrombosis in veins under 2 mm in diameter (38).
FIGURE 77-7 DIEP flap dissection from lateral to medial. A: Schematic drawing
demonstrating typical position of distal ends of the sensory components of respective
intercostal nerves (ICN 10 to 12) exiting the fascia and entering the flap. The exact
location and length of the fascial incision depends on the location of the chosen
perforators. B: Blue ink–labeled lateral perforators and adjacent intercostal nerves
10 to 12, and one additional sensory branch lateral to intercostal nerve 11. (Figure B
from Ducic I, Yoon J, Momeni A, et al. Anatomical considerations to optimize sensory
recovery in breast neurotization with allograft. Plast Reconstr Surg Glob Open
2018;6:e1985.)

FIGURE 77-8 Preserved segmental rectus abdominis motor nerves during DIEP flap
dissection.
FIGURE 77-9 End-to-end anastomoses of the deep inferior epigastric vessels to the
internal mammary vessels, and direct microneurorrhaphy between the anterior
(medial) cutaneous branch of the 4th intercostal nerve in the chest and the 11th
sensory intercostal nerve harvested with the contralateral DIEP flap. A discarded
segment of internal mammary artery has been used over the microneurorrhaphy as
a neural conduit.

Following the vessel anastomosis, a microneurorrhaphy is usually


performed between the anterior (medial) cutaneous branch of the 4th
intercostal nerve in the chest and the 10th, 11th, or 12th sensory intercostal
nerve branch harvested with the contralateral DIEP flap (Fig. 77-9). The
lateral 4th intercostal nerve is occasionally used as a recipient nerve. As
stated above, great care must be taken when maximizing length of the
harvested sensory nerve as these nerves originate from a mixed
sensory/motor nerve plexus (34) and careful interfascicular dissection is often
required to maximize the length of the harvested sensory nerve to ensure the
motor component is preserved. Significant prior abdominal surgery and
resultant scarring may preclude the inclusion of a sensory intercostal nerve
with the flap, or may only allow harvest of a short nerve segment.
FIGURE 77-10 Tension-free dual nerve autologous neurotization between the 4th
sensory intercostal nerve in the chest and the 10th and 11th sensory intercostal
nerves harvested with the contralateral DIEP flap. A discarded segment of internal
mammary artery has been used as a neural conduit at the microneurorrhaphy site.

Sensory neurotization can be performed either as a totally autologous


reconstruction (direct coaptation between the flap sensory nerve and the
recipient nerve in the chest), or with an interposition nerve graft. While the
traditional recipient nerve for breast neurotization is the lateral cutaneous
branch of the 4th intercostal sensory nerve (23), our preferred technique
involves complete skeletonization of the anterior (medial) cutaneous
intercostal sensory nerve in the parasternal area which facilitates tension-free
coaptation and flap insetting. The nerve is readily identifiable during
exposure of the internal mammary recipient vessels. As previously
mentioned, exposure is facilitated by resecting a small segment of
costochondral junction (3rd or 4th). Sometimes the transected end of the
nerve is easily identified near the base of the mastectomy skin flap in the
parasternal region. Often there is cautery artifact at the site of the nerve
transection. The nerve end is grasped and the overlying soft tissues are
dissected away to allow the freed nerve to be reflected laterally. Typically
this provides a recipient nerve which is several centimeters long. The
transected end of the nerve is then trimmed back to healthy nerve prior to
microneurorrhaphy to the sensory nerve harvested with the flap (Fig. 77-9).
Dual neurotization can also be performed (Fig. 77-10) using a variety of
recipient (medial and lateral) and flap nerve combinations. Occasionally, a
bridging nerve graft is required due to the short length of the segmental
sensory nerve harvested with the flap. In these instances we use a processed
human nerve allograft (Avance, manufactured by Axogen, Alachua, FL) as a
bridging graft (Figs. 77-11 and 77-12). Interrupted epineural 9-0 nylon
technique is used for all nerve repairs. Nerve intubation with a conduit is also
routinely performed using either discarded segments of epigastric or internal
mammary artery or vein (Figs. 77-9, 77-10 and 77-12), or a neural connector
tube (manufactured by Axogen, Alachua, FL) (Fig. 77-13).
Shaping and insetting of the flap and closure of the donor site are
performed simultaneously. Any poorly perfused mastectomy skin is resected
after evaluation with intraoperative angiography. Likewise, in the case of a
delayed reconstruction, any poor-quality skin is resected. Much of the
deepithelialization of the flap can be performed on the abdomen prior to
transfer of the flap to the chest to save time.
FIGURE 77-11 Bridging of a short donor nerve to the 4th sensory intercostal nerve
in the chest. A 50-mm Avance nerve allograft (manufactured by Axogen, Alachua,
FL) has been used to allow a tension-free nerve coaptation.

The flap must be positioned as medial as possible and anchored with


medial and/or lateral tacking sutures if necessary to prevent migration of the
flap. Tacking sutures are placed between the superficial fascia on the flap and
the chest wall soft tissues. Shaping and inset must also ensure that pedicle
position does not change as the flap is repositioned or with gravity
postoperatively. It is crucial to control the footprint of the reconstructed
breast at the time of the initial reconstructive procedure, as well as to
maximize lower pole fullness. It is usually fairly straightforward to address a
relatively deficient upper pole with subsequent fat grafting whereas a
deficient lower pole is typically harder to improve without the addition of an
implant.
The DIEP flap obviates the need for mesh in the donor-site fascial closure,
however we do reinforce significantly attenuated fascia (e.g., in patients with
complex prior abdominal surgical histories) with a Strattice (manufactured by
Allergan PLC, Dublin, Ireland) acellular dermal matrix onlay to minimize the
risk of a postoperative bulge.
Progressive tension sutures allow advancement of the upper abdominal
flap inferiorly. This not only decreases tension at the closure site but can also
effectively lower the position of the final donor-site scar. Like quilting
sutures, progressive tension sutures also close down dead space minimizing
the risk of a postoperative seroma. Fascial plication is performed as required
to optimize abdominal aesthetics though in most patients this is limited to the
upper abdomen to address supraumbilical rectus diastasis.

FIGURE 77-12 Bridging of the 3rd sensory intercostal nerve in the chest to the 10th
sensory intercostal nerve harvested with a contralateral DIEP flap. A 70-mm Avance
nerve allograft (manufactured by Axogen, Alachua, FL) has been used. When using
a contralateral DIEP flap, we rotate the flap approximately 135 degrees on inset so
the tail of the flap recreates the axillary tail of the new breast. In this position, the
location of 10th intercostal sensory nerve harvested with the DIEP flap may lack
sufficient length to permit primary tension-free coaptation to the medial intercostal
recipient nerve making a long nerve graft necessary. Alternatively, using a lateral
ICN (4th or 5th) as the recipient nerve can obviate the need for a nerve graft in this
setting.

The final component of an aesthetic donor-site closure is the


umbilicoplasty. The umbilicus can rarely be placed and inset too high. A long
umbilical stalk can facilitate superior placement, effectively increasing the
distance between the umbilicus and the final donor-site scar and further
giving the illusion of an even lower abdominoplasty-type scar. A low-lying
umbilicus and a high-riding donor-site scar is the worst combination, leading
to a final result that can make patients feel they have been “bisected” when
they look in the mirror rather than feeling they have truly benefitted from a
simultaneous abdominoplasty. We favor a narrow vertical ellipse for the
umbilical inset but this should be tailored to match the remaining abdominal
habitus. Anchor sutures between the umbilical stalk and the anterior
abdominal wall, along with defatting at the inset site are used to recreate
hooding and maximize the cosmetic result of the umbilicoplasty.

FIGURE 77-13 A neural connector tube made of porcine intestinal submucosa


(manufactured by Axogen, Alachua, FL).
INTRAOPERATIVE AND POSTOPERATIVE CARE
Highly skilled and highly motivated personnel in the operating room are the
cornerstones of performing successful microsurgical breast reconstruction.
Institutional support at all levels from the hospital CEO to the OR director,
staff nurses, anesthesia technicians, and orderlies is critical to success. While
regular meetings with hospital administration are important to ensure that
appropriate support is given to staff and to obtaining the latest equipment, of
more importance is direct communication with the operative team of
personnel who care for the patients each day. Although perioperative care is
critical in all surgical procedures, success in free tissue transfer can be
undone in a matter of moments by a careless transport team unconcerned
with patient positioning. Though the surgeon is always in charge, from a
practical standpoint, much work is delegated to all our ancillary personnel
and it cannot be stressed enough that this educational process is highly hands
on and requires constant maintenance. Needless to say, these procedures
cannot easily be performed at smaller hospitals on a limited, occasional basis,
unlike implant reconstructions that can largely be handled by a single surgeon
at almost any institution.
Skill and efficiency improve with time and cumulative experience of the
operative team. Attention to detail of many critical perioperative factors is
required, not just by the surgeon, but every member of a highly skilled and
trained microsurgical team including the anesthesiologist, circulating nurse,
and operative assistants.
Once the operation is completed and the patient transferred to the
postanesthesia care unit (PACU), monitoring of the flap and patient is
accomplished via clinical examination, pencil Doppler, and the use of T-Stat
transcutaneous tissue oximetry (manufactured by Spectros, Campbell, CA).
The T-Stat reports capillary-weighted oxygen saturation which is closely
related to local venous saturation, along with oxygen hemoglobin
concentration. Though initial measurements can vary widely, trends in values
are most important. Early reexploration is indicated if oximetry
measurements fall significantly, or hemoglobin concentration rises rapidly
(usually a sign of venous compromise). Such changes typically precede
clinical signs and symptoms associated with flap compromise.
We do not admit patients to the surgical intensive care unit. Patients are
transferred to a dedicated surgical floor where routine flap monitoring and
postoperative care are administered by specialist “breast nurses” we have
trained. We have implemented postoperative protocols for flap monitoring,
patient mobilization, and advancement of diet. Starting in PACU immediately
after surgery, the patient receives two baby aspirin (162 mg) per day, which
is discontinued at the end of 1 week. Lovenox is also started on the morning
of the first postoperative day and continued until the patient is discharged.
Surgical nurses have been trained to recognize venous outflow obstruction
or occlusion of arterial inflow in the flap, and a breast or abdominal
hematoma. The nursing staff has been instructed to promptly notify the
surgeon on call if one of the above complications is observed, or if there are
any questions regarding patient care. A surgical team is always available in
any event requiring emergent return to the operating room.
Since the introduction of our ERAS protocol, an increasing number of our
patients are being discharged from the hospital on postoperative day 2,
irrespective of unilateral or bilateral status. Preoperatively, patients are given
information packets containing detailed instructions for the postoperative
period. These information packets are accompanied by intensive teaching by
our practice nursing staff. Setting patient expectations is key. Discharge
instructions are reiterated to the patient by the hospital nursing staff and our
PAs on the day of hospital discharge. Patient education is an ongoing
process; adherence to perioperative clinical pathways minimizes the length of
hospital stay, decreases overall recovery time, and improves patient comfort
and outcomes.
Revision of the reconstructed breast and donor site along with symmetry
procedures of the contralateral breast are typically performed 3 to 6 months
after the initial reconstruction or after the patient has completed
chemotherapy and radiation therapy if these are required. Stage 2 typically
includes revision of the reconstructed breast, nipple reconstruction, alteration
of the native breast with mastopexy, reduction mammoplasty, or
augmentation mammoplasty for optimal symmetry, ancillary fat grafting
procedures to address residual small flap and chest wall defects or to add
volume, and abdominal donor-site scar revision. Usually these procedures are
grouped together and performed in an outpatient setting. If an extensive
revision of the reconstructed breast is necessary, the nipple reconstruction
may be deferred to a later date, usually as an office procedure. 3D
Micropigmentation (tattooing) of the nipple areolar complex, follows several
months later to complete the breast reconstruction.

CASES

CASE 1

This patient presented following right mastectomy and irradiation to the


right chest wall (Fig. 77-14A). Over the past several years, rates of
contralateral prophylactic mastectomy (CPM) in unilateral cancer
patients have increased significantly, particularly in the United States.
We have seen an increasing number of patients opting for CPM at the
time of autologous delayed reconstruction. This poses additional
problems of symmetry which was nicely achieved in this patient. She
chose to undergo a left prophylactic skin-sparing mastectomy and
bilateral reconstruction with neurotized DIEP flaps (right delayed, left
immediate). Stage 2: The revision procedure included bilateral breast
revision with autologous fat grafting, a left vertical mastopexy, bilateral
nipple areolar reconstruction, and abdominal donor-site revision with
liposuction. Stage 3: Bilateral nipple areolar micropigmentation was
performed as the final stage of the reconstruction in the office under local
anesthetic (Fig. 77-14B).
FIGURE 77-14

CASE 2

This high-risk patient presented following right mastectomy and chest


wall irradiation, and with significant ptosis of the left breast (Fig. 77-
15A). She underwent a left prophylactic skin-sparing mastectomy and
bilateral neurotized DIEP flap breast reconstruction (right delayed, left
immediate). Stage 2: Three months later we performed bilateral breast
revision incorporating autologous fat grafting, a left vertical mastopexy,
bilateral nipple reconstruction, and abdominal scar revision. Stage 3:
Bilateral nipple areolar micropigmentation was performed in the office 4
months after stage 2 to complete her reconstruction (Fig. 77-15B).
FIGURE 77-15

CASE 3

Nipple-sparing mastectomy has its place in both prophylactic mastectomy


patients with a genetic susceptibility for cancer, but also in DCIS and
early-stage invasive disease (Fig. 77-16A). In this patient, bilateral
nipple-sparing mastectomies allowed for an excellent reconstructive
result (Fig. 77-16B). Patients should be well-informed about any
potential increased risk of future disease secondary to nipple areolar
preservation, and the need for appropriate continued surveillance and
follow-up.
FIGURE 77-16

CASE 4

This high-risk patient with a strong family history underwent bilateral


nipple-sparing mastectomies with immediate DIEP flap breast
reconstruction (Fig. 77-17A). Bilateral breast autologous fat grafting and
abdominal donor-site scar revision were performed secondarily (stage 2)
to improve the final cosmetic results (Fig. 77-17B).
FIGURE 77-17

CASE 5

This patient presented from an outside institution following left breast


implant reconstruction (Fig. 77-18A). She was very unhappy with her
breast asymmetry and the overall “look and feel” of the reconstructed
breast. She opted for removal of her left breast implant and further
reconstruction with a neurotized DIEP flap. DIEP flap skin was
incorporated into the left breast skin envelope to restore the normal breast
diameter. A right vertical mastopexy was performed for improved
symmetry at stage 2 along with left nipple areolar reconstruction. Left
nipple areolar micropigmentation was subsequently performed in the
office to complete her reconstruction (Fig. 77-18B).
FIGURE 77-18
RISKS OF THE PROCEDURE
Reconstructive breast surgery using microsurgical tissue transfer is associated
with all the risks inherent in surgery in general. Bleeding, infection,
hematoma, and seromas can and do occur. The literature is replete with
discussions and trials using tissue glues to prevent seroma and antibiotics to
prevent infections. We have found that good surgical hemostasis, proper use
of drains, preoperative antibiotics given 30 minutes prior to incision and
discontinued after 24 hours, maintenance of normothermia and euvolemia,
and use of thromboembolism prophylaxis are all critical. Protocols change
frequently as new evidence-based studies come on line; however most of
these studies must be extrapolated to our patient population.
Clinically significant bleeding, hematoma, and infections vary year by year
between 3% and 5%. Reoperative rates also range between 3% and 5%.
Despite the successes over the past several decades in free tissue transfer, flap
losses still occur due to hematoma, malposition of the pedicle, edema, and
arterial or venous thrombosis. Our annual flap loss rate is less than 1%. Fat
necrosis may occur in some patients but is rarely clinically significant. This
may be excised at the revision stage if it is problematic.
CONCLUSION
Our practice has transitioned from the free TRAM flap in the early 1990s to
the muscle-sparing free TRAM flap, based on three to four perforators, and
ultimately to the DIEP flap, usually based on one or two perforators. While
we perform approximately 150 implant-based reconstructions annually, our
core service is microsurgical autologous breast reconstruction. We currently
perform over 700 perforator flap breast reconstructions annually, the vast
majority of which are DIEP flap reconstructions.
Routine flap sensory neurotization has been an integral component of
abdominal-based breast reconstruction in our practice for many years with
excellent anecdotal results. Further studies are necessary to determine the
optimal method of nerve coaptation, clarify the indications for use of
allografts, elucidate the optional timing and methods for objective
quantification of sensory restoration, and identify the effects on patient-
reported outcomes.
The role of autologous tissue breast reconstruction with the DIEP flap
continues to expand. In addition to being used for reconstruction following
mastectomy for a definitive breast cancer, these and other perforator flaps are
being increasingly utilized for breast reconstruction in several other settings:
prophylactic mastectomy; partial mastectomy defects; mastectomy for severe
fibrocystic disease with symptoms recalcitrant to dietary and drug therapy;
the congenitally deformed breast; and even to correct severe, recurrent
contracture and periprosthetic atrophy associated with breast augmentation.
Whether to perform the breast reconstruction as an immediate or delayed
procedure in the face of postmastectomy radiation continues to be a sticking
point for our practice (39,40). Despite radiation protocols, much depends on
patient biology and the radiation oncologist’s approach. Some radiation
oncologists, simply put, are just more “breast reconstruction friendly” and are
willing to consider maneuvers that decrease flap morbidity without
compromising cancer care, such as foregoing a boost. Even with the
significant advances in radiation therapy we still occasionally see severe
shrinkage and distortion of the DIEP flap following external beam radiation.
Though rare, this can require partial excision of the flap and repeat
breast/chest wall reconstruction with another autologous reconstruction
method. Lumpectomy followed by local delivery of radiation via a device
such as the MammoSite catheter has also occasionally produced partial breast
deformities requiring flap reconstruction.
In cases where the patient’s treatment plan includes postmastectomy
radiation we still generally prefer to delay reconstruction unless specific
radiation oncologists are involved in the patient’s treatment. Neoadjuvant
radiation therapy is an attractive approach currently being studied which
avoids radiating the flap while preserving the benefits of immediate
reconstruction (41). Thorough communication throughout the
multidisciplinary team is always crucial in ensuring optimal patient care, but
there is no better example than the close communication needed with the
radiation oncologist in cases requiring radiation therapy.
The passage of state and federal laws mandating coverage for breast
reconstruction procedures on the part of insurers has been beneficial to those
plastic surgeons in private practice wishing to perform this service. However,
rising malpractice premiums and other overhead costs, laborious interactions
with insurers, and declining reimbursements increasingly make breast
reconstruction more difficult to accomplish in a private practice setting. To
maintain breast reconstruction as a significant part of a private practice all
members of the practice must strive for efficiency, low complication rates,
and a high level of patient satisfaction (42,43). Best practices must be
developed and periodically reevaluated. Increasing efficiency and keeping
overhead costs as low as possible will make microsurgical breast
reconstruction more tenable financially, regardless of the reimbursement
level.

REFERENCES

1. Ochoa O, Chrysopoulo M, Nastala C, et al. Abdominal wall stability and


flap complications after deep inferior epigastric perforator flap breast
reconstruction: does body mass index make a difference? Analysis of
418 patients and 639 flaps. Plast Reconstr Surg 2012;130:21e–33e.
2. Shridharani AM, Magarakis M, Stapleton SM, et al. Breast sensation
after breast reconstruction: a systematic review. J Reconstr Microsurg
2010;26:303–310.
3. Beugels J, Cornelissen AJM, Speigel AJ, et al. Sensory recovery of the
breast after innervated and non-innervated autologous breast
reconstruction: a systemic review. J Plast Reconstr Aesthet Surg
2017;70:1229–1241.
4. Weissler JM, Koltz PF, Carney MJ, et al. Sifting through the evidence: a
comprehensive review and analysis of neurotization in breast
reconstruction. Plast Reconstr Surg 2018;141:550–565.
5. Nahabedian MY, Tsangaris T, Momen B, et al. Infectious complications
following breast reconstruction with expanders and implants. Plast
Reconstr Surg 2003;112:467–476.
6. Kroll SS, Evans GRD, Reece GP, et al. Comparison of resource costs
between implant-based and TRAM flap breast reconstruction. Plast
Reconstr Surg 1996;97:364–372.
7. Miller SH. Comparison of costs between implant-based and TRAM flap
breast reconstruction. Plast Reconstr Surg 1996;98:916–917.
8. Spear SL, Mardini S, Ganz JC. Resource cost comparison of implant-
based breast reconstruction versus TRAM flap breast reconstruction.
Plast Reconstr Surg 2003;112:101–105.
9. Blondeel PN, Vanderstraeten GG, Monstrey SJ, et al. The donor site
morbidity of free DIEP flaps and free TRAM flaps for breast
reconstruction. Br J Plast Surg 1997;50:322–330.
10. Nahabedian MY, Manson PN. Contour abnormalities of the abdomen
after transverse rectus abdominis muscle flap breast reconstruction: a
multifactorial analysis. Plast Reconstr Surg 2002;109:81–87.
11. Blondeel PN. Discussion: contour abnormalities of the abdomen after
transverse rectus abdominis muscle flap breast reconstruction: a
multifactorial analysis. Plast Reconstr Surg 2002;109:88–90.
12. Nahabedian MD, Dooley W, Singh N, et al. Contour abnormalities of
the abdomen after breast reconstruction with abdominal flaps: the role of
muscle preservation. Plast Reconstr Surg 2002;109:91–101.
13. Kroll SS, Schusterman MA, Reece GP, et al. Abdominal wall strength,
bulging, and hernia formation after TRAM flap breast reconstruction.
Plast Reconstr Surg 1995;96:616–619.
14. Parrett BM, Caterson SA, Tobias AM, et al. DIEP flaps in women with
abdominal scars: are complication rates affected? Plast Reconstr Surg
2008;121(5):1527–1531.
15. Beugels J, Heuts E, Piatkowski de Gryzymala A, et al. Neurotisation in
the deep inferior epigastric artery perforator (DIEP) flap breast
reconstructions: our technique and results. Eur J Surg Oncol
2016;42:S103–S104.
16. Magarakis M, Venkat R, Dellon LA, et al. Recovery of sensation in the
reconstructed breast. Plast Reconstr Surg 2011;127:54.
17. Isenberg JS, Spinelli H. Further experience with innervated autologous
flaps in postoncologic breast reconstruction. Ann Plast Surg
2004;52:448–451.
18. Yap LH, Whiten SC, Forster A, et al. Sensory recovery in the sensate
free transverse rectus abdominis myocutaneous flap. Plast Reconstr
Surg 2005;115:1280–1288.
19. Temple CF, Tse R, Bettger-Hahn M, et al. Sensibility following
innervated free TRAM flap for breast reconstruction. Plast Reconstr
Surg 2006;117:2119–2127.
20. Cornelissen AJM, Beugels J, van Kujik SMJ, et al. Sensation of the
autologous breast improves quality of life: a pilot study. Breast Cancer
Res Treat 2018;163:687–695.
21. Temple CL, Ross DC, Kim S, et al. Sensibility following innervated free
TRAM flap for breast reconstruction: Part II. Innervation improves
patient-rated quality of life. Plast Reconstr Surg 2009;124:1419–1425.
22. Cornelissen AJM, Beugels J, Lataster A, et al. Comparing the sensation
of common donor site regions for autologous breast reconstruction to
that of a healthy breast. J Plast Reconstr Aesth Surg 2018;71:327–335.
23. Spiegel AJ, Menn ZK, Eldor L, et al. Breast reinnervation: DIEP
neurotization using the third anterior intercostal nerve. Plast Reconstr
Surg Glob Open 2013;1:e72.
24. Puonti HK, Jääskeläinen SK, Hallikainen HK, et al. A new approach to
microneurovascular TRAM-flap breast reconstruction: a pilot study. J
Plast Reconstr Aesthet Surg 2011;64:346–352.
25. Pisano SM, Ledoux PR, Nastala C. Breast reconstruction in private
practice. Semin Plast Surg 2004;18:157–173.
26. Batdorf NJ, Lemaine V, Lovely JK, et al. Enhanced recovery after
surgery in microvascular breast reconstruction. J Plast Reconstr Aesthet
Surg 2015;68:395–402.
27. Kaoutzanis C, Ganesh Kumar N, O’Neill D, et al. Enhanced recovery
pathway in microvascular autologous tissue-based breast reconstruction:
should it become the standard of care? Plast Reconstr Surg
2018;141:841–851.
28. DellaCroce FJ, Blum CA, Sullivan SK, et al. Nipple-sparing
mastectomy and ptosis: perforator flap breast reconstruction allows full
secondary mastopexy with complete nipple areolar repositioning. Plast
Reconstr Surg 2015;136:1e–9e.
29. Puonti HK, Jääskeläinen SK, Hallikainen HK, et al. Improved sensory
recovery with a novel dual neurorrhaphy technique for breast
reconstruction with free muscle sparing TRAM flap technique.
Microsurgery 2017;37:21–28.
30. Hembd A, Teotia SS, Zhu H, et al. Optimizing perforator selection: a
multivariable analysis of predictors for fat necrosis and abdominal
morbidity in DIEP flap breast reconstruction. Plast Reconstr Surg
2018;142:583–592.
31. Sbitany H, Mirzabeigi MN, Kovach SJ, et al. Strategies for recognizing
and managing intraoperative venous congestion in abdominally based
autologous reconstruction. Plast Reconstr Surg 2012;129:809–815.
32. Ochoa O, Pisano S, Chrysopoulo M, et al. Salvage of intraoperative
deep inferior epigastric perforator flap venous congestion with
augmentation of venous outflow: flap morbidity and review of the
literature. Plast Reconstr Surg Glob Open 2013;1:e52.
33. Chatterjee A, Krishnan NM, Van Vliet MM, et al. A comparison of free
autologous breast reconstruction with and without the use of laser-
assisted indocyanine green angiography: a cost-effectiveness analysis.
Plast Reconstr Surg 2013;131:693e–701e.
34. Rozen WM, Ashton MW, Murray ACA, et al. Avoiding denervation to
rectus abdominis in DIEP flap harvest: the importance of medial row
perforators. Plast Reconstr Surg 2008;122:710–716.
35. Ducic I, Yoon J, Momeni A, et al. Anatomical considerations to
optimize sensory recovery in breast neurotization with allograft. Plast
Reconstr Surg Glob Open 2018;6:e1985.
36. Kroll SS. Fat necrosis in free transverse rectus abdominis myocutaneous
and deep inferior epigastric perforator flaps. Plast Reconstr Surg
2000;106:576–583.
37. Bajaj AK, Chevray PM, Chang DW, et al. Comparison of donor-site
complications and functional outcomes in free muscle-sparing TRAM
flap and free DIEP flap breast reconstruction. Plast Reconstr Surg
2006;117(3):737–746; discussion 747–750.
38. Hansen SE, Mitchell MB, Palivela N, et al. Smaller diameter
anastomotic coupling devices have higher rates of venous thrombosis in
microvascular free tissue transfer. Plast Reconstr Surg 2017;140:1293–
1300.
39. Rogers N, Allen RJ. Radiation effects on breast reconstruction with the
deep inferior epigastric perforator flap. Plast Reconstr Surg
2002;109:1919–1924; discussion 1925–1926.
40. Billig J, Jagsi R, Hamill JB, et al. Should immediate autologous breast
reconstruction be considered in women who require postmastectomy
radiation therapy? a prospective analysis of outcomes. Plast Reconstr
Surg 2017;139:1279–1288.
41. Hughes K, Noeh D. Neoadjuvant radiotherapy: changing the treatment
sequence to allow immediate free autologous breast reconstruction. J
Reconstr Microsurg 2018;34:624–631.
42. Collins ED. Discussion, reconstructive breast surgery: referring
physician knowledge and learning needs. Plast Reconstr Surg
2002;110:1451–1454.
43. Heinz TR, Cowper PA, Levin LS. Microsurgery costs and outcome.
Plast Reconstr Surg 1999;104:89–96.
CHAPTER 78

Profunda Artery Perforator Flaps


ANITA T. MOHAN | REUBEN A. FALOLA | MICHEL SAINT-CYR
HISTORY
The commonest donor site for autologous reconstruction with perforator flaps
is the abdomen, however in some cases there is inadequate donor tissue or
other indications making this site unavailable. The medial thighs and buttocks
have provided a second-line option for autologous reconstruction, but can be
fraught with disadvantages, including donor-site scar deformity or cosmesis,
a short vascular pedicle, and need for patient repositioning for flap inset. The
posterior thigh region is an often underused donor site but has perforators
originating from the femoral and popliteal artery that supply large cutaneous
areas (Figs. 78-1 and 78-2) that can be used for soft tissue reconstruction
with a robust vascularity for pedicled and free-flap reconstruction (1–10)
(Case 1). Posteromedial perforators from the profunda artery form can form
the basis of posteriorly based thigh flaps, also previously described as
adductor magnus, posterior thigh, posteromedial thigh flaps, or profunda
artery perforator (PAP) flaps, that have been used for locoregional tissue
reconstruction, pressure sores (1,11–15), and as free flaps for lower extremity
(16), head, and neck reconstruction (2,3,17) and now has growing role in
autologous breast reconstruction (4). Allen et al. were the first to describe the
PAP flap for breast reconstruction as a secondary donor site when abdominal
donor-site tissue was unavailable or contraindicated (4,7). It has since
become increasingly popular and is emerging as an alternative to the
transverse upper gracilis (TUG) flap, with growing number of published case
series, and anatomical and radiologic studies of the vascular territories.
FIGURE 78-1 Anatomic illustration of “Hot spots” to show density of perforators in
the posterior thigh region originating from the profunda artery.
FIGURE 78-2 Anatomical study using 3D-rendered computed tomographic
angiography to demonstrate the vascular territory of the profunda artery perforator
flap in a human cadaver.
FIGURE 78-3 Anatomical dissection of the right thigh and harvest of the profunda
artery flap harvest to demonstrate the first and second perforators originating from
the profunda artery passing through the adductor magnus muscle.
INDICATIONS
The PAP flap is an appropriate choice for women wanting to undergo
autologous breast reconstruction for small to medium volume breasts (300 to
400 g on an average approximately) (Case 2), particularly if abdominal
donor-site tissue is inadequate or contraindicated. The flap can be used as a
stacked flap (Case 3) for unilateral breast reconstruction. It can be used in
thin patients with a BMI <21 and can afford a skin paddle measuring 4 to 7
cm in width. There may be insufficient abdominal donor-site tissue in some
women, or women may have undergone previous abdominal liposuction or
surgery, previously failed transvers rectus abdominus myocutaneous
(TRAM)/deep inferior epigastric perforator (DIEP)/or superficial inferior
epigastric artery (SIEA) flaps, or abdominal surgeries making the use of the
abdominal donor site unavailable. The donor site will fall just below the
inferior gluteal crease and takes advantage of excess upper posterior thigh fat
that form a roll of excess tissue and is accentuated in pear-shaped women.
The scar is usually concealed within a swimsuit and allows for contouring
and lift of the thigh area. The flap is a perforator flap and obviates need for
muscle, and avoids any sciatic nerve exposure.
CONTRAINDICATIONS
There are no specific contraindications, but preoperative imaging should be
considered in any patient who has had significant trauma, surgery, or
resultant scarring that may have led to potential damage or alteration to the
blood supply in the lower extremity and this region.
PREOPERATIVE PLANNING
Perforators arise from the medial branches of the profunda artery and
commonly pass through the adductor magnus muscle (see Fig. 78-2). The
“hot spot” for dominant perforators lies within 13 cm of the gluteal crease
(see Fig. 78-1), within the boundary between the posterior border of the
gracilis muscle and posterior midline of the thigh. The proximal perforator is
found between 6 and 10 cm from the inferior gluteal crease, but a second and
third large perforator may be identified in the midthigh (Fig. 78-3).
Lower extremity CTA (Fig. 78-4) can provide useful additional
information to evaluate the blood supply and presence of perforators in the
posterior thigh region, however this is not mandatory. Prior to surgery and
with the patient in standing position, the inferior gluteal crease, adductor
longus tendon, the anatomical landmark of the gracilis muscle can be marked.
A hand-held Doppler can be used to identify potential perforators.
Traditionally for breast reconstruction, the skin paddle is designed in a
transverse orientation, but can be modified to maximize volume or recruit
posteromedial tissue if required (Fig. 78-5).

FIGURE 78-4 Computed tomographic angiography (CTA) of bilateral thighs with


demonstration of large perforator passing through the adductor magnus muscle
posterior to gracilis (blue arrows).
FIGURE 78-5 Illustration of potential modification of flap designs for profunda
artery perforator flaps. The Transverse T-PAP is the most traditional flap design for
breast reconstruction.
OPERATIVE TECHNIQUE
The flap can be raised in a supine frog-leg, prone, or lateral decubitus
position (Fig. 78-6). The flap is raised in a subfascial plane from an anterior
to posterior dissection, providing a pedicle length of 8 to 13 cm and large
caliber vessels for microanastomosis. Often the second cutaneous perforator
has a larger caliber and longer pedicle, therefore an anterior exploratory
incision allows for an initial evaluation of perforators so that the flap design
can be readjusted as necessary. When stacking multiple flaps in a single
breast, it is important to keep the internal mammary vessels long (Fig. 78-7).
In autologous breast reconstruction, the PAP flap was designed based
using a transverse skin paddle. Preoperative imaging helped identify suitable
skin perforators, which were confirmed by handheld Doppler. The superior
border of the flap was marked just inferior to the gluteal fold. The inferior
border of the flap was marked approximately 7 to 8 cm below the superior
border of the flap, but this was adjusted based on perforator location and skin
laxity and the pinch test. An elliptical flap design was drawn which did not
extend beyond the visible lateral and the medial extension was limited to the
midlateral line. The flap was raised in a supine frog-leg, prone or can be
harvested in a lateral decubitus position. The flap was raised in a subfascial
plane from an anterior to posterior dissection, providing a pedicle length of 8
to 13 cm and large caliber vessels for microanastomosis. Often the second
cutaneous perforator had a larger caliber and longer pedicle, therefore an
anterior exploratory incision allowed for an initial evaluation of perforators
so that the flap design could be readjusted as necessary. Beveling laterally
and inferomedially recruited additional volume. Care was taken to avoid
disturbing the gluteal fold and buttock contour superiorly and dissection into
the lymphatic basin anteriorly. The donor site was closed in multiple layers
with progressive tension sutures, over a closed-suction drain.
FIGURE 78-6 Intraoperative photographs of a profunda artery perforator (PAP)
flap harvest in a supine position. A: Transverse skin paddle designed and incised,
gracilis muscle seen at the medial aspect of the flap. B: Demonstration of subfascial
dissection and identification of perforators over gracilis and adductor magnus. C: It
is useful to separate the gracilis and adductor magnus muscle for better pedicle
exposure. D: Perforators identified for flap.
INTRAOPERATIVE CARE
The flap can be harvested in the lithotomy or supine positioning with the legs
on extremity boards or in a frog-legged position, with the hip and knee
flexed, and thigh abducted.
POSTOPERATIVE CARE
The donor sight is closed over a drain that can be removed when the output is
less than 20 to 30 mL/day, for two consecutive days. An incisional wound
vacuum dressing can be placed on the donor site intraoperatively and
removed prior to discharge (∼3 days) if there are any concerns for poor
wound healing, such as a tight closure (18). Patients are encouraged to
ambulate on postoperative day zero. Sitting or activities that place direct
pressure on the donor site should be avoided for 3 to 4 weeks after surgery.
Alternatively, prefashioned seating and positioning cushions can be used to
minimize pressure points and occurrences of wound dehiscence.
Compression garments may be used postoperatively to minimize swelling
and improve patient comfort (18). Compression garments can be used 4 to 6
weeks after surgery and weaned as tolerated.

FIGURE 78-7 Intraoperative photograph of a stacked profunda artery perforator


flap (PAP) anastomosis to proximal and distal internal mammary vein and artery.
A: The pedicle vessels have been kept long to increase the ease of stacked flap
anastomosis in a single breast. B: Stacked flap sutured into place with minimal
tension and good perfusion.
OUTCOMES
The PAP flap is a safe and consistent second option for breast reconstruction,
with complication rates comparable to that of free flaps for breast
reconstruction (18). A retrospective of 101 consecutive PAP flaps reported a
mean flap weight was 425 g +/− 153 g, ranging from 170 to 815 g, an
average pedicle length of 10.3 +/− 3 cm and an average number of 1.7 +/−
0.8 (range, one to four) perforators included in the flap. Reported
complications included total flap loss (2%), donor-site cellulitis (5.9%), or
donor-site wound dehiscence (10.9%) (18). Another retrospective review of
164 consecutive PAP flaps reported a success rate of 99%, with
complications including hematoma (1.9%), seroma (6%), fat necrosis (7%),
and donor-site infection (1.9%) (19). Finally, a meta-analysis by Qian et al.
of 12 studies including 516 PAP flaps reported a pooled surgical success rate
of 99% (95% CI: 97% to 100%) and an overall complication rate of 23%
(95% CI: 18% to 27%). Out of all complications, wound dehiscence was the
most common with incidence of 6% (95% CI: 4%–9%), followed by seroma
2% (95% CI: 0%–6%), and hematoma 1% (95% CI: 0%–2%). Partial
necrosis and flap loss (Case 4) accounted for 2% (95% CI: 0%–5%) and 1%
(95% CI: 0%–3%), respectively (19). The advantages of the PAP flap include
thick donor tissue, a reliable blood supply with a long pedicle and adequate
caliber, and a favorable donor site (20). For contour irregularities or scars that
can develop postoperatively, aesthetic revision can be performed using the
posterior thigh advancement flaps. The outcomes suggest that in select cases,
TUG variants may be considered more than just a secondary option for
autologous breast reconstruction.

CASES

CASE 1

Presented in Figure 78-8 an intraoperative view of a thin patient with


previous history of radiation therapy for a left breast carcinoma. Note the
area of anticipated profunda artery perforator (PAP) flap insetting and
immediate fat grafting of the medial upper pole. Flap design along the
medial posterior thigh, with marking of the PAP, as identified on the
computed tomography scan and with Doppler probe. Intraoperative
dissection of the pedicle within the adductor magnus. Flap harvest, with a
pedicle length in excess of 10 cm, provides greater freedom in flap
insetting. Fat grafting is used to provide volume enhancement of the
upper and medial pole of the left breast in an immediate fashion.

FIGURE 78-8

CASE 2

Patient with a history of immediate reconstruction, with subpectoral


tissue expanders’ placement, and “Y” closure of the mastectomy skin
flaps to limit the incisions within her anticipated areola size. She
underwent subsequent radiation therapy to the left breast with a slight
migration of her tissue expander in a cephalad direction on the right side.
The tissue expanders were removed 1 year later and replaced with
bilateral profunda artery perforator (PAP) flaps. Note the high-riding
inframammary fold (IMF) in the irradiated left breast compared to the
right. She underwent subsequent revisions including aggressive fat
grafting to the irradiated left breast, in order to lower the IMF. There was
improved symmetry after final fat grafting (Fig. 78-9A–F).
Secondary revisions after delayed reconstruction with PAP flaps,
included more fat grafting to the bilateral breast and bilateral nipple
areolar complex reconstruction (Fig. 78-9G–I).

FIGURE 78-9

CASE 3

Illustrated in Figure 78-10 is a thin patient who underwent a bilateral


implant salvage procedure utilizing bilateral PAP on the right and
bilateral DIEP flaps on left for a total of four flaps. Multiple flap
combinations are possible (DIEP, PAP, TUG, superficial circumflex iliac
artery (SCIA)). In cases of limited donor-site availability, the use of
stacked flaps can provide additional volume in one operation.

FIGURE 78-10

CASE 4

This case illustrates a 48-year-old patient who previously underwent


bilateral nipple-sparing mastectomy and immediate breast reconstruction
with buried profunda artery perforator (PAP) flaps (Fig. 78-11). Three
weeks postoperatively the left flap was compromised in motor vehicle
accident, with a seatbelt injuring the left breast. The left PAP flap was
subsequently removed, and she underwent delayed reconstruction with an
extended, fat grafted, autonomous only latissimus dorsi flap, after release
of the underlying scar tissue. She underwent additional revisional surgery
with more bilateral nipple reconstruction, areolar resizing to 5 cm,
bilateral fat grafting to the breasts (250 cc each), and bilateral axillary
dermatolipectomy.
FIGURE 78-11
CONCLUSION
The PAP flap has been recognized as an addition to the armamentarium of
autologous breast reconstruction. It can often be utilized in patients with a
slim body habitus and can be harvested in a supine position and affords a
two-team approach. It has a reliable skin paddle with a long pedicle and large
caliber vessels for anastomosis. These features have some advantages over
other secondary donor sites for breast reconstruction such as the TUG or
gluteal flaps. Possible modifications in the skin paddle design can take
advantages of recruiting greater volume of tissue in the posteromedial thigh
or maximizing areas of soft tissue redundancy.

REFERENCES

1. Angrigiani C, Grilli D, Thorne CH. The adductor flap: a new method for
transferring posterior and medial thigh skin. Plast Reconstr Surg
2001;107(7):1725–1731.
2. Scaglioni MF, Kuo YR, Yang JCS, et al. The posteromedial thigh flap
for head and neck reconstruction: anatomical basis, surgical technique,
and clinical applications. Plast Reconstr Surg 2015;136(2):363–375.
3. Wu JCW, Huang JJ, Cheng MH. Comparison of posteromedial thigh
profunda artery perforator flap and anterolateral thigh perforator flap for
head and neck reconstruction. Plast Reconstr Surg 2015;136(4
Suppl):48–49.
4. Allen RJ, Haddock NT, Ahn CY, et al. Breast reconstruction with the
profunda artery perforator flap. Plast Reconstr Surg 2012;129(1):16e–
23e.
5. Hunter JE, Lardi AM, Dower DR, et al. Evolution from the TUG to PAP
flap for breast reconstruction: comparison and refinements of technique.
J Plast Reconstr Aesthet Surg 2015;68(7):960–965.
6. Wong C, Nagarkar P, Teotia S, et al. The profunda artery perforator
flap: investigating the perforasome using three-dimensional computed
tomographic angiography. Plast Reconstr Surg 2015;136(5):915–919.
7. Haddock NT, Greaney P, Otterburn D, et al. Predicting perforator
location on preoperative imaging for the profunda artery perforator flap.
Microsurgery 2012;32(7):507–511.
8. Satake T, Muto M, Ko S, et al. Breast reconstruction using free posterior
medial thigh perforator flaps: intraoperative anatomical study and
clinical results. Plast Reconstr Surg 2014;134(5):880–891.
9. Mohan AT, Zhu L, Sur YJ, et al. Application of posterior thigh three-
dimensional profunda artery perforator perforasomes in refining next-
generation flap designs: transverse, vertical, and S-shaped profunda
artery perforator flaps. Plast Reconstr Surg 2017;139(4):834e–845e.
10. Saad A, Sadeghi A, Allen RJ. The anatomic basis of the profunda
femoris artery perforator flap: a new option for autologous breast
reconstruction—a cadaveric and computer tomography angiogram
study. J Reconstr Microsurg 2012;28(6):381–386.
11. Hallock GG. The propeller flap version of the adductor muscle
perforator flap for coverage of ischial or trochanteric pressure sores. Ann
Plast Surg 2006;56(5):540–542.
12. Hallock GG. The buttock crease adductor magnus peninsular perforator
flap as another local flap option for repair of the ischial pressure sore
transverse adductor magnus flap. Plast Reconstr Surg
2013;132(1):183e–184e.
13. Homma K, Murakami G, Fujioka H, et al. Treatment of ischial pressure
ulcers with a posteromedial thigh fasciocutaneous flap. Plast Reconstr
Surg 2001;108(7):1990–1996; discussion 1997.
14. Song YG, Chen GZ, Song YL. The free thigh flap: a new free flap
concept based on the septocutaneous artery. Br J Plast Surg
1984;37(2):149–159.
15. Koshima I, Soeda S, Yamasaki M, et al. The free or pedicled
anteromedial thigh flap. Ann Plast Surg 1988;21(5):480–485.
16. Sakai S, Shibata M. Free adductor perforator flap in lower leg
reconstruction. J Plast Reconstr Aesthet Surg 2006;59(9):990–993.
17. Heredero S, Sanjuan A, Falguera MI, et al. The thin profunda femoral
artery perforator flap for tongue reconstruction. Microsurgery
2019;40(2):117–124.
18. Haddock NT, Gassman A, Cho MJ, et al. 101 consecutive profunda
artery perforator flaps in breast reconstruction: lessons learned with our
early experience. Plast Reconstr Surg 2017;140(2):229–239.
19. Qian B, Xiong L, Li J, et al. A systematic review and meta-analysis on
microsurgical safety and efficacy of profunda artery perforator flap in
breast reconstruction. J Oncol 2019;2019:9506720.
20. Allen RJ Jr, Lee ZH, Mayo JL, et al. The profunda artery perforator flap
experience for breast reconstruction. Plast Reconstr Surg
2016;138(5):968–975.
CHAPTER 79

Transverse Upper Gracilis Flaps


ANITA T. MOHAN | REUBEN A. FALOLA | MICHEL SAINT-CYR
HISTORY
The musculocutaneous gracilis flap was first reported in 1972 by Orticochea
(1), and had been subsequently used as a free flap for head and neck, upper
and lower extremity and genitoperineal reconstruction, and facial
reanimation. The skin paddle was traditionally designed longitudinally with
unreliable distal perfusion, however Yousif et al. (1993) performed
anatomical injection studies and showed that perforators had a tendency to
travel in a horizontal direction with perforators posterior to the gracilis
muscle and this led to redesign of the skin paddle (2). This provided the basis
for the transverse myocutaneous gracilis (TMG), also known as the
transverse upper gracilis (TUG) flap, that has gained popularity utilized in
breast reconstruction particularly in Europe (2–7). This modification of using
a transverse skin paddle design afforded a more robust proximal blood
supply, obviating the problems of distal skin paddle necrosis, and allowing
for a faster dissection. A notable disadvantage however, has been lower flap
volume (case 1) compared to its abdominal and gluteal counterparts, limiting
this technique for small- to moderate-sized breasts. The TUG flap can be
used in cases where other donor sites, such as the abdomen are
contraindicated, or in those patients who would like to avoid scars in the
abdominal, gluteal, or back region. The potential skin territory is thought to
extend from the rectus femoris to the biceps femoris. Selective angiographic
studies of the dominant pedicles (Fig. 79-1) have demonstrated vascular
cutaneous territories of 400 cm2 and tendency for perfusion territory to
extend more posteriorly in reference to the gracilis muscle (8). There is
concern with regard to skin viability at the margins with a vertically
orientated flap and this may be somewhat improved with inclusion of a
second vascular pedicle (8–11). Modifications have been used in the design
including harvesting the flap from a more posterior location to recruit the
bulkier posterior thigh tissue allowing an extended TMG flap harvest (4,8), or
within the design including diagonal upper gracilis (DUG) (12), L-shaped, S-
shaped, or trilobed designs (8,13,14) that allow larger skin paddles to be
harvested. These variants in technique allow for further tissue recruitment.
Saint-Cyr et al. have shown this surgical approach to be appropriate to gain
flap volume without increased morbidity (8).
INDICATIONS
The technique is more commonly utilized in autologous reconstruction of
small- to medium-sized breasts. It can be used in bilateral reconstruction or
stacked for a unilateral reconstruction. It is also dependent on body habitus
and availability of adequate tissue laxity within the upper thighs. Medial
thigh tissue often directly correlates well with body mass index, and therefore
is a good option if abdominal or alternative donor sites are not available.

FIGURE 79-1 Anatomical study using 3D rendered computed tomographic


angiography to demonstrate the vascular territory of the gracilis flap in a human
cadaver. Note the paucity of vascularity in the anterior to the gracilis muscle.
Maximal vascularity is present in the medial and posterior portions of the thigh, and
in the vertical component of the gracilis muscle, which indicates the area of ideal skin
paddle perfusion and design. (Reprinted with permission from Wong C, Maia M, Bailey
S, et al. The extended transverse musculocutaneous gracilis (TMG) Flap: 3D CT
Angiography and Clinical Series. Plast Reconstr Surg. 2010;126:92.)
CONTRAINDICATIONS
A history of previous liposuction to the medial thighs may present as a
potential increased risk for perforator flap harvest; this is not an absolute
contraindication. Previous thighplasty, reconstruction of large breasts, and
delayed reconstructions have been described as contraindications for this flap
choice selection (3,5,15). However, a thorough history, clinical examination,
and appropriate counselling of the patient is essential and the use of
preoperative and intraoperative imaging techniques may provide additional
information for planning and assessment of the viability of the flaps when
harvested (16).
PREOPERATIVE PLANNING
The gracilis is a flat type II (Mathes and Nahai) muscle flap of the medial
thigh which lies between adductor longus and sartorius anteriorly, and
semitendinosus posteriorly. In the presence of adductor longus and magnus,
this muscle is expendable. The dominant pedicle arises from the ascending
branch of the medial circumflex artery or directly from the profunda femoris
and enters the muscle belly on its deep surface in the upper third, at 9 to 12
cm inferior to the pubic tubercle. Usually two or three vascular pedicles enter
the muscle, the most proximal usually being the dominant pedicle, and
arising between adductor longus and brevis before reaching the muscle. The
dominant pedicle can provide up to 6 to 7 cm in the length. On entering the
gracilis muscle it divides into ascending, descending, transverse branches
running in parallel with the longitudinal muscle fibers and commonly
anastomosing with the second vascular pedicle. Musculocutaneous
perforators generally predominate in both size and number. The dominant
pedicle provides musculocutaneous perforators to the overlying skin in the
proximal third of the muscle and direct fasciocutaneous vessels from the
medial circumflex artery, or superficial femoral artery in the distal portions of
the muscle (minor pedicles).
FIGURE 79-2 Intraoperative markings of position of the gracilis muscle and
marking of the transverse upper gracilis (TUG) flap.

For operative markings, the adductor longus tendon can be palpated


following forced adduction and a line can be drawn to delineate the insertion
anteriorly from the pubic tubercle to the medial femoral condyle. The central
axis of the gracilis muscle is 2 to 3 cm posterior to this line, however the
boundaries of the gracilis muscle can be palpated from the septum between
adductor longus and gracilis, and the muscle can be marked out as shown in
Figure 79-2. The skin paddle superior border is roughly 1 to 2 cm below the
upper thigh crease concealing the donor TUG flap specifically (cases 2 and
3), skin paddles can be raised up to approximately 16.5 × 11 cm or more, but
dependent on skin laxity. The maximal anterior extension of the horizontal
skin paddle is approximately 5 cm anterior to the gracilis, or 1 to 2 cm
anterior to the lateral edge of adductor longus (Fig. 79-3), avoiding damage
to any lymphatics or creating a noticeable scar. The vertical height of the flap
can vary from 5 to 10 cm that is determined by skin laxity. Maximal pinching
should be checked in adduction and abduction of the thigh to prevent closing
tension. A horizontal pinch test is undertaken to design the vertical
component of the skin paddle if required and 7 cm is usually sufficient for
closure. When combined with a vertical skin paddle, this can create a trilobed
(Fig. 79-4), “L”-shaped skin paddle (Fig. 79-5), or “S”-shaped paddle (Fig.
79-6). Table 79-1 provides a summary of the gracilis myocutaneous flap
design modifications for breast reconstruction, patient selection criteria, and
advantage and disadvantages associated with each flap design.

FIGURE 79-3 Intraoperative view showing partial dissection of the TUG flap
pedicle. After the initial skin incision in performed we see the adductor longus
muscle and the gracilis muscle, just posteriorly to it. Note here the accessory
saphenous vein, which should be retained in order to minimize any risk of lower
extremity swelling. There is very slight volume contribution to the flap from the
anterior portion of the skin paddle, just lateral to the adductor longus; therefore,
dissection of this area should be superficial to avoid damage to the lymphatic basin
above the femoral triangle, and the risk of lower extremity lymphedema. Most of the
volume of the flap is concentrated posteriorly and medially. Care should also be
taken to not extend the incision too high along the groin, anterior to the adductor
longus.
FIGURE 79-4 Intraoperative photograph of a trilobed design incorporating both a
horizontal and vertical component in the skin paddle.
FIGURE 79-5 Intraoperative photograph of an L-shaped transverse myocutaneous
flap harvested for breast reconstruction and weighing approximately 400 g.
FIGURE 79-6 Intraoperative markings and dissection of an S-shaped skin paddle in
the proximal medial thigh and subsequent orientation of the gracilis muscle. Note
here that this flap design incorporates maximal vertical and horizontal skin laxity of
the thigh for maximum harvest volume. This dissection resulted in a 700-g
myocutaneous flap, which can easily be coned for better contouring. S-shaped design
of the donor site also facilitates an oblique closure without any potential wound-
healing problem associated with T-junction closure.

TABLE 79-1 Summary of Modifications of Gracilis Flap for Breast


Reconstruction With Subcutaneous and Skin Paddle Extension as Proposed
by Saint-Cyr et al.
When designing the trilobed pattern, it is important to keep the base of
each lobe relatively broad which would result in an oval shape at the center of
the flap. When wanting to incorporate horizontal and transverse laxity (Fig.
79-7), the authors of this chapter would prefer the “S” design to avoid the
problematic T-junction at the donor site resultant from the trilobed design.
The vertical incision should be placed at the anterior border of the gracilis
and stopped at midthigh level. The posterior extension of the flap is carried
out midway between the medial midaxial line and posterior thigh midline.
Any extension beyond this point may increase the risk of fat necrosis,
damage to posterior cutaneous nerves, and flap-related complications. With
inclusion of a vertical component, the posterior extension can usually be
shortened to the midaxial line. Estimated additional soft tissue recruitment
through skin undermining can also be marked out preoperatively (Fig. 79-8).
Table 79-1 provides an overview of flap designs for the transvers gracilis
myocutaneous flaps.
FIGURE 79-7 Preoperative view of the vertical upper gracilis (VUG) flap donor site.
Left: Skin laxity tissues in the donor site favor an S-shaped skin paddle. Right:
Postoperative view of the TUG flap donor site. Note the impact of the vertical
component of the S-shaped flap on postoperative aesthetics in the thighs. Improved
contour is noted especially in patients with preoperative redundant thigh tissue.

FIGURE 79-8 Intraoperative photograph demonstrating a transverse upper gracilis


(TUG) skin flap design with a marked-out area for additional 4 cm of soft tissue
recruitment.
OPERATIVE TECHNIQUE
Flap harvest is performed supine in a lithotomy position with thighs and legs
on extremity boards. The superior inguinal crease incision is made 2 to 5 cm
anterior to anterior border of the gracilis, extending posteriorly to the medial
midaxial line. The septum is identified between the adductor longus and the
gracilis to locate the pedicle and adjustments to the skin paddle can be made
according to its position. Next, the inferior skin incision is made.
Undermining the skin inferior to the lower incision can be performed to
recruit subcutaneous fat, in a beveled fashion to recruit subcutaneous tissue
medially and posteriorly. However, undermining is limited at the widest
portion of the skin paddle to minimize risks of wound dehiscence.
Incorporation of subcutaneous tissue outside the boundaries of the skin
paddle should be kept over the gracilis muscle and posteriorly to gain
additional flap volume. The greater saphenous vein should always be
preserved and not incorporated within the flap, however accessory branches
may be ligated and there should be minimal disruption of the lymphatics
anteriorly. There may be a tendency for the subcutaneous tissue and skin to
droop posteriorly in relation to the gracilis muscle, for heavier patients (17).
Small proximal and distal V-shaped incisions can be used in these patients, to
first identify the muscle, and then tailor the dissection of the skin paddle
appropriately (17). Once the skin paddle is dissected, the gracilis muscle can
be harvested based on the medial circumflex femoral vascular pedicle with
maximal possible muscle length to gain the largest volume. Fat grafting
directly to the gracilis muscle distal to the skin paddle can also increase
volume.
For the inset, the flap is folded, or a limb is rotated onto itself to form a
“teardrop” and shaped to become a breast mound (Figs. 79-9 and 79-10). The
skin paddle limbs of the extended flaps can be rotated either clockwise or
counterclockwise, yielding the shape desired. The anterior limb, when
present, may be tucked under the flap or beside it to create the deep section of
the breast mound, thus providing medial fullness and better projection.
Shaping of the flap can be tailored to the reconstructive requirements of the
patient. In addition, the resultant “dog-ear” of skin projecting anteriorly can
be used together with rib cartilage for immediate nipple reconstruction at the
time of flap inset. The donor-site closure is similar to that of a medial thigh
lift. The superficial fascia of the lower edge of the wound is secured to Colles
fascia superiorly in order to prevent traction on the labia or scar migration. A
decision-making guide proposed by Saint-Cyr to choose the appropriate skin
paddle and flap design based on patient characteristics is shown in Figure
79-11.

FIGURE 79-9 Intraoperative photograph of shaping of an extended transverse


upper gracilis myocutaneous flap to create a teardrop-shaped breast mound for
breast reconstruction, seen here with immediate nipple reconstruction. Note that a
small piece of costochondral cartilage can be harvested and placed in the nipple
reconstruction for additional projection.
FIGURE 79-10 Intraoperative view of an S-shape skin paddle design of an upper
gracilis myocutaneous flap. A corresponding fully dissected flap from a different
case is shown, as well as subsequent coning in order to reproduce the original breast
shape and enhance projection.

Intraoperative Care
The flap can be harvested in the lithotomy or supine positioning with the legs
on extremity boards or in a frog-legged position, with the hip and knee
flexed, and thigh abducted.
Postoperative Care
The donor site is closed over a drain that can be removed when the output is
less than 20 to 30 mL/day for 2 to 3 consecutive days. Patients are
encouraged to ambulate on postoperative day zero. Sitting or activities that
place direct pressure on the donor site should be avoided for 3 to 4 weeks
after surgery. Alternatively, prefashioned seating and positioning cushions
can be used to minimize pressure points and occurrences of wound
dehiscence. Compression garments may be used 4 to 6 weeks after surgery
and weaned as tolerated.
FIGURE 79-11 Example of reconstructive algorithm for decision making to optimize
flap design based on variations of the gracilis myocutaneous flaps for breast
reconstruction previously described by Saint-Cyr et al. (8).

CASES

CASE 1
Illustrated above is patient who underwent immediate right breast
reconstruction with a transverse upper gracilis (TUG) flap, with
anastomosis of the internal mammary vessels. Postoperatively, there was
insufficient flap volume and projection, cephalad migration and
asymmetry of the inframammary fold (IMF), and skin envelope
contracture. This produced IMF asymmetry and a lack of volume
projection. She underwent serial fat grafting of the right TUG flap and
skin envelope, in order to maximize volume and lower the IMF. Each
subsequent serial fat grafting resulted in the lowering of the IMF and
provided improvements in breast volume projection. She eventually
required a contralateral symmetry procedure, which involved mastopexy
augmentation.

CASE 2
The above is the case of a patient who underwent bilateral T-shaped
transverse upper gracilis (T-TUG) flaps. She had excess skin in the
vertical and horizontal direction of the inner thighs and did not wish to
have an abdominally based reconstruction. Postoperatively, we noted
large skin paddles, ptotic breasts, and a slight asymmetry with regard to
projection and breast volume. She underwent secondary revision with
vertical mastopexy and fat grafting to improve symmetry. This was
followed by bilateral nipple areolar complex reconstruction. Note that the
vertical component of the T-TUG should be designed so as not to be
visible from an anterior–posterior direction and should be posterior
enough to be well concealed.

CASE 3

Illustrated above is a thin patient, status post bilateral skin-sparing


mastectomy and immediate reconstruction with transverse upper gracilis
(TUG) flaps. Note preoperative markings, where the anterior component
of the skin flap is kept relatively medial and does not enter the territory of
the femoral triangle, to minimize any risks of injury to the lymphatics in
the region. The minimal volume in this area does not contribute greatly to
flap size, and scars here are more noticeable; therefore, anterior extension
of the skin paddle should be avoided. The donor-site flap design and
orientation are based on available volume and skin laxity. Top Row:
Preoperative markings of donor site. Bottom Row: Preoperative and
postoperative view of breasts after TUG flap reconstruction and
subsequent fat grafting.
OUTCOMES
The extended TUG flap has consistent vascular reliability, with enough tissue
for reconstruction of small- to moderate-sized breasts. In a retrospective
study of 12 extended transverse gracilis flaps, the average flap weight was
386 g, yielding up to 750 g on the large size (8). Donor-site harvest allowed
for removal of redundant thigh skin and functional thighplasty, and in
massive weight loss cases patients would benefit from a circumferential thigh
lift. Complications, though uncommon, include wound dehiscence,
hematomas, seromas, and fat necrosis. These are not specific to any one
surgical technique, and functional loss of the gracilis muscle is minimal (18).
A systematic review conducted by Kang et al., of outcomes in the major
gracilis flaps, including TUG, V-TUG, and longitudinal gracilis
myocutaneous (LGM) flaps, analyzed a total of 485 gracilis flaps in 335
patients from 1966 to 2015. The study found that V-TUG flaps provided the
largest mean flap weights, requiring the no additional lipofilling or implant
placement. In contrast 50.6% of TUG flaps required additional fat grafting or
prosthetic augmentation. A low incidence of donor-site morbidity was
exhibited in all flap types. V-TUG and LGM flaps reported no flap losses,
and 2.3% total flap loss and 2.0% partial loss was found in all TUG flaps
(19).
CONCLUSION
The TUG flap can reconstruct small to moderate-sized breasts particularly
when abdominal flaps are not feasible. The extended TUG can optimize
recruitment of posterior and medial thigh subcutaneous tissue and provide a
conspicuous donor site. The gracilis has consistent anatomy and can be
rapidly harvested. By consideration of anatomy, adaptations to the traditional
skin paddle design for the extended TUG permitted versatility within the
reconstruction and not just limited to small-sized breast reconstructions.

REFERENCES

1. Orticochea M. The musculo-cutaneous flap method: an immediate and


heroic substitute for the method of delay. Br J Plast Surg
1972;25(2):106–110.
2. Yousif NJ. The transverse gracilis musculocutaneous flap. Ann Plast
Surg 1993;31(4):382.
3. Arnež Z, Pogorelec D, Planinšek F, et al. Breast reconstruction by the
free transverse gracilis (TUG) flap. Br J Plast Surg 2004;57(1):20–26.
4. Fattah A, Figus A, Mathur B, et al. The transverse myocutaneous
gracilis flap: technical refinements. J Plast Reconstr Aesthetic Surg
2010;63(2):305–313.
5. Wechselberger G, Schoeller T. The transverse myocutaneous gracilis
free flap: a valuable tissue source in autologous breast reconstruction.
Plast Reconstr Surg 2004;114(1):69–73.
6. Schoeller T, Huemer GM, Wechselberger G. The transverse
musculocutaneous gracilis flap for breast reconstruction: guidelines for
flap and patient selection. Plast Reconstr Surg 2008;122(1):29–38.
7. Schoeller T, Wechselberger G. Breast reconstruction by the free
transverse gracilis (TUG) flap. Br J Plast Surg 2004;57(5):481–482.
8. Saint-Cyr M, Wong C, Oni G, et al. Modifications to extend the
transverse upper gracilis flap in breast reconstruction: clinical series and
results. Plast Reconstr Surg 2012;129(1):24e–36e.
9. Whitaker IS, Karavias M, Shayan R, et al. The gracilis myocutaneous
free flap: a quantitative analysis of the fasciocutaneous blood supply and
implications for autologous breast reconstruction. PLoS One
2012;7(5):e36367.
10. Hallock GG. The conjoint medial circumflex femoral perforator and
gracilis muscle free flap. Plast Reconstr Surg 2004;113(1):339–346.
11. Whetzel TP, Lechtman AN. The gracilis myofasciocutaneous flap:
vascular anatomy and clinical application. Plast Reconstr Surg
1997;99(6):1642–1652; discussion 1653–1655.
12. Dayan E, Smith ML, Sultan M, et al. The diagonal upper gracilis (DUG)
flap. Plast Reconstr Surg 2013;132:33–34.
13. Peek A, Müller M, Ackermann G, et al. The free gracilis perforator flap:
anatomical study and clinical refinements of a new perforator flap. Plast
Reconstr Surg 2009;123(2):578–588.
14. Wong C, Mojallal A, Bailey SH, et al. The extended transverse
musculocutaneous gracilis flap: vascular anatomy and clinical
implications. Ann Plast Surg 2011;67(2):170–177.
15. Saint-Cyr M, Shirvani A, Wong C. The transverse upper gracilis flap for
breast reconstruction following liposuction of the thigh. Microsurgery
2010;30(8):636–638.
16. Mohan AT, Wong C, Saint-Cyr M. The Transverse upper gracilis flap
for breast reconstruction following liposuction of the thigh. In: Shiffman
M, Di Giuseppe A. (eds). Liposuction. Berlin, Heidelberg:Springer;
2016:561–566. doi:10.1007/978-3-662-48903-1_55
17. Park JE, Alkureishi LW, Song DH. TUGs into VUGs and friendly
BUGs: transforming the gracilis territory into the best secondary breast
reconstructive option. Plast Reconstr Surg 2015;136(3):447–454.
18. Mathes DW, Kenkel JM. Current concepts in medial thighplasty. Clin
Plast Surg 2008;35(1):151–163.
19. Kang V, Robinson E, Barker E, et al. Myocutaneous gracilis free flaps
in microsurgical breast reconstruction: a systematic review comparing
variations of the upper gracilis flap. J Reconstr Microsurg
2017;33(09):630–635.
20. Wong C, Maia M, Bailey S, et al. The extended transverse
musculocutaneous gracilis (TMG) flap: 3D CT angiography and clinical
series. Plast Reconstr Surg 2010;126:92.
CHAPTER 80

The Lumbar Artery Perforator Flap:


An Alternative to DIEAP Flap for
Breast Reconstruction
MOUSTAPHA HAMDI | GIUSY FATIGATO
HISTORY
The lumbar artery perforator (LAP) free flap is an excellent alternative in
autologous breast reconstruction for those patients who are not eligible for
the deep inferior epigastric perforator (DIEP) flap, which is still considered
the gold standard. Musculocutaneous and adipofascial flaps of the lumbar
region have been described since the 1970s (1), also known as “reverse
latissimus dorsi flaps,” they were used as pedicled flaps to reconstruct lower
lumbar soft tissue defects and decubitus ulcers (2,3). The LAP flap was first
described in the literature by Kroll and Rosenfield in 1988 as a new type of
flap based on unnamed perforators arising near the midline of the lower back
region for the coverage of lumbosacral defects, thus reducing the donor site
morbidity associated with traditional musculocutaneous flaps (4). In 1999,
Kato et al. reported a cadaveric and clinical study about the vascular territory
of LAPs, therefore validating the use of this vessel in harvesting LAP island
flaps and free flaps in this region (5). Since then, several studies have
described the anatomy of LAP flap based on perforators (6–11). In 2003, for
the first time, de Weerd et al. described the use of a free LAP flap for breast
reconstruction (12). To date, a few case series of LAP flaps for breast
reconstruction have been reported (11,13–15). For this purpose, LAP flap
may be a satisfactory option, providing a large amount of fat tissue harvested
from the so-called “love handles” in the lumbar and flank regions. For these
reasons in our practice, the LAP flap is a reliable second choice for breast
reconstruction, despite flap dissection may be more challenging and time
consuming compared to other alternatives. The LAP flap can be also used as
a sensate flap by harvesting the nervi clunium superiores and anastomosing
the sensory nerve of the flap to the fourth intercostal nerve (14).
ANATOMY
The four pairs of lumbar arteries (LAs) arise from either side of abdominal
aorta and they travel behind the psoas major muscle (Fig. 80-1). The upper
three LAs run laterally and backward between the quadratus lumborum and
the erector spinae muscles while the fourth pair of arteries normally runs
anterior to the quadratus lumborum muscle (5,6,10). The arteries then give
rise to perforators that pierce the thoracolumbar fascia just lateral to the
erector spinae muscle and supply the skin and the subcutaneous tissue in this
region. The course of LAs is variable, however perforator vessels arising
from the first pair of LAs are more likely to be musculocutaneous, whereas
perforators arising from the fourth LAs are more likely to have a
septocutaneous course, emerging between the erector spinae muscle and
quadratus lumborum.

FIGURE 80-1 Anatomy. The lumbar arteries (LAs) arise from either side of the
abdominal aorta and they travel behind the psoas major muscle. The upper three
LAs run laterally and backward between the quadratus lumborum and the erector
spinae muscles.

In our anatomical study, based on multidetector computed tomographic


scan findings in 20 patients, the fourth LA was the most reliable for having
perforators (L3 and L4 perforators were dominant in 90% of investigated
patients) (11). The mean diameter of lumbar vessel perforator (artery and
vein) was 2.8 ± 0.3 mm (6,11).
The mean point of perforation of the lumbar fascia by the lumbar vessel
perforator lay at 7.22 cm (range 5 to 9 cm) from the midline (5). The mean
pedicle length is described to vary between about 5 and 7 cm (6,11,14).
INDICATION
LAP flap can be a good alternative in patients who are not suitable for a
DIEAP flap breast reconstruction because of unavailable abdominal donor
site: insufficient abdominal tissue, aggressive liposuction, previous
abdominoplasty or excessive abdominal scar. Other candidates for LAP flap
breast reconstruction are patients who already underwent a failed DIEAP flap
or who developed a secondary tumor in contralateral breast after DIEAP flap
(11). LAP flap is also indicated in BRCA-positive young women who want
immediate reconstruction after preventive mastectomy and who lack
abdominal bulk for bilateral reconstruction (14).
CONTRAINDICATION
Contraindications to LAP flap reconstruction are similar to those of other
types of free tissue transfer and include previous incisions across donor sites
that might compromise vascular sources, as in circumferential lower body lift
or previous Latissimus Dorsi reconstruction with distal placement of skin
paddle over the lumbar area, aggressive liposuction of the love handles area,
and finally lack of the amount of available tissue. Patients’ comorbidities
such as smoking, advanced age, diabetes mellitus, and peripheral vascular
disease, should be assessed because they may contribute to delayed wound
healing, fat necrosis, and partial/total flap loss.
PREOPERATIVE PLANNING
Preoperative evaluation should include the same workup as for any other free
flap autologous breast reconstruction technique. Given the variability of
perforator size, course and length (Fig. 80-2), all patients should undergo a
preoperative computed tomographic angiography (CTA) of the lumbar and
thoracic regions. This enables the surgeon to evaluate the branching pattern
and course of the perforator (septocutaneous or musculocutaneous), thus
identifying the most appropriate perforator (Fig. 80-3), and also to assess the
patency of the internal mammary recipient vessels (8). The perforators are
marked by the radiologist using a grid system in which the midline along the
spinal process represents the y-axis, while the x-axis is a horizontal line
connecting the highest points on both iliac crests (Fig. 80-2). The dominant
perforator is marked and confirmed by a unidirectional Doppler. Bilateral
LAP flap cases are time consuming because of multiple position change
during the surgery. Therefore, bilateral LAP cases are always performed, in
our hands, in two stages with a minimum of 3 months between operations
(see Case 2, Fig. 80-11) (11).
FIGURE 80-2 Distribution of the dominant perforators. Position of origin and site of
penetration through the lumbar fascia are indicated in millimeters to the 0,0
intersection. (Redrawn from Hamdi M, Craggs B, Brussaard C, et al. Lumbar artery
perforator flap: an anatomical study using multidetector computed tomographic scan and
surgical pearls for breast reconstruction. Plast Reconstr Surg 2016;138:343–352.)

The patient is marked in a standing position (Fig. 80-4A). The posterior


midline and iliac crest is marked initially and then the dominant LAP is
identified and confirmed by unidirectional Doppler. A fusiform skin island is
drawn over the perforators slightly obliquely above the iliac crest pointing
toward the anterior superior spine to resemble an upper buttock lift scar (Fig.
80-4B,C). The drawings should not pass the posterior midline, and they are
designed to eventually meet up with an abdominoplasty scar laterally (Fig.
80-5A,B). The size of the flap is judged using the pinch test. Nevertheless,
the skin island should be kept as small as possible to avoid problems with
donor site closure; skin island of 8 to 10 cm can be easily closed primarily. In
the last few years, a more anterior design of the flap was introduced in order
to reduce the incidence of seroma by preserving the lymphatic drainage over
the thick deep fascia over the paraspinal muscle (11).
FIGURE 80-3 Preoperative computed tomographic angiography (CTA) of the
lumbar region to evaluate the branching pattern and course of the perforator
(septocutaneous or musculocutaneous).

FIGURE 80-4 A–C: Preoperative markings. The patient is marked in a standing


position. The skin island is drawn over the perforators slightly obliquely above the
iliac crest pointing toward the anterior superior spine to resemble an upper buttock
lift scar.

FIGURE 80-5 A, B: Donor site. The flap’s design was extended to the
abdominoplasty scar. On the right lower back is the scar from the previous LAP
flap.
OPERATIVE TECHNIQUE
The flap can be harvested in either a prone position or in a lateral decubitus
position (Fig. 80-6A,B). If the patient lies in the lateral decubitus position,
the flap is most easily harvested from the back toward the abdomen with the
surgeon standing at the posterior side of the patient (posterior approach). The
anterior approach is also used when the perforator is more laterally located. It
allows a two-team approach for the simultaneous preparation of the
mastectomy site and for the harvesting of a deep inferior epigastric
interposition graft if necessary. In case of prone decubitus, the operation
starts with the patient in supine decubitus while the mastectomy site is
prepared, the recipient vessels are dissected and a deep inferior epigastric
pedicle interpositional graft is harvested. Subsequently, the patient is turned
to a prone position for flap dissection. The flap is harvested from lateral to
medial with the surgeon standing at the ipsilateral side. While anastomosis of
the interposition graft is performed, a second team closes the donor site and
repositions the patient in a supine position for revascularization and shaping
of the flap (11,14).
After incising the skin and subcutaneous tissue, the thoracolumbar fascia is
opened medially over the erector spinae muscle (Fig. 80-7). The fascia is
elevated with a retractor to identify the sensory nerves and the perforators.
While directly visualizing the perforators, the flap is elevated from
anterolateral to medial in a subfascial plane. To obtain sufficient pedicle
length, the selected perforator with its concomitant vein is dissected down
between the erector spinae and quadratus lumborum muscles. At this stage,
the lumbar pedicle length and diameter are evaluated. Regardless of the
pedicle length and size obtained, the dissection should stop at the level of the
processus transversus vertebrae to avoid injury to the spinal nerves (11).
Indeed, postoperative quadriceps weakness and L3–L4 paresthesia have been
reported probably due to neuropraxia caused by an extensive dissection
beyond the processus transversus (14). To harvest more subcutaneous tissue,
the flap is raised beveling superiorly and inferiorly, creating a gluteal
extension in the adipose tissue. During undermining, care should be taken to
leave the fat layer above the superficial fascia in order to avoid donor site
depression. The flap is then freed from the abdominal deep fascia. If a
vascular graft is used, the flap is preferably positioned as it is harvested to
benefit from the cranial beveling which will supply the upper pole fullness of
the breast, whereas the thick inferior gluteal beveling gives volume and
projection to the breast. Because of these typical features, the LAP flap does
not need to be shaped and remodeled to obtain a natural breast contour.

FIGURE 80-6 A, B: Patient’s positioning on lateral decubitus which allows two-team


approach for flap harvesting and preparing of the recipient site. The perforators
were marked according to the CT-scan findings and confirmed by unidirectional
Doppler.

The flap can be also harvested with a sensory nerve if required. The nervi
clunium superiores follows the perforators, can be isolated for up to 10 cm of
length, and anastomosed to the fourth intercostal nerve if one desires to
reinnervate the flap. The severing of the nervi clunium superiores can lead to
hypesthesia of the upper buttock, which is rarely bothersome to the patient
(14).
FIGURE 80-7 The selected perforator is dissected down between the erector spinae
and quadratus lumborum muscles.
FIGURE 80-8 Flap is harvested. The LAP flap shows a short pedicle length (less
than 6 cm) and small caliber.

If the length of the pedicle is adequate (≥6 cm) and/or the artery diameter
is more than 0.5 mm, the anastomosis is performed in a similar manner as for
a DIEP flap. If the length or the caliber of the pedicle are not suitable, a
vascular interposition graft will be necessary (11) (Fig. 80-8). Harvesting the
deep inferior epigastric segment is straightforward and allows a longer
pedicle with a better size match to the diameter of the recipient vessels. The
anastomoses between the vascular graft and the LA and vein are done on a
separate surgical table (Fig. 80-9).
The internal mammary vessels are dissected simultaneously using a two-
team approach. However, due to the short lumbar perforator length, the
internal mammary vessels are dissected over 3 to 4 cm after removal of one
costal cartilage. This makes the microanastomosis easier.
FIGURE 80-9 A vascular artery–vein bypass is harvested from the left deep inferior
epigastric vessels, thereby creating a 12-cm pedicle length and better caliber match
with the IM recipient vessels.

Nevertheless, microanastomosis can still be done with costal cartilage


removal if the intercostal space is wider than 1.5 cm (11).
Once the microanastomosis is done with the internal mammary vessels, the
flap is fixed temporarily with surgical staples to the mastectomy skin. The
patient is then turned to the supine position for shaping of the breast. The
subcutaneous tissue is fixed to the pectoralis major muscle at the axillary side
and to the inframammary fold. The flap is deepithelialized depending on the
reconstruction type. In some cases, the entire flap is used; in others, the distal
part of the flap is trimmed if there are signs of venous congestion or
ischemia. The flap is used as a hammock within the mastectomy pocket
without the need for folding the flap onto itself. As the LAP flap donor site is
prone to seroma, a careful closure of the donor site is mandatory. In order to
reduce seroma, skeletonizing the iliac crest should be avoided and only
limited undermining, mainly inferior, resembling an upper buttock lift, is
required. Quilting sutures are sometimes used, as well as fibrin glue. Long-
acting local anesthetic is injected subfascially to reduce postoperative pain.
Two suction drains are left in the donor site until they give less than 20 cc/24
hrs or a maximum of 10 days postoperatively.
INTRAOPERATIVE CARE
Prophylactic treatment of low–molecular-weight heparin (LWMH) is usually
given the night before surgery and intermittent pneumatic compressive (IPC)
devices are placed on the legs during surgery and continued until the next day
after surgery to prevent deep venous thrombosis (DVT). Standard anesthesia
monitors are placed, and general anesthesia is administered. An intravenous
prophylactic dose of antibiotic is given, and a urinary catheter is inserted.
Standard sterile antiseptic skin prep and draping are used. Attention is paid to
the protection of all pressure points and placement of an arm roll is
mandatory for patients positioned in the lateral decubitus.
POSTOPERATIVE CARE
An abdominal binder or lipopanty is applied at the donor site for 4 to 6 weeks
postoperatively. Drains are left in the donor site until they produce less than
20 mL/24 hrs or for a maximum period of 10 days postoperatively.
Mobilization of the patient starts on the second postoperative day. Secondary
corrections such as nipple reconstruction, breast remodeling with fat grafting,
and contralateral breast symmetrization are performed 3 to 6 months after the
primary surgery. If necessary, donor site symmetrization is also performed at
that time by contralateral flank liposuction to enhance waist contour.

CASES

CASE 1

A 58-year-old patient presented for autologous breast reconstruction. She


underwent left mastectomy followed by radiotherapy. The patient had
abdominal liposuction few years before the mastectomy which prevented
harvesting of DIEP because of lack of abdominal tissue. She was a good
candidate for LAP flap breast reconstruction (Fig. 80-10).
FIGURE 80-10 A 58-year-old patient presented for autologous breast
reconstruction. She underwent left mastectomy followed by radiotherapy. A–
C: Preoperative view. The patient is not suitable for a DIEAP flap breast
reconstruction because of abdominal liposuction few years before the
mastectomy. D–F: Two-year postoperative view after left LAP flap. G: Two-
year postoperative view of the donor site. The scar is above her underwear
but does not disrupt the buttocks and waistline contour is improved.
CASE 2

A 53-year-old patient who had previous abdominoplasty later underwent


bilateral mastectomy with implant reconstruction. She was unsatisfied
with the results, therefore she was a candidate for reconstruction with
bilateral LAP flaps (Fig. 80-11). We planned bilateral LAP in two stages
with 3 months between operations.
FIGURE 80-11 A 53-year-old patient unsatisfied with the result of implant
reconstruction, underwent sequential reconstruction with bilateral lumbar
artery perforator flaps. The patient was not suitable for a DIEAP flap breast
reconstruction because of previous abdominoplasty. A–C: Preoperative view.
The patient has already undergone first step autologous reconstruction of
right breast with right LAP flap. D: Flap harvesting. The selected perforator
is dissected down between the erector spinae and quadratus lumborum
muscles. E: The left lumbar artery perforator flap was harvested with a
pedicle length less than 6 cm and a small artery diameter and it had almost
the same weight of the prosthesis. F: A vascular artery–vein bypass was
harvested from the left deep inferior epigastric vessels, thereby creating a 12-
cm pedicle length and better artery diameter match with the internal
mammary recipient artery. G, H: Two-year postoperative view after
sequential bilateral LAP breast reconstruction. I, J: Two-year postoperative
view of the donor site. The scar is above her underwear but does not cause
shape deformities and it gives a pleasing flank contouring.
GENERIC RISKS
Generic risks of the procedure are partial/complete flap necrosis,
hematoma/seroma formation, infection, and delayed wound closure in both
donor and recipient sites. The seroma can lead to prolonged drainage, serial
aspiration, and need for excision of seroma capsule. Delayed wound healing
can also be problematic and impact upon the timing of adjuvant treatments.
OUTCOMES
The LAP flap has increasingly gained popularity over the last few years
despite the fact that flap dissection is more challenging and time consuming
compared to other alternatives. Mean operating times vary between 270 and
424 minutes (11,15). The size of a LAP flap is usually ample to create a
breast of sufficient volume. The mean flap size is about 142 cm2 (dimensions
22 × 5.28 × 6.5 cm) and mean flap weight is 495 g (range 366 to 730 g).
Additional lipofilling to improve breast contour can be used to improve the
quality of skin damaged from preoperative irradiation.
In the study by Peters et al. including 35 LAP flaps, six flaps had to be
revised as a consequence of venous thrombosis (17%). Flap necrosis occurred
in three cases only (5.7%) (13). A larger series of 100 LAP flaps for breast
reconstruction in 72 patients has been recently published by Opsomer et al.
(14). With a mean follow-up time of 30 months, they reported a total flap
revision rate of 22%. The indications for revision were hematoma (3%),
venous thrombosis (14%), or arterial thrombosis (6%). Flap necrosis occurred
in 9% of the cases. This high revision rate can be attributable to a necessary
steep learning curve because of the difficult flap dissection, even in expert
hands. Furthermore, the need for an interpositional graft, which means an
additional anastomosis and longer operative time, is another possible risk
factor. The need of interpositional graft is reported to vary between 57% and
80% of the cases (11,14). This is usually harvested from the deep inferior
epigastric artery and vein through a small Pfannenstiel incision. Other options
are the thoracodorsal vessels or the descending branch of the lateral
circumflex iliac artery. Another possible explanation of the reported high
revision rate is the fact that, as the LAP is a secondary choice flap for breast
reconstruction, it is often performed in tertiary reconstruction after flap
failure. As we reported in a previous publication, the tertiary reconstruction
after a total flap failure is always a challenging and higher-risk procedure
(16). In our series, there were no cases requiring revision of
microanastomoses and no cases of flap failure or flap necrosis. A high
seroma rate at the donor site is relatively common, varying from 17% to 78%
(11,14). In the most recent cases, postoperative seromas are largely avoided
by several measures: (1) less flap skin harvested, (2) minimal undermining,
(3) a more anterior design of the flap, and (4) a meticulous closure technique
(11). As described above, quadriceps weakness and paresthesia in the
territory of L3–L4 (10) can be a temporary complication, reported in 3% of
the patients; it spontaneously resolves after intensive physical therapy (14).
Despite the technical difficulties, the LAP flap has remarkable advantages
such as soft and pliable fat tissue and pleasant contour of the donor site. The
lumbar and flank regions offer an optimal fat quality and furthermore the
teardrop shape mimics the native breast glandular tissue and usually does not
require further modeling. Since LAP flap is designed over a transition area
between the back and the buttock, harvesting of a significant amount of tissue
in the so-called “love handles” region is possible without causing shape
deformities, but on the contrary creating a pleasing flank contouring.
However, contralateral liposuction may be required in unilateral cases. The
resulting donor site scar is often too high to be hidden with typical underwear
and this may limit indication in young women or in patients not willing to
have a visible scar (11).
CONCLUSIONS
For patients who are not eligible for DIEAP flap, the LAP flap represents a
reliable alternative for autologous breast reconstruction. Surgical challenges
could be a difficult dissection, an inadequate length of the pedicle and a
possible size mismatch. The major advantages of LAP flap are the fat tissue
quality and the donor site contour. The lumbar and flank regions offer an
optimal fat quality, soft and pliable, and therefore flap shaping is easier and
usually does not require further modeling. Furthermore, LAP flap has lower
donor site morbidity and despite the visible scar, the flanks can be beautifully
contoured.

REFERENCES

1. Hill HL, Brown RG, Jurkiewicz MJ. The transverse lumbosacral back
flap. Plast Reconstr Surg 1978;62(2):177–184.
2. Bostwick J, Scheflan M, Nahai F, et al. The “reverse” latissimus dorsi
muscle and musculocutaneous flap: anatomical and clinical
considerations. Plast Reconstr Surg 1980;65:395–399.
3. Stevenson TR, Rohrich RJ, Pollock RA, et al. More experience with the
“reverse” latissimus dorsi musculocutaneous flap: precise location of
blood supply. Plast Reconstr Surg 1984;74:237–243.
4. Kroll SS, Rosenfield L. Perforator-based flaps for low posterior midline
defects. Plast Reconstr Surg 1988;81(4):561–566.
5. Kato H, Hasegawa M, Takada T, et al. The lumbar artery perforator
based island flap: anatomical study and case reports. Br J Plast Surg
1999;52(7):541–546.
6. Offman SL, Geddes CR, Tang M, et al. The vascular basis of perforator
flaps based on the source arteries of the lateral lumbar region. Plast
Reconstr Surg 2005;115(6):1651–1659.
7. Lui KW, Hu S, Ahmad N, et al. Three-dimensional angiography of the
superior gluteal artery and lumbar artery perforator flap. Plast Reconstr
Surg 2009;123(1):79–86.
8. Kiil BJ, Rozen WM, Pan WR, et al. The lumbar artery perforators: a
cadaveric and clinical anatomical study. Plast Reconstr Surg
2009;132:1229–1238.
9. Aho J, Laungani AT, Herbig KS, et al. Lumbar and thoracic perforators:
vascular anatomy and clinical implications. Plast Reconstr Surg
2014;134:635e–645e.
10. Bissel MB, Greenspun DT, Levine J, et al. The lumbar artery perforator.
3-dimensional anatomical study and clinical applications. Ann Plast
Surg 2016;77(4):469–476.
11. Hamdi M, Craggs, B, Brussaard C, et al. Lumbar artery perforator flap:
an anatomical study using multidetector computed tomographic scan
and surgical pearls for breast reconstruction. Plast Reconstr Surg
2016;138:343–352.
12. de Weerd L, Elvenes OP, Strandenes E, et al. Autologous breast
reconstruction with a free lumbar artery perforator flap. Br J Plast Surg
2003;56(2):180–183.
13. Peters KT, Blondeel PN, Lobo F, et al. Early experience with the free
lumbar artery perforator flap for breast reconstruction. J Plast Reconstr
Aesthet Surg 2015;68(8):1112–1119.
14. Opsomer D, Stillaert F, Blondeel P, et al. The lumbar artery perforator
flap in autologous breast reconstruction: initial experience with 100
cases. Plast Reconstr Surg 2018;142:1e–8e.
15. Honart JF, Leymarie N, Sarfati B, et al. Lumbar artery perforator flap
for breast reconstruction. Ann Chir Plast Esthet 2018;63(1):25–30.
16. Hamdi M, Andrades P, Thiessen F, et al. Is a second free flap still an
option in a failed free flap breast reconstruction? Plast Reconstr Surg
2010;126:375–384.
CHAPTER 81

Goldilocks Mastectomy for Immediate


Reconstruction Without Implants
LISA CASSILETH | HEATHER RICHARDSON
HISTORY
Described in 2012 and named after the storybook character who chose the
“just right” porridge option over ones that were “too hot” and “too cold,” the
Goldilocks mastectomy seeks to create a third option for breast
reconstruction that combines the safety and accessibility of simple
mastectomy with the aesthetic of reconstruction (1). As patients with breast
cancer increasingly live full lives, they may prioritize the appearance of their
breasts. In response to patient demand of improved aesthetics, we have
expanded Goldilocks mastectomy to accommodate both skin-sparing and
nipple-sparing mastectomy techniques.
Like a bowl of cold porridge, standard simple mastectomy without
reconstruction aims to remove as much tissue as possible but has a poor
aesthetic result. Simple mastectomy has major medical and surgical
advantages over traditional breast reconstruction that cannot be denied. It has
a low complication rate, it is technically simple, and requires only a simple
skin ellipse excision with creation of the mastectomy flap and closure. There
are no expensive materials or instruments required, such as a microscope,
venous couplers, tissue expanders, implants, or acellular dermal matrix.
Simple mastectomy takes little operative time to perform, requiring usually 1
hour or less. It requires only one surgeon, versus a team. Finally, it is
available to all patients, regardless of comorbidities or history of radiation.
Some patients who appreciate these distinct advantages, however, may feel
that while a breast is not critical to lifestyle or identity, they do not want a
deformed appearance. Simple mastectomy without reconstruction creates a
tight, hollow central portion and lateral and medial fullness at the ends of the
incisions, which is the exact opposite of the form of a normal female breast’s
central fullness, tapering medially and laterally.
Traditional breast reconstruction is the “hot porridge” option, potentially
offering the appearance of a normal breast. All breast reconstruction options
today involve either a flap or an implant. A flap involves a distant donor site
along with its comorbidities and risks, a longer more complicated surgery,
and chance of partial or complete flap loss. The use of expanders and
implants involves multiple surgeries, a lifetime device with maintenance, and
a higher risk profile (e.g., infection, long-term implant leakage, capsular
contracture, and poor symmetry with the contralateral natural breast in
unilateral procedures).
Goldilocks offers an “in-between” reconstruction option that, for some,
may be “just right.” The basic goal of breast reconstruction is to recreate the
fullness of a breast mound. The Goldilocks procedure achieves this without
the introduction of an artificial implant or the harvesting of autologous tissue
from a distant site with its associated issues. Realizing that there could be a
middle ground that creates the appearance of a breast by utilizing tissue
present in the mastectomy flap itself and directly adjacent fat, the Goldilocks
mastectomy was devised as a means to address the needs of women facing
mastectomy who either can’t have or don’t want to have implant- or flap-
based reconstruction.
In keeping with utilizing local tissue rearrangement, the Goldilocks
technique has recently been enhanced with a reliable nipple-sparing
technique and a method for utilizing fat lateral to the breast, perfused by the
lateral intercostal artery perforators, also known as the LICAP flap. These
modifications have allowed preservation of the nipple, improvement in
aesthetic outcome, and increased size, providing the necessary malleability to
handle various patient desires and body types.
INDICATIONS
From an oncologic safety point of view, any candidate suitable for a skin- or
nipple-sparing mastectomy can be considered for Goldilocks mastectomy. As
with typical mastectomy/reconstruction, skin and subcutaneous tissue should
be removed as needed to meet oncologic safety, and not spared simply in
order to improve cosmetic outcome. The Wise pattern is flexible and can be
adapted to accommodate skin excisions in the mastectomy flap at different
locations.
For patients who are not candidates for skin- or nipple-sparing
mastectomies due to health issues, prior radiation or extensive disease,
Goldilocks mastectomy can be considered in lieu of simple (amputation
style) mastectomy, as long as there would be enough residual tissue to create
a Wise-pattern closure and the patient could tolerate additional operative
time, which should not be more than double the length of time for a simple
mastectomy and closure.
The ideal patient for Goldilocks mastectomy has (1) breast ptosis such that
the nipple rests at the IM fold in the standing position or below, designated as
grade III or grade IV ptosis, (2) a well-developed plane of dermal fat that is
safe to remain as local flap volume, and (3) expectations in line with having a
significant decrease in breast size (Table 81-1).
Two types of Goldilocks candidates are typically encountered. The first
type is interested in this method of breast reconstruction because it has lower
risks than typical reconstruction, no permanent prosthetic materials, no
harvest site for free flaps, and does not require multiple surgeries. The second
type of patient is one who is considered high risk for standard forms of
reconstruction, and can therefore be offered the Goldilocks, avoiding
exposure to any additional risks.
Contraindications to Goldilocks mastectomy include: disease presence in
the lower pole skin, especially IM fold region, that would prevent viable
superficial blood flow to the remaining inferior pole tissue; disease presence
in the upper pole skin that would prevent adequate residual skin to close the
Wise pattern; and prior, recent transverse or curvilinear incisions (such as that
for lumpectomy) that would interrupt the dermal and subcutaneous blood
flow and leave unperfused tissue vulnerable to necrosis, especially along the
IM fold. Prior breast lift and/or reduction may be a relative contraindication,
depending on the length of time from surgery. Patients desiring nipple
preservation who are deemed oncologically sound should be counseled that
the reconfiguration of tissue makes preservation of adequate blood flow to
the nipple dependent on a diminished supply, with a chance of nipple loss.

TABLE 81-1 List of Reasons to Consider Goldilocks Mastectomy


Obese patient
Macromastia
Prior radiation history
Need for post mastectomy radiation therapy (PMRT)
Medical comorbidities associated with higher complication rates such as
smokers, diabetics, collagen vascular disease, coagulopathies, chronic
steroid or antirejection medicine use
Pt aversion to artificial implants, complex surgeries
Patients with past surgical history making distal flap sites unsuitable
Patients desiring simplified approach
Age
PREOPERATIVE EVALUATION AND PLANNING

Counseling and Patient Selection


The Goldilocks mastectomy can be applied to almost any breast size or
shape. Patients who want breast reconstruction, but for whom flap surgery or
tissue expanders are deemed too high risk, are good candidates for the
procedure. Patients who have educated themselves regarding breast
reconstruction may refuse traditional techniques and seek out a no-flap, no-
implant option. Some patients are obviously suited to Goldilocks because of
large, ptotic breast size and desire to be smaller. Any patients whose disease
presentation and history makes this feasible can be counseled to its pros and
cons.
The Goldilocks mastectomy will have the best aesthetic outcome in a
patient with a larger, ptotic breast, and in such a patient, it will often have a
cosmetic result similar to a reduction mammaplasty with mastopexy. This is
thanks to the inherent ability of the Wise-pattern closure to recruit excess
dermal fat that would normally be removed during a mastectomy. The fat is
layered centrally, giving the appearance of a breast. The new “breast” will be
created from the residual dermal volume, and although more dermal fat
means more workable volume, the technique can be adequate for smaller-
breasted women. This will always be an improvement over traditional
mastectomy, as a standard transverse elliptical incision that is tight centrally
has a tendency toward residual volume at the lateral and medial periphery,
which is the antithesis of the form of a human breast.
In deciding any surgical approach, patient education and expectation
management is paramount. It can be difficult to estimate the volume that will
be present on physical examination alone. A patient with a larger breast who
has a thinner dermal fat pad may have less residual fullness than a patient
with a smaller breast, but a thicker plane of fat. When discussing the
procedure with patients, it should be emphasized that there is little control
over the resulting projection and size of the reconstructed breast. If the
patient feels that the final result is too small, fat grafting and delayed implant
placement are reasonable, low-risk procedures that can provide increased size
but require additional procedures in the future after healing has completed.
Work-Up
A standard preoperative work-up as for any mastectomy should take place
with optimization of any health issues for those without cancer and choosing
to proceed with an elective prophylactic surgery for whatever reason.
Imaging may be done by the discretion of the physician. MRI is not required
necessary but can be helpful in advanced warning of disease presence in skin
or nipple that would require including these with the mastectomy specimen as
well as ensuring the absence of contralateral disease. An MRI within 6
months of surgery can be considered for those with documented mutations
(2). Patients with areas of concern on an MRI with plans for upcoming
bilateral mastectomy surgery are counseled to choose between immediate
biopsy to discern the nature of the abnormality or to consider addition of
sentinel lymph node (SLN) biopsy on the affected side in case occult
malignancy is present. Those with cancer should have a full history and
physical and should be counseled on unilateral versus bilateral approaches, as
there will be significant asymmetry if the contralateral side is left alone.
Preoperative and Perioperative Considerations
Photographic documentation of preoperative, perioperative, and
postoperative appearance is necessary to gauge results and effectiveness, and
to communicate the wide array of outcomes with patients. While this might
not be standard procedure in the office of a general surgeon, a photographic
protocol should be adopted by any surgeon regularly offering breast
intervention.
A plastic surgery colleague, if available to assist with planning and closure,
can be a great asset for the general surgeon just beginning to utilize the
Goldilocks mastectomy, as the Wise-pattern closure is used with standard
breast reduction and is familiar to plastic surgeons. If the nipple-sparing
option is used, this involves the creation of a pedicled flap and is usually
performed as a joint plastic surgery/general surgery case in our practice. An
additional modification to recruit lateral fat is often desirable to give
increased breast volume. In addition, with unilateral mastectomy, a
contralateral reduction improves symmetry and is often performed
concomitantly.
Standard preoperative clearance for safe practices for any patient should be
followed. Any patient deemed healthy enough to withstand simple
mastectomy without reconstruction should also be healthy enough for
Goldilocks mastectomy, considering the additional length of operative time
for the deepithelialization and closure.
In the operating room, the patient should be positioned and secured to
allow for raising into a sitting position intraoperatively to assess the
configuration of the flap and to address symmetry as applicable. It is also
helpful to have a skin stapler available to tailor tack the configuration, excise
dog-ears, and adjust any area requiring more deepithelialization prior to
committing to final sutures. Prep should be bilateral, and extend to the axilla
and lateral tissue to the table surface as the removal of dog-ears and
recruitment of lateral fat are more likely to be needed than not.
OPERATIVE TECHNIQUE
MARKING
The markings are performed with the patient in an upright position, arms at
her sides. The first mark is the inferior mammary crease. The mark will start
at the medial edge of the overhanging breast and transverse laterally to the
obvious edge of the breast tissue. When a flap of fatty tissue continues onto
the back, either a LICAP flap to recruit this tissue or a longer incision to
remove the dog-ear will need to be designed. A vertical line should then be
placed at the aesthetic center of the breast. This is the midline of the breast
and it is along this line that the vertical limb and the nipple, if preserved, will
be placed. Next, the new inframammary crease (IMC) is marked. It should be
placed where the breast skin overlaps the inferior mammary crease. The
nipple location can be estimated by measuring up 5 cm from the proposed
new location of the inferior mammary crease, along the vertical breast
midline. The location can be adjusted after the flap has been inset and tailor
tacked into position. Finally, the angle of the Wise pattern’s vertical limbs is
estimated by matching the length of the proposed new inferior mammary
crease across the breast to the length of the existing mammary crease on the
chest wall. This angle is necessary to allow a breast shape and to give a space
for the volume that is recruited under the new mastectomy flap. It is
important to note that the markings are not exactly the same for a Wise-
pattern reduction mammaplasty, as the plastic surgeon has been taught to
leave more skin in place as there is remaining breast to accommodate in a
breast reduction. The markings for a Goldilocks are simpler, as the closure
only need to contain the remaining bulk of the dermal fat and not an actual
breast.
If a LICAP flap is planned, an ellipse is marked just lateral to the breast
tissue. It is important not to undermine in this area during the mastectomy
portion, as the lateral intercostal perforators will be cut and the tissue cannot
be used.
DEEPITHELIALIZATION BEFORE VERSUS AFTER MASTECTOMY
Deepithelialization is the removal of the epithelium while preserving the
dermis. This preserves the subdermal plexus, which is the blood supply to the
dermal flap used. This process is often underappreciated, as it can be
technically difficult and time consuming. Most surgeons familiar with the
process of deepithelialization will agree that this is most easily accomplished
with tension on the skin, keeping the plane still and firm to maintain the
proper depth. This is usually best accomplished before the mastectomy has
been performed as the presence of the underlying tissue provides helpful
resistance to maintain tension. For those that perform deepithelialization first,
there may be overall time saved and an easier process, but with the
deepithelialization first comes commitment to the markings made. Surgeons
accustomed to a certain tension on the flap for the mastectomy dissection will
find that the lack of epidermis creates much more elasticity and “give” when
separating the dermal fat plane from the parenchyma. It may be harder to stay
in the correct plane with the difference in tissue texture and should be
important to not contuse, rip, or perforate the flap as you are attempting to
separate it from the breast mound.
If the mastectomy is performed first, and skin left intact, the Goldilocks
marking lines can be scratched to keep them from being wiped away during
what is usually a surgery fraught with oily residue that makes inked skin
markings difficult to keep in place. The lateral superior marking is used for
easiest access. Keeping a distinct and sharp angle for the vertical limb is very
helpful when constructing the final superior flap pattern and affixing the new
midline to the horizontal limb. The deepithelialization is then performed
second, which many find more difficult as the dissected flaps have little
natural tension.
FLAP CREATION
The ideal mastectomy flap is at the junction of the dermal fat pad and the
breast tissue, and varies from patient to patient. One might think the methods
used to separate the breast tissue from overlying dermal fat and skin are fairly
limited and provide consistent results from practitioner to practitioner, but
this is not the case. Methods of dissection and rates of injury/necrosis vary
widely (3,4). Average and expected rates appear to fall between 5% and 15%,
but have been stated as high as 40% in some papers. Those who create a
more aggressive dissection plane that includes much of the dermal fat plane
with the specimen will likely find the Goldilocks technique lacking in
aesthetic outcome. The fat plane on the mastectomy flap should not be
resected with the mastectomy specimen. This will preserve the plexus that
will supply the remaining mastectomy skin and also provide the bulk needed
to create a breast mound. Proper parenchymal removal should be completed,
and any tissue involved with malignant disease should be excised with proper
oncologic technique. These two practices are not mutually exclusive in the
creation of healthy mastectomy flaps, which are made up of more than simply
dermis but should include the subdermal fat and the blood supply that
perfuses the dermis. The breast tissue can be fully removed while subdermal
fat is preserved. This provides a healthy mastectomy flap, including the
critical blood supply that the subdermal fat offers.
In fatty breasts, the breast tissue and the dermal fat may be difficult
visually to distinguish from each other. Preoperative imaging, such as
mammography and ultrasound, can often be helpful to gauge the potential
thickness of the fat plane and aid in estimation of residual fat volume.
Observed breast size and density cannot be relied upon in order to predict the
final size of a Goldilocks reconstruction. Large-breasted women may have
thin dermal planes with parenchyma adjacent to areas of dermis with little
residual volume to be left behind, while seemingly small-breasted women
may have breasts consisting of small central islands of glandular tissue with
thick and well-developed fat planes that can be easily preserved and
reconfigured into a breast mound (Fig. 81-1).
ASSEMBLY OF THE MOUND WITH NIPPLE EXCISION
Once the mastectomy flaps have been created and the lower pole has been
deepithelialized, the lower pole of the breast should be detached from the
upper pole. If you are comfortable with your markings and are willing to
commit to them from the start, the mastectomy can be performed with even
better visualization than usual by incising the entirety of the transverse
marking and essentially bisecting the breast. Once the upper and lower poles
have been divided, the deepithelialized portion can now be inset to create
bulk in front of the pectoral muscle. It will be a unique size and shape in each
patient (and even when comparing left to right in a bilateral case). The most
common approach to assembling the mound is to suture the superior medial
border of the lower flap to the pectoral fascia. Longer and more redundant
lower pole flaps can be folded, carefully watching for reduction in blood
flow, to create more centromedial bulk. Shorter, wider flaps may not need to
be affixed to the chest wall at all, but may be able to be rested against the
pectoralis and will fall into a natural position under the upper pole with ease.
Once the lower pole is secured, the upper pole should be tacked with a
simple suture or skin staple to the T-junction site on the border of the
deepithelialized tissue to become the new IM fold. This is typically 10 to 12
cm from the sternum and should be measured for symmetry. Sitting the
patient upright to assess for drape and symmetry is very helpful and should
be done during initial assembly, prior to suturing (Fig. 81-2).
FIGURE 81-1 Original Goldilocks mastectomy in steps (A) preoperative Wise-
pattern markings, (B) residual tissue after mastectomy has been performed, (C)
deepithelialized lower pole on right, divided upper and lower pole with drain in place
on left, (D) upper pole position over lower pole to create neo breast mound.

FIGURE 81-2 Before and after bilateral Goldilocks mastectomy with in situ SWIM
nipple-sparing technique.
FIGURE 81-3 On-table marking for bilateral Goldilocks with in situ SWIM nipple-
sparing technique in a patient with recurrent left breast cancer, treated previously
with lumpectomy and radiation.

Prior to closure, drains are placed through a separate stab incision and can
be left over or under the lower flap as deemed fit, or into the axilla as may be
needed with axillary tissue sampling. The skin should then be secured with a
standard multilayer closure. The incision length of the IM fold and the newly
created central-T should be documented (Fig. 81-3).
NIPPLE PRESERVATION WITH LOCAL FLAP
In situ preservation of the nipple is possible and can be performed in two
ways. For patients with a short IMC-to-nipple distance, the nipple is simply
left on the inferior flap and the skin around it is deepithelialized. The nipple
is then brought through to the proper position at the top of the Wise angle
(Fig. 81-4). If the IMC-to-nipple distance is too long, which will be the case
in almost all large-breasted patients, then the nipple should be rotated into
position using a pedicled flap based on the superior mammary perforators.
The flap is designed by allowing the breast skin to hang laterally and marking
the location of the internal mammary arteries from their origin at the medial
intercostal space. The pedicle should be as wide as possible. The pedicle is
then freed from the IMC and the superomedial Wise triangular flap, and then
can be seated into position.
LICAP ADDITION
Further bulk and aesthetic improvement can be accomplished with the
addition of the LICAP flap. The LICAP flap is an often-forgotten but useful
type IV flap that can be harvested from excess axillary fat present in almost
every large-breasted mastectomy. An ellipse just lateral to the breast is
designed based on the location of the inferior mammary crease, similar to
where the dog-ear is naturally located. The perforators are typically located 2
cm posterior to the anterior mammary line. The flap is dissected
posteriorly/laterally first, carefully preserving the perforators as the dissection
is moved more medially. After the perforators have been located, the medial
soft tissue can be freed to allow for increased mobility. Multiple pedicles will
be present, especially for wide flaps. The flap can be deepithelialized and
then stacked with the new Goldilocks breast mound.

FIGURE 81-4 Intraoperative view of divided superior and inferior mastectomy flaps
with nipple in place.
MULTIPLE FLAP INSETS/CREATION OF BREAST MOUND
When the dissection is complete, there may be two to four stacked flaps
composed of deepithelialized dermis and the underlying dermal fat: the
LICAP flap, the inferior pole deepithelialized flap, the pedicled
inframammary nipple flap, and the Wise flaps. When planning the flaps, take
into account the resulting thickness and leave some excess epidermis of 2 to 3
cm on the Wise flaps in order to accommodate the stacked, sometimes bulky
flaps and avoid any excess tightness. To avoid fat necrosis, avoid torque on
the pedicles. Flap perfusion can be checked by trimming the tip of the flap
with the tissue in its sutured position. If small, bright-red points of arterial
perfusion are not seen, consider trimming the flap until the blood flow
appears viable. Free nipple grafting should be considered if the blood flow to
the nipple appears compromised.

FIGURE 81-5 Deepithelialized LICAP flap maneuvered from its lateral position to
help add volume in the mastectomy defect.

Nipple Preservation With Free Graft


Free nipple grafting has been utilized successfully (5,6) with a Goldilocks
mastectomy reconstruction. Any patient with poor blood flow to the nipple
flap, who would have otherwise been considered for nipple preservation in a
full reconstruction setting, can be considered for nipple grafting instead.
While free nipple grafting is fairly straightforward, it can result in loss of
areolar pigmentation and lack of nipple projection (Figs. 81-5 to 81-8) (7).
AFTER CARE
Postoperative wound management is not dissimilar to that of a simple
mastectomy. There is surprisingly little T-zone necrosis seen, but as with
breast reduction surgery, this watershed area is the most common site of
healing difficulties. Postoperative instructions should explain basic drain care
and place appropriate restrictions on activity, similar to a simple mastectomy
postoperative regimen.

FIGURE 81-6 The nipple on the SWIM flap pedicle divided from the flap with
redundant material added to the mound at the mastectomy defect.
FIGURE 81-7 Assembly and fixation of the tissues into the breast mound.
FIGURE 81-8 The superior flap has been tacked into its final configuration and the
skin excised to make room for the nipple areolar complex on its perfused SWIM
pedicle from the inferior medial portion to be sutured in place.
FIGURE 81-9 Before and after bilateral Goldilocks mastectomy with SWIM nipple
preservation.

Follow-Up
While ultrasound is cited as a useful tool in screening postoperative
mastectomy patients in general, mammography is not a standard
recommendation after mastectomy (8,9). Because other treating physicians
may incorrectly surmise that Goldilocks patients still have intact breasts due
to the natural appearance of the results, they should be notified that radiation
treatment and/or screening mammography are unnecessary in these patients.
As more patients accrue, data may show in the future that screening
modalities are helpful. Individual patients with disease patterns more
concerning for locoregional recurrence should be considered for tailored
follow-up imaging plans that may include MRI or mammography on a case-
by-case basis.
FIGURE 81-10 Before and after bilateral Goldilocks mastectomy with SWIM nipple
preservation. History of left lumpectomy with radiation treated for recurrent cancer.
Note some uneven pigmentation of the areola due to minimal superficial ischemia of
the areolar margin during healing.

FIGURE 81-11 Before and after bilateral Goldilocks mastectomy with SWIM nipple
preservation. Note some uneven pigmentation of the areola due to minimal
superficial ischemia of the areolar margin during healing.

Adjunctive Procedures
Once the patient has healed, if nipples were not preserved, a variety of
options are available to improve the final appearance, including prosthetic
silicone nipples, nipple reconstruction, and tattooing, just as with non–nipple-
sparing mastectomy reconstruction. Options are also available for patients
who feel that the final volume is not adequate, including external superficial
breast prostheses, fat grafting, and breast implants. Even if it is expected that
there will be an unsatisfactory final volume at the completion of the
procedure, delayed implant placement after Goldilocks mastectomy may have
benefits over attempting immediate, implant-based reconstruction in obese
women (10).
RESULTS
Final results are dependent on the patient’s habitus as well as surgical
technique. Patients may choose a unilateral or bilateral approach. Those who
choose a unilateral mastectomy are counseled that they will have asymmetry
if they do not have the contralateral breast adjusted or make use of a
prosthesis. The initial publication describing the Goldilocks mastectomy
described 32 patients (50 breasts) and reported that rate of complications
(seroma, cellulitis, wound healing difficulty, fat necrosis) was similar to that
of traditional mastectomy techniques. No instances of locoregional
recurrence were reported (11).
Additional applications of the technique have been explored to include a
patient with giant juvenile fibroadenoma (6) and to incorporate nipple
preservation with free nipple grafting (5,10). The limitations were notably
reported for smaller-breasted women in Japan (Figs. 81-9 to 81-11) (12).
CONCLUSION
Patients who cannot have, or do not want to have full breast reconstruction
after mastectomy, should be offered the Goldilocks mastectomy. Many of the
patients in this category are elderly or obese with ptotic breasts. This makes
them uniquely suited to utilize their own natural tissue that would have been
discarded with a large mastectomy specimen, tissue that would have been
spared if they had undergone full reconstruction. The elderly and obese
patient population is expected to grow and with it a likely increase in breast
cancer diagnoses (13).
The Goldilocks mastectomy offers a new, valuable option that may be
“just right” for some women who are facing breast cancer. For the surgeon
who chooses to include this technique in their armamentarium, the effort may
prove worthwhile to their patients.

REFERENCES

1. Rabin RC. Going Flat After Mastectomy. The New York Times; 2016.
2. Ehsani S, Strigel RM, Pettke E, et al. Screening magnetic resonance
imaging recommendations and outcomes in patients at high risk for
breast cancer. Breast J 2015;21(3):246–253.
3. Patel KM, Hill LM, Gatti ME, et al. Management of massive
mastectomy skin flap necrosis following autologous breast
reconstruction. Ann Plast Surg 2012;69(2):139–144.
4. Robertson SA, Jeevaratnam JA, Agrawal A, et al. Mastectomy skin flap
necrosis: challenges and solutions. Breast Cancer (Dove Med Press)
2017;9:141–152.
5. Schwartz JC, Skowronski PP. Total single-stage autologous breast
reconstruction with free nipple grafts. Plast Reconstr Surg Glob Open
2015;3(12):e587.
6. Ter Louw RP, Bruce SB, Nahabedian MY. Partial breast reconstruction
with Goldilocks technique after excision of giant fibroadenoma: a case
report. Plast Reconstr Surg Glob Open 2017;5(1):e1200.
7. Doren EL, Van Eldik Kuykendall L, Lopez JJ, et al. Free nipple
grafting: an alternative for patients ineligible for nipple-sparing
mastectomy? Ann Plast Surg 2014;72(6):S112–S115.
8. Farajado LL, Roberts CC, Hunt KR. Mammographic surveillance of
breast cancer patients: should the mastectomy site be imaged? AJR Am J
Roentgenol 1993;161(5):953–955.
9. Lee JH, Kim EK, Oh JY, et al. US screening for detection of
nonpalpable locoregional recurrence after mastectomy. Eur J Radiol
2013;82(3):485–489.
10. Schwartz JC. Goldilocks mastectomy: a safe bridge to implant-based
breast reconstruction in the morbidly obese. Plast Reconstr Surg Glob
Open 2017;5(6):e1398.
11. Richardson H, Ma G. The Goldilocks mastectomy. Int J Surg
2012;10(9):522–526.
12. Ogawa T. Goldilocks mastectomy for obese Japanese females with
breast ptosis. Asian J Surg 2015;38(4):232–235.
13. Torre LA, Siegel RL, Ward EM, et al. Global cancer incidence and
mortality rates and trends—an update. Cancer Epidemiol Biomarkers
Prev 2016;25(1):16–27.
CHAPTER 82

Neurotization of the Autologous Flap


KASIA KANIA | ALDONA J. SPIEGEL
HISTORY
The breast plays a pivotal role in female body image, femininity, and
sexuality. Its significance lies on a spectrum of varying importance and
differing attitudes for women. These attitudes toward the breast can range
from more positive, such as, an expression of confidence, self-worth, and
power, to more negative, an expression of shame or embarrassment. Breast
sensation is integral to intimacy, as both an erogenous zone and an autoerotic
point of view. After a mastectomy, this important perception becomes absent
and fractures the corporeal imagery of a woman.
The well-known Homunculus, a representation of the body mapped on the
brain described by Penfield in 1937, was based on early direct cortical
stimulation studies on epileptic patients and findings in the primary and
secondary somatosensory cortex (1,2). His studies focused primarily on
males and did not bring attention to female anatomy on the map. It took
several decades for researchers to study the female body with the help of
functional MRI. In 2013, several researchers proposed two versions of the
somatosensory “hermunculus,” depicting findings from human female
mapping studies and showing alternative localizations for the genitalia along
the dorsal somatosensory cortex and the medial wall (3). They further
emphasized that brain plasticity may occur during different reproductive life
stages, such as, pregnancy, menopause, and the ovarian cycle, creating
changes in somatotopy, size, and variability of representation on the brain
map.
Based on the hermunculus, breast sensation plays a vital sensory role for
women. When performing an operation that can significantly alter normal
sensation of the breast, a discussion on how this will affect the patient should
not be disregarded. Often, many patients are unaware that they will have
absent or greatly reduced sensation in the reconstructed breast. Although, by
definition, the breasts are a secondary erogenous zone, a subset of women
may consider the breast as a primary source of pleasure. Given the emergence
of methods that may avoid complete destruction of breast and nipple
sensation, loss of sensation should be discussed with patients prior to
mastectomy. Furthermore, there is a trend toward improved patient
satisfaction with better sensation after reconstruction (4). When comparing
innervated to noninnervated breast patients, improved scores were seen in
physical function, body pain, general health, social functioning, and
emotional role. The physical score summarizing all physical domains
improved overall. These findings suggested that breast sensation plays a
multifaceted role in patient recovery and should be part of the reconstructive
goal (Fig. 82-1) (5).
The sensory innervation of the breast is mainly derived from the
anterolateral and anteromedial branches of the thoracic intercostal nerves T3-
T5. All of these nerves are typically transected during a mastectomy. The
lateral nerves travel lateral to the pectoralis muscle and enter the breast gland.
The medial nerves typically travel in the subcutaneous tissue and are more
superficial. Due to this location, they can be preserved during a nipple-
sparing mastectomy, maintaining sensation with an oncologically sound
mastectomy. Although spontaneous recovery of sensation has been reported
in the reconstructed breast, the results have been inconsistent. Lack of
sensibility of the reconstructed breast can have variable importance to
patients. Lack of protective sensation, often presenting as a burn, has been
reported in noninnervated TRAM and latissimus dorsi flaps (6). The literature
generally suggests that sensory recovery is superior and occurs earlier in
innervated flaps when compared to noninnervated flaps, but there are
limitations in the studies regarding pressure measurements using
monofilaments and lack of reproducible data. Semmes–Weinstein
monofilaments have significant variability within and between devices from
different manufacturers. Moreover, the actual bending force vary despite
standard values. These deficiencies make it very difficult to gather
standardized data among different groups of patients at various institutions. A
newer device called the Pressure-Specified Sensory Device (PSSD), now the
Acroval, provides a more reproducible method of data collection with one-
and two-point static discrimination. The somatosensory measurement device
combines nerve density assessment with pressure threshold sensitivity to
provide numerical pressure readings (7).
FIGURE 82-1 Nerve supply. The main innervation to the nipple and areola is from
the lateral 4th intercostal nerve. There are also medial intercostal branches that
supply innervation. (From Hall-Findlay EJ. Vertical reduction mammaplasty. In: Thorne
CT, Gurtner GC, Chung K, et al., eds. Grabb and Smith’s Plastic Surgery. 7th ed.
Philadelphia, PA: Wolters Kluwer; 2013:604.)

The pattern of postoperative sensory return has been examined in


noninnervated breast flaps, showing an increase in sensation in the peripheral
skin in both pressure and temperature measurements, suggestive of nerve
growth into the flap periphery (8). In innervated breast flaps, pressure
threshold measurements were lower in both peripheral and central regions,
suggestive of both peripheral nerve ingrowth and flap innervation via the
intercostal nerve. Temperature discrimination was significantly greater in the
central nipple area relative to the areola and peripheral skin, suggestive of a
greater contribution to reinnervation by the intercostal nerve than by
peripheral nerve ingrowth (9). Although Blondeel et al. have qualitatively
observed sensory reinnervation originating from the center of the innervated
flap, the literature lacks quantitative evidence (9). However, a recent paper by
Spiegel et al. demonstrated objective documentation of different patterns of
regional sensory recovery in innervated and noninnervated flaps (10).
NEUROTIZATION TECHNIQUES
Restoration of breast sensation has not been considered a reconstructive goal
until recent years. With the lack of data and the observation of spontaneous
sensory recovery, neurotization was viewed as a lengthy process with
variable results. However, with proper technique, neurotization is fast and
feasible without the addition of significant operative time.

FIGURE 82-2 Deep inferior epigastric perforator flap with vessel anastomosis and
nerve coaptation. (From Spiegel AJ, Menn ZK, Eldor L, Kaufman Y, Dellon AL. Breast
Reinnervation: DIEP neurotization using the third anterior intercostal nerve. Plast
Reconstr Surg Glob Open 2013;1:e72.)

At most institutions, the deep inferior epigastric perforator (DIEP) flap is


the first-line choice for autologous reconstruction, thus we will describe its
neurotization in detail (Fig. 82-2).
The traditional donor nerves for DIEP flap neurotization are the T11-T12
sensory branches. These mixed segmental nerves run obliquely and anteriorly
to the deep inferior epigastric vessels and split into a sensory and motor
branch at variable distances. The pure sensory branches join with perforating
DIEP vessels and run in parallel to innervate the abdominal skin. The donor
nerve is identified with the most inferior lateral perforator vessels, typically
corresponding to the largest caliber segmental nerve. The nerve is dissected
and divided at the level of the fascia as a pure sensory nerve. To increase
length, the donor nerve can also be dissected below the fascia up to the point
of the motor nerve branch. The cutaneous sensory branches harvested with a
DIEP flap allow preservation of the motor innervation to the rectus
abdominus muscle, avoiding additional donor-site morbidity. Great care is
taken to preserve the motor branches to the rectus muscles, which enter the
rectus muscles laterally, by dissecting the sensory branch no farther than its
branch point with the motor contribution.
The recipient nerves used by the senior author are the fourth lateral and
third medial intercostal nerves, due to their role in breast sensation. The
fourth lateral intercostal nerve is frequently injured during mastectomy and
can be difficult to dissect during delayed reconstructions. Furthermore,
coaptation is performed away from the flap recipient vessels, requiring
repositioning of the microscope. Due to relative lack of length, flap inset and
shaping can also be challenging. Therefore, the third medial intercostal nerve
has been most routinely used by this author, due to its predictability,
proximity in the microsurgical field, and ease of dissection near the flap
recipient vessels in the 3rd rib interspace. Typically, a rib-sparing dissection
approach is used, where a small slip of pectoralis muscle is elevated and
excised. The intercostal muscle is then carefully resected to visualize the
internal mammary artery and vein. In the majority of cases, the recipient
vessels are dissected without resection of the rib. The anterior branch of the
3rd intercostal nerve is found at the junction of the inferior portion of the 3rd
rib and the sternum. To maximize the length of the recipient nerve, it is
dissected along its course as it travels with the pectoral intercostal perforator
to innervate the breast skin. Often, the nerve dissection proceeds up to the
end of the nerve where it is transected during the mastectomy. The recipient
nerve is dissected, transected medially, and mobilized to give it the longest
length in preparation for coaptation (Fig. 82-3) (10).
Nerve coaptation can be performed directly, or via autografts, allografts, or
nerve conduit tubes depending on the gap and surgeon preference. The ideal
repair of a peripheral nerve is a direct end-to-end coaptation of proximal and
distal nerve with a tension-free repair. When a gap precludes a direct repair,
autografts are the gold standard. Traditionally, harvesting an autograft
requires an extraoperative procedure, and create potential donor-site
morbidity. However, due to its segmental innervation, an autograft of at least
3 cm can be harvested from the DIEP flap donor site. Most of the lower
perforators, which are rarely used for flap perfusion, have an accompanying
nerve which may be dissected as an autograft and preserved for use if a gap is
present.
FIGURE 82-3 Epineural repair for nerve coaptation. (From Agnew SP, Ko JH.
Primary nerve repair and nerve graft for traumatic nerve injuries. In: Chung KCC, ed.
Operative Techniques in Hand and Wrist Surgery. Philadelphia, PA: Wolters Kluwer;
2019:252.)

Nerve conduits provide a bridge for regeneration of axonal pathways


across a lesion, while providing optimal mechanical and biochemical cues for
tissue regeneration. They are limited by gap distance, and were found to be
comparable to nerve autografts in the repair of digital nerves with defects up
to 3 cm in a prospective randomized clinical study. In the hand literature,
some studies have shown that nerve conduits can be used for gaps and have
similar outcomes to autograft technique by aiding in the directional growth or
alignment of the fascicle growth cone (11–14). In an animal study, conduit-
based nerve repairs had greater resistance to tension compared with primary
repairs (15).
Allografts provide an alternative option to primary repair or autograft.
They retain their nerve tissue scaffold and are made to be nonimmunogenic
by a variety of processing methods. They share the length restriction of
artificial conduits, but strategic modifications to acellular grafts may permit
axonal regeneration beyond these limits. Nerve conduit tubes are typically
synthetic silicone chambers or tubes made of biomaterials, such as,
polyglycolic acid or type I collagen.
NEUROTIZATION OUTCOMES
In a retrospective study by this author, neurotization of the DIEP flap using
the 3rd anterior intercostal nerve resulted in sensory recovery that was
statistically significantly improved in the flap skin and better than in the
native mastectomy skin. Sensibility recovered in DIEP flaps neurotized using
the nerve conduit was significantly better than in the corresponding areas of
the DIEP flaps neurotized by direct coaptation. This finding could suggest
that, using a nerve conduit, a small gap between the nerve endings allows for
the fascicles to realign appropriately. Sensation testing was performed using a
PSSD, which uses a more reproducible method of data collection with one-
and two-point static discrimination. However, it does have limitations. The
PSSD relies on the individual testing sensation and is dependent on when the
patient presses the button. Despite these limitations, it is the most accurate
and reliable method of testing sensation, which can be subjective relative to
motor function. In the future, functional MRI (fMRI) could potentially be
used to objectively test sensation. The nine areas of skin tested with the
PSSD were mastectomy skin and flap skin.
Several recent findings offer a new outlook on breast flap neurotization. In
order to quickly and routinely perform neurotization, the 3rd medial
intercostal nerve can be a reliable and convenient recipient nerve in relation
to the recipient vessels in one microsurgical field. With this technique,
neurotization adds minimal operative time, with estimates of 5 to 10 minutes
for donor nerve harvest, 5 minutes for donor nerve dissection, and 5 minutes
for coaptation in a proficient surgeon.
In our study mentioned above, increased sensory return in the flap skin of
immediate compared to delayed neurotized DIEP flap breast reconstructions
has been observed. There was a similar improvement observed between
immediate versus delayed nonneurotized flaps. However, when adjusted for
follow-up in months, this effect disappeared for nonneurotized but not for
neurotized flaps, suggesting that sensory recovery is improved and faster in
immediate versus delayed neurotized flaps irrespective of follow-up duration.
Sensory recovery was significantly different for flap skin between innervated
and noninnervated delayed DIEP flaps, even after adjustment for follow-up.
Sensory recovery in delayed flaps is especially important as a larger amount
of flap skin is required to reconstruct the breast envelope. The sensibility of
the reconstructed breast was not significantly different between innervated
and noninnervated immediate DIEP flap breast reconstructions, but the flap
skin and total skin did have increased sensation or lower pressure threshold
scores, suggesting that low sample size is a potential limitation. Immediate
flaps trended toward significance and will require a large sample size to show
effect. This effect was clearly more pronounced in delayed reconstruction.
For those patients who are not candidates for abdominal-based breast
reconstruction, neurotization can be performed for thigh-based flaps provided
the nerves are of adequate caliber. For superior gluteal artery perforator
(SGAP) and inferior gluteal artery perforator (IGAP) flaps, the superior
cluneal and inferior cluneal nerves can be used, respectively. For the
transverse upper gracilis (TUG) and profundal artery perforator (PAP) flaps,
a medial sensory branch of the femoral nerve can be used. For the lateral
thigh perforator (LTP) flap, branches of the lateral femoral cutaneous nerve
can be used for innervation.16
CONCLUSION
Breast flap neurotization during reconstruction is a feasible, simple, and fast
procedure that does not contribute to morbidity and can be performed
routinely. There have been promising results showing that neurotization
improves sensory return to flap skin, which builds on studies that have found
greater patient satisfaction with improved sensation after reconstruction. If
breast sensation is a vital component of sexuality and satisfaction for the
patient, neurotization should be an integral part of microsurgery planning.

REFERENCES

1. Schott GD. Penfield’s homunculus: a note on cerebral cartography. J


Neurol Neurosurg Psychiatry 1993;56(4):329–333.
2. Penfield W, Rasmussen T. The Cerebral Cortex of Man. New York: The
Maxmillian Company; 1950.
3. Di Noto PM, Newman L, Wall S, et al. The hermunculus: what is known
about the representation of the female body in the brain. Cereb Cortex
2012;23(5):1005–1013.
4. Cornelissen AJM, Beugels J, Van Kuijk SMJ, et al. Sensation of the
autologous reconstructed breast improves quality of life: a pilot study.
Breast Cancer Res Treat 2018;167(3):687–695.
5. Temple CLF, Ross DC, Kim S, et al. Sensibility following innervated
free TRAM flap for breast reconstruction: part ii. innervation improves
patient-rated quality of life. Plast Reconstr Surg 2008;124:1419–1425.
6. Faulkner HR, Colwell AS, Liao EC, et al. Thermal injury to
reconstructed breasts from commonly used warming devices: a risk for
reconstructive failure. Plast Reconstr Surg Glob Open
2016;4(10):e1033.
7. Lavery LA, Lavery DE, Lavery DC, et al. Accuracy and durability of
Semmes-Weinstein monofilaments: what is the useful service life?
Diabetes Res Clin Pract 2012;97(3):399–404.
8. Lehmann C, Gumener R, Montandon D. Sensibility and cutaneous
reinnervation after breast reconstruction with musculocutaneous flaps.
Ann Plast Surg 1991;26:325–327.
9. Blondeel PN, Demuynck M, Mete D, et al. Sensory nerve repair in
perforator flaps for autologous breast reconstruction: sensation or
senseless? Br J Plast Surg 1999;52:37–44.
10. Spiegel AJ, Menn ZK, Eldor L, et al. Breast reinnervation: DIEP
neurotization using the third anterior intercostal nerve. PRS Glob Open
2013;1(8):e72.
11. Ducic I, Fu R, Iorio M. Innovative treatment of peripheral nerve injuries.
Ann Plast Surg 2012;68:180–187.
12. Mackinnon SE, Dellon AL. Clinical nerve reconstruction with
bioabsorbable polyglycolic acid tube. Plast Reconstr Surg 1990;85:419–
424.
13. Weber RA, Breidenbach WC, Brown RE, et al. A randomized
prospective study of polyglycolic acid conduits for digital nerve
reconstruction in humans. Plast Reconstr Surg 2000;106:1036–1045;
discussion 1046–1048.
14. Ducic I, Safa B, DeVinney E. Refinements of nerve repair with
connector-assisted coaptation. Microsurgery 2017;37:256–263.
15. Rasappan K, Rajaratnam V, Wong Y. Conduit-based nerve repairs
provide greater resistance to tension compared with primary repairs: a
biomechanical analysis on large animal samples. Plast Reconstr Surg
Glob Open 2018;6:e1981.
16. Tuinder SMH, Beugels J, Lataster A, et al. The lateral thigh perforator
flap for autologous breast reconstruction: a prospective analysis of 138
flaps. Plast Reconstr Surg 2018;141(2):257–268.
CHAPTER 83

Management of the Failed Free Flap


MAURICE Y. NAHABEDIAN
HISTORY
According to the 2018 statistics compiled by the American Society of Plastic
Surgery, autologous breast reconstruction accounted for 18.1% of all breast
reconstruction performed in the United States (1). This includes pedicle flaps
such as the transverse rectus abdominis musculocutaneous (TRAM) and the
latissimus dorsi flap as well as free tissue transfer that includes the free
TRAM, deep inferior epigastric perforator (DIEP), and superficial inferior
epigastric artery (SIEA) flap as well as the gluteal and thigh-based flaps.
During the early years of microvascular breast reconstruction, flap success
rates ranged from 95% to 98%; however, current refinements with
microvascular techniques typically have resulted in flap success rates of 98%
to 99%. Flap failure has become a relatively uncommon event when
performed by experienced surgeons; however, when flap failure occurs, it can
be a devastating complication both for the patient and the operating surgeons
(Fig. 83-1). Whenever, considering autologous reconstruction, the possibility
of flap failure must be discussed with the patient and as such a backup plan
must be considered. In some cases, anatomic factors such as poor-quality
donor or recipient vessels for the microvascular anastomosis will prevent a
microvascular operation from being completed. In these cases, alternative
options such a prosthetic reconstruction or a pedicle flap reconstruction
should be discussed prior to the operation. In situations when flap demise
occurs following completion of the operation, options typically include
prosthetic or another flap.
FIGURE 83-1 A photograph of a failed flap following attempted salvage with leech
therapy.

This chapter will review reasons for flap failure as well the common
options following flap failure (Fig. 83-1).
FACTORS ASSOCIATED WITH MICROVASCULAR ANASTOMOTIC FAILURE
Published free flap failure rates for breast reconstruction vary between 0.3%
and 6% (2–5). Previous studies have demonstrated that the most common
cause of postoperative flap failure is due to issues related to the vein;
however, other events related to the arterial anastomosis, bleeding and
kinking of the pedicle have been described (4–6). Las et al. in a review of
1,530 free flaps performed in 1,247 patients have demonstrated that partial
and total flap failure rates were 5.5% and 4.5%, respectively (6).
Compromised flap circulation was responsible for flap failure and related to
previous radiotherapy, venous anastomosis revision, gluteal artery perforator
(GAP) flap choice, and postoperative bleeding. Sanati-Mehrizy et al.
evaluated risk factors leading to flap failure using the National Surgical
Quality Improvement Program (NSQIP) database and evaluated 1,921
patients that had microvascular free flaps (7). The study included patients
with flap reconstruction from various regions of the body; however, among
those patients having breast reconstruction with free flaps, BMI (adjusted
odds ratio 1.075, P < 0.012), and smoking (adjusted odds ratio 3.35, P <
0.02) were independent variables associated with flap failure.
The question of operative time and whether the reconstruction is unilateral
or bilateral and its relationship to flap failure has been studied. Previous work
by our group has demonstrated that unilateral failures following bilateral
reconstruction (3.5%) is more common that failure following unilateral
microvascular reconstruction (2.1%) (5). Although bilateral failure did not
occur in our series of 171 patients, it can occur. Of the 12 flap failures, 11 of
12 were subsequently reconstructed with prosthetic devices although
autologous options can also be considered depending upon patient
expectation and desire. The question of whether or not operative time can
impact the success of microvascular breast reconstruction has been evaluated
by Kwok et al. who reviewed 691 microvascular free flap breast
reconstruction using the NSQIP database (8). They were not able to
demonstrate a difference in flap failure based on unilateral or bilateral
reconstruction despite a median increase in the operative time of 78 minutes
with bilateral reconstruction. The authors did note, however, that for each
hour of increased operative time, there was a 17% increase in the odds of
having flap failure (p < 0.001). Based on the NSQIP database, the authors
were not able to demonstrate a significant association between preoperative
radiation therapy and flap failure when the radiation was delivered within 3
months of reconstruction (p = 0.33).
Also related to the topic of surgery length is whether or not the operation is
performed by a single surgeon or with two cosurgeons. Haddock et al. have
demonstrated that a single-surgeon reconstruction had significantly longer
OR time compared to the two-surgeon model where both surgeons were
present for the entire operation (678 vs. 485 minutes, P < .0001) (9). In
situations where the two surgeons were not present for the entire operations,
operative times were still reduced compared to the single-surgeon model (678
vs. 527 minutes, P < .0001). In addition, length of stay was reduced to 3.9
days versus 5 days (P < .001) using two surgeons. Patient-related
complications did not correlate with the number of surgeons.
PREVENTATIVE MANEUVERS TO MINIMIZE FLAP FAILURE
Given that venous related issues are responsible for the majority of flap
failures, it is important to consider maneuvers that will augment or maintain
venous circulation in the event of primary venous anastomotic insufficiency.
Thus, preservation of the superficial inferior epigastric vein during the
dissection and elevation of a DIEP or muscle-sparing free TRAM flap is
important. Al Hindi et al. retrospectively reviewed 198 DIEP flap breast
reconstructions over an 8-year period (10). Following DIEP flap
reconstruction, 7.5% of patients had an episode of intraoperative venous
compromise as opposed to 6.5% who had venous compromise noted
postoperatively. Of all patients, 15.1% had postoperative complications with
a flap failure rate of 2.5%. Of these flap failures, 2%: were due to venous
thrombosis and 0.5% were due to arterial thrombosis. In those patients that
had the venous insufficiency addressed with a second venous anastomosis at
the time of the reconstruction, all flaps survived without partial loss. All the
flap failures occurred in the cohort where venous augmentation was
performed at the take-back operation.
The role of preoperative vascular imaging of the abdominal wall
perforators is an important consideration when attempting to optimize
success and minimize flap failure. Both computerized tomographic
angiography (CTA) and magnetic resonance angiography (MRA) have been
described for this purpose (11,12). In a recent review of 240 DIEP flaps
performed in 202 patients, preoperative CTA demonstrated more abnormal
venous connections between the deep and superficial venous systems in flaps
that demonstrated venous congestion when compared to controls (66.7% vs.
8%, p < 0.0001) (13). In patients that had normal venous connections on
CTA, the likelihood of venous congestion was far less (26.7% vs. 80%, P <
0.001).
Postoperative monitoring and its relationship to the success or failure of
microvascular flap reconstruction has been studied. Current methods of
monitoring flaps postoperatively include a handheld Doppler, implantable
Doppler, and near-infrared spectroscopy (14). The utility of these devices is
surgeon dependent and all have demonstrated efficacy and accuracy. The
question of how long flaps should be monitored to improve the likelihood of
success has been studied. Zocalli et al. have evaluated their own experience
with 335 free flaps for breast reconstruction and demonstrated that hourly
flap monitoring was important up to the third postoperative day (15). The
correlations between the times of complication onset and the flap salvage
rates in all groups were significant. Of 31 flaps that were explored, 18 of 31
were explored within the first 24 hours and 9 of 31 were explored between 24
and 48 hours. Flap salvage rates were 66% and 55%, respectively. Our
personal protocol is to monitor microvascular flaps every 15 minutes for the
first 4 hours, then hourly for the next 20 hours using a handheld Doppler.
Monitoring continues at 4-hour intervals for the next day or two until
discharge.
It has been suggested that tertiary care facilities with intensive care units
(ICU) may have fewer flap failures than specialty surgery hospitals that do
not have ICU facilities. Vemula et al. have studied differences in outcomes
between two such facilities (16). The results of the study were that salvage
and failure rates were similar when comparing the two institutions and that
the presence of an ICU did not matter so long as the staff had the expertise to
expertly manage these patients. Flap failure rate was 1.78% at the specialty
surgery hospital and 1.19% at the tertiary care facilities. There were no
predictors that correlated with increasing the chances of flap failure.
RECONSTRUCTIVE OPTIONS
Secondary reconstruction of the failed flap can be performed using various
methods that include the use of prosthetic devices, pedicle flaps, such as the
latissimus dorsi or the thoracodorsal artery perforator flap as well as second
free flaps. The choice will depend on various factors that include patient
desire, prior radiation therapy, availability of recipient vessels for a second
free flap, and the quality of the skin over the chest wall. In some cases, there
may be an open wound that will require an autologous option and in other
cases there may be viable and healthy adipocutaneous layer that will be
amenable to prosthetic reconstruction. The next few sections will review
these options.
PROSTHETIC RECONSTRUCTION
The most common option following failure of a free flap is to consider
prosthetic reconstruction. Prosthetic devices in this setting usually include
tissue expanders but can in some situation be performed with permanent
implants. In most cases, the adipocutaneous layer will require expansion in
order to create a breast mound; however, in the event of flap failure and
nipple-sparing mastectomy, a permanent implant may be possible.
Prosthetic reconstruction in the setting of prior radiation therapy is
challenging because of the fibrosis and the relative inelasticity of the
adipocutaneous layer. In these situations, autologous reconstruction is
preferred; however, if the patient lacks suitable donor site or does not want
autologous reconstruction, serial fat grafting to prepare the skin can be
considered (17). The role of fat grafting is to provide additional fat and to
better condition the skin by introducing stem cells to promote angiogenesis
and improved elasticity.
Delayed prosthetic reconstruction following flap failure can be performed
by placing the device in the prepectoral or subpectoral position. In patients
that have been previously radiated the prepectoral position can be considered
but usually following autologous fat grafting. Placing a prosthetic device
under a radiated pectoralis major muscle usually results in reconstructive
failure due to the inability to adequate stretch the radiated muscle. In patients
that have not been radiated, the prosthetic device can be placed in the
prepectoral or subpectoral position. Prior to 2015, the subpectoral position
was the author’s preferred position; however, prepectoral placement is now
preferred. The use of acellular dermal matrix can also be considered to
provide additional soft tissue support and to compartmentalize the device.
Figure 83-2 illustrates a patient that had bilateral breast reconstruction with
DIEP flaps resulting in left-sided failure. She subsequently underwent two-
stage prosthetic reconstruction with long-term success.
PEDICLE FLAP RECONSTRUCTION
The use of a pedicle flap following failure of a microvascular breast
reconstruction is frequently considered, especially in the setting of prior
radiation therapy. The most common flap in this setting is the latissimus dorsi
flap primarily because it is very robust and in close proximity to the
mastectomy defect. This flap is ideal in cases where the primary recipient
vessels were the internal mammary artery and vein because the thoracodorsal
artery and vein are intact. However, if the recipient vessels for the failed flap
were the thoracodorsal vessels, the likelihood of using this flap is diminished
unless the serratus branch to the latissimus dorsi muscle was preserved.
The latissimus dorsi flap can be used for both breast and chest wall
reconstruction (18,19). The primary determinant is whether or not a chest
wall wound exists. If there is a nonhealing radiated wound, the latissimus
dorsi musculocutaneous flap is typically used for soft tissue coverage and not
necessarily to create a breast mound. However, if the soft tissue quality is
good and there is no open wound, the latissimus dorsi flap can be shaped to
create a breast. In most cases, the latissimus dorsi flap is combined with a
prosthetic device because the flap itself is usually too small to achieve the
desired volume or symmetry. Thus, this flap is often combined with a
prosthetic device, usually a tissue expander or permanent implant. In the
event of prior radiation therapy or infection, the author’s preference is to
perform a two- or three-stage reconstruction where the latissimus dorsi is
performed first followed a few months later by placement of a prosthetic
device. The reason for this staged approach is to allow the soft tissues to heal
before placement of an implant to minimize the risk of infection or undo
pressure on the incisions. Figure 83-3 illustrates a patient that had a failed
superior gluteal artery perforator flap (SGAP) that was subsequently
reconstructed with a TWO-stage latissimus dorsi musculocutaneous flap and
implant.
Figure 83-4 illustrates a patient that had a failed DIEP flap that
subsequently underwent successful three-stage latissimus dorsi flap and
implant reconstruction.
MICROVASCULAR FLAP RECONSTRUCTION
The option of a second free flap following initial free flap failure can be
considered but is the least common option. In some cases, it may be due to
the lack of a suitable recipient vessel or because the patient does not want to
risk a second failure. In some patients that have had failed free flap
reconstruction, the etiology is a hypercoaguable state that places any
microvascular anastomosis at risk of thrombosis. Wang et al. reviewed 2,032
flaps and found that a hypercoagulable state existed in 41 patients that
included factor V Leiden mutation, protein C deficiency,
hyperhomocysteinemia, antiphospholipid antibody syndrome, prothrombin
gene mutation, factor VIII elevation, anticardiolipin antibody syndrome, and
essential thrombocytosis (20). The study demonstrated that the rate of
thrombosis was 20.7% and occurred in 12 flaps. The overall rate of flap
failure in patients with a hypercoaguable state was 15.5% and the salvage rate
following postoperative thrombosis 0%.
FIGURE 83-2 A: A postoperative photograph following a failed left DIEP flap. B: A
left tissue expander was placed in the partial subpectoral position demonstrating
marked asymmetry with the right DIEP flap. C: A postoperative photograph
following left implant exchange and right breast revision burying the flap
demonstrating improved symmetry. D: Bilateral nipple reconstruction was
performed with CV flaps. E: Eleven-year follow-up demonstrating reasonable
symmetry. F: Animation deformity of the left breast was creating distortion and
discomfort. G: Preoperative markings for a left prepectoral conversion procedure
and right breast revision. H: Postoperative photograph demonstrating almost perfect
volume and contour symmetry of the left implant and the right DIEP flap. I: Left breast
lateral view demonstrating natural contour. J: Right breast lateral view demonstrating
natural contour.

Hamdi et al. have reviewed their experience with second free flaps in 688
patients that had autologous reconstruction of whom 14 required tertiary
breast reconstruction (21). In 8 patients a second free flap was performed that
included five SGAPs, three transverse myocutaneous gracilis flaps, and one
deep inferior epigastric artery perforator flap. Twenty-two percent of these
flaps (2/9) also failed requiring additional surgery. The authors recommend
careful screening of patients to rule out any hypercoaguable states prior to
attempting a second free flap.
CONCLUSION
Flap failure is a devastating complication for patients and for the surgeons.
Most studies that have evaluated the responses of patients following
complications have focused on adverse events such as infection or delayed
healing but have not focused on the psychological effects of total flap failure.
Recent studies have found that initially there is sadness, disappointment, and
shock; however, with the passage of time, many women were able to get back
to their normal lives and accept the flap failure (22). Others, however, have
reported feeling of disfigurement that in some cases adversely affected their
self-esteem and relationships. In the event of a flap failure, it is important for
the surgeon to explain what happened and provide an explanation regarding
why. Perhaps the most important message of this chapter is that it is critically
important to discuss the possibility of flap failure preoperatively to prepare
the patient in the event of this unlikely occurrence and to mention that there
are backup options in the event of failure.
FIGURE 83-3 A: A postoperative photograph demonstrating failure of a left SGAP
flap and previous radiation therapy. B: The left breast is reconstructed with a
latissimus dorsi musculocutaneous flap. C: Preoperative markings for placement of a
left breast implant and right breast mastopexy for symmetry. D: Three-year follow-
up with a left latissimus dorsi and implant and a right mastopexy. E: Left breast
lateral view demonstrating natural contour. F: Right breast lateral view
demonstrating natural contour.
FIGURE 83-4 A: Postoperative image of a patient following left mastectomy and
radiation. B: A left breast reconstruction with a DIEP flap failed following attempted
salvage. C: The left breast was reconstructed with a latissimus dorsi
musculocutaneous flap. D: The second stage of the reconstruction involved placing a
tissue expander under the latissimus dorsi flap. E: The patient was diagnosed with
right breast cancer and had a nipple-sparing mastectomy and tissue expander
placement. F: Preoperative marking for bilateral removal of the tissue expanders
and placement of silicone gel implants as well as left breast fat grafting. G: One-year
follow-up photograph status post bilateral implants and left fat grafting
demonstrating improved volume and contour symmetry.

REFERENCES

1. American Society of Plastic Surgeons—2018 procedural statistics.


www.plasticsurgery.org. Accessed November 11, 2019.
2. Selber JC, Kurichi JE, Vega SJ, et al. Risk factors and complications in
free TRAM flap breast reconstruction. Ann Plast Surg 2006;56:492–
497.
3. Tran NV, Buchel EW, Convery PA. Microvascular complications of
DIEP flaps. Plast Reconstr Surg 2007;119:1397–1405; discussion 1406–
1408.
4. Nahabedian MY, Momen B, Manson PN. Factors associated with
anastomotic failure after microvascular reconstruction of the breast.
Plast Reconstr Surg 2004;114:74–82.
5. Rao SS, Parikh PM, Goldstein JA, et al. Unilateral failures in bilateral
microvascular breast reconstruction. Plast Reconstr Surg
2010;126(1):17–25.
6. Las DE, de Jong T, Zuidam M, et al. Identification of independent risk
factors for flap failure: a retrospective analysis of 1530 free flaps for
breast, head and neck and extremity reconstruction. J Plast Reconstr
Aesthet Surg 2016;69:894–906.
7. Sanati-Mehrizy P, Massenburg BB, Rozehnal JM, et al. Risk factors
leading to free flap failure: analysis from the national surgical quality
improvement program database. J Craniofac Surg 2016;27:1956–1964.
8. Kwok AC, Edwards K, Donato D, et al. Operative time and flap failure
in unilateral and bilateral free flap breast reconstruction. J Reconstr
Microsurg 2018;34:428–435.
9. Haddock NT, Kayfan S, Pezeshk RA, et al. Co-surgeons in breast
reconstructive microsurgery: what do they bring to the table?
Microsurgery 2018;38:14–20.
10. Al Hindi A, Ozil C, Rem K, et al. Intraoperative superficial inferior
epigastric vein preservation for venous compromise prevention in breast
reconstruction by deep inferior epigastric perforator flap. Ann Chir Plast
Esthet 2019;64:245–250.
11. Masia J, Clavero JA, Larranaga J, et al. Preoperative planning of the
abdominal perforator flap with multidetector row computed
tomography: 3 years of experience. Plast Reconstr Surg 2008;122:80e–
81e.
12. Masia J, Kosutic D, Cervelli D, et al. In search of the ideal method in
perforator mapping: noncontrast magnetic resonance imaging. J
Reconstr Microsurg 2010;26:29–35.
13. Davis CR, Jones L, Tillett RL, et al. Predicting venous congestion
before DIEP breast reconstruction by identifying atypical venous
connections on preoperative CTA imaging. Microsurgery 2019;39:24–
31.
14. Nahabedian MY. Overview of perforator imaging and flap perfusion
technologies. Clin Plast Surg 2011;38(2):165–174.
15. Zoccali G, Molina A, Farhadi J. Is long-term post-operative monitoring
of microsurgical flaps still necessary? J Plast Reconstr Aesthet Surg
2017;70:996–1000.
16. Vemula R, Bartow MJ, Freeman M, et al. Outcomes comparison for
microsurgical breast reconstruction in specialty surgery hospitals versus
tertiary care facilities. Plast Reconstr Surg Glob Open 2017;5:e1514.
17. Rigotti G, Marchi A, Galie M, et al. Clinical treatment of radiotherapy
tissue damage by lipoaspirate transplant: a healing process mediated by
adipose-derived adult stem cells. Plast Reconstr Surg
2007;119(5):1409–1422; discussion 1423–1424.
18. Kokosis G, Khavanin N, Nahabedian MY. Latissimus dorsi
musculocutaneous flap for complex breast reconstruction: indications,
outcomes and a proposed algorithm. Plast Reconstr Surg Global Open
2019;7:e2382.
19. Friedman O, Fliss E, Inbal A, et al. Latissimus dorsi flap: a winning
hand for breast reconstruction salvage. Isr Med Assoc J 2019;21:260–
264.
20. Wang TY, Serletti JM, Cuker A, et al. Free tissue transfer in the
hypercoagulable patient: a review of 58 flaps. Plast Reconstr Surg
2012;129:443–453.
21. Hamdi M, Andrades P, Thiessen F, et al. Is a second free flap still an
option in a failed free flap breast reconstruction? Plast Reconstr Surg
2010;126:375.
22. Higgins KS, Gillis J, Williams JG, et al. Women’s experiences with flap
failure after autologous breast reconstruction: a qualitative analysis. Ann
Plast Surg 2017;78:521–525.
CHAPTER 84

Management of Donor-Site
Complications
DEVINDER SINGH | LUTHER H. HOLTON III | LAUREN ANTOGNOLI | SALMAN CHAUDRY
HISTORY

Relevant Anatomy
Since first described in 1979, the transverse rectus abdominis myocutaneous
(TRAM) flap has become a reliable choice in autologous-based breast
reconstruction (1). Over the last 30 years, significant advancement has been
made in autologous breast reconstruction with multiple flap choices including
the deep inferior epigastric perforator (DIEP) flap, muscle-sparing free
TRAM (MS-TRAM) flap, transverse myocutaneous gracilis (TUG) flap,
thoracodorsal artery perforator (TDAP) flap, muscle-sparing latissimus dorsi
(MSLD) flap, superior and inferior gluteal artery (SGAP/IGAP) flaps, and
profunda artery perforator (PAP) flap (2). Irrespective of flap choice, the goal
of autologous breast reconstruction is to recreate a breast mound that is soft,
durable, and aesthetically pleasing while minimizing donor-site morbidity.
The DIEP flap is currently a popular flap for patients undergoing
autologous breast reconstruction who otherwise are unable to undergo
implant-based reconstruction (IBR), fear IBR, or have failed IBR (typically
due to radiation). It provides the largest amount of skin that can be harvested
while also providing an incidental abdominoplasty. The focus of this chapter
is on the management of donor-site morbidity in DIEP flap patients, but the
ideas presented are generally applicable to other autologous donor sites.
The key component in creating and designing any flap revolves around its
blood supply. Critical to the design of each of the above-named flap options
for breast reconstruction is identification and preservation of appropriate
blood supply to the requisitioned soft tissue. With the DIEP flap, the skin and
subcutaneous tissue as well as its blood supply is removed and transplanted
to create a new breast. An understanding of abdominal wall vasculature and
perfusion is essential to perioperative planning. Preoperative imaging such as
3D-CT angiogram of the donor site can help identify a dominant perforator,
suggest superficial dominance, and reduce the amount of fascial disruption
created during harvest. This has important implications for the most feared
complication of all, donor-site hernia or bulging. In addition, familiarity with
the lower abdominal wall perfusion zones is critical to minimizing skin
necrosis upon final closure (1,3).
The pedicle to the DIEP arises from the external iliac artery and travels
superiorly. It commonly travels along the lateral aspect of the rectus and
undergoes variable branching patterns prior to entering the rectus abdominis
muscle (4). Here it takes a short intramuscular course before piercing the
anterior rectus sheath on its way to the subcutaneous fat and skin. Most
perforators are found within 3 cm of the umbilicus and once into the
subcutaneous tissue there is considerable branching. The perforators can
further be described as medial or lateral row perforators. Medial perforators
tend to extend perfusion across midline whereas lateral row perforators tend
to have little or less reliable midline crossover (4,5). The Hartrampf zones of
perfusion describe perfusion zones of the lower abdominal flap and are well
known in the literature. Hartrampf described these zones based on direct
observation of TRAM flaps and surgeons often use the system when
describing perfusion to the free flap version of this tissue. In this classic
description, zone I is the ipsilateral medial region of the dominant perforator,
zone II is the contralateral medial zone. Zones III and IV are adjacent to
zones I and II, respectively. Holms et al. described the perforasomes with
zone II and III in reverse order, illustrating the perfusion pattern consistent
with a lateral row perforator (6). Being aware of medial and lateral row
perforators can help guide which sections of the flap to preserve and which
can be discarded. However, despite the orientation of perfusion zones, it is
well accepted to locate the largest perforator to use for DIEP flap
reconstruction (5).
EXISTING SCARS
During initial consultation, it is important to be aware of any prior abdominal
surgical scars. This can affect whether or not DIEP reconstruction is
possible, as well as identifying possible areas of decreased perfusion
affecting the flap as well as the remaining tissue involved in donor-site
closure and healing. Generally, patients with prior abdominoplasty are not
eligible for DIEP-based reconstruction as the key perforator vessels are
already typically sacrificed (7,8). Furthermore, extra care must be taken in
patients with prior subcostal/Kocher or upper abdominal transverse incisions.
In the presence of these scars there is an increased risk for complications
related to wound healing as perfusion patterns may be absent or altered (9). If
there is limited blood supply originating from the more cephalad abdominal
skin and patients undergo DIEP flap harvest with sacrifice of the lower
abdominal blood supply to create the flap, the remaining area between the old
and new waistline scars is at very high risk for ischemia, especially given the
tension required to close in abdominoplasty fashion. Therefore, patients with
prior subcostal or upper transverse incisions are not appropriate candidates
for lower abdominal autologous flap reconstruction as the risk for wounding
is too high (7).
PREOPERATIVE IMAGING
There are various techniques to help identify the ideal perforator(s) for
harvest. The use of ultrasound can help provide information on size, location,
and flow of the dominant perforator, as well as thickness of adipose tissue.
When used preoperatively ultrasound can help to create a roadmap of the
dominant perforator(s) for harvest. The use of CT angiography has become
more popular among surgeons as it provides a detailed view of perforator
size, location, and its course from the external iliac artery through the rectus
muscle (4). MR angiography may also be used for preoperative assessment
and planning but tends to be less available and more expensive (2).
The use of near-infrared laser assisted indocyanine green (ICG) fluorescent
angiography can also be used to help identify perfusion patterns within the
flap intraoperatively (10). It provides a color map or gray scale of areas of
highest perfusion and identifies the extent of a perforator’s perfusion zone.
This, in turn, can guide flap design and elucidate which parts of the flap
can/should likely be discarded (2) (Fig. 84-1).
HERNIA RATES AND PREVENTION TECHNIQUES
Hernia rates after autologous breast reconstruction has been extensively
investigated. Hernia development after reconstruction have serious potential
consequences for patients including prolonged recovery and the need for
complex additional surgery not to mention the increased cost to the
healthcare system. Overall hernia rates have remained about 0.5% for DIEP-
based reconstruction (11). Understandably, TRAM flaps have significantly
higher hernia rates compared to DIEP flaps as there is a greater disruption or
use of the anterior fascia. Furthermore, MS-TRAM flaps tend to have higher
hernia rates compared to DIEP flaps for similar reason (12). The wide range
of reported rates likely reflects differences in technique, small sample sizes,
inconsistent definitions of hernia, and variability in length of follow-up.
FIGURE 84-1 Pre-operative view for bilateral deep inferior epigastric perforator
flap.

The incorporation of mesh is not commonly used in DIEP flaps given there
is minimal sacrifice of the anterior fascia. Mesh reinforcement of DIEP flap
donor sites is relatively uncommon since there is typically minimal sacrifice
of fascia in this technique. In free TRAM and MS-TRAM flaps the addition
of mesh has been shown to significantly reduce the rates of hernia and bulge
(up to 70% in unilateral and 84% in bilateral reconstruction), making
hernia/bulge rates similar to the rates seen with DIEP flaps (13,14). Given
less (or no) harvest of the anterior fascia during DIEP flap harvest, the fascia
can be closed primarily with relatively little tension. Our preference for
primary closure of rectus fascia is to use a running continuous, knotless no. 1
PDS unidirectional barbed suture (Stratafix, Knotless Tissue Control Device,
Johnson & Johnson).
While a trend toward a higher rate of hernia/bulge exists when comparing
bilateral to unilateral DIEP flaps, the data does not show a statistically
significant difference. This difference may reflect a general sense that
bilateral fascia donor sites may require mesh reinforcement whereas
unilateral cases may not (14).
While many studies discuss rates of hernia or bulge formation, very few
discuss the rates of operative repair. Mennie et al. reported 3-year hernia
repair rates among DIEP, Free TRAM, and Pedicled TRAM at 1.65, 3.18,
and 4.91, respectively (15).
SURGICAL SITE OCCURRENCES OF DIEP FLAP DONOR SITES
There are five main surgical site occurrences (SSOs) that complicate the
abdominal donor site in DIEP flap reconstruction: surgical site infections
(SSIs), seroma, hematoma, necrosis, and dehiscence. It is important to
consider the etiology, incidence, and risk factors for SSO when planning a
DIEP flap reconstruction and to discuss the possibilities of SSO with patients
preoperatively. The surgeon must have a strong understanding of the causes
and treatments of these complications as well as an understanding of the
maneuvers and modalities available to mitigate their occurrence.
Far more SSO data exists from cosmetic abdominoplasty series than from
series evaluating abdominally based free flaps closed in abdominoplasty
fashion. Some methods to reduce SSO in abdominoplasty can be extrapolated
to DIEP flap donor sites given the many similarities in dissection. However,
it is imperative to understand that prevention and management of DIEP flap
donor-site complications have their own unique considerations (Fig. 84-2).
Surgical Site Infection
The authors utilize a specific enhanced recovery after surgery (ERAS)
protocol to decrease the incidence of SSI in DIEP flap patients. These
perioperative measures include patient bacterial decolonization at home with
chlorhexidine gluconate (CHG) wipes or CHG-containing shower gel the
night before surgery, using CHG prep in the OR, and preop antibiotic
prophylaxis to cover common skin flora. Patients are not routinely placed on
antibiotics in the postoperative period. Once patients are ambulatory (the
authors’ ERAS protocol begin patient ambulation on postoperative day one),
they are ordered to shower daily to decrease general skin bacteria count.
FIGURE 84-2 On-table view after microvascular flap transfer and closure of
abdominal donor site.

Inadequate tissue perfusion is likely central to many DIEP donor-site


complications. Perfusion can be assessed intraoperatively using laser
angiography using ICG (10). The authors utilize SPY Intraoperative
Perfusion Assessment System (Stryker) to evaluate perfusion to the umbilicus
and abdominal skin and underlying fat after the flap is harvested and
abdominal flap is raised so that areas of poor perfusion can be debrided, thus
reducing risk of necrosis and development of infection from that particular
area. However, it is not always possible to debride all areas that appear
poorly perfused without then requiring tremendous tension of closure, which
then leads to poor perfusion of a different etiology.
Finally, the Prevena (KCI, San Antonio, TX) negative pressure incisional
dressing has recently been granted an FDA indication for reduction of
superficial infection and seroma: “When used with legally marketed
compatible dressings, PREVENA 125 and PREVENA PLUS 125 Therapy
Units are intended to aid in reducing the incidence of seroma and, in patients
at high risk for postoperative infections, aid in reducing the incidence of
superficial SSI in class I and class II wounds” (16). The clinical benefits of
this dressing will be discussed in last section of chapter.
Seroma and Hematoma
Seroma is a collection of serous fluid within a localized space after DIEP flap
that is typically beneath the skin and fat flap and above the fascia.
Harvest of a DIEP flap and subsequent creation of the superior abdominal
skin and fat flap requires extensive dissection and disruption of abdominal
lymphatics and vasculature. Once the skin and fat flap (not the DIEP flap) is
raised and dead space is created between the skin/fat and anterior rectus
fascia, flap motion and concomitant shearing within the newly created dead
space become key factors in formation of seroma. Although seroma has been
traditionally been considered lymphatic drainage, serous collections in the
immediate postoperative period are largely comprised of inflammatory
exudate and only begin to resemble lymph after 2 weeks (17). As the patient
becomes more ambulatory and the abdominal flap moves in relation to the
underlying fascia, mechanical shear disrupts early healing and drives
inflammation, which in turn increases vascular and lymphatic permeability,
resulting in fluid collections (18,19). Thus, flap immobilization is an integral
mechanism to minimize fluid accumulation, and can be achieved with
quilting/progressive tension sutures (PTS), drains, and/or other modalities
which are explored in the section that follows.
Seroma is the most commonly reported complication of abdominoplasty,
occurring in approximately 10% of patients (18–21). Incidence of seroma
following DIEP flap reconstruction is only about 5% (22). Risk factors for
seroma formation in abdominoplasty type closure—both cosmetic and DIEP
flap reconstruction—include high BMI (1), smoking (even after 45 days of
abstinence from tobacco) (1), extensive dissection (18,19,22), and previous
supraumbilical scars (18).
While smaller seromas can be self-limited and clinically insignificant,
larger seromas can have serious deleterious effects. Buildup of fluid
underneath the abdominal flap can cause increased pressure that increases
tension on the incision, increasing the risk of wound dehiscence and flap
necrosis. Left untreated, seroma may result in formation of a fibrous
pseudobursa which may cause discomfort and bulging (18). Should a seroma
become infected, this further increases the risk of fascial dehiscence and flap
necrosis, and patient may require percutaneous drainage, operative incision
and drainage, or even flap debridement. Infected seroma, namely those which
cause fascial dehiscence, can also lead to hernia, which come with significant
morbidity and require surgical repair. All of these complications lead to
prolonged recovery time, increased cost for both patient and provider (i.e.,
more clinic visits and possible interventions), and delay in patient return to
normal activity. Furthermore, complications from seroma can delay wound
healing altogether, which can potentially interrupt postoperative adjuvant
cancer treatment (18).
Dissection and Cautery
Extensive dissection is a known risk factor in seroma development.
Dissection of superficial inferior epigastric vein (SIEV) for additional
anastomosis for “venous superdrainage” to reduce venous congestion
increases risk of seroma, especially when performed bilaterally (10).
Literature suggests that dissection above Scarpa fascia in the lower abdomen
when performing abdominoplasty can decrease the incidence of seroma by
avoiding disruption of lymphatics (18,19,22), but there are no current studies
that examine similar dissection in DIEP flap harvest.
Studies suggest that electrocautery can lead to increased seroma formation
via increased tissue disruption and inflammatory response (23). Standard
monopolar electrocautery uses electrical current that passes through a single
electrode to cut and coagulate tissue at temperatures up to 350°C.
Plasmakinetic cautery uses pulsed radiofrequency which, when in contact
with tissue, dissects by means of an electrically conductive cloud of ions and
water vapor at lower temperatures (40° to 170°C) (24). The majority of
dissection of DIEP flap reconstruction is performed with electrocautery
devices, but some surgeons may opt to use plasmakinetic cautery to reduce
seroma. However, there is no significant difference in incidence of
postoperative donor-site seroma with use of plasmakinetic cautery versus
conventional electrocautery in abdominal free flap dissection (25).
Fibrin Sealants
Fibrin sealants are topical hemostatic adjuncts that mimic the final step in the
coagulation cascade. When applied to tissue, these agents form a fibrin clot
on the tissue onto which it is applied. There are multiple types of fibrin
sealant that contain thrombin but differ in other hemostatic components. Two
commonly used fibrin sealants include TISSEEL and FLOSEAL.
TISSEEL Fibrin Sealant (Baxter) is a two-component topical hemostatic
adjunct composed of human thrombin and human sealer protein which, when
combined, result in the conversion of soluble fibrinogen into fibrin. TISSEEL
is completely resorbed within approximately 10 to 14 days. Using the proper
application systems per manufacturer recommendations, TISSEEL is
aerosolized and can be sprayed into the donor site prior to closure.
FLOSEAL Hemostatic Matrix (Baxter) is another topical fibrin sealant that
contains human thrombin, but in contrast to TISSEEL, contains gelatin
granules which swell to tamponade bleeding and facilitate the formation of a
mechanically stable clot. FLOSEAL is completely resorbed in approximately
6 to 8 weeks.
While developed for intraoperative hemostasis, use of fibrin sealants has
evolved to include stabilization of anastomoses and adhesion of adjacent
tissues to eliminate dead space. The majority of literature regarding the use of
fibrin sealants in DIEP flap reconstruction focuses on its use to decrease
seroma and hematoma in the breast. Fibrin sealants can also be used to
stabilize the microvascular anastomosis, thus decreasing rates of
postoperative breast drainage and flap loss (26). However, there are no
current studies that solely focus on the use of fibrin sealants to reduce donor-
site complications. Thus, we again turn to studies that examine the use of
fibrin sealant in abdominoplasty.
Multiple studies suggest reduced incidence of seroma after abdominoplasty
with use of fibrin sealant (27–29). Studies comparing use of drains, fibrin
sealant, or PTS/quilting sutures to reduce seroma formation, all three
modalities significantly reduced seroma between postop days 15 and 30.
However, incidence of seroma was significantly higher in patients with fibrin
sealant (28). Furthermore, a more recent meta-analysis suggests that fibrin
sealant has no impact on seroma formation following abdominoplasty (21).
Utilization of both fibrin sealants and drains can be counterproductive in
seroma prevention, as the sealant is often thought to clog drains, this
hindering fluid evacuation from beneath the abdominal flap.
Drains
Multiple abdominal drains are commonly placed at the DIEP flap donor site
to allow drainage of accumulating fluid and are often sequentially removed
over the next 1 to 2 weeks as drain output decreases. It is widely accepted
that drains reduce incidence of seroma in the DIEP flap donor site, but the
“drain-free DIEP flap reconstruction” may obviate the need for drains when
PTS are used after DIEP flap harvest (30). This is discussed in more detail
below.
Progressive Tension Sutures
PTS are sutures placed between the abdominal flap and underlying fascia
with advancement of the flap in a proximal to distal direction, thus using
mechanical fixation of the flap to control two potential causes of seroma—
dead space and flap movement (18). By closely approximating the abdominal
flap and fascia, dead space is minimized, and fluid collections are
compartmentalized and more easily absorbed, thus reducing the incidence of
clinically significant seroma. Use of PTS can decrease the rate of seroma to
as low as 1.7% (31). PTS also allow for “tension-free” closure along the
waist by evenly distributing tension over the entire abdominal flap instead of
relying on the umbilical inset and low transverse incision for closure (18).
PTS can be placed in an interrupted or running fashion. Interrupted PTS
can be placed more precisely and more easily removed and replaced to adjust
symmetry and distribution of tension (4). Both absorbable and nonabsorbable
sutures have been used (18).
While PTS can be used in conjunction with drains, there is no advantage to
using both drains and PTS (17,30). In fact, the idea of “drain-free” DIEP flap
reconstruction is based on PTS eliminating the need for drains, as there is no
difference in complication rates in patients with only PTS compared to
patients who received PTS and drains (30). Studies show decreased volume
of seroma in patients who received PTS compared to patients with fibrin
sealant or drains (28).
Another advantage of PTS includes decreased patient dependence on tight
compressive binders or garments in the weeks after surgery (19). With
decreased mechanical shifting and shearing of the abdominal flap relative to
underlying fascia, patients may be able to ambulate sooner and walk upright
earlier after surgery, which theoretically could decrease risk of VTE in the
immediate postoperative period (4). Elimination of drains may also increase
patient independence after surgery as well as increase patient satisfaction
(30).
Despite multiple benefits, PTS are not without complications and must be
used at the surgeon’s discretion. PTS can be technically difficult to place and
require an assistant who is able to progressively advance the abdominal flap
with even distribution of tension while the surgeon places symmetric sutures.
Placement of PTS by experienced surgeons adds an average 23 minutes to
operative time but can be longer with trainees or surgeons who do not
routinely place PTS (18). Finally, in approximating the abdominal flap to the
underlying fascia, PTS can cause skin dimpling that is aesthetically
displeasing and may also weaken the underlying fascia.
Dehiscence and Necrosis
Incidence of wound dehiscence at the waistline incision in DIEP flap surgery
ranges from 3.5% to 14% (32). As with other SSOs, its etiology is
multifactorial in nature and depends on patient-related factors as well as
intraoperative and postoperative factors. In general, patients at increased risk
for wound dehiscence include females over the age of 65, BMI ≥30, diabetes
mellitus, tobacco use, and COPD (32). However, some literature suggests
that BMI, diabetes, and smoking are not significantly associated with wound
dehiscence, and adjuvant chemotherapy are some of the greatest risk factors
for this complication (30). These factors should be taken into careful
consideration when identifying candidates for DIEP flap reconstruction, and
patients must be counseled on their individual risk factors and encouraged to
optimize their health in the weeks to months leading up to surgery (i.e.,
smoking cessation, weight loss). Many surgeons have specific BMI cutoffs
and will not operate on smokers, as their risk for dehiscence—among other
perioperative complications—is increased. The authors have a BMI cutoff of
35 kg/m2.
An important intraoperative factor that increases a patient’s risk of wound
dehiscence is duration of surgery greater than 2.5 hours. DIEP flap donor
sites are at particular risk for dehiscence due to surgery duration, as
essentially all DIEP flap surgeries last greater than 3 hours (32). The
principal postoperative factor that places patients at increased risk for wound
dehiscence is suture line tension, which can be caused by increased
intraabdominal pressure (i.e., coughing, ventilation) (32), inadequate flexion
in the immediate postop period, seroma formation, and flap underperfusion
(18). Negative pressure wound therapy (NPWT) is a useful adjunct to reduce
tension on the incision and will be discussed later in this chapter (Fig. 84-3).
DIEP donor-site necrosis is primarily caused by poor perfusion of the
abdominal flap. Perfusion can be hindered by pre-existing abdominal scars
(19), so obtaining a careful past surgical history and performing a thorough
preop abdominal examination is imperative when selecting DIEP flap
candidates. Pressure on the abdominal flap (i.e., seroma, hematoma) can also
hinder perfusion and lead to donor-site necrosis (18).
Consequences of wound dehiscence and necrosis in DIEP donor sites are
like those of other SSOs: poor aesthetic outcome, increased risk of infection,
increased costs for both patient and provider, as well as emotional and
physical burden for the patient. While some minor wound dehiscence can be
managed as an outpatient, major wound dehiscence—namely fascial
dehiscence—may require surgical intervention, prolonged hospitalization,
and long-term wound care.
FIGURE 84-3 Application of closed incision negative pressure therapy dressing to
aid in healing of the flap donor site.
BARBED SUTURES
Barbed sutures are self-anchoring monofilament sutures that allow for even
distribution of tension along suture lines via circumferential, unidirectional
barbs. Barbed sutures are more expensive than traditional suture, but have the
advantage of knotless wound closure, decreased suture time, as well as
progressive and even tension when suturing (33). There is conflicting data
regarding decrease in SSO when using barbed suture, as some literature
suggests that while there are significantly fewer total wound complications
when using barbed suture compared to standard monofilament suture, there is
no difference in incidence of wound infection, wound dehiscence, seroma, or
hematoma (33).
NEGATIVE PRESSURE INCISION MANAGEMENT
The use of negative pressure for incisional therapy is often referred to in the
literature as closed incision negative pressure therapy (ciNPT), and is an
adjunct used to reduce donor-site morbidity. Prevena (KCI, San Antonio, TX)
typically remains on the incision for 5 to 7 days and helps healing by a
variety of mechanisms including: reducing tension across the suture line,
stabilizing soft tissues, reducing edema in the peri-incisional tissues,
improving blood flow at the margin, and evacuating some fluid. These
mechanisms offer multiple clinical benefits for patients including decreased
rates of seroma, infection, skin necrosis, dehiscence, postoperative pain, and
even formation of more narrow scars (Fig. 84-4).
FIGURE 84-4 Post-operative follow up demonstrating well healed autologous breast
reconstruction including donor site without complication.

The DEPRES study is a randomized controlled study observing NPWT in


patients undergoing autologous breast reconstruction. It showed a significant
reduction in dehiscence rate of 25% when VAC dressing was used for 7 days
compared to the standard incision management with Steri-Strips (32). These
results are further supported by retrospective studies observing patients
undergoing reduction mammoplasty and implant-based breast reconstruction
which again show significant reduction in rates of infection, dehiscence,
necrosis, and seroma (34,35). The advantage of NPWT has shown
comparable outcomes with a variety of flap types including the latissimus
dorsi flap, which is an alternative to DIEP flaps (36). While there are a
variety of incisional VAC dressings, the author recommends the use of
Prevena which uses −125 mm Hg of negative pressure over the wound
surface for 7 days. Patients can be sent home with the dressing in place and
have it removed in clinic. It is worth noting that there is an increased cost for
the VAC dressing. However, the increased cost outweighs the risk of
reoperation for complications. Moreover, there have been studies showing an
overall cost savings with the use of incisional VAC dressing (37). As
mentioned previously, Prevena is the only such dressing with an FDA
indication to reduce incidence of seroma and superficial SSI.

REFERENCES

1. Holmström H. The free abdominoplasty flap and its use in breast


reconstruction. An experimental study and clinical case report. Scand J
Plast Reconstr Surg 1979;13(3):423–427.
2. Mohan AT, Saint-cyr M. Anatomic and physiological fundamentals for
autologous breast reconstruction. Gland Surg 2015;4(2):116–133.
3. Hartrampf CR. The transverse abdominal island flap for breast
reconstruction. A 7-year experience. Clin Plast Surg 1988;15(4):703–
716.
4. Hamdi M, Rebecca A. The Deep Inferior Epigastric Artery Perforator
Flap (DIEAP) in breast reconstruction. Semin Plast Surg.
2006;20(2):95–102.
5. Wong C, Saint-cyr M, Mojallal A, et al. Perforasomes of the DIEP flap:
vascular anatomy of the lateral versus medial row perforators and
clinical implications. Plast Reconstr Surg 2010;125(3):772–782.
6. Holm C, Mayr M, Höfter E, et al. Perfusion zones of the DIEP flap
revisited: a clinical study. Plast Reconstr Surg 2006;117(1):37–43.
7. Chang DW. Breast reconstruction with microvascular MS-TRAM and
DIEP flaps. Arch Plast Surg 2012;39(1):3–10.
8. Parrett BM, Caterson SA, Tobias AM, et al. DIEP flaps in women with
abdominal scars: are complication rates affected?. Plast Reconstr Surg
2008;121(5):1527–1531.
9. Shermak MA, Mallalieu J, Chang D. Do preexisting abdominal scars
threaten wound healing in abdominoplasty? Eplasty 2010;10:e14.
10. Gurtner GC, Jones GE, Neligan PC, et al. Intraoperative laser
angiography using the SPY system: review of the literature and
recommendations for use. Ann Surg Innov Res 2013;7(1):1.
11. Butler DP, Plonczak AM, Reissis D, et al. Factors that predict deep
inferior epigastric perforator flap donor site hernia and bulge. J Plast
Surg Hand Surg 2018;52(6):338–342.
12. Vyas RM, Dickinson BP, Fastekjian JH, et al. Risk factors for
abdominal donor-site morbidity in free flap breast reconstruction. Plast
Reconstr Surg 2008;121(5):1519–1526.
13. Wan DC, Tseng CY, Anderson-dam J, et al. Inclusion of mesh in donor-
site repair of free TRAM and muscle-sparing free TRAM flaps yields
rates of abdominal complications comparable to those of DIEP flap
reconstruction. Plast Reconstr Surg 2010;126(2):367–374.
14. Chang EI, Chang DW. Reply: comprehensive analysis of donor-site
morbidity in abdominally based free flap breast reconstruction. Plast
Reconstr Surg 2015;135(1):227e.
15. Mennie JC, Mohanna PN, O’donoghue JM, et al. Donor-site hernia
repair in abdominal flap breast reconstruction: a population-based cohort
study of 7929 patients. Plast Reconstr Surg 2015;136(1):1–9.
16. U.S. Food and Drug Administration. PREVENA 125 and PREVENA
PLUS 125 Therapy Units, Negative pressure wound therapy device for
reduction of wound complications. April 19, 2019.
https://www.accessdata.fda.gov/cdrh_docs/reviews/DEN180013.pdf
17. Andrades P, Prado A. Composition of post-abdominoplasty seromas.
Aesthetic Plast Surg 2007;31(5):515–518.
18. Jabbour S, Awaida C, Mhawej R, et al. Does the addition of progressive
tension sutures to drains reduce seroma incidence after abdominoplasty?
A systematic review and meta-analysis. Aesthet Surg J 2017;37(4):440–
447.
19. Pollock TA, Pollock H. Progressive tension sutures in abdominoplasty: a
review of 597 consecutive cases. Aesthet Surg J 2012;32(6):729–742.
20. Nahas FX, Ferreira LM, Ghelfond C. Does quilting suture prevent
seroma in abdominoplasty? Plast Reconstr Surg 2007;119(3):1060–
1066.
21. Ardehali B, Fiorentino F. A meta-analysis of the effects of
abdominoplasty modifications on the incidence of postoperative seroma.
Aesthet Surg J 2017;37(10):1136–1143.
22. Nedomansky J, Nickl S, Radtke C, et al. Venous superdrainage in DIEP
flap breast reconstruction: the impact of superficial inferior epigastric
vein dissection on abdominal seroma formation. Plast Reconstr Surg
2018;141(2):206e–212e.
23. Yilmaz KB, Dogan L, Nalbant H, et al. Comparing scalpel,
electrocautery and ultrasonic dissector effects: the impact on wound
complications and pro-inflammatory cytokine levels in wound fluid
from mastectomy patients. J Breast Cancer 2011;14(1):58–63.
24. Dogan L, Gulcelik MA, Yuksel M, et al. The effect of plasmakinetic
cautery on wound healing and complications in mastectomy. J Breast
Cancer 2013;16(2):198–201.
25. Chow WTH, Oni G, Ramakrishnan VV, et al. The use of plasmakinetic
cautery compared to conventional electrocautery for dissection of
abdominal free flap for breast reconstruction: single-centre, randomized
controlled study. Gland Surg 2019;8(3):242–248.
26. Andree C, Munder BI, Behrendt P, et al. Improved safety of autologous
breast reconstruction surgery by stabilisation of microsurgical vessel
anastomoses using fibrin sealant in 349 free DIEP or fascia-muscle-
sparing (fms)-TRAM flaps: a two-centre study. Breast 2008;17(5):492–
498.
27. Pilone V, Vitiello A, Borriello C, et al. The use of a fibrin glue with a
low concentration of thrombin decreases seroma formation in
postbariatric patients undergoing circular abdominoplasty. Obes Surg
2015;25(2):354–359.
28. Bercial ME, Sabino Neto M, Calil JA, et al. Suction drains, quilting
sutures, and fibrin sealant in the prevention of seroma formation in
abdominoplasty: which is the best strategy?. Aesthetic Plast Surg
2012;36(2):370–373.
29. Toman N, Buschmann A, Muehlberger T. Fibrin glue and seroma
formation following abdominoplasty. Chirurg 2007;78(6):531–535.
30. Nagarkar P, Lakhiani C, Cheng A, et al. No-drain DIEP flap donor-site
closure using barbed progressive tension sutures. Plast Reconstr Surg
Glob Open 2016;4(4):e672.
31. Antonetti JW, Antonetti AR. Reducing seroma in outpatient
abdominoplasty: analysis of 516 consecutive cases. Aesthetic Surg J
2010;30(3):418–427.
32. Muller-Sloof E, De Laat HEW, Hummelink SLM, et al. The effect of
postoperative closed incision negative pressure therapy on the incidence
of donor site wound dehiscence in breast reconstruction patients:
DEhiscence PREvention Study (DEPRES), pilot randomized controlled
trial. J Tissue Viability 2018;27(4):262–266.
33. De Blacam C, Colakoglu S, Momoh AO, et al. Early experience with
barbed sutures for abdominal closure in deep inferior epigastric
perforator flap breast reconstruction. Eplasty 2012;12:e24.
34. Galiano RD, Hudson D, Shin J, et al. Incisional negative pressure wound
therapy for prevention of wound healing complications following
reduction mammaplasty. Plast Reconstr Surg Glob Open
2018;6(1):e1560.
35. Gabriel A, Sigalove S, Sigalove N, et al. The impact of closed incision
negative pressure therapy on postoperative breast reconstruction
outcomes. Plast Reconstr Surg Glob Open 2018;6(8):e1880.
36. Bi H, Khan M, Li J, Pestana IA. Use of incisional negative pressure
wound therapy in skin-containing free tissue transfer. J Reconstr
Microsurg 2018;34(3):200–205.
37. Gabriel A, Maxwell GP. Economic analysis based on the use of closed-
incision negative-pressure therapy after postoperative breast
reconstruction. Plast Reconstr Surg 2019;143(1S Management of
Surgical Incisions Utilizing Closed-Incision Negative-Pressure
Therapy):36S–40S.
CHAPTER 85

Secondary Procedures for the


Autologous Reconstructed Breast
JAUME MASIà | CRISTHIAN D. POMATA
HISTORY
Breast cancer is the most frequently diagnosed cancer among women and the
second most common cancer worldwide (1). Despite the incidence rates vary
substantially by race/ethnicity and age, some statistical analyses estimate that
approximately 12.4% of women will be diagnosed with female breast cancer
at some point during their lifetime (2). Moreover, women with breast cancer
are likely to have long-term survival, relative rates of 80% after 15 years (3).
Following the standard treatment, surgery is usually one of the first lines of
attack against breast cancer. When patients cannot be treated with breast-
conserving surgery, total mastectomy may be necessary to remove all the
breast and sometimes nearby tissue, performed whenever possible, via skin-
sparing, areolar-sparing, or nipple-sparing approaches. Furthermore, patients
with a high risk of getting second cancer often prefer to have a double
mastectomy to remove both breasts for prophylactic reasons (4).
There is enough evidence that mastectomy has an important impact on
patient self-esteem and body image perception (5–7). For this reason,
reconstruction of the female breast after a mastectomy is an integral part of
treatment for breast cancer that improves patient satisfaction, psycho-social
well-being, quality of life, and sexuality (8). The ideal goal is to replace the
resected breast tissue with something similar in terms of size, shape, and
texture, giving a feeling of a natural breast, stable over time which can best
achieve symmetry with the contralateral side or act as a substitute to those
lost in case of bilateral mastectomies.
Autologous tissue transfer is the most advanced reconstruction technique
which can provide skin, subcutaneous fat and sometimes muscle, to create a
more natural breast. The most common donor site is the abdomen which
includes the deep inferior epigastric artery perforator (DIEAP), superficial
inferior epigastric artery perforator (SIEAP), and the transverse rectus
abdominis musculocutaneous flaps (TRAM). However, there are a larger
variety of flaps available for autologous breast reconstruction such as the
thoracodorsal artery perforator (TDAP) and the latissimus dorsi
musculocutaneous flaps (LDM) from the back, the superior and inferior
gluteal artery perforator flaps (SGAP, IGAP) from the buttocks, the profunda
artery perforator (PAP) and the transverse upper gracilis flaps (TUG) from
the thighs (9).
In general, the initial reconstruction with vascularized tissue transfer offers
a satisfying aesthetic result but, it is just the first step in achieving a full and
natural breast reconstruction. Despite surgeon’s artistic experience in creating
a made-to-measure breast, obtaining a definite result in just one procedure is
not frequent because the flap usually undergoes an adaptation process into the
surrounding chest tissue, then rarely retains its original shape, size, or
position. Moreover, if the nipple–areola complex is removed during
mastectomy, the reconstruction should also be per-formed in a posterior
stage. Consequently, secondary procedures to refine the reconstructed breast
are frequently necessary (10).
PLANNING A SECONDARY PROCEDURE
Before initial breast reconstruction with autologous tissue, it is important that
the surgeon clearly explains to patients that they may need at least one or two
refinements to achieve the expected results (11). Whereas secondary
procedures are part of the autologous breast reconstruction, largely influenced
by the aesthetic perspective, the decision for surgical revisions always should
be taken based on the desires of the patient. Sometimes we have to deal with
women highly critical with the results, eager to undergo another procedure,
conversely, we can find exhausted patients who are not willing to proceed or
even satisfied with the asymmetries. Therefore, good communication is
essential to understand the patient’s expectations.
In order to define the surgical planning, a precise assessment should be
performed by patient and surgeon observation to identify the asymmetries
between both breasts and to determine the type of technique that may be
more appropriate. Contour irregularities, volume discrepancy, asymmetrical
inframammary fold position, and reconstruction of the nipple–areola
complex, are the common indications for secondary procedures for the
autologous reconstructed breast. In unilateral cases, the normal breast rarely
needs revision since the augmentation, mastopexy, or reduction
mammaplasty is always addressed in the initial intervention (12).
Secondary refinement procedures should be performed once the healing
process following the first stage of flap breast reconstruction is complete. The
optimal time is between 4 and 6 months. When adjunctive cancer-related
treatment is involved, secondary procedures take even longer until the
therapy is completed. However, the timing should be specifically determined
in each case.
BREAST MOUND REVISION
The most frequent reason for the revision is the contour asymmetries between
both breasts related to an overall or localized volume disproportions. A
common irregularity is a step-off that occurs at the interface between the
native chest wall and the breast mound (Figs. 85-1 and 85-2). Besides, an
excess or deficiency of flap volume in the superior and medial areas can
result in a slightly over- or undercorrected cleavage. Insufficient projection
can be associated with the lack of a conical shape of the autologous flap
tissue. Also, a deficiency of tissue in the medial part of the breast mound
associated with an excess of tissue in the lateral part is a common problem
when the thoracodorsal artery and vein are used as recipient’s vessels because
the flap is inset more laterally to minimize tension on the pedicle and the
anastomoses. Defects like dimpling, denting and concavity, can be also
associated with peripheral fat necrosis, extensive scarring or postoperative
radiation. Overall excess or deficiency of volume almost always will need a
secondary balancing procedure.
The goal of breast mound revision is to refine the shape and size,
employing several different techniques as a tool to sculpt the autologous
reconstructed breast. The main used methods include fat grafting, suction
lipectomy and direct tissue excision. Each procedure has its specifics purpose
for modeling the reconstructed breast, besides, a combination of these
techniques can usually be performed safely during breast mound revision.
Nevertheless, there are other less frequently used techniques to be
considered at the moment of a secondary revision regarding volume
augmentation, adding projection, restoring skin and subcutaneous tissue after
complications, or reorganizing the breast mound. All these procedures have
certain situations for which it would be the method of choice, that will be
explained forward.
FIGURE 85-1 A: A 36-year-old woman after bilateral mastectomy. B, C: Following
delayed bilateral breast reconstruction with SGAP flaps. Note the step-off at the
interface between the native chest wall and the breast mound. Secondary procedure:
fat grafting the transition zone of the upper part of both breast mounds.
FIGURE 85-2 A 30-year-old woman following bilateral nipple-sparing mastectomy
and immediate bilateral breast reconstruction with SGAP flaps. Secondary
procedure: fat grafting the upper lateral part of both breasts (green).

Contour Remodeling by Adding Volume


Fat Grafting
Autologous fat grafting is probably the most important technique in
secondary revisions and represents the ideal filler due to its relative ease of
use, biocompatibility, low morbidity, and longevity. This promising and
novel procedure provides a stable and natural improvement of the breast
mound contour and skin quality.
The fat can be harvested from numerous sites, including abdomen, thighs,
trochanter, flank, lower back, and knees. Usually, the donor site is infiltrated
with a tumescent solution, consisting of a local anesthetic and epinephrine in
saline solution, then the fat is procured using manual aspiration or
conventional liposuction device. Low harvest pressure and larger cannula
diameters are associated with higher yields of viable adipocytes. Before
grafting, the fat is typically processed by filtration, centrifugation,
decantation or washing, to eliminate tumescent fluid, free oil and debris,
obtaining a viable adipocytes concentration; however, no one method of
preparation has been shown to be the most effective (13).
The placement of the processed fat in specific spots along the breast
mound and chest wall is an excellent method to correct the shape in the upper
medial and lateral parts (Figs. 85-2 and 85-3) (14), as well as adding
projection in the central part (Figs. 85-4 and 85-5). Fat grafting is also used
in radiated breasts with skin damage because of the ability of fat and stem
cells to regenerate, hydrate, and revascularize damaged skin (15).
In general, less than 60 to 80 cc of fat is enough to correct minor contour
defects, injected in small aliquots and placed in multiple planes in the
subcutaneous tissue. Sometimes, a subdermal dissection of the slight
retractions of the skin on the relief’s areas or at the level of the incision scar,
with an 18-gauge needle, can be useful before fat grafting to improve the skin
contouring. When overall breast mound augmentation is necessary, volumes
of 150 to 200 cc of fat can be effectively placed within the flap itself due to
the tissue is soft and supple (Fig. 85-6).

FIGURE 85-3 A: A 52-year-old woman after unilateral mastectomy. B: Following


delayed breast reconstruction with DIEAP flap and contralateral mastopexy.
Secondary procedure: fat grafting the upper medial part of the breast mound (green)
and throughout the scar (red) previous subdermal dissection with an 18-gauge
needle. C: Final result after nipple reconstruction and areola tattooing.

FIGURE 85-4 A: A 39-year-old woman after unilateral mastectomy. B: Following


delayed breast reconstruction with DIEAP flap. Secondary procedure: fat grafting
the central part of the breast mound to add projection, and the contour defect in the
superior part of the chest wall (green), combined with liposuction of the excess
volume on the upper lateral part of the breast mound (red). The nipple
reconstruction is performed in an ulterior stage.

Implants
The use of a prosthetic device is another easy way to increase the
reconstructed breast volume. Implant size and profile will vary for each
patient based on the body characteristics and the desired end result. A low-
profile implant is wide and relatively flat in appearance but often provides
more cleavage, whereas, a higher-profile implant is narrow at the base but
provides a great central projection.
FIGURE 85-5 A: A 55-year-old woman after total mastectomy of the right side and
contralateral prophylactic mastectomy with implant-based reconstruction. B:
Following bilateral breast reconstruction with DIEAP flaps. Secondary procedure:
fat grafting the central part of the right breast mound to add projection (green),
combined with liposuction of the excess volume in the upper medial part of the right
breast mound (red), and direct resection of tissue from the lower part of the left
breast mound. C: Following the first revision and planning the final refinement:
liposuction of the excess volume in the medial part of the right breast mound and
nipple reconstruction.
FIGURE 85-6 A 40-year-old woman following left breast reconstruction with DIEAP
flap. Secondary procedure: overall breast mound augmentation and central
projection by fat grafting. Lowering the inframammary fold by subdermal
undermining with an 18-gauge needle and then fat grafting.

In general, implants volume that ranges from 80 to 140 cc is enough to


correct an overall volume discrepancy and achieve the desired shape, size, or
projection. The prosthesis can be easily placed under the flap in a small
pocket to avoid malposition, and far enough away of the pedicle to avoid
injury when the internal mammary vessels are used for a recipient site.
Furthermore, capsular contracture can occur but is effectively camouflaged
by the overlying flap tissue.
Despite most women prefer an autologous breast reconstruction to avoid
alloplastic materials, adding more volume to the flap by implants is possible
but is performed less and less since the use of fat grafting has become the
procedure of choice due to its highly effectivity as a filler and its natural
permanent results.

Local Perforator Flaps


Despite breast reconstruction with autologous tissue transfer is a reliable
surgical technique with a high rate of overall success, complications like
partial flap necrosis can occur in 2.5% to 7% of cases (16,17), therefore, a
secondary surgical revision will be necessary to correct contour deformities.
The use of local perforator flaps is an excellent salvage option that provides
skin and subcutaneous tissue to restore breast mound shape and volume after
partial flap loss (18).
The choice of the perforator flap will depend on the location of the defect
and the volume of tissue to be replaced. From an anatomic standpoint, the
TDAP and the lateral intercostal artery perforator (LICAP) flaps are the most
appropriate for defects in the lateral aspect of the breast mound (Fig. 85-7),
instead, the contralateral internal mammary artery perforator (IMAP), the
ipsilateral anterior intercostal artery perforator (AICAP), and the superior
epigastric artery perforator (SEAP) flaps are suitable techniques for defects
on the medial quadrants of the chest.
Contour Remodeling by Removing Volume
Suction Lipectomy
Liposuction is a minimally invasive procedure that became the most popular
method of body contouring. This procedure is the simplest approach when
small to moderate reduction is required to re-sculpt specific areas of the
reconstructed breast without markedly changing its shape or creating an
additional scar. Besides, decreasing the volume can sometimes make the
breast mound appear more ptotic and natural in shape.
FIGURE 85-7 A: A 37-year-old woman with partial flap necrosis after breast
reconstruction with DIEAP flap. B: Following a secondary reconstruction using a
local perforator flap (TDAP) to provide skin and subcutaneous tissue to restore the
breast mound shape and volume, and nipple reconstruction.

A common application of suction lipectomy in secondary autologous


breast revision is to precisely reshape areas with slightly excess volume on
the medial, superior, and lateral part of the breast mound (Figs. 85-4B and
85-5B,C). Gentle liposuction can also help to smooth the edges of the flap
blending the transition points to the chest wall. In general, these refinements
can be performed by traditional suction-assisted liposuction after tumescent
infiltration containing very dilute epinephrine to avoid contour alteration by
bleeding and make the remodeling more effective. However, in case of fat
necrosis, the ultrasound-assisted liposuction can offer an advantage in
softening the firmness mass within the autologous flap tissue with a very
precise and controlled maneuver (19).

Direct Tissue Excision


When a more radical reduction in size is necessary, direct parenchymal
excision may be convenient to achieve an optimal reshaping of the
reconstructed breast mound (Fig. 85-8). The excessive lateral tissue is a
common problem after autologous breast reconstruction that can be corrected
by suction lipectomy and skin resection.
When the autologous reconstruction results in a breast that is too ptotic,
wise pattern or standard vertical mastopexy is a good alternative to reduce the
overall size and adding central projection. In the same way, resection of a
triangle of skin and subcutaneous tissue from the lower part of the
reconstructed breast is also a good alternative to correct the shape and
projection (Fig. 85-5B). Trimming or removing the remaining flap skin
paddle, undermining a plane under the mastectomy skin, and then burying the
flap is also an alternative to lifting the breast mound. A large depressed scars
or skin retractions can be corrected by simply excising, elevating, and
advancing of the borders the skin flaps to ameliorate the contour.
Contour Remodeling by Flap Rearrangement
In some cases, an excess of tissue in one part of the breast mound will be
combined with a deficiency of tissue elsewhere in the breast. A local tissue
rearrangement can be performed by shifting the excess tissue to the part that
is requires it by using a subcutaneously based V-to-Y island flap (20). When
a more extensive reorganization of the breast mound is needed, the flap can
be elevated along one plane just overlying the chest wall and another plane
below the subdermal plexus of the skin, and then advance or rotate to fill in
the area of tissue deficiency. This approach involves extensive dissection to
raise and mobilize the subcutaneous flap by taking the risk of damaging the
pedicle to the flap. Whereas fat grafting and liposuction have demonstrated to
be the very effective and safeties techniques in adding and decreasing volume
in different spot in the same breast mound, flap rearrangement is rather
indicated to correct a very pronounce asymmetrical distribution of the flap
into the chest (Fig. 85-9) or correct small deficiency of tissue in specific spot
combined with a nearby excess of tissue.
INFRAMAMMARY FOLD CORRECTION
The inframammary fold is a crucial factor in reconstructing the appearance of
the female breast. A well-positioned and defined inframammary fold
contributes to transforming the amount of autologous tissue transferred into a
natural-appearing breast. Consequently, during secondary revision often
could be necessary to raise or lower the fold to symmetrize with the
contralateral side.

FIGURE 85-8 A: A 45-year-old woman after bilateral breast reconstruction with


DIEAP flaps. Secondary procedure: fat grafting the transition zone in the upper pole
between the native chest wall and the breast mound of the left side (green), and
direct excision of the skin and subcutaneous tissue in the right breast mound (green).
B: Final results after one more stage for nipple reconstruction, and areola tattooing.
FIGURE 85-9 A 53-year-old woman after unilateral breast reconstruction with
DIEAP flap and contralateral reductive mammoplasty. Secondary procedure: flap
rearrangement and creating the lateral inframammary fold.

Raising the inframammary fold can be a challenge and several surgical


techniques have been described for it. A common method consists of
undermining the tissue of the chest and upper abdominal wall through the
inferior incision, then advancing the lower thoracic flap superiorly and
anchoring the dermis to the chest wall with the use of barbed sutures (21,22).
Another method to create the inframammary fold without skin and soft
tissue advancement is by performing transcutaneous fixation of the
inframammary fold, at the desired level (23).
On the other hand, lowering the inframammary fold can be easily per-
formed by deepithelizing the skin of the chest wall, inferiorly, until the desire
position, then dissect the reconstructed breast above the pectoralis fascia and
repositioning down at the level of the new fold by suturing directly to the
chest wall.
Another interesting method to lowering the inframammary fold is by direct
dissection of the undersurface of the chest wall tissue through the inferior
mastectomy flap incision and then fat grafting (Fig. 85-9). A less invasive
procedure to avoid incisions can be done by multiple subdermal undermining
with an 18-gauge needle and then lipofilling (Fig. 85-6).
NIPPLE–AREOLA RECONSTRUCTION
Nipple–areola reconstruction is usually the final stage of breast
reconstruction. This procedure should be performed when the patient is
satisfied with the final shapes, sizes and symmetry between breasts is
achieved. When the reconstructed breast will not change significantly with
the revision, nipple reconstruction can be done at the end of the second-stage
procedure. Instead, if the revision of the reconstructed breast will
significantly change its size or shape, then it would be better to postpone the
procedure in order to avoid the risk that the previously chosen location may
turn out to be inadequate (see Fig. 85-5).
The challenge of nipple reconstruction is to create a three-dimensional
structure from a two-dimensional surface (24). There are numerous
techniques described for nipple reconstruction associated with high patient
satisfaction, including various local flaps (C-V, star, and skate flaps) and
nipple-sharing techniques (25). Instead, the most commonly employed
technique for areola reconstruction involves skin grafting, tattooing, and/or a
combination of these (see Figs. 85-3 and 85-8). Most nipple–areola complex
reconstruction can be performed in an office setting with or without local
anesthesia.
Areolar tattooing is usually performed 3 to 5 months following the nipple
reconstruction. In women who have had radiation, surgical nipple–areola
reconstruction is usually not advised, therefore 3D nipple–areolar tattooing is
an excellent option (26).
POSTOPERATIVE CARE
Usually, no complex postoperative care is required after secondary
procedures for the autologous reconstructed breast but there are some
recommendations about local compression. When lipofilling, local perforator
flap or nipple reconstruction has been performed, it is advisable to avoid
compression in those areas not even tight-fitting clothing. Instead, if the
patient underwent liposuction, inframammary fold elevation or direct tissue
excision, compressive supportive brassiere should be used for a few weeks
postoperatively.
In general, almost all secondary revisions can be safely performed under
local anesthesia or sedation, therefore, in a day hospital. In some cases of
more extensive revisions under general anesthesia, the patient can even spend
a night before discharge.
OUTCOMES ASSESSMENT
The full effects of secondary revisions can be noted from the second or third
month. In general, patients are happy and satisfied with the results after one
revision, which commonly includes the nipple–areola reconstruction.
Nevertheless, some patients return for predictably further revisions.
Volumetric or positional asymmetry can always result from over- or
undercorrection. Complications after secondary procedures are rare but could
happen, especially in fat grafting augmentations, which could result in oil
cysts or fat necrosis due to the excessive injection into one zone.
Sometimes, breast cancer treatment has a big impact on a patient’s
perception of her body, becoming more critical about the results,
emphasizing the aesthetical part, even more than the typical cosmetic patient.
When constant unexpected revisions are required, it is preferable to approach
with special care. Surgeon and patient should always agree on any
asymmetry and the possibility to correct it through surgery. If multiple
revision is not enough to achieve patient satisfaction, it is always a good
option to ask for a second opinion in order to approach it in a new perspective
or even make sure that nothing more should be done.
CONCLUSION
Secondary procedures are part of the autologous reconstructed breast which
involve multiples surgical techniques that the surgeon can employ as tools to
symmetrize both breasts. A suitable period of waiting for surgical refinement
should be at least 3 months. There is no precise algorithm that can be useful
for every breast reconstruction revision since a combination of different
procedures may usually be necessary to sculpt the breast mound, therefore
secondary refinement can represent a challenge for the surgeon from an
artistic point of view. Despite the patient is aware that one or two revisions
will be necessary to achieve the expected results, it is important to highlight
that if the flap is properly inserted and shaped during the initial
reconstruction, and in unilateral cases, the normal breast is addressed to
symmetrize to the reconstructed breast whenever necessary, secondary
revisions can be less complex and less frequent.

REFERENCES

1. Bray F, Ferlay J, Soerjomataram I, et al. Global cancer statistics 2018:


GLOBOCAN estimates of incidence and mortality worldwide for 36
cancers in 185 countries. CA Cancer J Clin 2018;68(6):394–424.
2. DeSantis CE, Ma J, Goding Sauer A, et al. Breast cancer statistics, 2017,
racial disparity in mortality by state. CA Cancer J Clin 2017;67(6):439–
448.
3. American Cancer Society. Breast Cancer Facts & Figures 2017–2018.
Atlanta: American Cancer Society, Inc; 2017.
4. Zurrida S, Bassi F, Arnone P, et al. The changing face of mastectomy
(from mutilation to aid to breast reconstruction). Int J Surg Oncol
2011;2011:980158.
5. Chen CL, Liao MN, Chen SC, et al. Body image and its predictors in
breast cancer patients receiving surgery. Cancer Nurs 2012;35(5):E10–
E16.
6. Monteiro-Grillo I, Marques-Vidal P, Jorge M. Psychosocial effect of
mastectomy versus conservative surgery in patients with early breast
cancer. Clin Transl Oncol 2005;7(11):499–503.
7. Ghali H, Fendri S, Ayedi I, et al. Perception of self-esteem and body
image among women with breast cancer of a University Hospital in
Tunisia. J Adv Med Med Res 2017;23:1–12.
8. Zhong T, McCarthy C, Min S, et al. Patient satisfaction and health-
related quality of life after autologous tissue breast reconstruction: a
prospective analysis of early postoperative outcomes. Cancer
2012;118(6):1701–1709.
9. Nahabedian MY, Patel K. Autologous flap breast reconstruction:
surgical algorithm and patient selection. J Surg Oncol 2016;113(8):865–
874.
10. Nahabedian MY. Symmetrical breast reconstruction: analysis of
secondary procedures after reconstruction with implants and autologous
tissue. Plast Reconstr Surg 2005;115(1):257–260.
11. Beahm EK, Walton RL. Revision in autologous breast reconstruction:
principles and approach. Clin Plast Surg 2007;34(1):139–162.
12. Nahabedian MY. Managing the opposite breast: contralateral symmetry
procedures. Cancer J 2008;14(4):258–263.
13. Gabriel A, Champaneria MC, Maxwell GP. Fat grafting and breast
reconstruction: tips for ensuring predictability. Gland Surg
2015;4(3):232–243.
14. Kanchwala SK, Glatt BS, Conant EF, et al. Autologous fat grafting to
the reconstructed breast: the management of acquired contour
deformities. Plast Reconstr Surg 2009;124(2):409–418.
15. Debald M, Pech T, Kaiser C, et al. Lipofilling effects after breast cancer
surgery in post-radiation patients: an analysis of results and algorithm
proposal. Eur J Plast Surg 2017;40(5):447–454.
16. Gill PS, Hunt JP, Guerra AB, et al. A 10-year retrospective review of
758 DIEP flaps for breast reconstruction. Plast Reconstr Surg
2004;113(4):1153–1160.
17. Blondeel PN. One hundred free DIEP flap breast reconstructions: a
personal experience. Br J Plast Surg 1999;52(2):104–111.
18. Hamdi M, Rasheed MZ. Advances in autologous breast reconstruction
with pedicled perforator flaps. Clin Plast Surg 2012;39(4):477–490.
19. Hassa A, Curtis MS, Colakoglu S, et al. Early results using ultrasound-
assisted liposuction as a treatment for fat necrosis in breast
reconstruction. Plast Reconstr Surg 2010;126(3):762–768.
20. Kroll SS, ed. Breast mound revision surgery. In: Breast Reconstruction
with Autologous Tissue. New York: Springer; 2000:293–311.
21. Ryan JJ. A lower thoracic advancement flap in breast reconstruction
after mastectomy. Plast Reconstr Surg 1982;70(2):153–160.
22. Terao Y, Taniguchi K, Tomita S. A new method for inframammary fold
recreation using a barbed suture. Aesthetic Plast Surg 2015;39(3):379–
385.
23. Buccheri EM, Zoccali G, Costantini M, et al. Breast reconstruction and
inframammary fold reconstruction: a versatile new technique. J Plast
Reconstr Aesthetic Surg 2015;68(5):742–743.
24. Nahabedian MY. Nipple reconstruction. Clin Plast Surg
2007;34(1):131–137.
25. Satteson ES, Brown BJ, Nahabedian MY. Nipple-areolar complex
reconstruction and patient satisfaction: a systematic review and meta-
analysis. Gland Surg 2017;6(1):4–13.
26. Halvorson E, Cormican M, West M, et al. Three-dimensional nipple-
areola tattooing: a new technique with superior results. Plast Reconstr
Surg 2014;133:1073–1075.
CHAPTER 86

Radiation and Autologous Breast


Reconstruction: The Role of Delayed-
Immediate Reconstruction
KATHLEEN A. HOLOYDA | ALVIN C. KWOK | JAYANT P. AGARWAL

Breast reconstruction following surgical treatment of breast cancer is a


complex, personal decision for the breast cancer patient. It has become
increasingly complex with the multiple choices for these patients, including
immediate or delayed reconstruction, implant-based reconstruction, and
autologous reconstruction. Adjuvant chemotherapy or postmastectomy
radiation therapy (PMRT) further complicates this decision. PMRT is
associated with superior locoregional control, disease-free survival, and
overall survival in node-positive breast cancer patients. For many patients
with early-stage breast cancer, the need for PMRT is not determined until the
final pathology has been evaluated. The delivery of PMRT to an immediately
reconstructed breast can adversely affect the aesthetic outcome. However, if
immediate breast reconstruction is not performed and no PMRT is needed,
the aesthetic benefit of immediate breast reconstruction in the setting of a
skin-sparing mastectomy is lost. In this chapter, we discuss a two-stage
approach, delayed-immediate reconstruction, that allows for excellent
oncologic and aesthetic outcomes in breast cancer patients requiring PMRT
and in those whose need for PMRT is not known at the time of mastectomy.
HISTORY
Radiation therapy was first described in the early 1900s by Wilhelm Conrad
Roentgen (1). The first report of radiation treatment to the breast was in the
1930s and involved the placement of radium needles and external beam
radiation therapy. Initially, radiation therapy was used to treat presumed
residual disease or to treat disease that had previously been deemed
inoperable. There were many challenges to early radiation therapy. Some of
these included the inability to detect locoregional disease and the reliance
upon bony targets and surface anatomy instead of specific soft tissue targets
thus making it difficult to know whether the radiation beam was successfully
treating the cancer mass and whether or not other critical organs were being
exposed to unnecessary radiation (2).
An initial concern with PMRT following immediate breast reconstruction
was that the reconstructed breast may interfere with delivery of PMRT and
unnecessarily increase the amount of radiation exposure to the patient’s heart
and lungs (3). Advances in radiation physics as well as computer technology
allowed for more precise delivery of radiation to the cancer being treated (1).
PMRT was shown to improve survival in 1997 by Overgaard et al. They
randomized 1,708 women with pathologic stage II or III who had undergone
mastectomy to either receiving chemotherapy and radiation or just
chemotherapy alone. Multivariate analysis demonstrated that PMRT
improved disease-free survival and overall survival (4).
In 2014, the Early Breast Cancer Trialists’ Collaborative Group
(EBCTCG) pooled patient level data from 22 randomized trials comparing
mastectomy with or without adjuvant radiation therapy and showed that
PMRT reduced locoregional recurrence by 19% and mortality by 9% for
breast cancer patients with four or more positive lymph nodes. Based upon
these data, the National Cancer Center Network (NCCN) recommends that
breast cancer patients who undergo mastectomy and have greater than or
equal to four positive nodes undergo PMRT. For patients with one to three
positive lymph nodes, the NCCN recommends that PMRT should be
“strongly considered” while taking into account patient comorbidities,
pathologic risk factors, and tumor characteristics. In patients with large
tumors (>5 cm) but no nodal disease, PMRT demonstrated no survival
benefit compared to mastectomy alone but there was an increased risk of
locoregional failure with mastectomy alone compared with those who
underwent PMRT (5,6). The American Society for Therapeutic Radiology
and Oncology (7), the American Society of Clinical Oncology (8), and Health
Canada’s Canadian Breast Cancer (9) Initiative recommend PMRT for
advanced breast cancer patients (those with T3 or T4 tumors or at least four
positive lymph nodes).
CLINICAL COMPLICATIONS ASSOCIATED WITH PATIENTS UNDERGOING
BREAST RECONSTRUCTION AND PMRT
While radiation therapy after mastectomy may improve overall survival, it
also causes vascular injury which can impair wound healing. Studies have
shown increased intimal–medial thickness of the carotid artery and narrowed
carotid lumens in head and neck cancer patients 1 year after radiation therapy
(10). Increased arterial stiffness has been demonstrated in Hodgkin
lymphoma survivors who have been treated with radiation (11). Stiffness and
contraction of vascular structures is thought to be secondary to a
proinflammatory state that is caused by the activation of nuclear factor-κ β
when blood vessel walls are irradiated (12).
On a biochemical level, certain cytokines are overexpressed following
radiation therapy. These include transforming growth factor-β, vascular
endothelial growth factor, tumor necrosis factor-α, interferon-γ, interleukin-1,
and interleukin-8 (13). Nitric oxide in normal tissue helps to promote wound
healing by induction of collagen deposition, though levels of nitric oxide are
noted to be reduced in irradiated wounds (14). The decreased collagen
deposition could account for the decreased strength of irradiated wounds
(15). Matrix metalloproteinases (MMPs) are central to the remodeling phase
of wound healing and these are found to be decreased in irradiated wounds as
well (16). The decreased MMP levels could explain the diminished ability of
soft tissue to reconstitute (15).
Keratinocytes and fibroblasts are particularly affected by radiation and are
crucial for epithelialization and remodeling in wounds, respectively.
Keratinocytes change their expression of various cytokines, thus altering their
ability to reepithelialize a wound. After radiation therapy, fibroblasts deposit
disorganized collagen bundles (15).
Like other cancer therapies, radiation therapy can result in complications
(8). While PMRT does not cause immunosuppression or feelings of illness,
there can be both acute and chronic toxicities. The acute toxicity usually
occurs within the first 3 months of radiation treatment. The most common
side effect is fatigue, sore throat, and radiation dermatitis. Radiation
dermatitis is characterized as skin erythema, hyperpigmentation, rash, and
dryness followed by moist desquamation, and usually develops gradually as
more radiation treatments are delivered. The peak of acute toxicity is usually
within the first 1 to 2 weeks after radiation therapy. Topical moisturizers can
be used help the skin heal. It usually takes about 2 to 4 weeks after treatment
for skin to heal but most patients will have some residual long-term skin
hyperpigmentation and/or associated subcutaneous fibrosis within the
treatment field (5).
Chronic toxicities include the long-term sequelae of radiation therapy to
the breast and chest wall. These make up hyperpigmentation and fibrosis of
the chest wall, radiation pneumonitis, rib fracture, lymphedema, radiation-
induced heart disease, hypothyroidism, and a low risk for secondary
malignancy (5).
TIMING OF PMRT
While immediate breast reconstruction itself does not delay adjuvant cancer
therapies, major complications can delay the delivery of adjuvant therapies
and these complications more commonly occur after immediate breast
reconstruction than after mastectomy alone (17). PMRT that is initiated
within 8 weeks of surgery in locally advanced breast cancer patients who
have undergone neoadjuvant chemotherapy has been shown to be associated
with better disease-free survival and better overall survival when compared to
those who initiate their radiation therapy at 8 to 16 weeks and >16 weeks
(18). Flores-Balcázar et al. demonstrated no difference in survival with delay
of adjuvant radiation therapy in patients with early-stage breast cancer but did
show a statistical decrease in disease-specific survival in patients with locally
advanced breast cancer receiving radiation therapy after a delay of at least 60
days (19). The initiation of radiation therapy should occur within 8 weeks of
surgery in order to provide the greatest overall and disease-specific survival.
PMRT AND ITS EFFECTS ON BREAST RECONSTRUCTION
Breast reconstruction can be performed using implant-based techniques or
using autologous tissue. It can also be carried out in either an immediate,
delayed, or delayed-immediate fashion. In the setting of PMRT each
reconstructive method has different benefits and risks.
Implant-Based Reconstruction and PMRT
Breast implant-based reconstruction is currently the most common method of
breast reconstruction in the United States (20). In efforts to reduce the
number of procedures undergone, increasing numbers of patients are electing
to undergo immediate breast reconstruction. Despite advances in the
pathologic determination of a specimen, the patient often needs to wait 1 to 2
weeks following their mastectomy before they will definitely know if they
need radiation therapy. If immediate reconstruction is performed, the need for
radiation is frequently unknown until after surgery. This leads to two
potential problems: (1) increased rates of complications and (2) a suboptimal
aesthetic result.
Careful patient selection is important for immediate breast reconstruction.
Axillary lymph node status remains an important determining factor with
regard to the need for PMRT. The possibility of PMRT requirement should
be thoroughly investigated prior to mastectomy and immediate breast
reconstruction. Clinicopathologic factors identified patients who were 50
years of age or younger, patients with tumors larger than 2 cm, and patients
with lymphovascular invasion on initial biopsy specimen to be at highest risk
for harboring axillary metastases (21).
Ideal timing and duration of PMRT can reduce the adverse effects on
breast implant-based reconstruction. There is significant risk of complications
associated with implant-based breast reconstruction following PMRT. PMRT
increases rates of infections, capsular contracture, implant loss, and
reconstructive failure in patients undergoing breast implant-based
reconstruction (22–24). Berbers et al. performed a systematic review that
demonstrated implant-based reconstructions had significantly higher total
complication rates if performed after radiation therapy (48.7%) than if
performed before radiation therapy (19.6%) (25). Magill et al. performed a
meta-analysis which examined seven studies including 2,921 patients (520
PMRT, 2,401 control). Patients who had immediate implant-based breast
reconstruction and PMRT had significantly increased rates of capsular
contracture (OR 10.21, p < 0.0001), revisional surgery (OR 2.18, p = 0.002),
and reconstructive failure (OR 2.52, p = 0.0007) compared to patients who
didn’t have PMRT. Patients who had PMRT also had reduced satisfaction
(OR 0.29, p = 0.0003) and poorer cosmetic outcome (OR = 0.28, p = 0.005)
(26). It is also important to note that patient-reported outcomes have
demonstrated decreased satisfaction and quality of life in breast-implant
based reconstruction with PMRT (27,28).
Autologous Tissue-Based Reconstruction and PMRT
Chetta et al. used the MarketScan database to characterize the postoperative
morbidity following reconstruction of the irradiated breast. They selected
breast cancer patients who had undergone mastectomy, radiation therapy, and
breast reconstruction from 2009 to 2012. In the United States, the vast
majority (80%) of irradiated patients underwent implant-based breast
reconstruction. Overall rates of complications were 45.3% for implant-based
reconstruction and 30.8% for autologous reconstruction. Implant-based
reconstructions had a failure rate of 29.4% compared to 4.3% in patients who
underwent autologous reconstruction. After controlling for confounders using
a multivariate logistic regression model, irradiated patients with implant-
based reconstruction had two times the odds of having any complication and
11 times the odds of failure compared with irradiated patients who had
autologous-based reconstruction (29).
Autologous tissue has been considered the mainstay of breast
reconstruction in the irradiated field (30). Autologous breast reconstruction
decreases the risk of reconstructive loss compared to implant-based breast
reconstruction by 92% (31). The most common issues found with PMRT
delivered prior to reconstruction were intraoperative vascular complications
and technical challenges for the surgeon without changes in clinical outcomes
including fat necrosis, delayed vascular complications, or flap loss (32). For
patients undergoing autologous breast reconstruction and PMRT, there is also
an increased risk of poor aesthetic outcomes. PMRT to autologous tissue is
associated with fibrosis, volume loss, fat necrosis, and distortion of breast
shape (33,34). The rates of revision surgery range between 16% and 35%
when PMRT is delivered to autologous breast reconstruction (35).
Irradiated patients who undergo autologous breast reconstruction have
been shown to have superior patient-reported outcomes and satisfaction
compared to those who undergo implant-based breast reconstruction (36). In
the setting of PMRT, delayed autologous reconstruction demonstrated
improved satisfaction and better aesthetic outcome compared to those who
underwent immediate DIEP flap reconstruction (37). Berbers et al.
demonstrated that while there was no significant difference in overall rates of
complication when comparing patients who had PMRT before or after their
autologous reconstruction, flap fibrosis rates were significantly higher in the
immediate reconstruction group compared to those whose reconstruction
occurred after radiation therapy (36.0% vs. 2.7%) (25). Another systematic
review by Khansa et al. demonstrated that patients who underwent radiation
to their autologous reconstructions had significantly more fat necrosis
compared to those who underwent PMRT prior to their reconstruction (22.3%
vs. 11.0%) (38). The additional flap fibrosis and fat necrosis seen with PMRT
after immediate autologous reconstruction may be contributing to the
decreased aesthetic and patient satisfaction.
Immediate Breast Reconstruction and PMRT
Indications for PMRT have broadened and as such, there have been
increasing rates of PMRT. An increased number of patients that undergo
radiation therapy are also undergoing breast reconstruction (39,40). The
growing indications for PMRT and the greater number of patients who pursue
breast reconstruction have increased the need to critically examine the
outcomes after breast reconstruction in patients undergoing radiation therapy.
Radiation oncologists create treatment plans to cover target regions such as
the chest wall and regional lymph nodes with the prescribed radiation dose
while trying to avoid other structures such as the contralateral breast, the
heart, and the lungs (41). In 2006 Motwani et al. from the MD Anderson
Cancer Center observed that more than half (52%) of patients with immediate
breast reconstruction had radiation treatment plans that were compromised
compared with 7% of matched controls who had no reconstruction (42).
More recent data has challenged this traditional paradigm that
reconstruction compromises the quality of radiation therapy. Ohri et al. at
Memorial Sloan-Kettering Cancer Center in 2012 demonstrated that implant-
based reconstruction does not adversely affect PMRT when internal
mammary nodes are not treated. In their analysis they studied 247 women
who underwent PMRT and found that there were similar doses of radiation
delivered to the heart, lower doses of radiation to the lung, and excellent
chest wall coverage when compared to those without reconstruction except
for the group where the internal mammary nodes were treated (43). In 2013,
Chung et al. at the University of Michigan demonstrated that when using
three-dimensional planning techniques, quality radiation treatments can be
achieved even when internal mammary nodes are targeted (44).
Immediate Versus Delayed Breast Reconstruction
Breast reconstruction can be performed immediately at the same time as
mastectomy or at a later time, known as “delayed breast reconstruction.”
Immediate breast reconstruction is becoming more common following
reports demonstrating superior overall aesthetic outcomes, lower costs, and
improved psychosocial well-being (45–47). More than 70% of breast
reconstructions performed in the United States are immediate breast
reconstructions (48,49).
Patient selection is important for immediate breast reconstruction. Delayed
reconstruction is typically recommended for women with significant
comorbidities, planned PMRT, inflammatory breast cancer, or women who
are psychologically unprepared to decide about reconstruction (50). Women
with significant comorbidities may be poor surgical candidates at the time of
oncologic resection and therefore optimization of medical comorbidities is
recommended prior to reconstruction. Delayed breast reconstruction is also
recommended for women who require PMRT because immediate breast
reconstruction followed by PMRT is associated with higher complication
rates (51–53). Some women diagnosed with breast cancer are unable to
decide about breast reconstruction at the time of their cancer diagnosis due to
the psychological stress of their diagnosis (49). While immediate breast
reconstruction is associated with improved psychosocial well-being
postoperatively, immediate breast reconstruction patients also tend to suffer
from higher levels of anxiety (54,55).
In a prospective, multicenter study, Yoon et al. demonstrated demographic
differences between women who underwent immediate and delayed
reconstruction. The delayed cohort tended to be older with higher body mass
index (BMI) and a higher prevalence of diabetes mellitus. They also
discovered that women undergoing delayed breast reconstruction more
commonly underwent unilateral reconstruction and autologous reconstruction
(49).
The decision to pursue immediate versus delayed breast reconstruction
involves a multidisciplinary team including the breast surgeon, the plastic
surgeon, the medical oncologist, the radiation oncologist, and the patient.
Factors to consider include quality of mastectomy flaps, need for PMRT, and
psychosocial well-being of the patient. When counseling patients, it is
important to discuss potential complications of immediate and delayed breast
reconstruction. Previous studies report varied results. Immediate breast
reconstruction in the setting of PMRT is associated with higher rates of
reconstruction failure, mastectomy flap necrosis, delayed wound healing,
infection, and tissue fibrosis compared to delayed reconstruction
(49,51,56,57). Yoon et al. reported no significant difference in the rates of
complications between delayed and immediate breast reconstruction. Delayed
autologous reconstruction is associated with significantly fewer
complications compared to immediate autologous breast reconstruction in the
setting of PMRT (49).
When taking into account patient-reported outcomes, delayed
reconstruction patients report significantly lower BREAST-Q scores
preoperatively. Delayed breast reconstruction patients also scored lower on
the Physical Function and Anxiety subscales of the PROMIS-29 and on the
preoperative EORTC Body Image and Sexual Functioning subscales. There
was no statistically significant difference in these scores 2 years
postoperatively (49). When comparing immediate and delayed autologous
breast reconstruction in the setting of PMRT, there is no significant
difference in complication rates at 2 years from final reconstruction. The
psychosocial concerns of the patient are important considerations when
deciding between immediate and delayed breast reconstruction.
Delayed-Immediate Breast Reconstruction
The concept of the delayed-immediate autologous breast reconstruction was
born from the debate regarding timing of autologous breast reconstruction in
the setting of PMRT. Some surgeons believe that immediate breast
reconstruction is ideal and that the flap can withstand PMRT. Other surgeons
find it unacceptable to radiate the flap given fibrosis, volume loss, fat
necrosis, and distortion of breast shape (30). Studies of autologous tissue
reconstruction indicate that reconstruction should be delayed in patients who
are known at the time of mastectomy to require PMRT (34,52). As discussed,
recommendations for PMRT are often not known until the final pathology of
the mastectomy specimen has been evaluated. It is difficult to determine at
the time of mastectomy and sentinel lymph node biopsy whether lymph node
micrometastases are present (21). The diagnosis of breast cancer is more
commonly based on minimally invasive techniques like fine-needle
aspiration and stereotactic core biopsy, as compared to open excisional
biopsy. These minimally invasive techniques limit the ability to assess for
local invasion within the breast parenchyma. To address this issue, breast
reconstruction could always be delayed until the completion of PMRT. If this
policy were universally accepted, patients who do not require PMRT would
be denied the aesthetic benefit of immediate breast reconstruction. Delayed-
immediate breast reconstruction provides a balance of optimal aesthetic
outcomes and effective PMRT (Fig. 86-1).
Patient selection for delayed-immediate breast reconstruction includes
patients whose requirement for PMRT is unknown at the time of mastectomy.
For delayed-immediate breast reconstruction, the reconstruction is performed
in two stages. During stage I, a tissue expander is placed at the time of
mastectomy in the prepectoral or subpectoral position and filled to the
surgeon’s discretion.
Position of the tissue expander depends on several factors. Submuscular
reconstruction has the advantage of muscle coverage in the event of
mastectomy skin necrosis and reduces risk of implant exposure (58). The
position of the pectoralis muscle above the implant also facilitates healing of
the mastectomy scar (3). Placement of the tissue expander above the
pectoralis major muscle, otherwise known as prepectoral reconstruction, has
become increasingly popular. Prepectoral placement is appropriate for
patients with adequate mastectomy skin flaps and if the tumor was not
adjacent to or involving the pectoralis muscle fascia. Sbitany et al. have
demonstrated that prepectoral placement of a tissue expander and subsequent
PMRT does not result in increased rates of necrosis, dehiscence, infection, or
explantation compared to submuscular reconstruction (59). Prepectoral tissue
expanders with replacement by implants have demonstrated excellent
physiologic and aesthetic outcomes in patients following PMRT with
minimal complications (60).
The tissue expander functions to preserve the breast skin envelope and
important anatomic landmarks like the inframammary fold and avoids the
need to stretch thin mastectomy skin flaps. The shape is preserved, not
stretched. Stretching of mastectomy skin flaps can lead to increased
contraction in the setting of radiation. Stretching the mastectomy skin flaps
can lead to expander exposure or worse aesthetic outcomes, like
telangiectasia formation of the breast reconstruction (3). In patients who do
not require PMRT, preservation of the breast skin envelope enables plastic
surgeons to achieve aesthetic outcomes similar to those obtained with
immediate breast reconstruction (61,62). In patients who do require PMRT,
radiation therapy is initiated after full expansion, allowing for “skin-
preserving” delayed reconstruction.

FIGURE 86-1 Schema for delayed-immediate breast reconstruction. (Modified from


schema from Kronowitz S, Hunt K, Kuerer H, et al. Delayed-immediate breast
reconstruction. Plast Reconstr Surg 2004;113(6):1617–1628.)
After stage I is complete, the final pathology report must be reviewed. If
PMRT is not indicated, stage II of delayed-immediate autologous
reconstruction can be performed tissue expansion has been performed. The
timing of tissue expander exchange for permanent implant an vary. Some
advocate for early exchange. This allows for the mastectomy flaps to
maintain their elasticity, while avoiding delays to chemotherapy. The tissue
expander prevents retraction of mastectomy skin and loss of the breast shape
(58). Symmetry with the contralateral breast is more easily obtained when
stage II reconstruction is performed within 2 weeks of stage I, as scar capsule
formation around the expander is not yet complete (3).
The two-stage delayed-immediate breast reconstruction offers several
advantages over standard techniques of immediate breast reconstruction. The
second stage allows for revision of the inframammary fold and debridement
of nonviable mastectomy skin flaps prior to the insetting of the autologous
tissue flap, thus preventing permanent scarring of the breast skin and
distortion of the breast shape that can occur after immediate breast
reconstruction when mastectomy skin necrosis is allowed to heal by
secondary intention.
If radiation therapy is indicated after the mastectomy and the first stage of
reconstruction, the tissue expander and chest wall are irradiated. The reason
for the two-stage reconstructive approach is to pathologically stage patients
with clinically node-negative breast cancer and to precisely evaluate the
presence of axillary lymph node micrometastases (58). If immediate breast
reconstruction was performed and PMRT is required due to pathologic
evaluation of the lymph nodes, it may adversely affect the aesthetic outcome
(33,51,52). The tissue expander remains filled during systemic adjuvant
chemotherapy and may or may not be deflated prior to radiation (63). During
this time, a mature scar capsule forms around the tissue expander prior to
PMRT (3). This mature capsule is desirable in the setting of PMRT because it
preserves the breast volume during radiation therapy. An inflated tissue
expander improves the aesthetic outcome (58).
In delayed-immediate reconstruction, tissue expanders can be deflated if
needed in order to facilitate a more effective adjuvant radiation treatment
plan. Unfortunately, deflation of expanders during radiation therapy has been
shown to increase overall complications and reconstruction failure rate
compared with keeping the expanders inflated. The most common reason for
reconstruction failure is the inability to reexpand because of skin fibrosis and
contracture (64). This is thought to be caused by changes in blood flow that
result from deflation of the tissue expander, particularly to the lower pole.
Animal studies suggest increased skin fibrosis and contracture rates with
PMRT delivery to a deflated tissue expander. Rabbit models have
demonstrated that partial deflation of expanders and subsequent radiation
therapy increases epidermal atrophy, dermal inflammation and fibrosis,
neovascularization and vascular changes, as well as capsule thickness (65).
Stage II autologous breast reconstruction is performed after the patient has
recovered from PMRT. Options for stage II include free muscle sparing, and
pedicled transverse rectus abdominis myocutaneous flap, deep inferior
epigastric perforator flap, gluteal artery perforator flap, and latissimus dorsi
with implant reconstruction. During this procedure, the tissue expander is
removed and the breast pocket is prepared for the free flap transfer. It is
important not to wait much longer than 3 months after the completion of
PMRT, as clinically the capsule surrounding the tissue expanders begin to
contract. This contraction distorts the breast anatomy, which was preserved
by the two-stage approach: the expanders move superiorly up the chest wall
and displace the inframammary fold. Revision of these changes is
challenging in an irradiated field.
Intraoperatively, the breast pocket is prepared with a partial capsulotomy
or capsulectomy depending on the thickness or degree of capsular tightness.
If submuscular placement of the tissue expander is performed and there is
excessive animation deformity, the second stage of reconstruction can be
used as an opportunity to change planes and reattach the pectoralis major
muscle to the chest wall. The reattachment preserves pectoralis major muscle
function. By removing the tissue expander from a submuscular position and
then reattaching the muscle, a noncapsular surface is present for flap
adherence. The delayed-immediate autologous reconstructed breast rarely
requires revision (3). The skin envelope is preserved, thus decreasing the skin
requirements for the autologous free flap. Generally, standard delayed breast
reconstruction following PMRT has extensive skin requirements because the
breast skin envelope was not preserved and the entire irradiated lower pole
requires excision and replacement by the tissue flap.
Patients undergoing delayed-immediate autologous breast reconstruction
have significantly better breast contour, size, position, and overall aesthetics
compared to those who have delayed autologous breast reconstruction (66).
Another advantage of the delayed-immediate breast reconstruction is that the
patients rarely require revision. If revision is required, it is seldom
complicated because the autologous tissue flap has been spared radiation (3).
Most immediate breast reconstruction procedures followed by PMRT and
standard delayed breast reconstruction procedures do require revision. In the
setting of previously irradiated tissue, these revisions can be associated with
wound healing problems.
FIGURE 86-2 Delayed-immediate breast reconstruction in a 63-year-old female. A:
Preoperative assessment. Patient was diagnosed with a 2.2 cm grade I invasive ductal
carcinoma. B: Patient underwent left skin-sparing mastectomy, sentinel lymph node
biopsy, and port placement. For stage I of her delayed-immediate breast
reconstruction, submuscular tissue expander placement was performed during the
same operation. C: Patient underwent PMRT and 5 months after her initial
operation, she underwent right hemi-abdomen DIEP reconstruction of the left breast
after removal of the tissue expander and left capsulectomy. The free flap was
positioned above the pectoralis major muscle. D: Final breast reconstruction, 3
months status post stage II delayed-immediate breast reconstruction.

Bilateral delayed-immediate reconstruction is technically less challenging


because not as much skin is required for reconstruction of bilateral breasts.
For patients that do not have the option of an abdominal-based or gluteal flap
for reconstruction, the latissimus dorsi may also be used in the delayed-
immediate setting. A small skin island may be designed because of the
advantages described above, thus limiting donor-site morbidity (Fig. 86-2).
CONCLUSION
Rate of PMRT is increasing in patients with early-stage breast cancer.
Whether or not breast cancer patients will require PMRT remains unclear at
the time of mastectomy, as the decision to use PMRT is based upon final
pathologic evaluation. While immediate breast reconstruction is beneficial
from a psychosocial standpoint to breast cancer patients (52,67), it is not
always appropriate. The aesthetic outcome of the reconstructed breast may be
altered by the use of PMRT (58). The incidence of late complications after
immediate, autologous reconstruction and PMRT is higher compared to
patients with PMRT and delayed reconstruction (51).
Delayed-immediate breast reconstruction confers the advantage of having a
tissue expander placed immediately, so the initial psychosocial effects
associated with delayed breast reconstruction are obviated. Delayed-
immediate patients that do not require PMRT have comparable complication
rates compared to those who undergo standard immediate breast
reconstruction. However, the delayed-immediate patients that do require
PMRT have fewer complications compared to those undergoing standard
reconstruction following PMRT. This likely can be attributed to the preserved
skin envelope and the decreased skin requirement of the stage II
reconstruction. Any mastectomy skin flap necrosis is debrided at the time of
stage II reconstruction, allowing for better aesthetic outcomes in delayed-
immediate breast reconstruction patients compared to immediate breast
reconstruction patients.
By delaying stage II breast reconstruction until after PMRT, aesthetic
outcomes are improved (3). The aesthetic outcomes in the delayed-immediate
technique are approaching those with immediate breast reconstruction
without PMRT. The preservation of the skin envelope increases the
reconstructive surgeon’s ability to achieve symmetry with the contralateral
breast, thereby reducing the risk of contralateral symmetry procedures.
Revision is also less likely in the delayed-immediate reconstruction, as the
autologous tissue flap is not irradiated. It provides women time to deal with
their new diagnosis of breast cancer without forcing them to make a decision
about immediate reconstruction, while allowing them to receive PMRT with
an acceptable aesthetic outcome. Delayed-immediate autologous breast
reconstruction is a safe and acceptable technique for breast cancer patients
undergoing PMRT.

REFERENCES

1. Society AC. Evolution of cancer treatments: radiation.


https://www.cancer.org/cancer/cancer-basics/history-of-cancer/cancer-
treatment-radiation.html. Accessed April 23, 2019.
2. Bradly J, Mendenhall N. Novel radiotherapy techniques for breast
cancer. Ann Rev Med 2018;69:277–288.
3. Kronowitz S. Delayed-immediate breast reconstruction: technical and
timing considerations. Plast Reconstr Surg 2010;125(2):463–474.
4. Overgaard M, Hansen P, Overgaard J, et al. Postoperative radiotherapy
in high-risk premenopausal women with breast cancer who receive
adjuvant chemotherapy. Danish Breast Cancer Cooperative Group 82b
trial. N Engl J Med 1997;337(14):949–955.
5. Remick J, Amin NP. Postmastectomy breast cancer radiation therapy.
StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2020.
https://www.ncbi.nlm.nih.gov/books/NBK519034.
6. EBCTCG (Early Breast Cancer Trialists’ Collaborative Group), McGale
P, Taylor C, et al. Effect of radiotherapy after mastectomy and axillary
surgery on 10-year recurrence and 20-year breast cancer mortality:
meta-analysis of individual patient data for 8135 women in 22
randomised trials. Lancet 2014;383(9935):2127–2135.
7. Harris J, Halpin-Murphy P, McNeese M, et al. Consensus statement on
postmastectomy radiation therapy. Int J Radiat Oncol Biol Phys
1999;44:989–990.
8. Recht A, Edge S, Solin L, et al. Postmasectomy radiotherapy: clinical
practice guidelines of the American Society of Clinical Oncology. J Clin
Oncol 2001;19:1539–1569.
9. Truong P, Olivotto I, Whelan T, et al; Steering Committee on Clinical
Practice Guidelines for the Care and Treatment of Breast Cancer.
Clinical practice guidelines for the care and treatment of breast cancer:
16. Locoregional post-mastectomy radiotherapy. CMAJ 2004;170:1263–
1273.
10. Faruolo M, Fiorentino A, Gallucci G, et al. Intimal-medial thickness and
carotid arteries lumen in irradiated patients for head and neck cancer:
preliminary data of an observational study. Clin Transl Oncol
2013;15:861–864.
11. van Leeuwen-Segarceanu EV, Dorresteign L, Vogels O, et al. Arterial
stiffness is increased in Hodgkin lymphoma survivors treated with
radiotherapy. Leuk Lymphoma 2013;54:1734–1741.
12. Halle M, Ekstrom M, Farnebo F, et al. Endothelial activation with
prothrombotic response in irradiated microvascular recipient veins. J
Plast Reconstr Aesthet Surg 2010;63:1910–1916.
13. Dormand E, Banwell P, Goodacre T. Radiotherapy and wound healing.
Int Wound J 2005;2(2):112–127.
14. Schaffer M, Weimer W, Wider S, et al. Differential expression of
inflammatory mediators in radiation-impaired wound healing. J Surg
Res 2002;107(1):93–100.
15. Haubner F, Ohmann E, Pohl F, et al. Wound healing after radiation
therapy: review of the literature. Radiat Oncol 2012;7:162.
16. Gu Q, Wang D, Gao Y, et al. Expression of MMP-1 in surgical and
radiation-impaired wound healing and its effects on the healing process.
J Environ Pathol Toxicol Oncol 2002;21(1):71–78.
17. O’Connell R, Rattay T, Dave R, et al. The impact of immediate breast
reconstruction on the time to delivery of adjuvant therapy: the iBRA-2
study. Br J Cancer 2019;120(9):883–895.
18. Silva S, Pereira A, Marta G, et al. Clinical impact of adjuvant radiation
therapy delay after neoadjuvant chemotherapy in locally advanced breast
cancer. Breast 2018;38:39–44.
19. Flores-Balcázar C, Flores-Luna H, Villarreal-Garza C, et al. Impact of
delayed adjuvant radiotherapy in the survival of women with breast
cancer. Cureus 2017;10(7):e3071.
20. El-Sabawi B, Carey J, Hagopian T, et al. Radiation and breast
reconstruction: algorithmic approach and evidence-based outcomes. J
Surg Oncol 2016;113:906–912.
21. Kronowitz S, Chang D, Robb G, et al. Implications of axillary sentinel
lymph node biopsy in immediate autologous breast reconstruction. Plast
Reconstr Surg 2002;109:1888–1896.
22. Tallet A, Salem N, Moutardier V, et al. Radiotherapy and immediate
two-stage breast reconstruction with a tissue expander and implant:
complications and esthetic results. Int J Radiat Oncol Biol Physiol
2003;57:136–142.
23. Cordeiro P, Albornoz C, McCormick B, et al. The impact of post
mastectomy radiotherapy on two-stage implant breast reconstruction: an
analysis of long-term surgical outcomes, aesthetic results, and
satisfaction over 13 years. Plast Reconstr Surg 2014;134:588–595.
24. Ho A, Bovill E, Macadam S, et al. Postmastectomy radiation therapy
after immediate two-stage tissue expander/implant breast reconstruction:
a University of British Columbia perspective. Plast Reconstr Surg
2014;134:1e–10e.
25. Berbers J, van Baardwijik A, Houben R, et al. ‘Reconstruction: before or
after postmastectomy radiotherapy?’ A Systemic review of the literature.
Eur J Cancer 2014;50(16):2752–2762.
26. Magill L, Robertson F, Jell G, et al. Determining the outcomes of post-
mastectomy radiation therapy delivered to the definitive implant in
patients undergoing one- and two-stage implant-based breast
reconstruction: a systematic review and meta-analysis. J Plast Reconstr
Aesthet Surg 2017;70(10):1329–1335.
27. Cowen D, Gross E, Rouannet P, et al. Immediate post-mastectomy
breast reconstruction followed by radiotherapy: risk factors for
complications. Breast Cancer Res Treat 2010;121:627–634.
28. Eriksson M, Anveden L, Celebioglu F, et al. Radiotherapy in implant-
based immediate breast reconstruction: risk factors, surgical outcomes,
and patient-reported outcome measures in a large Swedish multicenter
cohort. Breast Cancer Res Treat 2013;142:591–601.
29. Chetta M, Aliu O, Zhong L, et al. Reconstruction of the irradiated
breast: a national of claims-based assessment of postoperative
morbidity. Plast Reconstr Surg 2017;139(4):783–792.
30. Nelson J, Disa J. Breast reconstruction and radiation therapy: an update.
Plast Reconstr Surg 2017;140(5S):60S–68S.
31. Lee K, Mun G. Prosthetic breast reconstruction in previously irradiated
breasts: a meta-analysis. J Surg Oncol 2015;112:468–475.
32. Fosnot J, Fischer J, Smartt J, et al. Does previous chest wall irradiation
increase vascular complications in free autologous breast
reconstruction? Plast Reconstr Surg 2011;127:496–504.
33. Rogers N, Allen R. Radiation effects on breast reconstruction with the
deep inferior epigastric perforator flap. Plast Reconstr Surg
2002;109:1919–1924.
34. Spear S, Ducic I, Low M, et al. The effect of radiation on pedicled
TRAM flap breast reconstruction: outcomes and implications. Plast
Reconstr Surg 2005;115:84–95.
35. Rochlin D, Jeong A, Goldberg L, et al. Postmastectomy radiation
therapy and immediate autologous breast reconstruction: integrating
perspectives from surgical oncology, radiation oncology, and plastic and
reconstructive surgery. J Surg Oncol 2015;111:251–257.
36. Jagsi R, Momoh A, Qi J, et al. Impact of radiotherapy on complications
and patient-reported outcomes after breast reconstruction. J Natl Cancer
Inst 2018;110(2):157–165.
37. O’Connell R, DiMicco R, Khabra K, et al. Comparison of immediate
versus delayed DIEP flap reconstruction in women who require
postmastectomy radiotherapy. Plast Reconstr Surg 2018;142(3):594–
605.
38. Khansa I, Momoh A, Patel P, et al. Fat necrosis in autologous abdomen-
based breast reconstruction: a systematic review. Plast Reconstr Surg
2013;131(3):443–452.
39. Frasier L, Holden S, Holden T, et al. Temporal trends in
postmastectomy radiation therapy and breast reconstruction associated
with changes in National Comprehensive Cancer Network Guidelines.
JAMA Oncol 2016;2(1):95–101.
40. Agarwal S, Kidwell K, Farberg A, et al. Immediate reconstruction of the
radiated breast: recent trends contrary to traditional standards. Ann Surg
Oncol 2015;22(8):2551–2559.
41. Ho A, Hu Z, Mehrara B, et al. Radiotherapy in the setting of breast
reconstruction: types, techniques, and timing. Lancet Oncol
2017;18(12):e742–e753.
42. Motwani S, Strom E, Schechter N, et al. The impact of immediate breast
reconstruction on the technical delivery of postmastectomy
radiotherapy. Int J Radiat Oncol Biol Phys 2006;66:76–82.
43. Ohri N, Cordeiro P, Keam J, et al. Quantifying the impact of immediate
reconstruction in postmastectomy radiation: a large, dose-volume
histogram-based analysis. Int J Radiat Oncol Biol Phys
2012;84(2):e153–e159.
44. Chung E, Marsh R, Griffith KA, et al. Quantifying dose to the
reconstructed breast: can we adequately treat? Med Dosim
2013;38(1):55–59.
45. Khoo A, Kroll S, Reece G, et al. A comparison of resource costs of
immediate and delayed breast reconstruction. Plast Reconstr Surg
1998;101(4):964–968.
46. Wilkins E, Cederna P, Lowery J, et al. Prospective analysis of
psychosocial outcomes in breast reconstruction: one-year postoperative
results from the Michigan breast reconstruction outcomes study. Plast
Reconstr Surg 2000;106(5):1014–1025; discussion 1026–1027.
47. Elder E, Brandberg Y, Bjorklund T, et al. Quality of life and patient
satisfaction in breast cancer patients are immediate breast
reconstruction: a prospective study. Breast 2005;14(3):201–208.
48. American Society of Plastic Surgeons. “2015 Reconstructive Plastic
Surgery Statistics.” Plastic Surgery Statistics. American Society of
Plastic Surgeons. 2016. www.plasticsurgery.org
49. Yoon A, Qi J, Brown D, et al. Outcomes of immediate versus delayed
breast reconstruction; Results of a multicenter prospective study. Breast
2018;37:72–79.
50. Ananthakrishnan P, Lucas A. Options and considerations in the timing
of breast reconstruction after mastectomy. Cleve Clin J Med
2008;75(1):S30–S33.
51. Tran N, Chang D, Gupta A, et al. Comparison of immediate and delayed
free TRAM flap breast reconstruction in patients receiving post-
mastectomy radiation therapy. Plast Reconstr Surg 2001;108(1):78–82.
52. Williams J, Carlson G, Bostwick J 3rd, et al. The effects of radiation
treatment after TRAM flap breast reconstruction. Plast Reconstr Surg
1997;100(5):1153–1160.
53. von Smitten K, Sundell B. The impact of adjuvant radiotherapy and
cytotoxic chemotherapy on the outcome of immediate breast
reconstruction by tissue expansion after mastectomy for breast cancer.
Eur J Surg Oncol 1992;18(2):119–123.
54. Harcourt D, Rumsey N, Ambler N, et al. The psychological effect of
mastectomy with or without breast reconstruction: a prospective,
multicenter study. Plast Reconstr Surg 2003;111(3):1060–1068.
55. Roth R, Lowery J, Davis J, et al. Quality of life and affective distress in
women seeking immediate versus delayed breast reconstruction after
mastectomy for breast cancer. Plast Reconstr Surg 2005;116(4):93–
1002; discussion 1003–1005.
56. Seth A, Silver H, Kirsch E, et al. Comparison of delayed and immediate
tissue expander breast reconstruction in the setting of post-mastectomy
radiation therapy. Ann Plast Surg 2015;75(5):503–507.
57. Behranwala K, Dua R, Ross G, et al. The influence of radiotherapy on
capsule formation and aesthetic outcome after immediate breast
reconstruction using biodimensional anatomical expander implants. J
Plast Reconstr Aesthet Surg 2006;59(10):1043–1051.
58. Kronowitz S, Hunt K, Kuerer H, et al. Delayed-immediate breast
reconstruction. Plast Reconstr Surg 2004;113(6):1617–1628.
59. Sbitany H, Gomez-Sanchez C, Piper M, et al. Prepectoral breast
reconstruction in the setting of postmastectomy radiation therapy: an
assessment of clinical outcomes and benefits. Plast Reconstr Surg
2019;143(1):10–20.
60. Sigalove S. Prepectoral breast reconstruction and radiotherapy—a closer
look. Gland Surg 2019;8(1):67–74.
61. Kronowitz S, Kuerer H. Advances and surgical decision-making for
breast reconstruction. Cancer 2006;107:893–907.
62. Kronowitz S, Robb G. Breast reconstruction with postmastectomy
radiation therapy: current issues. Plast Reconstr Surg 2004;114:950–
960.
63. Clemens M, Kronowitz S. Current perspectives on radiation therapy in
autologous and prosthetic breast reconstruction. Gland Surg
2015;4(3):222–231.
64. Woo K, Paik J, Bang S, et al. The impact of expander inflation/deflation
status during adjuvant radiotherapy on the complications of immediate
two-stage breast reconstruction. Aesthetic Plast Surg 2017;41(3):551–
559.
65. Ozden B, Guven E, Aslay I, et al. Does partial expander deflation
exacerbate the adverse effects of radiotherapy in two-stage breast
reconstruction? World J Surg Oncol 2012;10:44.
66. Veld EH, Long C, Sue G, et al. Analysis of aesthetic outcomes and
patient satisfaction after delayed-immediate autologous breast
reconstruction. Ann Plast Surg 2018;80(55 Supplement 5):S303–S307.
67. Billig J, Jagsi R, Qi J, et al. Should immediate autologous breast
reconstruction be considered in women who require postmastectomy
radiation therapy? A prospective analysis of outcomes. Plast Reconstr
Surg 2017;139:1279–1288.
CHAPTER 87

Abdominal-Based Breast
Reconstruction—Optimizing Aesthetic
Results
ANDRES MASCARO | SUSANA BENITEZ
HISTORY
The pursuit to perfect postmastectomy breast reconstruction has been
growing steadily for the past few decades. Results have improved, and
expectations continue to increase as surgical techniques and options for
autologous breast reconstruction have evolved. Although plastic surgeons
have been performing surgery to improve breast aesthetics for several
decades, postmastectomy breast reconstruction did not become widely
popular until the latter part of the 20th century. Today, breast reconstruction
is a critical part of the comprehensive treatment plan and recovery of the
patient with breast cancer. The psychological benefits of postmastectomy
breast reconstruction have been shown to improve the overall satisfaction,
body image, self-esteem, and quality of life, as well as decrease anxiety and
depression (1).
Plastic surgeons these days have a huge variety of alloplastic and
autologous breast reconstruction options. Better understanding of flap
physiology and anatomy has provided an increasing number of flap options.
Advances in microsurgical techniques have provided surgeons with the
ability to reconstruct a breast mound using autologous tissue that not only
looks and feels like the native breast but also has sensation (2).
This improvement in the aesthetic results of the reconstructed breast has
led to a growing demand by patients for breast reconstruction
postmastectomy. With that being said the donor-site aesthetics has not always
gone hand in hand with the increasing aesthetic results of the breast and
sometimes is relegated to be a secondary result and given less importance.
AESTHETIC CONSIDERATIONS
Breast reconstruction with free autologous abdominal tissue (Free transverse
rectus abdominis musculocutaneous [TRAM], free muscle sparring
transverse rectus abdominis musculocutaneous [MS-TRAM], or deep inferior
epigastric artery [DIEP], superficial inferior epigastric vein [SIEA] flaps)
initially described by Holmström (3) and later perfected/evolved by Allen and
Treece (4) has since become a popular choice. This is attributed to its
generally good outcomes and relatively little donor-site morbidity (5). In
spite of this, some serious drawbacks regarding donor-site aesthetics may
occur (Fig. 87-1).
As patients’ expectations increase and greater awareness arises regarding
not only breast reconstruction, but the impact reconstructive procedures have
on the aesthetic body contour, the reconstructive surgeon has had to focus on
the overall aesthetic outcomes including not only breast aesthetics but the
donor site as well. A healthier lifestyle involving a growing concern about
body image, better eating habits, and exercise has also had an impact on
surgical aesthetic results.
The main reasons for dissatisfaction with the appearance of the abdomen
after reconstruction with an abdominal-based free flap are known to be dog-
ears, abdominal overhang, and, in particular, a visible donor-site scar too high
to be easily concealed by normal undergarment or swimwear. Additional
contour abnormalities and widened and pigmented scars due to wound issues
and excess tension at closure may also be problematic (6,7).
Another factor that affects patient satisfaction is the appearance of the
umbilicus and the umbilical scar itself. Many methods that aim to avoid these
dissatisfactory abdominal features have been described (8,9) including
midline marking and intraoperative dog-ear excision. However, little effort
has been made to lower the abdominal scar, because the upper border of the
flap has to include the periumbilical tissue.
This is a critical point, because as mentioned earlier an abdominal scar that
is too high is one of the most important reasons for patients hesitating to
accept an abdominal flap as an option for their breast reconstruction.
The current approach undertaken by many reconstructive surgeons,
specially at the beginning of their careers, is to pursue a “successful”
reconstruction of the breast by any means possible and that may sometimes
come at the cost of disregarding the final aesthetic result of the abdominal
donor site.
The main focus of this chapter is not to present a new and original
technique of autologous breast reconstruction using abdominal tissue, but to
describe a slightly different angle on how to approach a very well-known
reconstructive option (Fig. 87-2).
With this we attempt to bring up for consideration and thought that the
underlying goal is not only to focus on achieving a good final aesthetic result
on the breast but at the same time pursue an optimal result on the abdominal
donor site. By this manner the whole trunk is considered as a unit in the final
aesthetic outcome and hopefully better reaches the needs of patients.
The main premise of this approach resides in performing the lower incision
not more than 5 to 6 cm above the vulvar cleft which places the final
abdominal scar in a low position where it will be inconspicuous, at the same
time leaving no lateral dog-ears during the initial surgery and reconstructing
the neo-umbilicus with the same techniques utilized in cosmetic
abdominoplasties.
This may imply (in occasions) performing the upper incision in a location
at the level of the umbilicus or even below the umbilicus, so that the
abdomen can close with acceptable tension. This is done even if the
umbilicus scar remains behind as part of the upper abdominoplasty flap. In
our opinion this vertical scar is usually well tolerated by most patients.
FIGURE 87-1 Preoperative frontal view of a slim patient with limited abdominal
donor tissue.
FIGURE 87-2 Postoperative frontal view of the same patient as in Figure 87-1 after
right breast reconstruction with abdominal free tissue transfer.
INDICATIONS/CONTRAINDICATIONS AND PATIENT SELECTION
The TRAM flap was first proposed by Hartrampf et al. in 1982, with the idea
of recycling the tissue that would normally be discarded during abdominal
lipectomy (10); in other words, the TRAM flap was a byproduct of the
standard abdominoplasty that involved umbilicus rebuilding. During the
evolution of the TRAM flap to the DIEP or SIEA flap, its design continued to
include the umbilicus. Indeed, when the prototype of the DIEP flap was
introduced in 1991 by Koshima et al. (11), they called it a “paraumbilical
perforator-based flap.” This history has led to a mindset where it is very hard
to think of free TRAM or DIEP flaps without assuming that they would
involve periumbilical tissue. Furthermore, the most reliable perforators have
been proven to be located near the umbilicus (12); as a result, it was believed
that including the periumbilical tissue into the flap is essential for flap safety.
However, when we plan the DIEP/TRAM flap we rely on the fact that
many perforators can be found far below the umbilicus, some of which are
comparable to paraumbilical perforators, namely, they are large enough to
potentially be the main perforator.
The surgeon should always be aware that a lower DIEP flap approach may
increase the risk of poor perfusion/fat necrosis or venous congestion of the
flap. When the surgeon is faced with the situation where the lower portion of
the deep inferior epigastric (DIE) system has a paucity of good dominant
perforators and only presents several smaller perforators he or she should
have a low threshold to perform a free MS-TRAM and incorporate several
small perforators instead of pursuing a DIEP.
Having a very low threshold for doing a MS-TRAM versus a DIEP is a
point of contingency to performing this approach.
The overall outcomes of DIEP flaps versus MS-TRAM flaps are still a
point of controversy. There exists data that strongly supports no functional
postoperative differences between DIEP flaps versus free MS-TRAM flaps
and that they have comparable results (13). At the same time there is recent
data being published that states that from a patient satisfaction standpoint
there are some differences favoring a DIEP flap (5).
It is our opinion that to perform this technique some concessions have to
be done. If anatomically feasible we always attempt a DIEP flap as our first
option, but as mentioned above we have a low threshold to perform a free
MS-TRAM. This thought process is of great importance because it should be
preoperatively discussed in great detail with any patient that desires to
undergo an abdominally based breast reconstruction but specially with a
patient that has high aesthetic expectations for the abdominal donor-site
results.
The evaluation of the perforator anatomy is always confirmed
preoperatively by using a computed tomographic angiography (CTA) scan.
The use of a preoperative CTA scan for the visualization of perforators
from the DIE system is nearly mandatory when attempting this approach. The
knowledge of the perforator anatomy allows for an honest preoperative
discussion with the patient and gives a more realistic sense of likelihood that
this approach will succeed.
In certain cases, the aforementioned perforators located lower to the
umbilicus may not always be present. These patients would not be ideal
candidates to attempt this type of approach and they should be counseled
preoperatively that if they still want to pursue an abdominally based breast
reconstruction a standard DIEP/MS-TRAM will be performed, and the donor
scar may be located in a higher and less conspicuous position.
As mentioned earlier, venous congestion is a possibility when performing
this technique. This risk can be minimized or eliminated by supercharging the
SIEV system. If available and of an appropriate caliber we always dissect and
attempt to preserve the SIEV as a backup if venous congestion is
encountered.
These observations emphasize the importance of perforator evaluation by
using CTA and preoperative mapping with Doppler tracing.
When the decision has been made to perform a free MS-TRAM versus a
DIEP the amount of rectus fascia excised with the flap is usually minimal. It
is our practice to attempt to spare as much fascia as possible. Unfortunately,
in some cases it is required to excise more fascia than when compared with a
DIEP. When performing a bilateral free MS-TRAM it is our practice to
always place a polypropylene mesh as an underlay behind the anterior rectus
fascia to support the abdominal wall. It is our anecdotal experience that this
may contribute in minimizing abdominal wall complications such as hernias
and bulges.
As mentioned above the location of the lower incision is critical in
obtaining a favorable aesthetic result. This comes with the drawback that to
be able to close the abdomen with acceptable tension the umbilicus scar may
potentially remain behind as part of the superior abdominoplasty flap. This is
a point that also should be very clearly discussed with the patient in the
preoperative visit.
Patients with excess skin and fat tissue at the lower abdomen are usually
good candidates for a standard breast reconstruction using abdominal tissue.
Alternate techniques such as the one presented render inconsequential under
these circumstances due to the fact that there is enough substrate to work with
cephalad and there is freedom to place the lower incision in a low and ideal
location.
However, many patients who have available but yet limited amount of
donor-site tissue, desire to have a small-sized breast reconstruction and have
very high expectations regarding the donor site are deemed to be the ideal
candidates and could potentially benefit from this approach.
MARKING
Markings start with the patient in the upright standing position but most
importantly the patient is also evaluated in both a sitting or bent position to
determine how much excess abdominal pannus is available. These simple yet
critical maneuvers allow us to have a preoperative estimation of the donor
tissue as well as wound closure tension. We try to avoid markings on the
table, with the only exception of confirming that the lower incision is located
no more than 5 to 6 cm above the vulvar cleft.
In the upright position, the midline is marked from the sternum to the
vulvar cleft and a point 5 to 6 cm above the vulvar cleft is marked on the
midline. A horizontal line is then marked at this level and extended laterally
following the lowest abdominal skin crease. Lower and upper undergarment
and/or swimsuit edges are also taken into consideration at this point to avoid
visible incisions.
The patient is again seated and the excess pannus is evaluated, a tentative
mark is drawn on the superior extent of the flap just above the umbilicus as a
mirror image of the lower mark connecting both inferior lines. This final
lower abdominal elliptical design from hip to hip is confirmed for closure in
the same sitting position by grasping the skin from the umbilicus to the pubis
(Figs. 87.3 to 87.6).
FIGURE 87-3 Frontal view of proposed markings for upper incision. Markings for
lower incision and distance from vulvar cleft. (Courtesy of Claudio Milanes.)
FIGURE 87-4 Lateral view of proposed markings for upper incision. Markings for
lower incision and distance from vulvar cleft. (Courtesy of Claudio Milanes.)

FIGURE 87-5 Frontal view of preferred position (sitting or bent) to determine the
amount of available tissue that can be used as donor for transfer to the breast.
(Courtesy of Claudio Milanes.)
FIGURE 87-6 Lateral view of preferred position (sitting or bent) to determine the
amount of available tissue that can be used as donor for transfer to the breast.
(Courtesy of Claudio Milanes.)
OPERATIVE TECHNIQUE
Unlike most standard techniques, we perform the lower incision first. Doing
the lower incision first is critical. It ensures that the scar will remain in a
predefined low and conspicuous location.
Unfortunately this carries the potential problem that it does not allow the
surgeon to use the superior abdominoplasty flap (after dissection and
elevation of the flap to the xiphoid process) as a reference to mark and
determine the location of the lower incision and be able to perform a tension-
free closure.
The capability of correctly determining the location of the superior incision
is just as important because it will achieve a tension-free closure avoiding
unsightly and poorly aesthetic widened scars. This location is determined
during the preoperative marking and is based on the assessment of the patient
in the upright and sitting position.
The lower incision is taken down to fascia, and the SIEVs are identified,
preserved, and dissected free as proximal as possible. Midline incision is
done if bilateral.
Dissection over the abdominal fascia is done from lateral to medial
identifying and preserving all perforators. Based on the preoperative CTA but
more importantly on the in vivo evaluation of the encountered perforators an
assessment of the perfusion of the flap is done. If a single large perforator is
identified that has a palpable pulse and is low enough, all the other remaining
perforators are temporarily occluded with vascular clamps. Perfusion is
assessed both clinically and with ICG fluorescence angiography (if
available). If there is any question regarding the perfusion of the flap, we
have a very low threshold for incorporating more perforators and pursuing a
MS-TRAM to ensure optimal perfusion of the flap.
Once the adequate perforator(s) are selected, the dissection and elevation
of the flap (DIEP vs. MS-TRAM) is done. The details of the techniques used
for dissection of a DIEP or MS-TRAM are beyond the scope of this chapter
and can be found in Chapters 75 and 77. If doing a DIEP, the fascial incision
is kept as small as possible and just enough to ensure adequate dissection of
the DIE pedicle to a point where vessel diameter matches with the internal
mammary vessels. If performing a MS-TRAM the excision of fascia is kept
at a minimum. A polypropylene mesh is always used as underlay under the
rectus fascia when closing and is described in the section that follows.
The closure of the abdomen is sometimes relegated to the less experienced
members of the surgical team. This usually occurs to gain time in the overall
procedure while the main surgeon is performing the microsurgical portion of
the case. The ideal case scenario is that breast reconstruction using free tissue
transfer should be done by two surgical teams. There is strong data that
supports better outcomes (14). In our practice the closure of the abdomen is a
critical portion of the case and it is usually performed by one of the senior
members of the team that has extensive experience in cosmetic
abdominoplasties.
ABDOMINAL CLOSURE
Abdominal donor-site closure is performed by following the same principles
and care of a cosmetic abdominoplasty with the exception of additional
pannus thinning or rectus muscle plication. We believe this is optimized
when a two-team surgical approach is utilized routinely.
Before closure, hemostasis is obtained and the cavity irrigated with normal
saline solution. It is our practice to routinely use a polypropylene mesh to
reinforce our abdominal wall closures. The mesh is placed as an underlay
behind the anterior rectus sheath and is sutured with interrupted 2-0
polypropylene sutures to the medial and lateral boundaries of the rectus
abdominis compartment. After the mesh is secured the anterior rectus fascia
defect is repaired with 2-0 Prolene running sutures. Once the mesh is in place
and the rectus fascia closed the operating room table is flexed at the waistline
and legs elevated leaving the patient in a beach chair position. The upper skin
flap is then advanced to the lower incision. If excess tension is observed at
this point extra undermining of the superior pannus abdominal flap is
performed until adequate closure tension is obtained. Two Jackson–Pratt
drains are inserted, and temporary staples are placed to align the wound edges
and minimize dog-ears. A three-layer plane-by-plane closure is initiated with
3-0 Vicryl interrupted sutures to the deeper subcutaneous layers, 4-0 Vicryl
to the subdermal plane, and a final 4-0 Prolene intradermal layer for final skin
closure. Staples are removed and wound dressing with Jelonet, micropore,
and gauze is placed.
UMBILICUS
A horizontal umbilicoplasty is used for closure. The future neoumbilical site
is marked at the midline and positioned at the height of the original
umbilicus. This is determined before abdominal flap closure by direct
visualization when advancing the upper skin flap. Once abdominal closure is
completed a horizontal elliptical skin resection is performed at the mark
according to the size of the remaining umbilicus.
Minimal fat undermining of the flap surrounding the future neoumbilical
site is done and double plane closure is performed with interrupted 4-0 Vicryl
deep fixating sutures to the abdominal wall and interrupted 5-0 nylon Gillies-
type sutures to the skin.
POSTOPERATIVE CONSIDERATIONS
Postoperative management of patients that undergo this technique is not very
different from any other patient that undergoes a DIEP/MS-TRAM
procedure. The patients usually spend two nights in the ICU for flap
monitoring and then are transferred to a general surgical floor and are usually
discharged on postoperative day 5. The details of the postoperative flap
monitoring protocol is beyond the scope of this chapter. The only key
element that is imperative to mention is the fact that we use a very strict HOB
(head of bed) elevation of at least 40 degrees during their hospital stay and
when discharged home patients are instructed to maintain an elevation of 30
degrees of the HOB for at least a week.

REFERENCES

1. Jeevan R, Browne JP, Gulliver-Clarke C, et al. Surgical determinants of


patient-reported outcomes following postmastectomy reconstruction in
women with breast cancer. Plast Reconstr Surg 2014;134:810e–821e.
2. Weissler JM, Koltz PF, Carney MJ, et al. Sifting through the evidence: a
comprehensive review and analysis of neurotization in breast
reconstruction. Plast Reconstr Surg 2018;141(3):550–565.
3. Holmström H. The free abdominoplasty flap and its use in breast
reconstruction. Scand J Plast Reconstr Surg 1979;13:423–427.
4. Allen RJ, Treece P. Deep inferior epigastric perforator flap for breast
reconstruction. Ann Plast Surg 1994;32:32–38.
5. Erdmann-Sager J, Wilkins EG, Pusic AL, et al. Complications and
patient-reported outcomes after abdominally based breast reconstruction:
results of the mastectomy reconstruction outcomes consortium study.
Plast Reconstr Surg 2018;141(2):271–281.
6. Lee TJ, Jeong WS, Eom JS, et al. Adjuvant chemotherapy reduces the
incidence of abdominal hypertrophic scarring following immediate
TRAM breast reconstruction. Breast Cancer Res Treat 2013;137:767–
771.
7. Stalder MW, Accardo K, Allen RJ, et al. Aesthetic refinement of the
abdominal donor site after autologous breast reconstruction. Plast
Reconstr Surg 2015;136(3):455–461.
8. Niddam J, Bosc R, Lange F, et al. DIEP flap for breast reconstruction:
retrospective evaluation of patient satisfaction on abdominal results. J
Plast Reconstr Aesthet Surg 2014;67:789–796.
9. Greminger RF. The mini-abdominoplasty. Plast Reconstr Surg
1987;79:356–365.
10. Hartrampf CR, Scheflan M, Black PW. Breast reconstruction with a
transverse abdominal island flap. Plast Reconstr Surg 1982;69:216–225.
11. Koshima I, Moriguchi T, Fukuda H, et al. Free, thinned, paraumbilical
perforator-based flaps. J Reconstr Microsurg 1991;7:313–316.
12. Ireton JE, Lakhiani C, Saint-Cyr M. Vascular anatomy of the deep
inferior epigastric artery perforator flap: a systematic review. Plast
Reconstr Surg 2014;134:810e–821e.
13. Selber JC, Fosnot J, Nelson J, et al. A prospective study comparing the
functional impact of SIEA, DIEP, and muscle-sparing free TRAM Flaps
on the abdominal wall: part II. Bilateral reconstruction. Plast Reconstr
Surg 2010;126(5):1438–1453.
14. Weichman KE, Lam G, Wilson SC, et al. The impact of two operating
surgeons on microsurgical breast reconstruction. Plast Reconstr Surg
2017;139(2):277–284.
CHAPTER 88

Autologous Tissue Breast


Reconstruction in the Thin Patient
REBECCA KNACKSTEDT | RISAL DJOHAN
HISTORY
After mastectomy, reconstructive options include autologous or prosthetic-
based reconstruction. Numerous studies have demonstrated higher
satisfaction after autologous reconstruction as compared to prosthetic
reconstruction for women of all BMIs (1). Even though abdominally based
donor sites for autologous reconstruction remain most popular, women with a
paucity of abdominal tissue may not be suitable to have autologous
reconstruction (2,3). However, thin women often also have limited breast
envelope with thin subcutaneous tissue, making prosthetic based-
reconstruction equally challenging.
INDICATIONS
While the argument persists regarding the optimal autologous donor site
(4–6), the fact remains that not all patients are candidates for abdominally
based autologous breast reconstruction. However, when patient preference or
oncologic treatment demands autologous tissue, a surgeon must be equipped
with alternate approaches for reconstruction. Thus, alternative sites for
autologous tissue and ways to augment autologous tissue are paramount in
providing aesthetic reconstruction (7).
With the increasing concern of breast implant–associated anaplastic large
cell lymphoma (BIA-ALCL) or other breast implant illness, there has been
increasing interest among patients requiring mastectomy to undergo
autologous reconstruction. In thin patients, this can be a challenging situation
as there is limited skin laxity and soft tissue volume to replace missing breast
tissue. Sound clinical consideration in surgical planning in flap design and
harvest of tissue is critical in these patients. The limited and often lack of skin
laxity can create difficulty in closing the donor site, especially if flap
dimensions are increased to gain volume. If not careful, this can lead to
wound dehiscence and complications, and this must be addressed with the
patients preoperatively. Proper preoperative discussions must emphasize the
reasonable achievable volume and shape of reconstruction while balancing
potential donor-site complication.
CONTRAINDICATIONS
Contraindications for autologous breast reconstruction include patient
morbidities that do not allow for safe surgery or bleeding diatheses that
would compromise flap success.
PREOPERATIVE PLANNING
Preoperatively, some surgeons opt to pursue imaging, such as computed
tomography angiography (CTA) to delineate vascular supply to the chosen
flap. This is especially pertinent in patients who may have undergone prior
operations or liposuction in the region from which tissue will be transferred.
In the thin patient, this may be particularly useful, especially if a large
volume of soft tissue is to be transferred based on one or two perforators. A
CTA can help delineate which is the dominant perforator to a given flap and
technical feasibility of including multiple perforators to decrease
postoperative vascular compromise.
OPERATIVE TECHNIQUE
ABDOMINALLY BASED RECONSTRUCTION
It has been demonstrated that even in women with BMIs less than 23,
abdominally-based flap:mastectomy weight ratios of greater than 1 are
feasible. To achieve this, dissection is typically extended past the midline to
allow for more soft tissue transfer in unilateral breast reconstruction,
depending on the extent of perfusion.
Several studies have focused on stacked, bipedicled or extended abdominal
flaps for unilateral reconstruction, but, once again, this is often not an option
for women requiring bilateral reconstruction (8–14). When bilateral
reconstruction is desired, the recently reported stacked hemi-abdominal
extended perforator (SHAEP) flap allows for incorporation of the tissue
lateral to the typical deep inferior epigastric perforator (DIEP) dissection
(15).
In one study that retrospectively analyzed women who had undergone
abdominally based breast reconstruction with subgroup analysis based on
BMI, there was a lower rate of infection, abdominal wound healing, seromas,
and fat necrosis compared to women with larger BMIs (16). Thus, autologous
option is a promising option for thin women, but additional donor sites may
need to be considered.
LATISSIMUS DORSI
The latissimus dorsi (LD) flap is a commonly used pedicled flap for breast
reconstruction in patients who are not abdominally-based reconstruction
candidates. With LD breast reconstruction, the implant forms the bulk of the
reconstructed flap and this impact on final breast shape must be considered
(17). The anatomical basis for the LD flap has been well described and two
studies have performed sensate LD breast reconstruction. In one report, the
authors utilized an intercostal perforator nerve or the thoracodorsal nerve as
the recipient nerve and the lateral ramus of the 4th intercostal as the donor
with a nerve graft (18). Another used the lateral cutaneous branch of 7th
thoracic nerve as the recipient and the lateral cutaneous branch of 4th
intercostal as the donor, with and without nerve grafts (19). In thin women,
implant supplementation for desired volume augmentation may not be
needed, as modest additional volume of can often time be achieved with
lipografting.
SUPERIOR GLUTEAL ARTERY PERFORATOR
The superior gluteal artery perforator (SGAP) flap is an option for breast
reconstruction that utilizes excess tissue in the upper gluteal region. It is
considered a safe and reliable flap that has been utilized in women with BMIs
of an average of 22.5 (20). The dissected flap can be dissected to be more
than 100% of the mastectomy weight, demonstrating that adequate tissue can
be procured from this region (21). One study investigated providing
neurotized SGAP flaps for breast reconstruction with a dorsal lumbar
segmental nerve as the recipient and the anterior ramus of the lateral branch
of the 4th intercostal as the donor, without nerve grafts (22).
INFERIOR GLUTEAL ARTERY PERFORATOR
The inferior gluteal artery perforator (IGAP) flap relies on excess skin and
subcutaneous fat in the inferior gluteal region. Donor-site morbidity is
minimal, no sacrifice of muscle is required, and the scar can be hidden in the
natural inferior crease. The only contraindication for this flap is prior regional
liposuction (21,23–25).
In one study, a sensate flap was dissected by utilizing branches of the
posterior cutaneous femoral nerve (25).
ANTEROLATERAL THIGH AND TENSOR FASCIA LATA
The anterolateral thigh (ALT) and tensor fascia lata (TFL) flaps, although not
commonly utilized, have been successfully reported for breast reconstruction
(26,27) and take advantage of excess fat and skin in the “saddlebag” region.
Reported advantages include long perforators, easy flap dissection, and
decreased morbidity and faster recovery compared to abdominally based
flaps (28,29). However, available skin is limited and a balancing procedure is
often required.
LATERAL THIGH
The lateral thigh flap is also known as the lateral femoral circumflex artery
perforator flap. This is a modification of the TFL flap and its anatomy has
been studied retrospectively in DIEP protocol CTAs (30). The posterior
septum between the TFL and gluteus medium muscle is identified to allow
for dissection of perforators. During dissection, the lateral femoral cutaneous
nerve is identified and saved, and could potentially be utilized for sensate
reconstruction. This flap has been used successfully for breast reconstruction
with a median weight of 348 g (28,31,32).
TRANSVERSE MYOCUTANEOUS GRACILIS
The transverse myocutaneous gracilis (TUG) flap utilizes excess skin and fat
in the posterior thigh and upper buttock region based on the gracilis branch
from the medial femoral circumflex artery. Patients with small to medium
breasts with excess skin and fat in this region are good candidates for TUG
reconstruction (33–39). Variations of the TUG flap include the diagonal and
vertical upper gracilis (DUG and VUG, respectively) flaps (40).
MEDIAL CIRCUMFLEX FEMORAL ARTERY PERFORATOR
The medial circumflex femoral artery perforator (MCFA) flap is a flap based
on perforators from the main feeding vessel to the gracilis muscle (41,42).
This variation does not require sacrifice of the gracilis muscle. The MCFA
passes between the adductor longus and brevis and extends its first branch to
the adductor longus. This flap has been used successfully for breast
reconstruction with an average flap weight of 202 g and mean transplanted
flap weight of 177 g (43).
POSTERIOR MEDIAL THIGH
The posterior medial thigh (PMT) is a fasciocutaneous flap based on
perforators from the deep femoral system that mainly exit through the
adductor magnus muscle. This flap is ideal for a small to moderate breasts,
but it has not been widely employed (44).
PROFUNDA ARTERY PERFORATOR
The profunda artery perforator (PAP) flap utilizes excess skin and fat below
the gluteal crease based on a perforating vessel from the profunda artery that
pierces the fascia within 8 cm of the gluteal crease (45). In a study of 96
patients, the average flap weight was 367.4 g and the average pedicle length
was 10.2 cm (46).
LUMBAR ARTERY PERFORATOR
The lumbar artery perforator (LAP) flap utilizes excess skin over the lateral
iliac crest (47,48) and has been described as being harvested up to 12 × 24
cm (49). One report suggested that sensory nerves follow the perforators and
could be dissected if a sensate flap was desired (48).
RUBEN FAT PAD
Ruben fat pad utilizes fat in the iliac region, based on the deep circumflex
iliac artery and its myocutaneous perforators. Perforators travel over the iliac
crease and enter the subcutaneous tissue over or lateral to the crest (50).
ADJUNCTIVE PROCEDURES
Although autologous reconstruction has been performed successfully in
women with a lower BMI, this approach often requires additional adjunctive
surgeries (1). One option to provide additional soft tissue is through fat
grafting (51). However, unless transferred with a high surface area-to-volume
ratio, fat necrosis and oil cyst formation may result (52–56). This
complication has been reduced as refinements in technique have been
proposed, but some degree of palpable fat-related change remains
unavoidable (57–61). The rate of reported fat necrosis ranges in the literature
from 5% to 11% (62–66).
Another option to provide increased tissue projection is to augment the
autologous reconstruction with an implant. This can be done secondarily as
an outpatient revisionary surgery or as part of the initial reconstructive
surgery (2,3,17).
During the operation, if there is any concern for vascular compromise, ICG
fluorescence can be utilized to determine tissue perfusion. This information
can then be used in real time to determine if there is adequate perfusion or if
tissue requires resection.
INTRAOPERATIVE/POSTOPERATIVE CARE
To circumvent flap loss and allow for the early detection of flap compromise,
patients are sent to a nursing floor with staff well trained in monitoring flaps.
Flaps undergo checks every hour for 24 hours and then every 2 hours for the
next 24 hours. Checks involve both visual inspection and Doppler signal
investigation.

CASES

CASE 1

In Figure 88-1, a patient who presented for delayed autologous left breast
reconstruction underwent a DIEP flap utilizing all four zones perfused
with two perforators to allow for adequate volume. This tissue transfer
allowed for a durable and symmetric result.

FIGURE 88-1 Autologous reconstruction in a woman with minimal


abdominal tissue. This patient presented after prior left mastectomy for
delayed reconstruction (A). Reconstruction was performed using a DIEP flap
incorporating all four zones perfused with two robust perforators (B). This
achieved adequate breast tissue with good symmetry at 10-year follow-up
despite weight gain (C).

CASE 2
In Figure 88-2, a patient with minimal abdominal tissue underwent a left
DIEP previously and after right mastectomy, desired subsequent
autologous reconstruction. A TUG flap was performed to allow for
reasonable symmetry and a hidden donor site.

FIGURE 88-2 Autologous reconstruction in a woman with minimal


abdominal tissue. This patient with left breast cancer desired autologous
reconstruction but had a paucity of abdominal adiposity (A). She initially
underwent left breast mastectomy with unilateral DIEP reconstruction (B).
She was subsequently found to have suspicious lesions on the right and
underwent a right mastectomy with TUG reconstruction (C). This was able to
achieve reasonable symmetry and a hidden donor site (D) at 7-year follow-up.
GENERIC RISKS
As with all autologous-based reconstruction, generic risks include loss of flap
and risk of DVT or PE. Flap monitoring was previously addressed. To
prevent blood clots, which can be common due to surgical dissection and
immobilization, all patients are placed on appropriate anticoagulation
postoperatively, typically subcutaneous heparin injections three times a day.
OUTCOMES
In our experience, providing autologous breast reconstruction in a patient
with minimal adiposity can be successfully performed through the utilization
of alterative donor sites, augmentation of reconstruction with implants, or fat
transfer.
CONCLUSION
While autologous breast reconstruction in a thin woman can be a surgical
challenge, appropriate preoperative discussions and strategic surgical
planning can lead to aesthetic and symmetric results.

REFERENCES

1. Weichman KE, Broer PN, Thanik VD, et al. Patient-reported satisfaction


and quality of life following breast reconstruction in thin patients: a
comparison between microsurgical and prosthetic implant recipients.
Plast Reconstr Surg 2015;136(2):213–220.
2. Miller MJ, Rock CS, Robb GL. Aesthetic breast reconstruction using a
combination of free transverse rectus abdominis musculocutaneous flaps
and breast implants. Ann Plast Surg 1996;37(3):258–264.
3. Serletti JM, Moran SL. The combined use of the TRAM and
expanders/implants in breast reconstruction. Ann Plast Surg
1998;40(5):510–514.
4. Butler PD, Wu LC. Abdominal perforator vs. muscle sparing flaps for
breast reconstruction. Gland Surg 2015;4(3):212–221.
5. Murphy BD, Kerrebijn I, Farhadi J, et al. Indications and controversies
for abdominally-based complete autologous tissue breast reconstruction.
Clin Plast Surg 2018;45(1):83–91.
6. Opsomer D, van Landuyt K. Indications and controversies for
nonabdominally-based complete autologous tissue breast reconstruction.
Clin Plast Surg 2018;45(1):93–100.
7. Weichman KE, Tanna N, Broer PN, et al. Microsurgical breast
reconstruction in thin patients: the impact of low body mass indices. J
Reconstr Microsurg 2015;31(1):20–25.
8. Ali RS, Garrido A, Ramakrishnan V. Stacked free hemi-DIEP flaps: a
method of autologous breast reconstruction in a patient with midline
abdominal scarring. Br J Plast Surg 2002;55(4):351–353.
9. Hamdi M, Khuthaila DK, Van Landuyt K, et al. Double-pedicle
abdominal perforator free flaps for unilateral breast reconstruction: new
horizons in microsurgical tissue transfer to the breast. J Plast Reconstr
Aesthet Surg 2007;60(8):904–912; discussion 913–914.
10. Beahm EK, Walton RL. The efficacy of bilateral lower abdominal free
flaps for unilateral breast reconstruction. Plast Reconstr Surg
2007;120(1):41–54.
11. DellaCroce FJ, Sullivan SK, Trahan C. Stacked deep inferior epigastric
perforator flap breast reconstruction: a review of 110 flaps in 55 cases
over 3 years. Plast Reconstr Surg 2011;127(3):1093–1099.
12. Patel NG, Rozen WM, Chow WT, et al. Stacked and bipedicled
abdominal free flaps for breast reconstruction: considerations for
shaping. Gland Surg 2016;5(2):115–121.
13. Chang EI, Kronowitz SJ. Dual-pedicle flap for unilateral autologous
breast reconstruction revisited: evolution and optimization of flap design
over 15 years. Plast Reconstr Surg 2016;137(5):1372–1380.
14. Kroll SS. Bilateral breast reconstruction in very thin patients with
extended free TRAM flaps. Br J Plast Surg 1998;51(7):535–537.
15. Beugels J, Vasile JV, Tuinder SMH, et al. The stacked hemiabdominal
extended perforator flap for autologous breast reconstruction. Plast
Reconstr Surg 2018;142(6):1424–1434.
16. Kantak NA, Koolen PG, Martin C, et al. Are patients with low body
mass index candidates for deep inferior epigastric perforator flaps for
unilateral breast reconstruction? Microsurgery 2015;35(6):421–427.
17. Fisher J, Hammond DC. The combination of expanders with autogenous
tissue in breast reconstruction. Clin Plast Surg 1994;21(2):309–320.
18. Isenberg JS, Spinelli H. Further experience with innervated autologous
flaps in postoncologic breast reconstruction. Ann Plast Surg
2004;52(5):448–451; discussion 451.
19. Yano K, Hosokawa K, Takagi S, et al. Breast reconstruction using the
sensate latissimus dorsi musculocutaneous flap. Plast Reconstr Surg
2002;109(6):1897–1902; discussion 1903.
20. Baumeister S, Werdin F, Peek A. The sGAP flap: rare exception or
second choice in autologous breast reconstruction? J Reconstr
Microsurg 2010;26(4):251–258.
21. Granzow JW, Levine JL, Chiu ES, et al. Breast reconstruction with
gluteal artery perforator flaps. J Plast Reconstr Aesthet Surg
2006;59(6):614–621.
22. Blondeel PN. The sensate free superior gluteal artery perforator (S-
GAP) flap: a valuable alternative in autologous breast reconstruction. Br
J Plast Surg 1999;52(3):185–193.
23. LoTempio MM, Allen RJ. Breast reconstruction with SGAP and IGAP
flaps. Plast Reconstr Surg 2010;126(2):393–401.
24. Allen RJ, Levine JL, Granzow JW. The in-the-crease inferior gluteal
artery perforator flap for breast reconstruction. Plast Reconstr Surg
2006;118(2):333–339.
25. Struckmann V, Peek A, Wingenbach O, et al. The free fasciocutaneous
infragluteal (FCI) flap: outcome and patient satisfaction after 142 breast
reconstructions. J Plast Reconstr Aesthet Surg 2016;69(4):461–469.
26. Kaplan JL, Allen RJ, Guerra A, et al. Anterolateral thigh flap for breast
reconstruction: review of the literature and case reports. J Reconstr
Microsurg 2003;19(2):63–68.
27. Rosenberg JJ, Chandawarkar R, Ross MI, et al. Bilateral anterolateral
thigh flaps for large-volume breast reconstruction. Microsurgery
2004;24(4):281–284.
28. Tuinder S, Baetens T, De Haan MW, et al. Septocutaneous tensor
fasciae latae perforator flap for breast reconstruction: radiological
considerations and clinical cases. J Plast Reconstr Aesthet Surg
2014;67(9):1248–1256.
29. Elliott LF, Beegle PH. The lateral transverse thigh free flap: an
alternative for autogenous-tissue breast reconstruction. Plast Reconstr
Surg 1990;85(2):169–178; discussion 179–181.
30. Maricevich MA, Bykowski MR, Schusterman MA 2nd, et al. Lateral
thigh perforator flap for breast reconstruction: computed tomographic
angiography analysis and clinical series. J Plast Reconstr Aesthet Surg
2017;70(5):577–584.
31. Kind GM, Foster RD. Breast reconstruction using the lateral femoral
circumflex artery perforator flap. J Reconstr Microsurg 2011;27(7):427–
432.
32. Tuinder SMH, Beugels J, Lataster A, et al. The lateral thigh perforator
flap for autologous breast reconstruction: a prospective analysis of 138
flaps. Plast Reconstr Surg 2018;141(2):257–268.
33. Werdin F, Haug DM, Amr A, et al. Double transverse myocutaneous
gracilis free flaps for unilateral breast reconstruction. Microsurgery
2016;36(7):539–545.
34. Craggs B, Vanmierlo B, Zeltzer A, et al. Donor-site morbidity following
harvest of the transverse myocutaneous gracilis flap for breast
reconstruction. Plast Reconstr Surg 2014;134(5):682e–691e.
35. Locke MB, Zhong T, Mureau MA, et al. Tug ‘O’ war: challenges of
transverse upper gracilis (TUG) myocutaneous free flap breast
reconstruction. J Plast Reconstr Aesthet Surg 2012;65(8):1041–1050.
36. Wechselberger G, Schoeller T. The transverse myocutaneous gracilis
free flap: a valuable tissue source in autologous breast reconstruction.
Plast Reconstr Surg 2004;114(1):69–73.
37. Schoeller T, Huemer GM, Kolehmainen M, et al. A new “Siamese” flap
for breast reconstruction: the combined infragluteal-transverse
myocutaneous gracilis muscle flap. Plast Reconstr Surg
2005;115(4):1110–1117.
38. Fansa H, Schirmer S, Warnecke IC, et al. The transverse myocutaneous
gracilis muscle flap: a fast and reliable method for breast reconstruction.
Plast Reconstr Surg 2008;122(5):1326–1333.
39. Fattah A, Figus A, Mathur B, et al. The transverse myocutaneous
gracilis flap: technical refinements. J Plast Reconstr Aesthet Surg
2010;63(2):305–313.
40. Dayan JH, Allen RJ Jr. Lower extremity free flaps for breast
reconstruction. Plast Reconstr Surg 2017;140(5S Advances in Breast
Reconstruction):77S–86S.
41. Peek A, Müller M, Ackermann G, et al. The free gracilis perforator flap:
anatomical study and clinical refinements of a new perforator flap. Plast
Reconstr Surg 2009;123(2):578–588.
42. Peek A, Muller M, Exner K. [The free gracilis perforator flap for
autologous breast reconstruction]. Handchir Mikrochir Plast Chir
2002;34(4):245–250.
43. Shibuya M, Satake T, Nakasone R, et al. Breast reconstruction using
free medial circumflex artery perforator flaps: intraoperative anatomic
study and clinical results. Breast Cancer 2017;24(3):458–464.
44. Satake T, Muto M, Ko S, et al. Breast reconstruction using free posterior
medial thigh perforator flaps: intraoperative anatomical study and
clinical results. Plast Reconstr Surg 2014;134(5):880–891.
45. Saad A, Sadeghi A, Allen RJ. The anatomic basis of the profunda
femoris artery perforator flap: a new option for autologous breast
reconstruction—a cadaveric and computer tomography angiogram
study. J Reconstr Microsurg 2012;28(6):381–386.
46. Allen RJ Jr, Lee ZH, Mayo JL, et al. The profunda artery perforator flap
experience for breast reconstruction. Plast Reconstr Surg
2016;138(5):968–975.
47. de Weerd L, Elvenes OP, Strandenes E, et al. Autologous breast
reconstruction with a free lumbar artery perforator flap. Br J Plast Surg
2003;56(2):180–183.
48. Peters KT, Blondeel PN, Lobo F, et al. Early experience with the free
lumbar artery perforator flap for breast reconstruction. J Plast Reconstr
Aesthet Surg 2015;68(8):1112–1119.
49. Roche NA, Van Landuyt K, Blondeel PN, et al. The use of pedicled
perforator flaps for reconstruction of lumbosacral defects. Ann Plast
Surg 2000;45(1):7–14.
50. Hartrampf CR Jr, Noel RT, Drazan L, et al. Ruben’s fat pad for breast
reconstruction: a peri-iliac soft-tissue free flap. Plast Reconstr Surg
1994;93(2):402–407.
51. Laporta R, Longo B, Sorotos M, et al. Breast reconstruction with
delayed fat-graft-augmented DIEP flap in patients with insufficient
donor-site volume. Aesthetic Plast Surg 2015;39(3):339–349.
52. Chan CW, McCulley SJ, Macmillan RD. Autologous fat transfer—a
review of the literature with a focus on breast cancer surgery. J Plast
Reconstr Aesthet Surg 2008;61(12):1438–1448.
53. Niemela SM, Miettinen S, Konttinen Y, et al. Fat tissue: views on
reconstruction and exploitation. J Craniofac Surg 2007;18(2):325–335.
54. Boschert MT, Beckert BW, Puckett CL, et al. Analysis of lipocyte
viability after liposuction. Plast Reconstr Surg 2002;109(2):761–765;
discussion 766–767.
55. Peer LA. The neglected free fat graft, its behavior and clinical use. Am J
Surg 1956;92(1):40–47.
56. Veber M, Tourasse C, Toussoun G, et al. Radiographic findings after
breast augmentation by autologous fat transfer. Plast Reconstr Surg
2011;127(3):1289–1299.
57. Gir P, Brown SA, Oni G, et al. Fat grafting: evidence-based review on
autologous fat harvesting, processing, reinjection, and storage. Plast
Reconstr Surg 2012;130(1):249–258.
58. Kasem A, Wazir U, Headon H, et al. Breast lipofilling: a review of
current practice. Arch Plast Surg 2015;42(2):126–130.
59. Agostini T, Lazzeri D, Pini A, et al. Wet and dry techniques for
structural fat graft harvesting: histomorphometric and cell viability
assessments of lipoaspirated samples. Plast Reconstr Surg
2012;130(2):331e–339e.
60. Coleman SR. Facial recontouring with lipostructure. Clin Plast Surg
1997;24(2):347–367.
61. Coleman SR, Saboeiro AP. Fat grafting to the breast revisited: safety
and efficacy. Plast Reconstr Surg 2007;119(3):775–785; discussion
786–787.
62. Largo RD, Tchang LA, Mele V, et al. Efficacy, safety and complications
of autologous fat grafting to healthy breast tissue: a systematic review. J
Plast Reconstr Aesthet Surg 2014;67(4):437–448.
63. De Decker M, De Schrijver L, Thiessen F, et al. Breast cancer and fat
grafting: efficacy, safety and complications—a systematic review. Eur J
Obstet Gynecol Reprod Biol 2016;207:100–108.
64. Agha RA, Fowler AJ, Herlin C, et al. Use of autologous fat grafting for
breast reconstruction: a systematic review with meta-analysis of
oncological outcomes. J Plast Reconstr Aesthet Surg 2015;68(2):143–
161.
65. Spear SL, Coles CN, Leung BK, et al. The safety, effectiveness, and
efficiency of autologous fat grafting in breast surgery. Plast Reconstr
Surg Glob Open 2016;4(8):e827.
66. Groen JW, Negenborn VL, Twisk DJWR, et al. Autologous fat grafting
in onco-plastic breast reconstruction: a systematic review on oncological
and radiological safety, complications, volume retention and
patient/surgeon satisfaction. J Plast Reconstr Aesthet Surg
2016;69(6):742–764.
CHAPTER 89

Enhancing Volume in Autologous


Reconstruction
ALEXANDRA MAERTENS | BENJAMIN SARFATI
HISTORY
Breast reconstruction poses a real challenge for surgeons. Recreating breasts
in women using autologous reconstruction requires sound judgement and
skill.
Two contrasting techniques are available, either prosthetic or autologous
reconstructions.
Prosthetic reconstruction is the most commonly used technique. It may
include a two-step procedure using tissue expanders (later replaced by an
implant), or a one-step reconstruction with the immediate placement of the
implant during the mastectomy. One-step reconstructions have been
associated with higher rates of complications/revisions (1); however,
excellent aesthetic outcomes can be achieved with appropriate planning and
selection of patients.
Finally, autologous breast reconstruction has become increasingly popular
for breast reconstruction and has revolutionized aesthetic results. It is
commonly used (2). Autologous breast reconstruction can be performed
immediately or delayed. The timing of reconstruction is generally based on a
range of intrinsic and extrinsic factors related to patient and surgeon
preferences (3).
Unlike prosthetic reconstructions, results are more natural, aesthetic,
stable, and sustainable over time (2), with long-term higher levels of patient
satisfaction, and none of the traditional complications of implants (4).
Several autologous breast reconstruction techniques have been described.
Free flaps (deep inferior epigastric perforator [DIEP], profunda artery
perforator [PAP]) are commonly used. DIEP is extremely advantageous as it
imitates the shape and projection of the native breast and generally provides
sufficient volume without compromising the donor site. It is our gold
standard. For small to medium volumes, we favor a gracilis muscle or PAP
flap. In our practice, we no longer use buttock flaps (IGAP, SGAP) as this
requires two surgical positions and involves fairly significant sequelae at the
donor site.
The autologous pectoralis major pedicled flap plays an important role,
although its usefulness is limited by its inability to provide sufficient breast
volume. It is often combined during the initial surgery with a concomitant
implant or lipofilling.
Finally, and more anecdotally, autologous breast reconstruction can
sometimes be achieved exclusively via injections of adipose tissue.
Variables that determine appropriate reconstruction include the patient
habitus, smoking history, breast ptosis, skin viability after mastectomy, and
the need for additional radiotherapy and/or chemotherapy.
These various techniques have greatly increased the possibility of creating
more natural and aesthetically appealing breasts. However, symmetry
remains a concern for some patients who have undergone autologous
breast reconstruction. Although contralateral breast symmetry procedures
have been extensively described in the literature, very few publications focus
on secondary revision in autologous breast reconstruction. Consequently, an
element of uncertainty exists regarding the timing and appropriate technique
for revision procedures that do not endanger the viability of the flap (5).
Unlike the large number of studies examining the different removal
techniques for the various flaps, as well as modelling techniques, vascular
anatomy and abdominal wall imaging, there are far fewer studies exploring
the range of surgical techniques aimed at improving the aesthetic result of
flaps.
In our practice, despite careful preoperative planning and a vigilant
surgical technique, 40% of pure autologous breast reconstructions using a
flap require secondary aesthetic retouching.
The aim of these retouches is to obtain symmetry and a projection
corresponding to the native breast and/or contralateral breast (4).
In this chapter we will focus on retouching flap reconstructions to increase
the volume of the flap and fill the neckline to improve the aesthetic result.
TIMING
It is important to allow sufficient time before considering retouching the
autologous reconstruction. In fact, postsurgical oedema will take several
weeks to settle, and the skin will then gradually relax. It is estimated that the
flap will attain its final shape 4 to 6 months after the first surgery (6). A delay
of at least 3 months is required before retouching an autologous
reconstruction, as it is important to let the flap settle and reach its final
volume before considering any corrections.
In addition, particularly in the case of perforating flaps, it is important to
wait for the flap to become fully autonomous before considering any
retouching procedure that may traumatize the main perforator flap. In fact,
even in case of injury to the main pedicle flap, no secondary extensive
necrosis of the flap will be observed (7). A 3-month period is also required
(8).
Thus, autologous flaps can only be retouched 3 months after surgery.
Moreover, it is important to plan the volume before surgery.
Some teams use 3D stereophotogrammetry imaging techniques that can be
used during surgery and are low cost, and can be used to design, plan, and
help evaluate the required volume to ensure its qualitative and quantitative
improvement (4,9), resulting in high levels of patient satisfaction.
For immediate or delayed unilateral and bilateral breast reconstructions, a
breast mould may be considered as a useful and inexpensive addition to the
autologous breast reconstruction procedure. However, if the patient does not
have sufficient volume at the donor site or is not satisfied with the natural
appearance of her breast, the process of manufacturing a 3D printed model
offers little added value. Therefore, patients should be preselected before this
technique is used (9).
OPERATIVE TECHNIQUES
Volume correction is indicated for patients who do not have enough volume
at the donor site, to those who require double reconstruction, to macromastia,
or to retouching to perfect the symmetry. Although it is possible to reduce the
contralateral breast, sometimes this is not enough.
Several techniques are described for improving the aesthetic results of
autologous breast reconstructions.
INCREASING VOLUME AND PROJECTION

Breast Implants (Fig. 89-1)


Some teams propose increasing the volume by combining the autologous
reconstruction with a prosthetic implant to improve symmetry. This may
require the placement of a breast implant at either the same time as the flap,
or secondarily (10).
Reconstruction in patients with macroplasty can be difficult; insufficient
flaps for a very large breast imprint and lipofilling and, although it is possible
to modify the contralateral breast, this is inadequate. Teams will combine
flaps and implants in such indications.
The flap may help reduce the increased adverse effects associated with the
combination of an implant and radiotherapy; however, the risks of
nonautologous reconstruction remain.
This option is mainly carried out with a pectoralis major flap, though in
most cases it does not provide a sufficient volume (11).
Although very effective in increasing the volume and projection of the
reconstruction, our team does not perform this technique. Adding an implant
to a DIEP changes the paradigm of the autologous reconstruction, by
introducing implant reconstruction risks. In fact, when we decide to perform
an autologous breast reconstruction, we prefer avoiding inserting a foreign
body, as this combines the disadvantages of the flaps (need for an additional
scar) and implants (foreign body, contracture, infection, changes over time),
which may require the removal of the implant (12).

FIGURE 89-1 A: Delayed breast reconstruction with a DIEP flap (few sessions of fat
grafting are planned to increased volume of the flap). B: Same patient after massive
weight loss. The patient doesn’t have enough fat to enhance the flap. C: Results after
implant behind the flap and breast symmetrisation.
FIGURE 89-2 A: Immediate breast reconstruction with a DIEP flap. Partial necrosis
of the flap occurred with reduction of around 50% of the flap’s volume. B: Result
after one session of fat grafting (250 cc).

Exceptionally, when the patient has lost a lot of weight and it is impossible
to find sufficient volume to collect and reinject fat, an implant can be put in
place.
Our preferred technique is lipofilling. We do not routinely use implants to
increase the volume of our autologous reconstructions.
Fat Injections (Fig. 89-2)
Autologous fat grafts are frequently used both in aesthetic cases as well as
reconstruction cases.
Fat grafts (Fig. 89-3) can be used exclusively as an autonomous form of
reconstruction or to complement another reconstruction procedure and add
extra volume, to correct asymmetries, or to further refine an aesthetic result
by improving breast size and contour, and they have had a major impact on
reconstruction results (3).
A fat graft offers many features that make it an ideal filling material for
breasts. It is nontoxic, biocompatible, easy to use, and inexpensive. It also
provides a natural feel and appearance (3).
Initially, fat grafts were not widely accepted due to concerns about
oncologic safety and tumor surveillance, as it was feared that breast fat grafts
could interfere with the early detection of breast cancer via mammography;
the effectiveness of the technique was also questioned. Despite initial
criticism and reluctance, there is growing evidence that fat grafts can be used
safely and effectively in breast reconstructions (13).
It is now generally accepted that well-performed large-volume fat grafts
are both safe and effective (14–16).
Lipofilling may be carried out concomitantly with the removal and
placement of the flap, in the case of reconstruction using an autologous
pectoralis major (17); or, at a later date, within a period of 3 months. For
perforator flaps, we prefer to carry out lipofilling at a later stage, the same
deadline is respected when we multiply the sessions (Fig. 89-3).
The injection of fat concomitant with the lifting of a pectoralis major flap
may be carried out at the level of the pectoralis major muscle, its skin paddle,
and the pectoralis major muscle.
For fasciocutaneous perforator flaps, concomitant lipofilling may only be
performed at the level of the pectoralis major muscle.
Autologous fat transfers as a secondary procedure is a powerful addition to
enhancing the aesthetic outcome of the reconstructed breast and donor site
(18). It may be easily combined. With additional lipofilling, it may be
possible to broaden the indications and propose
autologous reconstructions with a flap even in very thin patients (19).
In fact, it is common to observe a lack of volume at the neckline a few
months after a flap reconstruction, but also to correct an external slash, to
restore shape to the lower part of the breast, and to correct a retractable scar.

FIGURE 89-3 A: Final result after the second session of fat grafting (350 cc). B: 3D
tattoo of the areola by Mrs. Alexia Cassar.

Adipose tissue is removed from the usual sites (abdomen, flanks,


trochanteric regions, inner thighs) based on the distribution of the fat zones of
the patient. Fat is aspirated using a 4-mm liposuction cannula, connected to a
400-ml Redon bottle, connected to a liposuction device. The fat is then
centrifuged.
The transfer of adipose tissue occurs in a radial and retrograde fashion and
across all areas (subcutaneous, fatty, muscular, and retromuscular tissue),
using a 2-mm injection cannula, surmounted by a 10-mm syringe (20,21). Fat
injections performed at the flaps are systematically combined with a rigotomy
procedure using 18-gauge needles (22). This will release adherences to the
deep tissues, increase the amount of fat injected per session, and increase the
projection.
In our experience, we have never observed complete flap necrosis during
remote lipofilling or any voluminous haematoma suggestive of injury to the
main pedicle.
Lipofilling is a safe, simple, and effective technique (23) with satisfactory
and long-term results.
It is our standard technique for increasing the volume of a flap or its
projection. It allows both the volume and projection to be corrected but also
corrects deformities of the breast contour, irregularities, and adhesions (24).
Autologous Flap Combination
However, the improvement in volume may also arise beyond retouching in
patients who are not ideal candidates, such as patients who do not have
adequate donor tissue and still require this reconstruction option or during
bilateral reconstructions (1).
For these patients, lipofilling is not sufficient and a flap combination may
be proposed to offer additional volume while still using an exclusive
autologous reconstruction option.
Various teams have performed these double (free or pedicled) flaps.
Sjoberg et al. suggest combining a pedicle lateral intercostal artery
perforator (LICAP) with a DIEP in a reconstruction to increase the size of the
chest and improve the aesthetic results (25).
Combinations with a LICAP flap have been used in women with
insufficient abdominal flap tissue in relation to the desired breast size.
The LICAP flap provided additional volume and allowed better projection
and ptosis of the new breast.
The overall rate of complications with LICAP flaps was 26%; all
complications were minor.
In some patients with insufficient abdominal flap tissue, the combination
of a free abdominal flap and a pedicled LICAP flap is an interesting option to
increase chest size and enhance the aesthetic result. Additional symmetry
surgery may still be required.
Free flaps were also combined: DIEP–gracilis, DIEP–PAP, or double
gracilis.
This combination of two separate pedicled or free flaps for a single
reconstruction is not a new concept for breast reconstruction. In 1992, Arnez
and Scamp described a bipedicled TRAM procedure and, in 1993,
Pennington et al. first described the reconstruction of a breast with a TRAM
flap combined with a periumbilical perforator as the second flap (26,27).
With the introduction and evolution of DIEP, the use of this flap for the
unilateral reconstruction of large volumes has been reported as being safe and
effective. Alternatively, other techniques have been published for combining
flaps, such as the PAP flap for unilateral reconstruction and have been
performed successfully.
Mayo and Al, propose bilateral reconstructions with four flaps (DIEP +
PAP) (28).
A PAP flap is used most frequently as a second-line flap due to its long
pedicle, ease of collection, and low morbidity at the donor site. This
combination appears to be safe and effective and provides superior aesthetic
results for bilateral autologous breast reconstructions when the abdomen does
not provide sufficient volume (29).
This type of reconstruction with overlaid DIEP/PAP flaps should be
considered when the abdomen alone does not provide the necessary
volume. A two-person microsurgery team is required, using anterograde and
retrograde internal breast vessels as well as recipient vessels, and maintaining
the supine position throughout surgery, which provides the necessary efficacy
without additional complications. In addition, the aesthetics of the DIEP/PAP
combination are very positive.
This double-flap technique is effective and is particularly indicated if the
donor site is inadequate.
Despite the combination of flaps, the majority of patients required
additional surgery to improve breast symmetry. The most common
procedures are either symmetry of the contralateral breast or retouching the
breast reconstructed by lipofilling.
Autologous Reconstruction and Radiotherapy
Some teams combine radiotherapy with autologous treatment, but the long-
term aesthetic results are not positive; moreover, there is an obvious change
in volume. The volume reduction was 12.3%, compared to 2.6% without
radiotherapy. For this reason, in patients undergoing radiotherapy, an
overcorrection of 14% is recommended to improve the aesthetic results (30).
It is difficult to predict changes in breast volume and shape over time (31).
BREAST REDUCTIONS
As it is not possible to control the involution of the flaps, we may need to
overcorrect the volume during surgery. It may therefore be necessary to
perform reduction retouches.
Fat Removal—Mastopexy
An autologous mastopexy technique is a useful option for secondary refining
procedures in breast reconstruction. It provides a reliable and predictable
method for adjusting the inframammary fold, increasing projection, and
treating excess ptosis. It has a low complication rate and can be safely and
reliably performed as early as 3 months after the initial reconstruction (5).
This procedure can also be associated with skin excisions. Leaving a skin
paddle in place allows an optimal monitoring of the flap immediately after
surgery.
Liposuction
For small excesses without irregularities and without the need for cutaneous
procedures, liposuction of the flap is an option, which allows us to refine
reliably in situ without complications after a period of 3 months.
Liposuction can also be used to establish the inframammary fold.
CONCLUSION
The aesthetic result of the flaps relies on the technique and experience of
each surgeon.
Symmetry remains a concern for patients and corrections can be
considered once the flap has been left in place and has attained its final
volume. A period of 3 months must be respected, which also allows the flap
to become autonomous without compromising its vitality.
Lipofilling is the most widely used technique. It is safe and reliable and
allows tailored retouches of the autologous breast reconstructions and has a
low morbidity rate.

REFERENCES

1. Chu MW, Samra F, Kanchwala SK, et al. Treatment options for bilateral
autologous breast reconstruction in patients with inadequate donor-site
volume. J Reconstr Microsurg 2017;33(5):305–311.
2. Kroll SS. Why autologous tissue? Clin Plast Surg 1998;25(2):135–143.
3. Stark RY, Mirzabeigi MN, Vonderhaar RJ, et al. Utilizing large volume
fat grafting in breast reconstruction after nipple sparing mastectomies.
Gland Surg 2018;7(3):337–346.
4. Chae MP, Rozen WM, Patel NG, et al. Enhancing breast projection in
autologous reconstruction using the St Andrew’s coning technique and
3D volumetric analysis. Gland Surg 2017;6(6):706–714.
5. Troy J, Little A, Kuykendall L, et al. Flap-mastopexy in autologous
breast reconstruction: timing and technique. Ann Plast Surg
2018;80(4):328–332.
6. Bricout N. Chirurgie du sein. Paris: Springer-Verlag; 1992.
7. Bradshaw K, Wagels M. Perfusion of muscle flaps independent of the
anatomical vascular pedicle: pedicle autonomy. J Plast Reconstr Aesthet
Surg 2017;70(11):1547–1555.
8. Brinkman JN, Timman R, Gopie JP, et al. Aesthetic outcome after
implant and DIEP flap breast reconstruction: an exploratory, prospective
comparison of 25 cases. J Plast Reconstr Aesthet Surg
2015;68(7):1018–1019.
9. Hummelink S, Verhulst AC, Maal TJJ, et al. Applications and
limitations of using patient-specific 3D printed molds in autologous
breast reconstruction. Eur J Plast Surg 2018;41(5):571–576.
10. Schwartz JC. Unilateral reconstruction of the large breast: combining
prosthetic and autologous methods for improved symmetry. Plast
Reconstr Surg Global Open 2019;7(2):e2154.
11. Delay E, Gounot N, Bouillot A, et al. Autologous latissimus breast
reconstruction. A 3-year clinical experience with 100 patients. Plast
Reconstr Surg 1998;102(5):1461–1478.
12. Chang DW, Barnea Y, Robb GL. Effects of an autologous flap
combined with an implant for breast reconstruction: an evaluation of
1000 consecutive reconstructions of previously irradiated breasts. Plast
Reconstr Surg 2008;122(2):356–362.
13. Villani F, Caviggioli F, Giannasi S, et al. Current applications and safety
of autologous fat grafts: a report of the ASPS Fat Graft Task Force.
Plast Reconstr Surg 2010;125(2):758–759.
14. Blondeel PN, Hijjawi J, Depypere H, et al. Shaping the breast in
aesthetic and reconstructive breast surgery: an easy three-step principle.
Part II—Breast reconstruction after total mastectomy. Plast Reconstr
Surg 2009;123(3):794–805.
15. Hitier M, Ho Quoc C, La Marca S, et al. Tolerance and efficacy of
lipomodelling as an element of breast symmetry in breast reconstruction.
Ann Chir Plast Esthet 2014;59(5):311–319.
16. Delay E, Garson S, Tousson G, et al. Fat injection to the breast:
technique, results and indications based on 880 procedures over 10
years. Aesthet Surg J 2009;29(5):360–376.
17. Delay E, Florzac AS. Reconstruction mammaire par lambeau de grand
dorsal autologue. Ann Chir Plast Esthet 2018;63(5–6):422–436.
18. Choi M, Small K, Levovitz C, et al. The volumetric analysis of fat graft
survival in breast reconstruction. Plast Reconstr Surg 2013;131(2):185–
191.
19. Russe E, Kholosy H, Weitgasser L, et al. Autologous fat grafting for
enhancement of breast reconstruction with a transverse myocutaneous
gracilis flap: a cohort study. J Plast Reconstr Aesthet Surg
2018;71(11):1557–1562.
20. Coleman SR. Long-term survival of fat transplants: controlled
demonstrations. Aesthetic Plast Surg 1995;19(5):421–425.
21. Ihrai T, Clough KB, Nos C, et al. The « fat trap »: a simple method for
the harvesting of large amounts of adipose tissue during liposuction.
Plast Reconstr Surg 2010;126(4):206e.
22. Rigotti G, Marchi A, Galiè M, et al. Clinical treatment of radiotherapy
tissue damage by lipoaspirate transplant: a healing process mediated by
adipose-derived adult stem cells. Plast Reconstr Surg
2007;119(5):1409–1422; discussion 1423–1424.
23. Zhu L, Mohan AT, Vijayasekaran A, et al. Maximizing the volume of
latissimus dorsi flap in autologous breast reconstruction with
simultaneous multisite fat grafting. Aesthet Surg J 2016;36(2):169–178.
24. Russe E, Kholosy H, Weitgasser L, et al. Autologous fat grafting for
enhancement of breast reconstruction with a transverse myocutaneous
gracilis flap: a cohort study. J Plast Reconstr Aesthet Surg
2018;71(11):1557–1562.
25. Sjoberg T, De Weerd L. The pedicled LICAP flap combined with a free
abdominal flap in autologous breast reconstructions. Plast Reconstr Surg
Global Open 2018;6(1):e1562.
26. Arnez ZM, Scamp T. The bipedicled free TRAM flap. Br J Plast Surg
1992;45(3):214–218.
27. Pennington DG, Nettle WJ, Lam P. Microvascular augmentation of the
blood supply of the contralateral side of the free transverse rectus
abdominis musculocutaneous flap. Ann Plast Surg 1993;31:123–126;
discussion 126–127.
28. Mayo JL, Allen RJ, Sadeghi A. Four-flap breast reconstruction: bilateral
stacked DIEP and PAP flaps. Plast Reconstr Surg Glob Open
2015;3(5):e383.
29. Mayo JL, Allen RJ, Sadeghi A. Flour-flap breast reconstruction:
bilateral stacked DIEP and PAP flaps. Plast Reconstr Surg Glob Open
2015;3(5):e383.
30. Myung Y, Son Y, Nam TH, et al. Objective assessment of flap volume
changes and aesthetic results after adjuvant radiation therapy in patients
undergoing immediate autologous breast reconstruction. PLoS One
2018;13(5):e0197615.
31. Borrelli MR, Patel RA, Sokol J, et al. Fat chance: the rejuvenation of
irradiated skin. Plast Reconstr Surg Glob Open 2019;7(2):e2092.
SECTION VI

Fat Grafting
90 Does Fat Grafting Increase the Risk of Breast Cancer?
91 Indications and Controversies in Fat Grafting of the Partial Mastectomy
Defect
92 Fat Grafting in Implant-Based Breast Reconstruction
93 Fat Grafting in Autologous Breast Reconstruction
94 Total Breast Reconstruction With Autologous Fat Grafting and Tissue
Expansion
CHAPTER 90

Does Fat Grafting Increase the Risk of


Breast Cancer?
SHERI S. WANG | FRANCESCO M. EGRO | ASIM EJAZ | KACEY G. MARRA | LAUREN E.
KOKAI | J. PETER RUBIN
HISTORY
Autologous fat grafting (AFG) to the breast has been increasingly used over
the last two decades thanks to the standardization in fat grafting technique,
increase in graft retention, and the increasing evidence on outcomes and
safety (1,2). AFG has been shown to improve scar appearance, pain,
radiation-induced fibrosis, patient satisfaction, and aesthetic outcomes (3,4).
In 2007, the Fat Grafting Task Force was initiated to evaluate the safety and
efficacy of fat grafting to the breast for oncologic reconstruction. Due to the
uncertainty of long-term impact of AFG to the breast, in 2011, the American
Society of Plastic Surgeons (ASPS) issued a statement encouraging caution
when performing fat grafting, urging careful patient selection, vigilant cancer
surveillance, and pre- and post-AFG radiologic and clinical examination.
This sentiment was echoed internationally by the French, Italian, and U.K.
plastic surgery societies.
Since then, the Postmastectomy Fat Graft ASPS Guiding Principles found
that the “quality of evidence to date indicates that fat grafting to the
postmastectomy breast with no native breast tissue is a safe and effective
modality in breast reconstruction” (1,5,6). Current evidence also shows that
when compared with other breast procedures, AFG has a smaller impact on
radiologic screening and does not impair cancer surveillance (5,6). In 2013,
62% of ASPS members reported regularly using fat grafting for
reconstructive breast surgery (7). As the popularity of fat grafting has
continued to grow, this percentage has also increased. In this chapter, we will
outline the radiologic implications of AFG on cancer surveillance and current
evidence regarding AFG on breast cancer recurrence.
DOES FAT GRAFTING INTERFERE WITH BREAST CANCER DETECTION?
Because the appearance of necrotic fat can resemble cancerous lesions on
imaging, there have been concerns that fat necrosis can interfere with
subsequent cancer surveillance. Early studies use the rate of
microcalcifications and cyst formation as a proxy for interference with cancer
surveillance. However, due to differences in the radiologic grading criteria,
rates of calcification varies widely (3.9% to 25.6%) (5,8). Despite the
increase in calcification compared to naïve breasts, literature suggests that fat
grafting does not impair future breast cancer detection and does not increase
the rate of biopsy compared to other surgical procedures (5,6,9). Rubin et al.
demonstrated that mammography findings after AFG showed significantly
lower rates of scarring (17.6% in AFG vs. 85.6% in reduction mammaplasty),
lower levels of benign calcification (17.1% vs. 27.2%), less mass distortion
(2.8% vs. 13.6%), and lower rates of biopsy (6.5% vs. 15.2%) compared to
reduction mammoplasty (Fig. 90-1) (6). Furthermore, AFG does not
significantly increase the BI-RADS score compared to preoperative imaging
(10).
FIGURE 90-1 Mammography highlighting scarring after reduction mammaplasty
(top left), oil cyst from fat necrosis following reduction mammaplasty (top right), and
oil cyst following breast lipoaugmentation (bottom). (Reproduced from Rubin JP, Coon
D, Zuley M, et al. Mammographic changes after fat transfer to the breast compared with
changes after breast reduction: a blinded study. Plast Reconstr Surg 2012;129(5):1029–
1038.)

Moving forward, it is critical for the breast imaging community to arrive at


a standardized interpretation of images and management guidelines. Multiple
studies have highlighted the importance of a establishing a “baseline” using
preoperative mammography and comparing it to postoperative imaging after
6 to 12 months (5,10). We recommend establishing a multidisciplinary care
team consisting of a fellowship-trained, dedicated breast radiologist, an
oncologic breast surgeon, and a plastic surgeon to ensure consistent, quality
patient care (6).
PRECLINICAL STUDIES: DOES FAT GRAFT INCREASE BREAST CANCER
RECURRENCE?

Composition of Lipoaspirate
The rejuvenative properties of AFG have been linked to the bioactivity of
adipocyte and other cellular components of the lipoaspirate (2–4). Adipocytes
play an important role in endocrine and immune regulation through secretion
of adipokines, cytokines secreted by adipocytes, such as adiponectin and
leptin (11,12). During liposuction, various stromal vascular cells are also
harvested including fibroblasts, immune cells, pericytes, and endothelial
progenitors (13). When the stromal vascular fraction (SVF) is isolated and
cultured, adipose stem cells (ASCs), which resemble multipotent
mesenchymal stem cells, adhere to the flask and can secrete cytokines and
growth factors that affect angiogenesis, cell proliferation, and inflammation
(13,14). The main safety concern focuses on the possibility of AFG altering
the tumor microenvironment to promote cancer proliferation (13,15,16).
AFG and ASCs on Growth Factor and the Tumor
Microenvironment
Numerous adipokines have been linked to tumor proliferation (8).
Immediately after surgery, the lack of blood supply to the newly grafted fat
cause hypoxic conditions, leading to the upregulation of hypoxia-inducible
factor-1α (HIF-1α), vascular endothelial growth factor (VEGF), insulin-like
growth factor-1 (IGF-1), etc. These growth factors could potentially alter the
recipient tissue bed, promoting tumor proliferation through the creation of a
microenvironment conducive to cancer growth (8). As such, some studies
found that tumor cells alter cocultured adipocyte phenotype resulting in a
positive feedback loop that increases tumor progression and migration (8,17).
Other studies found that AFG and ASCs coculture limited cancer
proliferation and resulted in more differentiated cancer cells (15,18,19). Tsuji
et al. found that fat graft was associated with decreased Ki67, a marker of cell
proliferation, staining in MDA-MB-231 cancer cells and decreased
proliferation in BT-474 cancer cells (20). These findings were reaffirmed by
a follow-up study conducted by Silva et al., who found that mice treated with
AFG had lower tumor volume and lower Ki67 activity than the control (21).
While there is no consensus on the effect of AFG and ASCs on cancer
proliferation in preclinical breast cancer studies, their tumor suppressive
effects have been noted in other cancer models (22). There has been an
initiative to combine AFG with localized chemotherapeutics to produce a
cancer suppressive reconstruction method with some early success (23).
Based on preclinical studies, the effect of AFG and ASCs on growth factor
and the tumor microenvironment remains inconclusive.
Limitations of Preclinical Studies
The mixed results in preclinical studies are likely due to the limitations posed
by the current cancer models. Donnenberg et al. point out that current models
do not reflect tumor “heterogeneity, dormancy, reactivation of occult tumor
cells.” In particular, they highlight that the most models use aggressive
tumors that would not be considered suitable for reconstruction in a clinical
setting (16,24). Another limitation comes from the cell lines used in the
majority of preclinical studies (25,26). Cellular characteristics change over
time in culture, from passages, and through the freeze thaw cycle (27). In
particular, two of the most commonly used breast cancer cell lines, MCF7
and MDA-MB-231 were both isolated in the 1970s from Caucasian women
(13). More recent attempts to isolate breast cancer cell lines have found the
isolated cells to have “extremely low tumorgenicity” compared to these
established cell lines (28). Furthermore, the engrafted cells are often
delivered using Matrigel, which has shown to increase “tumor-initiating
capacity,” particularly in large cell numbers (29). In addition, the dose of
ASC enrichment in preclinical studies is “order of magnitude higher than
could ever be obtained in clinical situations” (13,30). Preclinical studies are
important and can provide us with insight into the mechanism of AFG–cancer
cell interaction. However, we also encourage careful interpretation of the
results due to the limitations of current cancer models.
CLINICAL EVIDENCE: DOES FAT GRAFT INCREASE BREAST CANCER
RECURRENCE?

Observational Studies
Although animal and in vitro studies are inconclusive, clinical studies are in
consensus and demonstrate that there is no significant difference in cancer
recurrence between patients treated with and without AFG. Using outcome
measures of locoregional recurrence (LRR), distant recurrence (DR), and
mortality, early observational studies compared the rate of recurrence after
AFG to the general rate of recurrence after oncologic treatment (8).
For early-stage breast cancer, the 10-year LRR is around 13% after
mastectomy (MST) and around 12% for breast-conserving therapy (BCT)
(31). In a multicenter review of 513 patients who underwent AFG as part of
breast reconstruction, Petit et al. found 1.5% LRR per year and 1.9% DR per
year (32). The follow-ups were on average 39.7 months between oncologic
surgery and AFG and 19.2 months after AFG. Similar figures were found in
study conducted by Silva-Vergara et al. in 195 breast cancer patients who
received AFG. The LRR was 1.08% and DR was 0.71% per year with an
average interval between oncologic surgery and AFG of 36 months and an
average interval after AFG of 31 months (33). Seth et al. also found that AFG
did not alter the rate of recurrence in 886 patients in a retrospective review
with average follow-up of 24 months after initial AFG (34). Other clinical
studies also found that AFG does not increase the rate of recurrence (8).
Rigotti et al. compared LRR in patients in the periods before and after they
received AFG. Average time between oncologic surgery and AFG was 23
months with an average follow-up of 60 months after AFG. LRR was 0.91%
in the period before AFG and 0.72% after AFG. However, we caution
comparing these two percentages directly as there is a known higher risk of
recurrence immediately following oncologic surgery, which is not accounted
for in the analysis (35). In general, observational studies suggest that the LRR
following AFG is 0% to 3.9% per year, which is not a significant increase
from 1% to 2% per year without AFG (8,36,37). However, the rate of breast
cancer recurrence is multifactorial and depends on the cancer type,
phenotype, stage, treatment, and the follow-up timeline (31). The
aforementioned studies are observational and thus limited by the lack of a
case-controlled group.
Case-Controlled Studies
Case-controlled studies appear to corroborate the observational findings
(Table 90-1). The first results were reported by Petit et al. in 2012 using the
European Institute of Oncology database (36). In the 321 patients reviewed,
the median interval between oncologic surgery and AFG was 56 months and
interval after AFG was 26 months. Petit found no increase in recurrence with
AFG in an all-comers analysis. Shortly after, Petit et al. followed up with
another retrospective case control study of 322 patients that showed no
difference in the incidence of LR (p = 0.49), RR (p = 0.23), DR (p = 0.67), or
contralateral breast cancer (p = 0.51) (38,39). The average interval between
oncologic surgery and fat grafting was 4.6 months, and patients were
followed for 4.6 years after AFG.

TABLE 90-1 Summary of Case-Controlled Series

Other case-controlled studies have found that AFG does not increase the
rate of recurrence when used for breast cancer reconstruction. In a review of
329 case-controlled patients, Gale et al. found no significant increase in LRR
and DR when patients were treated with AFG (41). Similarly, Kronowitz et
al. completed a retrospective study of 719 well-matched patients and found
no difference in the LRR or DR based on AFG-treated MST or BCT groups
(42). Mestak et al. also conducted a prospective case-controlled study of 32
patients which found no significant difference in recurrence rates (43). A
recent study conducted by Silva-Vergara et al. examined 195 patients with an
average of 48 months between oncologic surgery and AFG and an average of
40 months of follow-up after AFG (33). Similar to other studies, they found
no difference between AFG and controls with 1.02% LRR per year in the
AFG group versus 1.17% per year in control. In 2018, Mazur et al. conducted
a case-controlled study in 56 patients with SVF-enriched AFG and found the
LRR to be 3.70% and 4.13% in SVF-enriched AFG and control, respectively
(45). Most recently, Krastev et al. published a case-matched study of 287
patients with breast cancer and found LRR over 5 years to be 2.8% and DR to
be 7.7% in the AFG group (46). In the control group, the LRR was 3.6% and
the DR was 7.0% over 4.4 years. There was no significant difference in the
LRR, DR, and breast cancer–related mortality between the AFG and control
groups.
Does Immediate Versus Staged Reconstruction Affect
Outcome?
While immediate reconstruction offers a timelier solution to the cosmetic
impact of the oncologic surgery, staged reconstruction can be beneficial.
After primary oncologic surgery and medical treatment, breast cancer
recurrence peaks around 24 months, independent of reconstruction methods
(47). The risk of recurrence will be higher with closer proximity to oncologic
surgery regardless of the reconstructive method chosen. In an observational
study of 65 patients who underwent immediate AFG after BCT, Damin et al.
found the LRR and DR to be similar to that of BCT without AFG. The LRR
was 3.07% and DR was 7.69% (48).
Petit et al. found a higher LRR when the first AFG procedure was
performed within 36 months of cancer surgery (8). Similarly, Silva-Vergara
reported an increased LRR when AFG was performed in the first 36 months
after primary cancer surgery (p = 0.014) (33). However, this Silva-Vergara
study is limited by lack of a control group, and the reported recurrence rates
are similar to what would be expected in the same early time period if AFG
was not performed. A study by Stumpf et al. in 167 patients with immediate
AFG reconstruction after oncologic resection found no increase in local
recurrence or systemic recurrence. However, this study is limited by the lack
of a case control.
There is no official statement from regulatory bodies guiding AFG timing.
Whether from the concern of initial higher LR or the potential effect of AFG,
many groups have made recommendations on staging the reconstruction from
24 to 55 months postoperative from the oncologic surgery (8,41,42).
Delaying surgery until at least 24 months post oncologic surgery can spare
the patient from undergoing additional reconstruction if further oncologic
surgery is needed. Regardless of the type of reconstruction, it is critical to
discuss the need to complete therapy and have consistent follow-up with the
primary oncology team before considering AFG.
Does the Type of Primary Breast Cancer Surgery (BCT vs.
MST) Affect Outcome?
Another common concern is that the addition of AFG will increase the
recurrence rate in the setting of retained cancer, particularly for patients
undergoing BCT. This concern was first raised by observational studies
which reported a slightly higher rate of LRR recurrence after BCT compared
to MST, 2.78% versus 1.75% (32). However, the majority of case-controlled
studies do not indicate that there is increased risk of recurrence when AFG is
combined with BCT versus MST. Kronowitz et al. conducted a case-
controlled study in 719 patients, 639 with MST and 79 with BCT, for 32
months before AFG and 28 months after AFG. They found there was no
significant increase in LRR in the BCT group compared to MST or the case-
matched controls (42). Silva-Vergara et al. also found no increase in LRR
between BCT versus MST both when the analysis was analyzed with respect
to surgery type and histologic type (33). In a case-cohort study by Myckatyn
et al. in 3,271 patients, there was no increase in time to disease recurrence
with AFG (49). Gale et al. found that LRR was slightly higher in the BCT
group compared to the MST group, 2.1% versus 1.1%, respectively but it was
not significant (p = 0.533). Findings by Petit et al. had similar rates of LRR
of 2.2% after BCT (36).
Does Cancer Type Affect Outcome?
Intraepithelial neoplasm, high Ki-67, HER-2, BRCA, and stage 3 to 4 cancers
have all been linked with higher recurrence in the general population (50). It
has been theorized that AFG might interact differently with more aggressive
cancers which could potentially increase recurrence rates. However, due to
the limited number of patients in existing studies with these aggressive
subtypes, it remains unclear whether or not AFG might pose an increased risk
for a subset of patients with aggressive tumors.
Petit et al. found a higher LRR in patients with intraepithelial neoplasia
when treated with AFG—the control group had no such increase (36). They
followed with another retrospective study of 59 patients with intraepithelial
neoplasms and 118 case-matched controls. They found that the 5-year
cumulative incidence of local recurrence was 18% with and 3% without AFG
(p = 0.02) (8). The authors note that study is limited by the relatively small
sample size and repeated use of certain patients in their previous study. Petit
also found that lipofilling increased the risk of local recurrence in women
<50 years, with high-grade neoplasia, Ki-67 ≥14, or who had undergone
quadrantectomy. Of note, Petit et al. did not mention intraepithelial neoplasm
in their 2017 case-controlled study of 322 patients. Other groups have not
validated the findings in Petit’s initial study. Studies performed by
Kronowitz, Gale, Silva-Vergara et al. found no increase in the LRR when
patients diagnosed with in situ cancer were treated with AFG. However, due
to the relatively small sample size of these studies (719, 221, and 195
respectively), they lack sufficient power to draw conclusions.
Silva-Vergara (33) and Kronowitz (42) also performed subset analyses of
cancer phenotypes and found that AFG increased the LRR for HER-2
positive tumors. Interestingly, Kronowitz found that patients who had
undergone hormonal therapy had a higher rate of LRR after AFG compared
to patients who had not undergone hormonal therapy (p = 0.038) (42). This
relationship was not found in other case-controlled or case-cohort studies
(44,51). Some experts have also cautioned against performing AFG in BRCA
patients (50), and Riggio et al. recommend against the treatment of stage 3 to
4 breast cancer with AFG (52). However, these recommendations have not
yet been examined in clinical studies. Given limited literature and lack of
consistent findings, caution should be exercised in patients with aggressive
tumors.
Does Cell-Enriched AFG Affect Outcome?
Studies have investigated the effect of ASCs on cancer recurrence. In a case-
matched study of 56 patients who received SVF-enriched AFG and 252
patients who did not receive reconstruction, there was no increase in
recurrence at 3 years. The cancer recurrence in SVF-enriched AFG was 3.7%
and cancer recurrence in the control was 4.13% (45). Pérez-Cano et al. also
investigated the effect of ASC-enriched fat grafting for partial MST defects
in the RESTORE-2 trial, a prospective, single-armed, multicenter clinical
trial. Although the patients were only followed up for 12 months, there was
no reported local cancer recurrence (53). A prospective study comparing
LRR and DR in SVF-enriched AFG (n = 41), AFG (n = 64), and control
group (n = 64) found that there was no increase in LRR or DR in SVF-
enriched AFG (2.4%, 7.3%, respectively) or the AFG group (4.7%, 3.1%,
respectively) compared to controls (3.1%, 3.1%, respectively) (54). The
patients were followed up for approximately 6 years post AFG. In a sample
of 10 patients treated with ASC-enriched AFG, Ito et al. found no recurrence
(55). Moving forward, a multicentered, robust clinical trial is needed to test
the safety and efficacy of cell-enriched AFG.
CONCLUSION
While preclinical studies are divided regarding the safety of AFG and ASCs
in proximity to cancer cells, clinical evidence suggests that AFG is safe to
use for breast reconstruction after oncologic surgery for both BCT and MST.
The ASPS and the Plastic Surgery Foundation are working in coordination
with their principal investigators Mehrara and Rubin to build a multicentered
database for plastic surgeons in the United States, Brazil, and Canada. The
General Registry of Autologous Fat Transfer will prospectively collect
information about initial cancer diagnosis, AFG therapy, and outcomes for
patients undergoing AFG as part of reconstruction following oncologic
surgery. These collaborative efforts will provide data to better guide clinical
and regulatory decisions.

REFERENCES

1. Coleman SR, Saboeiro AP. Fat grafting to the breast revisited: safety
and efficacy. Plast Reconstr Surg 2007;119(3):775–785; discussion
786–787.
2. Coleman SR. Structural fat grafting: more than a permanent filler. Plast
Reconstr Surg 2006;118(3 Suppl):108S–120S.
3. Rigotti G, Marchi A, Galiè M, et al. Clinical treatment of radiotherapy
tissue damage by lipoaspirate transplant: a healing process mediated by
adipose-derived adult stem cells. Plast Reconstr Surg
2007;119(5):1409–1422; discussion 1423–1424.
4. ELFadl D, Garimella V, Mahapatra TK, et al. Lipomodelling of the
breast: a review. Breast 2010;19(3):202–209.
5. Carvajal J, Patiño JH. Mammographic findings after breast
augmentation with autologous. Aesthetic Surg J 2008;28(2):153–162.
6. Rubin JP, Coon D, Zuley M, et al. Mammographic changes after fat
transfer to the breast compared with changes after breast reduction: a
blinded study. Plast Reconstr Surg 2012;129(5):1029–1038.
7. Kling RE, Mehrara BJ, Pusic AL, et al. Trends in autologous fat grafting
to the breast: a National Survey of the American Society of Plastic
Surgeons. Plast Reconstr Surg 2013;132(1):35–46.
8. Waked K, Colle J, Doornaert M, et al. Systematic review: the
oncological safety of adipose fat transfer after breast cancer surgery.
Breast 2017;31(2017):128–136.
9. Lindegren A, Chantereau MW, Bygdeson M, et al. Autologous fat
transplantation to the reconstructed breast does not hinder assessment of
mammography and ultrasound: a cohort study. World J Surg
2016;40(5):1104–1111.
10. Veber M, Tourasse C, Toussoun G, et al. Radiographic findings after
breast augmentation by autologous fat transfer. Plast Reconstr Surg
2011;127(3):1289–1299.
11. Schäffler A, Schölmerich J, Buechler C. Mechanisms of disease:
adipokines and breast cancer—endocrine and paracrine mechanisms that
connect adiposity and breast cancer. Nat Clin Pract Endocrinol Metab
2007;3(4):345–354.
12. Zuk PA, Zhu M, Mizuno H, et al. Multilineage cells from human
adipose tissue: implications for cell-based therapies. Tissue Eng
2001;7(2):211–228.
13. Sivak WN, Rubin JP. Vol. 1 Ch. 20—Reconstructive Fat Grafting. 4th
ed. London: Elsevier Inc.; 2017.
14. Kokai LE, Marra K, Rubin JP. Adipose stem cells: biology and clinical
applications for tissue repair and regeneration. Transl Res
2014;163(4):399–408.
15. Schweizer R, Tsuji W, Gorantla VS, et al. The role of adipose-derived
stem cells in breast cancer progression and metastasis. Stem Cells Int
2015;2015;120949.
16. Donnenberg VS, Zimmerlin L, Rubin JP, et al. Regenerative therapy
after cancer: what are the risks? Tissue Eng Part B Rev 2010;16(6):567–
575.
17. Dirat B, Bochet L, Dabek M, et al. Cancer-associated adipocytes exhibit
an activated phenotype and contribute to breast cancer invasion. Cancer
Res 2011;71(7):2455–2465.
18. Millet E, Haik J, Ofir E, et al. The impact of autologous fat grafting on
breast cancer: an experimental model using magnetic resonance
imaging. Isr Med Assoc J 2016;18(5):283–285.
19. Moltó-García R, González-Alonso V, Villaverde-Doménech ME, et al.
Effect of human fat graft on breast cancer metastasis in a murine model.
Plast Reconstr Surg 2017;139(5):1119–1128.
20. Tsuji W, Valentin JE, Marra KG, et al. An animal model of local breast
cancer recurrence in the setting of autologous fat grafting for breast
reconstruction. Stem Cells Transl Med 2017;7(1):125–134.
21. Silva MMA, Kokai LE, Donnenberg VS, et al. Oncologic safety of fat
grafting for autologous breast reconstruction in an animal model of
residual breast cancer. Plast Reconstr Surg 2019;143(1):103–112.
22. Qiao L, Xu Z, Zhao T, et al. Suppression of tumorigenesis by human
mesenchymal stem cells in a hepatoma model. Cell Res 2008;18(4):500–
507.
23. Scioli MG, Artuso S, D’Angelo C, et al. Adipose-derived stem cell-
mediated paclitaxel delivery inhibits breast cancer growth. PLoS One
2018;13(9):e0203426.
24. Zimmerlin L, Donnenberg AD, Rubin JP, et al. Regenerative therapy
and cancer: in vitro and in vivo studies of the interaction between
adipose-derived stem cells and breast cancer cells from clinical isolates.
Tissue Eng Part A 2011;17(1–2):93–106.
25. Eterno V, Zambelli A, Pavesi L, et al. Adipose-derived mesenchymal
stem cells (ASCs) may favour breast cancer recurrence via HGF/c-Met
signaling. Oncotarget 2013;5(3):613–633.
26. Rubio D, Garcia S, De la Cueva T, et al. Human mesenchymal stem cell
transformation is associated with a mesenchymal-epithelial transition.
Exp Cell Res 2008;314(4):691–698.
27. Gillet JP, Varma S, Gottesman MM. The clinical relevance of cancer
cell lines. J Natl Cancer Inst 2013;105(7):452–458.
28. Kuo WL, Ueng SH, Wu CH, et al. Establishment of two basal-like
breast cancer cell lines with extremely low tumorigenicity from
Taiwanese premenopausal women. Hum Cell 2018;31(2):154–166.
29. Lewis MT, Landua JD, Adams HC, et al. A mystery wrapped in an
enigma: Matrigel enhancement of mammary cell growth and
morphogenesis. J Mammary Gland Biol Neoplasia 2012;17(2):99–101.
30. Rosing JH, Wong G, Wong MS, et al. Autologous fat grafting for
primary breast augmentation: a systematic review. Aesthetic Plast Surg
2011;35(5):882–890.
31. Clemons M, Danson S, Hamilton T, et al. Locoregionally recurrent
breast cancer: incidence, risk factors and survival. Cancer Treat Rev
2001;27(2):67–82.
32. Petit JY, Lohsiriwat V, Clough KB, et al. The oncologic outcome and
immediate surgical complications of lipofilling in breast cancer patients:
a multicenter study—Milan-Paris-Lyon experience of 646 lipofilling
procedures. Plast Reconstr Surg 2011;128(2):341–346.
33. Silva-Vergara C, Fontdevila J, Descarrega J, et al. Oncological
outcomes of lipofilling breast reconstruction: 195 consecutive cases and
literature review. J Plast Reconstr Aesthetic Surg 2016;69(4):475–481.
34. Seth AK, Hirsch EM, Kim JYS, et al. Long-term outcomes following fat
grafting in prosthetic breast reconstruction: a comparative analysis. Plast
Reconstr Surg 2012;130(5):984–990.
35. Rigotti G, Marchi A, Stringhini P, et al. Determining the oncological
risk of autologous lipoaspirate grafting for post-mastectomy breast
reconstruction. Aesthetic Plast Surg 2010;34(4):475–480.
36. Petit JY, Botteri E, Lohsiriwat V, et al. Locoregional recurrence risk
after lipofilling in breast cancer patients. Ann Oncol 2012;23(3):582–
588.
37. Agha RA, Fowler AJ, Pidgeon TE, et al. The need for core outcome
reporting in autologous fat grafting for breast reconstruction. Ann Plast
Surg 2015;77(5):506–512.
38. Petit JY, Maisonneuve P, Rotmensz N, et al. Fat grafting after invasive
breast cancer: a matched case-control study. Plast Reconstr Surg
2017;139(6):1292–1296.
39. Petit JY, Maisonneuve P, Rotmensz N, et al. Safety of lipofilling in
patients with breast cancer. Clin Plast Surg 2015;42(3):339–344.
40. Petit JY, Rietjens M, Botteri E, et al. Evaluation of fat grafting safety in
patients with intra epithelial neoplasia: a matched-cohort study. Ann
Oncol 2013;24(6):1479–1484.
41. Gale KL, Rakha EA, Ball G, et al. A case-controlled study of the
oncologic safety of fat grafting. Plast Reconstr Surg 2015;135(5):1263–
1275.
42. Kronowitz SJ, Mandujano CC, Liu J, et al. Lipofilling of the breast does
not increase the risk of recurrence of breast cancer: a matched controlled
study. Plast Reconstr Surg 2016;137(2):385–393.
43. Mestak O, Hromadkova V, Fajfrova M, et al. Evaluation of oncological
safety of fat grafting after breast-conserving therapy: a prospective
study. Ann Surg Oncol 2016;23(3):776–781.
44. Silva-Vergara C, Fontdevila J, Weshahy O, et al. Breast cancer
recurrence is not increased with lipofilling reconstruction: a case-
controlled study. Ann Plast Surg 2017;79(3):243–248.
45. Mazur S, Zołocinska A, Siennicka K, et al. Safety of adipose-derived
cell (stromal vascular fraction—SVF) augmentation for surgical breast
reconstruction in cancer patients. Adv Clin Exp Med 2018;27(8):1085–
1090.
46. Krastev T, Van Turnhout A, Vriens E, et al. Long-term follow-up of
autologous fat transfer vs conventional breast reconstruction and
association with cancer relapse in patients with breast cancer. JAMA
Surg 2019;154(1):56–63.
47. Cheng L, Swartz MD, Zhao H, et al. Hazard of recurrence among
women after primary breast cancer treatment—a 10-year follow-up
using data from SEER-Medicare. Cancer Epidemiol Biomarkers Prev
2012;21(5):800–809.
48. Biazus JV, Stumpf CC, Melo MP, et al. Breast-conserving surgery with
immediate autologous fat grafting reconstruction: oncologic outcomes.
Aesthetic Plast Surg 2018;42(5):1195–1201.
49. Myckatyn TM, Wagner IJ, Mehrara BJ, et al. Cancer risk after fat
transfer: a multicenter case-cohort study. Plast Reconstr Surg
2017;139(1):11–18.
50. Skendelas JP, Lee C, Mangino A, et al. Unusual recurrence of breast
cancer in a BRCA-variant patient after fat grafting. Clin Case Reports
2018;6(12):2457–2462.
51. Yang G, Sau C, Lai W, et al. Cancer Recurrence After Fat Transfer
(CRAFT)—a multicenter case-cohort study. Plast Reconstr Surg
2015;344(6188):1173–1178.
52. Riggio E, Bordoni D, Nava MB. Oncologic surveillance of breast cancer
patients after lipofilling. Aesthetic Plast Surg 2013;37(4):728–735.
53. Pérez-Cano R, Vranckx JJ, Lasso JM, et al. Prospective trial of adipose-
derived regenerative cell (ADRC)-enriched fat grafting for partial
mastectomy defects: the RESTORE-2 trial. Eur J Surg Oncol
2012;38(5):382–389.
54. Calabrese C, Kothari A, Badylak S, et al. Oncological safety of stromal
vascular fraction enriched fat grafting in two-stage breast reconstruction
after nipple sparing mastectomy. Eur Rev Med Pharmacol Sci
2018;22(15):4768–4777.
55. Ito S, Kai Y, Masuda T, et al. Long-term outcome of adipose-derived
regenerative cell-enriched autologous fat transplantation for
reconstruction after breast-conserving surgery for Japanese women with
breast cancer. Surg Today 2017;47(12):1500–1511.
CHAPTER 91

Indications and Controversies in Fat


Grafting of the Partial Mastectomy
Defect
MAURICE Y. NAHABEDIAN | ALLEN GABRIEL
HISTORY
The benefits of autologous fat grafting following total breast reconstruction
with autologous tissue or prosthetic devices have been clearly established in
numerous clinical studies. Fat grafting has been used successfully to correct
contour abnormalities, provide additional volume, and to improve the quality
of the skin following radiation therapy. Most surgeons agree that fat grafting
is safe and effective for these purposes and there is little controversy
regarding its use following total mastectomy. The main reason for this is that
the breast tissue has been almost completely removed and there is little
mammographic confusion.
The benefits of fat grafting following partial mastectomy or breast-
conservation therapy (BCT) are less well established and are associated with
some degree of controversy and skepticism (1). The primary reason for this is
that the combination of normal breast tissue and autologous fat may create
some degree of mammographic confusion and that the radiated breast
parenchyma may be less amenable to contour correction. In addition, some
surgeons may be hesitant to introduce fat and stem cells into a breast that has
had prior breast cancer due to the fear and risk of promoting a local
recurrence.
This chapter will review the indications and controversies associated with
autologous fat grafting following BCT.
INDICATIONS
The primary indications for autologous fat grafting following breast
conservation are to correct any contour abnormalities, provide additional
volume for symmetry, and to improve the quality of the radiated skin.
Caveats to these indications are that the process of fat grafting is not always
predictable and that the results may vary from good to no difference (2).
Thus, patient selection is an important criterion when considering fat grafting
for this purpose. It is important to assess the degree of radiation damage to
the skin and to assess the amount of deep fibrosis within the parenchyma.
Patient expectations must be assessed and ensured that they are realistic.
Patients must be made aware that fat grafting of radiated tissue may require
between one to four sessions depending on the quality of the tissues and the
expectations of the patient.
CONTOUR IRREGULARITIES AND RADIATION CHANGE

Mechanisms of Action
The ability of autologous fat to correct contour abnormalities and improve the
quality of the radiated skin is dependent upon a variety of factors that
includes adipocyte viability, injection technique, recipient site vascularity,
and the adipose-derived stem cell (ADSC) concentration. The benefits of
ADSC for tissue regeneration have been studied and found to enhance the
efficacy of adipocytes used in fat grafting (3,4). Rigotti et al. have further
examined the role of ADSCs and adipocytes clinically in radiated patients
and demonstrated an increased ability to regenerate damaged subcutaneous
tissues (5). They proposed that fat grafting in radiated tissues precipitated
capillary ingrowth and maturation of stem cells into mature adipocytes and
vascular cells by 1 month. By 6 months adipocyte maturation was complete
and by 1 year a normal capillary circulation was evident.
Technique
By definition, breast conservation is associated with radiation; thus, all
secondary fat grafting procedures are performed in a radiated territory.
Following BCT, it is important to consider the soft tissue toxicity associated
with radiation therapy. The acute toxicity of radiation includes skin rash,
dermatitis, and erythema while chronic effects range from radiation-induced
fibrosis, fat atrophy, telangiectasia, and damage to small vessels. The
complexities of fat grafting in radiated tissues are well known; therefore,
special techniques must be considered in order to achieve success. Khouri has
described the technique of external expansion as a means of enhancing
vascularity, expansion of the breast parenchyma, and to enhance fat graft
retention (6). Khouri has also described the technique of percutaneous
aponeurectomy that is performed to release the scar tissue between the
subcutaneous fat and the dermis (7). Failure to do so will result in significant
resistance to fat injection, adipocyte disruption, and increased fat resorption.
The specific location of fat placement is another important consideration.
The ideal location is to inject the fat into the subcutaneous fat layer and avoid
the breast parenchyma. The actual spot of the lumpectomy or partial
mastectomy is usually dense due to scar tissue and injection of fat into this
area is not recommended. Placement of fat into the pectoralis major muscle
can be considered but it should be remembered that the Food and Drug
Administration and the ASPS Fat Grafting Task Force have recommended
that fat be injected where fat normally resides. It is recommended to use a
small-bore cannula ranging in diameter from 1 to 1.5 mm to inject the fat.
Thus, the recommended technique for fat grafting the BCT defect is to
perform a percutaneous aponeurectomy and then graft the fat into the
subcutaneous space with a narrow-bore cannula.
Outcomes
Outcomes following lipofill in the setting of prior BCT have been reported.
van Turnhout et al. reported on 109 patients and 114 breasts that had a
median number of two fat grafting sessions (range, 1 to 6) (8). The mean time
from breast-conserving surgery (BCS) to fat grafting was 44 months (range,
12 to 42 months). In all patients, the preoperative mammography showed no
local lesions. Fat was infiltrated in the subcutaneous plane from deep to
superficial. The mean amount of fat injected into the breast for each session
was 78 cc. The second session of fat grafting was associated with an increase
in 16% relative to the first session. Locoregional recurrence did not occur in
any patient. Postoperative outcomes were assessed using a blinded four-
member panel of experts that independently evaluated standardized digital
pre-and postoperative photographs. Aesthetic improvement was observed in
all patients with a mean score of the overall breast cosmesis that improved
from 5.1 ± 1.2 before fat grafting, to 7.2 ± 1.1 out of 10 after fat grafting (p <
0.01). All patients demonstrated improvement in symmetry, shape, and
volume.

CASES

CASE 1

A 48-year-old female 2 years following right upper outer quadrant


lumpectomy and radiation therapy desiring more symmetry is shown in
Figure 91-1.
FIGURE 91-1 Preoperative view (A–C) of a 48-year-old female 2 years
following right upper outer quadrant lumpectomy and radiation therapy
desiring more symmetry. Postoperative view 12 months (D–F) following fat
grafting to the right breast x2. Postoperative view 24 months (G–I).

CASE 2

A 59-year-old female 4 years following right upper outer quadrant


lumpectomy and radiation therapy desiring more symmetry is shown in
Figure 91-2.
FIGURE 91-2 Preoperative view (A–C) of a 59-year-old female 4 years
following right upper outer quadrant lumpectomy and radiation therapy
desiring more symmetry. Postoperative view 6 months (D–F) following fat
grafting to the right breast x1. Postoperative view 12 months (G–I) following
second fat grafting and left mastopexy. Postoperative view 24 months (J–L)
following fat grafting. Postoperative view 36 months (M–O) following fat
grafting.
CONTROVERSIES

Breast Imaging
One of the controversies surrounding fat grafting the breast-conservation
patient is the issue of imaging and whether or not there will be
mammographic confusion. This topic was addressed by Rubin et al. who
studied 27 women who had fat grafting to the breast and compared them to
23 women who had reduction mammaplasty (9). The average volume of fat
injected per patient was 526.5 cc. Experienced radiologists reviewed all of
the preoperative and postoperative mammograms and demonstrated no
significant differences for oil cysts (31.5% vs. 25.5%), benign calcifications
(27.2% vs. 17.1%), and calcifications warranting biopsy (1.6% vs. 4.6%)
between the breast reduction and lipoaugmentation cohorts, respectively. The
authors concluded that fat grafting to the breast produced fewer radiographic
abnormalities, a more favorable Breast Imaging Reporting and Data System
score, and less aggressive follow-up recommendations when reviewed by
breast radiologists.
Juhl et al. reviewed 49 patients who had autologous fat grafting following
BCS (10). Patients had one to three fat grafting procedures with a mean
volume of 135 ± 74 cc. Breast imaging was performed at a mean of 9 months
(range, 2 to 25 months) following the final grafting procedure. Comparison of
mammograms before and after fat grafting demonstrated calcifications in
21%, oil cysts in 85%, and increased scarring in 3%. Biopsy was required in
5 patients. There was a significant improvement based on breast aesthetic
appearance, body image, and scar quality. No patient had a major
complication and 3% of patients experienced a minor complication.
Mann et al. reviewed outcomes following fat grafting for BCT deformities
in 37 women (11). The mean number of sessions was 1.5 (range, 1 to 4) and
the mean volume of injected fat was 146 cc (range, 30 to 530 cc). The mean
time from BCT to fat grafting was 40.8 months and the mean follow-up after
fat grafting was 29.5 months. Four patients required a biopsy after a
suspicious palpable lesion was noted on imaging. The pathology was benign
in all cases. The authors concluded that there was a risk of unnecessary
biopsy following fat grafting but that the complication rates were low at that
fat grafting was a safe option for the correction of BCT deformities.
Oncologic Safety
The oncologic safety of fat grafting to the native breast parenchyma
continues to be studied. Concerns about cancer detection as well as
promotion of cancer remain topics of discussion. Some of this is borne of the
aromatase theory based on the fact that adipocytes will express aromatase
that is an enzyme involved in the synthesis of estrogen. Some breast tumors
are estrogen sensitive (12,13). Other factors that have posed concerns include
the induction of angiogenesis following fat grafting. The fear is that
angiogenesis may fuel tumorigenesis. The presence of ADSCs in lipoaspirate
has been postulated to stimulate tumor metastasis.
In a prospective clinical study, Brenelli et al. studied 59 patients who had
fat grafting following BCT (2). Patient stage at the time of BCT was stage 0
(11.8%), stage I (33.8%), or stage IIA (23.7%). Abnormal breast imaging was
demonstrated in 20% of the postoperative mammograms and 8% of those
patients had biopsy. There were three local recurrences noted in this series of
patients during the mean follow-up period of 34 months. These recurrences
were considered true and not related to the fat grafting.
In a systematic review of 43 studies, Groen et al. were able to isolate 21
studies that reviewed 3,020 patients and provided outcomes related to
oncologic safety (14). Meta-analysis demonstrated a local recurrence rate of
2.5% (95% confidence interval [CI]) and a distant recurrence rate of 2.0%
(95% CI). There was no difference in the local or distant recurrence rates
between mastectomy and BCT patients (p = 0.69). The histologic subtype of
the recurrent tumor was the same as that of the primary tumor. Based upon
the available evidence, the conclusion of this systematic review was that
autologous fat grafting after mastectomy or BCT did not seem to increase the
risk of cancer recurrence. They also found that local and distant recurrence
rates following breast conservation and fat grafting were lower than in
patients who had mastectomy and immediate breast reconstruction.
In another prospective study, Mestak et al. compared local recurrence rates
in patients that had BCT with or without postoperative lipofill for correct
contour deformities (15). The control (no fat graft) and study group (fat graft)
were matched for the following variables: histology, estrogen and
progesterone receptors, adjuvant hormone therapy, disease-free interval from
the initial BCT, and disease-free interval from the lipofilling. The primary
end point was tumor recurrence. Local recurrence was demonstrated in 2 of
32 cases (6.25%) in the lipofill group and in 2 of 41 cases (4.88%) in the
control group. Distant metastases were detected in all 4 cases. There was no
difference in the local recurrence rate between the two cohorts (p = 0.593).
Fat Retention
Fat retention in the radiated patient following BCT has been persistent topic
of discussion. Many surgeons have opined that fat retention is less in radiated
patients and more fat grafting sessions are necessary in order to achieve a
desired result. Others have stated that the fibrosis is deeper in the breast
parenchyma and that fat grafting will have minimal effect on correcting the
underlying problem. The amount of time required from completion of
radiation to fat grafting will vary from patient to patient depending upon the
degree of radiation change and fibrosis. Most surgeons feel that at least 1
year should elapse prior to considering the improvement of contour or skin
quality; however, the actual time should be based on when the soft tissues
have completely matured.
In a study designed specifically to answer the question of fat retention in
various types of breast reconstruction, Choi et al. used three-dimensional
imaging at various time intervals following fat grafting to assess retention
volume (16). The study group included autologous, prosthetic, and
oncoplastic reconstruction. Volumetric imaging was performed on
postoperative days 7, 16, 49, and 140. Various iterations were analyzed. The
first comparison was radiated versus nonradiated breasts. The mean volume
of fat injected into the breast was 97 cc for the nonirradiated breasts and 105
cc for the nonradiated breasts. In the radiated patients, fat grafting was
performed approximately 1.5 years after radiation. Volume retention at 140
days was 43.3% in the nonradiated breasts and 41.7% in the radiated breasts.
No statistical difference was demonstrated at the specified time intervals
between the two cohorts.
The second relevant analysis compared breasts based on the type of
reconstruction that included autologous, prosthetic, and lumpectomy. At
postoperative day 7, the lumpectomy reconstruction subset had statistically
significant higher-volume retention than the autologous reconstruction
subset. At 140 days, the fat retention was 56.3% for lumpectomy, 42.2% for
implant, and 31.4% for autologous. The third relevant analysis compared
volume of injected fat. The fat volumes were stratified as large volume (mean
151 cc, range 111 to 216 cc), intermediate volume (mean 93 cc, range 75 to
108 cc), and small volume (mean 51 cc, range 12 to 72 cc). Fat retention at
140 days was 52.3% for large-volume cohort, 38.1% for the intermediate-
volume cohort, and 27.1% for the small-volume cohort. The authors
concluded that fat retention is volume and time dependent and that patients
receiving higher volumes of injected fat had less volume loss and greater
volume retention.
Volume of fat retention was also evaluated in a systematic review of 43
studies of which two had data of fat retention volumes (14). One study used
MRI and the other used three-dimensional analysis combined with
computerized tomography. The mean injected volume was 128 cc and the
percentage of volume gain relative to the injected volume after a minimal
period of 1 year postoperatively was 63.7%. The study compared fat grafting
in radiated and nonradiated patients as well as demonstrated a 76.8% volume
retention in 681 nonradiated patients with a mean follow-up of 20 months
compared to 63.8% volume retention in 16 patients following radiation with a
mean follow-up of 24 months.
Complications
Complications following breast conservation and fat grafting are uncommon
and include oil cysts, fat necrosis, microcalcifications, and
macrocalcifications with an overall complication rate of 8.4% (14). The
incidence of fat necrosis was increased in patients following fat grafting
compared to those without fat grafting (9.0% vs. 4.7%, respectively) (14). In
addition, more biopsies were performed based on suspicious radiologic
findings in patients following fat grafting compared to no fat grafting (3.7%
vs. 1.6%, respectively) (14). Other studies have similarly demonstrated low
complication rates following fat grafting in the breast conservation patient
(11).

REFERENCES

1. Delay E, Guerid S, Muruta AC. Indications and controversies in


lipofilling for partial breast reconstruction. Clin Plastic Surg
2018;45:101–110.
2. Brenelli F, Rietjens M, De Lorenzi F, et al. Oncological safety of
autologous fat grafting after breast conservative treatment: a prospective
evaluation. Breast J 2014;20(2):159–165.
3. Moseley TA, Zhu M, Hedrick MH. Adipose-derived stem and
progenitor cells as fillers in plastic and reconstructive surgery. Plast
Reconstr Surg 2006;118(3 Suppl):121S–128S.
4. Ejaz A, Greenberger JS, Rubin PJ. Understanding the mechanism of
radiation induced fibrosis and therapy options. Pharmacol Ther
2019;204:107399.
5. Rigotti G, Marchi A, Galie M, et al. Clinical treatment of radiotherapy
tissue damage by lipoaspirate transplant: a healing process mediated by
adipose-derived adult stem cells. Plast Reconstr Surg 2007;119:1409–
1422; discussion 1423–1424.
6. Khouri RK, Schlenz I, Murphy BJ, et al. Nonsurgical breast enlargement
using an external soft-tissue expansion system. Plast Reconstr Surg
2000;105:2500–2512; discussion 2513–2514.
7. Khouri RK, Smit JM, Cardoso E, et al. Percutaneous aponeurotomy and
lipofilling: a regenerative alternative to flap reconstruction? Plast
Reconstr Surg 2013;132:1280–1290.
8. Van Turnhout AA, Fuchs S, Lisabeth-Brone K, et al. Surgical outcome
and cosmetic results of autologous fat grafting after breast conserving
surgery and radiotherapy for breast cancer: a retrospective cohort study
of 222 fat grafting sessions in 109 patients. Aesth Plast Surg
2017;41:1334–1341.
9. Rubin JP, Coon D, Zuley M, et al. Mammographic changes after fat
transfer to the breast compared with changes after breast reduction: a
blinded study. Plast Reconstr Surg 2012;129:1029–1038.
10. Juhl AA, Redsted S, Engberg Damsgaard T. Autologous fat grafting
after breast conserving surgery: breast imaging changes and patient-
reported outcome. J Plast Reconstr Aesth Surg 2018;71:1570–1576.
11. Mann RA, Ballard TNS, Brown DL, et al. Autologous fat grafting to
lumpectomy defects: complications, imaging, and biopsy rates. J Surg
Res 2018;231:316–322.
12. Fraser JK, Hedrick MH, Cohen SR. Oncologic risks of autologous fat
grafting to the breast. Aesthet Surg J 2011;31(1):68–75.
13. Simpson ER. Sources of estrogen and their importance. J Steroid
Biochem Mol Biol 2003;86:225–230.
14. Groen JW, Negenborn VL, Twisk DJWR, et al. Autologous fat grafting
in onco-plastic breast reconstruction: a systematic review on oncological
and radiological safety, complications, volume retention and
patient/surgeon satisfaction. J Plast Reconstr Aesthet Surg 2016;69:742–
764.
15. Mestak O, Hromadkova V, Fajfrova M, et al. Evaluation of oncological
safety of fat grafting after breast-conserving therapy: a prospective
study. Ann Surg Oncol 2016;23:776–781.
16. Choi M, Small K, Levovitz C, et al. The volumetric analysis of fat graft
survival in breast reconstruction. Plast Reconstr Surg 2013;131:185–
191.
CHAPTER 92

Fat Grafting in Implant-Based Breast


Reconstruction
JOHN HIJJAWI
HISTORY

Changes in Breast Reconstruction Expectations


The past 15 years have seen a revolution in the results that can be achieved
with breast reconstruction. This revolution has created great opportunity, but
equally great challenge for plastic surgeons. Gone are the days of “you’ll
look good in clothing” as the final comment in a reconstructive consult. The
expectations that patients have of their surgeons, and that plastic surgeons
have of themselves, have increased dramatically.
Technology is responsible for these changes in large part. Regarding
surgical techniques the advent of perforator flaps, CT angiography, acellular
dermal matrices, form-stable implants, and more restrained mastectomy
techniques have all contributed to better results.
Technology in the form of the internet and social media have also
contributed. Many patients do not sit in isolation lamenting a bad result or
wishing they had a more natural breast reconstruction. They frequently take
to social media outlets or the internet to seek information on better
techniques, engage with other breast reconstruction patients, evaluate
potential surgeons, and complain about poor results. All of this has pushed
the bar higher.
THE IMPACT OF PREPECTORAL BREAST RECONSTRUCTION ON FAT
GRAFTING
Implant-based breast reconstruction has rapidly shifted from a total or partial
submuscular technique, to a muscle-preserving prepectoral technique for
many surgeons. Mastectomy reconstruction remains the main focus for most
plastic surgeons. Implant-based reconstruction is by far the most common
method in breast reconstruction–focused practices around the world.
The benefits of prepectoral breast reconstruction are clear in the early
stages of this move away from submuscular approaches. The elimination of
animation deformity alone has been a major advance, even though further
long-term results will need to be evaluated. However, the move to prepectoral
implant-based breast reconstruction has not come without challenges (1). The
expense of larger sheets of acellular dermal matrices and the higher potential
for visible implant rippling are two of the problems that continue to challenge
surgeons. Autologous fat grafting is one of several techniques that promise to
help reduce visible implant rippling in both prepectoral and dual plane
reconstruction.
The safety and efficacy of autologous fat grafting in mastectomy patients
continues to be carefully studied, but has gained increasing acceptance. We
are in an era where the results of fat grafting techniques in an increasing
variety of clinical scenarios are being evaluated, and the indications for those
techniques are expanding. Autologous fat grafting has become a key adjunct
in both flap and implant-based mastectomy reconstruction, the reconstruction
of breast-conservation deformities, and in rare cases total breast
reconstruction with fat grafting alone.
FAT HARVEST TECHNIQUES
A great deal of attention has been given to the process of harvesting fat and to
the optimization of the techniques and instrumentation involved. The
majority of studies comparing various techniques of fat harvest rely on in
vitro cell viability assays or a histologic examination of adipocytes for
structural integrity as their end points rather than the in vivo assessment of fat
graft viability (2). These types of studies can certainly answer whether or not
a particular harvest technique damages adipocytes immediately upon harvest,
but they do not answer what the impact of those techniques might be on graft
viability after reinjection.
In 2000, Rohrich et al. compared the impact of a variety of liposuction
methods on the structural integrity and in vitro viability of human adipocytes
(3).
Shiffman et al. evaluated the impact of increasing suction pressure on
adipocytes in 2001 (4). That study looked at the histologic appearance of
adipocytes and found that if aspiration pressures were kept below 700 mm
Hg, damage to adipocytes could be avoided.
Ozsoy compared a variety of cannula sizes on in vitro adipocyte viability
in 2006 (5). This study found that the larger the size of the cannula used to
harvest fat, the better the viability of the adipocytes harvested. This seems
like a logical conclusion given the reduced shear stress on cells being
aspirated through larger-aperture cannulas. However, one needs to consider
the impact of large particle size on the viability of fat once grafted. Larger
globules of fat will certainly protect the adipocytes at the center of the
globule from shear stress and direct trauma. However, they will also insulate
those same adipocytes from the nutrition and neovascularization needed to
maintain long-term viability. On the other end of the spectrum, a very small
cannula aperture will induce significant shear on adipocytes at a given
suction pressure.
FAT PREPARATION
Centrifugation has long been an integral part of preparing fat grafts for
reinjection. Many of the studies looking at the impact of centrifugation have
used the speed of the centrifuge, or revolutions per minute (RPMs) as a
variable data point. This ignores the impact of the centrifuge’s moment arm
on the amount of G forces being applied to the fat. Kurita et al. addressed this
in 2008 when they looked at the impact of varying G forces on the in vivo
viability of human fat injected into athymic mice. That study found that the
greatest graft retention was seen when the aspirated fat was reinjected
without any centrifugation at all (6). The authors did find that when the goal
was to isolate stem cells, a moderate centrifugation was superior to no
centrifugation.
The widespread adoption of large-volume fat grafting was originally slow
in part due to efficiency issues. Many surgeons considered the time and effort
involved in harvesting more than 100 cc of fat in small aliquots, draining that
fat on absorbent pads or centrifuging it, and placing it back into syringes for
reinjection to not be worth the trouble. Gabriel et al. looked at the use of a
commercial filtration system, the Revolve system, (Allergan) and whether
that system could help expedite the harvest and preparation of fat grafts (7).
They found that with the use of the Revolve system, and more likely with the
elimination of centrifugation and the multiple transfers it requires, they could
harvest more fat in less time. They found that with the Revolve they could
more than double their fat harvest yield in about one-third of the time it took
using centrifugation.
There will always be a great deal of variety in how surgeons choose to
pursue different operations. However, there is a growing body of literature
that can point surgeons in the right direction and at least help avoid
techniques that at best waste time by adding steps that don’t demonstrate a
benefit or at worst are directly damaging to adipocytes. Ultimately, the
harvest technique has to reproducible, minimize morbidity to the patient and
harvested adipocytes, and involve procedures that can be performed
efficiently.
REINJECTION OF FAT
The fundamental principle of reinjection is gentle handling of the tissue and
the avoidance of creating large pools of fat. Gentle pressure on the syringe
during reinjection is a first step. Pressure is typically steady and slow enough
that the fat is released in a “string of beads” and not as a depot. The proper
selection of cannulas for reinjection is also important. As with harvesting fat,
cannulas that are too narrow may lead to shear forces on the fat that harm
viability. However, if the speed of reinjection remains well controlled this is
probably less of an issue than it is with harvest using a liposuction machine.
The concept of depositing the fat “one adipocyte at a time” so that every
grafted adipocyte is surrounded by the native tissue in the recipient bed, has
been put forward by Rigotti et al. While this is not technically feasible, the
idea illustrates the importance of maximizing contact of the grafted fat with
the recipient bed to improve the odds of successful revascularization.
There is a lingering misperception that prepectoral reconstruction
eliminates the possibility of fat grafting around implants because there is no
longer a plane to graft into. With dual plane or submuscular implant
reconstruction, fat can be grafted either between the pectoral muscle and the
skin flap, or directly into the muscle. In fact, there is an excellent plane
available for fat grafting when prepectoral breast reconstruction is performed
with acellular dermal matrix support. Most commonly, authors have
described ADM wrap technique that covers the entire anterior surface of the
tissue expander with ADM. The amount of posterior coverage varies.
Once tissue expander to implant exchange is performed, there is a very
healthy plane in between the ADM and the skin flap that can support up to
150 cc of fat transfer if that fat is carefully distributed around the entire skin
flap (8).
ACCESS OPTIONS
The subdermal plane can be directly accessed through the incision made to
perform the tissue expander to implant exchange. This facilitates direct
visualization of the plane and virtually eliminates the possibility of grafting
into the implant pocket. If grafting is performed after removing the expander,
but before placing the implant the entire pocket is easily observed.
An alternate method is to create a small access incision with a 16-gauge
needle and then gently dilate that incision with progressively larger Coleman
cannulas. This can be achieved with one needle and two cannulas.
Occasionally, fat can be reinjected through small tumescent injection
cannulas that are typically longer than Coleman cannulas. This increases the
reach of the cannula and the area that can be grafted through each access
incision.
Regardless of how the subdermal plane is accessed, it is important to
adhere to the reinjection technique described above with gentle pulsating
injection on withdrawal only. This creates a string of beads rather than pools
of fat that are unlikely to be revascularized.
PATIENT SAFETY
Two of the greatest risks to patients undergoing large-volume fat grafting
include hypothermia and thromboembolism. It can be challenging to expose
both recipient sites and adequate donor sites in these patients. The surgical
can sometimes extend from the sternal notch to the patella. With alcohol-
based prep solutions, this creates an ideal environment for heat loss.
Prewarming patients prior to their entry to the operating room, maintaining
reasonable ambient temperatures in the operating room, and employing
perioperative warming strategies are all useful in avoiding hypothermia. We
have found the use of circulating warm-fluid warming pads and sterile forced
air warming blankets to be useful.
The application of sequential compression devices can also be a challenge
when the operative field is broad. We have found the use of sterile towels and
sterile elastic bandages to be helpful in allowing the application and
maintenance of sequential compression devices throughout these procedures.
THE IMPACT OF FAT GRAFTING ON BREAST CANCER RECURRENCE
As soon as surgeons began grafting fat into breasts the Plastic Surgery
community warned of the potential dangers of inducing novel or recurrent
cancers. The potential for human fat to generate estrogen is well recognized,
and laboratory studies have demonstrated the ability of highly manipulated
adipose-derived stem cells (ASCs) to induce breast cancer cell growth
through growth-factor mediated pathways in an in vitro setting (3,9,10). The
other area of concern is the potential for pluripotential cells to differentiate
into undesired cell lines. As a result, there has been concern that grafting
additional fat to a breast that has already been treated for cancer might be ill
advised. The critical question is whether fat harvested by means developed to
obtain viable structural fat is comparable to fat harvested and treated to
amplify the concentration and biologic activity of ASCs (11). The average
plastic surgeon performing fat grafting is generally not using techniques to
amplify or concentrate ASCs. In fact, any procedures that amplify ASCs
should be performed under an IRB-approved protocol.
Brenelli and the Milan Group evaluated recurrence rates in their 2014
study of 59 patients treated with fat grafting for BCT deformities and found
that with 3-year follow-up 4% had some locoregional recurrence (12). Petit
found in 2011 that with a shorter follow-up of 19 months in a similarly-
treated group of 143 patients, only 1.3% had a locoregional recurrence (13).
In 2012 Petit directly matched a group of unreconstructed BCT patients with
a group of BCT patients treated with fat grafting (13). The 973 patients in this
study were matched for disease severity and at 26-month follow-up the fat-
grafted group had a recurrence rate of 2.4% while the BCT-only group had a
recurrence rate of 2.9%. Kaoutzanis et al. at the University of Michigan
focused on lipofilling in postmastectomy patients (14). They evaluated 167
breast reconstructions undergoing fat grafting in 108 patients with a mean
follow-up of 20 months. They found that 31.7% of patients underwent breast
imaging after lipofilling, a relatively high number. However, that imaging
resulted in only 2.4% of breasts undergoing biopsy with an additional 2.4%
of breasts undergoing biopsy for palpable lesions. Of the entire study group
of postmastectomy patients undergoing lipofilling there were no cases of
locoregional recurrence. The findings of this study which included a 31%
imaging rate for only a 2.4% biopsy rate represents a potential opportunity to
improve upon the utilization of postmastectomy breast imaging in patients
undergoing lipofilling procedures.
Silva-Vergara et al. published the results of their experience with
lipofilling both mastectomy and breast-conservation patients in 2014 (15). In
195 consecutive patients and 319 lipofilling procedures they observed a
locoregional recurrence rate of 3.1% over the course of the study. Follow-up
in the two groups were 74 months for the mastectomy group and 31 months
for the breast-conservation group. Of interest, the pathology was invasive
carcinoma in 81.6% of this study population. Blondeel et al. from Belgium
have published a meta-analysis of 18 clinical studies revealing regional
recurrence rates of between 0% and 3.9% per year in women undergoing
autologous fat grafting after having BCT. They note the disconnect between
the results of clinical studies that demonstrate a significant degree of safety
and conversely experimental studies that clearly suggest the potential to
induce cancers. Based on the clinical evidence available it is clear that the use
of autologous fat grafting in patients previously treated with BCT is safe but
requires ongoing study.
FAT GRAFTING AS AN ADJUNCT TO IMPLANT AND AUTOLOGOUS
MASTECTOMY RECONSTRUCTION
As noted in the introduction to this chapter, the expectations of patients
undergoing breast reconstruction have grown in recent years. Creating a more
natural-feeling breast without an autologous flap remains challenging. The
addition of fat grafting to an implant reconstruction offers the potential for
significant improvement in the outcomes for patients over implant
reconstruction alone. In 2017 Komorowska-Timek reported a study of 85
patients with implant reconstruction undergoing 117 fat grafting procedures
(16). This group included radiated and a smaller number of nonirradiated
patients. Overall complications reached 27% and implant-related
complications reached 22%. The authors observed fat necrosis, oil cysts, and
capsular contracture as some of the more common complications. However,
it is difficult to separate the mechanism of contracture in this study group
given the presence of irradiated patients.
Seth et al. at Northwestern University reported on a large number of
patients undergoing implant-based reconstruction with or without fat grafting
(17). In 1,202 breasts reconstructed with an implant-based approach they
found no difference in locoregional recurrence or survival whether or not the
patients underwent adjunctive fat grafting.
In a similar study, Cohen et al. from New York University looked at a
broader group of mastectomy patients (18). This study included both patients
reconstructed with implants and those reconstructed with an autologous
approach. When divided into those treated with adjunctive fat grafting and
those not undergoing fat grafting, the recurrence rate was 2.5% and 1.9%,
respectively. This was with at least a 38-month follow-up in the non–fat-
grafted group and a 44-month follow-up in the fat-grafted group.
CONCLUSION
The indications and utility of autologous fat grafting are growing rapidly. The
ability to place very precise amounts of tissue into precise locations is a
powerful tool. There is of particular interest in the implant-based
reconstruction patient population given the fact that fat grafting can be
performed as a solo procedure in many cases. When compared to a flap
procedure, the combination of implant reconstruction and fat grafting is likely
to appeal to a large number of women. The rapid, predictable volume of an
implant with the addition of autologous fat to create a softer breast is a
powerful combination.
As with all procedures performed in cancer patients, it is imperative we
closely follow the safety and outcomes over years. The existing data
consistently support the use of autologous fat grafting as a safe adjunct to
implant-based breast reconstruction. The positive impact on the lives of
breast cancer patients will likely continue to expand as we understand these
procedures better.

REFERENCES

1. Sigalove S, Maxwell GP, Sigalove NM, et al. Prepectoral implant-based


breast reconstruction: rationale, indications, and preliminary results.
Plast Reconstr Surg 2017;139:287–294.
2. Zimmerlin L, Donnenberg AD, Rubin JP, et al. Regenerative therapy
and cancer: in vitro and in vivo studies of the interaction between
adipose-derived stem cells and breast cancer cells from clinical isolates.
Tissue Eng Part A 2011;17:93–106.
3. Rohrich RJ, Morales DE, Krueger JE, et al. Comparative lipoplasty
analysis of in vivo-treated adipose tissue. Plast Reconstr Surg
2000;105:2152–2158; discussion 2159–2160.
4. Shiffman MA, Mirrafati S. Fat transfer techniques: the effect of harvest
and transfer methods on adipocyte viability and review of the literature.
Dermatol Surg 2001;27:819–826.
5. Ozsoy Z, Kul Z, Bilir A. The role of cannula diameter in improved
adipocyte viability: a quantitative analysis. Aesthet Surg J 2006;26:287–
289.
6. Kurita M, Matsumoto D, Shigeura T, et al. Influences of centrifugation
on cells and tissues in liposuction aspirates: optimized centrifugation for
lipotransfer and cell isolation. Plast Reconstr Surg 2008;121:1033–
1041; discussion 1042–1043.
7. Gabriel A, Maxwell GP, Griffin L, et al. A comparison of two fat
grafting methods on operating room efficiency and costs. Aesthet Surg J
2017;37:161–168.
8. Rubin JP, Coon D, Zuley M, et al. Mammographic changes after fat
transfer to the breast compared with changes after breast reduction: a
blinded study. Plast Reconstr Surg 2012;129:1029–1038.
9. Perez-Cano R, Vranckx JJ, Lasso JM, et al. Prospective trial of adipose-
derived regenerative cell (ADRC)-enriched fat grafting for partial
mastectomy defects: the RESTORE-2 trial. Eur J Surg Oncol
2012;38:382–389.
10. Waked K, Colle J, Doornaert M, et al. Systematic review: the
oncological safety of adipose fat transfer after breast cancer surgery.
Breast 2017;31:128–136.
11. Lohsiriwat V, Curigliano G, Rietjens M, et al. Autologous fat
transplantation in patients with breast cancer: “silencing” or “fueling”
cancer recurrence? Breast 2011;20(4):351–357.
12. Brenelli F, Rietjens M, De Lorenzi F, et al. Oncological safety of
autologous fat grafting after breast conservative treatment: a prospective
evaluation. Breast J 2014;20:159–165.
13. Petit JY, Lohsiriwat V, Clough KB, et al. The oncologic outcome and
immediate surgical complications of lipofilling in breast cancer patients:
a multi-center study—Milan-Paris-Lyon experience of 646 lipofilling
procedures. Plast Reconstr Surg 2011;128(2):341–346.
14. Kaoutzanis C, Xin M, Ballard TN, et al. Autologous fat grafting after
breast reconstruction in postmastectomy patients: complications, biopsy
rates, and locoregional cancer recurrence rates. Ann Plast Surg
2016;76:270–275.
15. Silva-Vergara C, Fontdevila J, Descarrega J, et al. Oncological
outcomes of lipofilling breast reconstruction: 195 consecutive cases and
literature review. J Plast Reconstr Aesthet Surg 2016;69:475–481.
16. Komorowska-Timek E, Turfe Z, Davis AT. Outcomes of prosthetic
reconstruction of irradiated and nonirradiated breasts with fat grafting.
Plast Reconstr Surg 2017;139:1e–9e.
17. Seth AK, Hirsch EM, Kim JY, et al. Long-term outcomes following fat
grafting in prosthetic breast reconstruction: a comparative analysis. Plast
Reconstr Surg 2012;130:984–990.
18. Cohen O, Lam G, Karp N, et al. Determining the oncologic safety of
autologous fat grafting as a reconstructive modality: an institutional
review of breast cancer recurrence rates and surgical outcomes. Plast
Reconstr Surg 2017;140:382e–392e.
CHAPTER 93

Fat Grafting in Autologous Breast


Reconstruction
NIMA KHAVANIN | KRISTEN P. BRODERICK | JUSTIN M. SACKS
HISTORY
Autologous fat transfer has assumed an important position in the plastic
surgeon’s armamentarium as a means for correcting asymmetries and contour
irregularities and/or augmenting the soft tissues across a wide range of
clinical indications. First described for the correction of facial deformities (1),
fat transfer was famously applied to the breast in 1895 when Czerny
attempted the transfer of a lipoma to the chest for breast reconstruction (2).
The application of fat grafting became more widespread with the advent of
liposuction in the 1980s (3). Shortly thereafter, concerns regarding its safety
in the setting of cancer recurrence and surveillance limited its application in
the breast until a 2007 paper by Coleman and Saboeiro demonstrated its long-
term safety in 17 patients (4,5).
Today, fat grafting is used frequently in both prosthetic and autologous
reconstruction. Particularly in the setting of autologous reconstruction, small-
volume transfers are useful during revision in order to camouflage step-offs
at the junction of the flap and chest wall and other contour irregularities.
Large-volume fat grafting into the flap and/or pectoralis muscle can be
performed before, during, or after flap transfer in order to augment relatively
small flaps and potentially avoid the need for an implant or stacked free flap
(6–8).
INDICATIONS
The indications for fat transfer in the autologously reconstructed breast are
numerous. Fat grafting to the flap and/or pectoralis muscle at the time of flap
transfer is typically indicated when the flap lacks adequate volume and/or
projection for an aesthetic reconstruction (Fig. 93-1). A considerable volume
of fat can be transferred in order to manipulate flap size and shape and avoid
the need for a tissue expander and/or implant. Total autologous
reconstruction with a flap (typically latissimus dorsi myocutaneous flap) and
fat grafting (6–15) is particularly relevant given the recent concerns regarding
breast implant–associated anaplastic large cell lymphoma, or BIA-ALCL, and
breast implant illness (16,17).
Small-volume fat grafting is used commonly as a revision procedure
wherever a contour irregularity or asymmetry exists (Fig. 93-1). Common
areas in autologous breast reconstruction include the junctions where the flap
edge meets the native chest wall. We also refer to these as superior pole
deformities.
CONTRAINDICATIONS
Contraindications to fat grafting the autologously reconstructed breast are
relative and must often be considered on a case-by-case basis. Specific
considerations include the presence of a coagulation disorder, the use of
anticoagulant and/or antiplatelet medications, disorders of lipid metabolism,
severe chronic disease states, acute infection, acute organ failure, strong
personal history of venous thromboembolism, and the presence of unrealistic
expectations/body dysmorphia (18).

FIGURE 93-1 A: left oblique, (B) center, and (C) right oblique views of a 52-year-old
female with a history of previous left nipple-sparing mastectomy and implant-based
reconstruction with subsequent right mastectomy with abdominally based
autologous tissue reconstruction presented for evaluation and revision. She was most
bothered by the global asymmetry in volume between the two breasts as well as the
sharp transition between the full upper lateral aspect of the right breast/flap and
chest wall.

The availability of donor fat is an important consideration when weighing


a patient’s candidacy for fat grafting. The evaluation of fat deposits should
bear in mind that approximately a quarter to one-third of the volume
harvested will be lost during centrifugation and/or preparation of the fat for
injection, and that another third to one-half will be resorbed within the weeks
to months following transfer. When a single donor site does not contain
enough volume, fat from several areas can be combined at the expense of
increased operative sites and time.
OPERATIVE TECHNIQUE
PREOPERATIVE PLANNING
The preoperative evaluation should include a focused history and physical
examination in order to determine the area of treatment within the breast or
flap and the location of natural fat deposits. At our institution, the preferred
donor sites for fat grafting include the flanks, abdomen, and thighs, and a
decision is ultimately made based on physical examination and patient
preference (Fig. 93-2). Several studies have demonstrated no association
between donor site and fat graft retention and/or histology (19,20).
FIGURE 93-2 Preoperative markings for planned fat grafting to the upper, medial
and lateral poles of the left breast for volume augmentation and to the upper pole of
the right breast in order to smoothen the transition between the chest wall and flap.
Donor sites were marked in the abdomen as well as the lateral right breast.
FAT HARVEST
The selected donor areas are infiltrated with a tumescent solution containing
lidocaine and epinephrine in order to reduce bleeding and postoperative
bruising, and 15 minutes are allowed to pass in order to achieve
vasoconstriction. A blunt-tipped harvesting cannula is inserted into the
subcutaneous space through a stab incision made with a no. 15 blade. Under
moderate suction, the adipose tissues are mechanically disrupted and
aspirated by passing the cannula through the tissues in an even, sweeping
motion in order to avoid postoperative contour irregularities. Preliminary
studies have suggested improved viability of fat grafts harvested through a
larger liposuction cannula (6-mm diameter vs. 2 or 4 mm) (21). Care should
be taken to limit aspiration of the superficial tissues and to avoid zones of
adherence including the lateral gluteal depression and gluteal crease (22).
When fat is harvested from bilateral donor sites, the risk of asymmetry can be
minimized by keeping track of volumes of tumescent solution injected and
tissues aspirated from each side and through regular inspection/palpation of
the donor sites.
FAT PROCESSING
Several techniques have been described for processing the lipoaspirate before
injection into the recipient tissues. Although there are animal studies
suggesting the superiority of fat processing on Telfa gauze to centrifugation
(23), this technique may not be feasible for large volumes of lipoaspirate and
these findings have not been sufficiently replicated in human trials (24,25).
At this time, our preference is to use the Revolve (LifeCell Corp.,
Bridgewater, NJ, USA) system, which provides a combination of filtration of
the lipoaspirate with serial washing and spinning. In our hands, the system
allows for the rapid and facile processing of a relatively large volume of fat.
Preclinical studies have demonstrated low amounts of free oil and blood with
the Revolve without any adverse effects on fat retention when compared to
decanting and centrifugation (26).
Fat Transfer
Although no consensus exists on the best techniques for retention of the
grafted adipose tissue, several guiding principles have been described to
optimize postoperative outcomes. Long-term retention of fat grafting is
believed to be associated with several patient-related factors including age, a
history of trauma and/or radiation to the recipient area, and the severity of
surrounding structural defects (24). It was initially believed that injections
into muscle would fare better than the dermis or subcutaneous space because
of increased vascularization (27), however, this hypothesis has not yet been
borne out in more recent trials (28).
The processed lipoaspirate is distributed into 10-mL Luer-Lok syringes in
preparation for injection with a 17-gauge blunt cannula (29). The use of
larger-diameter injection cannulas has been associated with a greater
susceptibility to central necrosis as the dimension of fat deposits becomes
more difficult to manage with 14-gauge or larger cannulas (30). When fat
grafting is used as a means for secondary revision, injection ports are created
using a 16-gauge hypodermic needle surrounding the area of interest on the
breast. Injection cannulas are inserted into the subcutaneous space and/or
muscle, and small deposits of fat are created in a systematic and controlled
fashion throughout the area of interest. As described by Coleman, adipose
tissue should only be injected during withdrawal of the cannula in order to
allow the tissues to fall into a natural plane (29). Fat grafts injected at a slow
rate (0.5 to 1 cc/sec) experience a lower shear stress and subsequently a
higher retention rate than grafts injected at a faster rate (3 to 5 cc/sec) (31).
When fat grafting is used to globally augment a flap in a single-stage
reconstruction, processed adipose tissues can be directly injected into the
target muscle and/or subcutaneous tissues following flap elevation and before
final inset and skin closure.
POSTOPERATIVE CARE
Patients are instructed on a strict postoperative compression regiment to
minimize edema and the risk of seromas and/or hematomas. This includes the
use of compression garments for 4 weeks after surgery. They can be worn
during the day for comfort and compression.
Patients are seen for follow-up initially at 1 week postoperatively and
subsequently every 3 months until they have demonstrated a complete
recovery from their operation.
GENERAL OUTCOMES
In the short term, patients often experience pain/discomfort and bruising
particularly at the donor site. It is not uncommon for bruising to be marked
and last up to 2 or even 3 weeks, and patients should be reassured that this is
not unusual. Cannula sites can typically be concealed in natural creased or
otherwise hidden areas and typically heal well.
Medium- and long-term complications can be divided into those that relate
to the donor site and those that relate to the breast. At the donor site, the most
common adverse event is the presence of a postoperative contour irregularity
in about 2.6% of cases (32). Several considerations have been proposed in an
attempt to minimize this risk, including: the use of small cannulas,
predominant aspiration of the deep tissues, a “crisscrossing” pattern of
liposuction, turning off suction when removing the cannula, and constant-use
visual and tactile feedback (33). Seromas can occur, particularly in the setting
of large-volume liposuction that creates large subcutaneous cavities (34).
Other complications, including infection, are rare and occur in less than 1%
of cases (35). Systemic complication related to lidocaine toxicity and/or fluid
shifts are less likely with the small lipoaspirate volumes seen for fat grafting
(36).
At the breast, overaggressive lipofilling can result in fat necrosis, oil cyst
formation, and calcifications if large volumes are injected into a single area
or if fat is injected into poorly vascularized bed. Although the overall
prevalence of these conditions is low within the literature (∼4.5%), it is
important to consider the method of radiologic/clinical detection of a study,
as rates vary considerably based on the use of mammography, ultrasound,
and magnetic resonance imaging (15). While mastectomy patients do not
typically undergo screening of their reconstructed breast, the presence fat
necrosis in the form of a palpable lump can be distressing to many breast
cancer survivors. Nonetheless, these complications can be easily
differentiated from pathologic conditions by an experienced radiologist, and
in general fat grafting is considered to not obscure or alter breast imaging at
this time (37). Similarly, postmastectomy fat grafting is not believed to
significantly affect a patient’s risk for cancer recurrence (4).
Fat Grafting in Latissimus Dorsi Breast Reconstruction
The latissimus dorsi myocutaneous flap is a reliable and commonly used
method for both immediate and delayed breast reconstruction. Despite its
reliable blood supply and relative ease of dissection, its principle limitation is
a limitation in the volume and projection of the transferred tissue (7). Many
surgeons overcome this limitation by combining the latissimus dorsi flap with
a tissue expander and/or implant, however this predisposes patients to all of
the risks of a breast implant, including: rupture, capsular contracture,
infection, BIA-ALCL, and breast implant illness (16,17,25).
More recently several authors have described combining the latissimus
dorsi flap with fat grafting, either in a single stage or sequentially, in order to
ensure a more aesthetic, totally autologous breast reconstruction (7,8,12).
Sinna et al. (38) have presented the largest series to date, including 200
patients who underwent secondary fat grafting of previously reconstructed
breasts using the latissimus dorsi flap. In their study, a mean volume of 176
mL of fat was transferred with a satisfactory result in nearly 95% of patients.
Niddam et al. (7) built upon this work by presenting 20 patients who
underwent fat grafting into the pectoralis major at the same time as latissimus
dorsi–based breast reconstruction. A mean volume of 228 mL of fat was
injected into the pectoralis muscle with only 10% of patients requiring an
additional treatment of fat grafting (90 mL and 110 mL volume) during the
13-month average follow-up. Finally, Zhu et al. (8) presented a series of 10
patients in whom fat grafting was performed safely into the latissimus dorsi
flap at the time of the primary surgery. On average, 176 mL were infiltrated
into the latissimus muscle, the overlying skin paddle, the pectoralis muscle,
and even the mastectomy skin flaps without any incidence of flap ischemia or
necrosis. Their technique served as a proof of concept that immediate fat
grafting can be performed safely into a freshly harvested latissimus dorsi. A
separate of study of 18 patients demonstrated good or excellent outcomes as
rated by the patient in 80% of cases following a single-stage procedure (39).
Economides and Song further developed this concept in 2018 in their report
on 18 patients with an average fat transfer of 359.6 mL per flap without
major adverse events (12). Total autologous reconstruction with a latissimus
flap and fat grafting represents a feasible option for patients who desire
autologous reconstruction and are not candidates for or do not desire
alternative pedicled/microvascular options.
FIGURE 93-3 A: left oblique, (B) center, and (C) right oblique views of the
postoperative results demonstrating improved symmetry in breast volume.
Contouring of the upper and lateral poles of the right breast have assisted in
camouflaging the edges of the flap and creating a more natural, ptotic breast shape.

Fat Grafting in Abdominally Based and Other Autologous


Breast Reconstructions
Abdominally based procedures in autologous breast reconstruction, including
DIEP and TRAM flaps, are commonly used options because of relative
abundance of abdominal adiposity in the majority of patients that allows for
an appropriately sized reconstruction. Nonetheless, many patients still require
some degree of revision fat grafting in order to address specific areas that
lack fullness or demonstrate contour irregularities (Figs. 93-1 and 93-3). In
one large series of 374 breast free flaps including primarily DIEP and
profunda artery perforator flaps, 100 (26.7%) underwent revision with fat
grafting with an average 1.12 sessions (13). On an average, 146.8 mL of fat
was injected predominantly into the medial and superior medial poles,
presumably to blend the step-off at the junction of the flap and chest wall.
Similar findings have been demonstrated in patients who under fat grafting to
DIEP flaps at the same time as a vascular delay (6) and in patients who
underwent breast reconstruction with transverse myocutaneous gracilis flaps
and secondary fat grafting (40).
Overall, these findings highlight the power of fat grafting as an adjunct to
autologous breast reconstruction. As our combined experience with these
techniques continues to increase, it may be possible to still further expand the
indications for autologous breast reconstruction to include even relatively
lean patients.
REFERENCES

1. Neuber F. Fettransplantation. Chir Kongr Verhandl Deutsche Gesellsch


Chir 1893;22:66–68.
2. Czerny V. Plastischer Ersatz der Brustdruse durch ein Lipom. Zentralbl
Chir 1895;27:72–75.
3. Illouz YG. Body contouring by lipolysis: a 5-year experience with over
3000 cases. Plast Reconstr Surg 1983;72(5):591–597.
4. Katzel EB, Bucky LP. Fat grafting to the breast: clinical applications
and outcomes for reconstructive surgery. Plast Reconstr Surg
2017;140(5S Advances in Breast Reconstruction):69S–76S.
5. Coleman SR, Saboeiro AP. Fat grafting to the breast revisited: safety
and efficacy. Plast Reconstr Surg 2007;119(3):775–785; discussion 86–
87.
6. Laporta R, Longo B, Sorotos M, et al. Breast reconstruction with
delayed fat-graft-augmented DIEP flap in patients with insufficient
donor-site volume. Aesthetic Plast Surg 2015;39(3):339–349.
7. Niddam J, Vidal L, Hersant B, et al. Primary fat grafting to the
pectoralis muscle during latissimus dorsi breast reconstruction. Plast
Reconstr Surg Glob Open 2016;4(11):e1059.
8. Zhu L, Mohan AT, Vijayasekaran A, et al. Maximizing the volume of
latissimus dorsi flap in autologous breast reconstruction with
simultaneous multisite fat grafting. Aesthet Surg J 2016;36(2):169–178.
9. Darrach H, Kraenzlin F, Khavanin N, et al. The role of fat grafting in
prepectoral breast reconstruction. Gland Surg 2019;8(1):61–66.
10. Delay E, Guerid S. The role of fat grafting in breast reconstruction. Clin
Plast Surg 2015;42(3):315–323, vii.
11. Streit L, Drazan L, Schneiderova M, et al. Intraoperative fat grafting into
the pectoralis and latissimus dorsi muscles-novel modification of
autologous breast reconstruction with extended latissimus dorsi flap.
Acta Chir Plast 2017;59(2):72–81.
12. Economides JM, Song DH. Latissimus dorsi and immediate fat transfer
(LIFT) for complete autologous breast reconstruction. Plast Reconstr
Surg Glob Open 2018;6(1):e1656.
13. Weichman KE, Broer PN, Tanna N, et al. The role of autologous fat
grafting in secondary microsurgical breast reconstruction. Ann Plast
Surg 2013;71(1):24–30.
14. Nelissen X, Lhoest F, Preud’Homme L. Refined method of lipofilling
following DIEP breast reconstruction: 3D analysis of graft survival.
Plast Reconstr Surg Glob Open 2015;3(9):e526.
15. Spear SL, Coles CN, Leung BK, et al. The safety, effectiveness, and
efficiency of autologous fat grafting in breast surgery. Plast Reconstr
Surg Glob Open 2016;4(8):e827.
16. Collett DJ, Rakhorst H, Lennox P, et al. Current risk estimate of breast
implant-associated anaplastic large cell lymphoma in textured breast
implants. Plast Reconstr Surg 2019;143(3S A Review of Breast
Implant-Associated Anaplastic Large Cell Lymphoma):30S–40S.
17. Magnusson MR, Cooter RD, Rakhorst H, et al. Breast implant illness: a
way forward. Plast Reconstr Surg 2019;143(3S A Review of Breast
Implant-Associated Anaplastic Large Cell Lymphoma):74S–81S.
18. Donofrio LM. Techniques in facial fat grafting. Aesthet Surg J
2008;28(6):681–687.
19. Li K, Gao J, Zhang Z, et al. Selection of donor site for fat grafting and
cell isolation. Aesthetic Plast Surg 2013;37(1):153–158.
20. Varghese J, Griffin M, Mosahebi A, et al. Systematic review of patient
factors affecting adipose stem cell viability and function: implications
for regenerative therapy. Stem Cell Res Ther 2017;8(1):45.
21. Erdim M, Tezel E, Numanoglu A, et al. The effects of the size of
liposuction cannula on adipocyte survival and the optimum temperature
for fat graft storage: an experimental study. J Plast Reconstr Aesthet
Surg 2009;62(9):1210–1214.
22. Rohrich RJ, Smith PD, Marcantonio DR, et al. The zones of adherence:
role in minimizing and preventing contour deformities in liposuction.
Plast Reconstr Surg 2001;107(6):1562–1569.
23. Canizares O Jr, Thomson JE, Allen RJ Jr, et al. The effect of processing
technique on fat graft survival. Plast Reconstr Surg 2017;140(5):933–
943.
24. Strong AL, Cederna PS, Rubin JP, et al. The current state of fat grafting:
a review of harvesting, processing, and injection techniques. Plast
Reconstr Surg 2015;136(4):897–912.
25. Cleveland EC, Albano NJ, Hazen A. Roll, spin, wash, or filter?
Processing of lipoaspirate for autologous fat grafting: an updated,
evidence-based review of the literature. Plast Reconstr Surg
2015;136(4):706–713.
26. Ansorge H, Garza JR, McCormack MC, et al. Autologous fat processing
via the Revolve system: quality and quantity of fat retention evaluated in
an animal model. Aesthet Surg J 2014;34(3):438–447.
27. Nguyen A, Pasyk KA, Bouvier TN, et al. Comparative study of survival
of autologous adipose tissue taken and transplanted by different
techniques. Plast Reconstr Surg 1990;85(3):378–386; discussion 387–
389.
28. Rieck B, Schlaak S. In vivo tracking of rat preadipocytes after
autologous transplantation. Ann Plast Surg 2003;51(3):294–300.
29. Coleman SR. Structural fat grafting: more than a permanent filler. Plast
Reconstr Surg 2006;118(3 Suppl):108S–120S.
30. James IB, Bourne DA, DiBernardo G, et al. The architecture of fat
grafting II: impact of cannula diameter. Plast Reconstr Surg
2018;142(5):1219–1225.
31. Lee JH, Kirkham JC, McCormack MC, et al. The effect of pressure and
shear on autologous fat grafting. Plast Reconstr Surg 2013;131(5):1125–
1136.
32. Hanke CW, Bernstein G, Bullock S. Safety of tumescent liposuction in
15,336 patients. National survey results. Dermatol Surg
1995;21(5):459–462.
33. Chia CT, Neinstein RM, Theodorou SJ. Evidence-based medicine:
liposuction. Plast Reconstr Surg 2017;139(1):267e–274e.
34. Dixit VV, Wagh MS. Unfavourable outcomes of liposuction and their
management. Indian J Plast Surg 2013;46(2):377–392.
35. Lehnhardt M, Homann HH, Daigeler A, et al. Major and lethal
complications of liposuction: a review of 72 cases in Germany between
1998 and 2002. Plast Reconstr Surg 2008;121(6):396e–403e.
36. Chow I, Alghoul MS, Khavanin N, et al. Is there a safe lipoaspirate
volume? A risk assessment model of liposuction volume as a function of
body mass index. Plast Reconstr Surg 2015;136(3):474–483.
37. Gutowski KA, ASPS Fat Graft Task Force. Current applications and
safety of autologous fat grafts: a report of the ASPS fat graft task force.
Plast Reconstr Surg 2009;124(1):272–280.
38. Sinna R, Delay E, Garson S, et al. Breast fat grafting (lipomodelling)
after extended latissimus dorsi flap breast reconstruction: a preliminary
report of 200 consecutive cases. J Plast Reconstr Aesthet Surg
2010;63(11):1769–1777.
39. Brondi RS, de Oliveira VM, Bagnoli F, et al. Autologous breast
reconstruction with the latissimus dorsi muscle with immediate fat
grafting: long-term results and patient satisfaction. Ann Plast Surg
2019;82(2):152–157.
40. Russe E, Kholosy H, Weitgasser L, et al. Autologous fat grafting for
enhancement of breast reconstruction with a transverse myocutaneous
gracilis flap: a cohort study. J Plast Reconstr Aesthet Surg
2018;71(11):1557–1562.
CHAPTER 94

Total Breast Reconstruction With


Autologous Fat Grafting and Tissue
Expansion
KIMBERLY S. KHOURI | ROGER KHOURI
HISTORY
Traditionally, the only available options to reconstruct total mastectomy
defects were implants and flaps. Now, there is a third alternative that can
empower women to regenerate their lost breasts without any incision, flaps,
or implants. Total breast reconstruction by autologous fat transfer (AFT) is
the new regenerative option (1). AFT is able to restore aesthetically pleasing
breasts that feel and look just like the original, with the added benefit of
normal sensation, something mastectomy patients miss the most (2). Since
the limit to success in megavolume AFT is a recipient large enough to
accommodate the large graft amount, and since fat injection has limited
ability to expand tissues, external vacuum expansion (EVE) is a necessary
adjunct. Total breast reconstruction with EVE and AFT is the game changer.
It is minimally invasive and gradually grows back in situ a totally autologous
natural breast mound.
EVE + AFT is in vivo tissue engineering. EVE generates in situ a three-
dimensional (3D) vascularized and innervated graft recipient scaffold where
large amounts of carefully seeded lipoaspirate can survive to regenerate the
breast mound. Growing back a breast mound, however, takes time. We build
the mound in a stepwise fashion with three to six procedures performed in
succession over the course of 6 to 15 months. While the number of
procedures may seem to be a hindrance or deterrence to patients, each
grafting session is relatively minimally invasive and can be done in an
outpatient setting. While proponents of implants and flaps claim a one-step
approach advantage, objective statistics show that most actually require five
to six procedures to complete their reconstruction. Additionally, it is the
overall cost–benefit ratio and the quality of the final result that matters and
should be emphasized when educating patients and making reconstructive
decisions. In this chapter, we elaborate on the principles behind large-volume
AFT and describe our technique that adheres to these principles. The results
speak for themselves.
INDICATIONS
This procedure is indicated for any woman who wishes to avoid invasive flap
transfer procedures and alloplastic implants, and desires to truly restore her
body and recover the most natural looking and sensate breasts. After the
devastation of mastectomy, the option of invasive flap transfer surgery leads
to patch-like results and additional scars. Implants, while considered less
surgery, still involves the insertion of foreign materials, which can be an
unsettling option to many women.
For young patients with congenital hypoplastic breasts, this procedure is
also ideally suited. If a patient has a mastectomy that is irradiated and/or has
suffered scarring from prior reconstruction failures, then the patient has to
understand that regenerating a new breast out of that irritated and scarred
tissue will take at least a year and, although minimally invasive, at least five
procedures.
Since EVE is crucial to the success of this technique, inability or
unwillingness to comply with the EVE preparation protocol is a major
drawback. In order to face the potential hindrance of patient noncompliance,
patients test wear EVE in the office for 20 to 30 minutes. While they become
comfortable with wearing the device, we educate them on its proper use. We
require confirmation of feasibility and consistency with its wear. From our
clinical experience, we have found that most intelligent educated women
would rather bear the inconvenience of EVE for a few hours a day over a few
weeks than subject themselves to the traditional surgical alternatives.
About 25% of patients in our Center are in the medical profession
themselves or have immediate relatives in the medical field. Therefore, EVE
is for educated women who are willing to work with the surgeon and
personally contribute to the goal of achieving a superior outcome through a
sequence of less-invasive procedures. Features that render a patient ideally
suited for this procedure: 1) no previous radiation to the breast; 2) bilateral
mastectomies, so we grow both breasts symmetrically and simultaneously; 3)
mastectomy defect without extensive scars from multiple previous
reconstruction failures; 4) ample amounts of fat she would appreciate losing
in exchange for regaining her breasts; 5) adamant about not weakening her
abdominal wall, losing a shoulder muscle, or having a foreign body implant;
and 6) intelligent, educated and compliant, because she is responsible for
doing the work of expansion.
CONTRAINDICATIONS
Smoking is the only absolute contraindication. Fat grafting has very poor
outcome in smokers.
Additionally, blood thinners, anticoagulants, or any
vitamin/herb/supplement that may prolong bleeding time must be
discontinued well before the surgery.
PREOPERATIVE PLANNING
Preoperatively, patient selection and education are paramount and cannot be
understated. The patient must understand that successful results depend upon
her active contribution, and that regeneration takes time. Typically, patients
come preselected; these are the ones who have rejected the flap and implant
alternatives or have been referred to the senior author for salvage
reconstruction. Additionally, many patients have close ties to the medical
field or have used the resources online to read about this technique and have
thus chosen the minimally invasive option that yields the most natural and
sensate breasts. Despite patient’s familiarity with the surgeries, the senior
author, as well as the general practitioner, must explain the process of EVE +
AFT since patient compliance with EVE is the foundation of the entire
procedure.
As described above, in the office it is important to have patients test wear
EVE for at least 20 minutes to ensure that they can comply with its daily use
(Fig. 94-1). Additionally, unless she has had a total mastectomy, all patients
are required to have preoperative MRIs in order to exclude occult pathology
and obtain a baseline of breast tissue quality and volume.
FIGURE 94-1 Preparation of the mastectomy recipient site. Patient wearing the
external vacuum expander for a bilateral mastectomy reconstruction. Preoperative
education of wearing EVE is pivotal for patient compliance and reconstructive
outcome. EVE is a key component to successfully graft the large volumes required
for total breast reconstruction. The device consists of two domes with silicone gel
rims that maintain a vacuum seal against the skin and a vacuum pump controlled by
a microprocessor that regulates the pressure. Through EVE we are able to create the
space necessary for fat graft survival and eliminate the bottleneck phenomenon
observed without adequate expansion.
OPERATIVE TECHNIQUE
Fundamental Concepts
Total breast reconstruction with fat grafting using EVE + AFT involves no
incision; therefore, it has no conventional exposure and no tissue dissection.
However, there is much more to successful AFT than syringes, cannulas, and
strong arms. Furthermore, there is no single panacea that will guarantee
success. The final outcome depends upon a succession of chain-linked steps
that need to be individually optimized. The quality of the result hinges upon
the weakest link among these individual steps. Just as in free flaps, a perfect
anastomosis does not guarantee success, since failure can still occur from
many other reasons. Each step in this regenerative process has the potential
for demise and the bottleneck determines the fate of the reconstruction.
The analogy of a farmer applies to these steps: large-volume fat grafting is
akin to farming a field. The 4S of success the farmer needs for an optimal
crop are: good seeds, a large well-prepared soil, a careful sowing technique,
and good support for the planted seedlings. The outcome is limited by the
rate-limiting step, and investing in non–rate-limiting steps is futile. It is
important to consider the process in its entirety and to avoid focusing on only
one factor while disregarding the others.

FIGURE 94-2 Principles of Fat Delivery. Microdroplets with radii less than 1.6 mm
= 17 μL (V = 4/3 πr2) will completely revascularize and 100% survive. A 1-mL
spherical droplet has a radius of approximately 6.2 mm. At best, only its outer 1.6-
mm shell will survive, leaving behind a necrotic center with a 4.6-mm radius (volume
= 0.41 mL). Therefore, even a tiny 1-mL droplet will have at least 41% necrosis.
When injected continuously through a cannula, microdroplets become cylindrical
microribbons. Ribbons with radii wider than 1.6 mm will inevitably suffer central
necrosis. (Modified from Eto et al. Reprinted with permission from Khouri RK Jr, Khouri
RK. Current clinical applications of fat grafting. Plast Reconstr Surg 2017;140(3):466e–
486e.)

Free fat grafts require blood supply to survive. Just like the familiar 2D
skin grafts, close graft-to-recipient contact is essential for revascularization.
Arbitrary bolus fat injections to plump up a breast mound are doomed for
failure, since lack of restoration of blood supply results in widespread
necrosis (3). It has been well established that an inserted fat graft droplet has
three layers or zones (4).
The most peripheral zone in direct contact with the recipient bed will
readily revascularize through neoangiogenesis. However, neoangiogenesis is
a slow process, and less than 1 mm of the outermost shell can reestablish
blood supply before the deeper adipocytes succumb to hypoxia. The
following layer is the regenerative zone, where only the more hypoxia-
resistant adipose-derived stem cells (ASCs) or stromal vascular fraction can
survive until revascularization reaches them and regenerates a new adipocyte
population. The deepest layer lies the necrotic zone, where no cells can
survive (5,6). Even under ideal circumstances, the maximum depth of the
graft survival zones is 1.6 mm, and the rate-limiting step in this process is
oxygen diffusion (7). Thus, revascularization depends upon this critical graft-
to-recipient interface, and in large-volume fat grafting, only “microdroplets”
or “microribbons” in the 3-mm (1.6 × 2) range revascularize and survive. In
order to optimize this graft-to-recipient interface, large graft volumes must be
skillfully and precisely delivered in a 3D distribution as a fine mist of 17-µL
(4/3 πr2) microdroplets. Since we use cannulas, passes 3 mm wide of
microribbons that do not coalesce must be delivered. Larger droplets or
ribbons will invariably suffer central necrosis (Fig. 94-2).
Fat Harvesting: The Seeds
Seeds are obtained by simple liposuction. We favor extensive tumescence of
the donor sites (more than 1 L per donor area) to obtain nonbloody aspirates
that can rapidly sediment. We harvest in a closed system with a constant low-
pressure (300 mm Hg) spring-activated syringe suction to minimize trauma to
the adipocytes (Fig. 94-3). Although vacuum pumps can also deliver
controlled low pressure, they are more destructive because they expose the fat
to high air flow in the necessary long tubing before they splash and bubble in
the rigid collection containers. We harvest with a thin, 2.7-mm cannula with
12 holes 1 × 2 mm each. This allows us to harvest smaller fat droplets
through tiny puncture wounds that leave minimal scars. Our preferred
cannula also has winglets at the opening that invite more fat, while the rough
barbs help harvest more stromal vascular tissue (8–9). The cannula is inserted
using 14G needle punctures all around the donor site. We preform liposuction
with crisscrossing passes through these multiple entry sites that leave
minimal scar. Using this technique, we harvest a thin even layer out of a wide
surface to address patients with a low BMI and no localized fat deposits.
In addition to fat cells, the lipoaspirate contains fibroblasts, endothelial
cells, pericytes, white blood cells, platelets, and ASCs. In our experience, we
find it important to graft back the entire “soup” and not pure adipocytes.
While some advocate removing inflammatory cells and debris through
filtration or washing, others champion the opposite and add platelets that are
rich in inflammatory agents. However, since there is no conclusive evidence
for the clinical advantage of adding to or removing substances from the
harvested adipose tissue, we prefer to take a purist approach, and the leave
the graft with its surrounding microenvironment as minimally manipulated as
possible. There is even mounting evidence that the entire harvested
liposuction matrix is required for optimal clinical result.

FIGURE 94-3 Barbed Cannula. Using a thin, 2.7-mm cannula with 12 holes 1 × 2
mm each, we can harvest smaller fat droplets through small puncture wounds that
leave minimal to no scars. Our preferred cannula also has winglets that invite more
fat and rough barbs that help harvest a greater stromal vascular fraction. To
minimize scarring, we insert the cannula through 14G needle punctures around the
donor site and liposuction in a crisscrossing pattern through multiple entry portals.

We allow the lipoaspirate to gravity sediment in the collection bag for a


few minutes and simply drain the infranatant fluid and combine the
supernatant fat into a lipografting bag. Along with most surgeons with
extensive experience with large-volume fat transfer, we no longer use
centrifugation. This is supported by a recent prospective controlled
randomized study (10). We prefer to use the Lipografter system to perform
the graft harvesting, preparation, and reinjection in a closed system (Fig. 94-
4).
Recipient Site Preparation: The Soil
In 3D grafting, we cannot graft more than what the recipient can expand to
accommodate; the stoichiometry of graft particles to recipient sites must
match. In postmastectomy breast reconstruction, the recipient site capacity is
quite limited. EVE helps to “prepare the soil” by increasing tissue
compliance.

FIGURE 94-4 Harvesting the seeds using Lipografter. We prefer to harvest with a
low-pressure low–air flow device to minimize trauma. The K-VAC syringe has a
ribbon spring that maintains an even 300-mm Hg aspiration pressure along the
entire excursion of the plunger. Pushing the plunger back in recocks the spring and
the large-bore tissue valve (AT-Valve) interposed between the syringe and the
harvesting cannula automatically purges the aspirate to the collection bag. This
closed system allows us to efficiently harvest with a controlled low-pressure syringe
without wasting precious time decannulating, cannulating, and switching syringes
(Lipografter; Lipocosm, Miami, FL). In order to loosen up the tissues for a smoother
harvest and to obtain a nonbloody aspirate that will rapidly sediment, the donor site
has to be extensively and tightly tumesced.
This enlarges the amount of graft the mastectomy defect can accept
without crowding or increasing the interstitial pressure to jeopardizing levels
of perfusion. Mechanistically, EVE stretches blood vessels and promotes
angiogenesis, which primes the tissues for better revascularization (11,12).
Along with the blood vessels, sensory nerves are also stretched and it is this
neoneurogenesis that restores sensation to the regenerated breast mound.
EVE also creates the skin envelope required for forming a breast mound.
EVE is designed like a bra that is meant to be worn every day for a few
hours for 2 to 3 weeks prior to surgery. From our extensive empiric
experience, we determined that the optimal therapeutic dose that prepares the
breast for AFT is a minimum of 200 hours over the 15 days immediately
preceding the grafting with a vacuum pressure that alternates 60–0–60 mm
Hg for 3 minutes on and one minute off.
Fat Graft Delivery: The Sowing
Fat grafting for breast reconstruction is a blind procedure that requires
craftsmanship, artistry, and adherence to fundamental principles. The goal is
to deliver microribbons of fat into separate contiguous tunnels in separate
planes. It is important to avoid coalescence, and to maintain an organized
pattern of grafting so that there is no under- or overgrafted site. Just like the
liposuction technique, where the tip of the cannula is not visualized, but an
even and diffuse harvesting can be achieved through multiple entry sites and
crisscrossing passes; we graft the fat in a similar fashion. Like a sprinkler
system, the way to evenly deliver specks of water over a broad expanse is to
randomly spray out a fine mist through many sprinkler heads, rather than
massively pouring a stream out of a few large-bore hoses. With this multiple
fine sprinkler system arrangement, we achieve “evenness through
randomness” (Fig. 94-5).
Graft delivery is the least studied and therefore, most often weakest link in
the chain of successful AFT. If we inject fat without moving the cannula, the
result is a localized blob of fat. If, on the other hand, we retract the cannula a
long distance while injecting the same amount of fat, the result is a thin
ribbon. The width of the ribbon delivered is therefore a function of volume
injected per distance of cannula travelled. Recognizing that 3 mm is the
widest ribbon that can revascularize, we calculate its surface area to be
approximately 10 mm2. Therefore, to deliver 1,000 mm3 (1 mL) as a
cylindrical ribbon with a 10-mm2 base, the cannula has to move 100 mm or
10 cm. This is how we derive 1-mL graft/10 cm of cannula excursion as the
cardinal rule of fat graft delivery. Note that this rule applies regardless of the
cannula diameter, the size of its hole, the pressure of injection, or the rate of
injection in mL/sec. Since the surgeon driving the cannula through the tissues
does not advance it much faster than 10 cm/sec, the pressure and shear forces
at 1 mL/sec are minimal, and the graft is delivered atraumatically as a fine
mist in all planes and all directions with high survivability.
FIGURE 94-5 Grafting the mastectomy defect. We prefer to graft with a 14G, single
hole spatulated tip grafting cannula connected to a 3-mL grafting syringe by means
of the AT-Valve in grafting mode. Because the fat is directly aspirated from the bag,
the valve prevents the wasted motions of cannulating and decannulating multiple
syringes. Since fat grafting to the breast is a blind procedure, it requires
craftsmanship and adherence to fundamental principles. The goal is to deliver
microribbons of fat into separate planes, to avoid coalescence, and to maintain an
organized pattern of grafting so that there is no under- or overgrafted site. Using a
single-holed cannula, we diffusely deliver specks of fat and achieve “evenness
through randomness.” We prefer to use a curved cannula as it is better at following
the curved contour of the body and at going through different paths.
Over the years, we have developed several mottos of graft delivery
craftsmanship: “no injection without motion,” “inject ≤1 mL/10 cm of
cannula motion,” “sprinkle with precision,” “smaller syringe leads to greater
precision,” and “no two motions in the same direction.” The subdermal and
subcutaneous planes are the most preferred sites for grafting since they
expand most with EVE, and augmenting these most superficial planes yields
more projection than injection in the deeper planes. Grafting the pectoral
muscle is ideal in immediate reconstruction because with the restrictive fascia
removed, the muscle/graft construct can swell unimpeded by any increase in
interstitial pressure. Furthermore fat grafting the exposed muscle is no longer
a blind procedure because the thin graft ribbons can be carefully inserted in
between the teased muscle fibers under direct vision. Grafting the
retropectoral space should be performed cautiously with the tip of the curved
cannula pointing upward to avoid a pneumothorax (Fig. 94-6).

FIGURE 94-6 Graft to recipient interface is the most important factor in graft
survival. Driving the cannula forward and retracting it creates tunnels through the
tissues. Injection during retraction fills the tunnels with fat ribbons. Injection
without motion delivers a fat blob, while injecting the same amount while retracting
a long distance leaves behind a thin ribbon. Therefore, the size of the delivered
ribbon is a function of the injection volume delivered per cm of cannula motion. The
thickest fat graft ribbon that can survive by neovascularization is 3 mm wide, or
approximately 10 mm2. To deliver 1000 mm3 (1 mL) as a 10 mm2 wide cylinder, the
cylinder has to be 100 mm long (10 cm). This means the excursion of the cannula
through the tissues should be at least 10 cm for every 1 mL of graft injected.
Straightforward physics shows that this simple rule is independent of the cannula
size and of the rate of delivery in mL/min. To avoid blob deliver and cavity
formation, there should be “no injection without motion.” It is also important that
the cannula makes a new, different tunnel with every stroke. Otherwise, it will refill
the same tunnel passage. There should be “no two motions in the same direction.”
(Reprinted with permission from Khouri RK Jr, Khouri RK. Current clinical applications
of fat grafting. Plast Reconstr Surg 2017;140(3):466e–486e.)

Postgraft Care: The Support


Just as we would immobilize and splint any graft, we recognize that fat grafts
should also be splinted postoperatively. We therefore recommend
immobilizing the breast as long as possible, up to 10 weeks to prevent
deflation and the shrinking of natural recoil. We place an adherent
conforming splint that immobilizes the graft to help angiogenesis.
Furthermore, by counteracting recoil, the splint places the tissue under
tension and acts as a passive external expander. Alternatively, if the patient
does not tolerate the splint we resume EVE at the now constant 20 mm Hg.
This postgrafting care also preserves the postoperative swelling and creates a
chronic edema state that is apidogenic.12 Adhering to these straightforward
principles allows us to maximize the likelihood of obtaining consistently
favorable results.
Fundamental Concepts of Tissue Augmentation With Fat
Grafting
Percentage graft survival gives little insight to what truly matters in large-
volume augmentation. To regenerate a breast mound out of a mastectomy
defect, the goal is volume augmentation with healthy well-vascularized fat.
Small amounts grafted into a large recipient might have excellent percentage
survival, but will result in minimal augmentation. Therefore, percentage
volume augmentation, which is volume increase relative to the original
recipient site volume, is a much more relevant outcome measure than
percentage graft survival. In contrast to most of the literature, we submit that
the most relevant measure of success should be percentage volume
augmentation and not percentage graft survival (Fig. 94-7).
With ideal grafting conditions, the maximum percentage augmentation
with revascularized live fat can rarely exceed 50%. This is typically reached
at the peak of the recipient capacity to accept the graft. Grafting beyond
recipient capacity is counterproductive. Grafted fat does not significantly
stretch tissue, so we cannot expect it to behave like a tissue expander and at
the same time survive the pressure of expansion. In a primed and pre-
expanded recipient, more grafted fat can survive. Therefore, through EVE,
doubling or tripling the recipient capacity allows more of the diffusely
injected graft to occupy the expanded scaffold without crowding, confluence,
or increase in interstitial pressure. Our experience has shown that tripling of
the recipient volume through EVE prior to grafting typically results in
doubling of the original breast volume.
Practical Techniques That Adhere to Above Principles
Donor Site Marking
Our preferred harvesting site is the posterior flank and upper inner thighs.
The “no-harvest” zones include the buttocks and any contour concavity since
these are worsened by liposuction.

Preoperative Estimation of Graft Amount


The amount of graft harvested must match the recipient capacity. To estimate
recipient site capacity we resort to the “palm and pinch” technique. This
technique allows us to determine the surface, the thickness, and the
compliance of the recipient site. As a rough estimate of the recipient volume,
we employ the “palm measure.” Using the estimate of an average male
surgeon’s hand to be 20 cm from the tips of the fingers to the wrist and 10 cm
across, we use a flat palm over the recipient to measure the surface area as a
fraction or a multiple of a 200-cm2 palm.
We employ the “pinch measure” by pinching and folding over the
subcutaneous fat to give an estimate of tissue thickness and compliance. Even
the most lax, unscarred recipient can accept, at best, a doubling of thickness
before reaching maximal capacity. Since the average mastectomy surface
area is less than 300 cm2, and the average thickness is less than 2 cm, we
rarely ever graft more than 600 mL per breast. Considering the scarring effect
of the mastectomy, we actually rarely graft more than 400 mL of loosely
sedimented fat per breast.
FIGURE 94-7 Augmentation versus Percentage Survival. The amount of graft must
match the capacity of the recipient to accommodate and revascularize it. With small
graft amounts and excellent craftsmanship in graft delivery, percentage survival
(black curve) remains very high until the recipient reaches maximal capacity (blue
region). Beyond this point, percentage survival steeply drops. Even with optimal
insertion of microdroplets that do not coalesce, the added graft also increases
interstitial fluid pressure to levels that choke capillary perfusion. Similarly, with
small graft amounts, percentage augmentation (blue curve) is modest despite
excellent graft survival. With increasing graft amounts, percentage augmentation
increases until maximum capacity is reached. Beyond this point, additional grafting
is counterproductive as it causes more necrosis worsening augmentation. The goal is
to therefore stay as close as possible to recipient maximal capacity without
overgrafting and dramatically falling off the cliff. Pre-expansion with EVE increases
the maximal recipient capacity and shifts the curve to the right to increase maximum
percentage augmentation. A measure of percentage graft survival therefore gives
little insight to volume augmentation, only about this relative mismatch. Since
volume augmentation is what really matters, the more relevant measure of success
should be percentage volume augmentation. This important fact is counter to most of
the literature that erroneously still uses percentage survival as the standard
yardstick of success in fat grafting. (Reprinted with permission from Khouri RK Jr,
Khouri RK. Current clinical applications of fat grafting. Plast Reconstr Surg
2017;140(3):466e–486e.)

We use the same palm and pinch method to calculate donor-site


availability. This method is applicable even for thin patients since a 0.25-cm
layer of fat harvested over the surface area of a palm will yield 50 mL (200
cm2 × 0.25 cm). With our thin-cannula, multiple-needle puncture wound
entry, we can therefore safely harvest as a thin even layer 250 mL solely from
the anterior surface of a woman’s thigh that has five “palm measures.”
Patients are rarely turned away for lack of available fat. From clinical
experience, we prefer thin patients to overweight ones, as their fat has more
cells and less oil.

Recipient Site Marking


We mark the breast using a clock face for reference, from 12 noon and
proceeding in a clockwise fashion around the breast. In the lower half, we fan
out multiple radial passes a few degrees apart, placing microribbons of fat in
either the subdermal or deeper subcutaneous spaces. We generally alternate
each plane for odd- or even-numbered clock-face hours. The upper half is
reserved for the deepest muscular and submuscular planes. The 9 to 11
o’clock positions are ideal for grafting the pectoralis muscle.
We conceptually divide the recipient into layers or planes that need to be
evenly filled and distended. The ideal graft recipient construct should
conceptually resemble a mille-feuille, or Napoleon French pastry with 3-mm
graft layers alternating with recipient scaffold. We therefore plan to fill first
the most superficial, immediately subdermal layer, after which we fill a
subcutaneous fat layer a few millimeters deeper, then the muscular layer, and
finally the deepest submuscular.
To ensure that no fat cell is more than 1.5 mm from a recipient capillary,
we deliver less than 1 mL per 10 cm of cannula excursion. Realizing that this
degree of precision can only be achieved with small syringes we use a 3-mL
syringe with a 14G (2.4-mm) 25-cm long curved and spatulated-tip single-
hole cannula to deliver approximately 2.5 mL per complete cannula pass.
This adheres to the 0.1 mL/cm cardinal rule of fat grafting.

Grafting Technique
The entry sites are made using a 14G hypodermic needle and are allowed to
heal without stitches. Using 3-mL syringes for large-volume AFT requires
hundreds of syringe switches. In order to remain efficient and maintain
sprinkling microribbons of fat, we use a two-way large-bore tissue valve
(Lipografter; MTF, Edison, NJ) that transfers fat from the collection bag to
the syringe and then to the patient automatically, without the unnecessary
wasted time and motion of cannulating and decannulating.

Ancillary Procedures
Rigottomy: Contractures of the mastectomy tissue is seen after infection,
radiation, or scarring from previous surgery. Restoring a breast mound
necessitates the release of scar bands and a reorganization of the fibrous
framework. Direct scar excision and open surgical release must be avoided
since this will create cavities, which when grafted, will lead to a graft that
lacks a vascular recipient scaffold and a poor graft-to-recipient interface.
Cavity is the enemy of grafts. Large cuts to release restrictive scars lead to
cavities where the graft will die. To release and expand tethering scars
without creating cavities, the percutaneous needle mesh release or
“Rigottomy” was developed by Dr. Rigotti. Using 18G needles, or preferably
safer, nonhollow solid 1.1-mm cutting needles (K-Needles, Lipocosm,
Miami, FL), we inflict multiple short nicks inside the contracted tissue to
create a 3D mesh that can expand the scar with microcavities where the fat
graft can revascularize and survive. However, it is important to realize that
too much release will create large cavities and also destroy the recipient
scaffold. We are more liberal with Rigottomies if the patient has been well
prepared with EVE as it increases the capillary density to preserve a vascular
network despite more extensive meshing (Fig. 94-8).
FIGURE 94-8 Rigottomy. Cicatrix to matrix. Multiple small punctures can expand a
tight scar and turn it into a recipient scaffold for fat grafts. The result is a larger,
softer, construct with more fat and less scar. However, only microcavities created by
smaller punctures preserve graft-to-recipient contact and succeed. Larger cuts
create cavities where the graft will die from poor graft-to-recipient interface. It is
therefore important to avoid overmeshing which might lead to necrosis and more
scars. (Reprinted with permission from Khouri RK, Rigotti G, Cardoso E, et al.
Megavolume autologous fat transfer: part II. Practice and techniques. Plast Reconstr Surg
2014;133(6):1369–1377.)

Reverse Abdominoplasty and Fat Transfer or RAFT Procedure


The RAFT is an incision-free flap tissue transfer and a very valuable adjunct
to fat grafting the breast. Over the past three decades, the senior author has
advanced in his breast reconstruction practice from free flaps to free grafts to
incision-free flaps that complement the grafts. Realizing that even with the
best techniques, avascular grafts cannot reliably transfer as much tissue as
flaps we have refined a technique that allows us to percutaneously dissect and
transfer both a lateral thoracic flap and a reverse abdominoplasty flap without
any incision. The RAFT procedure consists of inserting a purse-string
suspension suture that can recruit 2 to 7 cm of circummammary skin and 100
to 250 mL of tissue that can mushroom up a significant breast mound and
define new breast folds. The required RAFT Suture (Lipocosm, Miami, FL)
is a specially designed 35-cm long double-pointed needle with no. 2 PDS
suture swaged 3 cm from one of the ends. The needle point is long and sabre-
like flat to act as rudder that maintains a constant depth throughout its long
passes in the subdermal plane of the new recruited mammary folds. It is
double pointed such that, by always keeping the tip of the needle in the
dermis, the thread never exits the skin and dimpling is avoided.
RAFT Suture Insertion and Flap Dissection: Starting just below the
midclavicle, we introduce the RAFT needle pointing it toward the sternum at
angle of Louis. We then steer it caudally in a deep plane just above the body
of sternum till the beginning of the median mammary fold. From there on, we
drive the needle more superficial to pursue a subdermal plane until the end of
the lateral mammary fold below the axilla. At this point, we pass the needle
deep under the pectoralis to exit at the subclavicular entry site and complete
the loop. Pulling the suture creates a purse- string recruitment effect.
Inserting the purse-string suture, however, is not enough. It is important to
dissect and elevate the flap in order to advance it without tension and to
create a wound injury interface for the tissues to heal and hold in their new
position. We achieve this with a Rigottomy procedure that mesh expands the
recruited abdominal and lateral thoracic tissues and, without making an
incision, undermines the advanced tissues under the new breast fold to better
define it. We usually insert two suture loops along the same path to ensure a
smooth mammary fold and a more secure fixation. The sutures should be tied
under no tension and the knot is simply passed through and suspended to the
pectoralis (Figs. 94-9 and 94-10).
FIGURE 94-9 A: Bilateral mastectomies with immediate breast reconstruction. We
planned to bank the nipples in her C-section scar because preserving them would
leave too much skin redundancy that will fold in and will be difficult to iron out in
subsequent stages. Note the mastectomy incisions, and the thigh liposuction donor
sites. We often harvest the fat during the mastectomy resection. B: Three days post
mastectomy. We grafted 300 mL of sedimented fat to each mastectomy defect. The
grafts were meticulously delivered as thin ribbons in between the exposed muscle
fibers. We also grafted a thin layer in the submuscular plane, the lateral thoracic
fascia, and the base of the skin flaps. We carefully avoided graft coalescence and lake
formations. The nipple are olar complex is grafted in the C-section scar and held
with tie over dressing. Note the moderate fullness already achieved with this
immediate grafting session. C: Result 2 months post mastectomy. By now the skin
flaps have adhered to the muscle and she is ready to start external expansion. She
has a moderate amount of fullness, but has residual skin folds in the inner lower
quadrants of her breasts. The patient is now given the external vacuum expander
(EVE) and instructed to use it for a total of 200 hours over the next 15 days in
preparation for her next grafting session. This will expand the skin envelope, stretch
out the folds, and generate a recipient scaffold for the grafts. D. She is now 12 weeks
post mastectomy and presents to her second grafting session still wearing the EVE
device.
GENETIC RISKS
Breast reconstruction with AFT + EVE is a series of small outpatient
procedures. Patients return to home on the same day as surgery and resume
light level activities within a week, which is unlike the massive physiologic
insult of an in-patient flap transfer.
The most common complication is fat necrosis. It is the result of
overgrafting, blob grafting, and cavity grafting. Small necrotic cysts will
resorb with time, moderate-sized cysts can be simply aspirated, and larger
cysts will lead to hard lumps that eventually calcify. Larger scars from fat
necrosis can be managed by resection and grafting again. Necrotic tissue, a
growth medium for bacteria, might lead to infection, ulceration, and more
tissue loss. Infection is rare, but it commonly occurs when there is tissue
necrosis from failure to revascularize or from too extensive of Rigottomies
that destroy the vascular network required for tissue perfusion. Fortunately,
unless infection ensues, failure of graft to survive is a relatively benign
complication treated by repeat fat grafting. In essence, if we fail to achieve a
satisfactory breast mound in three sessions of fat grafting, we might have to
graft once, or twice more to complete the reconstruction. However, the
radiated mastectomies will require at least two additional grafting sessions to
reverse the radiation damage to the tissues.

FIGURE 94-10 A: Appearance of the EVE expanded mastectomy defect prior to


grafting. She now has a much larger recipient, has stretched out the skin envelope
and partially released the abnormal folds caused by the skin excess. Notice the
expected areas of skin irritation around the breast caused by the EVE device. Its
absence is an indication she has not fully complied with use of the device. Harvesting
the fat from the posterior flanks will be performed in the prone position. We will
carefully evenly and diffusely graft 400 mL of dilute lipoaspirate through through 8
to 10 needle puncture sites all around the breast. B: Appearance 12 weeks later and
just prior to her third grafting session. (Second post mastectomy). This time, the
patient did not comply with the EVE device wear and has not expanded. We will
compensate for this by performing a Reverse Abdominoplasty Fat Transfer (RAFT)
procedure. This is an incision free flap recruitment of upper abdominal and lateral
thoracic tissue. The Outline of the RAFT purse string suture is marked in green. We
will harvest the fat from the abdomen and lateral chest to facilitate cephalic and
medial mobilization of these tissues. C: Appearance 3 days following that procedure.
Because she was not expanded, we grafted only 300 mL of dilute fat. The RAFT
purse string has helped mushroom out a breast mound, added about 150 mL of
stable graft tissue and defined nice mammary breast folds. D: One year later after a
minor touch up with transfer of the banked NAC. She has regrown in situ,
autologous, soft, sensate breasts without any additional scars while benefiting from a
few liposuction body contouring procedures.

Pneumothorax is a complication that still occurs in 1% of the procedures. It


is usually recognized in the recovery area by low-oxygen saturation and we
treat it with chest tube drainage for a couple of days.
CONCLUSION
In this chapter, an overview of preoperative patient selection, education, and
surgical markings as well as the established principles and techniques
necessary for achieving an optimal outcome are outlined. By adhering to
these techniques, total breast reconstruction with AFT can yield consistent
and highly satisfactory results. The outpatient and less-intensive, less–
complication-prone procedures reduce health care cost without compromising
quality.
Although many individual factors have been singled as being important for
graft survival, it is clear that no single additive or processing method serves
as a panacea. Like a famer planting seeds, the final outcome depends upon a
succession of chain-linked steps that need to be individually optimized: crops
will only grow when the farmer has obtained good seeds, has well prepared
the soil, adhered to a careful precise, diffuse, and even sowing technique, and
provided good support for the planted seedlings. Fat graft surgery must be
approached with the same degree of craftsmanship as microvascular free flap
surgery. Since the limit to success in megavolume AFT is a recipient large
enough to accommodate the large graft amount, and since fat injection has
limited ability to expand tissues, EVE is a necessary adjunct to large-volume
fat transfer. Finally, complementing free grafts with the RAFT incision free
flap has reduced the number of procedures required to achieve an optimal
result and has been the single most important addition to the breast
reconstruction armamentarium.

REFERENCES

1. Khouri KS, Khouri RK, Khouri RK. The third postmastectomy


reconstruction option—autologous fat transfer. JAMA Surg
2019;154(1):63–64.
2. Rabin R. After Mastectomies, an Unexpected Blow: Numb New
Breasts. New York Times. Jan 29 2017.
https://www.nytimes.com/2017/01/29/well/live/after-mastectomies-an-
unexpected-blow-numb-new-breasts.html
3. Del Vecchio D, Del Vecchio S. The graft-to-capacity ratio: volumetric
planning in large-volume fat transplantation. Plast Reconstr Surg
2014;133(3):561–569.
4. Eto H, Suga H, Aoi N, et al. The fate of adipocytes after
nonvascularized fat grafting: evidence of early death and replacement of
adipocytes. Plast Reconstr Surg 2012;129:1081–1092.
5. Khouri RK, Rigotti G, Cardoso E, et al. Megavolume autologous fat
transfer: part I theory and principles. Plast Reconstr Surg
2014;133(3):550–557.
6. Bourne DA, James IB, Wang SS, et al. The architecture of fat grafting:
what lies beneath the surface. Plast Reconstr Surg 2016;137(3):1072–
1079.
7. Khouri RK, Khouri RE, Lujan-Hernandez JR, et al. Diffusion and
perfusion: the keys to fat grafting. Plastic Surgery Global Open
2014;2(9):e220.
8. Lujan-Hernandez J, Lancerotto L, Nabzdyk C, et al. Induction of
adipogenesis by external volume expansion. Plast Reconstr Surg
2016;137:122–131.
9. Khouri RK, Khouri RK. Current clinical applications of fat grafting.
Plast Reconstr Surg 2017;140(3):466e–486e.
10. Caggiati A, Germani A, Di Carlo A, et al. Naturally adipose stromal
cell-enriched fat graft: comparative polychromatic flow cytometry study
of fat harvested by barbed or blunt multihole cannula. Aesthet Surg J
2017;37(5):591–602.
11. Kosowski T, Rigotti G, Khouri K. Tissue-engineered autologous breast
regeneration with Brava-assisted fat grafting. Clin Plast Surg
2015;42(3):325–337.
12. Khouri RK, Rigotti G, Cardoso E, et al. Megavolume autologous fat
transfer: Part II. Practice and techniques. Plast Reconstr Surg
2014;133:1369–1377.
SECTION VII

Augmentation & Augmentation Mastopexy &


Revisionary Augmentation
95 Augmentation Mammaplasty: General Considerations
96 Augmentation in Patient With Congenital Breast Deformity
97 Patient Education in Breast Augmentation
98 Inframammary Approach to Breast Augmentation
99 The Periareolar Approach to Augmentation Mammaplasty
100 Transaxillary Breast Augmentation
101 Subfascial Breast Augmentation
102 The Inframammary Approach to Augmentation Mammaplasty
103 Shaped Implant in Breast Augmentation
104 Light-Weight Implants in Breast Augmentation
105 Polyurethane Implants in Aesthetic Breast Surgery
106 Augmentation Mastopexy: General Considerations
107 Breast Augmentation Mastopexy—Safe and Simplified
108 Augmentation-Mastopexy With Shaped or Round Implants, Is There a
Difference?
109 Avoiding Pitfalls With Mastopexy-Augmentation
110 Management of Recurrent Ptosis Following Augmentation Mastopexy
111 Liposuction Mastopexy
112 Neopectoral Technique for Implant Malposition
113 Subpectoral “Dual-plane” Conversion for Treating Aesthetic Concerns
After Breast Augmentation
114 Secondary Revision of the Augmented Breast
115 Combining Lipofill and Small Implants for Breast Augmentation
116 Breast Revisionary Surgery and the Role of Acellular Dermal Matrix
and Bioabsorbable Mesh
CHAPTER 95

Augmentation Mammaplasty: General


Considerations
ALLEN GABRIEL | G. PATRICK MAXWELL

Glandular hypomastia may occur as a developmental or involutional process


and affects a significant number of women in the United States.
Developmental hypomastia is often seen as primary mammary hypoplasia or
as a sequela of thoracic hypoplasia (Poland syndrome) or other chest wall
deformity. Involutional hypomastia may develop in the postpartum setting
and may be exacerbated by breastfeeding or significant weight loss.
Compared to the norm, inadequate breast volume may lead to a negative
body image, feelings of inadequacy, and low self-esteem (1). These
disturbances may adversely affect a patient’s interpersonal relationships,
sexual fulfilment, and quality of life (2).
There has been a steady increase in breast augmentation surgery with the
emerging importance of body image, changes in societal expectations, and
the increasing acceptance of aesthetic surgery in the United States.
Augmentation mammaplasty is currently the most frequently performed
cosmetic surgical procedure in women in the United States and has been
since 2006 (3). In this chapter, we review the history, operative planning and
technique, and some perioperative and late complications of breast
augmentation. The evolution of modern breast implants is described and the
controversy surrounding the use of silicone gel in breast augmentation is
discussed.
HISTORY
The first report of successful breast augmentation appeared in 1895 in which
Czerny described transplanting a lipoma from the trunk to the breast in a
patient deformed by a partial mastectomy (4). In 1954, Longacre described a
local dermal fat flap for augmentation of the breast (5). Eventually, both
adipose tissue and omentum were also used to augment the breast. However,
the clinical results of using autogenous tissue for breast augmentation were
often unpredictable and unacceptable (6).
During the 1950s and 1960s, breast augmentation with solid alloplastic
materials was carried out using polyurethane, polytetrafluoroethylene
(Teflon), and expanded polyvinyl alcohol formaldehyde (Ivalon sponge).
Ultimately, the use of these materials was discontinued after patients
developed local tissue reactions, firmness, distortion of the breast, and
significant discomfort (7). Various other solid and semisolid materials have
been injected directly into the breast parenchyma for augmentation, including
epoxy resin, shellac, beeswax, paraffin, petroleum jelly, and liquid silicone.
Liquid silicone (polydimethyl siloxane) was originally developed in the
aeronautics industry during World War II. In 1961, Uchida reported the
injection of liquid silicone into the breast for breast augmentation (8).
Unfortunately, injection of liquid silicone resulted in frequent complications,
including recurrent infections, chronic inflammation, drainage, granuloma
formation, and even necrosis (9,10). Breast augmentation by injection of free
liquid silicone was abandoned in the United States in light of these
complications.
The modern breast implant is a two-component prosthetic device
manufactured with a nearly impermeable silicone elastomer shell filled with a
stable filling material, consisting of either saline solution or silicone gel. This
shell plus filler implant was originally developed by Cronin and Gerow in
1962 using silicone gel as the filling material contained within a thin, smooth
silicone elastomer shell (11). Since that time, both silicone gel– and saline-
filled implants have undergone several technical alterations and
improvements.
BREAST IMPLANT EVOLUTION

Saline-Filled Implants
The use of inflatable saline-filled breast implants was first reported in 1965
by Arion in France (12). The saline-filled implant was developed in order to
allow the noninflated implant to be introduced through a relatively small
incision, followed by inflation of the implant in situ (13). Although the
incidence of periprosthetic capsular contracture was lower with the saline-
filled implants compared to the earlier generation of silicone gel–filled
implants, the deflation rate was initially quite high. The original saline-filled
implants manufactured by Simiplast in France had a deflation rate of 75% at
3 years and was subsequently withdrawn from the market. In 1968, Heyer-
Schulte Company introduced its version of the inflatable saline-filled breast
implant (Mentor 1800) in the United States.
The thin, platinum-cured shell and the leaflet-style retention valve were
two features of the early saline-filled implants that contributed to their high
deflation rate (14). The silicone elastomer shell of the saline-filled implant
has been improved by making it thicker and by employing a new room-
temperature vulcanization process. This process is used in the manufacture of
all saline-filled implant shells currently available from Allergan (formerly
Inamed Corporation and McGhan Medical) and from Johnson & Johnson
(formerly Mentor Corporation [which acquired Heyer-Schulte]). The third
breast implant manufacturer in the United States, Sientra Inc., does not
produce saline-filled implants. The original Heyer-Schulte saline-filled
implant shell had a leaflet-style retention valve through which the implant
was inflated (15). A more reliable diaphragm valve was developed and is
currently incorporated into the shell of all modern saline-filled breast
implants.
Saline-filled implants are manufactured with a range of recommended fill
volumes. Mild breast asymmetry may be corrected by taking advantage of
this range of recommended fill volumes during placement of the implants.
Underfilling saline-filled implants may lead to increased deflation rates due
to folding or friction subjected to the implant shell and is not recommended.
Underfilling saline-filled implants may also lead to a wrinkled appearance or
rippling of the breast in certain positions. Saline-filled implants have
historically performed better when slightly overfilled and when placed under
thicker soft tissue coverage. Although these implants may be slightly
overfilled, aggressive overfilling may lead to a more spherical shape and
scalloping along the implant edge with knuckle-like palpability and unnatural
firmness. Another potential disadvantage of saline-filled implants is that the
consistency of these implants on palpation is similar to that of water instead
of the more viscous feel of natural breast tissue. Several types of saline-filled
breast implants are available from Allergan and Mentor with different surface
textures, shapes, and degrees of projection (Table 95-1). Of note, textured
implants from Allergan were withdrawn from the worldwide market on July
24, 2019 (16). The withdrawal was initiated after the U.S. Food and Drug
Administration (FDA) requested that Allergan recall all BIOCELL textured
breast implants and tissue expanders marketed in the United States due to the
risk of breast implant–associated anaplastic large cell lymphoma (BIA-
ALCL).
Silicone Gel–Filled Implants
Silicone Chemistry
Silicone is a mixture of semi-inorganic polymeric molecules composed of
varying lengths of polydimethyl siloxane [(CH3)2–SiO] monomer chains.
The physical properties of silicones are quite variable, depending on the
average polymer chain length and the degree of cross-linking between the
polymer chains (17). Liquid silicones are polymers with a relatively short
average length and very little cross-linking. They have the consistency of an
oily fluid and are frequently used as lubricants in pharmaceuticals and
medical devices. Silicone gels can be produced of varying viscosity by
progressively increasing the length of the polymer chains or the degree of
cross-linking. The consistency of silicone gels may vary widely from a soft,
sticky gel with fluid properties to a firm, cohesive gel exhibiting shape
retention or form stability, depending upon the polymer chain length and the
degree of cross-linking. Extensive chemical cross-linking of the silicone gel
polymer will produce a solid form of silicone referred to as an elastomer with
a flexible, rubber-like quality. Silicone elastomers are used for the
manufacture of facial implants, tissue expanders, and the outer shell of all
breast prostheses. The versatility of these compounds has made them
indispensable in aerospace engineering, medical devices, and the
pharmaceutical industry.

TABLE 95-1 Saline-Filled Breast Implants


Model Surface Shape Projection
Natrelle Style 68LP Smooth Round Low
Natrelle Style 68MP Smooth Round Moderate
Natrelle Style 68HP Smooth Round High
Mentor Style 1600 Smooth Round Moderate
Mentor Style 2000 Smooth Round Moderate plus
Mentor Style 2600 Siltex Textured Round Moderate
Mentor Style 3000 Smooth Round High
Mentor Style 2700 Siltex Textured Anatomic High
Contour
Mentor Style 2900 Siltex Textured Anatomic Moderate
Contour
Mentor Spectrum Style Smooth Round Moderate
1400
Mentor Spectrum Style Textured Round Moderate
2400 Siltex
Mentor Spectrum Style Textured Anatomic High
2500 Siltex Contour

Evolution of Silicone Gel–Filled Implants


The first-generation silicone gel–filled implant was introduced in 1962 by
Cronin and Gerow and was manufactured by Dow Corning Corporation (11).
The shell of the first-generation implant was constructed using a thick,
smooth silicone elastomer as a two-piece envelope with a seam along the
periphery (Table 95-2). The shell was filled with a moderately viscous
silicone gel. The implant was anatomically shaped (teardrop) and had several
Dacron fixation patches on the posterior aspect to help maintain the proper
position of the implant. Unfortunately, these early devices had a relatively
high contracture rate that encouraged implant manufacturers to develop
second-generation silicone gel–filled implants.
In the 1970s, the second-generation silicone implants were developed in an
effort to reduce the incidence of capsular contracture with a thinner, seamless
shell and without Dacron patches incorporated into the shell. These implants
were round in shape (nonanatomic) and filled with a less viscous silicone gel
to promote a natural feel. However, the second-generation breast implants
were plagued by diffusion or bleed of small silicone molecules into the
periprosthetic intracapsular space due to their thin, permeable shell and low-
viscosity, silicone gel filler. This diffused silicone may be encountered as an
oily, sticky residue surrounding the implant within the periprosthetic capsule
during explantation of older silicone-filled implants. Microscopic silicone
particles have been shown to be present within the periprosthetic tissues and
even within the draining lymphatics and axillary lymph nodes (18). The
phenomenon of silicone bleed has not been shown to create significant local
or systemic problems (19). However, long-term device failure issues have
plagued these second-generation devices due to the thin, weak, shell
composition.

TABLE 95-2 Evolution of Silicone Gel–Filled Breast Implants


First generation (1962–1970) Thick, two-piece shell
Smooth surface with Dacron fixation
patches
Anatomically shaped (teardrop)
Viscous silicone gel
Second generation (1970–1982) Thin, slightly permeable shell
Smooth surface (no Dacron patches)
Round shape
Less viscous silicone gel
Third generation (1982–1992) Thick, strong, low-bleed shell
Smooth surface
Round shape
More viscous silicone gel
Fourth generation (1993–present) Thick, strong, low-bleed shella
Smooth and textured surfaces
Round and anatomically shaped
More viscous (cohesive) silicone gela
Fifth generation (1993–present) Thick, strong, low-bleed shella
Smooth and textured surfaces
Round and diverse anatomic shapes
Enhanced cohesive and form-stable
silicone gel

aInaccordance with technical parameters established by the American Society for Testing
Methodology.
The development of the third-generation, silicone gel–filled implants in the
1980s focused on improving the strength and integrity of the shell in order to
reduce silicone gel bleed from intact implants and to reduce implant rupture
and subsequent gel migration. Inamed Corporation (now Allergan) developed
a multilayer implant shell in which a patented barrier coat material is
sandwiched between two layers of silicone elastomer (Intrashield). Mentor
Corporation (now Johnson & Johnson) also developed a shell for their
silicone gel–filled breast implants, which consists of a multilayered silicone
elastomer. These third-generation prostheses reduced gel bleed to an almost
immeasurable level and significantly lowered device shell failure rate.
After the FDA required the temporary removal of third-generation silicone
gel implants from the U.S. market in 1992, the fourth-generation gel devices
evolved for their market reintroduction. These silicone gel breast implants
were designed under more stringent American Society for Testing
Methodology and FDA-influenced criteria for shell thickness and gel
cohesiveness. Furthermore, the fourth-generation devices were manufactured
with improved quality control and with a wider variety of surface textures
and implant shapes (Table 95-3).
The development of the anatomically shaped, fourth generation of gel
implants was based on recognition that breast augmentation must account for
the individual patient’s breast shape and chest wall dimensions in order to
produce the most natural result. The shells of anatomically shaped breast
implants are manufactured with a textured surface to encourage ingrowth and
disorganization of the periprosthetic scar tissue and to reduce the incidence of
implant rotation and resulting breast deformity (20). Figure 95-1 shows
micrographs of the textured surface of several implants.
With the evolution of the fifth-generation silicone gel implants (Table 95-
3), the concept of anatomically shaped implants was carried to the next level.
The BioDimensional Planning System in which a matrix of 12 possible
combinations of implant height and projection was introduced for the specific
needs of the individual patient. These anatomically shaped (style 410)
implants, which are no longer available, came in a range of volumes and any
of the 12 combinations of low, moderate, and full height with low, moderate,
full, and extra projection. The Contour Profile Gel (CPG) implant has been
designed by the Mentor Corporation with a more rounded and projecting
lower pole and a flatter, more sloping upper pole to yield a more natural
breast shape in breast augmentation and reconstruction. The OPUS shaped
implants, manufactured by Sientra, are available with a classic, round, or oval
base which provide varying degrees of projection and are designed to mimic
the look of a natural breast.

TABLE 95-3 Silicone Gel–Filled Breast Implants

It is believed that as the gel flows inferiorly with gravity, the upper portion
of the implant collapses due to a relatively decreased volume in the upper
pole. To combat this characteristic of silicone gel–filled implants efforts have
been made to develop fifth-generation devices containing more cohesive
silicone gel that exhibits less flow and more form stability (Table 95-3). The
development of these fifth-generation devices has resulted from advances in
the technology of silicone gel.

The Approval of Silicone Gel–Filled Implants


In 1976, the U.S. Congress passed the Medical Device Amendment to the
Food, Drug, and Cosmetic Act, which gave the FDA authority over
implantable medical devices (14). Breast implants that were currently
available at that time or those that were “substantially equivalent” were
allowed to remain in use until the FDA could formally review their safety and
efficacy. In 1988, the FDA called for the manufacturers of silicone gel–filled
implants to submit premarket approval applications providing data that could
substantiate the claim of safety and efficacy for these devices. In November
1991, the FDA convened an advisory panel of experts to evaluate the
manufacturers’ data and to hold public hearings. The advisory panel
concluded that more research was needed to establish the safety and efficacy
of silicone gel–filled breast implants but that these devices should remain
available for use by the general population while the clinical trials were
carried out.
Instead of ratifying the panel’s recommendation, the FDA commissioner
called for a voluntary moratorium on the use of all silicone gel–filled
implants. Further evaluation by the advisory panel led the commissioner to
rule in April 1992 that silicone gel breast implants were not necessarily
unsafe, but that the law required more data than the manufacturers had
supplied to establish the safety and efficacy of these devices (14). Although
the news media and the general public regard this moratorium as a ban on the
use of silicone gel–filled implants due to their supposed hazardous nature,
their use has never been officially banned. From 1992 to 2006, the use of
silicone gel–filled implants for aesthetic breast augmentation and breast
reconstruction was restricted to patients with breast deformities who
participated in clinical trials. Criteria and eligibility for enrolment in the
silicone gel–filled breast implant Adjunct Study was developed both by
Mentor (now Johnson & Johnson) and Inamed (now Allergan) (Table 95-4).
The manufacturers continued to improve their gel-filled products and
presented the results of the silicone gel–filled breast implant Adjunct Study to
the FDA. On November 17, 2006, the FDA approved the new and improved
silicone gel–filled breast implants produced by the two manufacturers for
breast reconstruction and for cosmetic breast augmentation. The approval was
given with a number of conditions, including a requirement to complete 10-
year studies on women who have already received the implants and a 10-year
study on the safety of the devices in 40,000 women.
FIGURE 95-1 A: Polyurethane foam gains tissue adherence and delaminates from
the implant. No longer available in the United States, this texture fostered the
development of textured silicone surfaces. B: Biocell is an aggressive silicone
textured surface that adheres to surrounding tissue by an adhesive effect. C: Siltex is
a less-aggressive silicone textured surface that does not demonstrate any adhesive
effect and does not gain tissue adherence. D: TRUE Texture is different from the
other textured product in that it falls in between and looks to combine characteristics
from both of the other textured products (BioCell and Siltex). (A–C from Maxwell
GP, Hammond DC. Breast implants: smooth versus textured. Adv Plast Reconstr Surg
1993;9:209–220; D from Stevens WG, Calobrace MB, Alizadeh K, et al. Ten-year core
study data for Sientra’s Food and Drug Administration-approved round and shaped breast
implants with cohesive silicone gel. Plast Reconstr Surg 2018;141(4S Sientra Shaped and
Round Cohesive Gel Implants):7S–19S.)

Alternative Filling Materials


Manufacturers of breast implants have developed alternative filler materials
in response to concerns about the safety of silicone gel (21). In 1991, the
Bioplasty Corporation introduced the Misti Gold implant, which uses
polyvinylpyrrolidone (PVP) as the filling material. The PVP filling material
is described as a bio-oncotic gel and is believed to be more radiolucent than
silicone. NovaMed acquired Bioplasty and still markets the PVP-filled
implant under the name NovaGold outside the United States. The PIP
Corporation in France developed breast implants filled with a hydrated
polysaccharide gel (hydrogel). However, there have been reports of swelling
of hydrogel and PVP-filled implants postoperatively due to the osmotic
pressure gradient. In December 2000, the British Medical Devices Agency
issued an alert citing a lack of studies that demonstrate the safety of these
implants. In 1994, the LipoMatrix Corporation developed the Trilucent
implant, which was filled with a triglyceride derived from soybean oil (21).
However, problems developed with oil bleed, tissue irritation, and a foul,
rancid odor. These implants were withdrawn from the market in 1999, and
none of the alternative filling material implants are currently available in the
United States.

TABLE 95-4 Inclusion Criteria for Participation in the Silicone Gel–Filled


Breast Implant Adjunct Clinical Study

I. Patient is female, 18 yrs of age or older, willing to sign informed


consent, and willing to follow study requirements
II. Reconstructive breast surgery
a. Postmastectomy or other oncologic surgery involving the breast
b. Posttraumatic injury involving the breast
III. Congenital or developmental deformity of the breast
a. Congenital breast absence
b. Poland syndrome
c. Thoracic hypoplasia
d. Tuberous breast deformity
e. Pectus excavatum/carinatum
f. Scoliosis, isolated rib deformities
IV. Acquired deformity
a. Severe ptosis requiring mastopexy
b. Advanced periprosthetic capsular contracture (Baker grade III or IV)
V. Revision of ruptured breast implant
a. Implant rupture after augmentation mammaplasty
b. Implant rupture after reconstructive breast surgery
VI. Saline-filled implants deemed unsuitable for medical reasons
a. Skin too thin
b. Insufficient soft tissue coverage
c. Severe wrinkling of skin

Based on Adjunct Study Enrollment Form 1 (McGhan Medical Corp.) and Preoperative Patient History
Record CRF Page 2–1 (Mentor Corp.).

The Absence of Evidence-Based Medicine


Of interest, silicone-containing compounds are ubiquitous in everyday life.
The general public has been exposed to them for more than 50 years in
consumer products such as hairsprays, suntan lotions, and moisturizing
creams. Silicones are extremely resistant to the action of enzymes when
implanted into living tissue largely due to their hydrophobic nature (17). This
makes silicone compounds extremely stable and inert. Silicones are often
used in the consumer safety testing industry as the standard to which all other
products are compared for biocompatibility (17). While elemental silicon and
silicone particles are detected in periprosthetic tissues, the biologic
significance of this finding remains undetermined and uncharacterized (22).
In one study, no significant difference was found in levels of antisilicone
antibodies between patients who had silicone elastomer tissue expanders and
control subjects (23).
Several clinical studies have shown no difference in the incidence of
autoimmune diseases in mastectomy patients receiving silicone gel–filled
implants compared to patients who had reconstruction with autogenous tissue
(24–27). Even meta-analysis research combining data from more than 87,000
women has revealed no association between silicone breast implants and
connective tissue diseases (28). In the modern era of evidence-based
medicine, it seems that the only exception to the rule of science is in the use
of silicone gel–filled breast implants, where lawsuits and hysteria supersede
science. Notably, virtually all industrialized nations in the world except the
United States use silicone gel implants almost exclusively for breast
augmentation.
SURGICAL GOALS AND TREATMENT

Patient Assessment
The initial consultation for augmentation should begin with open-ended
questions about the patient’s goals and expectations for the procedure.
Patients today often spent some time researching the procedure either through
friends or through the internet. The surgeon should be able to form an
impression of the patient as a well-informed, psychiatrically stable person
with appropriately realistic expectations for the procedure. Any concerns
about the patient’s level of understanding, unrealistic expectations, or self-
esteem issues should be fully explored prior to proceeding with surgery (1).
Careful medical history and physical examination are essential for the
assessment of risk factors and candidacy for breast augmentation.
Preoperative mammography is recommended for patients older than 35 years
of age or patients of any age with significant risk factors for breast cancer.
The ideal size and shape of the female breast is inherently subjective and
relates to both personal preference and cultural norms. However, most
surgeons will agree that there are certain shared characteristics that represent
the aesthetic ideal of the female breast form. These characteristics include a
profile with a sloping or full upper pole and a gently curved lower pole with
the nipple areolar complex at the point of maximal projection (Fig. 95-2).
The breast structure may be thought of as the breast parenchyma resting on
the anterior chest wall surrounded by a soft tissue envelope made up of skin
and subcutaneous adipose. Clearly, the resulting form of the breast after
augmentation mammaplasty will be determined by the dynamic interaction of
the breast implant, the parenchyma, and the soft tissue envelope (29).
FIGURE 95-2 A: Measurable parameters that comprise the aesthetic breast form. B:
Following breast augmentation, the resultant breast form is composed of the
interaction among the character and compliance of the soft tissue envelope, the
volume and quality of the breast parenchyma, and the dimensions, volume, and
characteristics of the breast implant. (Redrawn from Maxwell GP, Hartley W. Breast
augmentation. In: Mathes SJ, Hentz VR, eds. Plastic Surgery. 2nd ed. Philadelphia, PA:
Elsevier; 2006.)

A thorough physical examination begins with observation and careful


documentation of any signs of chest wall deformity or spinal curvature. It is
imperative to document and draw attention to any asymmetry of breast size,
nipple position, or inframammary fold (IMF) position. Careful palpation of
all quadrants of the breast and axilla is required to rule out any dominant
masses or suspicious lymph nodes. While palpating the breast, the surgeon
should carefully assess the quantity and compliance of the parenchyma and
soft tissue envelope. The soft tissue pinch test is a useful method of
assessment in which the superior pole of the breast is gathered between the
examiner’s thumb and index finger and the thickness of the intervening tissue
is measured. In general, a pinch test result of less than 2 cm will often
indicate a need for subpectoral placement of the implant. It is also important
to characterize the amount, quality, and distribution of the breast parenchyma
as it may be necessary to reshape or redistribute the parenchyma to achieve
the desired shape of the breast mound. The elasticity of the skin should also
be characterized by observing its resistance to deflection and noting any signs
of skin redundancy or stretch marks. Allergan has developed the
BioDimensional preoperative planning system to facilitate patient assessment
and implant selection (Table 95-5). Johnson & Johnson has also developed
the BodyLogic breast implant sizing selection tool to enhance outcomes with
ease of implant confirmation. In addition, a system for breast implant
selection has been developed based on the patient’s tissue characteristics (T),
envelope (E), parenchyma (P), the implant (I), and the dynamics of soft tissue
and implant interaction (D), referred to as the TEPID assessment system (30).

TABLE 95-5 Preoperative Planning and Dimensional Analysis in


Augmentation Mammaplasty
1. Carefully analyze and measure the dimensions and shape of the existing
breasts.
2. Analyze the character and evaluate the adequacy of the soft tissue
envelope.
3. Develop an anatomically well-defined goal for the breast shape after
augmentation (e.g., more or less upper pole fullness).
4. Select implant size, shape, height, width, and projection to accomplish the
individual patient’s goals.
5. Select surgical approach (incision) and implant pocket location (i.e.,
subpectoral, subglandular, subfascial).
FIGURE 95-3 Preoperative assessment includes the measurements from
supersternal notch to nipple (SSN:N), nipple to inframammary fold (N:IMF), breast
width (BW), breast height (BH), and intermammary distance (IMD). The soft tissue
thickness and quality is also assessed with a soft tissue pinch test and further tissue
characterization. (Redrawn from Maxwell GP, Hartley W. Breast augmentation. In:
Mathes SJ, Hentz VR, eds. Plastic Surgery. 2nd ed. Philadelphia, PA: Elsevier; 2006.)

Precise measurements must be taken using the IMF, the nipple areolar
complex, and the suprasternal notch as key landmarks (Fig. 95-3). The
surgeon should measure the breast width (BW) at its widest point, the breast
height (BH), and the distance from the nipple areolar complex to the
inframammary fold (N:IMF). The distance from the suprasternal notch to the
nipple areolar complex (SSN:N) and the intermammary distance (IMD)
should also be documented. It is often helpful to make markings on the
patient in the seated position with a permanent marker just prior to surgery. It
is imperative to mark the original IMF, and it is a good idea to mark the true
midline of the anterior chest.
In addition to manual measurements, three- and four-dimensional systems
are available to facilitate the measurement process in addition to enhancing
the patients overall experience by increasing physician–patient interaction in
selecting the appropriate implant. The visual display of the implant selected
increases the confidence of the patient in the results that will be achieved.
The four-dimensional imaging system (Precision Light, Los Gatos, CA)
automatically measures and characterizes both the soft tissue and chest wall,
as this is an important step in surgical planning. There are times that minor
chest wall or soft tissue asymmetries are missed by manual measurement and
visualization. This new system captures all of the asymmetries preoperatively
so that appropriate preoperative planning can be performed and the patient is
advised with an accurate informed consent. This system is based on
biodimensional principles as previously described. As we continue to pursue
this approach to increasing patient safety and satisfaction while decreasing
reoperation rates, this system will serve as another tool in our armamentarium
to achieve these goals.
Operative Planning
Implant Position
The breast implant may be positioned in the subglandular position between
the breast parenchyma and the pectoralis major muscle or in the subpectoral
position between the pectoralis major muscle and the chest wall (Fig. 95-4).
In general, the position of the implant will be determined by the adequacy of
the nascent breast tissue. Subglandular implant placement should be
considered for patients with mild glandular hypomastia and an adequate soft
tissue envelope. Patients who undergo subglandular augmentation have less
perioperative discomfort and a shorter period of convalescence than those
undergoing subpectoral placement. Subglandular augmentation is believed to
yield a more natural-looking breast form because the overlying breast tissue
is less distorted than with subpectoral positioning. An additional advantage of
subglandular augmentation is that activation of the pectoralis major muscle
does not cause unnatural movement or deformation of the implant as is often
seen with subpectoral implants in active women (31). However, thin patients
with severe hypomastia will be at risk for palpability and even visibility of
the implant if it is placed in the subglandular position. This accounts for the
predominance of subpectoral implant placement in thin patients.
During subpectoral placement of the implant, it is often necessary to either
partially or totally release the inferior portion of the pectoralis major muscle
origin in order to achieve the needed expansion in the lower pole of the
breast. Frequently, implants placed in the subpectoral position are in reality
only covered with pectoralis major muscle in the superior and medial two-
thirds of the implant. This common situation may be more accurately
characterized as the partial subpectoral position (32). Infrequently, it may be
necessary to place the implant under both the pectoralis major muscle and the
serratus anterior muscle, which is called the total submuscular position.

FIGURE 95-4 A: When ample soft tissue is present, the implant may be placed over
the pectoral muscle in the subglandular or subfascial position. B: When inadequate
soft tissue is present, the implant is placed beneath the pectoral muscle in the
subpectoral or dual plane position. (Redrawn from Maxwell GP, Hartley W. Breast
augmentation. In: Mathes SJ, Hentz VR, eds. Plastic Surgery. 2nd ed. Philadelphia, PA:
Elsevier; 2006.)

In some cases, the interaction between the breast parenchyma and the
pectoralis major muscle may adversely affect the appearance of the resulting
augmented breast. For example, the breast mound may appear to hang
anteriorly and inferiorly off the pectoralis muscle, resulting in the Snoopy-
nose breast deformity (6). It is then necessary to perform a partial release of
the breast parenchyma from the pectoralis muscle, creating a plane of
dissection in both the subpectoral and subglandular planes (29). This dual
plane dissection allows the pectoralis muscle to retract superiorly or window-
shade upward while the breast parenchyma is redraped over the inferior
portion of the implant, avoiding deformity of the resulting augmented breast
(Fig. 95-5).
In certain patients, a subfascial implant position is an alternative option for
augmentation mammaplasty (33,34). Theoretically, placement of the implant
in the subfascial position between the anterior fascia of the pectoralis major
and the muscle itself may provide additional support to the overlying soft
tissue envelope, causing less distortion of the breast form and decreasing
mobility of the implant within the pocket. The long-term outcome studies of
breast augmentation employing this position are not yet available, but the
procedure is gaining popularity worldwide.

Implant Selection: Filling Material


Since the reintroduction of silicone implants to the U.S. market, the number
of their placements as compared to saline implants has gradually been
increasing. In our experience, breast augmentation with silicone gel–filled
implants consistently produces a softer, more natural feel on palpation and an
appearance that is superior to augmentation with saline-filled implants. The
superiority of silicone gel–filled implants seems to be widely accepted
internationally and silicone gel–filled implants are used almost exclusively
for primary breast augmentation.
Even though the safety of silicone implants has been shown in several
studies and the link to immunologic disorders have been disproven (35),
many patients still have the impression that saline-filled implants are
somehow safer than silicone–filled implants despite the lack of any scientific
data to support this notion. Saline-filled implants are a good alternative for
those patients who are convinced that silicone gel–filled implants are
potentially dangerous.

Implant Selection: Implant Size


The selection of the implant size is initiated during the preoperative
consultation period based on both the patient’s goals and the surgeon’s
assessment. In general, the critical factors in selecting a specific implant size
are the dimensions of the nascent breast, the compliance and characteristics
of the soft tissue envelope, and the desired volume for the resulting
augmented breast. The base width of the breast is related to the width of the
patient’s chest and is proportional to the overall body habitus. It is imperative
that this dimension is respected during augmentation in order to maintain the
normal anatomic landmarks such as the lateral breast fold in the anterior
axillary line and the IMD. The same is true for BH but to a lesser degree than
for BW. Violation of these landmarks may yield an unnatural and deformed
appearance. Generally, the surgeon should select an implant that is slightly
less wide than the existing breast (Fig. 95-6). Fortunately, implant
manufacturers are now producing implants with varying degrees of projection
for a given base width. In this way, the surgeon should be able to attain the
desired amount of projection by choosing a low-profile, moderate-profile, or
high-profile implant while preserving the normal aesthetic proportions of the
breast.
FIGURE 95-5 Subpectoral implant placement generally involves the release of the
pectoralis major muscle. This results in varying degrees of muscle coverage of the
upper portion of the implant and mammary glandular coverage of the lower portion.
The degree and location at which the pectoral muscle is divided will determine the
amount of relative muscle and glandular implant coverage. The term “dual plane”
has been used to describe this implant positioning. (Redrawn from Maxwell GP,
Hartley W. Breast augmentation. In: Mathes SJ, Hentz VR, eds. Plastic Surgery. 2nd ed.
Philadelphia, PA: Elsevier; 2006.)

Implant Selection: Implant Surface Texture


In 1970, Ashley reported a dramatically reduced incidence of capsular
contracture when using a silicone gel implant coated with a thin layer of
polyurethane foam (PUF) for breast reconstruction (36). The textured surface
was originally designed to promote ingrowth of the surrounding tissue and
help to maintain the position of the implant on the chest wall. Microscopic
examination of the PUF reveals an open, trabecular structure (Fig. 95-1A).
This structure elicits aggressive tissue ingrowth, which is believed to disrupt
and prevent the circumferential linear fibrosis associated with periprosthetic
capsular contracture (37). Examination of the PUF-coated prostheses after
implantation frequently revealed delamination of the coating and limited
mobility of the silicone gel–filled implant within the capsule. Despite this
fact, the periprosthetic capsules that formed were soft and did not produce
clinically relevant contractures. During the next two decades the PUF-coated
implants (Natural-Y, Même, Replicon) enjoyed increasing popularity with
plastic surgeons due to the aesthetically pleasing results and remarkably low
rates of capsular contracture (38–40). Concerns about the safety of PUF-
coated implants arose in response to the findings of a National Cancer
Institute study published in 1979 finding that mice fed extremely high doses
of 2,4-toluenediamine showed an increased incidence of breast cancer (41).
Ultimately, the manufacturer of the PUF-coated implants (Surgitek/Bristol-
Meyers-Squibb) failed to attain FDA premarket approval in April 1991, and
these implants were withdrawn from the U.S. market.
FIGURE 95-6 The width of the selected implant generally should not exceed the
width of the patient’s breast tissue. In this illustration, the breast width is 13 cm. An
implant is selected 12.5 cm in width and placed beneath the patient’s tissue. This
gives a resultant postoperative breast form of approximately 14.5 cm in width with
similar resultant dimensional changes in breast height and projection. (Redrawn from
Maxwell GP, Hartley W. Breast augmentation. In: Mathes SJ, Hentz VR, eds. Plastic
Surgery. 2nd ed. Philadelphia, PA: Elsevier; 2006.)

In light of safety concerns associated with PUF-coated devices, implant


manufacturers developed processes to create a textured surface on the
silicone elastomer shell of breast prostheses and tissue expanders. In 1986,
McGhan Medical (now Allergan) introduced the Biocell textured surface on
both silicone gel–filled and saline-filled breast implants (Fig. 95-1B). The
Biocell textured surface was created using a lost salt technique and produced
a coarse, open pore surface with a variable pore size of 300 to 600 μm and
average density of 3.1 pores/mm2 (37). This surface had been shown to
induce an aggressive tissue response, which caused adherence of the implant
to the periprosthetic capsule (42). This adhesive effect that was seen with the
Biocell textured implants was similar to that seen with the PUF-coated
implants but differed in that the textured surface did not delaminate from the
implant. Ultimately, the Biocell textured prosthesis remained relatively
immobile within the implant pocket but generally produced a soft,
noncontracted periprosthetic capsule. This was the genesis of the concept of
immobility with softness. The principle of immobility with softness yields a
relatively fixed location of the implant within the precisely fitted pocket and
contrasts dramatically with the great mobility of a smooth implant within a
significantly larger capsule pocket (Fig. 95-7). Several clinical studies have
shown a significantly lower incidence of capsular contracture with Biocell
textured surface implants than with smooth surface implants (37,42–44). As
mentioned earlier, all Biocell textured devices have been withdrawn from the
market.
In 1989, Mentor Corporation (now Johnson & Johnson) introduced the
Siltex textured surface on an inflatable saline breast prosthesis and on tissue
expanders, as shown in Figure 95-1C (45). The Siltex textured surface is
created as a negative imprint by contact with a texturing foam that produces a
dense pattern of raised irregular nodules ranging in height from 65 to 150 μm
and in width from 60 to 275 μm. The Siltex textured surface is less coarse
than the Biocell textured surface, as it does not exhibit the same degree of
adherence to the periprosthetic capsule seen with the Biocell implant.
Therefore, the Siltex textured surface implants exhibit more mobility within
the pocket but theoretically also reduce the risk of rippling visible on the
breast surface. Of importance, clinical studies have shown a significantly
lower incidence of capsular contracture with Siltex textured surface implants
than with smooth surface implants (45).
FIGURE 95-7 Pocket dissection is implant specific. A: When round, smooth implants
are used, a large pocket is dissected to allow implant mobility within the resultant
bursa. B: When anatomic implants are used, the pocket should be dissected very
precisely around the base dimensions of the implant, promoting tissue adherence and
implant immobility. (Redrawn from Maxwell GP, Hartley W. Breast augmentation.
In: Mathes SJ, Hentz VR, eds. Plastic Surgery. 2nd ed. Philadelphia, PA: Elsevier;
2006.)

Sientra’s textured devices are manufactured with a process that involves


volatilization of ammonium carbonate with heat (46). The textured surface,
TRUE Texture, is created using a proprietary texturing method that does not
use sodium chloride, sugar, soak/scrub, or pressure-stamping methods.
Scanning electron microscope of the TRUE Texture surface indicates that it
falls in between and combines characteristics from both of the other
manufacturers’ textured surfaces (Biocell and Siltex) (Fig. 95-1D). Similar to
other textured devices, TRUE Texture surface implants have also been
demonstrated to have a lower incidence of capsular contracture compared
with smooth surface implants.

Implant Selection: Implant Shape


It is important to reiterate the principle that the shape of the natural female
breast is not a semicircle or a hemisphere. Dimensional analysis of the
aesthetically pleasing breast form reveals a gently sloping upper pole and a
curved lower pole with the nipple areolar complex at the point of maximum
projection (Fig. 95-2). The typical round breast implant has its greatest
projection centrally with the remainder of the volume distributed evenly
along the base of the implant (Fig. 95.8A). In contrast, anatomically shaped
breast implants have a flatter upper pole with the majority of the volume and
projection in the lower pole (Fig. 95-8B). Thus, the anatomically shaped
implant of a given base width and volume will produce less upper pole
convexity than a round implant of the same base width and volume. This
characteristic of anatomically shaped implants can be extremely useful when
the patient desires a significant volume augmentation but has a relatively
narrow BW (47–49).
All three manufacturers have developed anatomically shaped breast
implants to address the need for more naturally shaped breast prostheses in
breast reconstruction and augmentation mammaplasty. Allergan had
developed the BioDimensional style 410 anatomically shaped, silicone gel–
filled breast prostheses, which are no longer available (Table 95-3). Mentor
Corporation has developed the MemoryShape series of anatomically shaped,
silicone-filled breast implants while Sientra has developed the Opus Curve
anatomically shaped silicone-filled breast implants. Obviously, it is
imperative that anatomically shaped implants be relatively immobile within
the implant pockets since rotation or inversion would produce a significant
breast deformity (50). Therefore, all anatomically shaped implants are
produced with a textured surface to promote either sufficient friction or tissue
ingrowth between the implant and the periprosthetic capsule to ensure
immobility of the implant.
FIGURE 95-8 A: When there is acceptable preoperative breast form, a round
implant may suffice for volumetric enhancement. B: When there is inadequate
breast form as well as volume deficit, an anatomic implant is preferable. (Redrawn
from Maxwell GP, Hartley W. Breast augmentation. In: Mathes SJ, Hentz VR, eds.
Plastic Surgery. 2nd ed. Philadelphia, PA: Elsevier; 2006.)
OPERATIVE TECHNIQUE
SURGICAL APPROACH
Preoperative markings are made with the patient in the upright position and
are useful as a reference point during the actual procedure (Fig. 95-3). The
surgeon should mark the chest midline in the frontal view from the
suprasternal notch to the xiphoid process, the existing IMFs, and the likely
position of the new IMFs as the proposed limits of the dissection. The patient
is then placed in the supine position, centered on the operating table with the
pelvis directly over the flexion point of the bed. The arms must be well
secured to the armboards, which are placed at 90-degree angles to the torso.
These preparations are required so that the patient may be placed in the
upright seated position as often as needed during the procedure. The sterile
preparation and draping of the anterior chest must provide visualization of the
patient’s shoulders as an important anatomic reference point.
The three types of incision that are commonly employed in augmentation
mammaplasty are inframammary, periareolar, and transaxillary incisions
(51). While the patient’s preference should be taken into consideration, the
ultimate choice of incision must allow the surgeon optimal visualization,
control of the dissection, and precise control of the implant. The potential
advantages and limitations of each approach should be discussed with the
patient (Table 95-6). The surgeon should become facile with each technique
so that the surgical approach can be tailored to the individual patient’s
anatomy.
The inframammary approach permits complete visualization of the implant
pocket with either subglandular or subpectoral placement, and was
popularized by Cronin and Gerow (11). The incision should be placed in the
predicted location of the new IMF, which is typically 1 to 2 cm below the
existing fold. Smaller incisions (1 to 3 cm) may be used for inflatable saline-
filled implants, but prefilled implants (silicone gel or saline) often require
incisions up to 5.5 cm in length. The incision should be designed with the
majority of the incision lateral to the breast midline, as this will place the
resulting scar in the deepest portion of the new IMF.
The periareolar approach for augmentation mammaplasty was described by
Jenny in 1972 and currently enjoys widespread use by plastic surgeons (52).
The periareolar incision is placed along the inferior portion of the areolar-
cutaneous juncture. The principal advantage of this incision is that the
resulting scar is usually well camouflaged and quite inconspicuous. The
periareolar approach allows easy adjustment of the IMF and direct access to
the parenchyma for scoring and release when the lower pole of the breast is
constricted. However, visualization and control of the dissection are typically
inadequate with the periareolar incision in patients with areolas less than 3
cm in diameter. Other disadvantages of this approach include the potential
risk of contamination if the lactiferous ducts are transected, the increased risk
of changes in nipple sensitivity, and the risk of a hypopigmented scar in
patients with darkly pigmented areolas.

TABLE 95-6 Incision Options in Breast Augmentation


Factor Axillary Periareolar Inframammary
Implant plane
Submuscular + + +
Subglandular − + +
Implant type
Saline round + + +
Saline shaped − + +
Silicone − + +
round/shaped
Preoperative breast
volume
High (>200 g) + + +
Low (<200 g) + + −
Preoperative breast
base position
High + + +
Low − + +
Breast shape
Tubular − + −
Glandular ptosis + + +
Ptosis (grade I– − + −
II)
Areolar
characteristics
Small diameter + − +
Light/indistinct + − +
Inframammary
crease
None + + −
High + + −
Low + + +
Secondary − + +
procedure

+, applicable; −, not generally recommended.


Adapted from Hidalgo DA. Breast augmentation: choosing the optimal incision, implant and pocket
plane. Plast Reconstr Surg 2000;105(6):2202–2216.
The transaxillary approach was described by Hoehler in 1977 and
popularized by Bostwick et al. (53). This procedure can be performed either
bluntly using the Montgomery dissector or using an endoscope for precise
visualization, together with dissection of the implant pocket. The
transaxillary approach avoids incisional scarring directly on the breast and
places the incision in the inferior and anterior area of the axilla. The
transaxillary incision usually provides adequate access when placing an
inflatable round breast implant. The placement of a large, prefilled implant or
an anatomically shaped device is more difficult with this approach, but is not
precluded.
Creating the Implant Pocket
The incision is made in the location determined during the preoperative
consultation period. The superficial fascial system (Scarpa), which is
contiguous with the inferior and lateral edge of the breast parenchyma, is
divided and the dissection is beveled cephalic to avoid fold tissue disruption
down to the anterior fascia of the pectoralis major muscle. Meticulous
hemostasis is maintained using the Bovie electrocautery device. A variety of
fiberoptically lighted retractors are available to aid visualization during the
procedure. The surgeon may wish to use a fiberoptically lighted headlight to
illuminate the operative dissection instead of a lighted retractor. Once the
anterior fascia of the pectoralis major muscle is identified, the dissection will
proceed either above or below the muscle, depending upon the planned
position of the breast implant. Alternatively, the dissection plane may be
developed between the anterior fascia of the pectoralis major and the muscle
itself in order to place the implant in the subfascial position.
When placing the implant in the subpectoral position, it is necessary to
identify the lateral border of the pectoralis major muscle as a key anatomic
landmark. The lateral edge of the muscle is carefully elevated to gain access
to the subpectoral pocket. This plane is developed superiorly, medially, and
inferiorly by dividing the loose areolar connective tissue between the muscle
and the chest wall. Perforating branches of the internal mammary artery are
frequently encountered medially within the pocket and need to be carefully
coagulated using the extended tip on the electrocautery or the insulated
DeBakey forceps. The inferior origin of the pectoralis major muscle may
need to be partially or totally divided in order for the pocket to accommodate
the subpectoral implant (Fig. 95-5). The extent to which the inferior origin of
the pectoralis muscle is divided (or attenuated) is determined by the location
of the origin in the individual patient, the dimension of the patient’s breast,
and the height of the implant. Conversely, the lateral portion of the implant
pocket should be developed using a blunt dissection technique. In this way,
the third, fourth, and fifth intercostal cutaneous nerves, which provide
sensory function to the nipple areolar complex, may be preserved.
The subpectoral implant pocket is then copiously irrigated with a triple-
antibiotic–containing saline solution or a povidone-iodine solution. The
pocket is carefully inspected again to ensure meticulous hemostasis. When
placing prefilled implants, it is generally helpful to first insert an adjustable
implant sizer, inflate it to planned volume, and place the patient in a seated
position. Careful observation at this point will allow confirmation of the
appropriate implant volume and identification of minor asymmetries
intraoperatively. The prefilled implant or the deflated implant is then placed
in the implant pocket, making sure that the point of maximal projection is
centered beneath the nipple. Once the implant is in the proper position and
inflated to the appropriate volume, a multilayer closure is accomplished using
absorbable suture material and sterile paper tape is applied longitudinally
over the incision. Typical results of augmentation mammaplasty with round,
smooth, saline-filled implants placed in the subpectoral position are shown in
Figure 95-9. Results following breast augmentation with round, smooth,
silicone gel–filled implants placed in the subpectoral position are shown in
Figure 95-10.

FIGURE 95-9 A: The patient is shown preoperatively B: Supersternal notch-to-


nipple measurements are 22 cm, breast widths are 13.5 cm, and breast heights are
12.5 cm. Based on these dimensions and the patient’s desire for saline implants,
implants of 12.7 cm are selected from the data chart. These are 360-cc implants filled
to 375 cc per side. The implants are placed subpectorally with pectoral release. The
implants are placed subpectorally due to a soft tissue pinch test of less than 2 cm. C:
The result is shown with the round, smooth saline implant in the dual plane.
In patients with adequate soft tissue coverage, the subglandular position
may yield the optimal aesthetic result (Fig. 95-11). Placement of the implant
in the subglandular position involves development of the plane between the
posterior aspect to the breast parenchyma and the anterior fascia of the
pectoralis major muscle. It is imperative to maintain meticulous hemostasis
and avoid injury to the lateral intercostal cutaneous nerves during the
dissection. A larger pocket is created for smooth, round implants to allow
mobility of the implant within the pocket (Fig. 95-7A). For textured
anatomically shaped implants, the pocket is precisely dissected to snugly
accommodate the implant. Selection of the final implant volume, adjustments
of the implant pocket, irrigation, and closure are carried out in the fashion
described previously.
Postoperative Care
In the overwhelming majority of cases, augmentation mammaplasty is
performed as an outpatient procedure. Patients are given prescriptions for oral
analgesics and a 3-day course of prophylactic oral antibiotics. Patients are
allowed to remove operative dressings and shower as desired starting on
postoperative day 2. The first follow-up visit is scheduled for 3 to 5 days after
the procedure. If smooth (nontextured) implants were used, initiation of
implant mobility exercises is recommended at this time. If the patient is at
risk for superior implant displacement, a circumferential elastic strap may be
used to apply continuous downward pressure during the early postoperative
period. Patients are usually able to return to work a few days after surgery but
are not permitted to resume rigorous exercise for 2 to 3 weeks. Additional
follow-up visits are scheduled at 4 to 6 weeks, 3 months, and 1 year. The
importance of postoperative photographic documentation and critical analysis
of the operative outcomes cannot be overemphasized.
FIGURE 95-10 A: This athletic patient desiring proportionate breast enhancement is
shown preoperatively. B: Supersternal notch-to-nipple dimensions are 20 and 20.5
cm, nipple intermammary fold asymmetries are 6.0 and 5.5 cm, breast widths are
12.5 cm, and breast heights are 12 cm. C: The resultant breast form meets the
patient’s aesthetic and functional goals.
MANAGEMENT OF THE AUGMENTED PATIENT

Perioperative Complications
Alterations of nipple sensitivity after augmentation mammaplasty may be
manifested as either anesthesia or hyperesthesia and are believed to result
from traction injury, bruising, or transection of the lateral intercostal
cutaneous nerves. The incidence and severity of nipple sensation changes
vary considerably with the surgical approach employed. The periareolar
approach is generally associated with the highest rate of changes in nipple
sensation, while the transaxillary approach is associated with a significantly
lower incidence. The frequency of changes reported in the literature varies
widely, but patients should be advised that the risk of permanent alterations
in nipple sensitivity is about 3% to 5% for all approaches (54).
Periprosthetic seroma fluid is usually resorbed by the soft tissues within
the first week of surgery (55). Persistent seromas, although very rare in
primary augmentation, may require ultrasound-guided aspiration or drainage
catheter placement. Diluting the antibiotic irrigation solution and minimizing
use of the electrocautery may help to prevent seroma formation. The
development of a hematoma after breast augmentation has several deleterious
effects in both the early and late postoperative periods, including pain, blood
loss, disfigurement, and capsular contracture (56). Preoperatively, patients
should receive a list of prescription and over-the-counter medications that
may contribute to excessive postoperative bleeding. It is imperative that the
patient discontinue any medications that impair clotting or platelet function at
least 1 week prior to surgery. Obviously, maintenance of meticulous
hemostasis during the procedure is critically important, and blunt dissection
is to be used sparingly if at all to avoid hematoma formation. If a hematoma
does develop in the perioperative period, immediate evacuation of the
hematoma and exploration of the pocket is recommended. Unfortunately, the
source of the hematoma is only rarely identified at the time of the
exploration. Patients may occasionally present with a delayed hematoma 1 to
2 weeks or even months to years after augmentation, and frequently a history
of breast trauma is elicited. Expanding hematomas require exploration and
drainage regardless of the length of time from the augmentation.
Nonoperative management of small, nonexpanding hematomas is one option
but places the patient at a higher risk of subsequent periprosthetic capsular
contracture (56).
FIGURE 95-11 A: This young patient presented with significant bony,
musculoskeletal, and breast asymmetry. She desired a natural aesthetic breast form
with improvement in symmetry. B: Assessment shows nipple-to-supersternal notch
distances of 17 and 18 cm, breast widths of 11.5 and 12 cm, and the obvious
discrepancy in inframammary fold locations. C: The patient’s breast height of 8 cm
is noted with the significant depression in the chest wall. The right breast has a
constricted lower pole. The soft tissue pinch test is less than 2 cm. D: The asymmetric
augmentation result was accomplished with a 255-g style 410 MF implant and a 245-
g 410 MM implant in the left, placed through inframammary incisions in the
subpectoral or dual plane location. E: Preoperative oblique appearance. F:
Postoperative result with enhanced aesthetic breast form and better breast
symmetry.
Postoperative wound infection may present with a spectrum of severity
ranging from a mild cellulitis of the breast skin to a purulent periprosthetic
space infection. The organism Staphylococcus epidermidis is part of the
normal skin flora and is the most frequently identified pathogen in
postoperative wound infections. Patients are given prophylactic antibiotics
intraoperatively and postoperatively to reduce the risk of infection. Sterile
technique is maintained during the procedure, and the implant pocket is
irrigated with triple antibiotic solution containing 50,000 units of bacitracin,
1 g of cefazolin, and 80 mg of gentamicin per 500 mL of saline. Further
reduction of risk for bacterial contamination may be achieved by employing
the no-touch technique in which only the surgeon handles the implant with
fresh, powder-free gloves. The implant is then inserted carefully with the
surgeon’s choice of insertion technique. Our patients are also asked to shower
with antimicrobial soap (Hibiclens) 3 days prior to the operation followed by
5 to 10 days during the postoperative period. A significant number of
postoperative wound infections will respond to oral or intravenous antibiotics
if therapy is initiated very early in the course of the infection (55). If the
infection persists or progresses, then the implant should be removed and the
wound should be allowed to heal by secondary intention. Once the infection
has totally cleared, a secondary augmentation and scar revision should be
planned.
Mondor disease is a superficial thrombophlebitis of the breast that may
occur in up to 1% to 2% of augmentation patients (55). This process usually
affects the veins along the inferior aspect of the breast and occurs most
frequently with the inframammary approach. Fortunately, this is a self-
limiting process that usually resolves with warm compresses over a period of
several weeks.
Delayed Complications of Augmentation Mammaplasty
Periprosthetic Capsular Contracture
One of the most common delayed complications of augmentation
mammaplasty is the development of a palpable and deforming periprosthetic
capsular contracture. All surgical implants undergo some degree of
encapsulation due to the natural foreign-body reaction by the surrounding
tissues. Clinically significant periprosthetic capsular contracture is
characterized by excessive scar formation that leads to firmness, distortion,
and displacement of the breast implant. Histologic examination of these
contractures reveals circumferential linear fibrosis, which is especially severe
when formed in response to smooth shell implants (37). In 1975, Baker
proposed a clinical classification system of capsular contracture after
augmentation that is still commonly used to describe periprosthetic
contractures (57). This classification system is summarized in Table 95-7.
Capsular contracture remains one of the most common and most problematic
complications of augmentation mammaplasty, with an incidence reported
between 0.5% and 30%.

TABLE 95-7 Baker Classification of Capsular Firmness in Augmented


Breasts
Grade I (no palpable capsule) The augmented breast feels as soft as
an unoperated one
Grade II (minimal firmness) The breast is less soft, and the
implant can be palpated but is not
visible
Grade III (moderate firmness) The breast is harder, the implant can
be palpated easily, and it (or
distortion from it) can be seen
Grade IV (severe contracture) The breast is hard, tender, and cold;
distortion is often marked

While several factors have been identified that contribute to capsular


contracture, the precise etiology remains unknown. The hypertrophic,
circumferential linear scar probably involves stimulation of myofibroblasts
that are known to be present within the periprosthetic capsule. Irritation
caused by periprosthetic hematoma, seroma, or silicone gel bleed may incite
the capsular contracture (58). Other foreign body particles such as glove
powder, lint, or dust may also contribute to the process.
Several studies have suggested an infectious etiology for periprosthetic
capsular contracture (59,60). This theory describes a chronic subclinical
infection located immediately adjacent to the implant shell within a
microscopic biofilm that is relatively inaccessible to cellular and humoral
immune function (61,62). The appropriate treatment for the infectious
etiology would be total capsulectomy and placement of a new sterile breast
implant. The use of perioperative prophylactic antibiotics theoretically
reduces the risk of bacterial contamination and has become standard in
augmentation.
Many strategies have been employed to prevent periprosthetic capsular
contracture. One strategy has been the creation of a large implant pocket and
maintenance of this oversized pocket with implant displacement exercises.
The use of implants with textured surfaces has been described earlier in this
chapter and has been shown to reduce the rate of capsular contracture in
breast augmentation. Other efforts have focused on minimizing operative
trauma in order to reduce the risk of seroma or hematoma formation.
Seromas, hematomas, and even blood staining of the periprosthetic tissues
may incite capsular contracture. Any bleeding that does occur during the
dissection needs to be controlled, and the staining of the tissues with blood
should be diluted with copious irrigation fluid.
Some evidence has accumulated that leukotriene receptor antagonists,
which are used to treat asthma, may prevent and reverse the formation of a
periprosthetic capsular contracture (63). Specifically, zafirlukast (Accolate)
and montelukast (Singulair) have been shown to reverse clinical signs of
capsular contracture in patients taking the medication for asthma.
Treatment of established capsular contractures usually requires operative
intervention. Open capsulotomy involves scoring the capsule
circumferentially and anteriorly to adequately release and expand the soft
tissue envelope. With very thick fibrous capsules or with calcified capsules
containing silicone granulomas, it is often necessary to perform either a
partial or complete capsulectomy to correct the deformity (64,65). This is
often extremely effective in treating advanced grade IV capsular contractures,
especially when the implant is replaced with a saline-filled or a no-bleed
silicone gel–filled implant. Implant site change surgery has become popular
for treating established or recurrent capsular contracture. Recent evidence
also shows that the use of acellular dermal matrix (ADM) may be helpful in
both treating and possibly preventing capsular contractures. Although long-
term follow-up is still needed, use of ADM is showing promise in treating the
most common reason that the patients present for revisionary breast surgery.
The workhorse of revisionary breast surgery for the authors are the use of
ADM with or without the creation of the neopectoral pocket (66,67). For
those patients whose original implants were subglandular, a pocket change to
a subpectoral plane and lower pole coverage with ADM should be performed.
For those patients whose original implants were in a subpectoral, a
neopectoral pocket with the addition of ADM should be performed. For
patients who did have adequate breast tissue, a subfascial pocket with ADM
sling should be performed. This allows the newly placed implant to be
positioned in contact with normal, well-vascularized tissue instead of residual
scarred tissues.
All three manufacturers have reported their long-term follow-up data on
the rate of capsular contracture. Mentor’s MemoryShape Gel Implant core
study included 572 primary augmentation patients. At 10 years’ follow-up,
3.6% of patients had capsular contracture (68). Allergan’s Natrelle 410
anatomical form-stable silicone breast implant core study included 492
women who underwent primary augmentation mammaplasty. The capsular
contracture rate was 9.2% at 10 years’ follow-up (69). Sientra’s core study of
round and shaped breast implants with cohesive silicone gel included 1,116
primary augmentation patients. The rate of capsular contracture at 10 years
was 9.0% among textured devices and 17.5% among smooth devices (46).

Implant Rupture and Deflation


Any defect in the silicone elastomer shell of a saline-filled breast implant will
ultimately result in deflation of the implant. The saline filling material leaks
out of the implant and is harmlessly absorbed by the surrounding tissues.
Clinical recognition of deflation is usually made by the patient and virtually
always requires surgical explantation and replacement of the implant. A
history of recent trauma is frequently elicited with deflation, and true
spontaneous failure of the implant shell is relatively rare. Both manufacturers
of saline implants have reported their 10-year deflation rates for saline-filled
breast implants as part of the FDA postmarket approval process. The
deflation rate for the Mentor saline-filled implants was 24.7% in 1,097
patients with a 60% follow-up rate (70). For the Allergan saline-filled
implants, the deflation rate was 13.8% in 901 patients with a 91% follow-up
rate (71). The surgeon should, thus, advise any patient considering
augmentation mammaplasty with saline-filled implants to expect a deflation
rate of approximately 14% to 25% over a 10-year period.
The spontaneous rupture rates for silicone gel-filled prostheses have been
significantly more difficult to monitor (72,73). It is often difficult to
distinguish between silicone gel bleed and minor silicone gel leak when both
produce nearly identical clinical findings. Actual failure of the shell may
result in only a small amount of gel leak into the periprosthetic intracapsular
space. Leakage of silicone gel into the extracapsular tissues may occur only
as small herniations in isolated areas. Certainly, patients who have undergone
closed capsulotomies are at greater risk for gel leakage into the surrounding
tissues. Of interest, the constrictive force of the periprosthetic capsular
contracture itself may contribute to extrusion of the gel into the extracapsular
space. In the majority of gel implant ruptures, significant deformity of the
breast is not clinically obvious, with only a small amount of intracapsular or
extracapsular gel leakage (73). Instead, there may be only very subtle
changes in the implant shape or firmness even when frank rupture of the gel
implant shell is present.
Magnetic resonance imaging (MRI) of the breast is considered the state-of-
the-art technique for evaluating breast implant integrity. However, false
positives and false negatives occur when using breast MRI to assess silicone
gel–filled implants (74). The finding of silicone residue between the implant
shell and the periprosthetic capsule on MRI may often be misinterpreted as
evidence of implant rupture. Upon explantation, however, the implant shell is
often actually found to be intact and the residue represents only gel bleed.
Hölmich et al. showed that the majority of the second-generation implants
examined by MRI showed evidence of rupture despite the fact that the
patients were asymptomatic with this finding (74). Patients with evidence of
ruptured silicone gel–filled implants on MRI did not have increased
symptoms, autoimmune disease, or autoantibodies compared to patients
without MRI evidence of rupture. The authors concluded that silicone gel–
filled implant rupture is a relatively harmless condition, which only rarely
progresses and gives rise to notable symptoms (74).
Modern silicone gel is substantially more cohesive than the second-
generation gel and less likely to leak into the surrounding tissues, even when
the implant shell is ruptured. This cohesive silicone gel is described as being
form stable or as having shape retention with little or no gel flow and
immeasurable gel bleed. This raises the question of whether an actual rupture
of a modern silicone gel implant shell is relevant, since both gel leak and gel
diffusion are unlikely to occur even in the face of shell failure.

BIA-ALCL
BIA-ALCL is a rare form of lymphoma, a slow-growing type of non-
Hodgkin lymphoma, that has been associated specifically with textured breast
implants. It initially appears in the fluid between the capsule and implant but
can progress to involve the surrounding capsule and tissues, if left untreated.
The etiology or pathogenesis of BIA-ALCL is currently unknown but leading
theories include macrotextured devices with increased surface area, specific
bacterial biofilm, and genetic predisposition (75).
As of July 6, 2019, there have been 573 unique cases of BIA-ALCL
globally (76). Eighty-four percent of these cases were attributed to Allergan
BioCell textured implants. The risk of BIA-ALCL with Allergan textured
implants is, thus, approximately six times the risk of BIA-ALCL with other
textured implants. Based on these data, the FDA requested Allergan to
withdraw its textured devices from the market. There is a chapter dedicated
on ALCL and please refer to Chapter 122 for more detail.
CONCLUSION
We have reviewed the history and development of breast augmentation in the
United States. In addition, our aim has been to provide a method for patient
assessment, operative planning, and technique. Currently, there are several
alternatives when selecting the surgical approach and the specific type of
breast implant for a given patient. Ultimately, decisions about the size, shape,
surface texture, and filling material must be made in conjunction with the
recommendations of the surgeon and the desires of the patient. However,
there is not one strategy for achieving all of the goals of breast augmentation
for every patient. Recognizing that augmentation mammaplasty is both a
science and an art, it is imperative that the surgical approach, the creation of
the implant pocket, the implant selection, and the implant position must
always be tailored to the individual patient.

REFERENCES

1. Shipley RH, O’Donnell JM, Bader KF. Personality characteristics of


women seeking breast augmentation, comparison to small-busted and
average-busted controls. Plast Reconstr Surg 1997;60(3):369–376.
2. Baker JL Jr, Kolin IS, Bartlett ES. Psychosexual dynamics of patients
undergoing mammary augmentation. Plast Reconstr Surg
1974;53(6):652–659.
3. American Society of Plastic Surgeons. 2018 Plastic surgery statistics
report. Available at:
https://www.plasticsurgery.org/documents/News/Statistics/2018/plastic-
surgery-statistics-full-report-2018.pdf. Accessed November 18, 2019.
4. Czerny V. Plastic replacement of the breast with a lipoma [in German].
Chir Kong Verhandl 1895;2:216.
5. Longacre JJ. Correction of the hypoplastic breast with special reference
to reconstruction of the “nipple type breast” with local dermofat pedicle
flaps. Plast Reconstr Surg 1954;14:431–441.
6. Picha GJ, Batra MK. Breast augmentation. In: Achauer BM, Eriksson E,
Guyuron B, et al., eds. Plastic Surgery: Indications, Operations, and
Outcomes. 1st ed. St. Louis, MO: Mosby; 2000:2743–2756.
7. Institute of Medicine. Safety of Silicone Breast Implants. Washington,
DC: National Academy Press; 1999.
8. Uchida J. Clinical application of crosslinked dimethylpolysiloxane,
restoration of the breast, cheeks, atrophy of infantile paralysis, funnel-
shaped chest, etc. Jpn J Plast Reconstr Surg 1961;4:303.
9. Boo-Chai K. The complications of augmentation mammaplasty by
silicone injection. Br J Plast Surg 1969;22:281–285.
10. Ortiz-Monasterio F, Trigos I. Management of patients with
complications from injections of foreign materials into the breasts. Plast
Reconstr Surg 1972;50(1):42–47.
11. Cronin TD, Gerow FJ. Augmentation mammaplasty: a new “natural
feel” prosthesis. In: Transactions of the Third International Congress of
Plastic Surgery. Amsterdam: Excerpta Medica; 1963;41–49.
12. Arion HG. Presentation d’une prothese retromammaire. J Soc Fr
Gynecol 1965;35:421.
13. Regnault P, Baker TJ, Gleason MC, et al. Clinical trial and evaluation of
a proposed new inflatable mammary prosthesis. Plast Reconstr Surg
1972;50:220–226.
14. Young VL, Watson ME. Breast implant research: where we have been,
where we are, where we need to go. Clin Plast Surg 2001;28(3):451–
483.
15. Lavine DM. Saline inflatable prostheses: 14 years’ experience. Aesthet
Plast Surg 1993;17:325–330.
16. U.S. Food and Drug Administration. Allergan Recalls Natrelle Biocell
Textured Breast Implants Due to Risk of BIA-ALCL Cancer. Available
at: https://www.fda.gov/medical-devices/medical-device-
recalls/allergan-recalls-natrelle-biocell-textured-breast-implants-due-
risk-bia-alcl-cancer. Accessed November 18, 2019.
17. Brody OS. Silicone technology for the plastic surgeon. Clin Plast Surg
1988;15(4):517–520.
18. Barnard JJ, Todd EL, Wilson WG, et al. Distribution of organosilicone
polymers in augmentation mammaplasties at autopsy. Plast Reconstr
Surg 1997;100(1):197–203; discussion 204–205.
19. Thomsen JL, Christensen L, Nielsen M, et al. Histologic changes and
silicone concentrations in human breast tissue surrounding silicone
breast prostheses. Plast Reconstr Surg 1990;85(1):38–41.
20. Baeke JL. Breast deformity caused by anatomical or teardrop implant
rotation. Plast Reconstr Surg 2002;109(7):2555–2567.
21. Spear SL, Mardini S. Alternative filler materials and new implant
designs: what’s available and what’s on the horizon? Clin Plast Surg
2001;28(3):435–443.
22. Schnur PL, Weinzweig J, Harris JB, et al. Silicon analysis of breast
periprosthetic capsular tissue from patients with saline or silicone gel
breast implants. Plast Reconstr Surg 1996;98(5):798–803.
23. Robrich RJ, Hollier LH, Robinson JB. Determining the safety of the
silicone envelope: in search of a silicone antibody. Plast Reconstr Surg
1996;98(3):455–458.
24. Edworthy SM, Martin L, Barr SG, et al. A clinical study of the
relationship between silicone breast implants and connective tissue
disease. J Rheumatol 1998;25(2):254–260.
25. Gabriel SE, O’Fallon WM, Kurland LT, et al. Risk of connective-tissue
diseases and other disorders after breast implantation. N Engl J Med
1994;330(24):1697–1702.
26. Park AJ, Black RJ, Sarhadi NS, et al. Silicone gel-filled breast implants
and connective tissue diseases. Plast Reconstr Surg 1998;101(2):261–
268.
27. Schusterman MA, Kroll SS, Reece GP, et al. Incidence of autoimmune
disease in patients after breast reconstruction with silicone gel implants
versus autogenous tissue: a preliminary report. Ann Plast Surg
1993;31(1):1–6.
28. Sanchez-Guerrero J, Colditz GA, Karison EW, et al. Silicone breast
implants and the risk of connective-tissue diseases and symptoms. N
Engl J Med 1995;332(25):1666–1670.
29. Tebbetts JB. Dual plane breast augmentation: optimizing implant-soft-
tissue relationships in a wide range of breast types. Plast Reconstr Surg
2001;107(5):1255–1272.
30. Tebbetts JB. A system for breast implant selection based on patient
tissue characteristics and implant-soft tissue dynamics. Plast Reconstr
Surg 2002;109(4):1396–1409; discussion 1410–1415.
31. Biggs TM, Yarish RS. Augmentation mammaplasty: retropectoral
versus retromammary implantation. Clin Plast Surg 1988;15(4):549–
555.
32. Regnault P. Partially submuscular breast augmentation. Plast Reconstr
Surg 1977;59(1):72–76.
33. Graf RM, Bernardes A, Auersvald A, et al. Subfascial endoscopic
transaxillary augmentation mammaplasty. Aesthet Plast Surg
2000;24:216–220.
34. Graf RM, Bernardes A, Rippel R, et al. Subfascial breast implant: a new
procedure. Plast Reconstr Surg 2003;11l(2):904–908.
35. Van Nunen SA, Gatenby PA, Basten A. Post-mammoplasty connective
tissue disease. Arthritis Rheum 1982;25:694–697.
36. Ashley FL. A new type of breast prosthesis: preliminary report. Plast
Reconstr Surg 1970;45(5):421–424.
37. Barone FE, Perry L, Keller T, et al. The biomechanical and
histopathologic effects of surface texturing with silicone and
polyurethane in tissue implantation and expansion. Plast Reconstr Surg
1992;90(1):77–86.
38. Capozzi A, Pennisi YR. Clinical experience with polyurethane-covered
gel-filled mammary prosthesis. Plast Reconstr Surg 1981;68(4):512–
520.
39. Gasperoni C, Salgarello M, Gargani G. Polyurethane-covered mammary
implants: a 12-year experience. Ann Plast Surg 1992;29(4):303–308.
40. Herman S. The Même implant. Plast Reconstr Surg 1984;73(3):411–
414.
41. Hester TR, Tebbetts JB, Maxwell GP. The polyurethane-covered
mammary prosthesis: facts and fiction (II). Clin Plast Surg
2001;28(3):579–586.
42. Burkhardt BR, Eades E. The effect of Biocell texturing and povidone-
iodine irrigation on capsular contracture around saline-inflatable breast
implants. Plast Reconstr Surg 1995;96(6):1317–1325.
43. Hakelius L, Ohisén L. Tendency to capsular contracture around smooth
and textured gel-filled silicone mammary implants: a 5-year follow-up.
Plast Reconstr Surg 1997;100(6):1566–1569.
44. Tarpila E, Ghassemifar R, Fagrell D, et al. Capsular contracture with
textured versus smooth saline-filled implants for breast augmentation: a
prospective clinical study. Plast Reconstr Surg 1997;99(7):1934–1939.
45. Burkhardt BR, Demas CP. The effect of Siltex texturing and povidone-
iodine irrigation on capsular contracture around saline inflatable breast
implants. Plast Reconstr Surg 1994;93(1):123–128; discussion 129–130.
46. Stevens WG, Calobrace MB, Alizadeh K, et al. Ten-year core study data
for Sientra’s food and drug administration-approved round and shaped
breast implants with cohesive silicone gel. Plast Reconstr Surg
2018;141(4S Sientra Shaped and Round Cohesive Gel Implants):7S–
19S.
47. Bronz G. A comparison of naturally shaped and round implants. Aesthet
Surg J 2002;22(3):238–246.
48. Hobar PC, Gutowski K. Experience with anatomic breast implants. Clin
Plast Surg 2001;28(3):553–559.
49. Niechajef I. Mammary augmentation by cohesive silicone gel implants
with anatomic shape: technical considerations. Aesthet Plast Surg
2001;25:397–403.
50. Panettiere P, Marchetti L, Accorsi D. Rotation of anatomic prostheses: a
possible cause of breast deformity. Aesthet Plast Surg 2004;28:348–353.
51. Hidalgo DA. Breast augmentation: choosing the optimal incision,
implant and pocket plane. Plast Reconstr Surg 2000;105(6):2202–2216.
52. Jenny J. The areolar approach to augmentation mammaplasty. Int J
Aesthet Plast Surg 1972(fall).
53. Hoehler H. Breast augmentation: the axillary approach. Br J Plast Surg
1977;26:373–376.
54. de Cholnoky T. Augmentation mammaplasty: survey of complications
in 10,941 patients by 265 surgeons. Plast Reconstr Surg 1970;45:573–
577.
55. Handel N. Managing local implant-related problems. In: Spear SL, ed.
Surgery of the Breast: Principles and Art. 1st ed. Philadelphia, PA:
Lippincott-Raven;1998:953–968.
56. Williams C, Aston S, Rees TD. The effect of hematoma on the thickness
of pseudosheath around silicone implants. Plast Reconstr Surg
1975;56:194–198.
57. Baker JL Jr. Classification of spherical contractures. Presented at the
Aesthetic Breast Symposium, Scottsdale, Arizona, 1975.
58. Barker DE, Retsky MI, Schultz S. “Bleeding” of silicone from bag-gel
breast implants, and its clinical relation to fibrous capsule reaction. Plast
Reconstr Surg 1978;61(6):836–841.
59. Burkhardt BR. Fibrous capsular contracture around breast implants: the
role of subclinical infection. Infect Surg 1985;4:469.
60. Courtiss EH, Goldwyn RM, Anastazi GW. The fate of breast implants
with infections around them. Plast Reconstr Surg 1979;63:812–816.
61. Dobke MK, Svabn JK, Vastine VL, et al. Characterization of microbial
presence at the surface of silicone mammary implants. Ann Plast Surg
1995;34(6):563–569; discussion 570–571.
62. Virden CP, Dobke MK, Stein P, et al. Subclinical infection of the
silicone breast implant surface as a possible cause of capsular
contracture. Aesthet Plast Surg 1992;16:173–179.
63. Schlesinger SL, Ellenbogen R, Desvigne MN, et al. Zafirlukast
(Accolate): a new treatment for capsular contracture. Aesthet Surg J
2002;22(4):329–336.
64. Maxwell GP, Hammond DC. Breast implants: smooth versus textured.
Adv Plast Reconstr Surg 1993;9:209.
65. Maxwell GP, Hartley W. Breast augmentation. In: Mathes SJ, Hentz
VR, eds. Plastic Surgery. 2nd ed. Philadelphia, PA: Elsevier; 2006:1–
34.
66. Maxwell GP, Gabriel A. Use of the acellular dermal matrix in
revisionary aesthetic breast surgery. Aesthet Surg J 2009;29(6):485–493.
67. Maxwell GP, Birchenough SA, Gabriel A. Efficacy of neopectoral
pocket in revisionary breast surgery. Aesthet Surg J 2009;29(5):379–
385.
68. Hammond DC, Canady JW, Love TR, et al. Mentor contour profile gel
implants: clinical outcomes at 10 years. Plast Reconstr Surg
2017;140(6):1142–1150.
69. Maxwell GP, Van Natta BW, Bengtson BP, et al. Ten-year results from
the Natrelle 410 anatomical form-stable silicone breast implant core
study. Aesthet Surg J 2015;35(2):145–155.
70. Mentor. Saline-Filled & Spectrum™ Breast Implants Directions For
Use. Mentor, Irving, TX; 2015. Available at: http://cof.hr/wp-
content/uploads/2019/08/MENTOR_implantati_katalog_2018.pdf
71. Walker PS, Walls B, Murphy DK. Natrelle saline-filled breast implants:
a prospective 10-year study. Aesthet Surg J 2009;29(1):19–25.
72. Cohen BE, Biggs TM, Cronin ED, et al. Assessment and longevity of
the silicone gel breast implant. Plast Reconstr Surg 1997;99(6):1597–
1601.
73. Cook RR, Bowlin SJ, Curtis JM, et al. Silicone gel breast implant
rupture rates: research issues. Ann Plast Surg 2002;48(1):92–101.
74. Hölmich LR, Vejborg TM, Conrad C, et al. Untreated silicone breast
implant rupture. Plast Reconstr Surg 2004;114(1):204–214; discussion
215–216.
75. K Groth A, Graf R. Breast implant-associated anaplastic large cell
lymphoma (BIA-ALCL) and the textured breast implant crisis. Aesthetic
Plast Surg 2020;44(1):1–12.
76. U.S. Food and Drug Administration. Medical Device Reports of Breast
Implant-Associated Anaplastic Large Cell Lymphoma. Available at:
https://www.fda.gov/medical-devices/breast-implants/medical-device-
reports-breast-implant-associated-anaplastic-large-cell-lymphoma.
Accessed November 18, 2019.
CHAPTER 96

Augmentation in Patient With


Congenital Breast Deformity
GAURAV BHARTI | BILL G. KORTESIS | VASILEIOS VASILAKIS | MATTHEW H. ISAKSON
HISTORY
Tuberous deformities present along a continuum of severity and constitute
one of the most challenging breast conditions to surgically correct. Although
several terms have been used to characterize these deformities, including
tuberous breasts, lower pole hypoplasia, and constricted breasts, all describe
conditions within the same anatomic spectrum. Individuals with tuberous
breast deformity will generally have all components of the breast present
including parenchyma, areola, and nipple, however these structures have
abnormal relationships with one another. The parenchyma is most commonly
underdeveloped and there is variable herniation of breast tissue into the
areola and expansion of nipple areolar complex. These features create
significant asymmetries and the appearance of the breast is devastating to the
young women affected with any degree of tuberous breast deformities.
ANATOMIC BASIS OF THE DEFORMITY
The clinical features of the tuberous breast deformity are illustrated in Figure
96-1 and include a reduced breast base diameter, high and constricted
inframammary fold (IMF), breast hypoplasia, breast ptosis, areola
hypertrophy, and “herniation” or preferential expansion of the growing breast
bud into the areola. Asymmetry in shape and size between the two breasts is
frequently a significant component of the tuberous breast deformity.

FIGURE 96-1 The spectrum of clinical presentations seen in patients with the
tuberous breast deformity.

The breast parenchyma is contained within a fascial system. The


superficial fascial layer is continuous with the superficial fascial system of
the abdomen and covers the breast parenchyma. The deep fascial layer lies
deep to the breast, overlying the pectoralis fascia. There is absence of
superficial fascia at the level of the areola, which in conjunction with fascial
constrictions and suspensory ligament thickenings, results in the development
of the breast in a vertical direction into the nipple areolar space, leading to
tuberous appearance.
CLASSIFICATION
Several classification schemes have been described over the years. The early
work of Grolleau focused on the tuberous breast deformity in relation to
breast base, with type I having a deficient lower medial quadrant, type II
having a deficient lower pole, and type III being deficient in all four
quadrants. A fourth variant, type 0, has been described, and refers to an
isolated, temporary or permanent, areolar herniation associated with a normal
breast base.
Recently, Kolker et al. comprehensively expanded on this description and
focused their classification in the analysis of the six major clinical features of
the deformity:
Base—minor/moderate/severe
Inframammary fold—normal laterally, minor elevation medially/medial
and lateral elevation/elevation of entire fold, or fold absence
Skin envelope—sufficient/inferior insufficiency/global insufficiency
Breast volume—no deficiency, minimal deficiency, or
hypertrophy/moderate deficiency/severe deficiency
Ptosis—mild, moderate, or severe/non or mild/mild/moderate
Areola—enlargement/normal, mild or moderate herniation/severe
herniation
PRINCIPLES OF SURGICAL MANAGEMENT
All the aforementioned anatomic features of the deformity must be taken into
account in order to successfully reconstruct the tuberous breast. Type I, or
mild tuberous breast deformity, is the most common and type of presentation.
Even in the mildest forms, subtle IMF or other constriction is present
therefore high index of suspicion is warranted. This needs to be recognized
preoperatively in order to adequately release the soft tissue and IMF during
ptosis repair or augmentation of the hypoplastic breast. Technically, radial
incisions extending through the parenchyma to the dermis are required.
Provided there is enough overlying soft tissue, utilizing a prepectoral or
partial subpectoral pocket during augmentation will allow access to the
parenchyma in order to achieve the release (Fig. 96-2). Placement of the
implant in the subglandular plane will also enhance the stretch effect on the
base and remaining breast tissue. Occasionally, fat grafting is used to add to
the soft tissue and enable prepectoral placement. Typically, unless a tissue
expander is used, as in severe of hypoplasia and lack of skin envelope,
reconstruction is performed in one stage.
Although surgical technique depends on the severity of the tuberous
deformity, successful management relies on recognition of the following key
principles:
Release of all constriction points and thick bands in the radial and
horizontal plane with incisions extending through the tissue up to the
dermis
Complete obliteration of the native IMF, setting the new IMF at a lower
position
Reduction of the herniated breast parenchyma

FIGURE 96-2 A: The base of the breast in patients with tuberous breast
deformity can often be seen to have constricting bands tethering the
parenchyma and preventing normal breast expansion. B: By incising through
these tethering bands, the constriction through the base of the breast can be
released, allowing the breast to reexpand.

Areola reduction
Volume augmentation
Achieving contralateral symmetry
RECONSTRUCTION OF THE LOWER POLE AND BASE
As mentioned above, once the IMF is adequately released, fat can be used to
fill the lower poll, or in severe cases tissue expansion might be necessary.
Intraoperatively, if IMF and inferior pocket dissection do not provide enough
release of the lower pole, a tissue expander rather than an implant is placed.
Fat can be added to in the lower pole in combination with a mammary
implant. Various techniques of internal glandular reshaping have been
described and provide satisfactory volume and contour to reconstruct the
inferior pole and reconstitute the base. They mostly rely on central or
subareolar breast tissue to fill the lower breast pole and several flaps and
internal parenchymal release incisions have been described as means to
redistribute the breast tissue. These will reshape the breast and provide the
necessary volume and contour to the lower pole and IMF, however these are
often inadequate to adequately increase the volume of the tuberous breast,
and fat grafting or implant need to be added.
Two popular techniques with extremely low reoperation rates are the
modified Puckett technique by Oroz-Torres et al. of the unfolded subareolar
gland flap, which is based on lengthening of the subareolar flap via two L-
shaped releasing incisions in order to reconstitute the lower pole and new
IMF, and the modified inferior pole flap by Mandrekas et al. The latter
technique involves periareolar incision and deepithelialization and dissection
of the breast tissue off the deep fascia. With the breast tissue attached only at
its superior aspect, complete release and repositioning of the IMF is allowed.
This is followed by the formation of two long parenchymal pillars that are
folded toward one another, reshaping the breast and filling the inferior pole.
CONSTRICTION AND AREOLAR HERNIATION
It is commonly the herniation of the areola that creates the greatest and most
distressing deformity for the patient. Typically, a periareolar approach, with
or without periareolar mastopexy, allows for direct soft tissue release to
reduce the herniated breast parenchyma and relieve the pressure on the
areola. This is often combined with placement of an implant or tissue
expander. Ionescu et al. have described a simple three-layer suture technique
for very minor, type 0, deformities, which avoids incision and can be
combined with breast augmentation.
VOLUME CORRECTION
Autologous or alloplastic techniques are acceptable. Fat grafting has emerged
as an essential tool in the management of the full range of the tuberous breast
deformity. Although it is more commonly used to add volume to the lower
pole, we utilize it throughout the breast. The ability to uniformly distribute
and contour the breast depends in releasing all the fibrous constricting bands.
Abdominal fat is our preferred donor site, followed by the lateral and inner
thighs. As vascularized fat responds to weight changes, the patient is
educated as to the need for weight maintenance.
Even in severe presentations, fat grafting remains a useful tool for adding
volume and softening the contour of the breast mound. It is still imperative to
disrupt all constriction points and divide the thickened bands in order to
facilitate expansion. In mild to moderate cases, we favor a subcision
technique using a 14-gauge trocar to perform radial scoring until adequate
release is achieved. This prepares the recipient bed for fat transfer and allows
interposition of fat graft into these areas to further interrupt their continuity.
In more severe cases, invasive procedures are required in order to lower the
fold and expand the inferior pole of the breast. In cases of serial fat grafting,
we recommend at least 6 months between fat grafting sessions. The number
of fat grafting sessions required is dictated by the severity of the patient’s
deformity and discrepancy between current breast size and desired breast
size.
Placement of implant is our preferred method of restoring volume in the
hypoplastic breast. We must note that the approach is highly individualized
and often a tissue expander is preferred in order to reach ours and the
patient’s goal, or fat is used as an adjuvant at a later stage. We tend to favor
the IMF approach (and release) in patients with minimal areola hypertrophy
and herniation (Fig. 96-3). Our preference is one-stage implant reconstruction
using silicone-filled, round implants. Size selection depends on the
contralateral side, projection, width and height of the breast, and patient
preference.
As mentioned earlier, we aim for subglandular placement and we find that
a standard circumareolar mastopexy (always following implant placement) is
still indicated in most cases (Fig. 96-4). Sizers can be very useful, depending
on surgeon preference.
In cases of unilateral breast hypoplasia, a relatively popular option is to
place an expander in the prepectoral space and expand the device as both
breasts develop. An attempt to catch up with the normal breast is made early
in the expansion process to restore symmetry. Once development is complete
and the desired volume is achieved, release of constriction and periareolar
mastopexy/nipple reduction are performed at the time of the expanded
replacement with an implant.
FIGURE 96-3 A–C: Preoperative appearance of a 21-year-old female patient with a
mild tuberous breast deformity on the right with asymmetry. The left breast is
uninvolved. The preoperative plan includes placement of saline implant in the
subglandular plane on the right via an inframammary fold incision. A simultaneous
contralateral symmetrizing augmentation–mastopexy was performed. D–F:
Postoperative appearance of the single-stage reconstruction.
FIGURE 96-4 A–C: Preoperative appearance of a 20-year-old woman who presents
with an asymmetric bilateral moderate tuberous breast deformity. On each side the
inframammary fold is positioned high on the chest wall, the base of the breast is
constricted, and the breast has “herniated” through a narrow soft tissue window
creating a narrow projecting breast mound. D–F: Two-year postoperative
appearance after placement of 370-cc saline implants and simultaneous
circumareolar purse-string subglandular mastopexy.
COMPLICATIONS
Complications related to large implants and lack of adequate soft tissue
coverage are common, namely palpability and rippling. Preventive fat
injections to the soft tissue should be considered in high-risk patients.
Complications related to the periareolar mastopexy are attempted to reduce
with the use of Gore-Tex suture. Copious pocket irrigation with betadine and
the use of Keller funnel for “no-touch” implant placement are ways to reduce
infection.
A common complication is persistent IMF due to incomplete release. This
rarely self-corrects but improves with stretch effect of the implant. It can be
camouflaged with fat grafting to the breast base and lower poll and often
requires surgical release. Lack of support of the new IMF may lead to
implant malposition, which is difficult to correct and warrants reoperation.
POLAND SYNDROME
Poland syndrome describes a wide range of spectrum of mostly aesthetic
chest wall deformities. These range from simple (mild form) unilateral
mammary hypoplasia, axillary fold deficiency, and absence of the
sternocostal head of the sternocleidomastoid, to complex (severe form) cases
associated with absence of ipsilateral ribs, foreshortening of the hemithorax,
and axillary webbing.
FIGURE 96-5 A, B: Preoperative appearance of a 40-year-old woman with Poland
syndrome of the right breast. The sternal head of the pectoralis major muscle is
absent and there is hypoplasia of the right breast. C–E: Postoperative appearance
after breast augmentation using a cohesive anatomic silicone gel implant on the right
and a round, smooth silicone gel implant on the left. The shaped configuration of the
cohesive implant on the right provided enough control of the upper pole of the breast
to provide adequate symmetry with the opposite breast without creating a superior
pole step-off as might have occurred if a round implant had been used.

The goal of reconstruction is most commonly to correct the aesthetic


deformities via restoring volume, rather than functional as disabilities are
rarely associated with the thoracic deformities. Since chest wall deformities
are mostly aesthetic, reconstruction is typically performed in late adolescence
or adulthood to allow psychosocial development and avoid growth inhibition
secondary to reconstructive trauma. The reconstructive options are assessed
on a case-by-case basis and depend on the complexity of the deformities.
In female patients with mild form of Poland syndrome (Fig. 96-5), the
basis of reconstruction is mammary prosthesis. If additional volume is
needed, a latissimus dorsi flap can be transferred to help fill the chest wall,
supraclavicular hollowness or contour the axillary fold. Alternatively, TRAM
or latissimus dorsi flaps alone are viable options in adequately restoring
volume. In addition, the volume provided by the muscle can also serve to
soften the contours of the reconstructed breast mound. Contralateral
symmetrizing breast procedures are commonplace and should be performed
at a later stage.
In male patients with simple form of Poland syndrome, the latissimus dorsi
flap is the preferred reconstructive option, as its close origin and similar
function the pectoralis major muscle make it an ideal option and require little
patient reeducation. Prefabricated custom chest wall prostheses are an
unfavorable option in all patients as they are associated with very high levels
of dissatisfaction due to discomfort, contour irregularities, and migration.
In both men and women, complex chest wall deformities associated with
severe forms of Poland syndrome provide additional challenges and usually
require a multistage reconstructive process. Once the chest wall cartilage is
repaired and the chest wall flattened though, latissimus dorsi flap transfer is
the optimal reconstructive option. In women, implant placement in addition
to latissimus dorsi flap is often needed, followed by nipple areolar complex
reconstruction at a later stage.
CONCLUSION
Understanding the anatomic abnormalities of the tuberous breast is key in
successfully correcting the deformities. Individualized analysis of the
anatomic and clinical features determines the optimal approach for each
patient. Modern principles of aesthetic and reconstructive surgery play a key
role in forming the armamentarium for successful outcome. Multiple stages
might be required to achieve the aesthetic goals and symmetry.

SUGGESTED READINGS
Brown MH, Somogyi RB. Surgical strategies in the correction of the tuberous
breast. Clin Plast Surg 2015;42(4):531–549.
Costagliola M, Atiyeh B, Rampillon F. Tuberous breast: revised
classification and a new hypothesis for its development. Aesthetic Plast
Surg 2013;37(5):896–903.
Grolleau JL, Lanfrey E, Lavigne B, et al. Breast base anomalies: treatment
strategy for tuberous breasts, minor deformities, and asymmetry. Plast
Reconstr Surg 1999;104:2040–2048.
Ionescu R, Dima D, Antohi N. Intra-areolar pexy: the “compass rose” suture
technique for small and moderate areola herniation. Aesthet Surg J
2019;39(4):393–402.
Kolker AR, Collins MS. Tuberous breast deformity: classification and
treatment strategy for improving consistency in aesthetic correction. Plast
Reconst Surg 2015;135(1):73–86.
Mandrekas AD, Zambacos GJ. Aesthetic reconstruction of the tuberous
breast deformity: a 10-year experience. Aesthet Surg J 2010;30(5):680–
692.
Mathes SJ, Seyfer AE, Miranda EP. Congenital anomalies of the chest wall.
In: Mathes SJ, Hentz VR, eds. Plastic Surgery. Vol. 6, Trunk and Lower
Extremities. Philadelphia, PA: Saunders Elsevier; 2006:485–509.
Oroz-Torres J, Pelay-Ruata MJ, Escolán-Gonzalvo N, et al. Correction of
tuberous breasts using the unfolded subareolar gland flap. Aesthetic Plast
Surg 2014;38(4):692–703.
Seyfer AE, Fox JP, Hamilton CG. Poland syndrome: evaluation and
treatment of the chest wall in 63 patients. Plast Reconstr Surg
2010;126(3):902–911.
Seyfer AE, Icochea R, Graeber GM. Poland’s anomaly. Natural history and
long-term results of chest wall reconstruction in 33 patients. Ann Surg
1988;208(6):776–782.
Spear SL, Pelletiere CV, Menon N. One-stage augmentation combined with
mastopexy: aesthetic results and patient satisfaction. Aesthetic Plast Surg
2004;28(5):259–267.
CHAPTER 97

Patient Education in Breast


Augmentation
CAROLINE A. GLICKSMAN | SARAH E. FERENZ
HISTORY
Plastic surgeons who were in practice before the 1992 FDA moratorium on
silicone gel–filled breast implants remember a time when surgeons picked a
breast implant, patients underwent surgery, and the relationship between the
two ended shortly thereafter. By the start of the new millennium it became
evident that the status quo in breast augmentation would forever be changed.
The FDA began its regulation of breast implants as early as 1976 with the
passage of the Medical Device Amendments to the Federal Food Drug and
Cosmetic Act (FFDCA) of 1938. A medical device is deemed “safe” by the
FDA, “when it can be determined based on valid scientific evidence that the
probable benefits to health from the use of the device for its intended uses
and conditions of use, when accompanied by adequate directions and
warnings against unsafe use, outweigh the probable risks” (1). In the 1980s
the Center for Devices and Radiologic Health (CDRH) was developed and
several years later the FDA classified breast implants as class III medical
devices, allowing the FDA to demand data on breast implant safety for the
first time (2). As devices have evolved over the last 50 years, their improved
longevity and reliability have been well documented (3,4). Despite these
technologic advances, data on surgical outcomes and as reflected by revision
rates, still lag far behind (5).
Considerable effort has been placed on redefining breast augmentation as
more than just a surgical procedure. Peer-reviewed publications confirm that
markedly improved long-term outcomes can be achieved when there is
effective communication between the physician and the patient. The first step
in accomplishing improved outcomes in breast augmentation is
comprehensive patient education (6). Decisions made by both the surgeon
and the patient during the consultation phase of the breast augmentation
process may have more of an impact on the quality of the outcome and its
longevity than the device selected or the augmentation procedure itself. It is
during this educational process that surgeons have the best opportunity to
introduce informed consent documents that will hold patients accountable for
their decisions. An effective educational process must link understanding
with accountability, and what really matters is whether the patients
understand, accept, and take responsibility for their decisions (7).
This chapter focuses on analyzing the current informed consent issues in
the breast augmentation process as well as improvements to this process that
have been requested by the FDA and advocacy groups. It reviews essential
content suggested in the initial consultation, presented in a format that
patients will understand, while simultaneously integrating informed consent
documents into the patient’s educational experience. Useful educational tools
and models that can be used both in and out of the office are recommended as
well as suggested steps to be taken preoperatively, including the development
of certified patient decision aids (PDAs), to clearly document the patient’s
accountability for decisions made. Finally, this chapter reviews methods that
will help manage patient expectations with regard to the potential for yet
unknown risks and complications, the patient’s financial responsibilities for
potential complications or staged procedures, as well as expected long-term
follow-up as both the patient and the devices age.
PATIENT EDUCATION AND INFORMED CONSENT
In the medical setting, the term “informed consent” arose in the United States
in 1957. This terminology shifted the physician–patient relationship away
from the medical paternalism that had encompassed medicine and surgery for
centuries toward that of a duty to respect patient autonomy. The U.S. court
case of Cobbs v. Grant (1972) noted that the doctrine of informed consent is
“anchored” in four postulates. First, patients are generally ignorant of
medicine. Second, patients have a right to control their body and decide about
their medical treatment. Third, consent to treatment must be informed to be
effective. Fourth, patients depend on their physicians for truthful information
and must trust them (8). Informed consent in breast augmentation, therefore,
should have two main aims. The foremost goal should be to respect and
promote the patients’ autonomy; the second should be to be truthful and
protect them from harm. If we assume the provision that accurate, detailed
information has been provided in an understandable format, patients should
be assured of both of these aims. Only if the patient obtains a comprehensive
understanding of the possible benefits, harms, and alternatives to the
procedure through a process of shared decision making, can the patient give
adequate informed consent. In addition, with respect to breast augmentation,
we must also convey the fact that there remain unknown risks associated with
the procedure.
Successful communication plays the central role in physician–patient
relationships, and it has been shown to positively influence patient
satisfaction, compliance, medical outcomes, and the overall quality of the
patient experience (9). It is especially important for informed consent where
patients are allowed, and expected, to participate in the decision-making
process by weighing the benefits against the risks of recommended options
(10). To be able to become true and knowledgeable decision makers, patients
need to understand the basis and significance behind those recommendations
and discuss them with their physicians properly. The current practice of
obtaining informed consent is often centered on the legal duty of having the
patient sign a form. Signing does not always represent patient understanding.
Shared decision making has become an accepted process of two-way
communication. This occurs when physicians and patients collaborate
together to make well-informed decisions that aligns the best current
treatment options for the patient—including surgical and scientific
uncertainties regarding possible outcomes—with the values, desires, and
preferences of the patient (11). PDAs are now recognized as structured,
evidence-based, up-to-date educational tools that help facilitate informed
decision making by patients. The use of PDAs is accepted in many medical
and surgical fields yet at the time of this writing, none exist in aesthetic
plastic surgery. PDAs in plastic surgery may include information online or
provided by manufacturers in the form of patient brochures. Decision aids are
intended to provide the patient time to reread what has been discussed during
a consultation, and adequate time should be provided for patients to become
knowledgeable about their options.
Past decisions in aesthetic breast augmentation were generally made
according to the surgeon’s own preferences and values. Shared decision
making and the use of PDAs allow for real-time documentation of the
informed consent process and goes hand in hand with clinical research and
evidence-based outcome decisions. A leading barrier to the incorporation of
shared decision making in a breast augmentation practice is the fear that it
will add time and costs to the practice.
The U.S. Department of Health and Human Services now requires that all
consent forms be “in a language understandable to the subject or their
representative.” Many states require culturally sensitive informed consent
documents, as this process has also been shown to be compromised when
language or cultural barriers are present. It is also recommended that
documents and brochures be provided in writing that is understandable to the
reading level of eighth grade or lower (12).
One of the roles of the physician is to become an effective communicator.
Physicians and their staff must be able to deliver information in language that
is familiar to their patients and easy to understand, using common words
from everyday language. Studies have shown that medical language and
everyday language are seen as two separate languages (13). Most physicians
and caregivers can translate the necessary medical information into a
language that the patients can understand. An interactive communication loop
between the patient and physician or nurse educator should be used to
frequently check comprehension and recall while clarifying and tailoring the
information in repeated cycles to improve comprehension (14). Some studies
suggest that patient understanding might be improved if the consent forms
were short and easy to read. They suggest modifications to consent forms
with regard to content, writing style, format, and length (15). The FDA has
recommended a patient decision checklist to help women consider the
benefits and risks of breast implants (16). Others conclude that these
modifications to informed consent are no more successful than other
approaches to improving patient comprehension (17). In addition, the term
“fully” informed consent would require that every piece of information
available would be provided to every patient. No rational patient desires all
the information about a procedure or a device, nor is there sufficient time.
It is also particularly difficult to obtain true informed consent in breast
augmentation because there remain unknowns that have yet to be identified
(18). Patients should be provided with “reasonable” and “adequate”
information, which will always be less than all of the available information
(19). In breast augmentation we must also further define risks as either
surgical or implant-related risk. Although the patient’s signature on a single
surgical consent document might represent agreement, it does not always
imply understanding. An attempt to assess understanding should be made at
varying steps throughout the educational process and documentation recorded
at each step.
Several options have been suggested that create an integrated approach to
patient education and the informed consent process (7). Traditional informed
consent documents in breast augmentation surgery have been criticized for
being “a source of waste” in health care. In addition to providing multiple,
short, readable documents in a staged approach, physicians and their staff
should frequently check the patient’s level of understanding. The method of
“teach back” can confirm understanding. The physician or staff can ask the
patient to say in her own words what has been described, and ask again if the
patient’s words show incomplete or inaccurate understanding. Probably the
most important factor in ensuring a high level of patient understanding is the
quality of the time spent with the patient. When the surgeon and the staff are
dedicated to providing their patients with a breast augmentation process that
is specifically designed to ensure safe, predictable, long-lasting results with
the lowest chance of unnecessary revisions, patients should be given the
necessary time to make well-informed decisions. Many patients make their
surgical decisions too quickly and select surgical options without taking the
time to process the information they have received. Patients should, if
possible, always be given the opportunity to return for a second consultation.
Between the two visits they should be encouraged to read any educational
materials provided, go online, and even seek another surgical opinion if they
desire. There is however, a considerable amount of misinformation available
online and on social media, and patients should be given an opportunity to
discuss and ask questions about information and sites found online. For
women who want to be involved in the surgical decisions entailed in breast
augmentation, it is crucial that they are reassured that they have time to
evaluate their surgical options.
Much of the research focusing on the quality of patient decisions in
surgery has been associated with clinical trials of patient decision aids and
other decision support tools. The preoperative decisions in breast
augmentation are known as “preference-sensitive” decisions to reflect the fact
that although medical evidence is necessary to make decisions, it may not be
sufficient. The patient’s preferences are also necessary to make the
appropriate decision. It follows, however that “preference-sensitive” clinical
decisions can be defined as the extent to which the implemented choices
reflect the considered preferences of the well-informed patient. Therefore,
patients should be given ample opportunity to become well informed (20).
There has been a great deal of discussion in the plastic surgery literature and
at scientific meetings surrounding the balance between patient autonomy, that
is, the physician’s obligation to create the conditions necessary for
autonomous choice and an individual’s right to self-determination, and
beneficence, which is the physician’s responsibility to do what is best for the
patient. Beneficence is also the belief that physicians are expected to refrain
from causing harm in addition to having an obligation to help their patients.
While there has been a long tradition in Western medical ethics toward
focusing on autonomy, that prioritization has now been critiqued (21,22). The
ethical debate in breast augmentation arises when the patient’s autonomous
decisions conflict with the physician’s beneficent duty to look out for the
patient’s best interest, for example, if the physician wishes to prevent
avoidable breast augmentation complications that may eventually result in
potentially uncorrectable deformities. Both surgeons and patients may sense
this as a return to an era of paternalism and reject the concept of “doctor
knows best” with regard to patient education in breast augmentation.
However, if we accept that there are quantifiable evidence-based guidelines
that can minimize revision surgeries and optimize long-term results, then
there is a need to incorporate beneficent actions in the preoperative education
process. Patients may still proceed with autonomy during the informed
consent process involved in breast augmentation, provided they are
accurately informed and fully understand the long-term consequences of their
decisions. They must then also be willing to be held accountable for those
decisions.
THE INITIAL PATIENT CONSULTATION
With all of the available information available online, the education process
in breast augmentation generally begins well before the first consultation.
Surgeons have the opportunity to set in motion a comprehensive process of
patient education before the patient even steps foot into the physician’s
office. Most staff are proficient in credentialing their surgeons, but should
also be instructed with scripts that provide early information for patients that
will establish a pattern to be followed throughout the breast augmentation
experience. Both physicians and patients routinely use the Internet and social
media as a source of health-related information; however, websites and social
media are not monitored, and therefore the quality of information is variable.
Prospective breast augmentation patients need to be taught to distinguish
between credible sites, such as those developed by the plastic surgery
societies, manufacturers, and the FDA, from sites that are sponsored by
organizations that may misinform or engage in cyberbullying. A physician’s
website can be an excellent source of information about the practice, the
surgeon’s philosophy, and information about implant technology and surgical
facilities. Online information, however, is not intended to replace information
provided by the physician; it is in addition to information provided by the
practice. The sites visited by the patient before the initial consult should be
reviewed by the physician or nurse educator at the first visit to correct any
inaccuracies encountered (23).
If patient education is to be a staged repetitive learning process, it will
require participation from several members of the surgeon’s staff. Many large
practices have a patient educator who plays an active role in the educational
process. For smaller practices, it may be the responsibility of the surgeon and
a well-trained staff member to develop a detailed precise approach to patient
education and informed consent. Extremely well-thought-out programs that
integrate patient education and informed consent have been published (6).
Comprehensive informed consent documents should be developed by the
practice and incorporated directly into the preoperative educational process.
These documents are specifically designed to verify the patients
understanding of content and their acceptance of responsibility for their
decisions (Tables 97-1 to 97-3 Staged patient educator lists and Informed
Consent Checklist).
TABLE 97-1 Patient Educator Initial Consultation
Patient Name: ___________
Date of Initial Consult: ___________
General Information Covered at First Visit:
• My commitment to patient education and long-term follow-up;
• Information available on my website;
• Clinical evaluation—your medical history;
• Brief history of augmentation—a 50-yr history of saline and silicone
implants;
• Breast implant technology:
• Constantly changing alternatives—differences between manufacturers,
gel fills, textured vs. smooth, and clinical trial implants, if applicable;
• Limitations of implants—each has its own potential risks as well as
benefits;
• Do implants cause disease? Breast implant illness—the research, data, and
science of silicone implants;
• Breast implants (textured) and rare association with BIA-ALCL;
• FDA approvals in United States, CE mark in Europe;
• Breast implants and breast cancer;
• Breast implants and mammography:
• All implants may interfere with mammograms to some degree;
• Implants may require imaging as they age to detect rupture and patients
may be responsible for costs;
• Complimentary high resolution ultrasound is available in Dr.
Glicksman’s office to help image your implants as they age;
• Alternatives versus a single approach to breast augmentation:
• What are your incision alternatives: inframammary, axillary,
periareolar;
• What are the different implant pocket locations: subglandular, dual
plane, subfascial;
• Discuss all currently available implant choices in the United States:
saline or silicone, round gel—smooth and textured, Motiva clinical trial
if available;
• Manufacturers: Allergan, Sientra, and Mentor, Motiva clinical trial
while enrolling.
• The benefits of fitting the procedure and implant to your tissues to
minimize long-term risks, compromises, and complications
Size Selection:
• Determining the best size;
• Which is more important to you? Size or stable results and avoidance of
problems long-term? Creating a proportionate breast augmentation;
• How an implant’s size affects your tissues—now and later;
• Bra cup sizing—no guarantee on cup size, with a discussion on bra sizing
language. Where do you shop? Discussion on the differences between
manufacturers as well as the concept of sister sizes;
• Measuring your breast, understanding your tissues; effects of weight
changes, pregnancies, and aging;
• Importance of concentrating on shape, fill, and dimensions;
• Photos and planning the operation—selection of an implant;
• Vectra 3D simulation may be used for educational purposes only. No
warranty is expressed or implied by its use; and
• Simulated images may be provided via email after signing informed
consent for “View My Image” portal.
Risks of Breast Augmentation:
• Breast augmentation is a totally elective operation with risks and
uncontrollable factors not limited to the following:
• Bleeding or infection;
• Change in sensation of the breast, skin, and nipple areola;
• Unsatisfactory aesthetic results or scarring;
• Possible interference with cancer detection—future breast imaging may
require additional views;
• Rare risk of BIA-ALCL, a very rare type of lymphoma possibly related
to some textured implants and bacterial contamination;
• Complications may require additional surgery, longer recovery, and
additional costs;
• Discussion on what is known about avoiding capsular contracture, how
capsules form, and the role of bleeding, trauma, and infection, as well as
the higher risks associated with revision procedures;
• Correcting the hard breast: options if capsular contracture develops;
• Prophylactic antibiotics are recommended by Dr. Glicksman for any
procedures that breaches the skin or mucosa;
• Size will affect skin stretch, visibility, and palpability of your implant, and
duration of your results; size does matter;
• Size will be selected together after examination, measurements, photos,
and 3D Vectra imaging whenever possible; and
• It is extremely rare that Dr. Glicksman will need to change your implant
size after surgery.
• All costs for any surgery relating to factors the surgeon cannot predict or
control are the patient’s responsibility (surgeon fees, facility fees,
anesthesia, lab, time off work) including, but not limited to: capsular
contracture, rupture, hematoma, infection, stretch deformities,
asymmetries, late seromas, BIA-ALCL, and possible implant size
changes.
Patient Initials: ________ Date: ________
Surgeon’s Initials: ________ Date: ________
Patient educator 1 rev.8-19

TABLE 97-2 Patient Educator Second Consultation


Patient Name: __________
Date of Second Consultation: __________
Selection of an Implant:
• Measurements and photographs were obtained;
• Choice of implant size, style, fill, volume, and shape was discussed; and
• Benefits as well as trade-offs of selected implant was discussed.
The Operation—What’s It Like:
• Day surgery routine transportation to and from the Center, who will
accompany you;
• The facility and facility personnel: Northern Monmouth Regional Surgery
Center; and
• Anesthesia—safety of anesthesia, misconceptions, risks, our personnel,
and “no narcotic” policy.
After Surgery:
• Waking in recovery and discharge home with a responsible adult;
• Detailed instructions will be given to you when you leave the center; and
• Nurses will instruct you and your caregiver what to expect and do until
your first postoperative visit.
Recovery and Activity:
• A bra is provided for your recovery, you will leave the surgery center in a
soft comfortable bra;
• No aerobic exercise for 2 wks after surgery;
• We will schedule your postop visits, discuss your short-term and long-
term follow-up, and requirements for clinical trial patients.
• Significant other: any friend or relative who wishes to be included in
postoperative discussions with regard to your results must be present
for the educational portion of your consultations preoperatively.

I have read all educational material provided, and have been given the
opportunity to visit the website (www.drglicksman.com) for
additional information.
___________________________ Patient’s Initial
Written information provided to me was discussed in detail and all my
questions were answered to my satisfaction.
___________________________ Patient’s Initials
All informed consent documents discussed in detail with me and all my
questions answered to my satisfaction.
___________________________ Patient’s initials Date:
________________
___________________________ Dr. Glicksman’s initials Date:
_________________
Patient Educator Visit 2. 12—2018

An approach to education that documents decisions made between the


surgeon and patient after each topic has been discussed may produce a more
valid informed consent than a single consent document signed at the time of
payment for the procedure. Shorter documents, simplified in content, length,
and language are more reliable communication tools to help physicians
evaluate patient understanding. It is also extremely important to document
whether a spouse, significant other, or relative will be involved in the
decision-making process. That individual should be present for at least one of
the office educational visits if he or she is to be allowed to participate in any
postoperative discussions on the surgical outcome (7). Although it may not
be the preference or style of all breast augmentation practices to interject the
signing of multiple documents throughout the patient’s preoperative
experience, there should be a verbal discussion with clear written
documentation preoperatively that the patient understands the alternatives
offered and accepts trade-offs, risks, and possible short- and long-term
complications associated with her decisions. In addition, there should be
written documentation of the financial responsibilities that the patient may
encounter postoperatively for possible untoward complications, future
radiologic imaging, and the eventual replacement or removal of her implant.
PATIENT EDUCATION IN BREAST AUGMENTATION: TOOLS, TECHNOLOGY,
AND THE SENSES

Most surgeons develop their communication skills over the years and are
turning with increasing frequency to tools and technology to improve shared
decision making between the surgeon and patient. From the use of a simple
illustration on paper or a tablet, to the use of commercially available
customizable interactive imaging and patient education platforms, there is a
perceived need to reach out to patients with better educational tools so they
can make better-informed decisions (24). Most women seeking breast
augmentation are highly motivated to learn about the breast augmentation
process. Many patients present with little or no knowledge concerning the
history of breast implants and may have biases based on the media, personal
experiences, the experiences of friends, relatives, and social media. Today we
are accustomed to interactive educational tools that incorporate the patient’s
senses into the learning experience. Physicians can utilize both visual and
tactile tools to reinforce the messages presented. Visuals have proven to be an
important asset in improving patient–physician communications, enhancing
education, and advancing the informed consent process. Visuals can increase
patient satisfaction and comprehension while reducing the amount of time a
physician needs to spend explaining specifics, such as implant designs or fill.
Visual tools have also been shown to overcome virtually any literacy or
cultural barriers that a patient may display (25). The use of older-generation
silicone implants as well as textured and smooth devices as educational tools,
can be invaluable when discussing the important changes that have occurred
in implant technology over the last 50 years (3,26). The 1992 FDA
moratorium on silicone breast implants which lasted in the United States until
2006, as well as the 2019 FDA recall of textured surface devices, has
generated a cohort of women who maintain a preconceived notion on the
safety of breast implants (27,28).

TABLE 97-3 Informed Consent Visit 2


Name: ____________________________________________
Acceptance of Risks and Factors in Breast Augmentation that the Surgeon
Cannot Control
Surgeon Patient
• Additional surgery to your breasts and/or ___________ ____________
implant will be likely over the course of
your life
• Your implants are not considered lifetime ___________ ___________
devices and you will likely undergo
implant removal, with or without
replacement, during your lifetime
• Implants may require imaging as they age ___________ ___________
to detect rupture and patients may be
responsible for all costs at a radiology
facility
• You should inform your mammography ___________ ___________
technologist about the presence of your
implants. Additional views may be
necessary
• To monitor your breast implants for silent ___________ ___________
rupture, the FDA currently recommends
an MRI 3 yrs following surgery and then
every 2 yrs after that; this requirement
may change to ultrasound surveillance in
the future
• The scar tissue or capsule that normally ____________ ___________
forms around the implant may tighten
and develop a contracture, if severe; this
may require surgery
• All costs for any surgery relating to ___________ ___________
factors the surgeon cannot predict or
control are the patient’s responsibility
(surgeon fees, facility fees, anesthesia,
labs, time off work). This may include,
but is not limited to: capsular contracture,
infection, stretch deformities, scarring,
BIA-ALCL, and implant size changes,
yet unknown complications associated
with breast implants
• The Vectra 3-D imaging system is used as ____________ ___________
an educational tool for the sole purpose
of communicating with patients and no
warranty is expressed or implied by its
use
• Rare cases of BIA-ALCL (anaplastic large ____________ ___________
cell lymphoma) have been reported in
women with breast implants. Long-term
follow-up to watch for signs of late
infection, or swelling around an implant
is recommended
• The use of some silicone gel implants ____________ ___________
before the age of 22 is considered an off-
label use for congenital deformities,
asymmetry, or reconstruction
• Long-term follow-up appointments will be ___________ ___________
scheduled to follow your implants as
they age and this may include in-office
ultrasound
Consent for the Use of Silicone Gel and Saline Breast Implants
I have had adequate time to review and understand the information
presented both in the office and in the written and web materials provided
by Dr. Glicksman. My doctor has addressed my concerns and questions. I
have considered alternatives to breast augmentation surgery including the
use of padded bras or alternatives to enhancing the appearance of my
breasts.
I am choosing to proceed with silicone gel– or saline-filled breast
implant surgery
Patient Name (Printed): ____________
Patient Signature: ____________ Date: ____________
Surgeon Name (Printed): Caroline A. Glicksman, MD
Surgeon Signature: _____________ Date: _____________

FIGURE 97-1 A: Breast augmentation results at 3 months. B: Breast augmentation


results at 3 years.

A great deal of misunderstanding can be eliminated when patients are


given the opportunity to see and feel the older devices and compare them to
the latest generation of implants. Additionally, the concept of implant fill,
both percentage of fill and cohesivity or the elasticity of the gel can be taught
to patients and their significant others. Women seeking breast augmentation
are increasingly aware of the many implant choices available to them.
Providing the patient the opportunity to hold each device provides a tactile
dimension to their education. Surgeons should consider showing all available
implants, not just their favorites. Patients need to get a better understanding
of their implant choices which includes the benefits or trade-offs of each
device that the surgeon may be considering. Patients grasp onto much more
information when it is presented repeatedly, and making use of appropriate
communication materials and decision aids can improve communication for a
wide range of health literacy levels. Patients, together with their surgeon,
must eventually decide on the fill and projection of their implant and should
be informed of their options as well as the trade-offs of each choice. Utilizing
actual implants as an educational tool creates a more engaged and informed
patient.
A more common approach to patient education in breast augmentation has
been the use of “before” and “after” photos as both educational and
marketing tools. As of August 2019, a Google search will produce over
42,900,000 results for breast augmentation with images, up over 40 million in
the last 10 years. Patient photographs can increase patient comprehension as
well as the retention of information. What most patients fail to understand is
that pictures cannot document the tissue characteristics or the quantitative
measurements that make each patient unique, nor are they aware that the
images they are viewing are not always long-term results, with most images
online captured at less than 6 months to a year (Fig. 97-1). Viewing images
with a patient can however, provide invaluable insight into her desires, and is
an opportunity to educate women with respect to the need to reconcile those
desires with their individual tissues and dimensions. Moreover, most patients
have only a vague understanding of the possible short- and long-term risks
that may be a direct result of the choices made preoperatively, for example,
when the patient desires an implant far wider than her tissues will
accommodate, or when a mastopexy may also be recommended. Patient
images can be very informative when used to help patients understand terms
like capsular contracture, skin stretch, implant malposition, symmastia, and
visible wrinkling (Fig. 97-2). The use of images may also aid the discussion
of the possible incision length and location, and the potential risks associated
with scarring. These visual counseling tools are also useful in demonstrating
unclear concepts such as parenchymal thinning, skin stretch, and implant
malposition. What is more, images can be shown depicting revision
procedures often necessary to correct some of the discussed potential
complications, as well as those problems that may be uncorrectable. The goal
of using 2D images in patient education is not to discourage the patient from
undergoing a breast augmentation, but to enhance the patient’s knowledge
base when multiple treatment options exist, thereby making her better able to
make informed choices (Fig. 97-3).
FIGURE 97-2 Patient images can demonstrate the leading drivers for revision
surgery and the results of poor decisions. A: Oversized breast implants and their
consequences over time. B: Capsular contracture. C: “Bottoming out” or stretch
deformity. D: Stretch deformity. E: Inferior malposition.

Eager to enhance the patient learning experience even further and provide
the opportunity for patients to visualize a 3D simulation of their own possible
outcomes, many breast augmentation practices around the world are
embracing various forms of interactive surgical simulation software
integrated with 3D image capture technology. Each of the currently available
systems uses multiple stereoscopic cameras to produce a seamless 3D image
of the patient, stitching together the pixels to create a truly lifelike image
(29). Various computer algorithms identify key landmarks and can calculate
existing breast volumes as well as asymmetries of the breasts and chest wall
(Fig. 97-4).
The most important question is whether the time spent performing the 3D
simulation is a valuable addition to the process of patient education and
informed consent? How the simulations are performed, and by whom, can be
of great importance in differentiating those practices that use 3D capture to
market and sell surgery versus those that use the system to educate and
demonstrate possible outcomes. The use of 3D capture technology should not
replace a traditional physical examination and manual measurements. A
computer-generated assessment will produce valuable information about the
size, shape, and position of the patient’s breasts and chest wall. These
measurements help guide the selection of a small range of implants that will
be offered to the patient. Systems can be loaded with implant data from
multiple manufacturers and patients can be given the opportunity to view
various volumes, projections, and fills. Some software systems allow for the
creation of a Health Insurance Portability and Accountability Act of 1996
(HIPAA) compliant portal for patients to upload the images and view at
home with family or friends. The addition of 3D capture into the informed
consent process may help produce a more knowledgeable patient (Fig. 97-5)
(30).
FIGURE 97-3 The effects of soft tissue coverage, selection of implant fill, and pocket
location. Implants may become visible and palpable after weight loss and training,
here in a competitive body builder. A, B: Preoperative. C, D: 6 months
postoperative. E, F: 1 year postoperative.
FIGURE 97-4 Simulations used to educate patients preoperatively. A: 3D
simulations can demonstrate key differences between the breasts. B: Simulations can
demonstrate chest wall and breast asymmetries. C, D: Patients can be shown how the
location of the IMF may affect the shape of the breast even more than the projection
and shape of the implant itself.

Patients must eventually decide upon an implant shell, fill, size, pocket
location, and the location of the incision. Surgeons can decide which of these
educational modalities works best for his or her practice in an efficient
manner, ensuring an effective transfer of information to breast augmentation
patients. In addition, all of the tools can be of great value in the management
of patient expectations and help distinguish the realistic from the unrealistic
patient. The educational tools described can be used repetitively to address
vital issues and make certain that there is effective communication of risk.
The expectation is that a well-educated patient is going to make better
lifelong decisions and be willing to be held accountable for those decisions.
CONVEYING LIFELONG RISK IN BREAST AUGMENTATION
A key factor in any communication of risk is whether the patient pays
attention to, and understands the details. In general, it is believed that the
greater the elaboration of risk messages, the greater the likelihood that the
resulting perception of risk will influence behavior (31). The decision to
undergo a breast augmentation is entirely elective, and patients should be
presented with useful information to be able to make well-informed
decisions. Information should be provided in a clear, positive, and personally
relevant format. For most patients, risk is relative and terms like, “the risk of
capsular contracture is very low” may not be clear or convincing. Whenever
possible, risk should also be communicated numerically in absolute
proportions. Numeracy, the patient’s ability to use numerical information and
its relation to health behavior, is not uniform among all patients. Many
patients lack the numerical skills that are essential to maintain their health
and make informed medical decisions. Low numeracy may distort a patient’s
perception of the risks and benefits of breast augmentation and these patients
are more likely to be swayed by the effects of mood or how the information is
presented. In an era where patients have access to a great deal of medical
information most often presented numerically, not all patients are prepared to
understand risk in term of numbers alone. Surgeons often provide data from
published peer-reviewed scientific literature in breast augmentation, or
compare their own capsular contracture rates to the manufacturers reported
rates. This may help explain why certain steps will be taken that have been
confirmed by a consensus of expert opinion to avoid known possible
complications.
FIGURE 97-5 3D simulations are useful to demonstrate superior malposition and
inferior malposition. Simulations can also be used to demonstrate the effect of a
heavy implant on the tissues over time. A: IMF too high. B: IMF location
proportionate to implant base width, and volume. C: IMF too low.

Conveying information about rare risks, or risks of yet unknown


complications, may be more understandable to some patients when compared
to relatively well-known lifetime health risks such as, “the known risk of
breast implant associated anaplastic large cell lymphoma (BIA-ALCL) at this
time is 1:2,832 (.003%), as compared to the 1:8 (12%) risk of developing
breast cancer during your lifetime” (32). Patients should not be overwhelmed
with information that they cannot understand and it is recommended that all
information provided, as well as the decisions made between the surgeon and
the patient, should be completely and thoroughly documented (7).
The Longevity of Breast Implants
It should be conveyed that despite the advances in technology, no device,
saline or silicone, will last forever. Patients must be provided with the
manufacturer’s package insert, informed consent documents, and all implant
warranty information. The FDA website also includes current information
from the Centers for Devices and Radiological Health, including patient
labeling information from Allergan, Mentor, Sientra, and Ideal implants (33).
The direct link to the manufacturer’s website is also available for the most
recent data on rupture and capsular contracture rates, and patients should be
provided with these links so they can view them again at home (34). Breast
augmentation surgeons who routinely follow their patient’s outcomes should
be able to provide long-term data on their own revision rates, including
surgeries for capsular contracture, rupture rates, and other complications.
Patients should then be given the opportunity to compare data, focus on
realistic risks, and make better choices. Data on rupture and capsular
contracture rates can be overwhelming for many patients, but providing the
information through visuals, numerically, and verbally will improve the
process of risk communication.
Breast Imaging for Cancer Screening and Addition of Office-
Based High-Resolution Ultrasound for Evaluation of Silicone
Gel Implants
Several studies have addressed the question of whether breast implants
interfere with mammography and therefore delay cancer detection in women
with breast augmentation (35,36). Patients need to be informed that the
presence of breast implants may interfere with standard mammography.
Silicone gel–filled breast implants are radiopaque, and the physical presence
of the implant may obscure part of the breast tissue and deform breast
structure. The amount of interference varies depending on a variety of
factors, including the position of the implant, any capsular contracture, and
the density of the breast parenchyma. Although there is evidence that
subpectoral placement of the implant may improve the amount of tissue
visible on mammography as compared with subglandular placement, the
effect that the placement of the implant has on the sensitivity and specificity
of screening needs further study (36). Breast implants are not, however,
associated with an increased risk of breast cancer incidence or death. In 2011,
the FDA identified a possible association between breast implants and the
development of ALCL, and in 2016 the World Health Organization
recognized BIA-ALCL as a unique type of T-cell lymphoma. Recent
information regarding the association of BIA-ALCL and textured devices has
changed the perception of risk and what unknowns may occur in the future,
but it is difficult to determine the true incidence of BIA-ALCL because of a
lack of information on the actual number of patients with both smooth and
textured breast implants worldwide (37). Patients should be advised that
studies have shown that women with breast augmentation who developed
breast cancer had tumors with better prognostic characteristics, including
smaller size, lower grade, and more favorable estrogen receptor status
(38,39). This may be due to the fact that augmented women have less natural
breast tissue or because the implant provides a firm surface to palpate against
(39). The best information that we can provide to breast augmentation
patients suggests that although the sensitivity of screening mammography is
lower in asymptomatic women with breast augmentation, there is no evidence
that this results in more advanced disease at diagnosis compared with women
without augmentation (38,40). Women seeking breast augmentation should
be assured by the consistency of scientific studies which have determined that
women with implants are not diagnosed at a later stage, are not at increased
risk for recurrent breast cancer, and do not have a decreased length of
survival (41). To increase sensitivity, patients need to be informed that they
may require displacement-type views and possible additional images (42).
Under ideal conditions, up to 90% of the breast may be visualized using these
modified mammography techniques. Patients also need to recognize that
capsular contracture may make imaging not only more difficult, but also
more painful (43).
Although some implant ruptures can be diagnosed on physical
examination, the sensitivity of plastic surgeons who routinely perform breast
augmentation to diagnose rupture by clinical examination has been reported
at 30% (44), compared to 89% for magnetic resonance imaging (MRI) (45).
As of this writing, the FDA guidelines on breast imaging with MRI for the
detection of rupture are under question, as the high costs associated with MRI
as a screening tool are a considerable deterrent. Small, portable high-
resolution ultrasound (HRUS) devices are becoming increasing popular and
affordable for in-office imaging by plastic surgeons, and patients need to be
informed that implants need long-term imaging to detect ruptures or palpable
concerns (46). Women considering breast augmentation need to be
encouraged to participate in long-term follow-up with their physicians and be
enrolled in breast implant registries to help evaluate the long-term safety and
benefits of breast implants (47,48).
EDUCATION AND ITS ROLE IN THE MANAGEMENT OF PATIENT
EXPECTATIONS
If the preoperative educational experience is to be complete, a significant
portion of the consultation should be devoted to the management of the
patient’s postoperative expectations. Time spent prior to surgery should
include a discussion of what factors the surgeon can and cannot predict or
control. Patient expectations related to breast size are perhaps the most
common early postoperative area of potential conflict between patient and
surgeon. Allergan’s core study data from the FDA PMA studies, updated in
2007, disclosed that patient request for size change, reported at 23.4%, was
the second most common reason for revision surgery at 4 years (31,34).
Sientra’s 10-year data demonstrated a 19.3% size change at 10 years (5).
Reoperation for incorrect size can mean either that a patient desires a larger
size after surgery than was agreed on before surgery or the patient is unhappy
with implants that have been oversized for her tissues. Furthermore,
physicians need to inform their patients that no method of breast
augmentation exists that can accurately determine an exact postoperative
breast cup size. The current accepted system of determining bra size is so
inaccurate and varies so often it is of no true value. If one includes the many
different styles of bras, fabrics, and elastics and the lack of standardization
among brands, it is understandable why women struggle to find a
comfortable, well-fitting bra. Determining the correct bra size is more a
matter of educated guesswork and trial and error than of precise
measurements (49). Bra sizing varies worldwide and differs considerably
among manufacturers. In addition, many bra manufacturers, designers, and
bra shop fitters have their own techniques for sizing and fitting. Patients often
are given misleading information concerning both their back measurements
and cup size. Confusion exists when patients either underestimate or
overestimate their back size, and very few understand the concept of sister
sizes; for example, a 34C is equivalent to a 36B bra. In the United States, the
U.S. Standard Clothing Size sets some guidelines, but there is no formal
standard inch-based brassiere sizing system in the United States (50,51).
Studies have demonstrated, however, that reoperations for size change can be
virtually eliminated when the surgeon places a high value on patient
education and decision-making processes that emphasize potential long-term
complications over postoperative cup size (7).
Patients, who share in the selection of their breast implants based on their
individual tissue measurements make decisions that are knowledge based and
patient centered. Communication is crucial during the informed consent
process, as is the absolute need to document the patient’s implant selection in
writing. The education process can also continue postoperatively if patients
question their size or shape after surgery. Quality preoperative photos and
Vectra 3D images with computer generated measurements of existing
asymmetries are invaluable as teaching tools postoperatively. Patients often
forget “how small,” “how ptotic,” or “how asymmetric” they were before
surgery. Side-by-side photography offers patients the opportunity to validate
the decisions that were made together with the surgeon. Patients who
understand and participate in the implant selection process by and large
accept their improvements in breast size and shape postoperatively.
Before surgery, patients should also be provided with a clear and forthright
dialogue that addresses the very issues that can drain the gratification out of
the physician–patient relationship after surgery. One of these issues concerns
who will be responsible financially for the possible known and unknown
events that might occur after surgery (52). Financial responsibilities after
surgery may include surgical or implant-related complications costs
associated with potential radiologic evaluation of the implants as they age,
and eventual replacement or removal of breast implants. Defining the
potential financial risks that may occur over the patient’s lifetime and
whether the surgeon or patient will be financially responsible is imperative
before breast augmentation. These important issues should be delineated in
writing during the informed consent process. Finally, patients should be
aware of the physician’s policy on “out-points,” defining when implant
removal without replacement would be recommended to decrease further
surgical and financial risks (53).
CONCLUSION
For decades preoperative decisions in breast augmentation, including implant
selection, pocket location, and incisions, were based on either a surgeon’s
subjective preferences or the desires of the patient. Although physicians were
responsible for obtaining informed consent prior to the procedure, there failed
to be a means to assess whether the decisions made by the patient were fully
informed and reflected the patient’s preferences based on an adequate
communication of risk by the physician and staff. Data suggest that breast
augmentation surgeons should try to better understand the patient’s
knowledge base and decision quality so as to address any gaps in
comprehension before surgery. Patient decisions in breast augmentation are
considered “preference-sensitive” clinical decisions and should reflect
decisions made by a well-informed patient. The informed consent process
should include quality patient decision aids that hopefully will be certified in
aesthetic breast augmentation surgery someday. The simultaneous
introduction of informed consent documents into the educational process will
help hold patients accountable for autonomous decisions while preserving
their right to self-determination. Furthermore, debate continues with regard to
a plastic surgeon’s beneficent duty to recommend that the patient reconcile
her desires within the limitations of her tissues if data suggest that doing
otherwise may increase risks of revision surgeries and potential uncorrectable
deformities. Patient consultations are now turning toward more interactive
learning experiences, with the inclusion of verbal, visual, and tactile tools in
order to create a more engaged and informed patient. Considerable social
media attention has been focused on the safety of breast implants, and many
women seeking breast augmentation may have unsubstantiated biases that
may require a multimodality educational approach to surmount. The
management of patient expectations should also include what factors a
surgeon can and cannot control and who will be financially responsible for
possible untoward results.
Finally, the physician must convey to patients the lifelong risks of breast
augmentation, which may be complicated by the natural aging process or
systemic symptoms that may or may not be related to their breast implants.
Events such as weight gains and losses, childbearing and breastfeeding,
breast cancer risks, and eventually menopause are all natural events in a
woman’s life. Furthermore, patient education in breast augmentation does not
end with the surgical procedure and should continue over the years as new
health risks may emerge, new implants are introduced, or infrequently, when
implants are recalled from the U.S. market. Plastic surgeons should be aware
that the most frequent complaint of women who reported dissatisfaction with
breast augmentation surgery to the FDA was that they felt they had not
received adequate information before surgery (54). Changes proposed by the
FDA in 2019 include the development of patient decision checklists to help
ensure that patients considering breast implants have the information they
need to have thoughtful and balanced discussions about the risks and benefits
of breast implants (55). It is unlikely that the FDA, the media, or social media
will ever turn their attention away from this issue. Physicians can however,
make a difference by assuring that their patients are well informed with
regard to the known and unknown risks of breast augmentation surgery.

REFERENCES

1. Code of Federal Regulations, Title 21, Volume 8, Revised as of April 1,


2018, (21 CFR 860.7)
2. Federal Register, Volume 53, Number 122, Pages 23749–24010, June
24, 1988
3. Adams WP, Potter JK. Breast implants: materials and manufacturing
past, present, and future. In: Spear SL, ed. Surgery of the Breast:
Principles and Art. 2nd ed. Baltimore, MD: Lippincott Williams &
Wilkins; 2006:424–437.
4. Maxwell G, VanNatta B, Bengston B, et al. Ten-year results from the
Natrelle 410 anatomical form-stable silicone breast implant core study.
Aesthet Surg J 2015;35(2):154–155.
5. Stevens WG, Calobrace MB, Alizadeh K, et al. Ten-year core study data
for Sientra’s Food and Drug Administration-approved round and shaped
breast implants with cohesive silicone gel. Plast Reconstr Surg
2018;141(4S Sientra Shaped and Round Cohesive Gel Implants):7S–
19S.
6. Adams WP. The process of breast augmentation: four sequential steps
for optimizing outcomes for patients. Plast Reconstr Surg
2008;122(6):1892–1900.
7. Tebbetts JB, Tebbetts TB. An approach that integrates patient education
and informed consent in breast augmentation. Plast Reconstr Surg
2002;110(3):971–978; discussion 979–981.
8. Cobb v Grant [1972].8 Cal3rd 229, 104 Cal Rptr 505, 502 P21.
9. Stewart M. Effective physician-patient communication and health
outcomes: a review. CMAJ 1995;152:1423–1433.
10. Whitney SN, McGuire AL, McCullough LB. A typology of shared
decision making, informed consent, and simple consent. Ann Intern Med
2004;140:54–59.
11. Ubbink D, Santema T, Lapid O. Shared decision-making in cosmetic
medicine and aesthetic surgery. Aesthet Surg J 2016;36(1):NP14–NP19.
12. Davis TC, Crouch MA, Willis G, et al. The gap between patient reading
comprehension and the readability of patient education materials. J
Family Pract 1990;31:533–538.
13. Ong LM, de Haes JC, Hoos AM, et al. Doctor-patient communication: a
review of the literature. Soc Sci Med 1995;40:903–918.
14. Kusec S, Oreskovic S, Skegro M, et al. Improving comprehension of
informed consent. Patient Educ Couns 2006;60:294–300.
15. Beardsley E, Jefford M, Mileshkin L. Longer consent forms for clinical
trials compromise patient understanding: so why are they lengthening? J
Clin Oncol 2007;25:e13–e14.
16. FDA takes action to protect patients from risk of certain textured breast
implants; Requests Allergan voluntarily recall certain breast implants
and tissue expanders from market. Available at
https://www.fda.gov/news-events/press-announcements/fda-takes-
action-protect-patients-risk-certain-textured-breast-implants-requests-
allergan. Accessed August 12, 2019.
17. Flory J, Emanuel E. Interventions to improve research participants
understanding in informed consent for research: a systematic review.
JAMA 2004;292:1593–1601.
18. Wood S, Spear S. What do women need to know and when do they need
to know it? Plast Reconstr Surg 2007;120(7):135S–139S.
19. Veatch R. Implied, presumed and waived consent: the relative moral
wrongs of under and over-informing. Am J Bioeth 2007;7(12):39–54.
20. Sepucha K, Ozanne E, Silvia K, et al. An approach to measuring the
quality of breast cancer decisions. Patient Educ Couns 2007;65:261–
269.
21. Schneider CE. The Practice of Autonomy: Patients, Doctors, and
Medical Decisions. New York: Oxford University Press; 1998.
22. Tauber AI. Patient Autonomy and the Ethics of Responsibility.
Cambridge, MA: MIT Press; 2005.
23. Yermilov I, Chow W, Devgan L, et al. How to measure the quality of
surgery-related web sites. Am Surg 2008;74:997–1000.
24. Alston C, Berger Z, Brownlee S, et al. Shared decision-making
strategies for best care: Patient decision aids. Available at
https://nam.edu/perspectives-2014-shared-decision-making-strategies-
for-best-care-patient-decision-aids/. Accessed August 14, 2019.
25. Noland K, Juhn G. The Visual Health Experience: Tools, Technology,
and Information for Providers and Their Patients. Atlanta, GA: ADAM;
2001.
26. Young VL, Watson ME. Breast implant research: where we have been,
where we are, where we need to go. Clin Plast Surg 2001;28(3):451–
483.
27. Swami V. Body appreciation, media influence, and weight status predict
consideration of cosmetic surgery among female undergraduates. Body
Image 2009;6(4):315–317.
28. The FDA requests Allergan voluntarily recall Natrelle Biocell textured
breast implants and tissue expanders from the market to protect patients:
FDA safety communication. Available at https://www.fda.gov/medical-
devices/safety-communications/fda-requests-allergan-voluntarily-recall-
natrelle-biocell-textured-breast-implants-and-tissue. Accessed August
11, 2019.
29. Epstein M, Scheflan M. Three-dimensional imaging and simulation in
breast augmentation: what is the current state of the art? Clin Plast Surg
2015;42(4):437–450.
30. Canfield. Available at https://www.canfieldsci.com/imaging-
systems/vectra-m3-3d-imaging-system/. Accessed August 11, 2019.
31. Lipkus IM. Numeric, verbal, and visual formats of conveying health
risks: suggested best practices and future recommendations. Med Decis
Making 2007;27:696–713.
32. Collett D, Rakhorst H, Lennox P, et al. Current risk estimate of breast
implant-associated anaplastic large cell lymphoma in textured breast
implants. Plast Reconstr Surg 2019;143:(3S A Review of Breast Implant
Associated Anaplastic Large Cell Lymphoma):30S–40S.
33. U.S. Food and Drug Administration. Labeling for approved breast
implants. Available at https://www.fda.gov/medical-devices/breast-
implants/labeling-approved-breast-implants. Accessed August 11, 2019.
34. Hammond DC, Canady JW, Love TR, et al. Mentor contour profile gel
implants: clinical outcomes at 10 years. Plast Reconstr Surg
2017;140(6):1142–1150.
35. Allergan. Breast implant answers: understanding silicone gel-filled
breast implants. Available at http://www.breastimplantanswers.com/.
Accessed August 11, 2019.
36. Miglioretti DL, Rutter CM, Geller BM, et al. Effects of breast
augmentation on the accuracy of mammography and cancer
characteristics. JAMA 2004;291:442–450.
37. Seiber DA, Adams WP. What is your micromort? A patient-oriented
analysis of breast implant associated large cell lymphoma (BIA-ALCL).
Aesthet Surg J 2017;37(8):887–891.
38. Handel N, Silverstein MJ, Gamagami P, et al. Factors affecting
mammographic visualization of the breast after augmentation
mammaplasty. JAMA 1992;268:1913–1917.
39. Deapen D. Breast implants and breast cancer: a review of incidence,
detection, mortality, and survival. Plast Reconstr Surg 2007;120(suppl
1):70S–80S.
40. Clark CP 3rd, Peters GN, O’Brien KM. Cancer in the augmented breast.
Diagnosis and prognosis. Cancer 1993;72(7):2170–2174.
41. Hoshaw S, Klein P, Clark B, et al. Breast implants and cancer:
causation, delayed detection, and survival. Plast Reconstr Surg
2011;107(6):1393–1407.
42. Eklund GW, Busby RC, Miller SH, et al. Improved imaging of the
augmented breast. AJR Am J Roentgenol 1988;151:469–473.
43. Brown SL, Todd JF, Luu HD. Breast implant adverse events during
mammography: reports to the food and drug administration. J Women’s
Health 2004;13:371–378; discussion 379–380.
44. Hölmich LR, Fryzek JP, Kjøller K, et al. The diagnosis of silicone breast
implant rupture. Clinical findings compared to findings at magnetic
resonance imaging. Ann Plast Surg 2005;54(6):583–589.
45. Hölmich LR, Vejborg I, Contrad C, et al. The diagnosis of breast
implant rupture: MRI findings compared to findings at explanation. Eur
J Radiol 2005;53:213–225.
46. Bengston B, Eaves F. High resolution ultrasound in the detection of
silicone gel breast implant shell failure: background, in vitro studies, and
early clinical results. Aesthet Surg J 2012;32(2):157–174.
47. Allergan. BIFS. Breast Implant Follow-up Study. Available at
http://www.bifs.us/. Accessed August 11, 2019.
48. Pusic A. U.S. national breast implant registry (NBIR) and patient
registry and outcomes for breast implants and anaplastic large cell
lymphoma etiology and epidemiology (PROFILE) Status Update, U.S.
FDA. Available at https://www.fda.gov/media/123021/download.
Assessed August 11, 2019.
49. Prechter EA. A new method for determining bra size and predicting
post-augmentation breast size. Plast Reconstr Surg 1998;102(4):1259–
1265.
50. Apparel Search Company. US standard clothing sizes. Definition for the
clothing industry. Available at
http://www.apparelsearch.com/Definitions/Miscellaneous/US_standard_clothing_size
Accessed August 12, 2019.
51. Bengston B, Glicksman C. The standardization of bra cup
measurements: redefining bra sizing language. Clin Plast Surg
2015;42(4):405–411.
52. Wood SF, Spear SL. What women need to know and when do they need
to know it? Plast Reconstr Surg 2007;120:135S–139S.
53. Tebbetts JB. “Out points” criteria for breast implant removal without
replacement and criteria to minimize reoperations following breast
augmentation. Plast Reconstr Surg 2004;114:1258–1264.
54. Merkatz RB, Bagley GP, McCarthy EJ. A quantitative analysis of self-
reported experience among women encountering difficulties with
silicone breast implants. J Women’s Health 1993;2:105–109.
55. Statement from FDA Principal Deputy Commissioner Amy Abernethy,
MD PhD., and Jeff Shuren, MD, JD, director of the FDA’s Center for
Devices and radiologic health on FDA’s new efforts to protect women’s
health and help ensure the safety of breast implants, May 2, 2019.
Available at https://www.fda.gov/news-events/press-
announcements/statement-fda-principal-deputy-commissioner-amy-
abernethy-md-phd-and-jeff-shuren-md-jd-director-fdas/. Accessed
August 11, 2019.
CHAPTER 98

Inframammary Approach to Breast


Augmentation
M. BRADLEY CALOBRACE | CHET MAYS
HISTORY
Achieving a successful outcome in breast augmentation requires excellent
preoperative and intraoperative decision making and expert surgical
execution. Thoughtful consideration of the patient’s desired aesthetic result in
conjunction with the anatomic characteristics of her breast and chest wall
provides insight into the optimal surgical approach to achieve a successful
outcome. There are many incisional approaches to breast augmentation,
including inframammary, periareolar, transaxillary, and transumbilical. The
inframammary approach has increasingly become the preferred incisional
approach and is the most commonly performed today.
PREOPERATIVE PLANNING
One of the most critical steps in achieving excellence in breast augmentation
is the preoperative evaluation. The preoperative evaluation through a
thorough assessment should identify not only the appropriate implant to
achieve optimal results, but also the location of the incision, the implant
pocket, asymmetries of the breast, chest wall, and/or nipple areolar complex,
and the potential need to lower the inframammary fold (IMF). The
preoperative markings create a roadmap for the planned procedure (Fig. 98-
1).

FIGURE 98-1 Preoperative markings showing the Sternal notch-to-nipple distance,


breast width, inframammary fold, and dual plane plan.

Evaluation of the soft tissue coverage including quality of skin and breast
tissue, amount of breast parenchyma, the footprint of the breast, and the level
of ptosis is essential to determining the optimal pocket for implant placement.
Precise pocket creation and appropriate implant choice are the best
safeguards against postoperative implant malposition issues. Likewise, the
most common reason for revisional surgery after a breast augmentation is
capsular contracture (1,2). There is strong evidence that biofilm development
from bacterial contamination is a significant causative component in the
development of capsular contracture (3–6). Part of the operative planning,
therefore, should include efforts to minimize this risk when possible. Table
98-1 summarizes some of the implant and surgical technique options that
have been associated with lower capsular contractures (7–23).

TABLE 98-1 Associated With Reduced Capsular Contracture Rates


Associated With Reduced Capsular Contracture Incidence
No-touch technique (7–9)
Nipple shields (8)
Pocket irrigation with triple antibiotics (10)
Insertion sleeve (9)
Submuscular implant pocket (11–13)
Textured implants (11,13–18)
Inframammary incision (13–19)
Cohesive shaped implants (20–23)
OPERATIVE TECHNIQUE
PATIENT POSITIONING
Patients are placed on the operating room table in the supine position. The
arms are secured to the armboard with soft gauze wraps at 45 degrees to
stabilize the patient in the upright position (Fig. 98-2).
This relaxes the pectoralis muscle providing a more accurate assessment of
the implant position and the redraping of the overlying breast tissue.
Alternatively, some surgeons prefer placing the arms along the side of the
patient on the operative table, but an armboard at 90 degrees should be
avoided as it does not allow accurate assessment of the breast when the
patient is placed in the upright position.
INFILTRATION OF LOCAL
Prior to surgical preparation, 50 mL of a local field block is injected of 1/4%
lidocaine, 1/8% bupivacaine, and 1:400,000 epinephrine (see Table 98-2).
The injection is placed in the dermis along the planned incision line, and as a
field block with injections along the IMF, the medial pectoral border, the
anterior axillary line and finally deep to the breast parenchyma in a fanning
fashion throughout the area of planned pocket creation (Fig. 98-3).
These injections provide not only assistance in operative hemostasis, but
also in the management of postoperative pain.
SURGICAL PREP AND STERILE DRAPING
After local infiltration, nipple shields (created by placing a small piece of
Tegaderm over each nipple areolar complex) provide a barrier against
potential bacterial contamination (Fig. 98-4) (8).
The patient is prepped with chlorhexidine and draped to provide a sterile
field with the entire chest and bilateral breasts visible for assessment during
the procedure. The sterile dressings must be secured to prevent disruption in
the sterile field while placing the patient in the upright position.

TABLE 98-2 Breast Local Anesthetic Formula


Breast Local Anesthetic Formula
1/2% Lidocaine plain 25 mL
1/2% Lidocaine/1:200,000 25 mL
epinephrine
1/2% bupivacaine/1:200,000 25 mL
epinephrine
Injectable saline 25 mL
Total concentration: 1/4% 100 mL
lidocaine, 1/8% bupivacaine,
1:400,000 epinephrine
FIGURE 98-2 Patient positioning on operating room table with arms at 45 degrees.
FIGURE 98-3 Infiltration of breast of local with a 20-cc syringe and spinal needle.
FIGURE 98-4 Nipple shields over the entire NAC to provide a barrier to bacterial
contamination.

TABLE 98-3 Advantages to Placement of the IMF Incision


Advantages to Placement of an IMF Incision
• Well-hidden scar in the fold of the breast
• Incisional length is unlimited, thus can accommodate any and all implant
choices
• Excellent visualization for dissection of the implant pocket
• The ability to control the IMF position during incision closure
• Can be used for any complication revision
• Lower capsular contracture
• Minimal issue of a scar contracture creating deformity
• Potentially less nipple sensation changes
INFRAMAMMARY INCISION
The IMF has become the preferred incision location for most surgeons today.
There are many advantages (Table 98-3) and some disadvantages (Table 98-
4) which must be considered to ensure the appropriateness of the IMF
approach.
The size of the incision depends on the location, but in general should be
as small as possible and yet large enough to safely dissect the pocket and
place the implant without distortion or injury to the device. In general, the
incision length increases with increases in implant size, gel cohesiveness,
optimal fills, and texturization of the implant. Implant fractures of form-
stable cohesive implants and rupture or distortion of silicone implants have
been associated with attempting to place implants through incisions
inadequate to accommodate the implant. Additionally, the quality of the scar
is often better if a slightly larger scar is utilized, reducing the stretch and
retraction injury placed on the scar. Incision length ranges include: 3 to 4.5
cm for saline implants, 4 to 6 cm for silicone round implants, and 4.5 to 7 cm
for shaped cohesive silicone implants.
INFRAMAMMARY FOLD POSITIONING
Predicting the final position of the IMF is critical to determining the
placement of all breast incisions, but especially the inframammary incision.
This can be a challenging task as so many variables contribute to the final
position of the fold. The IMF is formed by the fusion of the anterior and
posterior leaves of the superficial fascia which is intimately associated with
the dermis at the lowest aspect of the inferior pole of the breast (24). During
preoperative markings, the native IMF is identified and marked in the sitting
position. The true IMF position is determined by performing an IMF
expansion test. The breast is grasped and autorotated inferiorly to identify the
inferior extent of the attachments of the IMF (Fig. 98-5).

TABLE 98-4 Disadvantages to Placement of an IMF Incision


Disadvantages to Placement of an IMF Incision
• The scar is located on the breast
• Scar may be more visible if breast fold is absent or if the scar becomes
pigmented
• Must determine final IMF position preaugmentation and place scar
precisely in planned new fold
• Scar position more vulnerable to irritation from the bra
FIGURE 98-5 Inferior autorotation of the breast to identify the inferior attachments
of the inframammary fold.

This is the best predictor of where the fold will naturally sit after breast
augmentation. The amount of lower pole skin required and the ultimate
position of the fold is a function of many factors, including the type of
implant (saline vs. silicone, round vs. shaped), size of implant, pocket
location, and the strength and stability of the soft tissue of the lower pole.
The distance measured from the nipple to true fold under maximal stretch
assesses the amount of lower pole skin available to accommodate the selected
implant. An acceptable standard that has been used is an implant with a base
diameter of 11 cm requires 7 cm, a base diameter of 12 cm requires 8 cm, and
a base diameter of 13 requires 9 cm (25). A more comprehensive evaluation
has been described using tissue-based planning principles (26). In the High
Five System analysis, variables are analyzed including implant volume,
patient’s base width, implant base width, anterior pulled skin stretch, and
nipple-to-fold (N-IMF) distance under maximal stretch. Based on the selected
implant, a reference chart provides the desired N-IMF distance, which if
longer than the measured distance, will require IMF lowering.
In determining fold position, our team has found three alternative methods
extremely useful. One method is using a formula to determine optimal N-
IMF distance with a formula using implant projection and height shown in
Table 98-5.

TABLE 98-5 Formula for Determining Optimal N-IMF Distance


Optimal N-IMF distance = ½ implant projection + ½ implant height

TABLE 98-6 Determining Optimal N-IMF Distance Based on Implant


Height and Fill Volume
Optimal N-IMF Base Diameter (cm) Volume (cc)
Distance (cm)
7 11 200
8 12 300
9 13 400

The other methods involve using either the base diameter or fill volume of
the implant to determine the optimal N-IMF distance shown in Table 98-6. If
the current N-IMF is shorter than the optimal distance, the fold will need to
be lowered.
If the desired N-IMF distance is equal or less than the measured N-IMF
distance, then the fold does not require lowering. The distance can be
adjusted based upon expectation for lower pole stretch postoperatively. It is
important to recognize that IMF lowering is less often required when placing
a larger smooth or saline silicone implant, especially if higher profile,
secondary to lower pole, stretches over time (27,28). However, when implant
choice or soft tissue characteristics predict less lower pole stretching, IMF
lowering may be required (13,29). Likewise, shaped implants are not only
textured but also have a greater volume of a more cohesive gel present in the
lower pole of the implant, thus requiring more lower pole skin to
accommodate the implant (20–23,30,31). Table 98-7 identifies some implant
and soft tissue characteristics that may be associated with greater need to
lower the IMF due to less postoperative stretching of the lower pole
(13,20–23,26–31).
INCISION
The inframammary incision provides direct access and visualization of the
pocket with the least injury to surrounding structures. After determining the
IMF position (either the native true fold position or the planned lowered
position), a paramedian line is drawn through the center of the breast and
bisects the newly drawn IMF. The incision’s medial extent begins 1 cm
medial to the paramedian line and extends laterally for the appropriate
distance as previously described (Fig. 98-6).

TABLE 98-7 Characteristics Associated With Less Stretching of the Lower


Pole
Characteristics Associated With Less Stretching of the Lower Pole
Textured implants
Cohesive implants
Shaped implants
Silicone compared to saline implants
Lower-profile implants
Smaller implants
Tight, firm breast skin
FIGURE 98-6 Thick black vertical line is the paramedian line through the center of
the breast. The red line is the IMF incision with its most medial extent 1 cm medial
to the paramedian line and extending laterally.

The initial incision is made with a 15 blade and then dissection is carried
out with electrocautery through the skin and subcutaneous tissue beveling
upward while rotating the breast off the chest wall. The dissection proceeds
subcutaneous for approximately 1 cm and then deep through the superficial
fascia and toward the lateral pectoral border deep on the chest wall. This
technique preserves a small cuff of superficial fascia at the incision which
helps to protect the IMF and will prove useful during closure (Fig. 98-7).
IMPLANT POCKET
There continues to be divergent thought as to the optimal pocket for breast
implants. The subglandular/subfascial pocket is the most natural for the
implant with avoidance of animation deformities seen with submuscular
implants, enhanced correction of constricted breast or ptotic breasts, ease of
dissection, and less postoperative discomfort for the patient (32–35). The
submuscular pocket advantages includ lower capsular contracture rates,
enhanced coverage of the implant minimize issues of wrinkling, provides a
more natural upper pole, and provides enhanced support for the breast
implant (11–13,32–34,36). Undoubtedly, the issues of wrinkling and need for
enhanced coverage with saline implants provided the impetus for
submuscular pockets becoming the preferred pocket by U.S. surgeons
(29,37,38). It has been widely accepted that an upper pole pinch test of 2 cm
is required to place an implant in the subglandular/subfascial pocket to reduce
the risk of upper pole implant visibility or wrinkling. With the availability of
silicone implants, both round and shaped, and simultaneous fat grafting,
optimal pocket choice may be even more elusive.
FIGURE 98-7 Cuff of superficial fascia which has been colored purple in the photo
for illustration purposes.

No matter which pocket is selected, it is helpful during the marking


process to identify as accurately as possible the pocket size necessary to
accommodate the selected implant. This will provide a pocket that maintains
the implant in a control position and minimizes the risk of postoperative
implant malposition. In breast augmentation with round implants, the
accurate placement of the IMF and control of the medial and lateral extent of
the pockets provide ideal implant positioning to achieve the desired cleavage
and minimize lateral migration of the implant (29). When using a shaped
implant, a controlled pocket including the superior extent is even more
essential to minimize the risk of implant rotation postoperatively (23,30,31).
DUAL PLANE SUBMUSCULAR POCKET
The importance of optimizing soft tissue coverage in breast augmentation can
be overstated. Inadequate coverage, often combined with oversized implants,
can lead to parenchymal atrophy and skin stretching resulting in wrinkling
and palpability of the implants and other associated breast deformities
(27,28). The dual plane, initially described by Tebbetts, maximizes coverage
and support of the breast implant while minimizing the disadvantages of
submuscular placement including animation deformities and pseudoptosis of
the breast tissue overlying the submuscular implant (i.e., waterfall deformity)
(36).
When performing a dual plane pocket, the lateral pectoral border is
identified, and fascia incised to expose the underlying muscle. Upward
retraction of the breast tissue will usually elevate the lateral border allowing
further dissection and placement of the retractor beneath the overlying
pectoralis muscle (Fig. 98-8).
A very helpful “rule” is to never cut through the muscle that cannot be
elevated. The inability to tent the muscle up off the chest wall may indicate
that the muscle fascia is extremely adherent, but more likely that the
identified muscle is actually not the pectoralis, but rather the serratus, rectus,
or an intercostal muscle. Continuing the dissection through an intercostal
could inadvertently penetrate the pleural space resulting in a pneumothorax.
Once the edge of the pectoralis is safely elevated and the subpectoral space is
identified, dissection is carried upward centrally to the superior extent of the
pocket. Dissection is then carried laterally to identify the pectoralis minor and
then carried directly over its fascia until the lateral border of the pocket is
reached. Dissection is then continued along the lateral border of the pocket,
identifying and staying superficial to the serratus muscle until the inferior
extent of the pocket at the IMF is reached. The muscle is then released along
the planned IMF, staying 1 cm superior to the fold to account for
postoperative caudal muscle descent (Fig. 98-9).
FIGURE 98-8 Elevation of the lateral border of the pectoralis major muscle.

Dissection directly at the fold will often lead to a fold that is lower than
planned as the muscle retracts inferiorly. As you carry your dissection
medially along the IMF it is critically important to stop the dissection at the
most medial extent along the sternum. A transition point (TP) occurs as you
taper the muscle release along the main body of the muscle into the transition
zone (TZ) toward the sternum. Preservation of the most caudal attachment of
the pectoralis muscle along the sternum is critical to minimize the chance of
window shading of the pectoralis with subsequent medial implant exposure
and animation deformities (Fig. 98-10).
FIGURE 98-9 Pectoralis major muscle release with electrocautery 1 cm above the
IMF.
FIGURE 98-10 The dark black line is the IMF. The blue dotted line represents the
release of the pectoralis major muscle 1 cm superior to the IMF. As you approach
the sternum with the muscle release you create a transition point (TP, thick blue line)
and begin to taper the muscle in a transition zone (TZ) up to the sternum. The thick
red line indicates where to stop the thinning of the muscle at the sternum.

The extent of the pocket is completed by defining the medial pectoral


border by dividing the accessory slips of pectoralis muscle that insert along
the ribs, preserving the main body of the muscle as it inserts along the
sternum. Dividing these muscles with electrocautery rather than blunt
dissection improves postoperative cleavage and maintains prospective
hemostasis.
The dual plane approach ultimately creates a subglandular pocket in the
inferior breast pocket. The levels of dual plane represent the amount of
muscle released from the inferior breast tissue and resultant inferior
subglandular pocket (Fig. 98-11).

FIGURE 98-11 Dual plane levels. Dual plane 1 is complete division of the pectoralis
major muscle (PMM) along the IMF. Dual plane 2 is release of the breast tissue off
the PMM up to the lower areola. Dual plane 3 is release of the breast tissue off the
PMM up to the upper border of the areola.

Division of the inferior pectoralis muscle just above the IMF during initial
pocket dissection created a dual plane level 1. The level of dual plane
required varies and each surgery can be tailored to provide the optimal level
based on soft tissue requirements and implant selection. In general, creating a
subglandular pocket inferiorly is required to either redrape the skin and breast
tissue more accurately over the implant or for expansion and exposure of the
lower pole, such as in a tuberous or constricted breast. The release of the
caudal edge of the muscle is performed incrementally, creating the least
amount of release that will adequately address the lower pole. Placement of a
retractor into the breast pocket and elevating superiorly while rocking the
breast tissue over the retractor will assist in assessing the effects of the
implant on the overlying skin and breast tissue once placed in the pocket
(Fig. 98-12). When a dual plane is created for expansion and exposure in a
tight envelope, the level will depend on the need to access the parenchyma
for scoring and expansion. This usually requires at least a level 2 and often a
level 3 dual plane to expose the retroareolar tissue.

FIGURE 98-12 Releasing the breast tissue off of the caudal edge of the pectoralis
major muscle to create the dual plane.
SUBGLANDULAR/SUBFASCIAL POCKET
The subglandular or subfascial pocket can be easily developed through the
inframammary incision and this dissection is performed without the need for
muscle division or dual plane creation. Once the incision is made and the
lateral pectoral border has been identified, the dissection is carried out either
above (subglandular) or deep to (subfascial) the pectoralis fascia. As the
dissection is carried medially in the subglandular plane, the midline can
quickly be violated due to the lack of sternal muscle attachments that usually
limits your dissection in the submuscular plane. When dissecting the
subfascial pocket, the fascial attachments assist in limiting the medial
dissection. This is important as inadvertent overdissection can lead to implant
medialization, visibility, and potentially symmastia. The pocket dissection
then proceeds to the extent of the desired pocket. The subfascial plane can be
a more challenging dissection as there is no natural plane present for this
dissection. The subfascial pocket is often preferred over a subglandular
pocket when shaped implants are used as it potentially provides a more
precise and stable pocket in the upper pole to avoid implant rotation.
Implant Placement
Once the pocket has been created, it is irrigated with triple-antibiotic betadine
solution (50 mL of povidone-iodine, 1 g of Cefazolin sodium, 50,000 units of
bacitracin mixed in 500 mL of normal saline) or 50% povidone-iodine saline
solution and hemostasis is assessed (10). It is the goal during the operation to
achieve prospective hemostasis with minimal blood staining, however a final
assessment is mandatory prior to implant placement. The implants are soaked
in the irrigation solution prior to insertion. Gloves are changed and rinsed
with the irrigation solution to remove any lint or powder.
The implant is then placed either manually or with the assistance of an
insertion sleeve such as the Keller funnel (Fig. 98-13) (9).
The opening of the funnel should be cut large enough to allow the implant
to pass easily through the funnel. The funnel provides a “minimal to no-
touch” technique which has been associated with lower capsular contracture
rates (7). The funnel allows for easier implant placement with potentially
smaller incision requirements compared to manual placement. Once the
implant is in the pocket, a finger-assisted assessment and manipulation of the
implant within the pocket is necessary to confirm its proper placement and
assure appropriate redraping of the breast parenchyma over the implant. This
maneuver is especially important with textured devices as these implants are
less mobile and less likely to stretch the pocket and thus a distortion or
wrinkling of the implant in a tight pocket may be permanent if not resolved
prior to closure. Repeated removal and insertions of the implant should be
avoided to minimize implant or incision damage, potential contamination,
and pocket overdissection.

FIGURE 98-13 Implant insertion with the Keller funnel for a “no-touch” technique
to minimize contamination.
CLOSURE
Prior to incision closure, the patient should be placed in the upright position
to assess implant position, fold position, symmetry, and the adequacy of the
dual plane (Fig. 98-14).

FIGURE 98-14 Patient sitting upright on the operating room table for final
assessment prior to closure.
FIGURE 98-15 Closure of the superficial (Scarpa) fascia from the superior edge to
the superficial fascia and deep fascia of the inferior edge to effectively lock down the
IMF.

Any additional adjustments of the dual plane can be accomplished after the
patient is placed back in the recumbent position by simply retracting the
breast tissue superiorly off the implant, identifying the caudal edge of the
muscle, and releasing it incrementally off the overlying breast tissue to the
desired level.
A significant advantage of the inframammary approach is the ability to
accurately and effectively control the fold position during closure of the
incision. The cuff of superficial fascia that was preserved during the initial
incision is utilized to secure the fold during closure. Although in our practice
all IMFs are “locked-down” during incisional closure, it could be argued that
a well-developed stable IMF that has not been violated or lowered during the
procedure is potentially stable and may only require a more superficial
closure. However, when the fold is unstable due to either inherent weakness
in the fold structure or from disrupting it with fold lowering, closure should
include stabilization of the fold structure. This is accomplished by securing
caudal edge of the Scarpa fascia present on the lower incisional edge to the
underlying deep fascial structures with an absorbable suture such as a 2-0
Vicryl (Fig. 98-15).
This is usually done by simply incorporating the superficial and deep
fascia together during a running closure. It may also be performed by first
placing three to four interrupted sutures on the lower flap securing Scarpa
fascia to the underlying deep fascia followed by closure of the incision. The
incision is closed in three layers:
1. Scarpa fascia superiorly to Scarpa fascia and the deep fascia inferiorly
2. Deep dermis
3. Subcuticular
POSTOPERATIVE MANAGEMENT
Patients are wrapped in an ace wrap for the first 24 hours followed by a
sports bra to be worn 23 hours a day for the next 4 weeks. Early range of
motion beginning in the recovery room is initiated for all patients which
includes shoulder rolls in both directions as well as elevation of the arms
outward to the sides and over the head. With smooth devices, implant
massage begins postoperative day 4 and includes displacing the implant
upward and downward in the pocket, crossing the arms and pulling the
implants inward to create cleavage, and downward pressure on the implants
to stretch the lower pole. Implant massage is contraindicated with textured
surface devices as it can irritate the pocket and potentially create serous fluid
around the implant. Likewise, the implants are placed in a controlled pocket
with the implant positioned appropriately at the base of the pocket and
displacement could lead to implant malposition or in the case of shaped
devices, rotation of the implant. Limited arm movement other than range of
motion is recommended for the first week. It is also advisable to limit
strenuous exercise for 6 to 12 weeks with textured implants to avoid early
seroma formation. Patients are allowed to resume regular bras after 4 weeks
but should continue with sports bra during bedtime for an additional 2 to 4
weeks to limit lateral implant migration while recumbent. Normal activity
resumes within a few days after surgery, but exercise and high impact activity
should be delayed for 3 to 4 weeks. Whereas smooth implants often seem
high initially and often require downward massage and/or the use of breast
bands or bandeaus, textured devices that are appropriately seated in the base
of the breast pocket should only occasionally require such maneuvers.

CASES

CASE 1

A 47-year-old female (Fig. 98-16) with no breast ptosis underwent


bilateral inframammary fold submuscular augmentation with textured
250-cc low-profile cohesive silicone implants.
FIGURE 98-16 A 47-year-old female with no breast ptosis underwent
bilateral inframammary fold submuscular augmentation with textured round
250-cc low profile cohesive silicone implants.

CASE 2

A 35-year-old female (Fig. 98-17) with no breast ptosis underwent


bilateral inframammary fold submuscular augmentation with textured
shaped 350-cc classic cohesive silicone implants.
FIGURE 98-17 A 35-year-old female with no breast ptosis underwent
bilateral inframammary fold submuscular augmentation with textured
shaped 350-cc classic cohesive silicone implants.

CASE 3

A 31-year-old female (Fig. 98-18) with grade I breast ptosis underwent


bilateral inframammary fold subglandular augmentation with textured
round 355-cc moderate-profile cohesive silicone implants.
FIGURE 98-18 A 31-year-old female with grade I breast ptosis underwent
bilateral inframammary fold subglandular augmentation with textured
round 355-cc moderate-profile cohesive silicone implants.

CASE 4

A 41-year-old female (Fig. 98-19) with grade I breast ptosis on the left
and grade II ptosis on the right underwent bilateral inframammary fold
subfascial augmentation with textured round 355-cc moderate-profile
cohesive silicone implants
FIGURE 98-19 A 41-year-old female with grade I breast ptosis on the left and
grade II ptosis on the right underwent bilateral inframammary fold
subfascial augmentation with textured round 355-cc moderate-profile
cohesive silicone implants.
CONCLUSION
The inframammary approach to breast augmentation is the preferred
technique by most surgeons today and begins with careful preoperative and
intraoperative decision making. Consideration of the patient’s desired
outcome, soft tissue, and chest wall characteristics, and the degree of ptosis
provide important information in determining the optimal implant, incision,
and pocket. The ability to create an accurate and symmetrical pocket that
allows for appropriate breast tissue redraping, efforts to minimize bacterial
contamination/biofilm formation, and the control of the pocket and IMF are
hallmarks of a reproducible and successful breast augmentation procedure.

REFERENCES

1. Spears SL, Murphy DK, Slicton A, et al. Inamed silicone breast implant
core study results at 6 years. Plast Reconstr Surg 2007;120:8S–16S;
discussion 17S–18S.
2. Cunningham B, McCue J. Safety and effectiveness of Mentor’s
MemoryGel implants at 6 years. Aesthetic Plast Surg 2009;33:440–444.
3. Araco A, Caruso R, Araco F, et al. Capsular contracture: a systematic
review. Plast Reconstr Surg 2009;124:1808–1819.
4. Virden CP, Dobbke MK, Stein P, et al. Subclinical infection of the
silicone breast implant surface as a possible cause of capsular
contracture. Aesthetic Plast Surg 1992;16:173–179.
5. Pajkos A, Deva AK, Vicery K, et al. Detection of subclinical infection
in significant breast implant capsules. Plast Reconstr Surg
2003;111:1605–1611.
6. Rieger UM, Mesina J, Kalbermatten DF, et al. Bacterial biofilms and
capsular contracture in patients with breast implants. Br J Surg
2013;100:768–774.
7. Mladick RA. “No-touch” submuscular saline breast augmentation
technique. Aesthetic Plast Surg 1993;17:183–192.
8. Wixtrom RN, Stutman RL, Burke RM, et al. Risk of breast implant
bacterial contamination from endogenous breast flora, prevention with
nipple shields, and implications for biofilm formation. Aesthet Surg J
2012:32:956–963.
9. Moyer HR, Ghazi B, Saunders N, et al. Contamination in smooth gel
breast implant placement: testing a funnel versus digital insertion
technique in a cadaver model. Aesthet Surg J 2012;32(2):194–199.
10. Adams WP, Rios JL, Smith S. Enhancing patient outcomes in aesthetic
and reconstructive breast surgery using triple antibiotic breast irrigation:
six-year prospective clinical study. Plast Reconstr Surg 2006;118(Suppl
7):46S–52S.
11. Stevens WG, Nahabedian MY, Calobrace MB, et al. Risk factor analysis
for capsular contracture: a 5-year Sientra study analysis using round,
smooth and textured implants for breast augmentation. Plast Reconstr
Surg 2013;132(5):1115–1123.
12. Schaub TA, Ahmad J, Rohrich RJ. Capsular contracture with breast
implants in the cosmetic patient: saline versus silicone. A systematic
review of the literature. Plast Reconstr Surg 2010;126:2140–2149.
13. Namnoum JD, Largent J, Kaplan HM, et al. Primary breast
augmentation clinical trial outcomes stratified by surgical incision,
anatomical placement and implant device type. J Plast Reconstr Aesthet
Surg 2013;66(9):1165–1172.
14. Barnsley GP, Siigurdson LJ, Barnsley SE. Textured surface breast
implants in the prevention of capsular contracture among breast
augmentation patients: a meta-analysis of randomized controlled trials.
Plast Reconstr Surg 2006;117:2182–2190.
15. Hakelius L, Ohlsen L. Tendency to capsule contracture around smooth
and textured gel-filled silicone mammary implants: a 5-year follow-up.
Plast Reconstr Surg 1997;100:1566–1569.
16. Burkhardt B, Eades E. The effect of biocell texturizing and povidone-
iodine irrigation on capsule contracture around saline-inflatable breast
implants. Plast Reconstr Surg 1995;96:1317–1325.
17. Coleman DJ, Foo IT, Sharpe DT. Textured or smooth implants for
breast augmentation? A prospective controlled trial. Br J Plast Surg
1991;44:444–448.
18. Malata CM, Felderg L, Coleman DJ, et al. Textured or smooth implants
for breast augmentation? Three year follow-up of a prospective
randomized controlled trial. Br J Plast Surg 1997;50:99–105.
19. Weiner RC. Relationship of incision choice to capsular contracture.
Aesthetic Plast Surg 2008;32:303–306.
20. Hammond DC, Migliori MM, Caplin DA, et al. Mentor contour profile
gel implants: clinical outcomes at 6 years. Plast Reconstr Surg
2012;129:1381–1391.
21. Maxwell GP, Van Natta BW, Murphy DK, et al. Natrelle style 410
form-stable silicone breast implants: core study results at 6 years.
Aesthet Surg J 2012:32:709–717.
22. Jewell ML, Jewell JL. A comparison of outcomes involving highly
cohesive, form-stable breast implants from two manufacturers in
patients undergoing primary breast augmentation. Aesthetic Surg J
2010;30:51–65.
23. Caplin DA. Indications for the use of MemoryShape breast implants in
aesthetic and reconstructive breast surgery: long-term clinical outcomes
of shaped versus round silicone breast implants. Plast Reconstr Surg
2014;134(3S):27S–37S.
24. Muntan CD, Sundine MJ, Rink RD, et al. Inframammary fold: a
histological reappraisal. Plast Reconstr Surg 2000;105:549–556;
discussion 557.
25. Teitelbaum S. The inframammary approach to breast augmentation. Clin
Plast Surg 2009;36:33–43.
26. Tebbetss JB, Adams WP. Five critical decisions in breast augmentation
using five measurements in 5 minutes: the high five decision support
process. Plast Reconstr Surg 2005;116:2005–2016.
27. Adams WP. The process of breast augmentation: four sequential steps
for optimizing outcomes for patients. Plast Reconstr Surg
2008;122:1892–1900.
28. Tebbetts JB, Teitelbaum S. High- and extra-high-projection breast
implants: potential consequences for patients. Plast Reconstr Surg
2010;126:2150–2159.
29. Calobrace MB, Kaufman DL, Gordon AE, et al. Evolving practices in
augmentation operative techniques with Sientra HSC round implants.
Plast Reconstr Surg 2014;134(Suppl 1):57S–67S.
30. Hammond DC. Technique and results using MemoryShape implants in
aesthetic and reconstructive breast surgery. Plast Reconstr Surg
2014;134(Suppl 3):16S–26S.
31. Schwartz MR. Algorithm and techniques for using Sientra’s silicone gel
shaped implants in primary and revision breast augmentation. Plast
Reconstr Surg 2014;134(Suppl 1):18S–27S.
32. Strasser EJ. Results of subglandular versus subpectoral augmentation
over time: one surgeon’s observations. Aesthet Surg J 2006;26:45–50.
33. Goes JCS, Landecker A. Optimizing outcomes in breast augmentation:
seven years of experience with the subfascial plane. Aesth Plast Surg
2003;27:178–184.
34. Serra-Renom J, Garrido MF, Yoon T. Augmentation mammoplasty with
anatomic soft, cohesive silicone implant using the transaxillary approach
at a subfascial level with endoscopic assistance. Plast Reconstr Surg
2005;116:640–645.
35. Graf R, Pace DT, Damasio RC, et al. Subfascial breast augmentation. In:
Innovations in Plastic and Aesthetic Surgery. Chapter 50. New York:
Springer; 2008:406–413.
36. Tebbetts JB. Dual plane breast augmentation: optimizing implant-soft-
tissue relationships in a wide range of breast types. Plast Reconstr Surg
2001;107:1255–1272.
37. Maxwell GP, Gabriel. The evolution of breast implants. Plast Reconstr
Surg 2014;134(Suppl 1):12S–17S.
38. Maxwell GP, Gabriel A. The evolution of breast implants. Clin Plast
Surg 2009;36:1–13.
CHAPTER 99

The Periareolar Approach to


Augmentation Mammaplasty
JULIANA E. HANSEN
HISTORY
The periareolar incision for augmentation mammaplasty allows for excellent,
direct access with an inconspicuous scar, making this a particularly versatile
approach. First described in the 1970s (1–4), this method provides central
access to the implant pocket and is compatible with all planes of dissection
and most types of implants (5). It is equivalent to or better than an
inframammary approach at preserving nipple sensation (6,7). The nipple-
areola junction appears to be a privileged area for scars; the resultant scar is
often inconspicuous. This is in contrast to inframammary incisions, where
dissatisfaction with scars may be more common (8). The location of the
periareolar incision is independent of the inframammary fold. Furthermore, it
is an excellent choice when lowering of the inframammary fold is desired
either at the first operation or subsequent operations (5). This incision does
not interfere with breast biopsies or mastectomy incisions performed through
or around the areola and is compatible with future mastopexy incisions by
simply extending the periareolar incision around the entire areola (3–5,8–14).
Finally, should the patient require revisionary surgery, the periareolar
approach can be used again for most procedures (15).
This approach does violate some breast parenchyma and may create
scarring within the breast, but in practice this is rarely a problem clinically or
radiographically (9,10,12,14). A periareolar scar may be more visible than an
inframammary scar in the upright patient but tends to be less visible when the
patient is supine. The scar is only visible when the entire breast is exposed;
otherwise the scar is hidden by even the most minimal amount of clothing.
The periareolar approach can be used in virtually all women, in breasts with
or without ptosis, and with most small or large areolas. As the amount of
breast parenchyma increases though, the periareolar incision becomes less
desirable because of the increasing amount of breast tissue that must be
traversed to reach the retromammary space. One concern of going through
the breast near the nipple is the increased likelihood of contamination of the
implant with breast bacterial flora. Such contamination has been speculated
to be a risk factor for infection or capsular contracture (16). Available
information regarding rates of capsular contracture after periareolar versus
other incision choices shows conflicting data. While a meta-analysis
demonstrated a significantly higher rate of capsular contracture after breast
augmentation with periareolar incision as compared to inframammary fold
(IMF) or transaxillary incisions (17), only seven studies were included
(16,18–23). Of those, three studies (18–20) showed no statistically significant
effect of periareolar incision on capsular contracture rates.
In breast augmentation, the choice of incision must be considered along
with several other decisions, including subpectoral versus subglandular
pocket placement, smooth versus textured and round versus anatomic implant
choice, and accompanying mastopexy or not. A periareolar incision facilitates
a future mastopexy. If the patient’s areola is large or the inframammary fold
is high, the periareolar approach is similarly appealing due to the ease of
exposure and vantage point for creating a lower fold. Even if the areola is
small, in cases where there is minimal glandular volume and the fold is
absent, it may be desirable to use the existing areola edge rather than estimate
the location of the incision at the site of the new fold to be created by the
breast implant. While remote incision placement, such as transaxillary and
transumbilical, may carry certain cosmetic advantages, the advantage is
minimal and in many situations it is more difficult and potentially less
accurate than the periareolar approach, even with the help of an endoscope.
The periareolar approach is direct, easy, and user friendly and does not
require special equipment (18,24).
TECHNIQUE
The preoperative markings are performed with the patient facing forward,
sitting or standing upright, with her arms at her sides. The breast meridian,
inframammary fold, and the location of the planned inframammary fold are
marked. In the operating room, before the infiltration of an epinephrine-
containing local anesthetic, the periareolar incision is marked precisely at the
junction of the areola and surrounding unpigmented breast skin. It is
important that this be performed prior to infiltration of any local anesthetic
and/or epinephrine-containing solution because these can distort or obscure
this border and make it more difficult to place the skin incision correctly. The
incision is placed directly inferior for most dissections (4). In general, we try
to avoid making the incision above the equator of the areola, and we center
the skin incision at the 6 o’clock position (13). An antibiotic-impregnated
adherent plastic dressing may be placed over the nipple but should not
obscure the precise areolar-cutaneous junction while marking. Perioperative
antibiotics are recommended as in most procedures involving prostheses, but
their use is optional.
The patient is positioned with the arms abducted no more than 90 degrees
and secured on padded arm boards or, tucked at the sides. The patient should
be positioned on the table to facilitate hip flexion with back raise. It is
essential that the patient’s shoulders be level to best judge the intraoperative
result when the patient is sat upright during the operation. Adequate lighting
is crucial for this procedure; use of an endoscope, headlight, lighted retractor,
or lighted electrocautery is recommended.
The region to be incised is infiltrated with a local anesthetic solution
containing epinephrine. After allowing adequate time for the epinephrine to
take effect, the skin incision is made through the dermis with a scalpel, and
electrocautery is then used to incise into the breast tissue (Fig. 99-1). Skin
hooks are placed on either side of the wound to provide the necessary
retraction. The dissection through the breast tissue proceeds either directly
posteriorly or by beveling inferiorly toward the chest wall (Fig. 99-2) (13).
This maneuver leaves adequate breast tissue caudally to facilitate wound
closure and preserves the skin and the breast contour. Rake retractors
followed by Army/Navy retractors are used as the dissection proceeds deeper
into the breast, toward the chest wall. When the pectoralis fascia is reached,
the breast tissue is mobilized off this layer, exposing the underlying fascia
and muscle in an area corresponding to the lower pole of the breast from the
inframammary fold inferiorly, to a point superiorly, which may vary
depending on the existing skin envelope and degree of ptosis (Fig. 99-3).
Inferiorly and inferolaterally, the dissection is subcutaneous down to the level
of the desired inframammary fold (Fig. 99-4). If a subglandular approach is
to be used, the remainder of the pocket is then precisely dissected under
direct vision with electrocautery, fiber-optic lighting, or endoscopy, and
Deaver retractors.

FIGURE 99-1 It is crucial to make the periareolar incision precisely along the edge
of the areola. If done accurately, this produces a nearly invisible scar over time. The
incision should be centered over the 6 o’clock position.
FIGURE 99-2 After the skin incision has been made, dissection begins with an
electrocautery cutting either directly posteriorly or obliquely through the breast,
aiming inferiorly while deepening the incision. For subpectoral augmentation, the
dissection proceeds more medially. We recommend against an initial superficial
dissection just beneath the skin, which is more likely to produce visible subcutaneous
scar distortion. As the dissection deepens, it is prudent to use a scalpel or heavy,
sharp scissors to completely divide the deeper aspect of the breast down to the
pectoral fascia in order to create a tunnel to perform the operation.

When performing a subpectoral augmentation, the inferior edge of the


exposed pectoralis muscle is then grasped with an Allis clamp. The lower
edge of the muscle is lifted up and separated from the underlying chest wall
by first creating a tunnel in the central portion of the subpectoral space. This
step provides access to the subpectoral plane (Fig. 99-5). The subpectoral
pocket is precisely enlarged using a combination of electrocautery and
minimal blunt dissection (Fig. 99-6). Care is taken to cauterize perforating
blood vessels before they are cut. Throughout this dissection, it is essential
that the utmost care be taken to avoid lifting either the serratus anterior or the
pectoralis minor muscles. The completed pocket is created by releasing the
entire length of the lower edge of the pectoralis major muscle so it is
confluent with the previously created lower pole subglandular pocket. After
the muscle has been completely divided along its lower border, the
subglandular dissection is finalized. Hemostasis is confirmed with fiber-optic
lighting and precision use of electrocautery, followed by irrigation of the
wound with a triple antibiotic and/or dilute Betadine solution. The skin
around the incision should then be re-prepped and the single surgeon who
will be handling the implant should don new, powder-free gloves.
FIGURE 99-3 After the fascia has been identified, the breast is reflected off the
underlying pectoralis major using cautery or sharp dissection. For subglandular
breast augmentation, the dissection continues until the entire planned pocket has
been created. A tissue expander or an inflatable implant can be used and inflated
with saline or air to help with the dissection and to identify areas that need further
release. For subpectoral augmentation, the breast inferior to the pectoralis muscle
should be dissected first, lifting that portion of the breast off the muscle just as in a
subglandular augmentation. The free inferior edge of the pectoralis muscle should be
exposed to allow access beneath it.
FIGURE 99-4 The inferior portion of the pocket should be created using primarily
sharp cautery dissection under direct visualization. Subtle adjustments can then be
made with blunt finger stretching and pulling or pushing movements. Anterior
traction on the overlying tissues helps with these maneuvers. Subglandular dissection
should proceed inferiorly down to the fold.
FIGURE 99-5 For subpectoral augmentation, the free edge of the pectoralis major
muscle is grasped using one or two Allis clamps and lifted up out of the wound
through the tunnel that has already been created.
FIGURE 99-6 Using fiber-optic lighting or an endoscope, the muscle is sharply and
carefully released using the electrocautery medially and inferiorly to create a pocket
with the desired shape.
FIGURE 99-7 Although there are legitimate drawbacks to all incisions, including the
periareolar one, this approach does not limit the size of incision, even in patients with
a small areola. Even with an areola measuring 25 mm (about the size of a quarter),
this allows the easy creation of a 4-cm incision along one-half of the areola
circumference.
FIGURE 99-8 A, B: A 51-year-old, 5 ft 7 in tall woman before breast augmentation.
C, D: The same patient 3 months after augmentation mammaplasty with a 375-mL
silicone gel implant placed in a dual-plane pocket through a periareolar incision. E:
Preoperative markings. Note that the inframammary fold is lowered from 7.5 to 8.5
cm. F: Patient at 3 months postop flexing her pectoral muscles to show her level of
animation deformity.
FIGURE 99-9 A, B: A 41-year-old, 5 ft 10 in tall woman before breast augmentation.
C, D: The same patient 6 months after augmentation mammaplasty with a 425-mL
high-profile, saline-filled implant placed in a dual-plane pocket through a
periareolar approach. E, F: The same patient 3 months after bilateral implant
exchange to a 700-mL high-profile, saline-filled implant placed in a dual-plane
pocket through a periareolar approach.

In the case of inflatable implants, air is aspirated from the prostheses, and
they are then rolled like a cigar from each side toward the valve and inserted
into the pocket. The implants are filled with the proper amount of saline or
other fluid, and with the fill tubes left in, the incision is tacked together and
the patient is placed in the sitting position. Only after the surgeon is satisfied
are the fill tubes removed, and valve closure is verified under direct vision
and/or digital palpation.
Silicone implants ideally are placed with a no-touch technique. A funnel is
extremely useful to prevent contamination of the implant as well during
placement through a periareolar incision. Additionally, use of a funnel
distributes the forces on the implant shell evenly as it is being inserted, thus
reducing the risk of tear.
After implant placement, the patient should be placed into a sitting position
and the breasts assessed for symmetry in terms of size, position, contour,
inframammary fold, and nipple height. The breast gland is then repaired with
several interrupted 2-0 or 3-0 PDS sutures on a taper needle. A 3-0 or 4-0
absorbable monofilament suture is then used for buried, interrupted dermal
sutures. Finally, a 3-0 or 4-0 absorbable monofilament suture is used for a
running intradermal closure. External tissue glue is then applied to the wound
as a surface dressing (14).
DISCUSSION
The periareolar approach works well with all types of implants: silicone or
inflatable, round or anatomic, textured or smooth. Because of its excellent
versatility and exposure, it often can adequately accommodate anatomic
implants. The use of inflatable implants allows the effective use of a
periareolar incision, even with the smallest of areola. Even in a small areola
of 25-mm diameter, a semicircular incision around the areola measures
approximately 4 cm in length (Figs. 99-7 to 99-9) (10). It is the logical choice
when eventual mastopexy is suspected but is not certain preoperatively (5).
This approach is also the best in cases of tuberous breast hypomastia because
it affords the possibility of periareolar skin or breast parenchymal excision, if
necessary (5). Secondary procedures requiring capsulectomy, implant
exchange, unilateral augmentation for symmetry, pocket size adjustments,
and correction of implant malposition can all be performed through the
periareolar incision.
ACKNOWLEDGMENTS
The author gratefully acknowledges the past contributions of Scott L. Spear,
Jeffrey M. Jacobson, and Elan Reisin.

REFERENCES

1. Williams JE. Experiences with a large series of silastic breast implants.


Plast Reconstr Surg 1972;49:253–258.
2. Jenny H. Areolar approach to augmentation mammaplasty. Plast
Reconstr Surg 1974;53:344.
3. Jones FR, Tauras AP. A periareolar incision for augmentation
mammoplasty. Plast Reconstr Surg 1973;51:641–644.
4. Gruber R, Friedman GD. Periareolar subpectoral augmentation
mammoplasty. Plast Reconstr Surg 1981;67:453–457.
5. Hidalgo DA. Breast augmentation: choosing the optimal incision,
implant, and pocket plane. Plast Reconstr Surg 2000;105(6):2202–2216;
discussion 2217–2218.
6. Okwueze MI, Spear ME, Zwyghuizen AM, et al. Effect of augmentation
mammaplasty on breast sensation. Plast Reconstr Surg 2006;117:73–83;
discussion 84–85.
7. Mofid MM, Klatsky SA, Singh NK, et al. Nipple-areola complex
sensitivity after primary breast augmentation: a comparison of
periareolar and inframammary incision approaches. Plast Reconstr Surg
2006;117:1694–1698.
8. Becker H. The intra-areolar incision for breast augmentation. Ann Plast
Surg 1999;42(1):103–106.
9. Biggs TM, Humphreys DH. Augmentation mammaplasty. In: Smith JW,
Aston SJ, eds. Grabb and Smith’s Plastic Surgery. 4th ed. Boston, MA:
Little, Brown; 1991:1145–1156.
10. Spear SL, Matsuba H, Little JW. The medial periareolar approach to
submuscular augmentation mammaplasty under local anesthesia. Plast
Reconstr Surg 1989;84:599–606.
11. Riefkohl R. Augmentation mammaplasty. In: McCarthy JG, ed. Plastic
Surgery. Vol. 6. Philadelphia, PA: Harcourt Brace; 1990:3879–3844.
12. Biggs TM, Cukier J, Worthing JF. Augmentation mammaplasty: a
review of 18 years. Plast Reconstr Surg 1982;69:445–452.
13. Spear SL, Bulan EJ. The medial periareolar approach to submuscular
augmentation mammaplasty under local anesthesia: a 10 year follow up.
Plast Reconstr Surg 2001;108(3):771–775.
14. Courtiss EH, Goldwyn RM. Breast sensation before and after plastic
surgery. Plast Reconstr Surg 1979;58:1–13.
15. Hammond D. The periareolar approach to breast augmentation. Clin
Plast Surg 2009;36(1):45–48.
16. Wiener TC. Relationship of incision choice to capsular contracture.
Aesthet Plast Surg 2008;32:303–306.
17. Li S, Chen L, Liu W, et al. Capsular contracture rate after breast
augmentation with periareolar versus other two (inframammary and
transaxillary) incisions: a meta-analysis. Aesthetic Plast Surg
2018;42:32–37.
18. Stutman RL, Codner M, Mahoney A, et al. Comparison of breast
augmentation incisions and common complications. Aesthetic Plast Surg
2012;36:1096–1104.
19. Benito-Ruiz J, Manzano ML, Salvador-Miranda L. Five-year outcomes
of breast augmentation with form-stable implants: periareolar vs
transaxillary. Aesthetic Surg J 2017;37(1):46–56.
20. Jacobson JM, Gatti ME, Schaffner AD, et al. Effect of incision choice
on outcomes in primary breast augmentation. Aesthet Surg J
2012;32(4):456–462.
21. Spear SL, Murphy DK. Natrelle round silicone breast implants: core
study results at 10 years. Plast Reconstr Surg 2014;133(6):1354–1361.
22. Stevens WG, Nahabedian MY, Calobrace MB, et al. Risk factor analysis
for capsular contracture: a 5-year Sientra study analysis using round,
smooth, and textured implants for breast augmentation. Plast Reconstr
Surg 2013;132(5):1115–1123.
23. McGuire P, Reisman NR, Murphy DK. Risk factor analysis for capsular
contracture, malposition, and late seroma in subjects receiving Natrelle
410 form-stable silicone breast implants. Plast Reconstr Surg
2017;139(1):1–9.
24. Yavuzer R, Basterzi Y, Tuncer S. Using tissue adhesives for closure of
periareolar incisions in breast reduction surgery. Plast Reconstr Surg
2003;112:337.
CHAPTER 100

Transaxillary Breast Augmentation


LOUIS L. STROCK
HISTORY
The transaxillary approach for breast augmentation has the appeal of allowing
for a breast implant to be placed with no incisions on the breast. The
approach was first reported in 1973 by Hoehler, who described the placement
of an implant in a partial subpectoral pocket using mainly blunt dissection
(1). While other early reports provided encouragement for this approach
based on short-term results, technical limitations became readily apparent that
limited its popularity (2). This led Tebbetts to describe a series of technical
refinements based on anatomic studies and long-term follow-up, seeking to
limit complications using this approach (3). Despite these efforts, this early
approach depended completely upon blunt technique with limited or no tissue
visualization and had limited appeal because of problems with implant
asymmetry and a general lack of technical control compared with the more
conventional inframammary and periareolar approaches.
More recent reports have called this long-standing resistance to the
transaxillary approach into question. Two single-surgeon, large patient series
have supported the transaxillary nonendoscopic approach as having very
consistent outcomes with very low rates of capsular contracture and
complications overall (4,5). Gryskiewicz reported higher satisfaction scores
reported by transaxillary patients compared with inframammary patients (5).
In their review article entitled “Evidence Based Medicine: Augmentation
Mammaplasty,” Lista and Ahmad suggested that the transaxillary incision
was equal to the inframammary approach as the preferred incisions for breast
implant placement (6). This article did not distinguish between the
endoscopic and nonendoscopic transaxillary approaches.
The addition of endoscopic assistance to the transaxillary approach, as first
described by Price et al., allowed for direct visualization of the tissue layers
to be released, helping to overcome the greatest limitation of the previous
transaxillary approaches that were based on blunt technique with no tissue
visualization (7,8). The improved visualization allowed for improved
hemostasis, improved control of inframammary fold (IMF) level and shape,
and the ability to precisely divide specific tissue layers according to the needs
of each patient. The added technical control afforded by endoscopic
assistance to the transaxillary approach for breast augmentation has been
reflected in multiple patient series reports (9–15). Additionally, technical
refinements have been described and demonstrated that allow for precise
technical control to maintain or modify the level and shape of the IMF during
implant placement using the transaxillary approach with endoscopic
assistance (16–21). This combined experience with improved technical
control suggests that the endoscopic approach for transaxillary breast
augmentation has become the standard for implant placement using a
transaxillary incision.
TRANSAXILLARY ENDOSCOPIC BREAST AUGMENTATION
The author is a strong advocate for the use of endoscopic assistance when the
transaxillary approach is used for breast augmentation, due to the added
technical control afforded by visualization of the specific tissue layers to be
divided. Nuances of incision design and device placement will be covered in
great detail, with the understanding that the tissue pocket creation and muscle
release technique is identical regardless of the type of implant to be used. The
transaxillary endoscopic approach will be presented in detail (16), followed
by a discussion of the nonendoscopic approach where the technique differs in
the tissue release phase of the procedure.
MARKINGS
Markings are routinely placed in the preoperative holding area with the
patient in the sitting position, and include breast and chest wall width, tissue
thickness, IMF position, IMF position planned, and exact incision location
(Fig. 100-1). The anatomic chest midline and midbreast meridian at the IMF
are marked with the patient in the sitting position and reconfirmed when the
patient is supine, under anesthesia on the operating table.

FIGURE 100-1 Preoperative markings. A: IMF marked to maintain level with breast
implant placement. B: Where the IMF is to be lowered, the existing IMF level is
marked, followed by new lower level to be used as guide for tissue pocket creation.
POSITIONING
The patient is placed in a supine position with the arms secured onto
armboards at 90 degrees. The procedure is performed under general
anesthesia with the aid of short-acting muscle relaxation. Draping is
performed as with routine breast augmentation, except that the surgeon must
be able to work above and below the shoulder on each side. The anesthesia
machine is located at the head of the bed, also with enough space to allow for
the surgeon to perform a majority of the procedure from a position above the
shoulder, facing the endoscopic equipment at the foot of the bed. In addition
to the endoscopic tower, all cautery and suction lines are directed toward the
foot of the bed (Fig. 100-2).
EQUIPMENT
The equipment used is that described by Price et al., consisting of an
endoscopic tower with monitor, endoscopic light source, recorder, and
camera. The camera is mounted to a 10-mm downward-angled endoscope
that slides into an Emory Breast Retractor (Cardinal Health) sheath with a
grooved handle that holds the fiberoptic light cord (4,5). The author prefers
use of Dingman-Agris dissectors for blunt refinements if needed (Fig. 100-3)
(5,8,12).
INCISIONS
The incisions for the procedure differ depending upon whether saline,
cohesive silicone gel, or highly cohesive silicone gel implants are to be used.
All marks are carefully made to be confined within the axilla and within the
hair -bearing skin. For small cohesive silicone gel or saline augmentation, an
incision 3 to 4 cm is marked in the axillary apex, within an existing skin
crease (Fig. 100-4A). Occasionally, a dominant skin crease is long enough to
permit a longer straight incision design. The cross mark is to facilitate correct
alignment of the closure (Fig. 100-4B). Alternatively, for larger cohesive
silicone gel augmentation, a boomerang-shaped incision design 4 to 5 cm in
length is used. This incision design is recommended by the author for all
device types as a good starting point to facilitate ease of use of the
endoscopic equipment. The markings for this incision begin with a dot
marked in the axillary apex. A line is then drawn anteriorly, in an existing
skin crease, just short of the posterior boundary of the pectoralis major
muscle. The posterior portion of the incision, beginning at the dot in the
axillary apex, is marked in a posterior and slightly superior direction. This is
the most versatile incision design, regardless of device type, based on the
author’s long experience with the approach (Fig. 100-4C). Additional
approaches that can be helpful that uses a modified hockey stick–shaped
incision or an elongated S centered in the deepest skin crease can be used for
placement of large highly filled cohesive silicone implants, highly cohesive
silicone gel implants or in patients who may have an especially narrow
segment of hair-bearing skin in the axilla, regardless of the implant to be used
(Fig. 100-4D).
FIGURE 100-2 Patient is positioned with arms out, allowing room for surgeon to
perform procedure from above shoulder. Note endoscopic tower at foot of operating
room bed.

FIGURE 100-3 A: Endoscopic instruments. B: Endoscopic setup with camera


mounted to endoscope, light source above into endoscope, with cord held in groove in
Emory Endoscopic Retractor (Cardinal Health).
FIGURE 100-4 A: Short incision 3 to 4 cm, in existing crease, used for small cohesive
silicone gel or saline breast implants. B: Silicone gel augmentation incision 4 to 5 cm,
extending from mark in axillary apex, into extended dominant crease within hair-
bearing skin. C: Silicone gel incision 4.5 to 5 cm, angled based on mark in axillary
apex, extended anteriorly within crease. Extended posteriorly at a superior angle in a
posterior direction, allowing for the incision to function longer than its actual length.
D: Silicone gel incision 4 to 5 cm, with anterior and posterior curved extensions. This
is most useful for placement of highly cohesive gel devices or for patients with
especially narrow segments of hair-bearing skin in the axilla, regardless of device
type to be placed.
FIGURE 100-5 A: Saline augmentation incision at 6 months. B: Silicone gel
augmentation incision at 4 months. C: Silicone gel augmentation incision in same
patient as B at 1 year.

These marks usually made in the preoperative holding are with the patient
in a sitting position to ensure proper incision placement behind the anterior
axillary fold. The longer or angled incision designs are especially helpful for
use in patients having cohesive gel devices or if the surgeon is early in use of
the axillary approach to facilitate visualization in the early technical steps of
the procedure. In the author’s experience, the shorter incision as used
routinely for saline augmentation is visible for up to 6 months, as compared
with 9 months for the longer incision options routinely used for silicone gel
augmentation. These incisions are typically difficult to see by 1 year after the
procedure (Fig. 100-5).
INITIAL DISSECTION
After incision placement, the initial dissection is performed in an immediate
subcutaneous plane, in an anterior direction using the electrocautery, until the
lateral border of the pectoralis major muscle is reached. Alternatively, scissor
dissection is preferred for entry into the subpectoral space when using the
shortest incision length for saline implant patients. Dissection in this
superficial plane is important to prevent damage to the intercostobrachial
nerve. The subpectoral space is then entered using facelift scissors,
developing the plane between the pectoralis major and the pectoralis minor
muscles. Alternatively, using the longer incision designs needed for silicone
gel device placement, a fiberoptic retractor is used to enter the subpectoral
space under direct vision. Gentle blunt finger movement is used to provide
additional limited dissection of the subpectoral space. This approach is
uniformly used in the placement of silicone gel implants of all types, as the
initial tissue tunnel that connects the incision to the subpectoral space must
be larger to allow for the placement of silicone gel devices as compared with
saline implants. This distinction is important because saline implants are
placed empty into the tissue pocket, and then filled with saline, as compared
with silicone gel devices that are prefilled during the manufacturing process
(Fig. 100-6).
POCKET CREATION I: OPTICAL CAVITY CREATION
The subpectoral dissection is an important phase of the procedure that largely
determines the ease of the endoscopic release of the pectoralis major muscle.
Emphasis is placed on creation of a clear optical field with little or no blood
staining. While the initial description of the endoscopic approach states
preference for blunt dissection to the pectoralis major muscle at the IMF, the
author prefers to avoid the occasional blood staining of tissue that can be seen
with that approach (4). The author prefers creation of the optical cavity by
sharp endoscopic dissection, releasing the areolar plane just deep to the
pectoralis major muscle using electrocautery with blended current (Fig. 100-
7) (12). This is accomplished by initial placement of the Emory retractor
(Cardinal Health) into the subpectoral space, followed by placement of the
endoscope through the retractor sheath following contact with defogging
solution. The spatulated cautery rod, with a J shape oriented outward in a
lateral direction, is used for the dissection. Suction is attached to the posterior
end of the cautery handle for smoke evacuation. This sequence is used for all
endoscopic portions of the procedure. Orientation is maintained by
identification of a rib, following which the tissue is released until the main
body of the pectoralis major muscle is identified clearly in all areas to be
addressed with the main muscle release (Fig. 100-8).
FIGURE 100-6 Initial dissection in subpectoral space as seen immediately following
placement of endoscope. For orientation, the view is of right breast pocket, medial is
left, lateral is right, ribcage lower end of field.

FIGURE 100-7 The optical field is created to allow for visualization of main body of
pectoralis major muscle for release.
FIGURE 100-8 External landmark checked relative to internal anatomy. This allows
precision in starting the muscle release relative to the level of the existing
inframammary fold.
POCKET CREATION II: PECTORALIS MAJOR MUSCLE RELEASE
The release of the pectoralis major muscle is started medially, carefully
correlating internal anatomy seen endoscopically with external reference
markings (Fig. 100-9A,B). This ensures the release will be performed at the
intended level relative to the IMF, a critical issue whether the fold level is to
be maintained or lowered. If the preoperative IMF level is to be maintained,
the pectoralis major release is started one inch above the level of the existing
IMF. Alternatively, if the IMF is to be lowered, then the muscle is released
just above the level of the existing IMF. The pectoralis release then proceeds
from medial to lateral, carefully rechecking the level of the muscle release
relative to the IMF. Hemostasis is meticulously maintained during the tissue
release. The retractor is elevated in a toe-up position to expose the tissue
release. The excellent visibility afforded by the combination of endoscopic
magnification and proper retractor elevation allows for specific release of
muscle and fascia layers as needed in a given patient (Fig. 100-9C,D). If the
IMF is to be lowered, the release is performed just superficial to the
prepectoral fascia of the lower muscle cuff, carefully correlating of external
landmarks and markings with internal anatomy. The release is continued
laterally to just past the base toward the lateral breast, or the lateral edge of
the pectoralis major muscle. While the sharp dissection is performed laterally
in some patients, this is carefully monitored to always avoid overrelease.
Sharp dissection is always carefully limited laterally, so as to avoid damage
to the sensory nerves in this area. Light blunt technique in this area is
preferred. Dingman-Agris dissectors are then used to confirm the medial and
lateral extent of the tissue release, which can then be refined with additional
endoscopic inspection and release. Hemostasis is carefully rechecked with the
aid of the endoscope at this time. The extent of the medial release is
rechecked with the endoscope, addressing any persistent accessory muscle
slips that may require division (Fig. 100-10). The medial release is rarely
extended above the level of the nipple. It is critically important that the main
body of the pectoralis major muscle not be overreleased medially, as
significant deformity can result that can be difficult to repair. The release site
is irrigated with antibiotic solution and local anesthetic agents per routine.
FIGURE 100-9 An endoscopic view of release, from medial to lateral, with clear
visualization to allow for specific tissue layer division. For orientation, medial is left,
lateral is right, ribcage down. B: Endoscopic view of prepectoral fascia on lower
muscle cuff; the plane to release and lower the IMF is immediately superficial to the
prepectoral fascia. C: External landmarks are rechecked, with new level of IMF and
the extent of dual plane tissue release confirmed. D: Medial muscle release is
rechecked, preserving main pectoralis major muscle superior to external reference
marking. Correlation of internal anatomy and external marking is reconfirmed.

FIGURE 100-10 Cohesive silicone gel implant in insertion sleeve, in preparation for
placement. A 1-inch Deaver retractor is used to hold open the entry into the tissue
tunnel. The device is placed with the aid of the insertion sleeve, serving to minimize
manipulation of the device and eliminating direct contact with the hair-bearing
axillary skin during implant placement.

The release of the pectoralis major muscle using endoscopic assistance is


straight forward if attention is paid to maintaining a clear optical field at all
stages of the procedure. This demands that attention be paid to the method
for entry into the subpectoral space, the method used for subpectoral
dissection to reach the main body of the pectoralis major muscle, and the
method of muscle release. Smoke evacuation must be working at all times to
maintain visibility, and hemostasis must be meticulously maintained during
the tissue release and rechecked following blunt refinements medially and
laterally. An adequate muscle cuff must be maintained in the direction of the
chest wall to allow for control of bleeding during release of the pectoralis
major muscle.
OPERATIVE TECHNIQUE
IMPLANT PLACEMENT
The technique for placement of cohesive silicone gel implant placement
begins with placement of a 1-inch Deaver retractor, pointed toward the
medial muscle release point, to hold open entry into the tissue pocket.
Alternatively, two 1-inch Deaver retractors can be placed perpendicular to
one another, one parallel to the clavicle, the other parallel to the lateral chest
wall, pulled simultaneously apart to permit introduction of the implant.
Insertion sleeves have routinely been used by the author to facilitate
placement and minimize exposure and contact of the breast implant with skin
and subcutaneous tissues during placement (see Fig. 100-10). The implant
must be laid flat against the ribcage and dropped to the base of the tissue
pocket along the IMF. Correct placement and position are confirmed
manually. Additionally, the device is assessed to ensure that the device was
not damaged during placement. An additional step of ensuring correct
orientation is needed if shaped gel devices are used. Inspection is then
performed as described above, with the patient’s back raised to 45- and 80-
degree sitting position to adequately inspect pocket dimensions, IMF level
and shape, and fully evaluate for symmetry of the augmented breasts.
The technique for saline implant placement begins with evacuation of air
from the device, followed by placement into antibiotic solution. A 1-inch
Deaver retractor is placed thorough the incision and into the subpectoral
space, pointed inferiorly and medially, toward the medial aspect of the base
of the breast. The implant is rolled with the fill tube in the center facing up,
and then placed beneath the retractor and into the soft tissue pocket. The
device is then carefully unrolled and filled to the desired volume. The patient
is placed in the 45- and 80-degree sitting position, allowing for the level and
shape of the IMF to be checked. Minor adjustments can be made using
Dingman-Agris dissectors, minimizing contact with the device. Alternatively,
the device can be deflated and removed, the pocket adjusted with endoscopic
visualization, and the implant replaced. As the surgeon gains more
experience with the technique, this is rarely if ever needed. The identical
procedure is performed on the contralateral side, with any adjustments
performed as needed for optimal symmetry.
Layered closure of incisions, with the use of a 2-0 Vicryl deep in the
subcutaneous tissue, followed by multiple PDS sutures in the deep dermis, is
then performed. One-inch Microfoam tape is placed along the IMF to help
stabilize the level and shape of the IMF, followed by placement of a pressure
dressing (22).
POSTOPERATIVE CARE
An important aspect of the transaxillary approach is that the space in the
upper area of the subpectoral space used for implant placement is not
otherwise needed and must be addressed in the early postoperative period by
the use of external pressure. This serves to close that space that will otherwise
tend to collect fluid or allow the implant to migrate superiorly into an
undesirable position. To obliterate this space, a pressure dressing is placed in
the operating room and maintained for 24 to 48 hours, followed by use of an
elastic wrap which is then used to maintain downward pressure for 5 to 7
days (Fig. 100-11). Other complications are essentially all those seen with
any of the other traditional inframammary or periareolar approaches to breast
augmentation.

FIGURE 100-11 Postoperative implant space stabilization using bra and elastic
wrap.
NONENDOSCOPIC APPROACH
The nonendoscopic technique can be performed in an identical fashion to the
technique described above, except that the tissue release is performed using
entirely blunt dissection. Once the subpectoral space is entered, Dingman-
Agris dissectors are used to complete development of the subpectoral space
to the main body of the pectoral muscle. After the initial pocket is created, the
pectoralis major muscle is bluntly separated using the Dingman-Agris
dissectors to the 6 o’clock position. Further blunt refinement of the lateral
pocket is then performed in a similar fashion. The IMF level and shape is
checked with the patient in the sitting position. Hemostasis is then checked
with a long fiberoptic retractor. Once satisfactory soft tissue pocket
dimensions and hemostasis have been accomplished, the implants are then
placed (4,5).
CONCLUSION
The transaxillary endoscopic approach to breast augmentation provides the
precision and technical control needed to obtain consistent and reliable results
when a transaxillary approach is selected for breast augmentation.
Endoscopic tissue visualization provides the consistent ability to perform
specific tissue release and control IMF level and shape in a way that is very
difficult, if not impossible, to accomplish without direct tissue visualization.
Experience with the transaxillary endoscopic technique permits this approach
to be used in patients with a variety of tissue types, patients with varying
needs for IMF position maintenance or modification, and patients seeking
augmentation with saline or silicone gel breast implants (Figs. 100-12 to 100-
15). In their recent review article entitled “Evidence Based Medicine:
Augmentation Mammaplasty,” Lista and Ahmad suggested that either the
inframammary or transaxillary incisions were preferred for breast implant
placement. These findings are consistent with the experience of the author,
who has spent many years performing breast augmentation offering a choice
to his patients between the transaxillary and inframammary approaches, with
the only distinction being the equipment used to create a tissue pocket
specific to the incision access selected by the patient. The transaxillary
endoscopic approach to breast augmentation can provide results as consistent
as those seen with the more traditional inframammary and periareolar
approaches, with the distinct advantage of leaving no incisions on the breast.
FIGURE 100-12 A: Preoperative photo of a 22-year-old woman who presented
seeking placement of cohesive silicone gel breast implants using the transaxillary
approach. She is noted to have mild asymmetry and well-defined IMF shape. B:
Preoperative markings show plan to lower IMF. C, D: Postoperative views 1 year
following transaxillary endoscopic breast augmentation using Mentor MemoryGel
Xtra moderate plus profile smooth wall cohesive I silicone gel implants, 405 cc.
FIGURE 100-13 A: Preoperative photo of a 38-year-old woman who presented
seeking placement of cohesive silicone gel breast implants using the transaxillary
approach. She is noted to have minimal to no breast tissue and no IMF definition or
shape. B: Preoperative markings show plan to create shape of the IMF and lower its
position. C, D: Postoperative views 1 year following transaxillary endoscopic breast
augmentation using Mentor MemoryGel Xtra moderate plus profile smooth wall
cohesive I silicone gel implants, 370 cc.
FIGURE 100-14 A: Preoperative photo of a 34-year-old woman with minimal ptosis
who presented for breast augmentation using the transaxillary approach. She is
noted to have low breast position with minimal ptosis. B: Preoperative markings
show plan to lower the IMF and increase dual plane tissue separation. C, D: One-
year postoperative views are shown following placement of 350-cc Mentor
MemoryGel moderate plus profile smooth round cohesive silicone gel implants.
FIGURE 100-15 A: Preoperative photo of a 32-year-old woman with low breast
position who presented requesting that shaped, highly cohesive gel implants be
placed using a transaxillary incision. B: Preoperative markings show minimal IMF
modification planned. C, D: Four-year postoperative views shown following
placement of 290-cc Mentor MemoryShape moderate plus profile shaped highly
cohesive silicone gel implants in a partial subpectoral pocket using a transaxillary
endoscopic approach.

REFERENCES

1. Hoehler H. Breast augmentation: the axillary approach. Br J Plast Surg


1973;26:373.
2. Wright JH, Bevin AG. Augmentation mammaplasty by the transaxillary
approach. Plast Reconstr Surg 1976;58(4):429–433.
3. Tebbetts JB. Transaxillary subpectoral augmentation mammaplasty:
long-term follow-up and refinements. Plast Reconstr Surg
1984;74(5):636–647.
4. Huang GJ, Wichmann JL, Mills DC. Transaxillary subpectoral
augmentation mammaplasty: a single surgeon’s 20 year experience.
Aesthetic Surg J 2011;31(7):781–801.
5. Gryskiewicz J, DeLuc R. Transaxillary nonendoscopic subpectoral
augmentation mammaplasty: a 10 year experience with gel vs saline in
2000 patients—with long-term patient satisfaction measured by the
breast-Q. Aesthetic Surg J 2014;34(5):696–713.
6. Lista F, Ahmad J. Evidence-based augmentation mammaplasty. Plast
Reconstr Surg 2013;132:1684–1696.
7. Price CI, Eaves FF, Nahai F, et al. Endoscopic transaxillary subpectoral
breast augmentation. Plast Reconstr Surg 1994;94(5):612–619.
8. Jones GE, Nahai F. Transaxillary breast augmentation. In: Spear SL, ed.
Surgery of the Breast: Principles and Art. 2nd ed. Philadelphia, PA:
Lippincott Williams & Wilkins; 2006:1311–1318.
9. Eaves FF. Breast augmentation: enhanced visualization with the
endoscopic transaxillary technique. Aesthetic Surg J 1999;19:162–164.
10. Graf RM, Bernardes A, Auersvald A, et al. Subfascial endoscopic
transaxillary augmentation mammaplasty. Aesth Plast Surg
2000;24:216–220.
11. Strock LL. Technical Refinements and Complication Avoidance in
Transaxillary Endoscopic Breast Augmentation. Boston, MA: Presented
at the American Society for Aesthetic Plastic Surgery Meeting; 2003.
12. Serra-Renom JM, Garrido MF, Yoon T. Augmentation mammaplasty
with anatomic soft, cohesive silicone implant using the transaxillary
approach at a subfascial level with endoscopic assistance. Plast Reconstr
Surg 2005;116(2):640–645.
13. Giordano PA, Roif M, Laurent B, et al. Endoscopic transaxillary breast
augmentation: clinical evaluation of a series of 306 patients over a 9-
year period. Aesthet Surg J 2007;27(1):47–54.
14. Tebbetts JB. Axillary endoscopic breast augmentation: processes
derived from a 28-year experience to optimize outcomes. Plast Reconstr
Surg 2006;118(7S):53S–80S.
15. Strock LL. Technical Refinements and Complication Avoidance in
Transaxillary Endoscopic Breast Augmentation: An Updated
Experience. San Diego, CA: Presented at the American Society for
Aesthetic Plastic Surgery Meeting; 2008.
16. Strock LL. “Live Surgery Video: Transaxillary Breast Augmentation.”
49th Annual Baker Gordon Symposium on Cosmetic Surgery. Plast
Reconstr Surg 2016.
17. Strock LL. “Transaxillary Breast Augmentation.”, Operative
Techniques in Plastic Surgery. In: Thorne C, Disa J, et al., eds. Elsevier;
2017.
18. Strock LL. “Transaxillary Breast Augmentation”, Atlas of Breast
Augmentation. In: Adams WP, ed. Elsevier; 2017.
19. Strock LL. “Transaxillary Breast Augmentation”, Clinics in Plastic
Surgery: Breast Augmentation. Bengston B, ed. Elsevier; 2015.
20. Sim HB, Sun SH. Transaxillary endoscopic breast augmentation with
shaped gel implants. Aesthet Surg J 2015;35(8):952–961.
21. Strock LL. Commentary on: transaxillary endoscopic breast
augmentation with shaped gel implants. Aesth Surg J 2015;35(8):962–
964.
22. Maxwell GP, Falcone PA. Eighty four consecutive breast
reconstructions using a textured silicone tissue expander. Plast Reconstr
Surg 1992;89(6):1022–1035.
CHAPTER 101

Subfascial Breast Augmentation


ALEX N. MESBAHI | LOUISA YEMC
HISTORY
Breast augmentation is currently the most popular cosmetic surgery
procedure, being the most frequently performed cosmetic surgery in 2018 (1).
Initially, breast augmentation was introduced with the implant being placed
in the subglandular plane. This plane offers the advantage of adequate breast
projection with a brief recovery period (2). The disadvantage with this
approach is the potential for implant palpability and visibility, as well as a
higher incidence of capsular contracture. To improve on these shortcomings,
the submuscular or dual plane approach was developed. This approach offers
greater soft tissue coverage and was shown to have less incidence of capsular
contracture. The main disadvantage with the dual plane approach is
animation deformity, which not only can distort the breast shape but also may
cause discomfort for the patient.
Wright and Bevin first described subfascial transaxillary breast
augmentation in 1976 (3). The procedure fell out of favor though due to
highly visible implant edges in the upper pole, especially in thin patients. In
the late 1990s, Graf reintroduced subfascial breast augmentation as the
procedure that would eliminate the disadvantages of both the subglandular
and dual plane approach while still providing an excellent aesthetic
outcome. The subfascial plane is created above the pectoralis muscle and
below the fascial layer thereby minimizing contact between the implant and
the breast gland (4). This approach offers a natural appearance with minimal
implant visibility or palpability in carefully selected patients. Animation
deformity is not a concern as a result of this placement and capsular
contracture incidence is believed to be less than subglandular augmentations
(Fig. 101-1). There is also a shorter recovery period when compared to using
the dual plane approach (5). In the ideal candidate with adequate soft tissue
coverage of the breast, it may offer excellent aesthetic outcomes with less
postoperative pain and recovery. Several publications have reported the
advantages of the subfascial approach, which avoids the dual plane, yet still
allows for adequate support (6–9).
INDICATIONS
There are certain considerations that should be made when evaluating a
patient for a subfascial augmentation. The soft tissue thickness in the upper
pole of the breast and at the inframammary fold (IMF) should be examined.
In a thin patient, the implant could be more palpable and visible when placed
in the subfascial plane (4). The pinch test was developed to help assess the
thickness of the breast tissue superficial to the pectoralis muscle to assist with
determining the ideal plane for an augmentation. It has been recognized that a
pinch test of less than 4 mm at the IMF and less than 3 cm at the upper pole
of the breast would not offer sufficient coverage of an implant and therefore
the subfascial approach would not be ideal. The upper pole should have a
thickness of ideally greater than 3 cm to potentially offer the best outcome
(Fig. 101-2) (10).
In very active patients that may utilize their chest muscles regularly, the
subfascial plane should be considered. This would include body builders,
swimmers, and exercise enthusiasts who would be disinclined to go through
surgery if it were to result in animation deformity in the long term. The
recovery time period is usually less than patients undergoing submuscular
breast augmentation since the pectoralis muscle function is not temporarily
disrupted. This is advantageous for those unwilling to disrupt their daily
routine significantly with surgery (Fig. 101-3).
The subfascial approach should also be considered in the reconstructive
patient who has undergone unilateral breast reconstruction for mastectomy as
a treatment for breast cancer. With the emerging popularity of implant-based
prepectoral mastectomy reconstruction, it is appropriate to consider
subfascial augmentation for the contralateral symmetry procedure.
Candidates that should not consider using the subfascial approach would
include those with very thin skin who do not support the parameters of the
pinch test. Also, if there is a history of a previous subglandular breast
augmentation, these patients should be carefully considered, as the subfascial
plane may be more difficult to visualize. This would be the result of scar
tissue and capsule development that could obscure the boundaries of the
subfascial plane.
FIGURE 101- This figure illustrates the subfascial (A, B) and dual plane (C, D)
augmentation patient at rest and with flexion of the chest to display animation
deformity.

FIGURE 101-2 The photos display a patient with adequate soft tissue thickness in
the preoperative setting (A, B). The same patient seen 3 months postoperatively
following subfascial breast augmentation with Allergan Style SCF 335-cc implants
(C, D). The patient was an ideal candidate for this approach as seen by the
appropriate tissue coverage following the augmentation.

FIGURE 101-3 The photos display a patient in the preoperative setting (A, B) and 3
months following a bilateral subfascial breast augmentation (C, D). The patient has
Allergan Style SRM 325 cc on the right and 240 cc on the left.
ANATOMY
It has long been debated whether the breast fascial system is distinct enough
to differentiate a subfascial augmentation from a subglandular (11). However,
there have been numerous descriptions regarding the specifics of breast
anatomy. The earliest of reports dates back to 1840 by Cooper who describes
the fascia mammae to contain two layers, one anterior to the gland and one
posterior to it (12). The breast has been described as an appendage of the skin
contained within layers of the superficial fascia. Later, Graf et al. described
the superficial fascia as containing two layers: superficial and deep. The
superficial layer is indistinct from the dermis and the deep layer is more
distinct and identified on the deep surface of the breast parenchyma. A loose
areolar layer between the deep layer of the superficial fascia and the fascia
covering the pectoralis major has also been described that continues on to
cover the rectus abdominus, serratus anterior, and external oblique muscles
(Fig. 101-4) (5,13).
The concept of the superficial fascia joining deeper structures to
compartmentalize fat and other tissue applies to other regions of the body as
well. Fusion zones of adherence in the face “exist as bilaminar membranes,
travel from the deep to superficial fascia, and determine the anatomic
boundaries of the fat compartments and anatomic spaces” (14). Similarly,
Rohrich et al. described zones of adherence between the superficial and
underlying deep fascia of the thigh and buttocks. With its anchorage to the
deep fascia the superficial fascia system shapes the soft tissue into buttocks,
hips, saddlebag areas, and the upper medial thigh fat pad (15).
FIGURE 101-4 The photo displays the dissection of the subfascial plane
intraoperative with the pectoralis fascia grasped in forceps and breast parenchyma
retracted.
FIGURE 101-5 The diagram displays the anatomy of the superficial fascial system.
(From Rehnke R, Groening R, Van Buskirk E, et al. Anatomy of the superficial fascia
system of the breast. Plast Reconstr Surg 2018;142(5):1135–1144.)

One of the most recent descriptions of breast anatomy was by Rehnke et


al., who described a more comprehensive theory of breast anatomy (16). The
superficial fascial system of the breast is described as containing two layers,
an anterior and posterior lamella which encompasses the breast
parenchyma. The layers connect and fuse to the deep fascia of the chest wall
in a circular zone of adhesion called the circummammary ligament. This
ligament connects the breast to the chest, compartmentalizes it, and allows
for support and structure to the breast. The pectoral fascia is thicker in the
upper breast which may be an advantage in limiting superior implant
displacement by forcing it down (Fig. 101-5) (13,17).
INCISION AND APPROACH
The axillary, inframammary, and areolar incisions can all be considered in
subfascial augmentation. The choice of incision should be based on the breast
anatomy as well as support the patient’s preference as clinically guided by the
surgeon for a safe and appropriate outcome. The subfascial plane can be
visualized with all approaches and involves dissection underneath the fascia
of the pectoralis major, serratus anterior, and rectus abdominis muscles.
When utilizing the axillary approach, a combination of blunt dissection and
electrocautery with endoscopic visualization can be used to create the
boundaries of the implant pocket (10). The axillary approach offers the
advantage of a less conspicuous incision and potentially better preservation
of nipple sensation (7). In addition, the axillary approach may be
advantageous in patients with a small areola or poor definition of the IMF
(8,18).
Aygit et al. reported on their experience of endoscopically assisted total
subfascial augmentations in 50 breasts with an average follow-up of 21
months. Anatomic, textured cohesive gel implants were used with a mean
implant size of 235 cc. Sixteen percent of the patients had grade II capsular
contracture with no cases of malposition, wrinkling, or rippling. A 96%
patient satisfaction was also reported (7). Use of the endoscope in
transaxillary augmentation allows for improved visualization, more precise
fascial elevation, and better hemostasis. However, it does require more
training, equipment, and potentially cost (19). Despite the potential
limitations of a blind dissection, others have reported successful
outcomes. Benito-Ruiz has described use of a cold light retractor only with
no bleeding after dissection (20).
Regardless of approach, the role of skin contamination, biofilm, and
inflammation in the development of capsular contracture must be considered,
especially in the subfascial augmentation (21). Aseptic maneuvers to reduce
bacterial exposure include pocket irrigation with antibiotic impregnated
solutions, nipple shields, use of funnels for implant insertion, and reprepping
the skin prior to implant placement. In a 6-year prospective study, triple-
antibiotic solution containing cefazolin, gentamicin, and bacitracin
demonstrated only a 1.8% capsular contracture rate in primary breast
augmentations (22). Antibiotic irrigations containing Betadine provide even
greater gram-negative coverage including bacterium Ralstonia pickettii which
has been linked to the development of breast implant–associated anaplastic
large cell lymphoma (BIA-ALCL) (23,24). Therefore, the use of Betadine in
the antibiotic solution is even more important when selecting textured
implants. The optimal antimicrobial solution to optimize bacterial coverage
while minimizing adverse wound healing effects is 10% Betadine with triple-
antibiotic solution (25,26).
The use of nipple shields is not presently considered the standard of care in
breast augmentation. However, the nipple can have bacterial contamination
even after surgical prep (27). Therefore, the use of nipple shields may be of
benefit to avoid implant contamination, especially when using an areolar
incision. It has been documented by Benito-Ruiz that nipple shields made no
difference in outcomes with the transaxillary approach (28). The use of a
shield can be surgeon preference with surgical practice (Fig. 101-6).
Use of an implant funnel is another method to minimize bacterial exposure
to the implant. A construct is used which avoids both direct handling of the
implant and direct skin exposure by funneling the implant directly into the
breast pocket. A multicenter preliminary report of over 1,100 breast
augmentations demonstrated that using the funnel led to significantly lower
rates of reoperation for capsular contracture (29). The additional cost of the
funnels and learning curve associated with its use must be weighed against
these potential benefits.
FIGURE 101-6 The photo displays the use of a Tegaderm over the nipple as a shield
to avoid implant contamination.
IMPLANT SELECTION
The subfascial augmentation can support the use of either saline or silicone
implants. Depending on the soft tissue thickness in the upper pole, a saline
implant should be chosen wisely as visible rippling and palpability is more
common than with a silicone implant. With the advancement of silicone
implants containing cohesive gel that is form stable, the likelihood of a
contour irregularity resulting from implant rippling is considerably less (6).
To minimize the risk of contour irregularity or more visible implant borders,
composite breast augmentation with fat grafting is a technique to consider
regardless of the type of implant. A survey of American plastic surgeons
conducted by the American Society of Plastic Surgeons (ASPS) in 2016
revealed that almost half of the surgeons combined fat grafting with primary
augmentation (30). This is especially useful in thinner patients when a
subfascial augmentation is planned. The fat is injected not for volume, but
rather to enhance the contour of the upper pole and parasternal regions of the
breasts (31,32). A 6-year retrospective review of primary composite
subfascial augmentations combining fat grafting and textured round implants
demonstrated low overall complication rates and relevantly, low capsular
contracture rates (33).
Implants can be found in a round or anatomic shape with options for a
textured or smooth surface. The implant chosen should be patient specific
and based on the aesthetic goals for the surgery and measurements of the
preoperative breast. The textured anatomic silicone implant has been a
common implant of choice in publications regarding subfascial
augmentation. Its benefits include a more natural appearance, adherence to
tissues for stability, and it can increase short nipple to IMF distances (34).
The main risk of using an anatomic implant is rotation (35). In addition,
recent investigations have found an association between textured implants
and BIA-ALCL. As documented by the U.S. Food and Drug Administration
(FDA), the lifetime risk of developing ALCL presently is a range between 1
in 3,817 and 1 in 30,000 women with textured implants (36). Currently, there
is no single known cause for BIA-ALCL. Inflammation initiated by possible
gram-negative bacterial contamination and the degree of implant texturization
have been implicated (37–41). While this concern is relatively new and still
under investigation, patients should be made aware of this issue when
selecting their implant.
POSTOPERATIVE CARE
While most plastic surgeons prescribe prolonged oral antibiotics
postoperatively, standardized guidelines on the use of prophylactic antibiotics
still do not exist (30).Guidelines recommended by the ASPS for implant-
based breast reconstruction suggest that a single intravenous dose of
antibiotics given within 60 minutes of incision and discontinued within 24
hours of surgery is sufficient unless a drain is present (42). A similar
approach to antibiotic usage should be considered in subfascial augmentation
(43).
Because the subfascial plane does not disrupt the pectoralis muscle
insertions, there is likely less need for narcotic pain medications long term. A
recent publication evaluating postoperative narcotic use in prepectoral
expander or implant-based mastectomy reconstruction found that patients in
the prepectoral group required significantly fewer days of postoperative
opioid medication than those in the dual plane reconstruction group (35). The
use of muscle relaxants in the postoperative period is also not necessary when
using the subfascial approach.
The surgical incision is usually dressed with either a surgical glue or tape.
Both can be exposed to water and showering is permitted 24 hours after
surgery or otherwise guided by the surgeon. Patients should avoid baths,
swimming, and submerging underwater for 1 month postoperatively.
Strenuous activity is avoided for the first 2 weeks with most patients
returning to normal activity by 4 weeks. Patients can often resume activity
sooner when using the subfascial plane, which is advantageous for the more
active individual.
Patients are encouraged to stay in a soft, comfortable, wireless bra as
tolerated postoperatively to support the new implants. Often, the surgical bra
provided at the time of surgery is sufficient for the first few weeks
postoperatively. Massage of breasts postop is often helpful to encourage
smooth implants to settle in the created pocket. Since the implant is
subfascial, the implants will likely settle sooner than when in the dual plane
(5).
CONCLUSION
The subfascial breast augmentation offers the advantages of the subglandular
and dual plane approaches combined without creating distortion of the breast
with animation. This approach potentially offers greater coverage of the
implant when compared to the subglandular approach and as a result, less
incidence of capsular contracture. In the ideal candidate, it can offer a shorter
recovery period with low complication rates (44).

REFERENCES

1. Plasticsurgery.org. 2018 National Plastic Surgery Statistics. 2019.


https://www.plasticsurgery.org/documents/News/Statistics/2018/plastic-
surgery-statistics-report-2018.pdf. Accessed April 30, 2019.
2. Spear SL. Surgery of the Breast, Principles and Art. 3rd ed.
Philadelphia, PA: Lippincott Williams & Wilkins; 2011.
3. Wright J, Bevin A. Augmentation mammaplasty by the transaxillary
approach. Plast Reconstr Surg 1976;58(4):429–433.
4. Graf RM, Bernardes A, Rippel R, et al. Subfascial breast implant: a new
procedure. Plast Reconstr Surg 2003;111(2):904–908.
5. Hunstad JP, Webb LS. Subfascial breast augmentation: a comprehensive
experience. Aesthetic Plast Surg 2010;34(3):365–373.
6. Sampaio Goes J, Munhoz A, Gemperli R. The subfascial approach to
primary and secondary breast augmentation with autologous fat grafting
and form-stable implants. Clin Plast Surg 2015;42(4):551–564.
7. Aygit A, Basaran K, Mercan E. Transaxillary totally subfascial breast
augmentation with anatomical breast implants. Plast Reconstr Surg
2013;131(5):1149–1156.
8. Serra-Renom J, Garrido M, Yoon T. Augmentation mammaplasty with
anatomic soft, cohesive silicone implant using the transaxillary approach
at a subfascial level with endoscopic assistance. Plast Reconstr Surg
2005;116(2):640–645.
9. Benito-Ruiz J, Raigosa M, Manzano M, et al. Subfascial breast
augmentation: thickness of the pectoral fascia. Plast Reconstr Surg
2009;123(1):31e–32e.
10. Park S, Sim H. Endoscopic transaxillary prepectoral conversion for
submuscular breast implants. Arch Plast Surg 2018;45(2):158–164.
11. Tebbetts J. Does fascia provide additional, meaningful coverage over a
breast implant? Plast Reconstr Surg 2004;113(2):777–779.
12. Cooper AP. On the Anatomy of the Breast. London: Longman, Orme,
Green, Brown, and Longmans; 1840. Available at
https://jdc.jefferson.edu/cooper/60/. Accessed April 6, 2019.
13. Jinde L, Jianliang S, Xiaoping C, et al. Anatomy and clinical
significance of pectoral fascia. Plast Reconstr Surg 2006;118(7):1557–
1560.
14. Pessa J, Kenkel J, Heldermon C. Periorbital and temporal anatomy,
“targeted fat grafting,” and how a novel circulatory system in human
peripheral nerves and brain may help avoid nerve injury and blindness
during routine facial augmentation. Aesthet Surg J 2017;37(8):969–973.
15. Rohrich R, Smith P, Marcantonio D, et al. The zones of adherence: role
in minimizing and preventing contour deformities in liposuction. Plast
Reconstr Surg 2001;107(6):1562–1569.
16. Rehnke R, Groening R, Van Buskirk E, et al. Anatomy of the superficial
fascia system of the breast: a comprehensive theory of breast fascial
anatomy. Plast Reconstr Surg 2018;142(5):1135–1144.
17. Tijerina V, Saenz R, Garcia-Guerrero J. Experience of 1000 cases on
subfascial breast augmentation. Aesthetic Plast Surg 2009;34(1):16–22.
18. Munhoz A, Fells K, Arruda E, et al. Subfascial transaxillary breast
augmentation without endoscopic assistance: technical aspects and
outcome. Aesthetic Plast Surg 2006;30(5):503–512.
19. Niechajev I. Improvements in transaxillary breast augmentation.
Aesthetic Plast Surg 2010;34(3):322–329.
20. Benito-Ruiz J. Subfascial breast implant. Plast Reconstr Surg
2004;113(3):1088–1089.
21. Adams W. Capsular contracture: what is it? What causes it? How can it
be prevented and managed? Clin Plast Surg 2009;36(1):119–126.
22. Adams W, Rios J, Smith S. Enhancing patient outcomes in aesthetic and
reconstructive breast surgery using triple antibiotic breast irrigation: six-
year prospective clinical study. Plast Reconstr Surg 2006;118(7
Suppl):46S–52S.
23. Jewell M, Adams W. Betadine and breast implants. Aesthet Surg J
2018;38(6):623–626.
24. Ryan M, Adley C. The antibiotic susceptibility of water-based bacteria
Ralstonia pickettii and Ralstonia insidiosa. J Med Microbiol
2013;62(Pt_7):1025–1031.
25. Wiener T. The role of betadine irrigation in breast augmentation. Plast
Reconstr Surg 2007;119(1):12–15; discussion 16–17.
26. Yalanis G, Liu E, Cheng H. Efficacy and safety of povidone-iodine
irrigation in reducing the risk of capsular contracture in aesthetic breast
augmentation. Plast Reconstr Surg 2015;136(4):687–698.
27. Wixtrom R, Stutman R, Burke R, et al. Risk of breast implant bacterial
contamination from endogenous breast flora, prevention with nipple
shields, and implications for biofilm formation. Aesthet Surg J
2012;32(8):956–963.
28. Benito-Ruiz J. Nipple shields in transaxillary breast augmentation. Ann
Plast Surg 2017;78(4):397–402.
29. Flugstad N, Pozner J, Baxter R, et al. Does implant insertion with a
funnel decrease capsular contracture? A preliminary report. Aesthet Surg
J 2015;36(5):550–556.
30. Hidalgo D, Sinno S. Current trends and controversies in breast
augmentation. Plast Reconstr Surg 2016;137(4):1142–1150.
31. Bravo F. Parasternal infiltration composite breast augmentation. Plast
Reconstr Surg 2015;135(4):1010–1018.
32. Serra-Mestre J, Fernandez Peñuela R, Foti V, et al. Breast cleavage
remodeling with fat grafting. Plast Reconstr Surg 2017;140(5):665e–
672e.
33. Kerfant N, Henry A, Hu W, et al. Subfascial primary breast
augmentation with fat grafting. Plast Reconstr Surg 2017;139(5):1080e–
1085e.
34. Kovacs L, Eder M, Zimmermann A, et al. Three-dimensional evaluation
of breast augmentation and the influence of anatomic and round
implants on operative breast shape changes. Aesthetic Plast Surg
2012;36(4):879–887.
35. Somogyi R, Brown M. Outcomes in primary breast augmentation: a
single surgeon’s review of 1539 consecutive cases. Plast Reconstr Surg
2015;135(1):87–97.
36. Clemens M. “BIA-ALCL Resources.” American Society Of Plastic
Surgeons. 2019. https://www.plasticsurgery.org/for-medical-
professionals/health-policy/bia-alcl-physician-resources/by-the-numbers
37. Hu H, Jacombs A, Vickery K, et al. Chronic biofilm infection in breast
implants is associated with an increased T-cell lymphocytic infiltrate.
Plast Reconstr Surg 2015;135(2):319–329.
38. Hu H, Johani K, Almatroudi A, et al. Bacterial biofilm infection
detected in breast implant–associated anaplastic large-cell lymphoma.
Plast Reconstr Surg 2016;137(6):1659–1669.
39. de Boer M, van Leeuwen F, Hauptmann M, et al. Breast implants and
the risk of anaplastic large-cell lymphoma in the breast. JAMA Oncol
2018;4(3):335–341.
40. Doren E, Miranda R, Selber J, et al. U.S. epidemiology of breast
implant–associated anaplastic large cell lymphoma. Plast Reconstr Surg
2017;139(5):1042–1050.
41. Loch-Wilkinson A, Beath K, Knight RJW, et al. Breast implant–
associated anaplastic large cell lymphoma in Australia and New
Zealand: high-surface-area textured implants are associated with
increased risk. Plast Reconstr Surg 2017;140(4):645–654.
42. Alderman A, Gutowski K, Ahuja A, et al. ASPS clinical practice
guideline summary on breast reconstruction with expanders and
implants. Plast Reconstr Surg 2014;134(4):648e–655e.
43. Wan D, Rohrich R. Modern primary breast augmentation. Plast
Reconstr Surg 2018;142(6):933e–946e.
44. Copeland-Halperin L, Yemc L, Emery E, et al. Evaluating postoperative
narcotic use in prepectoral versus dual-plane breast reconstruction
following mastectomy. Plast Reconstr Surg Glob Open
2019;7(2):e2082.
CHAPTER 102

The Inframammary Approach to


Augmentation Mammaplasty
STEVEN TEITELBAUM | ALLEN GABRIEL | G. PATRICK MAXWELL
HISTORY
When planning a breast augmentation, there are generally three preoperative
decisions that must be made. These include choosing the size and style of the
breast implant, choosing the pocket plane into which the implant will be
placed, and selecting an incision location to gain access to the breast. With
respect to the choice of incision, any incisional strategy for breast
augmentation must balance the sometimes-competing goals of providing
comfortable access to the breast, while placing the incision in the most
inconspicuous location possible. To this end, several different approaches
have been described, including incisions located around the areola, through
the nipple, in the axilla, and in the umbilicus. However, for many surgeons, it
is the inframammary fold approach that provides the best balance between
these two aspects of incision location. Perhaps the most important advantage
of the inframammary fold approach is that direct access to the breast is
provided, which facilitates accurate creation of the dimensions of the pocket
and precise control of bleeding. The resultant scar then falls strategically
within the inframammary fold crease where it remains unseen unless the
breast is lifted or the patient lies supine. The other incisions tend to variably
compromise operative exposure for dissection of the breast pocket either due
to incision length, as can be the case with periareolar or transnipple incisions,
or due to their remote location, as with the transaxillary and periumbilical
techniques. In addition, with these other incisions, pocket dissection is often
performed in a blunt fashion, which can compromise precise pocket
development and hemostasis. Also, if any patient develops complications
such as hematoma, capsular contracture, or shape distortion, the
inframammary approach may then be necessitated anyway to provide
adequate exposure to correct the problem. Therefore, despite the relatively
inconspicuous appearance of the other resulting scars, many surgeons find the
inframammary fold approach to be the most attractive option when
comparing operative exposure with scar quality and location.
INCISION PLANNING
Placing the incision so it will eventually fall directly in the resultant
inframammary crease requires that many factors be taken into account.
Perhaps the easiest situation to deal with is the patient who preoperatively has
enough breast volume to form a defined crease and enough skin to
accommodate the breast implant without recruiting upper abdominal skin to
assist in forming the lower pole of the breast. This also assumes the
inframammary fold location will not change. In these cases, the incision is
diagrammed directly in the fold, and it is made long enough to allow
adequate exposure for accurate pocket dissection and placement of the breast
implant. Incision length for saline implants ranges from 3 to 4 cm in most
cases, and for silicone gel implants, 4 to 5 cm. When the more cohesive
anatomically shaped silicone gel implants are used, incisions of up to 7 cm in
length may be required for larger implants. In these types of patients, the scar
will consistently and reliably fall directly in the fold postoperatively, and in
most cases, will be almost imperceptible (Fig. 102-1). When the existing skin
envelope of the breast is not adequate to easily accommodate the proposed
breast implant, skin from the periphery of the breast will be recruited, and a
new inframammary fold location will generally be created. This must be
taken into account when planning incision location. Direct measurement of
the base diameter of the proposed breast implant can assist in placing the new
fold. By using the radius measurement of the implant, a measurement from
the nipple to the proposed fold can be made to approximate the location of
the new fold. The elasticity of the skin must also be taken into account.
Assuming the lower pole breast skin will stretch to accommodate the breast
implant, this measurement is optimally made with the lower pole skin under
stretch to attempt to predict this proposed effect. Alternatively, a maneuver I
have found to be helpful in these types of patients is to gently lift the breast
skin envelope away from the chest wall, with mild tension directed from
above and with the patient supine, and observe where the new fold tends to
form. Placing the incision at the lower margin of this fold ensures the
resulting scar will fall in the new fold formed after the breast implant is
inserted (Fig. 102-2). In cases of severe restriction of the skin envelope of the
breast preoperatively, placement of the inframammary fold incision can be
difficult to gauge accurately. The location of the fold is almost always
lowered in these patients, and the lower pole breast skin tends to be relatively
inelastic so the stretch effect will be limited. As a result, direct measurement
of the distance from the nipple to the proposed fold is the best method to
predict the ultimate location of the new inframammary fold. This
measurement is again guided by the radius measurement of the width of the
proposed breast implant. There is still a tendency for the incision to ride up
on the lower pole of the breast in these types of patients, and an additional 0.5
to 1 cm lowering of the planned incision is generally used to increase the
likelihood that the scar will fall directly in the subsequent fold (Fig. 102-3).

FIGURE 102- A: Preoperative appearance of a woman with moderate breast volume


prior to breast augmentation through an inframammary fold incision. B: At 1 year,
the augmented breast falls over the fold, concealing the scar. C: Only with the breast
lifted and by looking from below can the well-healed scar be seen.
FIGURE 102-2 A: Preoperative appearance of a woman with minimal breast volume
and a short inframammary fold-to-nipple distance prior to breast augmentation. B:
By lifting the breast away from the chest wall, the redundancy in the skin can be
taken up to simulate what effect the breast implant will have on the soft tissue
envelope. C: By applying slight pressure from above, the exact location of the new
inframammary fold can be seen, which allows for accurate placement of the incision
so the resulting scar will fall precisely in the fold.
FIGURE 102-3 A: Preoperative appearance of a woman with essentially no breast
volume and no defined inframammary fold. B: Measurements based on the radius of
the proposed breast implant are made in each direction centered on the nipple. In
this fashion, the location for the new fold can be estimated. C: Postoperative result
showing accurate placement of the fold with good symmetry.

After the location of the desired fold is determined, the actual incision can
be located anywhere along this line. A common strategy to position the
incision is to drop perpendicular from the medial aspect of the areola or the
nipple to the proposed fold and then measure the desired distance laterally
along this line. I have found that an even more lateral location can be
desirable in some patients. By measuring from the lateral margin of the areola
and then extending laterally, the scar is even more difficult to see as the
breast falls over the fold (Fig. 102-4). This approach also has the added
benefit of allowing more of the inframammary fold to be addressed surgically
from above and to the side rather than when the incision is located directly in
the midportion of the fold. Accurately dissecting the fold to a desired level is
easier to do from this more remote location than when the incision is directly
in the center of the fold (Fig. 102-5).
FIGURE 102-4 A and B: A line is drawn extending from the lateral aspect of the
areola to the proposed inframammary fold. An incision of the desired length is then
measured along the fold laterally. This places the resulting scar low and lateral,
which is a location that heals well and is difficult to see postoperatively.

FIGURE 102-5 A: Working through an incision in the middle of the inframammary


fold can sometimes be cumbersome when it comes to controlling the dissection space
and positioning the location of the fold. Due to the proximity of the fold to the
incision, it is easy to lower the fold position too much and end up with an implant
that has a “bottomed-out” appearance. B: By moving the inframammary fold
incision to a more lateral location, the same access to the breast is provided, but it is
easier to directly dissect the implant pocket as it relates to the fold, which can
provide for greater control of fold location.
In cases where the native inframammary folds are asymmetric, it is
generally easier to maintain the position of the lowermost fold and then drop
the position of the higher fold as needed (Fig. 102-6). The effect of lowering
the fold on the position of the nipple and areola must also be taken into
account. In cases of significant fold asymmetry, the high fold cannot be
lowered to such a degree that the nipple areolar complex (NAC) becomes
malpositioned superiorly on the breast mound, relative to the other contours
of the breast. Here, it is best to raise the opposite fold, manipulate the NAC
position with periareolar surgery, or simply accept a persistent mild, but
improved, fold asymmetry.

FIGURE 102-6 A: Preoperative appearance of a woman with an inframammary fold


asymmetry. B and C: At surgery, the left inframammary fold will be lowered to
match the fold on the right. D and E: Postoperatively, after placement of smooth
round saline implants, the fold levels are symmetric with the breasts in repose and
with the arms elevated. F: The low and laterally placed scar has been correctly
positioned directly in the fold.
OPERATIVE TECHNIQUE
Utilization of an incision in the inframammary fold affords direct
visualization of the dissection plane required for breast augmentation. All
types of pocket dissection techniques are facilitated using this approach,
including subglandular, subfascial (1,2), partial subpectoral, dual plane (3–6),
and completely submuscular dissection spaces. After infiltrating the skin with
a dilute solution of local anesthetic with epinephrine, incision is made
through the skin. By angling upward to the underside of the breast,
inadvertent lowering of the inframammary fold can be avoided. A lighted
retractor is inserted and the desired pocket dissection is begun by expanding
the superior dissection in all directions for several centimeters. For partial
subpectoral or submuscular pockets, direct superolateral dissection will
expose the lateral margin of the pectoralis major muscle. The underside of the
muscle is elevated and then, by working from medial to superior to lateral,
the pocket is opened. Laterally, care must be taken to avoid inadvertent
overdissection because this space tends to open up easily. Through this
incision, the pectoralis major muscle can be easily and under direct vision
released along the inferomedial border of the pocket as desired. In addition, if
dual plane release of the overlying soft tissues is desired, the lower edge of
the muscle can be released from the overlying breast as needed.
Subcutaneous and subfascial pocket dissection also proceeds directly and
easily through an inframammary incision. The limits of pocket dissection are
readily identified and precise control of potential bleeding points is
accomplished without difficulty. In addition, structures that are optimally
preserved can be readily identified through the inframammary incision. In
particular, the large 2nd intercostal perforator off the internal mammary
artery in the superomedial portion of the pocket, as well as the lateral
intercostal nerves, can be visualized and protected. The pocket dissection is
continued until the dimensions of the pocket approximate the dimensions of
the desired implant. This is particularly important with respect to the medial
and lateral extent of the pocket dissection. If the pocket is too wide, the
implant will tend to fall off laterally under the arm when the patient is supine
and create a medial concavity in the breast. This finding can be a great source
of dissatisfaction in selected patients. After the pocket is developed, insertion
of the implant also proceeds without difficulty because the incision and the
pocket are in such close proximity. This is particularly advantageous with
silicone gel implants, which have a fixed volume and must be coaxed into the
pocket with gentle manipulation. In addition, with the anatomically shaped
cohesive silicone gel implants, ensuring proper orientation and positioning of
the shaped devices is facilitated because the orientation dots on the device
can be easily visualized and palpated through the incision. Textured devices
can sometimes be difficult to insert and position through remote incisions due
to friction between the rough implant surface and the soft tissues of the
breast. Again, the proximity of the breast pocket to the incision can help ease
implant insertion in these cases. After the pocket has been developed and the
implants properly positioned, the surgical wound is closed in layers, first
closing the deep fascia and dermis with interrupted 3-0 or 4-0 absorbable
monofilament sutures, and finally closing the skin incision with a running
subcutaneous suture.
CONCLUSION
When performing breast augmentation, precision and control of pocket
dissection and proper implant positioning are key factors in obtaining
aesthetic results with few complications. To this end, the inframammary fold
incision provides excellent operative exposure to accomplish both of these
goals. The scar heals well and is unobtrusive because it is hidden in the
inframammary crease. Thus, the inframammary approach is recommended as
a consistent and widely applicable method for performing augmentation
mammaplasty.

REFERENCES

1. Graf RM, Bernardes A, Rippel R, et al. Subfascial breast implant: a new


procedure. Plast Reconstr Surg 2003;111:904–908.
2. Góes JC, Landecker A. Optimizing outcomes in breast augmentation:
seven years of experience with the subfascial plane. Aesthetic Plast Surg
2003;27:178–184.
3. Tebbetts JB. Dual plane breast augmentation: optimizing implant—soft-
tissue relationships in a wide range of breast types. Plast Reconstr Surg
2001;107:1255–1272.
4. Tofield JJ. Dual plane breast augmentation. Plast Reconstr Surg
2001;108:2162–2164.
5. Ramirez OM, Heller MDL, Tebbetts JB. Dual plane breast
augmentation: avoiding pectoralis major displacement. Plast Reconstr
Surg 2002;110:1198.
6. Spear SL, Carter ME, Ganz JC. The correction of capsular contracture
by conversion to “dual-plane” positioning: technique and outcomes.
Plast Reconstr Surg 2003;112:456–466.
CHAPTER 103

Shaped Implant in Breast


Augmentation
PER HEDÉN
HISTORY
It is apparent for professionals in the aesthetic field of plastic surgery that
breast augmentation is one of the most requested procedures. The female
desire for breast enhancement dates back a long way in human history and
surgical procedures to perform this has been done well over 100 years (1).
With the introduction of silicone breast implants in 1962 by Gerow and
Cronin (2) the modern era of breast augmentation begun. In the 1960s, 70s,
and 80s relatively limited research was put into developing breast implants.
The exception to this was alterations of surface technology starting with
polyurethane coverage in 1968 followed by texturization of implants in the
late 1980s. A paradigm shift occurred, however, in 1994 when McGhan (later
an Inamed and now Allergan Co.) introduced anatomically shaped breast
implants with highly cohesive silicone filling. The use of these implants has
been thoroughly described in two previous editions of this book (3,4) and
also in other publications (5). Since the last edition of this book, great
changes have occurred in the use of shaped breast implants. The largest and
most dramatic alterations relate to increased knowledge about breast implant–
associated anaplastic large cell lymphoma (BIA-ALCL). This has resulted in
a reduced use of textured implants. Lately regulatory authorities in Europe
(Agence National de Securité de Medicament [ANSM]) have prohibited the
use of Allergan’s macrotextured Biocell surface (February 8, 2019). The
impact of this decision is not yet fully known at the writing of this book
chapter. However, it has obviously limited the use of certain shaped breast
implants, especially those available from Allergan (Style 410). The decision
from ANSM is to a large extent related to the recent increased knowledge
about BIA-ALCL. There is no doubt about the fact that the patient must be
well informed about the possibility of a connection between textured breast
implants and ALCL. However, it is also important to understand the benefits
of textured implants and, thereby, especially the difference between shaped
and round implants. It also deserves to be underlined that today’s knowledge
has confirmed that the frequency of ALCL is low, and this is for a disease
that is relatively benign if diagnosed early. Most patients developing ALCL
will be cured by implant removal and capsulectomy if the disease is confined
to the seroma fluid around the implant. Also, to abandon the uses of textured
implants in favor of only round smooth breast implants when the frequency
of ALCL is likely to be somewhere between 1/3,000 and 1/90,000 for
textured implants is clearly an overreaction. Obviously, this disease cannot be
compared to breast cancers as these diseases have totally different etiologies,
but it should be put in perspective that breast cancers are much more
malignant diseases and occur in a frequency of 1/9 in most developed
countries. It should also be remembered that double-blind studies have
confirmed that the capsular contraction frequency is considerably higher for
smooth implants if these are placed in the subglandular space compared to if
textured implants are used in the same position (6). Smooth round implants
are likely to have a reduced risk for ALCL but they have other problems such
as malpositioning and increased capsular contracture frequency which may
necessitate a reoperation and any reoperation risk should be compared to the
low risk for ALCL.
After the first anatomically shaped implants were introduced by Allergan
(formerly McGhan/Inamed) in 1994, many other manufacturers, for example,
Mentor, Sientra, GC Aesthetics, Sebbin, Polytech, Silimed, Perthese, Arion,
and Establishment Labs have also introduced anatomical shaped highly
cohesive silicone implants. Comparison of the difference between these
different manufacturer products goes beyond the scope of this chapter, but
the author has used several of these products with equally good outcomes.
DIFFERENCES BETWEEN ROUND AND SHAPED IMPLANTS
The debate relating to differences between round and shaped implants has
been intense and sometimes even slightly inflamed. Several studies have also
compared the result between these two different types of implants and not
seldomly have the results been conflicting (7–10). Several studies have
claimed that there are no differences in outcome when selecting an
anatomically shaped implant or a round one. Unfortunately, much of these
discussions have been too simplified, not taking into consideration all the
parameters that must be considered when doing these types of comparisons.
To be able to judge the differences after augmentation with a round or
anatomically shaped implant the conditions must be comparable: Thus, the
breasts have to have a similar shape and appearance. Breasts with thin tissue
cover should have implants placed under the muscle as with subglandular
placement, the implant shape is more visible. Also, the postoperative
situation when it comes to capsular activity must be similar where a
noncontracted breast best reveals the differences. If these differences are very
similar in the before and after pictures that are evaluated, then there is no
doubt that there are clear differences when comparing round and anatomical
implants. Some studies claiming that there are no differences in outcome
have not considered all of the variables needed for an objective comparison.
Examples of this is the Hidalgo and Weinstein study from 2017 claiming to
be a scientific level 1 randomized controlled trial. In fact, this study is only
partially controlled as anatomical and round implants were placed in the same
patients but in different breasts. This was done perioperatively and not
evaluated in final outcome. Furthermore, the actually used implant was
placed on the round side whereas sizers were mainly used on the anatomical
side. Thus, there are severe limitations to this study which should not be
regarded as level 1 scientific evidence.
In comparing round and anatomical implants there are, in fact, 10 different
considerations that must be made:
1. The slope of the upper pole: which clearly is different between a round
and anatomically shaped implant.
2. The implants height and width relation: In anatomical implants the width
and height ratio can be varied where the height in relation to width can be
higher, the same, or lower. In round implants, obviously, the width and
height ratio is always equal. Studies of what constitutes attractive breasts
(11) shows that they have more volume in the lower pole, which also
favors anatomical implants over round ones. In the attractive breast the
ratio of upper to lower pole volume should be 45%/55%. This means that
anatomically shaped implants can be placed 50% of its height distal to the
nipple areolar complex (NAC). If a round implant is placed with 50% of
its height distal to the NAC there will be too much volume in the upper
pole and not sufficient elevation of the NAC. For highly cohesive round
implants it is recommended to have 55% of the implant height (=
diameter) distal to the nipple projection point (please see section on
preoperative markings below). This difference between round and
anatomical implants affects how their lower pole is placed in relation to
the existing inframammary fold (IMF). An anatomically shaped implant
with lower height than its width, will be placed higher on the chest wall
whereas round ones have to be placed lower. Thus, round and full-height
anatomical implants have a higher risk for contour irregularity in the
lower pole if they are used in a patient with a short lower pole. Double-
bubble deformity risks can be minimized by selecting a low-height
anatomical implant in these cases (Fig. 103-1).
3. The implant projection (and thus the volume): If a lower-projecting
implant is used the difference between a round and anatomically shaped
implant is small compared to if extra-projecting implants are used.
4. Position of the implant in relation to the pectoralis muscle: If the upper
pole is covered with the pectoralis muscle this gives a smoother transition
between the implant and the surrounding tissue and muscle cover and
reduces the differences in appearances between a round and anatomical
implant.
5. The amount of glandular cover: Patients with thick glandular cover and
subcutaneous tissue conceals much more of the shape differences
between round and anatomically shaped implants. With thin tissue cover
these differences are much more apparent (Fig. 103-2A–D).
FIGURE 103- Anatomical implants can have variable width/height relation and are
placed 50% of the height distal to the NAC. Round implants, on the other hand,
always have the same height and width and should to achieve an ideal aesthetic
breast appearance be placed 55% distal to the NAC. This has implications on how
the implant is placed in relation to the IMF and thus for the risk of developing a
contour irregularity (“Double bubble”).
FIGURE 103-2 A, B: Before and after subfascial augmentation with a round
moderately projecting implant. A natural anatomical slope of the upper pole is
achieved as this round implant has a moderate projection and a thick tissue cover
(glandular pinch 4 cm at upper border of implant). C, D: Before and after
augmentation with a round moderately projecting implant. Compared to A and B a
more unnatural slope of the upper pole is achieved as the tissue cover is thin
(glandular pinch 1.5 cm at upper border of implant).

6. The implants vertical position in relation to the NAC: A too high–


positioned anatomical implant can provide more of an unnatural and
bulging upper breast slope than a round implant placed low.
7. The type of filling material and its cohesivity and elasticity: Highly
cohesive silicone filling with low elasticity maintains upper pole volume
much more than an implant with a much more elastic gel with less
cohesivity.
8. The degree of implant filling: There is a certain variability in the degree
of filling of silicone implants and a 100% filled implant will provide
more upper pole fullness, especially if this has low elasticity and high
cohesivity. An underfilled implant, exemplified by an underfilled saline
implant will not have the same volume, roundness, and artificial filling of
the upper pole.
9. The degree of capsular activity: Even moderate degree of capsular
activity can reduce the diameter of the implant and produce more cranial
displacement and roundness of the upper pole. With more pronounced
capsular contraction activity (Baker III and Baker IV) even anatomical
implants can create a very artificial and rounded upper pole compared to a
round implant without capsular contraction activity.
10. The observation angles: In the anterior–posterior (AP) view of breast
implants it may be very difficult to reveal shape differences between
breasts with round or anatomical implants, especially if these are not
excessively large. Oblique views and side views reveal the differences
much better.

On consideration of all of these parameters when comparing round or


anatomical devices, it is obvious that there under certain anatomical
situations are clear differences in outcome between round and anatomical
implants. There are also very clear indications to use anatomically shaped
implants and the beauty of modern plastic surgery is to have “a large tool
box” to choose from when selecting the optimal procedure for a patient.
There is no one size or one type of implant that fits all in modern breast
surgery and the selection should be done on a case-by-case basis. It is
commonly argued that the shape differences between round and anatomical
implants can be compensated with fat grafting and obviously this is true
when it comes to many of the different parameters discussed above.
However, it should be recognized that fat grafting is an additional procedure
which has additional costs and possible morbidity on both donor and
recipient area. In thin patients it can also be quite time consuming and
difficult to find sufficient amount of fat and this can make the procedure
considerably longer lasting and involves higher risks. Thus, it cannot be
stated that this solution would be suitable for most patients even though it can
have certain indications.
A final and very important additional consideration when comparing round
and anatomical implants is relating to surface technology. Anatomically
shaped implants should be textured to minimize malposition and rotation.
Round ones can obviously be smooth and microtextured. This has certain
benefits, but we should also recognize that even though smooth surface
implants may have reduced risk for developing seroma and possibly also
ALCL there is a back side to this coin and that is the risk for inferior and
lateral malposition. Implants with very little tissue adhesion or friction has
high risk for malpositioning which could necessitate secondary surgery and
additional risks for the patient.
Indications for Anatomically Shaped Implants
Shaped implants have many indications and can basically be used in any type
of breast augmentation. It is important to realize, however, that several
differences exist when using anatomical implants compared to older
traditional techniques used for round implants: The implant selection process
cannot be arbitrary and should be based on careful analysis and
measurements (see below). This is also true for the preoperative markings
that should be much more elaborate than what was used in the times when
only round implants were available. The surgical technique also differs as a
much more precise dissection and a snug-fitting implant pocket is necessary
to avoid complications. Proactive hemostasis to minimize bleeding is
recommended. In addition to this the postoperative regime should be different
as patients are not allowed to massage or move around the implant in the
pocket.
Bouncing exercise should also be avoided in the healing phase so the
implant pocket settles in a proper way around the implant. If all of these
considerations are followed, there is no doubt that anatomically shaped
implants can provide superior outcome under certain situations. Indications
for use of these devices are, for example:

tuberous breasts (Figs. 103-3 and 103-4)


breast with short lower pole and a well-defined gland
pseudoptotic breast
certain poorly shaped breasts with poor tissue cover
chest wall deformities, for example, a pectus excavates or bird chest
deformity (Fig. 103-5)
breast asymmetries; thanks to the greater variability of different
anatomically shaped implants, treatment of breast asymmetries offers
more alternatives than with round. Post mastectomy breast are extremely
severe asymmetries that favorably can be treated with anatomical
implants. For long-term stability of the result sometimes a radical
reduction augmentation on the remaining breast where a lower-
projecting implant is used in combination with more projecting implants
on the reconstructive side can give a much better long-term outcome
than unilateral implant reconstruction and contralateral
mastopexy/reductions

FIGURE 103-3 A, B: Tuberous breast with a short lower pole is usually a good
indication for anatomical implants as most volume is needed in the lower pole.
Before and after augmentation with moderate height full-projecting implants and
scoring of the lower pole glandular tissue to avoid a “double-bubble” deformity.

FIGURE 103-4 A, B: Tuberous breast and asymmetry with lower NAC on L breast.
Before and after augmentation with anatomical implants and L-sided internal lifting
(SIMA = scar-less internal mastopexy augmentation) where the gland internally is
sutured up to the pectoralis major before a submuscular implant placement.
FIGURE 103-5 Before (A–C) and after (D) breast augmentation with microtextured
anatomical implants. Preoperative markings (C). To answer how to position the
implant vertically on the chest wall in relation to the NAC (Question One) a nipple-
to-sternum (NS) line is drawn with arms on top of the head and half the height of the
anatomical implant is measured distally in the midline. With arms elevated again a
horizontal line parallel to the NS line is marked indicating the implants lower pole
position (ILP line). The second question (Question Two) to answer with the
preoperative markings is how much skin that is needed in the lower pole and thus
also where an IMF incision should be made. This relates to the length of the lower
ventral curvature of the implant from the nipple projection point on the implants
ventral surface down to its lower border (LVC value) plus how much glandular
tissue the patient has (in a typical breast augmentation this is between 1.3 and 1.5
cm, for small beasts it is 0.5 to maximally 1 cm less and for big breasts 0.5 to 1 cm
more).

Detailed description of indications for use of anatomically shaped implants


has previously been published (12).
Another reason for selecting anatomically shaped implants is that these
may reduce complications. It should be recognized that comparison of
complication rates is difficult due to the lack of high-quality comparative data
from single centers. However, when reviewing the 10-year follow-up data of
the CORE studies for anatomical implants by Allergan and Mentor, rates of
capsular contraction, implant malposition, and reoperations were lower with
anatomical implants compared to round ones (13–16).
The great number of different implant shapes of anatomical implants
available today makes customization in relation to patients’ biologic
conditions and desire possible.
Complications Related to the Use of Shaped Implants
It has been stated that shaped implants have higher frequency of certain
complications which includes rotation double capsule and seroma formation
(17–19) and recently BIA-ALCL (20–22).
The overall risk for these types of complications can however be
significantly reduced by optimizing the process of breast augmentation in
relation to implant selection, preoperative marking, surgical technique, and
postoperative management. Adams et al. reported no ALCL case in a series
of 42.000 macrotextured implants when adhering to a regime to minimize
implant contamination (23). In our early experience of anatomically shaped
implants (24) the frequency of rotation was low when adhering to the special
instructions for use of anatomical implants (0.4%).
With regard to late seroma the 10-year follow-up multicenter CORE
studies from Allergan 410 implants and Mentor contour profile implants only
showed 0.4% and 0.2% seroma, respectively (14,15).
There is no doubt that anatomically shaped implants in some cases are
strongly indicated and that round implants cannot satisfactorily substitute for
these. In the personal experience of the author, anatomically shaped implants
are associated with excellent long-term patient satisfaction and low
complication rates and it is felt that the drawbacks and limitations of
anatomically shaped implants strongly have been overstated by some
physicians.
THE PROCESS OF A BREAST AUGMENTATION PROCEDURE
A breast augmentation is so much more than the actual surgical procedure
and should more be regarded as a process. This first involves the important
patient communication where it is fundamental to understand patient’s
desires and expectations. This should be followed by a thorough examination
of the breast, chest, and surrounding tissues. Then a careful analysis of the
dimension and proportion of the breast including its width, height, and
envelope characteristics which results in a recommended implant shape and
volume, should be performed. Thus, implant selection in the 21st century
should take patient’s desires into consideration but it should also most
importantly be tissue based. For the patient it is important to understand that
there are limitations in what implant dimensions the tissue can accommodate
and that it is the physicians’ responsibility to select an implant that goes in
line with these limitations.
Having analyzed the “ideal” implant, 3D imaging is a useful tool to predict
what the likely outcome of the procedure would be and that this is in line
with the patient’s desires. This technology has been demonstrated to give
accurate predictions (24) but it may be inaccurate in patients with ptosis. In
addition to 3D imaging, trying an appropriate sizer in a tight-fitting sports bra
usually gives the patient a good understanding for what an outcome will be.
Using the actual implant in a sports bra is inadequate as this will be placed on
top of the existing breast and thus not take into consideration the convexity of
the breast underlying the implant. It will also underestimate the width of the
postoperative breast. For this reason, most implant manufacturers have
created sizer systems which limits these drawbacks. However, these also
have limitations as they do not predict the volume and dimensions in an exact
way. To minimize these limitations a patented technology; PREPLANT has
been developed by the author (Figs. 103-6 and 103-7).
In a double-walled bra a plastic bag is located in the bra’s outer pocket.
This is filled with the exact implant volume of a two-component self-curing
silicone (15 minutes). The sports bra with its liquid silicone is placed on the
patient and a hard-plastic cup with the calculated dimensions of the new
breast is placed on top of the liquid silicone to let it cure it in the desired
shape. The hard-plastic cups are available in a large number of different
dimensions in relation to calculated new dimensions of the breast. After 15
minutes the hard-plastic cups are removed and a soft but cured customized
sizer is then in place in the double-walled bra. The patient can then go home
to feel how it is to live with larger breasts, try her different clothes, show her
relatives, and experience how it is to have larger breasts in sports, etc.
Questionnaires to patients have documented that this is highly appreciated
technique and at least equally good for the patient as 3D imaging to make
their final decisions for the operation. This, not yet commercialized system,
hopefully can improve the communication process with patients further and
create even more confidence in the deciding for the procedure.
FIGURE 103-6 A: Before augmentation with an anatomical microtextured implant
(side views of same patient as in Fig. 103-7). B: With only a double-walled sport bra
(IPOMIA) and support garment. C: With a standard recommended sizer from the
manufacturer for the selected implant. D: With a custom-made PREPLANT sizer
after molding and shaping with an external hard plastic shell to control the shape of
the sizer while the two-component silicone mixture cures. E: Postoperative 6-month
follow-up.

FIGURE 103-7 A: Before augmentation with an anatomical microtextured implant


(AP views of same patient as in Fig. 103-6). B: Preoperative markings (see
description in text and Fig. 103-6). Arms elevated 45 degrees above horizontal plane
to simulate the nipple elevation that will be achieved with the augmentation. C:
Preoperative markings (see description in text and Fig. 103-6) with arms hanging.
Note shift in NS line, in this case with tight tissues and a relatively small breast a
relatively small shift of the nipple position. In patients with larger breast and laxer
tissues usually the nipple elevation is more pronounced (see Fig. 103-15). D: At
dismissal from the clinic 4 hours postoperatively. Note NS is now horizontal an equal
to the preoperative markings. E: Postoperative 6-month follow-up. F: Preoperative
simulation of result with custom-made sizer (PREPLANT—see Fig. 103-6). G:
Postoperative 6-month follow-up with the same double-walled sport bra (IPOMIA)
and support garment.

Having gone through this whole process of selecting the accurate implant,
the next step in the procedure is the adequate preoperative markings, the
surgical technique, and the correct postoperative management (see section
that follows).
Implant Selection
The “Akademikliniken Method,” the “AK Method,” or Simply the “2Q
Principle”
In the past implant selection was arbitrary and mainly based on the surgeon’s
experience and artistry. Unfortunately, this does not always provide good
results, especially in more complicated cases. With the introduction of
anatomical form-stable implants in the early 1990s it became necessary to
select implants dimensionally instead of volumetrically. The reason for this is
that form-stable anatomically shaped implants cannot be deformed to fit into
the wrong implant pocket size (Fig. 103-8). The implant and its pocket have
to fit snuggly and measurements of the breast became necessary. Today when
round implants with more elastic gel are used increasingly these can
obviously be deformed and used in a similar way as we used implants in the
past. However, with the evolution of dimensional thinking thanks to the
introduction of shaped anatomical implants dimensional thinking and
planning is also used for these round, more elastic implants.

FIGURE 103-8 Comparing how a low-cohesive non–form-stable implants can be


stuffed into a shape that is different compared to the implants’ intended shape. With
the introduction of anatomical form-stable implants this is not possible and with
their introduction in the mid-90s a completely different approach was needed.
Implant selection, preoperative markings, surgical technique, and postoperative
management had to be different. Without understanding of these principles many
surgeons had bad results and blamed the implants for this when in fact their
technique was to be blamed.
The way that the implants are selected, and the preoperative marking
principles have previously been described in detail in two different editions
of this book (3,4) and also in recent publications. The author has called this
implant selection process and preoperative marking principles the
Akademikliniken method or the AK method but also lately named it the 2Q
principle. This way of selecting implants uses the same principle in the
preoperative markings and it involves answering two fundamentally
important questions for any breast augmentation patient:
1. How should an implant be placed vertically in relation to the NAC on the
chest wall?
2. How long should the distance of skin be between the nipple and the IMF?

If surgeons keep these two principles and questions on top of their minds
when selecting implants and doing preoperative markings the frequency of
complications can be greatly minimized. Having developed these principles
since the 1990s and having held numerous preceptorships, live
demonstrations etc., the author has realized that the principles have been
regarded as very useful but at the same time very complicated by some
physicians. Therefore, a simplification has been introduced since the last
version of this book.
The selection of the ideal implant should always start with the suitable
footprint of the implant, thus its width and the height. If round implants are
used obviously the height and width are equal but with anatomically shaped
implants this can be varied. The height of the breast is important to consider
when it comes to selecting implant height and it is important to consider
where different implant heights end up in relation to the inferior border of the
gland but also in relation to the upper slope of the chest and breast. If the
breast has a well-defined dense gland, and a short lower pole and an implant
is placed well distal to this glandular border then the contour irregularity
“double bubble” has a high risk of occurring.

Question 1: The Implants Vertical Position on the Chest Wall in Relation


to the NAC
Analysis of the Implant Height
Fundamental and important observations from the author in the 1990s:
1. A correctly performed breast augmentation elevates the NAC. To
achieve this nipple elevation volume has to be placed in the lower pole of
the breast and the implant has to be placed correctly on the chest wall.
The nipple elevation is achieved by a breast augmentation similar to the
movement of a pendulum. The distance from the sternal notch to the
nipple does not change but volume loading pushing out the NAC moves
the NAC in a cranial direction like a pendulum of a clock (Fig. 103-9).
2. Horizontal transfer of the nipple position to the midline (the nipple-
sternum line [NS]) is useful for correct planning. As breasts are greatly
varying in amount and elasticity of the envelope and glandular tissue
planning along the midline of the breast is difficult compared to the
sternal midline where tissue variability is small and tissues relatively
fixed.
3. The postoperative nipple position can adequately be predicted
preoperatively by arm elevation. Having reviewed and examined
several hundred breast augmentation patients it was noted that an
adequate way of predicting the postoperative nipple elevation was done
by elevating the arms 45 degrees above the horizontal plane. A simple
way of doing this is to ask the patient to clasp her hands on top of the
head. This 45-degree elevation accurately predicts the postoperative
nipple position. With this position the nipple is transferred to the midline
and the analysis of implant position on the chest wall is done along the
sternum in the midline.

These principles are extremely important when selecting implant height.


Previously many surgeons used sternal notch-nipple distance measurements
to select implant height but this is an inadequate way of selecting the height
of the implant. It is better to measure where the upper border and lower
border of the implant height will be located on the chest wall and in relation
to the glandular border. As mentioned previously, for an adequate aesthetic
appearance of the breast 50% of anatomically shaped implants should be
placed distal to the NAC after the breast augmentation. Having predicted the
nipple position postoperatively with arm elevation and transferred this to the
midline, half of the implant height could thus be measured distally in the
midline. At the distal end of this midline measurement a horizontal line
parallel to the NS marking as described above defines the ideal position of
the lower implant border (Fig. 103-10). This inferior line is called implant
lower pole (ILP) line. If this line will be located well distal to the existing
IMF and glandular border it should always be considered how such a
violation affects the outcome (see section that follows).
In the implant selection the first recommended step is to measure the
height of the lower pole of the breast: The arms are elevated 45 degrees
above horizontal plane and the nipple position as well as the existing
submammary fold is transferred to the midline. When measuring the distance
between these two points in the midline this answers how high the lower pole
of the breast is. The ideal implant height is thus the double height of the
lower pole if an anatomical implant is used (55% of the diameter of a round
implant). This height should be kept in mind when selecting the footprint of
the implant. The second question to answer is the ideal width of the implant.

FIGURE 103-9 In the 1990s the author made three fundamental and important
observations for the principles of adequate implant selection and preoperative
markings. (1) A correctly performed breast augmentation elevates the NAC (this is
related to volume loading in the lower pole and acts as a pendulum and thus the
volume pushes the NAC outward and up. The sternal notch-to-nipple distance is
thereby, however, unaltered. If the implant is placed too high on the chest wall this
elevation of the NAC is not achieved, thus volume loading in the upper pole tends to
push down the NAC instead. (2) Planning the procedure on the breast tissue is
difficult as it is greatly variable when it comes to laxity, amount, shape, and
projection. In the midline of the chest the tissues are much less variable and fixed
and therefore transferring of the position of the NAC to the midline by doing a
nipple-to-sternum marking (NS line) is good for planning in the midline instead of on
the breast. (3) The nipple elevation achieved with a breast augmentation can be
accurately preoperatively predicted with arm elevation 45 degrees above the
horizontal plan.

Implant Width Analysis


It is not uncommon that surgeons state that an implant volume over 400 cc
usually should be avoided. It deserves to be remembered, however, that the
footprint of the implant has no volume and that patients with large chest
circumference (over 90 cm) will need a considerably wider implant base and
thus approximately a double implant volume than patients with a narrow
chest circumference (under 70 cm) to achieve a similar result.

FIGURE 103-10 Preoperative marking principles for an anatomical implant. First


step is to answer where to place the implant vertically on the chest wall in relation to
the NAC (Question One). A nipple-to-sternum (NS) line is drawn with arms on top of
the head and half the height of the anatomical implant is measured distally in the
midline. With arms elevated again a horizontal line parallel to the NS line is marked
indicating the implants lower pole position (ILP line). If a round high cohesive
implant is used 55% of the diameter (= the height) is instead measured distally in the
midline, thus for a 12 cm wide implant 6.6 cm should be measured distally in the
midline.

It is recommended to measure the chest circumference as an indication of


if this patient is likely to have a wide or narrow implant. The existing breast
width is measured with a caliper and in addition to this the tissue cover
should be analyzed. The tissue cover is measured at the height of the NAC, at
the border of where the implant is expected to be located and with a caliper
compressing the tissue to simulate the compression that the implant exerts on
the overlying tissue. This caliper measurement should preferably be done
both medially and laterally. As such a tissue pinch is a double fold of tissue
the actual cover is half of the measurement. Thus, the accurate way of
calculating tissue cover is the pinch medial and lateral added and then divided
by two. As tissue cover usually is relatively similar medial and lateral a
simplified way of doing this analysis is just to take one pinch measurement
and subtract this from the desired breast width which will provide the desired
implant width. The desired breast width is communicated with a patient,
preferably in front of a full-size mirror, where the estimated cleavage of 2 to
3 cm is demonstrated and the lateral protrusion respecting the axilla is shown.
This can also easily be demonstrated by compressing the breast tissue using
the flat end of the caliper to compress the breast between the caliper ends and
thereby using the caliper to show the estimated width of the breast after the
augmentation.
Based on the two above analyses the ideal footprint of the implant has been
decided and if an implant height have to be positioned distal to the existing
glandular border the following questions should be considered.
1. Is it risky to pass the border of the existing gland in this case or is the
gland so poorly defined that this does not matter?
2. If the border is not respected how much can it be passed without high risk
for a contour irregularity? Usually 3 to 5 mm is no problem.
3. If a well-defined glandular border is passed with the implant, how should
this be managed? —(a) Glandular scoring, (b) Fat grafting, (c) Modified
“Pucket” procedure.
4. Is it better to select a different implant height to have the lower border of
the implant closer to the existing fold?
5. Is it better to reposition the NAC and place the implant at the existing
glandular border?

Question Two: The Length of Skin Between the Nipple and the New IMF
Having defined the footprint of the implant, the patient should be aware of
the fact that this footprint has no volume whatsoever and that the final
implant volume is a function of the implant’s base plate and its projection.
Anatomically shaped implants with similar base plate as round ones usually
produce less volume with a similar projection as they have less volume in the
upper pole. The projection of the implant is greatly dependent on patient
preferences but is even more a decision that should be based on the covering
envelope. This is the second very important question to answer when
selecting implants.

FIGURE 103-1 The second question (Question Two) to answer with the preoperative
markings is how much skin that is needed in the lower pole and thus also where an
IMF incision should be made. This relates to the length of the lower ventral
curvature of the implant from the projection point of the NAC on the implants
ventral surface (LVC value) plus how much glandular tissue the patient has. The
length of skin added for to the LVC value is the difference between the purple and
the red line (if all the gland in this illustration was removed, then the purple line
would move in to the position of the red line and thus the difference in length
between these lines is of importance). This can be measured exactly by elevating the
arms 45 degrees and measure the convexity of the breast down to the ILP line (see
Figs. 103-10 and 103-13) and subtracting half of the height of the implants (in a
typical breast augmentation this is between 1.3 and 1.5 cm, for small breasts it is 0.5
to maximally 1 cm less and for big ones 0.5 to 1 cm more).

Obviously a more projecting implant with a larger footprint needs longer


distance of skin between the NAC and the new submammary fold. Also, the
amount of gland affects how long the distance should be (Fig. 103-11).
The amount of skin needed or filled in the lower pole of the breast relates
to the so called LVC value of the implant (the Lower Ventral part of the
implant thus the length of this Curvature). This is something that can easily
be measured on a millimeter paper where the vertical axis represents the
projection of the implant and the horizontal axis is half of the height of the
implant or as much of the implant that is estimated to be positioned distal to
the NAC after the procedure. This measurement has been performed for
several implant manufacturers’ implants and charts for different implants can
be provided by the author (Fig. 103-12).
FIGURE 103-12 The LVC values of any implant can be measured with a tape ruler
on a millimeter paper with the projection on one axis and as much of the implant
height that is placed distal to the NAC on the other axis (half the height for
anatomical implants). The LVC values for many different manufacturers’ implants
have been calculated by the author and are available in charts. As the way to
calculate length of skin that has to be added to the LVC value for the amount of
glandular tissue has been difficult for many surgeons to understand the author has
made a simplification adding the average 1.3 to 1.5 cm to a chart with the nipple-to-
new IMF distance (N-NIMF). Using this chart will make it very simple to answer
how much skin that is needed between the nipple and the IMF dependent on the
selected implant (for small breasts it is 0.5 to maximally 1 cm less and for big ones
0.5 to 1 cm more). In this illustration the LVC values and N-NIMF values for
Allergan’s Style 410 are demonstrated. These implants are no longer on the market
and similar charts for other implant manufacturer and implants are available.
FIGURE 103-13 The length of skin added to the LVC value can be measured exactly
by elevating the arms 45 degrees and measuring the convexity of the breast down to
the ILP line and subtracting as much of the implant that is placed distal to the NAC,
for an anatomical implant this is half the height of the implant.

The length of skin needed to be added to this LVC distance in relation to


the amount of glandular cover can be measured exactly: During arm elevation
of 45 degrees above horizontal plane the distance between the nipple and ILP
line as described above is measured and from this distance the “inside of the
breast” is subtracted—this is obviously equal to half the height of the implant
if half of the implant is placed distal to the NAC (Fig. 103-13).
Since this method was developed close to 20 years ago by the author it has
been presented in many different meetings and workshops and unfortunately
sometimes described as a good but difficult technique. For that reason, the
author modified the technique by analyzing how much length of skin was
added to the LVC value of the implant in the average breast augmentation
patient. Looking at several hundred breast augmentation patients it was found
that on average 1.34 cm is added for the amount of gland to the LVC value.
Therefore, charts were developed where the LVC value plus 1.5 was added
(1.6 mm more than the average thus). These nipple-to-new inframammary
fold distance (N-NIMF) charts represent the ideal distance of skin for a
specific implant in a “normal” breast augmentation. For surgeons who desires
to be more exact value 0.5 to 1 cm can be subtracted or added to this N-N
IMF distance if the breast is small, very small, or large/very large (Fig. 103-
12).

The Importance of Answering Questions One and Two in Any Breast


Augmentation
Having answered the questions about ideal vertical implant position on the
chest wall and the amount of skin needed in the lower pole, the ideal situation
for a breast augmentation is that the implant will be located in the existing
IMF and that the amount of skin needed comes exactly in the same position.
However, this is commonly not the case and when the skin is stretched
maximally the N-NIMF distance comes distal or proximal to the ILP line. If
the discrepancy between the ILP line and the amount of skin needed in the
lower pole of the breast is less than 2 cm the selected implant is usually
acceptable. If the distance is more than 2 cm the implant should not be used
or additional measurements such as a mastopexy or selection of a
smaller/larger implant is needed. To make an incision <2 cm distal to the ILP
line if a large implant is requested and the tissues are tight and to recruiting
skin to the lower pole can usually be done. The Scarpa fascia of the incision
is then in the end of the procedure sutured up to the thoracic fascia at the ILP
location (Fig. 103-14).
If patients request small implants and the tissues are lax the analysis above
may indicate that the incision should be done above the ILP line. The
dissection is then distal to the incision and beyond the ILP line. The incision
is then sutured down to thoracic fascia along the distally placed implant.
The same principles for implant selection can be used both for anatomical
and round implants. Round highly cohesive implants are however as
mentioned above placed slightly more distal to the NAC (55%) of the height,
thus 6.6 cm for a 12-cm implant diameter.
Preoperative Markings
The principles for preoperative markings should be the same as used for the
implant selection process described in detail above. In this section a more
summarized description of these principles will be given. Preoperative
photographic documentation including:
1. straight AP view picture,
2. 45-degree oblique pictures left and right,
3. straight left- and right-side view pictures,
4. AP picture with arms elevated above the head,
5. AP picture with tightening of the pectoralis muscle,
6. picture (a) and (d) after preoperative markings

FIGURE 103-14 Example of a big breast in a tight envelope. The vertical implant
position (Question One: NS line measuring distally as much of the implant that is
placed distal to the NAC and extending an ILP line laterally) is above the amount of
skin needed between the NAC and the new IMF (N-NIMF charts—see Figs. 103-11
to 103-13). When marking N-NIMF distance the skin should be stretched maximally.
If the discrepancy between these two lines is <2 cm the IMF incision can be sutured
up to the implants lower pole (ILP line) recruiting skin to the lower pole of the
breast. The Scarpa fascia of the incision is then sutured to the thoracic fascia along
the implant border. If the discrepancy is >2 cm the implant is too big for the
envelope. Same principles can be used in lax breasts where the ILP line frequently is
below the N-NIMF marking. In an ideal situation the ILP line comes at the
preoperative existing IMF and the N-NIMF distance with stretching of the lower
pole skin is in the same place.

To gain understanding for the healing process etc. it is also recommended


to take pictures postoperative at dismissal and at each follow-up.
The preoperative markings include the following steps:
1. Draw a line along the midline from the sternal notch to the xiphoid and
along the existing submammary fold.
2. Use the chest as a sketch board marking:
a. Selected implant type and volume and its width and height
b. The LVC value and/or the N-NIMF distance measurements according to
available charts (the LVC plus what is added for the amount of gland on
average 1.5 cm)
3. Ask the patient to elevate the arms 45 degrees above the horizontal plane
by clasping their hands on top of the head and transfer the nipple position
to the midline by drawing a NS line.
4. Lower the arms and measure in the midline from the medial part of the
NS line, half of the height of the anatomical implant distally with a
caliper.

Ask the patient to once again elevate their arms on top of the head and
transfer the distal midline marking laterally parallel to the NS line by drawing
an ILP line. These above steps have now answered the very important
question on how to ideally position the implant vertically on the chest wall
(Fig. 103-15). The horizontal position distally does not need any additional
measures as implants are placed symmetrically between the midline (2 to 3
cm intramammary distance) and axilla. The next step is marking of the ideal
position for an IMF incision which is equal to the amount of skin in the lower
pole of the breast. N-NIMF distance according to available charts or
measured on a piece of millimeter paper is the LVC of the implant plus what
is added for the amount of gland on average for a breast augmentation = 1.5
cm.
Stretch the lower pole of skin maximally and mark the N-NIMF distance.
Preferably and ideally this should come at the same place as the ILP line but
if slightly above or below (≤2 cm) the incision should be done above or
below the ILP line.
The length of the incision is marked and depends on implant type and
volume. The width and height of the implant and its position on the chest
wall is marked and this finalizes the preoperative markings.

FIGURE 103-15 A, B: Preoperative markings with arms elevated and hanging. Note
how the NS line shifts in this larger breast. C: Note also how the NS line with
hanging arms 4 hours postoperative is equal to preoperative NS line with elevated
arms. D: Follow-up 6 months postoperative.
OPERATIVE TECHNIQUE
With the introduction of anatomically shaped implants in the first half of the
1990s it became apparent that older and traditional surgical techniques could
not any longer be used and this resulted in a much more exact surgical
technique which today increasingly is used also for round breast implant.
Blunt dissection with oversized pockets used earlier for smooth-walled round
implants could result in rotation of anatomical devices. If the preoperative
markings have been done according to the description above the patient can
be put to sleep with arms at 90-degree angle facilitating the anesthesia and
the procedure. In secondary cases and mastopexy augmentation the patient
should be sleeping with the arms along the side as pre-operative vertical
positioning of the upper thorax after implant insertion is recommended in
many of these cases. With the preoperative markings described above this is
not necessary in primary cases as the planning accurately shows how to
position the implant without having the patient in a sitting position during
surgery.
After sterile draping, local anesthetics are applied. If this is liberal
circumferentially it reduces the postoperative pain and speeds up the
recovery. The author uses a solution of 160 cc made by adding 20 cc of 2%
plain Xylocain and 140 cc of saline plus 0.8 mg of Adrenaline. Two syringes
are used to speed up the injection and the pectoralis muscle is also injected to
reduce twitching during dissection. The length of the incision varies but with
use of the Keller Funnel this can be reduced approximately 1 cm compared to
the length needed without the Keller Funnel. Average length for a 300-cc
anatomical implant inserted with a Keller Funnel is 4.5 cm. Dissection is
done with a scalpel through the dermis and straight down to the thoracic
fascia which is followed in a proximal direction, 2 to 3 cm above the incision
the pectoralis fascia is elevated to visualize the lateral border of the pectoralis
muscle if a dual plan positioning is planned. The subfascial dissection is
continued to the areolar border in dual plane II dissection and past the areola
in dual plane III (Fig. 103-16). In dual plane IV dissection, a more extensive
subfascial dissection is done laterally almost to the upper border of the
implant (Fig. 103-17). This dual plane IV technique is mainly used for body
builders and the lateral muscle division is done at a much higher level
whereas the medial part of the muscle is kept to the same height along the
sternum as in dual plane II and III dissections (see below).

FIGURE 103-16 Performing the dual plane II and III procedure is the most common
technique in naturally shaped youthful breasts. The subglandular or subfascial
dissection on top of the pectoralis muscle is done to the level of the nipple areola
complex (II) or slightly above it (III). The muscle is then divided distally but well
above the lower pole of the implant (ILP) line to provide a rigid structure for the
later anchoring of the incision to the inframammary fold. The weakened lateral
pectoralis flap retracts and minimizes animation during pectoralis activity. The
nipple-sternum line in the midline is respected, and usually division of the muscle
should be kept well below this level (2 to 3 cm).

In patients with thick tissue cover and a pinch of more than 3 to 4 cm at the
calculated upper border of the implant a subfascial placement of the implant
can be done. In the majority of cases dual plane position, usually dual plane
II is recommended. After having done the dissection up to the NAC the
lateral border of the pectoralis muscle is grabbed with a forceps 2 to 3 cm
above the ILP line. This is essential to be able to emphasize the fold with a
suture at the end of the procedure. Dividing the muscle all the way down to
the IMF does not permit a good fixation of the IMF with sutures. The muscle
is divided in oblique fashion weakening the retracting pectoralis muscle in
the lateral inferior part. When reaching the submuscular plane the loose
areolar issue on the ribs is carefully preserved using proactive hemostasis
with electrocautery and a Colorado tip or insulated forceps. Usually the
dissection is blood free. The steps of dissection are from the lateral border of
the pectoralis muscle in the direction of the sternal notch. When reaching the
upper marked border of the implant (dissection height is checked with a
ruler) the dissection is carried on laterally on top of the pectoralis minor
muscle. After reached the lateral border of the pocket, the medial inferior
origin of the pectoralis muscle is divided. It is essential to always maintain
muscle cover distal to the NS line. Both NS and ILP lines are valuable
guidelines during the surgical procedure. The pectoralis muscle division is
done up to the inner border of where the implant will be positioned but
muscle is kept along the sternum well distal to the NS line. The width of the
pocket should not be checked with a finger as the pocket size is
overestimated, instead an instrument is placed under direct vision at the
border of the dissection and pushed vertical toward the skin surface to
confirm the width at the external markings of the implant width. After
controlling hemostasis, the pocket is irrigated with saline and antibiotic
solution and usually drains are not needed. The implant is inserted after glove
change and with the aid of a Keller Funnel to minimize contamination. The
implant package is irrigated with antibiotic solution before it is opened and
the implant is moved directly to the Keller Funnel. Care should be taken for
orientation of the shaped implant, so the vertical axis is in the desired
position. In some cases, a slight outward rotation of the vertical axis of the
implant is desired for compensation of the shape of the thorax. In other cases,
it is placed in a vertical position or even medialized. The procedure is
finalized by recreating the submammary fold. This is preferably done with a
barbed suture (e.g., Quill no. 0) which is placed exactly at the border of the
implant along the ILP line. A strong grip is taken into the thoracic fascia,
then through the Scarpa fascia along the lower border of the incision, and
then run along the inferior border of the implant. Reaching the end of the
incision, the Scarpa fascia of the upper incision line is brought down to the
thoracic fascia. Following two layers of this closure, the deep dermis is
closed with a running barbed suture (e.g., Monoderm 2-0) in a ridging
fashion to relax the deep dermis (Fig. 103-18). The superficial layer is then
closed with the other end of the barbed suture aiming for a perfect epidermal
repositioning of the epithelium (“PER technique”). The incision is then
closed with dressings, preferably brown Micropore tape or Steri-Strips.
Finally, the patient is put in a good support garment.

FIGURE 103-17 Dual plane IV techniques are useful in patients with severe ptosis or
in tuberous breasts. The subglandular or subfascial dissections in these cases are
more extensive, going well above the nipple areolar complex, and the muscle division
is higher laterally (close to the nipple level). The dissection of the pectoralis muscle is
more parallel to the muscle fibers, but in the midline the nipple-sternum line is still
respected by at least 2 to 3 cm. This creates a true subglandular position of the lower
pole of the implant without attachment to the ribs.
POSTOPERATIVE CONSIDERATIONS
To minimize postoperative discomfort the patients are recommended early
arm activation by placing of the arms on top of the head and carefully stretch
the pectoralis muscle. At the time of dismissal from the clinic, usually 3 to 4
hours postoperatively the patient should be able to stretch their arms straight
above the head. Most patients today express that they experience the pain
similar to that after severe exercise with a similar type of muscle ache, thus a
relatively minor discomfort. The patient is allowed to shower the day after
surgery but without removing the Micropore tape from the wound. This is
removed at the first postoperative visit 6 days after the surgery. It is
extremely important that patients with shaped implants have good support
garment; this is obviously also true for implants with smooth surface or
“nanosurface” technology where bottoming out and lateralization is a higher
risk. The support garment should provide good circumferential support and
the author favors the use of IPOMIA bras being the first lingerie brand
specifically constructed for patients with breast implants. Patients should
wear their support bra day and night for at least 3 weeks and then daytime for
3 months. Even if most patients are back to normal daily activities within 24
hours this does not include exercise. Leg exercise such as spinning is allowed
after 3 weeks but bouncing movements such as running should be avoided for
3 months postoperatively. Forever when bouncing and performing exercise
such as horseback riding, running, etc. patients should have very good
support garments. Patients who do not follow these recommendations have
higher risk for rotation and malposition.
FIGURE 103-18 Deep dermal suture relaxation and long postoperative surgical
taping (Micropore) prevents scar widening and counteracts scar hyperactivity. A, B:
The ridge suture is placed deeper at the wound edge and more superficial far away
from the wound edge. C, D: Example of primary healed hypertrophic scar 2 years
after partial mastectomy. Result only 6 months after ridged suturing. Note the small
hypertrophy in the only area of the scar that as a test was injected with
corticosteroids at the time of scar correction.

After final healing approximately 6 months postoperatively the patients are


welcome for an annual follow-up but most important for any woman is self-
examination of her breast. This should include a careful palpation in the
shower at least once per month. Women who learn to know their own breast
in this way usually note any changes earlier than done at follow-ups by
physicians. For women with textured implants it is of great importance to be
informed about the risk albeit low for ALCL and that this usually manifest
itself in a swollen breast. If this should occur, they should come for an
examination including ultrasound.
CONCLUSION
Anatomically shaped breast implants have clear indications and should in
spite of recent concern for ALCL be part of the alternatives for a breast
augmentation or reconstruction. When using anatomically shaped implants it
is necessary to understand how the implant selection process, preoperative
markings, surgical techniques, and postoperative management differ
compared to that in the use of other implants. If all of these steps are done in
a way recommended in this chapter, the outcome is usually very favorable
providing a natural-looking breast. The great variability of different implant
shapes makes customization in relation to the patient’s biologic conditions
and desires better than for other type of implant. Long-term high satisfaction
rate has been observed by the author having used these devices for nearly 25
years.
ADDENDUM FROM JANUARY 2020
Since this book chapter was written there has been some new regulatory
decisions affecting the use of anatomical breast implants. Due to the growth
of ALCL cases and studies showing a link between macrotextured surfaces
and the development of this disease Allergan Co. has made a voluntary
withdrawal of their implants with a BIOCELL® macrotextured surface. This
means that Allergan’s anatomical Style 410 implants are no longer available
on the market in most countries. In several countries also other
macrotextured implants have been banned. Any restriction on the use of
microtextured implants (e.g., Mentor CPG implants) does not exist as the risk
for developing of ALCL appears to be so much lower (1/86,000 vs. 1/3,000).
However, all the descriptions in this chapter on the benefits of anatomical
implants and how to select implants and perform preoperative markings are
valid for other available anatomical implants. It also deserves to be stressed
that the principles of implant selection and preoperative markings as
described in this chapter are equally important and suitable when it comes
to using round and smooth implant.

REFERENCES

1. Hedén P. Section 4, Chapter 96: Breast augmentation with anatomical,


high-cohesive silicone gel implants. In: Spear SL, ed. Surgery of The
Breast—Principles and Art. Vol. 2. Philadelphia, PA: Wolters
Kluwer/Lippincott Williams & Wilkins; 2006:1344–1366.
2. Hedén P. Breast augmentation with anatomic, high-cohesiveness
silicone gel implants (European experience). In: Spear SL, ed. Surgery
of the Breast: Principles and Art. 3rd ed. Philadelphia, PA: Wolters
Kluwer/Lippincott Williams & Wilkins; 2011:1322–1345.
3. Hedén P. Chapter 24: Form stable shaped high cohesive gel implants. In:
Elizabeth J. Hall-Findlay, Gregory RD, eds. Aesthetic and
Reconstructive Surgery of the Breast. UK: Saunders Elsevier; 2010:357–
386.
4. Hakelius L, Ohlsen L. A clinical comparison of the tendency to capsular
contracture between smooth and textured gel-filled silicone mammary
implants. Plast Reconstr Surg 1992;90(2):247–254.
5. Al-Ajam Y, Marsh DJ, Mohan AT, et al. Assessing the augmented
breast: a blinded study comparing round and anatomical form-stable
implants. Aesthet Surg J 2015;35:273–278.
6. Hidalgo DA, Weinstein AL. Intraoperative comparison of anatomical
versus round implants in breast augmentation: a randomized controlled
trial. Plast Reconstr Surg 2017;139:587–596.
7. Rubi CG, Lozano JA, Pérez-Espadero A, et al. Comparing round and
anatomically shaped implants in augmentation mammaplasty: the
experts’ ability to differentiate the type of implant. Plast Reconstr Surg
2017;139:60–64.
8. Arvind M, See M, Farhadi J. Can you tell the difference: Round vs
anatomical implants—A real-time global ballot. J Plast Reconstr Aesthet
Surg 2018;71:770–771.
9. Mallucci P, Branford OA. Concepts in aesthetic breast dimensions:
analysis of the ideal breast. J Plast Reconstr Aesthet Surg 2012;65:8–16.
10. Hedén P, Montemurro P, Adams WP Jr, et al. Anatomical and round
breast implants: how to select and indications for use. Plast Reconstr
Surg 2015;136:263–272.
11. Spear SL, Murphy DK; Allergan Silicone Breast Implant U.S. Core
Clinical Study Group. Natrelle round silicone breast implants: core
study results at 10 years. Plast Reconstr Surg 2014;133:1354–1361.
12. Maxwell GP, Van Natta BW, Bengtson BP, et al. Ten-year results from
the Natrelle 410 anatomical form-stable silicone breast implant core
study. Aesthet Surg J 2015;35:145–155.
13. Hammond DC, Canady JW, Love TR, et al. Mentor contour profile gel
implants: clinical outcomes at 10 years. Plast Reconstr Surg
2017;140:1142–1150.
14. Caplin DA. Indications for the use of Memory Shape breast implants in
aesthetic and reconstructive breast surgery: long-term clinical outcomes
of shaped versus round silicone breast implants. Plast Reconstr Surg
2014;134(3 Suppl):27S–37S.
15. Lista F, Tutino R, Khan A, et al. Subglandular breast augmentation with
textured, anatomic, cohesive silicone implants: a review of 440
consecutive patients. Plast Reconstr Surg 2013;132:295–303.
16. Hall-Findlay EJ. Breast implant complication review: double capsules
and late seromas. Plast Reconstr Surg 2011;127:56–66.
17. Spear SL, Rottman SJ, Glicksman C, et al. Late seromas after breast
implants: theory and practice. Plast Reconstr Surg 2012;130:423–435.
18. Hu H, Johani K, Almatroudi A, et al. Bacterial biofilm infection
detected in breast implant-associated anaplastic large-cell lymphoma.
Plast Reconstr Surg 2016;137:1659–1669.
19. Brody GS, Deapen D, Taylor CR, et al. Anaplastic large cell lymphoma
occurring in women with breast implants: analysis of 173 cases. Plast
Reconstr Surg 2015;135:695–705.
20. Loch-Wilkinson A, Beath KJ, Knight RJW, et al. Breast implant-
associated anaplastic large cell lymphoma in Australia and New
Zealand: high-surface-area textured implants are associated with
increased risk. Plast Reconstr Surg 2017;140:645–654.
21. Adams WP Jr, Culbertson EJ, Deva AK, et al. Macrotextured breast
implants with defined steps to minimize bacterial contamination around
the device: experience in 42,000 implants. Plast Reconstr Surg
2017;140:427–431.
22. Hedén P, Jernbeck J, Hober M. Breast augmentation with anatomical
cohesive gel implants: the world’s largest current experience. Clin Plast
Surg 2001;28(3):531–552.
23. Donfrancesco A, Montemurro P, Hedén P. Three-dimensional simulated
images in breast augmentation surgery: an investigation of patients’
satisfaction and the correlation between prediction and actual outcome.
Plast Reconstr Surg 2013;132(4):810–822.
24. Hedén P. Invited discussion on: tissue-based implant selection and
preoperative markings with the AK or Q2 method. Aesth Plast Surg
2020;44(1):24–27.
CHAPTER 104

Light-Weight Implants in Breast


Augmentation
MICHAEL SCHEFLAN | OREL GOVRIN-YEHUDAIN | DAEL GOVREEN-SEGAL | JACKY
GOVRIN-YEHUDAIN
HISTORY
Since the introduction of silicone gel–filled breast implants by Cronin and
Gerow into the United States in 1962, breast augmentation and reconstruction
mammaplasty have gained increasing popularity (1). Statistics compiled by
the American Society for Aesthetic Plastic Surgery have shown that the
number of breast augmentations, at 329,914 in 2018, has been increasing
each year in the last decade, with a 15.2% increase between 2014 and 2018
(2), and is now ranked as the most common surgical aesthetic procedure for
women in the United States (1,2). Also on the rise, is the number of patients
undergoing immediate, implant-based breast reconstruction following
mastectomy, with a dramatic increase in the United States from 27% in 2005
to 43% in 2014 (3,4). However, despite the widespread popularity, and well-
established safety profile of procedures involving breast implants (5,6) they
may be associated with a variety of postoperative complications and carry a
high incidence of revisionary surgeries. While there have been improvements
in surgical techniques, shells, and surfaces, and some properties of the fillers
—all implants available, since the introduction of the first silicone-filled
breast implant, have been of roughly the same density—1 mL of volume
equates to 1 g of weight (7–10). The recognition that a lighter-weight breast
implant would be advantageous for improved long-term outcomes for breast
augmentation and breast reconstruction patients fueled the reevaluation of
current thinking, namely, to uncouple weight from volume in order to
overcome the weight-dependent impact of mechanical forces on breast
tissues. Thus, the expected outcome of the light-weight breast implant
(LWBI) was to create the desired aesthetic results, while reducing the impact
of persistent and implant weight–induced complications associated with these
procedures (9,10).
WEIGHT AS A CENTRAL FORCE ACTING ON THE BREAST
The breast is an unstable and dynamic organ, composed of skin, fat, and
glandular tissues, influenced by endogenous and exogenous factors such as
gravity, age, hormonal status, and body mass index. Over the course of a
woman’s lifetime, through the different stages of puberty, pregnancy,
lactation, and menopause, the breasts change in size and shape. Over time,
the breast tissue becomes atrophic and the skin becomes thinner and its
elasticity reduced.
In an effort to comply with clinical limitations and satisfy patient demands
for increased volume, Tebbetts argued that size is one of the most critical
characteristics to be assessed when selecting a breast implant (11). Maxwell
et al. reported long-term and often permanent tissue deformities resulting
from breast augmentation, with adverse events including tissue atrophy,
accelerated ptosis, sensory loss, and inframammary fold migration (12).
Vegas and Martin del Yerro postulated that all these effects are directly
related to the biomechanical (viscoelastic) properties of soft tissues and their
response to loading and compressive forces. Moreover, secondary mastopexy
and related complications of revisional surgery chiefly stem from the
augmentation-induced modifications of the breast tissue (7).
Our extensive clinical experience, together with consideration of the
weight-dependent adverse effects, fundamental laws of physics, and
viscoelastic properties of soft tissues, led us to formulate the scientific
precept that it was the implant weight, rather than its volume, that stood
at the basis of breast tissue compromise and deformation (9).
HEAVIER BREASTS SAG MORE
The weight-dependent effects on the soft tissues of the breast are
demonstrated in Figure 104-1. We can see that when there are natural breast
asymmetries, the larger breast always sags more. Intuitively, we attribute the
sagging to the breast’s size, while in reality the underlying reason is the
breast’s weight.
WEIGHT IS THE DOWNWARD FORCE IN THE PRESENCE OF GRAVITY
In his second law of mechanics, Sir Isaac Newton described one of the most
fundamental laws of physics: F = ma (where F is the force, m is the mass,
and a is the acceleration). When the constant acceleration force is due to
gravity, Newton’s second law becomes F = mg (where g is gravity).
Consistent with the above equation, the formula expresses quite simply that
the force (weight) acting downward on an object is only dependent on the
mass of the object and the effect of gravity. As we can see, volume is not a
factor in this formula (9). Rather, we should remember that weight is the
force by which a body is pulled downward by gravity. In fact, a large portion
of our work as plastic surgeons is to repair the undesirable effects of gravity
that worsen over time.

FIGURE 104- Natural breast asymmetries prior to surgical intervention.


Asymmetries in natural breasts presurgery. The heavier breast sags more. (Images
courtesy of Dr. Jacky Govrin.)
THE FORCE EXERTED ON BREAST TISSUE IS IN DIRECT PROPORTION TO
WEIGHT
A spring-mass model provides a simple but effective approximation of elastic
systems, such as breast tissue. According to Hooke Law, we can see that the
degree of tissue stretching will be proportional to breast + implant mass
and inversely proportional to its stiffness (inelasticity). In a static, upright
posture, the weight of an implant will displace the breast downward with a
force proportional to the weight of the implant. The tissue’s stretch is linear
(within the elasticity limits of the tissue), and therefore, tissue displacement
will increase in direct correlation to the implant weight. The greater the
weight, the greater is the displacement. A heavier implant will therefore
result in increased forces and consequential stretch of the breast, as compared
with a lighter implant (Fig. 104-2) (9).
MOVEMENT AMPLITUDE IS IN DIRECT PROPORTION TO WEIGHT
When maintaining an upright, static posture, the pull of gravity on the breast
is constant and unidirectional. In dynamic states such as walking, descending
stairs, dancing, or running, accelerative forces result in significant breast
movement and tissue impact. According to Scurr et al., in breast kinematic
measurements made on a treadmill, the amplitude of breast movement is
multidirectional and in direct proportion to weight and not related to
volume (13).

FIGURE 104-2 Hooke law and breast tissue responses. The elastic tissue of the
breast is symbolized by a spring with constant k. The displacement is described as
ΔX = F/k, where ΔX is the displacement, F is the force applied, and k is the spring
constant (tissue stiffness). A heavier implant will result in increased forces and
consequential stretch of the breast, as compared with a lighter implant. Therefore, m
< M resulting in F1 < F2 and ΔX1 < ΔX2. (Reproduced with permission from G&G
Biotechnology Ltd. Haifa, Israel.)
BREAST REDUCTION
Macromastia’s secondary health problems (contact dermatitis, impaired
breathing, shoulder indentation, chronic back or neck pain, and ulnar
paresthesia), can be also effectively alleviated by resecting breast tissue
weighing 256 g or more (14,15). This is one clinical example that
demonstrates that even a small reduction in breast weight can adequately
reduce gravitational forces on the tissue, diminishing their long-term
detrimental effects and associated symptoms.
THE BREAST’S VISCOELASTIC RESPONSE
Following breast augmentation, both volume and weight are intertwined to
act on the soft tissues and create strain. This sudden increase in strain initially
triggers a stress–relaxation response where the breast tissues gradually
undergo relaxation and expand. As a result, the effect of the volume of the
implant gradually diminishes over time (Fig. 104-3A). In contrast, the effect
of weight of the implant results in a permanent and longstanding stress; it
does not diminish over time but rather persists throughout a woman’s lifetime
causing a continuous creep deformation (Fig. 104-3B) (7).
In fact, from now on, the weight of the implant should be considered the
dominant mechanical factor, affecting the breast tissue.
The persistent and constant stress induced by the implant weight creates
strain on the soft tissues of the breast, ultimately producing tissue atrophy,
accelerated ptosis, and inframammary fold breakdown as well as breast
deformity. The breast lacks a significant weight support mechanism.
Selecting implants with weights that challenge the elastic capacity of the
breast tissue, bears the risk of aggravation of all the aforementioned adverse
events, which may ultimately become irreversible. Consequently, contrary to
long-standing precepts that are largely based on the equivalence of the weight
and volume of traditional silicone and saline breast implants, the breast
implant’s weight, rather than its volume, is the critical variable affecting
breast augmentation outcomes (9).

FIGURE 104-3 Breast tissue stress–strain curves. A: Tissue stress in response to


implant volume is transient (weeks). When a breast (material) is loaded with an
implant (stress), it undergoes instant deformation by becoming an augmented breast.
Through the stress–relaxation response, the temporary stress resolves over time. B:
Tissue stress in response to implant weight is ongoing and permanent (years). The
continuous, time-dependent strain under a constant load is termed “creep.” Creep
deformation accumulates as a result of long-term stress induced by the persistent
presence of force (weight).
LONG-TERM ADVERSE EFFECTS ASSOCIATED WITH HIGHER IMPLANT
WEIGHT
Long-term stability of the augmented breast is directly correlated to the breast
tissues’ response to the weight of the implant. Therefore, to enhance the
safety of breast augmentation procedures and the duration of their outcomes,
presurgical planning must simultaneously address the characteristics of
supporting tissue and breast implant weight (9,10). This is because these two
factors contribute to many of the postoperative complications and side effects
in procedures involving breast implants (5,8,10,16).
TECHNOLOGIC INNOVATION AND PRECLINICAL DEVELOPMENT
The recognition of breast implant weight as a critical determinant of long-
term clinical outcomes, prompted the development of the first LWBI, B-
Lite® (G&G Biotechnology Ltd., Haifa, Israel & Polytech Health &
Aesthetics GmbH, Dieburg, Germany), which was able to uncouple weight
and volume for the first time (10). This sixth-generation, form-stable, silicone
gel LWBI was designed to be a light-weight alternative to traditional silicone
breast implants. The LWBI’s allows a reduction in implant weight of up to
30%, while maintaining the equivalent size, form, and function of traditional
breast implants. The addition of this light-weight implant to available implant
choices is expected to enable the surgeon to achieve the patient’s desired
breast size and shape without jeopardizing long-term tissue stability or
integrity induced by additional weight. Such avoidance of tissue compromise
and reoperation is projected to further improve both patient satisfaction and
long-term outcomes (9). The form-stable round or anatomical implant (Fig.
104-4) contains a continuous phase, reinforced, medical-grade silicone gel
filler enriched with inert, ultra–high-purity, hollow, borosilicate microspheres
chemically bound to, and encapsulated by, the gel network.
Microsphere spatial positioning in the LWBI is fixed by means of a
proprietary curing process. Furthermore, the microspheres are surface treated
to ensure that they remain affixed within the silicone gel. The resulting high-
strength bond between the microspheres and the gel is calculated to exceed
that of the cohesion forces within the gel, effectively creating gel-covered
microspheres and obviating the risk of both free microspheres migrating
and/or separating from the gel. In the unlikely event of shell degradation or
rupture, the gel–microsphere bond remains stable, without exposing bare
microspheres to the surrounding tissues. Taken together, the unbreakable
nature of the gel, the microspheres, and the microsphere–gel interactions
result in an implant with a marked mechanical gel strength with good
maintenance of the form and structure of the implant (Fig. 104-5). The light-
weight implants have an optimal fill and are form stable (9).
FIGURE 104-4 B-Lite® round and anatomical light-weight breast implants (LWBIs).
(Reproduced with permission from G&G Biotechnology Ltd. Haifa, Israel.)

The microspheres of the LWBI are size selected to achieve the desired
spatial distribution and concentration. The strictly enforced particle size
limitation (>30 μm) prevents leakage and migration through the intact shell.
Likewise, in the unlikely event of the implant’s rupture and direct contact of
its contents with the surrounding tissues, the microspheres are too large to
undergo phagocytosis or drainage through the lymphatic system and would,
at most, only elicit a local foreign body reaction as does regular silicone gel
(9). Borosilicate microspheres exhibit superior biologic, mechanical, and
chemical properties, such as crush resistance, biocompatibility, inertness, and
chemical resistance, making them a preferred biomaterial for implantable
devices. It is for this reason that borosilicate microspheres were selected as an
integral weight reduction component of the LWBI. Simultaneously, their
presence reduces the volume of gel required to fill the implant, further
lowering its silicone content. The gel is confined within a standard silicone
elastomer shell with an internal barrier layer, which is sealed with a patch
composed of the same silicone elastomer and barrier layer. The shell has been
in clinical use for years as part of an array of commercially available full-
mass implants that have been implanted safely in hundreds of thousands of
women. Both smooth and microtextured LWBIs are available and in clinical
use since 2013, and their long-term safety has been established. The
implant’s final shape is dictated by the outer shell, with anatomical and round
implants available in both smooth and textured forms (9).

FIGURE 104-5 Microsphere-enhanced silicone gel. Integration of silicone gel cross-


linked to borosilicate microspheres yields a reinforced gel. The magnified segment
shows the high cross-linking density at the surface of the microspheres, resulting in a
microsphere–gel adhesion strength exceeding the gel’s internal strength of cohesion.
Even in the unlikely event of rupture, microspheres will remain bound within the gel
and will not disperse. (Reproduced with permission from G&G Biotechnology Ltd.
Haifa, Israel.)

Extensive preclinical testing has been carried out on the LWBI by


independent test laboratories under good laboratory practice (GLP)
conditions and simulating worst case scenarios. Tests demonstrated that the
cohesion of the silicone gel filler is up to standard, as is the implant’s
resistance to fatigue, impact, and static rupture.
Following simulated gel exposure to bodily fluids, by means of submersing
the LWBI implant gel segments in saline and fetal bovine serum (FBS) for an
extended period of time, under repetitive mechanical manipulation, no visible
separation, swelling, or deterioration of the gel and no microsphere “escape”
was observed.
Crush strength tests demonstrated that the borosilicate microspheres in this
implant can withstand pressures of over 200 psi (>13 atm), far beyond the
pressure ranges women are exposed to following implantation, including
during flight and recreational diving. The light-weight implants are CE
approved (9). Experience gathered since 2013 reports a capsular contracture
incidence of less than 1% at 5 years. There have been no reports of LWBI
ruptures and no cases of breast implant–associated anaplastic large cell
lymphoma (BIA-ALCL).
INDICATIONS
The LWBI is indicated for:

Primary and revision breast augmentation (with or without mastopexy)


Primary and revision breast reconstruction following mastectomy
CONTRAINDICATIONS AND PRECAUTIONS
While there are no clear contraindications for light-weight implants it is
sometimes useful to have a full-weight implant settle in the breast’s lower
pole, specifically in situations of tight and constricted lower pole (tubular
breasts), and in some patients following skin-sparing mastectomies. In these
patients, the tight and narrow lower pole may prevent a light-weight implant
from properly settling down.
PREOPERATIVE PLANNING
All the preoperative considerations, patient factors, preoperative markings,
surgical technique, and implant selection process, are the same as when using
full-mass silicone implants.
INTRAOPERATIVE AND POSTOPERATIVE CARE
The LWBI is placed at the discretion of the surgeon into the partial
submuscular or subglandular planes using standard surgical techniques (9).
The implant is selected based on breast width, leaving a 1- to 2-cm soft tissue
rim on each side. Incision lengths and placement for the LWBI are
comparable to those applied for traditional form-stable silicone implants.
Women implanted with the LWBI have consistently reported less pain and
shorter recovery periods as compared to those undergoing augmentation with
a full-mass implant. This is regardless of implant volumes, and occasionally
larger incision and plane of insertion (17). Subsequent operative data from a
larger patient base is following similar trends.
Reduced postoperative pain may be explained by significantly reduced
pressure on the tissues. A 200-cc light-weight implant exerts approximately
the same pressure on the lower pole soft tissues as a 100-cc full-mass implant
(18).
OPERATIVE TECHNIQUE
The light-weight implant has been utilized in standard augmentation with or
without mastopexy, as well as in breast reconstruction following
mastectomy/lumpectomy, either as a direct-to-implant procedure or as a two-
stage reconstruction procedure. There is no difference in the surgical
technique with these implants.

FIGURE 104-6 Less pain and faster recovery in patients undergoing primary breast
augmentation with LWBI. First published in Govrin-Yehudain et al., Postsurgical
recovery indicators in patients undergoing primary breast augmentation with LWBI
or traditional implants. (Govrin-Yehudain O, Matanis Y, Govrin-Yehudain J. Reduced
pain and accelerated recovery following primary breast augmentation with lightweight
breast implants. Aesthet Surg J 2018;382(10):1092–1096.)
CLINICAL REPORTS

Clinical Survey Report (November 2017)


A clinical survey report of 790 procedures including a total of 1,580 light-
weight implants with a mean follow-up of 15 months (1 to 44 months),
demonstrated favorable satisfaction rates and acceptable overall safety.
Adverse event rates were similar to or lower than other breast implants. No
ruptures were reported by any of the six reporting surgeons. Twenty-one
reoperations (2.6%) were reported while only five of them (0.6%) could be
considered device related. The operating surgeons were very satisfied with
the LWBI (with a mean rating of 4.86 out of 5), as was their estimate of
patient satisfaction (4.85 out of 5). The high patient and surgeon satisfaction
were reported specifically with regard to the parameter of a natural look and
feel; one of the primary concerns of patients. Additionally, in a blinded test
led by the senior author (MS), three surgeons examined 30 patients (15 with
the LWBI and 15 with traditional implants) and were unable to differentiate
between implants based on their look and feel.
Retrospective Study (2018)
A retrospective observational single-center study was conducted comparing
postsurgical pain levels, recovery times, and satisfaction with the healing
process reported by 50 patients undergoing implantation of the LWBI versus
50 patients undergoing implantation of full-mass silicone breast implants
(19). Patients who received the light-weight implants consistently reported
lower pain levels, took less pain medication, and resumed their normal
routine faster as compared to those undergoing augmentation with a full-mass
implant (Fig. 104-6) (19).
Such postsurgical experiences of less pain and shorter recovery time have
been consistently linked to higher patient satisfaction. These findings of
minimized pain, may present considerable clinical advantages, in addition to
the long-term physiologic benefits of the light-weight implant (19).

CASES
Clinical outcomes with the LWBI are shown in a range of primary
augmentation procedures (Figs. 104-7 to 104-10), as well as breast
reconstruction (Fig. 104-11) and mastoplasty following massive weight
loss (MWL) (Fig. 104-12).

FIGURE 104-7 A 33-year-old woman before breast augmentation (top row),


5 years after augmentation with round, 325-cc bilateral B-Lite, subglandular
(bottom row). (Images courtesy of Dr Jacky Govrin.)

FIGURE 104-8 A 51-year-old woman before breast augmentation (top row),


5 and half years after augmentation with round, 440-cc bilateral B-Lite,
subglandular (bottom row). (Images courtesy of Dr. Jacky Govrin.)
FIGURE 104-9 A 23-year-old woman before breast augmentation (top row),
19 months after round, 460-cc right LWBI and 390-cc left B-Lite
subglandular and scar-less mastopexy technique left breast only (bottom
row). (Images courtesy of Dr. Jacky Govrin.)

FIGURE 104-10 A 25-year-old woman before breast augmentation (top row)


5 years after augmentation with round, 390-cc bilateral B-Lite, subglandular,
and right scar-less mastopexy technique (bottom row). (Images courtesy of
Dr Jacky Govrin.)
FIGURE 104-11 A-43 year-old woman (A, B) after bilateral prepectoral
direct-to-implant (DTI) reconstruction with B-Lite and TIGR® mesh (C, D).
After 3D tattoo (E). (Images courtesy of Dr. Stefano Pompei.)
FIGURE 104-12 A 49-year-old woman post obesity (-70 kg) (A). Six weeks
after mastoplasty with B-Lite (B–D). After 22 months (E–G). (Images
courtesy of Dr. Stefano Pompei.)
ADDITIONAL PRELIMINARY BENEFITS OF THE LWBI
Preliminary experience has shown that the LWBI has the following
additional benefits: (1) less gel bleed; (2) better performance in breast
imaging; and (3) improved breast kinetics.
Less Gel Bleed Versus Traditional Implants
Gel bleed is one of the most prevalent issues associated with breast
reconstruction and augmentation procedures (20). Diagnosis of gel bleed
poses a challenge as gel bleed can generally not be detected clinically. Gel
bleed presents in ultrasound imaging as a snow storm in axillary lymph nodes
and is considered to be one factor leading to capsule contracture, or clinically
palpable siliconomas (20–22). Gel bleed may not always be diagnosed on
mammography, ultrasound, or magnetic resonance imaging (MRI) (22).
Throughout the 1990s, both the structure of the shell and the cohesiveness of
the gel were altered in an attempt to create form-stable implants with a
reduced likelihood of gel bleed, capsular contracture, or implant rupture (21).
In addition, most implant designs incorporated barrier layers to slow down
the diffusion rate of low–molecular-weight liquid silicone across the
elastomer shell. These improvements have indeed reduced the incidence of
gel bleed (21). In the case of the LWBI, the microspheres displace a
significant part of the silicone gel and therefore reduce the overall amount of
silicone in the implant (9). Thus, the LWBI has the unique combination of a
barrier layer and a microsphere dense cross-linked silicone gel which reduces
the amount of potential bleed through an intact shell. Following the unlikely
event of a breast implant rupture, both the dryness of the light-weight implant
and the reduced diffusion gradient caused by the microsphere-enhanced
cohesive gel, can avert gel diffusion into the tissues. In order to examine the
resilience of the LWBI, internal research was conducted and published here
for the first time, to measure the rate of silicone moieties leaching out from
the network (with or without the presence of microspheres) under worst-case
scenario conditions. Approximately 0.5-cc chunks of gel were cut and placed
on dry absorption wipes for about 3 months. Plain and a light-weight gel
were tested. The area of each wet spot was recorded after 38, 55.5, 124, 418,
809, and 1,987 hours. The findings showed that the LWBIs demonstrated less
gel bleed when placed on absorbent paper, after as little as 5 days, and
produced a drier gel to the touch (Fig. 104-13) (18). Furthermore, the
traditional silicone gel in this experiment showed greatly increased (147%)
release of oil as compared to the drier light-weight microsphere-enhanced gel
(Fig. 104-14) (18).
While this data is preliminary, it provides reassurance to surgeons and
patients that the unique microsphere-enhanced gel in the light-weight
implants does seem to reduce gel bleed. Any such gel bleed into
extracapsular tissues can induce local inflammatory responses as well as risk
of dissemination through the lymphatic system, as has been reported with
other implants (23,24). The biologically inert microspheres contained in the
LWBI are unlikely to induce an inflammatory response, while the strictly
enforced particle size limitation (>30 μm) renders them too large to enter the
lymphatic system, thus preventing their dissemination elsewhere in the body
(9).
FIGURE 104-13 Samples of traditional silicone gel and LWBI microsphere-
enhanced gel on absorbent paper. Note the greatly increased oil spot under the
silicone-only specimen after as little as 5 days and the much drier gel of the LWBI.
(Reproduced with permission from G&G Biotechnology Ltd. Haifa, Israel.)
FIGURE 104-14 Oil release over time from LWBI gel as compared to traditional
silicone gel. The rate of solvent leach out of a gel containing microspheres is lower
than a gel not containing microspheres. This may indicate that an implant that
contains gel with microspheres will have reduced bleeding out of gel.

Better Performance in Breast Imaging


Diagnostic imaging such as ultrasonography, mammography, and MRI
imaging are used to evaluate implant integrity, detect abnormalities of the
implant and its surrounding capsule, and, of course, detect breast pathology
unrelated to implants. The presence of the implant may impair the
effectiveness of mammography or ultrasound imaging for breast cancer
detection (25). The inherent material composition of the light-weight implant
gel has been shown to improve breast imaging characteristics such as
radiolucency and decrease associated visual noise in ultrasound images (18).

LWBI and MRI


LWBI are MRI safe and compatible, having no ferromagnetic or conductive
components and showing no interference when compared to full-mass
implants (9).

LWBI and Ultrasonography


Ultrasonic breast imaging showed a higher definition of the shell with fewer
artefacts in the LWBI cohort (Fig. 104-15) (18).

LWBI and Mammography


On mammography, silicone implants are seen as opaque, oval masses so that
a separate envelope or accompanying folds are not visualized (24). An
additional concern, for patients and physicians alike, is the fact that silicone
implants, may interfere with the sensitivity of imaging, so specialized
“Eklund” views are required (24). The LWBI shows increased translucency
under mammography versus traditional implants (Fig. 104-16) (18).
The LWBI is more radiolucent than a pure silicone gel implant when
viewed in a mammogram. This improves the visibility of tissue in front of or
behind the implant, thus potentially increasing diagnostic capability. A pilot
study showed microcalcifications in patients diagnosed with breast cancer,
visible behind a LWBI and completely obscured underneath a regular
silicone implant (Fig. 104-17) (18).
Favorable Breast Kinetics
A lower-mass implant may impact breast kinetics by decreasing the
acceleration of the breast during dynamic activity, and subsequently the stress
exerted on the breast structures, implant, and implant capsule (26). A recent
preliminary study conducted in four patients (two with the LWBI and two
natural breasted), is the first to describe the dynamic behavior of implanted
breasts. The one heavier natural breasted participant consistently displayed
the greatest undulations for all nipple kinematics, in all directions, while the
opposite was true for the subglandular LWBI participant. The data suggests
that a reduced mass implant stabilizes the breast, thereby decreasing the
biomechanical load on the breast. The reductions in breast acceleration
identified during dynamic activity, coupled with a reduction in breast mass,
could result in biomechanical benefits. Such benefits may include reduced
ptosis over time and increased longevity of the desired outcomes. More
research is needed on the behavior of implanted breasts during dynamic
activity, as well as on comparing the biomechanical effects of the LWBI
versus traditional full-mass implants in the pre- and postimplant setting (26).

FIGURE 104-15 Ultrasound reverberations with traditional silicone implants versus


LWBIs. A: The ultrasound of the breast with the LWBI implant shows very little
visual noise or artefacts. The tissue, shell, and implant material are clear. B: The
ultrasound of the breast with the traditional silicone implant shows reverberations
seen as visual noise caused by the implant. This noise is seen extending significantly
into the area of the image expected to be anechoic. The noise also extends above the
shell creating a cloud-like snow over the tissue area of the image which is intended
for diagnosis. (Reproduced with permission from G&G Biotechnology Ltd. Haifa, Israel.)

FIGURE 104-16 Mammographic imaging with the LWBI versus a traditional


silicone implant A: The mammogram of the breast with the LWBI shows the implant
is relatively translucent. Breast tissue not obscured by the implant is visible in the
mammogram. B: The traditional silicone implant appears completely white (opaque
to x-ray) showing no detail of the tissue in front of it or behind it. Breast tissue not
obscured by the implant is visible in the mammogram. (Reproduced with permission
from G&G Biotechnology Ltd. Haifa, Israel.)

FIGURE 104-17 Mammogram views of breast cancer specimen presenting with


calcifications behind LWBI versus a traditional silicone implant. A: The test setup is
a lumpectomy breast cancer specimen on top of an implant. B: The barely
perceptible breast cancer specimen is seen behind a traditional silicone implant with
only the silhouette of the guide wires visible. C: Detailed information including
microcalcifications, indicated by red circles, can be clearly seen behind a LWBI. D:
Detailed information including microcalcifications, indicated by red circles, can be
seen with the enlarged negative image of the breast specimen behind a LWBI. The
LWBI is more radiolucent than a pure silicone gel implant when viewed in a
mammogram. This improves the visibility of tissue in front of or behind the implant,
thus potentially increasing diagnostic capability. (Reproduced with permission from
G&G Biotechnology Ltd. Haifa, Israel.)
CONCLUSION
The novel sixth-generation LWBI was developed to reduce the mechanical
stress and strain applied by the added weight, in combination with
gravitational and accelerative forces, on the natural soft tissue of the breast.
The unique implant design allows for a reduction in implant weight of up to
30% while maintaining the size, form, and function of traditional implants.
The reduced weight conserves tissue stability and longevity of results over
time by reducing the inherent stresses and strains imposed by standard
implants. Women with LWBIs report significantly less pain following
surgery than women with traditional silicone implants. Furthermore,
preliminary studies have suggested that women with LWBIs have a natural
look and feel that is no different than with standard silicone gel implants. The
safety profile of the light-weight implants to date has been reassuring with no
reports to date of rupture or BIA-ALCL. Nevertheless, these important
benefits require further rigorous investigation. The light-weight implants are
a class III device under European regulations, have surpassed all preclinical
safety tests, and are CE certified. Implantation of the LWBI holds promise to
reduce some of the side effects of silicone breast implants on breast tissues.
This in return may decrease the need for secondary surgeries and further
improve patient safety and satisfaction, both in primary and revision
augmentation, as well as in primary and revision breast reconstruction. Using
a market-leading shell manufactured in Germany (Polytech Health and
Aesthetics GmbH) with its long-term excellent safety record, together with a
robust microsphere-enhanced cohesive implant grade silicone gel, provides
strength and reduced risk of gel bleed while imparting a natural and
comfortable feel. As shown by initial reports, both patients and surgeons have
been highly satisfied with these new implants, and they can be implanted
effectively using standard-of-care procedures. Finally, improved visualization
of breast tissue during imaging means that the LWBI is likely to reduce
masking of any underlying pathology or implant rupture, and increase
diagnostic capability in ultrasound and mammographic imaging. The LWBI
is thus a new and innovative advance in breast implant technology with many
additional favorable advantages in breast augmentation and reconstruction.
REFERENCES

1. ISAPS International Study on Aesthetic/Cosmetic Procedures Performed


in 2017. Available online at https://www.isaps.org/medical-
professionals/isaps-global-statistics/. Last Accessed May 2, 2019.
2. Aesthetic Surgery National Data Bank Statistics. Available online at
https://www.surgery.org/sites/default/files/ASAPS-Stats2018_0.pdf.
Last Accessed June 20, 2019.
3. Ilonzo N, Tsang A, Tsantes S, et al. Breast reconstruction after
mastectomy: a ten-year analysis of trends and immediate postoperative
outcomes. Breast 2017;32:7–12.
4. Chang JM, Kosiorek HE, Dueck AC, et al. Trends in mastectomy and
reconstruction for breast cancer; a twelve year experience from a tertiary
care center. Am J Surg 2016;212(6):1201–1210.
5. El-Haddad R, Lafarge-Claoue B, Garabedian C, et al. A 10-year
prospective study of implant-based breast augmentation and
reconstruction. Eplasty 2018;18:e7.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5807774/pdf/eplasty18e07.pdf
Accessed June 10, 2019.
6. U.S. Food & Drug Administration. Update on the Safety of Silicone
Gel-Filled Breast Implants (2011)—Executive Summary. Available
online at
https://www.fda.gov/MedicalDevices/ProductsandMedicalProcedures/ImplantsandPr
Last Accessed May 2, 2019.
7. Vegas MR, Martin del Yerro JL. Stiffness, compliance, resilience, and
creep deformation: understanding implant-soft tissue dynamics in the
augmented breast: fundamentals based on materials science. Aesthetic
Plast Surg 2013;37(5):922–930.
8. Tebbetts JB, Teitelbaum S. High- and extra-high-projection breast
implants: potential consequences for patients. Plast Reconstr Surg
2010;126:2150–2159.
9. Govrin-Yehudain J, Dvir H, Preise D, et al. Lightweight breast implants:
a novel solution for breast augmentation and reconstruction
mammaplasty. Aesthet Surg J 2015;35(8):965–971.
10. Govrin-Yehudain O, Ascherman JA. Breast implant weight vs volume:
reappraising breast implant compatibility with tissue characteristics.
Plast Reconstr Surg 2019;143(4):901e–902e.
11. Tebbetts JB, Adams WP. Five critical decisions in breast augmentation
using five measurements in 5 minutes: the high five decision support
process. Plast Reconstr Surg 2005;116:2005–2016.
12. Maxwell GP, Van Natta BW, Murphy DK, et al. Natrelle style 410
form-stable silicone breast implants: core study results at 6 years.
Aesthet Surg J 2012;32(6):709–717.
13. Scurr JC, White JL, Hedger W. Supported and unsupported breast
displacement in three dimensions across treadmill activity levels. J
Sports Sci 2011;291:55–61.
14. Chadbourne EB, Zhang S, Gordon MJ, et al. Clinical outcomes in
reduction mammaplasty: a systematic review and meta-analysis of
published studies. Mayo Clin Proc 2001;765:503–510.
15. Thoma A, Sprague S, Veltri K, et al. A prospective study of patients
undergoing breast reduction surgery: health-related quality of life and
clinical outcomes. Plast Reconstr Surg 2007;1201:13–26.
16. Handel N. Secondary mastopexy in the augmented patient: a recipe for
disaster. Plast Reconstr Surg 2006;118(7 Suppl):152S–163S; discussion
164S–165S, 166S–167S.
17. Govrin-Yehudain O, Govrin-Yehudain J. Scarless mastopexy with
lightweight breast implants. Int J Surg Proced 2018;1(2):107.
18. G&G Biotechnology Ltd. Data on file. 3524 Patent Document.
19. Govrin-Yehudain O, Matanis Y, Govrin-Yehudain J. Reduced pain and
accelerated recovery following primary breast augmentation with
lightweight breast implants. Aesthet Surg J 2018;38(10):1092–1096.
20. Puskas JE, Luebbers MT. Breast implants: the good, the bad and the
ugly. Can nanotechnology improve implants? Wiley Interdiscip Rev
Nanomed Nanobiotechnol 2012;4(2):153–168.
21. Lee Y, Kim YS, Kim JY. Form-stable highly cohesive gel breast
implants. Arch Aesthet Plast Surg 2013;19(1):1–6.
22. Wiedenhoefer JF, Shahid H, Dronbluth C, et al. MR imaging of breast
implants: useful information for the interpreting radiologist. Applied
Radiol 2015;44(10):18–24.
23. Tikunas T, Howarth S, Godwin Y. Inflammatory changes of the nipple
areolar complex of a patient with PIP breast implants: a possible
immune response to free silicone from gel bleed? J Plast Reconstr
Aesthet Surg 2014;67(3):423–425.
24. Bachour Y, Heinze ZCM, Dormaar TS, et al. Poly implant Prothèse
silicone breast implants: implant dynamics and capsular contracture. Eur
J Plast Surg 2018;41(5):563–570.
25. Shah AT, Jankaharia BB. Imaging of common breast implants and
implant-related complications: a pictorial essay. Indian J Radiol
Imaging 2016;26(2):216–225.
26. Norris M, Jones M, Mills C, et al. The kinematics of breasts implanted
with a reduced mass implant: a preliminary report. Aesthet Surg J
2020;40(5):NP253–NP262.
CHAPTER 105

Polyurethane Implants in Aesthetic


Breast Surgery
STEFANO POMPEI | DORA EVANGELIDOU
HISTORY
Worldwide, silicone and saline-filled breast implants have been used for
breast augmentation and breast reconstruction since 1962. Variations in
silicone gel density, implant shape, and texturization of the surface have been
constantly altered in an attempt to minimize implant complications with the
most frequent being the capsular contracture (CC) and reoperation.
It is widely accepted nowadays, that polyurethane (PU) foam coating
minimizes CC and enhances postoperative stability of the implant within the
pocket. Textured implants were in fact developed with the aim to mimic the
shape of the PU foam and also its benefits in terms of reduction of CC rate,
however they were not able to reach this goal.
PU was not used for the first time in medicine. It has been used for medical
devices such as cardiovascular devices, catheters, and facial skeleton
implants for many decades now. PU-coated implants’ CE mark was
introduced in Europe in 1996 and approved for clinical use in the UK in
2005. Since then, they are widely used worldwide.
PU-coated implants gained ground since CC still remains a common
complication of breast augmentation and reconstruction in silicone shell
implants and this is still the primary reason for reoperation (1–4). Plastic
surgeons are in search of implants that are associated with lower rates of
complications (including CC) and decreased likelihood of revisional surgery.
In a 25-year study of 1,529 patients (3,495 implants), the first-generation of
PU-coated implants were associated with a relatively low risk of CC (3). This
might be attributed to the fact that during the formation of the capsule the PU
breaks down to become part of the forming capsule. The tiny particles of PU
biointegrated in the capsule do not allow the formation of an organized
capsule therefore traditional “one vector” contracture is prevented. Capsular
collagen fibers are arrayed in multiple directions to encapsulate the degraded
PU particles in a very disorganized architecture rendering one direction
tightening and firmness unlikely to occur (5). It is a very common conceptual
mistake to consider the PU-covered implants as macrotextured implants. The
PU foam that covers the implants provides them with a completely different
surface, and the mechanisms related to tissue adhesion as well as to fibrous
capsule formation differ totally from those of textured implants. PU is a
three-dimensional matrix that is incorporated and actually becomes part of
the capsule (6).
In fact, the microscopic presence of biointegrated PU particles is detected
within the capsule as long as 30 years after the implant insertion (1) and that
possibly explains the long-term protection against CC formation when these
types of implants are used.
INDICATIONS
Initially, PU-coated breast implants were used to treat CC. Their use was
recommended mainly in secondary breast surgeries where a more stable
implant was needed to secure a stable implant position in a larger pocket, to
prevent symmastia or lateral displacement and even to secure the viability of
the inframammary fold (IMF) since the multiple operations might
compromise its anatomy. The extra grip and stability this implant exhibits
ensures that there is no rotation of anatomically shaped implants and no
dislocation or displacement after a proper intraoperative placement.
Furthermore, all the effects above are achieved without any time-consuming
surgical technique. Surgical steps like reducing a large pocket or reinforcing
the IMF are seldom avoided when PU implant is used.
Nowadays, these exact characteristics render the PU-coated implant a
primary choice for aesthetic breast surgeries in:

primary breast augmentation


hybrid/composite implant with fat augmentation
secondary breast augmentation
augmentation mastopexy
symmastia correction
bottoming-out correction
pseudoptosis
tubular breast
congenital pathologies, that is, Poland syndrome
capsular contracture treatment
implant rotation correction
implant displacement/dislocation correction

In reconstructive breast surgeries PU-coated implants are indicated: (7)

subpectoral implant reconstruction with or without ADM/mesh (8)


prepectoral implant reconstruction with or without ADM/mesh
direct-to-implant one-stage reconstruction with or without ADM/mesh
second session of staged reconstruction
combined autologous and implant reconstruction
secondary breast reconstruction surgeries
CONTRAINDICATIONS
No absolute contraindication
PREOPERATIVE PLANNING
PU-coated implants are adaptable to every breast surgery and every type of
technique preferred by the surgeon. Preoperative planning of breast
augmentation with PU implants is a very important step ensuring the success
of the surgery (9).
Implant size is selected by the traditional method after taking into
consideration the chest wall width, IMF–nipple distance, sternal notch-to-
nipple distance, and the stretching capacity of the skin envelope. Assessment
of the skin and soft tissue characteristics of the entire envelope will determine
the pocket level, however the traditional upper pole pinch thickness test is
less important when PU implants are to be used. Submuscular plane is
traditionally chosen due to the lower risk of CC than the subglangular plane.
However, the protective characteristic of PU implant, renders this advantage
of the submuscular plane, obsolete. Therefore, when a pinch test is found to
be less than 2 cm hybrid/composite surgery with upper pole and presternal fat
grafting is sufficient enough to avoid involvement of the pectoralis muscle
and all the possible complications (i.e., animation deformity, higher
hematoma rate, etc.) that might arise with this pocket. We consider dual plane
(10) only if the patient is extremely skinny with low fat reserve and
extremely thin skin envelope to prevent more palpable or visible upper
implant edges. In fact, by using the hybrid augmentation with the fat grafting
in the upper and medial pole of the breast, we seldom use dual plane.
Incision location of the incision is selected after taking into consideration
patient’s preference and the need or not of periareolar nipple areolar complex
(NAC) modifications size and location and the need of mastopexy or not. The
authors’ preference is by default the inframammary fold (IMF) incision when
pure augmentation is planned as it ensures a less invasive approach by
reducing trauma and scarring within the gland and minimizes bacterial
contamination.
Regardless of the incision location or the need of mastopexy or not, IMF
estimation is considered of paramount importance when PU-coated implant is
chosen. Any method of estimation is considered valid and can be selected for
the preoperative marking of the new IMF.
OPERATIVE TECHNIQUE
As PU-coated implants have a wide spectrum of indications and can be used
in every single implant-based breast surgery the authors will avoid describing
every single operative technique as it has been already described in the
Operative Technique section of previous chapters. Instead, attention will be
drawn to the important steps that differentiate the use of these implants from
any other silicone shell implant.
A significant difference is that during the operation a surgeon must prepare
a large and generous pocket usually 1 to 1.5 cm larger than the implant
dimensions, so that the implant can settle in with ease to avoid curved edges
or rippling folds that can be caused by a tight pocket.
Contrary to the silicone shell implants, the PU coat exerts an adhesive-like
property to the tissues that it comes in contact with therefore its proper
intraoperative placement is of paramount importance. As it is virtually
impossible to dislocate, rotate, or even drop due to gravity after surgery a
surgeon must ensure that the implant is placed precise at the proper location
during the operation. The intraoperative maneuver of sitting up the patient
after securing the head, the neck, the anesthesia tube, and the arms should
always be performed after the implant placement in order to check the proper
position of the implant. If the implant is found to be in the proper anatomical
position then the surgeon can proceed with the next operative step. Having in
mind that property, one must also manually check the implant’s base to make
sure there is no fold and if using the anatomical shape to ensure that the
indication line is in alignment with the breast meridian line and in the proper
distance from the midsternal line. The authors recommend drain placement in
every type of breast surgery involving PU-coated implants. By keeping the
pocket dry and free of excess fluid and blood during the first postoperative
hours the foam remains in contact with the tissue of the pocket allowing the
“ingrowth” of tissue in the sponge-like foam. As a result, the aforementioned
properties of the PU foam are preserved and highlighted.
POSTOPERATIVE CARE
Postoperative care does not change significantly when PU-coated implants
are used. The routine of each surgeon for each type of surgery can be
performed unchanged with the only recommendation that drains are removed
when the fluid collection is 30 mL or less. In some rare cases a patient might
exhibit skin rash on the areas overlying the implants. No treatment is
recommended as this is a self-resolving erythema that will subside within
some days or few weeks.
A surgeon must have in mind that PU-coated implants feel firm and
immobile in the first few postoperative months, however they become softer
and completely naturally looking and feeling like within the third
postoperative month. Our patients are properly informed in advance,
therefore it never consisted a problem in our practice.

CASES

CASE 1

Shown in Figure 105-1A,B is a patient with bilateral grade 4 CC


associated with previous smooth implant. After revisional composite
augmentation mastopexy with PU-coated anatomic implants (Fig. 105-
1C,D).
FIGURE 105-1 A, B: Patient before procedure. C, D: Patient after procedure.

CASE 2

In this case, Figure 105-2A–C shows a patient with bilateral grade 4 CC


associated with previous smooth implant. After revisional augmentation
mastopexy with PU-coated anatomic implants (Fig. 105-2D–F).
FIGURE 105-2 A–C: Patient before procedure. D–F: Patient after procedure.
CASE 3

A patient with bilateral grade 3 CC associated with previous smooth


implant is shown in Figure 105-3A–C. After revisional breast
augmentation with PU-coated anatomic implants (Fig. 105-3D–F).
FIGURE 105-3 A–C: Patient before procedure. D–F: Patient after procedure.

CASE 4

Figure 105-4A shows a patient with bilateral micromastia and low-fat


reserves. In Figure 105-4B–D the patient’s breast augmentation with PU-
coated anatomic implants in a dual plane pocket is shown.
FIGURE 105-4 A: Patient before procedure. B–D: Patient after procedure.

CASE 5

A patient with bilateral micromastia and low-fat reserves is shown in


Figure 105-5A,B. Figure 105-5C,D shows the patient after breast
augmentation with PU-coated anatomic implants in a dual plane pocket.
FIGURE 105-5 A, B: Patient before procedure. C, D: Patient after procedure.

CASE 6

In Figure 105-6A–C a patient with right implant (textured) rotation and


lateral displacement. Shown in Figure 105-6D–F is the same patient after
the implant is removed and replaced with PU-coated one.
FIGURE 105-6 A–C: Patient before procedure. D–F: Patient after procedure.

CASE 7

A patient with bilateral macromastia is shown in Figure 105-7A,B.


Figure 105-7C,D shows the patient after composite subglandular breast
augmentation with PU-coated anatomic implants and fat grafting on the
upper poles.
FIGURE 105-7 A, B: Patient before procedure. C, D: Patient after procedure.

CASE 8

In Figure 105-8A,B a patient with bilateral breast atrophy is shown.


Figure 105-8C,D depicts the patient after subglandular breast
augmentation with PU-coated implants and fat grafting on the upper and
medial quadrants.
FIGURE 105-8 A, B: Patient before procedure. C, D: Patient after procedure.

CASE 9

A patient with bilateral breast ptosis is shown in Figure 105-9A,B. In


Figure 105-9C,D the patient is shown after subglandular composite
augmentation mastopexy with PU-coated anatomic implants.
FIGURE 105-9 A, B: Patient before procedure. C, D: Patient after procedure.

CASE 10

In Figure 105-10A–C a patient with bilateral breast ptosis and atrophy is


shown. The patient after subglandular composite augmentation
mastopexy with PU-coated anatomic implants is shown in Figure 105-
10D–F.
FIGURE 105-10 A–C: Patient before procedure. D–F: Patient after procedure.
OUTCOMES
From 2000 to 2019 more than 800 patients were implanted in our institution
with PU-coated implants for either aesthetic or reconstructive breast surgery.
In a retrospective study that we published in 2016 (7), 255 implants that were
used for primary breast augmentation were studied and followed up. Data
were collected from postoperative follow-up sessions at 2 weeks; 1, 3, 6, and
12 months; and annually thereafter. We recorded three cases of CC, two out
of which occurred after haematoma. It is proven that hematoma increases the
risk of CC, especially early-onset CC. CC was diagnosed in these breasts 8
and 12 months postoperatively and only one occurred spontaneously. Four
implants exhibited malposition, and that was due to poor intraoperative
placement. It is also important to highlight the low rate of seroma with
Microthane implants (0.8%), a complication that indicates possible
relationship with breast implant–associated anaplastic large cell lymphoma
(BIA-ALCL). Skin rash was recorded in 0.8% of the cases and resolved
spontaneously without any treatment.
In breast reconstruction, we recorded the Kaplan–Meier cumulative
incidence of CC following two-stage breast reconstruction was 8.1% (95%
CI) with a median follow-up of 9 years. The incidence of CC was 10.7%
(95% CI) with radiation therapy (RT) and 5.5% (95% CI) without RT,
respectively (4). This attribute did not appear to diminish over time.
It is well known that RT with textured implants increases the risk of high-
grade CC, however this complication can be strongly reduced using PU
implants.
The lower CC risk associated with these implants, as opposed to smooth or
textured implants, is well documented in the literature of aesthetic and
reconstructive breast surgery over the past years (4,5,11–15).
Since the first documentation of PU-covered implants by Ashley in 1970
(2) and 1972 (3), not only the vulcanization process has been improved but
also a barrier layer was added in the middle of the numerous silicone shell
layers. As fragments of PU foam have been incorporated in the capsular
tissue, the microtextured surface of the silicone shell is revealed partially.
The current generation of these devices involves a microtextured implants
under the PU coat, a combination that cannot be compared to any other
silicone shell texturization (6).
CONCLUSION
The safety of PU foam–coated implants has been demonstrated in clinical
practice for more than 50 years. The clinical papers published on PU implants
always asserted their benefits in terms of low incidence of the most common
adverse events.
PU-coated silicone gel implant can be used in any type of aesthetic or
reconstructive surgery, primary or secondary. Compared with textured
implants, PU implants are associated with a lower rate of CC, which is the
most common complication of breast aesthetic and reconstruction surgery
and a frequent reason for reoperation. This attribute of PU implants does not
diminish over time and is particularly attractive for patients who undergo RT.
Furthermore, the foam characteristics and properties render it a significant
tool in order to solve troubling complications and to standardize the results of
secondary breast surgeries.
These evidences confirm that PU implants are an effective alternative to
textured devices, which have failed to attain the benefits of the foam.

REFERENCES

1. Castel N, Soon-Sutton T, Deptula P, et al. Polyurethane-coated breast


implants revisited: a 30-year follow-up. Arch Plast Surg
2015;42(2):186–193.
2. Ashley FL. A new type of breast prosthesis. Preliminary report. Plast
Reconstr Surg 1970;45(5):421–424.
3. Ashley FL. Further studies on the Natural-Y breast prosthesis. Plast
Reconstr Surg 1972;49(4):414–419.
4. Pompei S, Arelli F, Labardi L, et al. Polyurethane implants in 2-stage
breast reconstruction: 9-year clinical experience. Aesthet Surg J
2017;37(2):171–176.
5. Handel N, Gutierrez J. Long-term safety and efficacy of polyurethane
foam-covered breast implants. Aesthet Surg J 2006;26(3):265–274.
6. Hamdi M. Association between breast implant-associated anaplastic
large cell lymphoma (BIA-ALCL) risk and polyurethane breast
implants: clinical evidence and European perspective. Aesthet Surg J
2019;39(S1):S49–S54.
7. Pompei S, Evangelidou D, Arelli F, et al. The modern polyurethane-
coated implant in breast augmentation: long-term clinical experience.
Aesthet Surg J 2016;36(10):1124–1129.
8. Pompei S, Evangelidou D, Arelli F, et al. The use of TIGR matrix in
breast aesthetic and reconstructive surgery: is a resorbable synthetic
mesh a viable alternative to acellular dermal matrices? Clin Plast Surg
2018;45(1):65–73.
9. Tebbetts JB. Dual plane breast augmentation: optimizing implant-soft
tissue relationships in a wide range of breast types. Plast Reconstr Surg
2006;118:81S–98S; discussion 99S–102S.
10. Nava MB, Rocco N, Tunesi G, et al. Decisional pathways in breast
augmentation: how to improve outcomes through accurate pre-operative
planning. Gland Surg 2017;6(2):203–209.
11. Handel N, Cordray T, Gutierrez J, et al. A long-term study of outcomes,
complications, and patient satisfaction with breast implants. Plast
Reconstr Surg 2006;117:757–767; discussion 768–772.
12. Handel N, Silverstein MJ, Jensen JA, et al. Comparative experience with
smooth and polyurethane breast implants using the Kaplan-Meier
method of survival analysis. Plast Reconstr Surg 1991;88(3):475–481.
13. Rancati A, Soderini A, Dorr J, et al. One-step breast reconstruction with
polyurethane-covered implants after skin sparing mastectomy. J Plast
Reconstr Aesthet Surg 2013;66(12):1671–1675.
14. Vázquez G. A ten-year experience using polyurethane-covered breast
implants. Aesth Plast Surg 1999;23(3):189–196.
15. Vázquez G, Pellón A. Polyurethane-coated silicone gel breast implants
used for 18 years. Aesth Plast Surg 2007;31(4):330–336.
CHAPTER 106

Augmentation Mastopexy: General


Considerations
ROBERT COHEN
HISTORY
Augmentation mastopexy surgery is justifiably considered one of the more
challenging aesthetic procedures, and its performance demands careful
assessment and planning, a three-dimensional conceptualization of the breast
tissues and chest wall anatomy, and long-term understanding of the soft
tissue/implant relationship. Having a broad range of surgical techniques
available to manage a wide array of anatomical variations (even between
breasts on the same patient) is also critical to success. Understandably, this
category of procedures can seem intimidating to surgeons as a result of the
many variables involved. However, when performed properly, this surgery
can create dramatic aesthetic improvements and produce a high degree of
patient satisfaction. By breaking down the process of planning, marking, and
performing this surgery into its essential parts, this chapter intends to present
universal building blocks that can be combined in progressively complex
ways in order to create a unified approach to augmentation mastopexy.
Candidates and Noncandidates
Augmentation mastopexy candidates are generally patients that suffer from
suboptimal breast volume (particularly in the upper pole) in combination with
ptosis, who are healthy enough to undergo surgery. While a mastopexy alone
will correct ptosis, the addition of volume should be considered when the
patient’s starting tissues are unlikely to create stable upper pole fullness due
to insufficient natural volume, weak soft tissues, low breast tissue density, or
poor skin elasticity. Barring medical contradictions, there are few surgical
contradictions to augmentation mastopexy as long as patient expectations are
matched properly with the reality of physics and the patient’s pre-existing
tissues, and the proper volume addition and skin resection pattern is selected
by the surgeon to maximize the chance of success. If patients have unrealistic
expectations (expecting a full mastopexy result without allowing the
necessary skin resection pattern), or pose an issue with postoperative
compliance (active smokers), surgery should be avoided. Situations beyond
the control of the patient and surgeon should also be addressed and factored
into the surgical plan in order to minimize failures and disappointments; for
example, reinforcement materials should be strongly considered or required
in patients with naturally weak tissues wanting larger volume augmentations.
PREOPERATIVE EVALUATION AND PATIENT EXPECTATION MANAGEMENT
The first, and one of the most important steps in the process of augmentation
mastopexy occurs with the initial meeting and patient assessment. This is the
time where the surgeon can obtain a solid understanding of the patient’s
concerns and aesthetic goals, and synthesize these concerns with the pre-
existing anatomy and with what may be realistically achieved in the operating
room. There are a vast number of anatomical variations that must be
addressed which include, but are not limited to: skin thickness and elasticity,
breast parenchyma volume and density, inframammary fold (IMF) position
and strength, degree of ptosis, breast base width and nipple areolar size, and
position on the breast mound. Understanding the patient’s specific concerns
and goals is paramount, as what aesthetically bothers a patient may differ
somewhat from what the assessing surgeon finds most problematic. A
detailed discussion in which surgical options are presented in conjunction
with a realistic physical assessment can save the surgeon from future
disappointment if expectations and results do not align (Figs. 106-1 and 106-
2).
A systematic series of questions, and attentive listening to each patient’s
answers, can be helpful to start the process of augmentation mastopexy
surgery and allows the surgeon to gain as much insight as possible into the
patient’s thoughts. A logical progression of questions might proceed as
follows: (1) Are your breasts too large, too small, or about right in terms of
volume? (2) If you wish to be larger, where would you want the increase in
fullness to be? (3) Are you concerned about loose or overhanging skin? (4)
Are you bothered by any breast asymmetry? (5) Do you have concerns about
the nipple areolar size, shape, or position? (6) Are you concerned about
excess fullness in the axillary areas or lateral chest? (7) Are you open to the
idea of adding implants? In the author’s practice, patients are also encouraged
to view the before and after photo gallery to visually express what their goal
appearance is.
FIGURE 106- Four patients with different degrees of ptosis will require varied
management appropriate to their anatomy. The first patient (A) has mild glandular
ptosis and can be corrected with an augmentation and circumareolar mastopexy.
The second patient (B) has grade 2 ptosis and is a more appropriate candidate for
augmentation with a vertical mastopexy. The third patient (C) has severe grade 2
ptosis and will benefit from augmentation or fat grafting with an inverted T scar
mastopexy. The final patient (D) has grade 3 ptosis and will require an inverted T
scar mastopexy with lower pole tissue resection and augmentation with implants or
fat grafting.

As augmentation mastopexy is a surgery that requires a degree of


maintenance over time, it is also critical to comprehend what type of lifestyle
the patient has and how surgery will fit into their daily routine. For example,
some patients are generally more willing to accept implant maintenance in
exchange for the aesthetic satisfaction of upper pole fullness, while others are
more willing to compromise and may prefer fat grafting to implants, giving
up some upper pole volume in exchange for less future surgery. Patients often
come into the evaluation with relatively poor or unrealistic information about
the surgery gleaned from social media feeds and anecdotes from friends.
During the first consultation, it is very important for the surgeon to educate
the patient regarding their anatomy and how loss of volume and ptosis
became an issue for them, with specific reference to genetics, anatomical
structures such as Cooper’s ligaments, weight loss or pregnancy changes, and
other such issues. Reinforcing the fact that surgery is not a permanent
solution and will need to be redone periodically over time is crucial to
avoiding future dissatisfaction.
FIGURE 106-2 This photo shows a patient with relatively constricted breasts that
are consistent with tuberous breast development. A: The white arrow represents the
patient’s actual base width while the red arrow represents the ideal base width. If
implants are selected in combination with the mastopexy, the ideal base width should
be used to determine the implant base width. If fat grafting is selected in addition to
the mastopexy (as was done in this case), the fat should be used to create a wider-
appearing breast to better match the ideal base width (B).
ANATOMICAL ASSESSMENT FOR AUGMENTATION MASTOPEXY
A detailed physical examination with attention to multiple anatomical
features is critical to success in augmentation mastopexy. Each anatomical
detail should not only be noted, but should be compared to the contralateral
side as various degrees of asymmetry are routinely present in most patients.
Multiple anatomical variations will need an “augmentation mastopexy” for
correction, but the actual techniques needed can be quite different, and will
be based primarily on the pre-existing anatomy. As with the initial
consultation questions, the physical assessment should proceed in a logical
and organized fashion in order to synthesize the best possible surgical plan
(Fig. 106-3).
Initial breast measurements are taken with a ruler and calipers, and
determine the sternal notch-to-nipple (S-N) distances, the nipple-to-nipple
(N-N) distance, the nipple-to-inframammary fold (N-IMF) distance on
maximum stretch, the actual and ideal breast base width diameters (BWDs),
upper and lower pinch thicknesses, and nipple positions relative to the IMFs.
Ideal base width is often considered the most crucial measurement as this sets
the proper size range for breast implants used during surgery. The base width
measurement should be determined by the ideal breast width (∼1.5 cm lateral
to the midline to the anterior axillary line), as opposed to the actual base
width in the situation of tuberous, or excessively narrow breasts. During this
portion of the examination, it can be helpful to speak each measurement out
loud as they are recorded, as the inevitable differences between each side
helps the patient realize that they are not totally symmetrical. Areolar sizes
and positions relative to the IMF should also be measured and noted.
Once the basic measurements are completed, a logical way to assess the
breasts is from a superficial to deep plane. This evaluation should include
skin quality and elasticity, general breast size, breast density, chest muscle
anatomy, and ribcage/sternal anatomy.
Skin elasticity is an important first assessment as patients with thicker,
tighter skin will hold their shape better after surgery. Patients demonstrating
striae, poor elasticity, or other skin strength issues will need to understand
that they face a higher risk of problems such as recurrent ptosis, stretch
deformities, and malpositions. Patients with poor skin strength should be
advised to consider implant and material reinforcement options that mitigate
the risk of these problems such as resorbable mesh, acellular dermal matrix
(ADM), or textured implants.

FIGURE 106-3 This picture is an example of a way to record breast measurements.


The top two lines are used to record base width, the triangle is used to sternal notch-
to-nipple distances as well as the nipple-to-nipple distance. The lower lines are used
to mark the IMF-to-nipple distance (on maximum stretch), and the upper and lower
breast pinch thicknesses can be noted on this picture as well.

After assessing the skin, the subcutaneous soft tissue thickness should be
evaluated because patients with a thinner layer of subcutaneous fat will be at
a higher risk for rippling and implant palpability. Considerations in this
patient population should include the use of higher-stability silicone gel
implants, avoidance of excessively large or heavy implants, the use of
reinforcement materials, and/or adding more padding via fat grafting if
possible.
After the subcutaneous tissue evaluation, the breast tissue density should
be assessed as this will also impact the final results and influence the surgical
plan. Low-density breasts with a large degree of adipose tissue provide less
stable upper pole volume, although they are easier to mold and redistribute
over an underlying implant, and are less likely to cause excessive projection.
Conversely, firmer breasts with a greater proportion of glandular tissue may
be more challenging to reshape, but they will more readily provide upper pole
fullness. Dense breast tissue can sometimes create excessive projection when
combined with an implant, and may need debulking or internal scoring for an
acceptable result. Patients with larger, dense breasts are often good
candidates for mastopexy with upper pole fat grafting, and this option should
be considered and discussed with the patient as a potentially simpler
substitute to augmentation with breast implants.
In addition to the breast tissue density, each breast’s volume, both alone
and in comparison with the contralateral side, should be evaluated. When
asymmetry is noted, options include differential implant sizes, tissue
debulking of the fuller breast, fat grafting of the smaller breast, or a
combination of these approaches. Generally, the most predictable way to
manage volume asymmetry in long term is to equalize the breast volume first
with resection so that similar implant sizes or fat grafting amounts can be
utilized.
Once the breast assessment is complete, the chest musculature should be
evaluated for symmetry, position, strength, and medial spacing. Patients with
very large, strong pectoralis major muscles will face a higher risk of
animation deformities, and should be considered for fat grafting or
subglandular/subfascial implant placement in order to remove the muscles
from the surgical equation. Patients with widely spaced pectoralis origins will
need to understand that their implant spacing may be wider than desired.
Once again, subglandular/subfascial placement may be considered, and
medial chest fat grafting can also be used to decrease the intermammary
distance if implants are placed in a subpectoral position.
Finally, the patient’s chest wall should also be evaluated, as this is the
platform on which the implants and breasts will sit. The chest wall should be
viewed from both the standing and supine “worm’s eye” view for maximum
accuracy. If a pectus carinatum or laterally sloping ribcage is noted, the
patient will be at higher risk for lateral implant migration. If a pectus
excavatum is present, a medial malposition is more likely. In both of these
situations, the use of reinforcement materials or textured implants should be
considered to reduce the risk of a malposition (Fig. 106-4). Differential
ribcage projection will affect implant projection, and often requires the use of
different implant profiles on each side to equalize breast projection while
maintaining a similar base width.
Once the general breast examination is completed, the ancillary structures
such as the nipples and the surrounding chest anatomy should be evaluated as
well. Many patients will benefit from liposuction of the axillary fat or lateral
chest to improve contouring. Additionally, patients with inverted or elongated
nipples should be offered aesthetic improvements with these issues as well
for the best overall results.
AUGMENTATION MASTOPEXY SURGICAL PLANNING—GENERAL OVERVIEW
After the detailed and focused history and physical examination is completed
as described above, the planning and execution for the augmentation
mastopexy can begin. Preoperative decisions will include (1) whether to use
implants or fat grafting to augment the breasts, (2) what size, profile, and
style implants are optimal for the patient’s anatomy and goals, (3) what plane
of dissection to utilize if implants are placed, (4) what skin excision pattern
will be needed, (5) what reinforcement materials, if any, will be used, and (6)
what ancillary procedures will be performed to maximize the aesthetic
outcome. Once these decisions are made, the plan should be performed in
surgery with some flexibility regarding implant choices and scar pattern
techniques if possible to allow for the best possible shape and symmetry.

FIGURE 106-4 A “Worm’s eye view” of the patient is important to assess for risk of
implant malposition (A). In this case, a laterally sloping ribcage places the patient at
higher risk for lateral malposition and as a result, extra precautions should be made
(such as the use of reinforcement material or textured implants) to minimize the risk
of reoperation (B).
AUGMENTATION MASTOPEXY SURGICAL PLANNING—IMPLANT SELECTION
The history and physical examination should clarify whether breast implants
are needed. As noted above, in select patients with more elastic skin and a
greater amount of dense glandular tissue, a mastopexy with fat grafting of the
upper poles may be the best option. With patients that have less natural
tissue, or want a fuller appearance with predictable volume maintenance, an
augmentation mastopexy with implants is generally the best option.
When the decision is made to utilize implants, the first basic choice is to
use saline or silicone implants. Saline implants are a reasonable option but
are generally more prone to rippling, a less natural look and feel, and higher
risks for a “water hammer” effect. These issues are reduced with the use of
cohesive silicone gel. With modern silicone implants using fifth-generation
gel, the implants can be soft yet still be very cohesive and are easily removed
in the case of a rupture. These implants are usually more appreciated by
patients for their more natural appearance and density.
The next basic implant choice is to use a smooth or textured surface. In the
United States, the majority of implants used have historically been smooth
shelled, while in Europe and most other countries around the world, the
majority of implants placed are textured. Each style of implant has its own set
of positive and negative attributes, although textured implants have become
more controversial due to breast implant–associated anaplastic large cell
lymphoma (BIA-ALCL).
Smooth implants generally have a thinner shell and are a more forgiving
and less-palpable implant style than textured. There is no current association
of BIA-ALCL with smooth implants. On the downside, the smooth surface is
less positionally stable and can be problematic for patients with angled
ribcages or anatomy that places them at higher risk for malposition.
Additionally, some studies have demonstrated higher rates of capsular
contracture with smooth implants, especially if placed in the subglandular
plane.
Textured implants are a very diverse category, as each brand has its own
unique form of texturing which ranges from friction-based microtexturing to
tissue ingrowth–promoting macrotexture, with varying risks of BIA-ALCL
that appear to increase with more aggressive texturing. These implants allow
for a greater degree of positional stability and open the option for anatomical
implants which preferentially expand the lower breast pole due to their
geometry and more form-stable gel. Anatomical implants can be particularly
useful when expansion of the lower pole is needed as in the case of tuberous
breasts. BIA-ALCL must be discussed in detail with patients considering
textured implants, and the risks of this illness weighed against the risk of
reoperation if smooth implants are used. If stability is needed but the patient
wishes to avoid texture, a reinforcement material is another reasonable
option.
Covering all details regarding implant selection, including the decision on
size, profile, and shape, is beyond the scope of this chapter, however it is
important to use biodimensional planning and accurate measurements to
ensure the tissue parameters and implants match well.
AUGMENTATION MASTOPEXY SURGICAL PLANNING—INCISIONS/PLANE
SELECTION
Once the implant style and (approximate) size has been chosen, the incision
location for the implant placement and the plane of dissection should be
selected. These decisions will be discussed separately from the selection of
the mastopexy skin patterns.
Implant placement should generally be placed through an inframammary
incision or a low vertical incision depending on what scar pattern is
ultimately selected for the mastopexy. This incisional approach allows
excellent direct access to the implant pocket, and also presents the cleanest
approach for implant placement as it avoids potential bacterial contamination
that can occur when passing through the milk ducts of the breast or the
axillary glands. Utilization of nipple shields, a funnel device, minimal
implant handling, and washes with antibiotic solution covering both gram-
positive and -negative bacteria is also important to minimize risk of a biofilm
which can lead to an increased risk of capsular contracture.
As far as decisions regarding the plane of the pocket dissection, the options
include subglandular, subfascial, dual plane, and total submuscular
approaches, although this latter option is rarely utilized due to the blunted
shape of the lower pole and additional muscle dissection. The dual plane is
most commonly used as it provides additional upper breast soft tissue
coverage, a more gradual slope to the upper pole, and good control of the
cleavage. For patients with strong, bulky pectoralis muscles who are at higher
risk for animation issues, or those simply wishing to avoid muscle dissection,
a subfascial or subglandular plane dissection is a reasonable option as well if
the subcutaneous tissue coverage is 2 to 3 cm or more with a skin pinch test.
Any of these tissue plane dissections can be combined with reinforcement
material if the tissues are weak and pose a risk for malposition or stretch
deformities.
AUGMENTATION MASTOPEXY SURGICAL PLANNING—CHOOSING THE
MASTOPEXY PATTERN
There is a wide range of anatomical variations that could be considered
ptotic-appearing breasts, which require different techniques for correction.
These variations include breasts with a low nipple areolar complex (NAC),
breasts with grade 2 and 3 ptosis, and breasts with glandular ptosis. Certain
patients will have enough breast asymmetry to warrant different mastopexy
techniques on each breast. In this section, the range of mastopexy skin pattern
techniques will be addressed, from the simplest option to the most extensive
approach (Fig. 106-5).

FIGURE 106-5 Cross view of breast anatomy including nipple and ducts, Cooper’s
ligaments, breast fat/parenchyma, chest muscles, and ribcage.
FIGURE 106-6 Two different patients with varying levels of pre-existing breast
tissue will potentially warrant alternative approaches depending on their goals. For
patients with less natural tissue (A, B), augmentation using implants in conjunction
with a mastopexy will be the best option. For patients with a larger degree of dense,
natural breast tissue (C, D) a mastopexy with upper pole fat grafting is often a lower-
maintenance option that can provide a good aesthetic outcome.

Mastopexy Pattern—Crescent Lift


The crescent lift is a very simple technique that, due to its very limited skin
resection, is quite modest in its usefulness and should only be applied to
achieve mild NAC elevations or to correct small NAC position asymmetries.
With this approach, a crescent of skin is removed from the area above the
areola corresponding to the 9:00 to 3:00 positions. Since only the upper
areola is addressed, attempting to elevate the NAC greater than 1 to 1.5 cm
will place the patient at risk for a distorted or elongated areolar appearance
(Fig. 106-6).
Mastopexy Pattern—Circumareolar Mastopexy
After a crescent lift, the next minimally scarring technique is the
circumareolar mastopexy, which involves skin resection around the entire
areola and can be used for many purposes, including tightening breast skin
over an implant framework, shifting the NAC positions on the breast mound,
reducing the size of areolas, and flattening out excessively projected or
“pointy” breasts. While this technique has garnered a reputation for poor
outcomes, this is primarily due to inappropriate applications where an overly
aggressive circumareolar skin resection is used when a vertical or inverted T
scar mastopexy would have been more appropriate. As noted earlier, this
technique applies compressive forces to the breasts, so while it is excellent
for “pointy” tuberous breasts, it is a poor technique choice for patients with
flatter breasts such as those with more significant grade 2 or grade 3 ptosis, or
glandular ptosis (Fig. 106-7).

FIGURE 106-7 Different types of ptosis including grade 1–3 and pseudo ptosis.
With the circumareolar mastopexy technique, while the inner incision is a
true circle designed with a 38- to 42-mm cookie cutter, it is important to
design the outer pattern to be approximately 0.5 to 1 cm longer in vertical
height than horizontal width as the lateral forces on the breast will otherwise
pull a concentric circle into a horizontally oriented oval over time. Depending
on the skin laxity, the areolas can generally be shifted by 2 to 2.5 cm
vertically, or they can be moved in other directions as needed depending on
how the outer oval pattern is located relative to the inner circular incision.
Thinner, weaker skin, which can be assessed with a simple skin pinch, can be
more aggressively resected as it will apply less outward force when the outer
oval is tightened with a purse-string suture. A more conservative skin
resection should be applied to patients with thick, elastic skin as the stronger
outward skin forces increase the risk for areolar scar spread.
Because this technique can be performed with simple skin
deepithelialization, the subdermal plexus can be preserved, allowing this
technique to be performed safely in patients with extremely thin tissues (Fig.
106-8).
Mastopexy Pattern—Vertical Mastopexy
One of the most powerful mastopexy techniques is the vertical mastopexy or
“lollipop scar” mastopexy. This approach provides multiple benefits
including the power to elevate the nipple as much as needed, tighten lower
pole horizontal skin excess, and resect lower breast pole tissue excess if it
poses a risk for a waterfall deformity. Additionally, the mechanics of the
vertical mastopexy elevates the IMF and creates more breast projection,
which can be helpful in patients with a relatively low breast footprint (Fig.
106-9).
Mastopexy Pattern—Inverted T Scar Mastopexy
The inverted T scar (“anchor scar”) mastopexy allows for a full, three-
dimensional reshaping of the breast and allows for resection of both
horizontal and vertical skin excess. Because of this, it represents the most
aggressive option for skin resection, and is best used for the correction of
more severe grade 2 and 3 ptosis. Like the vertical mastopexy, this scar
pattern allows for lower pole tissue debulking as needed, and can be used to
create a more balanced breast if a vertical mastopexy alone creates an
unaesthetically long distance (>6 to 7 cm) from the lower edge of the NAC to
the IMF. Unlike the vertical mastopexy, the IMF is generally not elevated,
but the inframammary scar tends to hide well in the patient’s pre-existing
inframammary crease (Fig. 106-10).
AUGMENTATION MASTOPEXY—UNIVERSAL MARKINGS
Because it can be difficult to assess exactly how much skin removal will be
necessary after implant placement, some flexibility regarding skin resection
should be maintained for single-stage augmentation mastopexy until the
implants are in place. To assist with this and ensure that good symmetry will
be achieved after surgery, the author developed a universal marking system
for breasts that creates the ability to adjust or change the degree of skin
resection without becoming disoriented to landmarks or losing the ability to
maintain symmetry even if the patient shifts somewhat under the drapes from
checking them in both the seated and supine positions (Fig. 106-11).
FIGURE 106-8 This is a patient with mild glandular ptosis and somewhat low set
and asymmetrical nipple areolar complexes (A). In addition to a silicone breast
augmentation, a crescent lift was performed in order to elevate the nipple position
(B). Asymmetrical skin excision on each side was performed to improve areola
positional symmetry (C, D).
AUGMENTATION MASTOPEXY OPERATIVE TECHNIQUES—IMPLANT
PLACEMENT
For single-stage augmentation mastopexy, the best order is implant
placement first with skin and tissue resection afterward. This has the dual
advantage of a “cleaner” implant placement, as well as knowing the final
volume of the breast before a commitment to the amount of skin excision is
made. An inframammary incision or a low vertical incision (in the case of a
vertical mastopexy) is made and dissection is continued down to the chest
wall. If a dual plane is used, the pectoralis major muscle edge is located and
carefully elevated and a precise pocket is created. Alternatively, a subfascial
or subglandular dissection may be performed. Nipple shields, antibiotic
washes, minimal implant handling, and glove changes should be performed
to minimize risk of bacterial contamination and subsequent capsular
contracture. Attention to the pocket dissection is key, and a bloodless cautery
dissection with precise dissection is important to avoid oversized pockets
which can lead to malposition, particularly in the lateral direction.
FIGURE 106-9 This is a patient with mild grade 2 ptosis that was corrected with a
silicone augmentation and circumareolar mastopexy to elevate the nipple position
and tighten the skin around the underlying implant framework (A–C). The final scar
is well hidden at the areolar edge (D–F).

If a dual plane dissection is performed, the pectoralis muscle should be


dissected at its inferior border across to the sternum to allow lower pole
expansion while avoiding upward release of the muscle origins to avoid
muscle “window-shading.” Sizers can be used for maximum accuracy,
however if the surgeon is confident with the preselected shape and size of the
implants, these can be placed without the use of sizers. If a dual plane 2 or 3
is needed for additional lower pole expansion, the release of the lower edge
of the pectoralis from the overlying parenchyma should be performed after
the pocket dissection is completed. With the implants in place, the skin can
be tailor tacked to ensure the proper amount of skin resection. The final
implants are then placed and the pocket closed off before the nipple shields
are removed and the mastopexy resection is started.
AUGMENTATION MASTOPEXY OPERATIVE TECHNIQUES—CRESCENT LIFT
The crescent lift is a simple technique, with the most common error being
excessive skin resection or overutilization of the technique to correct a
problem that requires a more extensive mastopexy. With this lift, an incision
is made from 9:00 to 3:00 at the upper areolar edges. A second curved
incision is made 1 to 1.5 cm above this and the crescent of excess skin can be
excised full thickness or even deepithelialized if the superior subdermal
plexus blood supply needs to be maintained.
FIGURE 106-10 This is a patient with grade 2 ptosis that had a silicone dual plane
breast augmentation with vertical mastopexies (A–C). During surgery, the option
was left open to perform an inframammary skin excision if needed, but a vertical
scar only can correct most grade 2 and lesser degrees of ptosis when the skin
envelope is partially filled with the implant volume (D–F).
AUGMENTATION MASTOPEXY OPERATIVE TECHNIQUES—CIRCUMAREOLAR
MASTOPEXY
The key to success with a circumareolar mastopexy is proper application of
the procedure. Understanding the dynamics of this technique and how it
affects the breast shape is crucial in understanding when it is appropriate to
use. As stated above, this is an inherently compressive technique, and the
degree of breast flattening increases with tighter, more elastic skin, and as the
pattern is made larger. Because of this, the technique should be avoided in
situations where more projection is needed, or where a significant amount of
lower pole skin needs to be resected, such as with the correction of moderate
grade 2 ptosis, grade 3 ptosis, and with significant glandular ptosis.
In addition to rounding out a “pointy” or overprojected breast, this
multipurpose technique can be used to adjust NAC position on the breast
mound, to reduce the overall size of the NAC, and to tighten loose skin over a
breast mound/implant framework (Fig. 106-12).
To perform this technique, the implants are placed first as described above.
Once the pockets are closed, each NAC is placed on maximum stretch and a
38- to 42-mm cookie cutter is used to mark the desired areola size. The final
desired position for the upper edge of the areola is marked on each side,
which should be symmetrical distances when measured down from the
sternal notch (using the 5-cm universal reference marks). The distance from
the original upper areola edge to the desired upper areola edge position
(generally up to 2.5-cm elevation) will likely be different as most NACs are
not naturally symmetrical. The distance from the lower edge of the resection
pattern to the IMF should be measured evenly as well so the distance
measures approximately 6 to 7 cm. By doing these markings, maximum
postoperative symmetry is obtained although the size of the resection patterns
will often vary side to side if there is pre-existing asymmetry. When the
upper and lower marks are completed, the outer, vertically oriented oval is
completed so it is 0.5 to 1 cm longer vertically than it is horizontally to create
a true circle at the end of closure (Fig. 106-13).
FIGURE 106-1 This patient had severe grade 2 ptosis due to involution and changes
after childbirth (A–C). For the optimal correction, a dual plane silicone
augmentation with an inverted T scar mastopexy was performed (D–F).

With regard to deciding the total safe amount of skin resection, this can be
decided by manually pinching the tissues to ensure the resection is not
excessively tight, or by temporarily tacking the skin with staples. If the
pattern seems too large to close properly, it should be redrawn more
conservatively on both sides. After the safety of the skin resection pattern
size is checked, the area within the pattern is deepithelialized and cautery is
applied to the dermis for hemostasis and to allow contraction of the dermis.
Once again, by maintaining the subdermal plexus, the blood supply remains
dependable, even in patients with thin tissues.
FIGURE 106-12 This is a universal marking system that can assist with any type of
augmentation mastopexy and allows for on-table adjustments as needed. A: The
midline is marked down from the sternal notch and the inframammary folds are
marked as well. B: A 3-cm wide “no-touch” zone is marked centrally, and the ruler
is then used to mark the breast meridians which are carried down onto the abdomen.
C: A large caliper is used to transpose the IMF onto the breasts, and the breasts are
swung (D) medially and (E) laterally with plumb lines drawn down to estimate the
safe degree of skin resection if a vertical or inverted T scar mastopexy is planned. F:
Five-cm hatch marks are drawn up from the transposed IMF mark so that if
adjustments are needed during surgery, the NAC symmetry can be maintained with
these measurements even if the patient shifts or tilts under the drape. G: A template
is used to mark the NAC position, with the NAC usually centered approximately 1 to
1.5 cm above the transposed IMF mark. H: Final preoperative marks are completed
with a ++ reminder marking on the larger breast side, and topographic marks for
axillary liposuction. Keep in mind, after the implant or sizer placement, the
mastopexy pattern should be temporarily tailor tacked with staples and the pattern
can be adjusted as needed for the best breast shape and symmetry. The gauze on this
patient’s arms was used to cover tattoos.

FIGURE 106-13 Illustration of a crescent lift technique where distance “x” should be
no more than 1–1.5 cm to avoid areolar distortion.

There are multiple ways to close the circumareolar mastopexy, however


for the sake of simplicity, the author’s technique will be described. The deep
dermal layer is circumferentially tightened by imbricating the dermis with a
running 3-0 PDS. This takes much of the tension off of the skin closure.
Next, a 3-0 Prolene is used as a “deep subcuticular” running purse-string
suture which involves both the outer areolar edge and the inner breast skin
edge. The knot is buried deeply under the imbricated dermis to minimize
suture spitting. Finally, the skin is run closed with a tension-free 4-0
Monocryl subcuticular closure. This multilayered approach minimizes scar
spread while the limited number of knots and use of monofilament reduces
the risk of suture spitting and wound healing issues (Fig. 106-14).
AUGMENTATION MASTOPEXY OPERATIVE TECHNIQUES—VERTICAL
MASTOPEXY
Marking for a vertical mastopexy can be performed in a relatively simple and
predictable way, however the surgeon should always tailor tack the skin and
check the patient in both the supine and upright position before making
incisions to ensure that the amount of skin removal is appropriate. To
perform the on-table markings (after the implants are placed), a template is
made by cutting a rectangle of paper taken from the sterile paper towels that
come with the surgical gowns and marking a circle using a 38- to 42-mm
cookie cutter. The circle is then cut out and the lower template is split evenly
from the bottom to the lower circle. Once the template is made, it is centered
where the NAC should be after the mastopexy is completed. This ideal
position will be affected by the implant size and skin elasticity, but generally
the upper edge of the pattern (corresponding to the upper edge of the future
areola) is set at a position 5 cm above the transposed IMF. An alternative way
to conceptualize this is that the new nipple is usually centered 1 to 2 cm
above the transposed IMF mark. As noted above, this should be checked and
adjusted as needed after tailor tacking with staples becomes more
experienced.
Once the template is centered appropriately on the breast, the keyhole
pattern is spread open and a gentle curve is drawn on the breast with its
lowest point being at the IMF. Once again, measurements will differ patient
to patient, however the distance from corner to corner where the circle
portion of the pattern is opened usually measures close to 5 cm wide, and the
greatest distance of horizontal skin resection is usually 6 to 8 cm (Fig. 106-
15).
After the pattern for the first breast is finalized, the second breast will be
easier to mark as the surgeon can refer to measurements on the first breast
unless there is significant asymmetry. The second breast should be tailor
tacked as well and the breasts compared for aesthetics, symmetry, and
volume.
FIGURE 106-14 Illustration of a circumareolar mastopexy technique including
markings. The outer pattern should be 0.5-1 cm longer vertically than horizontally to
avoid horizontal distortion. If the NAC positions are asymmetrical, the patterns can
be offset so that distance “x” (the distance from the upper edge of the outer pattern
to the first reference mark) and “y” (the distance from the lower edge of the outer
pattern to the IMF) are equal.
FIGURE 106-15 Illustration of a vertical mastopexy technique including markings.
The dermis is released at the dotted line to create a superior pedicle with minimal
undermining. Distance “x” and “y” will vary between patients but as a general rule
“x” will often be close to 5 cm and “y” will be close to 7–8 cm.

After the skin patterns are finalized, cross marks with a pen are useful to
allow for accuracy when lining up the skin during closure. Staples are
removed and the pattern is deepithelialized after the areolas are marked with
a 38- to 42-mm areolar marker and scored. Much like with the circumareolar
mastopexy, the dermis can be cauterized for hemostasis and to contract the
tissues. The areolas are released inferiorly at the dermal level, leaving them
based on a minimally undermined superior dermoglandular pedicle.
Generally, very little deep dissection is needed to elevate the areolas,
allowing safe surgery even on patients with thin tissues.
In cases where bulky lower pole tissues increase the risk of a waterfall
deformity, the lower pole parenchyma can be resected to allow a tighter wrap
of the soft tissues over the implants, leaving some deeper tissue intact to
avoid exposure of the implants. Interrupted buried 3-0 PDS is placed to close
the vertical pillars. A new 3-0 PDS suture is then buried at the 6:00 point of
the areolar keyhole and run down the vertical closure as a deep dermal suture
and back up the vertical portion of the pattern as a subcuticular suture to both
imbricate the deep dermis and close the skin.
When the areolar incision is reached, the 3-0 PDS is continued as a deep
dermal suture to set the areola up for final closure. If, at this point, the areolas
are asymmetrical or irregular in shape, the cookie cutter can be used to
remark the areolas and the skin resection can be refined. Final circumareolar
closure is then performed with a 4-0 Monocryl in running subcuticular
fashion. The final appearance should have an areola centered on the breast
mound measuring 38 to 42 mm, and a distance of approximately 6 to 7 cm
from the lower edge of the areola to the IMF.
AUGMENTATION MASTOPEXY OPERATIVE TECHNIQUES—INVERTED T
SCAR MASTOPEXY
The marking and execution of an inverted T scar mastopexy is performed in a
similar way to the vertical mastopexy, however this surgery is needed when
the vertical length of the lower breast is too long for a vertical only (the
distance from the lower NAC edge to the IMF is greater than 7 to 8 cm) and
therefore the lower breast pole skin must be removed transversely in order to
shorten this distance. Generally, marks are made approximately 7 cm down
from the lower corners of the areolar keyhole and connected to another mark
made at the patient’s pre-existing IMF to create a horizontally oriented
elliptical pattern of skin resection. In addition to removing skin, the lower
pole tissue can also be resected in order to create a sharper IMF and reduce
the risk of a waterfall deformity. Closure on the lower pole skin resection is
performed with a 3-0 PDS as a deep dermal running suture from the medial
point to the lateral point of the IMF incision, and the same suture is then run
back to the medial point in subcuticular fashion to complete the skin closure
(Fig. 106-16).
AUGMENTATION MASTOPEXY—FAT GRAFTING
For patients wishing to avoid implants, or those with favorable anatomy
(significant amounts of breast tissue with good skin elasticity), fat grafting is
a viable alternative to the use of breast implants. In this situation, the
mastopexy is performed first, using the same techniques described earlier in
this chapter. One adjustment concerning mastopexy without implants is that
when the nipple location is selected, it is generally centered closer to the true
transposed IMF than when implants are used (0.5 to 1 cm higher than the
transposed IMF with mastopexy only vs. 1 to 2 cm higher with augmentation
mastopexy).

FIGURE 106-16 Illustration of an inverted T scar mastopexy including markings.


The dermis is released at the dotted line to create a superior pedicle with minimal
undermining. The lower pole skin is resected as an ellipse to avoid an NAC to IMF
distance of more than 7–8 cm. The lower pole breast tissue can also be debulked as
needed to create a sharper IMF and to reduce the risk of recurrent ptosis.

Once the mastopexy is almost completed, tumescent infiltration is infused


into the areas designated for fat harvest. The closure is completed while
waiting for the epinephrine effect, and liposuction is then performed with the
fat processed using the surgeon’s preferred system. The fat is then injected in
multiple thin threads in multiple planes to increase exposure of fat cells to the
surrounding blood supply and improve the survival of the grafts. The primary
area of grafting tends to be the upper poles and medial breasts in the
subcutaneous plane for the most visible improvements, although this will
vary with patient anatomy. For the best long-term symmetry, asymmetrical
breasts should be equalized with regard to shape and volume first (as opposed
to performing unequal volumes of fat grafting), so if more fat is resorbed than
expected the patient will maintain symmetry. Once again, patients should be
examined both supine and upright during this process to ensure the most
aesthetic results (Fig. 106-17).
FIGURE 106-17 This patient developed breast ptosis after childbirth but wished to
avoid implants (A–C). In surgery an inverted T scar mastopexy and abdominoplasty
were performed and fat was harvested from the flanks and abdomen with power-
assisted liposuction. Approximately 155 cc of fat was grafted to the right upper
breast and 125 cc to the left upper breast due to preoperative asymmetry (D–F).
AUGMENTATION MASTOPEXY—REINFORCEMENT MATERIALS
For patients that present with weak natural tissues and poor skin elasticity,
the risk of implant malposition and stretch deformities can be increased,
particularly if the patient seeks larger implants. In these cases, the use of a
reinforcement material such as an ADM or resorbable mesh should be
considered. While these materials add cost to the surgery, they can add
additional structural strength that is not present in the native tissues,
offloading the weight of the implant from the skin. The material should
generally be used to reinforce the inferolateral breast, and if a dual plane is
used, the upper edge of the material can be sutured to the pectoralis muscle
edge as a pectoralis extension, creating an “internal support bra.” This
concept will be easy to explain to the patient, and most will appreciate the
recommendation, even if they choose to avoid the materials. For patients at
extremely high risk of a malposition or other complication due to poor
tissues, the author will sometimes refuse to perform augmentation mastopexy
surgery unless a reinforcement material is used to minimize the risk of early
reoperation. Discussion of the various types and properties of reinforcement
materials are outside the scope of this chapter, however any surgeon using
them should be aware of their pros and cons, and should also be able to
explain their reasoning behind why they selected one product over another.
ANCILLARY PROCEDURES—NIPPLE REDUCTION, INVERTED NIPPLE
CORRECTION, LIPOSUCTION
Addressing and correcting small irregularities of the breasts can sometimes
be the difference between an adequate and an excellent result, and
demonstrates to patients a higher level of attention and expertise by the
surgeon even if they decide not to pursue these options. These ancillary areas
include the nipples themselves, the axillary fat, and the lateral chest.
The NAC is a focal point of the breast when patients are in the nude, and
as a result, they should be assessed for optimal aesthetics. Some patients will
present with oversized, ptotic, or excessively projected nipples due to
genetics or breastfeeding. In these cases, a nipple reduction is indicated to put
it in harmony with the overall breast mound. Although multiple techniques
have been reported, the method preferred by the author involves skin removal
circumferentially at the nipple base, maintaining blood supply to the nipple
tip via the deeper vascularized soft tissue. The skinned nipple tissue is then
telescoped into the areola and sutured at its base with 5-0 Monocryl in
interrupted buried and running subcuticular fashion (Fig. 106-18).
As opposed to elongated nipples, inverted nipples are usually due to
foreshortened milk ducts or tighter connective tissue that applies inward
forces on the nipples. The degree of this issue will vary, with grade 1
inversion indicating a nipple that is usually everted but sometimes inverted,
grade 2 indicating nipples that are usually inverted but sometimes everted,
and grade 3 indicating nipples that are always inverted. To correct inverted
nipples, the author uses a monofilament suture to temporarily place traction
on the nipple itself. A 3-mm incision is made at the base of the nipple where
it connects with the areola and tenotomy scissors are then used to divide the
deeper ducts and structures, thus mobilizing the nipple. The skin of the nipple
is palpated with a gloved finger during this dissection to ensure that the
internal dermis is not cut accidentally. Finally, a 4-0 PDS is placed as an
internal purse-string suture to make the diameter of the nipple base (where it
connects to the areola) smaller than the nipple itself so it cannot reinvert and
the skin is closed with a simple interrupted suture. It is important for patients
to understand that if this technique is used, their ability to breastfeed will
essentially be eliminated, so this must be taken into consideration (Fig. 106-
19).
Liposuction as an adjunct to breast surgery can be helpful in creating a
more aesthetic contour to the breast periphery. The most common area
needing liposuction is the axillary fat area which can be present even in
thinner patients. By debulking this area in patients with excess fat, a more
elegant S-curve can be created for the lateral breast. In patients with wider
chests or those that demonstrate a lateral chest roll, lipocontouring can create
a narrower, more aesthetically pleasing chest shape. In certain cases, the
inframammary incision must be extended laterally as well to remove loose
skin after liposuction. In general, liposuction should be performed after the
implant placement and mastopexy is complete, but extreme care should be
taken to avoid implant damage with the liposuction cannula (Fig. 106-20).
AUGMENTATION MASTOPEXY—POSTOPERATIVE CARE
Augmentation mastopexy does not require a very complicated postoperative
care routine. As with all breast surgery, deep breathing, early ambulation, and
bowel care are all important. Gentle range of motion exercises, including
slow arm elevation and rotation of the shoulders, should be initiated the day
of (or the morning after) surgery to reduce pain and stiffness and improve
mobility of the upper extremities. Brief showers can be initiated within 48
hours after surgery. Drains are generally not used unless the patient needed
an ADM. Steri-Strips are taken off after 1 week and scar care such as a
topical silicone product is started approximately 2 weeks postoperatively.
Exercise other than light walking is avoided for 1 month and slowly restarted
after that, avoiding or minimizing chest building exercises permanently if
implants are placed under the pectoralis major muscles.
FIGURE 106-18 This patient developed ptosis of the nipples after breastfeeding (A–
C). In addition to a dual plane silicone augmentation, a nipple reduction was marked
and performed in order to shorten the nipple projection and correct the nipple ptosis
for the optimal aesthetic result (D–F).

FIGURE 106-19 This patient was unhappy with her inverted nipples of which the
right side was more severe (A). An inverted nipple correction was performed with
transaction of the foreshortened milk ducts and an internal purse-string suture was
used to stabilize the results (B).

FIGURE 106-20 This patient was noted to have significant axillary fat which was
disproportionate to her body and negatively impacted the lateral curve of her breasts
(A). Axillary liposuction was performed at the same time as her breast augmentation
in order to create a smoother and more aesthetic silhouette (B).
OUTCOMES AND COMPLICATIONS
The majority of augmentation mastopexy complications can be minimized
with proper biodimensional planning and well-executed surgery. Many
problems such as malpositions and stretch deformities can be reduced by
avoiding oversized implants and using reinforcement materials if needed.
Waterfall deformities are reduced by debulking the lower pole tissues, or
avoiding implants and using fat grafting for augmentation. Capsular
contractures are minimized with extremely sterile and precise implant
placement techniques, antibacterial washes, and closing the pockets prior to
performing the mastopexy. Hematomas and seromas are reduced with precise
pocket dissection using the electrocautery and avoiding excessive blunt
dissection.
Understanding the blood supply of the breast, minimizing undermining,
and maintaining a subdermal plexus to the NAC helps to avoid tissue
necrosis, and multilayered closures with deep sutures offloading tension from
the skin reduces the risk of dehiscence and wound healing complications.
Proper mastopexy pattern selection reduces the risk of contour issues, and
tailor tacking prior to committing to incisions avoids the risk of overresecting
the skin.
As stated in the beginning of this chapter, it is critical to have an in-depth
discussion with patients about realistic outcomes for their anatomy so their
expectations match the results. Many concerning situations can be avoided
simply with careful patient selection.
CONCLUSION
Despite the wide array of anatomical presentations and problems that need to
be solved with augmentation mastopexy surgery, the process can be separated
into logical steps that—when followed carefully—can make the entire
process straightforward and enjoyable for both surgeons and patients.
Starting with the initial patient evaluation and conversations, followed by the
formulation of an appropriate and safe surgical plan, the execution of that
plan in the operating room, and proper postoperative management, the
surgeon can guide patients through a process that can have dramatic impacts
on their quality of life and self-confidence, while minimizing the chance of
complications and disappointment.

SUGGESTED READINGS
Adams WP Jr, Rios JL, Smith SJ. Enhancing patient outcomes in aesthetic
and reconstructive breast surgery using triple antibiotic breast irrigation:
six-year prospective clinical study. Plast Reconstr Surg 2006;117:30–36.
Barnsley GP, Sigurdson LJ, Barnsley SE. Textured surface breast implants in
the prevention of capsular contracture among breast augmentation patients:
a meta-analysis of randomized controlled trials. Plast Reconstr Surg
2006;117:2182–2190.
Benelli I. A new periareolar mammaplasty: the “round block” technique.
Aesthet Plast Surg 1990;14:93–100.
Bengtson B, Ringler SC, George ER, et al. Capsular tissue: a new local flap.
Plast Reconstr Surg 1993;91(6):1077–1079.
Bestwick J III. Plastic and Reconstructive Breast Surgery Vol. I. St. Louis,
MO: Quality Medical Publishing; 2000.
Calobrace MB, Herdt DR, Cothron KJ. Simultaneous augmentation/
mastopexy: a retrospective 5-year review of 332 consecutive cases. Plast
Reconstr Surg 2013;131:145–156.
Calobrace M, Schwartz M, Zeidler K, et al. Long-term safety of textured and
smooth breast implants. Aesthet Surg J 2017;38:38–48.
Calobrace MB, Stevens WG, Capizzi PJ, et al. Risk factor analysis for
capsular contracture: a 10-year study using round, smooth, and textured
implants for breast augmentation. Plast Reconstr Surg 2018;141(4S Sientra
Shaped and Round Cohesive Gel Implants):20S–28S.
De la Fuente A, Martin del Yerro JL. Periareolar mastopexy with mammary
implants. Aesthet Plast Surg 1990;16:337–341.
Delay E, Garson S, Tousssoun G, et al. Fat injection to the breast technique,
results and indications based on 880 procedures over 10 years. Aesthet
Surg J 2009;29:360–376.
Deva AK. Reply: breast implant-associated anaplastic large cell lymphoma in
Australia and New Zealand: high-surface-area textured implants are
associated with increased risk. Plast Reconstr Surg 2018;141(1):177e–
178e.
Elliott LF. Circumareolar mastopexy with augmentation. Clin Plast Surg
2002;29:337–347.
Ersek RA, Ersek SC. Circular cinching stitch. Plast Reconstr Surg
1991;88:350–352.
Frame J. The waterfall effect in breast augmentation. Gland Surg
2017;6(2):193–202.
Grolleau JL, Lanfrey E, Lavigne B, et al. Breast base anomalies: treatment
strategy for tuberous breasts, minor deformities and asymmetry. Plast
Reconstr Surg 1999;104:2040–2048.
Gruber RP, Jones HW. The “donut” mastopexy: indications and
complications. Plast Reconstr Surg 1980;65:34–38.
Hammond DC, Khuthaila DK, Kim J. The interlocking Gore-Tex suture for
control of areola diameter and shape. Plast Reconstr Surg 2007;106:804–
809.
Handel N. Augmentation mastopexy. In: Spear SL, ed. Surgery of the Breast:
Principles and Art. Philadelphia, PA: Lippincott-Raven; 1998:921–937.
Hester TR, Ghazi BH, Moyer HR, et al. Use of dermal matrix to prevent
capsular contracture in aesthetic breast surgery. Plast Reconstr Surg
2012;130:126S–136S.
Karnes J, Morrison W, Salisbury M, et al. Simultaneous breast augmentation
and lift. Aesthet Plast Surg 2000;24:148–154.
Maxwell GP, Birchenough SA, Gabriel A. Efficacy of pectoral pocket in
revisionary breast surgery. Aesthet Surg J 2009;29(3):379–385.
Maxwell GP, Gabriel A. Use of the acellular dermal matrix in revisionary
aesthetic breast surgery. Aesthet Surg J 2009;29(6):485–493.
Persoff MM. Vertical mastopexy with expansion augmentation. Aesthet Plast
Surg 2003;27:13–19.
Puckett CL, Meyer VH, Reinisch JF. Crescent mastopexy and augmentation.
Plast Reconstr Surg 1985;75:533–539.
Regnault P. Breast ptosis. Definition and treatment. Clin Plast Surg
1976;3:193–203.
Seiser DA, Adams WP. What’s your micromort? A patient-oriented analysis
of Breast Implant-Associated Anaplastic Large Cell Lymphoma (BIA-
ACCC). Aesthet Surg J 2017;37(8):887–891.
Spear SL. Augmentation/mastopexy: “surgeon, beware.” Plast Reconstr Surg
2003;112:905–906.
Spear SL, Boehmler JH, Clemens MW. Augmentation/mastopexy: a 3-year
review of a single surgeon’s practice. Plast Reconstr Surg 2006;118:136S–
151S.
Spear SL, Carter ME, Ganz JC. The correction of capsular contracture by
conversion to “dual-plane” positioning: technique and outcomes. Plast
Reconstr Surg 2003;112:456–466.
Spear SL, Carter ME, Ganz JC. The correction of capsular contracture by
conversion to “dual-plane” positioning: technique and outcomes. Plast
Reconstr Surg 2006;118 (7 suppl):103S–113S; discussion 114S.
Spear SL, Davison SP. Breast augmentation with periareolar mastopexy.
Oper Techn Plast Reconstr Surg 2000;7:131–136.
Spear SL, Dayan JH, Bogue D, et al. The “neosubpectoral” pocket for the
correction of symmastia. Plast Reconstr Surg 2009;124:695–703.
Spear SL, Giese SY, Ducic I. Concentric mastopexy revisited. Plast Reconstr
Surg 2001;107:1294–1299.
Spear SL, Kassan M, Little JW. Guidelines in concentric mastopexy. Plast
Reconstr Surg 1990;85:961–966.
Spear SL, Pelletiere CV, Menon N. One-stage augmentation combined with
mastopexy: aesthetic results and patient satisfaction. Aesthet Plast Surg
2004;28:259–267.
Spear SL, Seruya M, Clemens MW, et al. Acellular dermal matrix for the
treatment and prevention of implant-associated breast deformities. Plast
Reconstr Surg 2011;127:1047–1058.
Stevens WG, Calobrace MB, Cohen R, et al. Sientra high-strength cohesive
textured round implant technique: roundtable discussion. Aesthet Surg J
2015;35(S1):S11–S21.
Stevens WG, Freeman ME, Stoker DA, et al. One-stage mastopexy with
breast augmentation: a review of 321 patients. Plast Reconstr Surg
2007;120:1674–1679.
Stevens WG, Macias LH, Spring M, et al. One-stage augmentation
mastopexy: a review of 1062 simultaneous breast augmentation and
mastopexy procedures in 615 consecutive patients. Aesthet Surg J
2014;34:723–732.
Stevens WG, Nahabedian MY, Calobrace MB, et al. Risk factor analysis for
capsular contracture: a 5-year Sientra study analysis using round, smooth,
and textured implants for breast augmentation. Plast Reconstr Surg
2013;132(5):1115–1123.
Stevens WG, Spring M, Stoker DA, et al. A review of 100 consecutive
secondary augmentation mastopexies. Aesthet Surg J 2007;27(5):485–492.
Stevens WG, Freeman M, Stoker DA, et al. One-stage mastopexy with breast
augmentation: a review of 321 patients. Plast Reconstr Surg
2007;120(6):1674–1679.
Stevens WG, Stoker DA, Freeman ME, et al. Is one-stage breast
augmentation with mastopexy safe and effective? A review of 186 primary
cases. Aesthet Surg J 2006;26(6):674–681.
Tebbetts JB. Dual plane breast augmentation: optimizing the implant-soft
tissue relationships in a wide range of breast types. Plast Reconstr Surg
2001;107:1255–1272.
Tebbetts JB. Discussion: capsulorrhaphy revisited: a simple technique for
complex problems. Plast Reconstr Surg 2005;1(115):302.
Tebbetts JB, Adams WP. Five critical decisions in breast augmentation using
five measurements in 5 minutes: the high five decision support process.
Plast Reconstr Surg 2005;116:2005–2016.
Tebbetts JB, Teitelbaum S. High-and extra-high-projection breast implants:
potential consequences for patients. Plast Reconstr Surg 2010;126:2150–
2159.
Tebbetts JB. Breast implant selection based on patient tissue characteristics
and dynamics: the TEPID approach. Plast Reconstr Surg
2002;190(4):1396–1409; discussion 1410–1415.
CHAPTER 107

Breast Augmentation Mastopexy—


Safe and Simplified
ROD J. ROHRICH | AMY S. XUE
HISTORY
From its outset, the single-stage augmentation mastopexy is designed to
address the deflated, ptotic breast, where augmentation alone would result in
a high-riding implant with residual glandular and nipple ptosis, and
mastopexy alone would correct only the nipple position but frequently
accentuate the volume loss. Gonzalez-Ulloa (1) first described combining
subglandular augmentation using a prefabricated Polystan material with
concurrent mastopexy. Regnault described a similar one-stage technique
using the Cronin Silastic prostheses (2). Both aimed to achieve volume
expansion and nipple reposition in a single operation, and both reported good
outcomes.
Since its advent, the one-stage augmentation mastopexy gained significant
popularity, particularly in the early 2000s, and underwent many variations,
including evolution to the modern-day breast implants and mastopexy
techniques. However, with its popularity came the notoriety of being one of
the most litigated plastic surgery operations during that time. Complication
rate, as high as 21% (3), has been reported, with disastrous outcomes,
including complete loss of implant and tissue necrosis. This culminated in Dr.
Spear’s impassioned letter warning surgeons that the complication risk is
“not the sum … of the two individual parts but rather a substantially greater
risk when (the two procedures) are performed either at the same time or in
tandem” (4). His advice was “Surgeon, Beware.”
WHAT IS THE PROBLEM?
The difficulty lies in the need to carefully balance the expansive force of
augmentation with the reductive force of mastopexy, in the setting of
compromised blood supply. Due to this inherent mechanical contradiction,
the end goals of both procedures (volume and nipple position) become
unpredictable, particularly in the long run. Mastopexy tightens the envelope,
and makes the initial implant choice difficult. Depending on the size of the
implant, augmentation often lifts the nipple, which may be displaced further
in the long term as the weight of the implant bottoms out.
In addition, devascularization and denervation risks are both higher when
compared to each individual procedure due to need for more soft tissue
rearrangement. Infection risk is also expected higher for the same reason
(3,4). In 2006, Spear et al. reported a 10-fold increase in complications of
primary augmentation/mastopexy at 3-year follow-up when compared to
primary augmentation alone (5). Khavanin et al. demonstrated a pooled
complication rate of 13.1% in a meta-analysis of 4,856 cases, and a 10.7%
reoperation rate (3).
PRINCIPLES TO ENSURE SAFETY AND RELIABILITY
Due to these known issues, many surgeons opt for a more cautious staged
approach to management of the ptotic deflated breast. However, this requires
two separate procedures, and two separate general anesthesia, which is not
without its own risks. Over the past several years, many surgeons published
techniques to improve safety and reliability of the one-stage augmentation
mastopexy (6–9). Most advocate the need to be conservative in implant
choice, skin resection, and undermining. The one-stage procedure has since
become notably safer. There are several primary principles to keep in mind
when performing this operation (Table 107-1).

TABLE 107-1 Operative Details


Preoperative Considerations
Mild to moderate ptosis (<4-cm elevation) is favorable for single stage
Severe ptosis (>4-cm elevation), consider two stage
Implant selection no more than 300 cc
Operative Steps
Wise pattern with 8 cm vertical limb
Narrow splay angle
Wide central or inferior pedicle (8 cm)
Subpectoral pocket by splitting muscle
Thick medial and lateral skin flaps (2 cm)
Limited undermining

Clear Patient Expectation, Careful Selection


Due to the unique set of limitations associated with this operation, patient
selection and management of expectations are important to ensure that the
patient’s goal aligns with what can be safely accomplished. In essence, a
patient with concurrent breast ptosis and deflation chooses between size and
shape. If the patient prioritizes size and desires a large augmentation, a staged
procedure starting with augmentation as first stage is more appropriate, as a
larger implant would be needed, which would affect the degree of ptosis both
in the short term and long term. Any residual ptosis can be addressed in a
second stage.
The one-stage augmentation/mastopexy better serves patients who
prioritize restoration of shape. This population often presents seeking a
“breast lift.” Discussion must be clear that although mastopexy alone can
reposition the nipple and create a youthful-appearing breast shape, it cannot
reliably correct volume deflation, particularly not in the superior pole. An
implant would be necessary.
For patients requiring significant elevation of the nipple areolar complex
(>4 cm), a staged procedure starting with mastopexy should be strongly
considered to prevent perfusion-related complications. An augmentation can
be performed as needed in a second stage.
Precise Marking, Conservative Resection
Precise preoperative marking and intraoperative commitment to these
markings are necessary to optimize predictability of the outcome and
minimize intraoperative time. Marking (Fig. 107-1) includes a wide central
pedicle with Wise-pattern skin resection, which is often required for this
patient population, due to both horizontal and vertical excess in breast skin
envelope. The vertical limb is at least 8 cm in length with a narrow splay
angle hugging the areolar border to guarantee a conservative but adequate
skin resection. Nipple elevation should be less than 4 cm. To minimize
devascularization and associated wound healing complications, skin flaps
should be thick. Undermining should be as needed to allow tension-free
redraping and closure.
FIGURE 107- Preoperative marking.

Prudent Implant Selection, Subpectoral Placement


Selection of implant size should be conservative enough to provide superior
pole fullness, not for gross volume augmentation. Since the primary objective
of surgery is to reshape the breast to correct ptosis, mastopexy is performed
before augmentation. Therefore, the skin envelope after the mastopexy is the
true limitation to implant size. Preoperative selection is based upon breast
base width, and usually implants less than 300 cc are used. Some surgeons
favor performing augmentation first before mastopexy. In our experience,
this often leads to selection of a large implant that may not be appropriate for
the tissue envelope. A large implant limits tissue mobility, thereby
compromising the outcome of the mastopexy. In addition, large implants
exert more pressure on the overlying tissue, and may lead to perfusing
complications, poor healing, and more bottoming out in the long run.
Subpectoral placement of implant is performed by splitting the pectoralis
major longitudinally at the lateral two-third of the muscle. This allows
reliable control of the pocket without compromising blood supply to the
breast parenchyma and nipple (Fig. 107-2).

FIGURE 107-2 Subpectoral placement of implant.


FIGURE 107-3 New nipple position should be down and out intraoperatively (top left
and right). New nipple-to-inframammary fold distance is purposefully shortened by
1 to 2 cm to accommodate for postoperative elongation (bottom left and right) by 7
months. Notice that both the vector of the nipple and inferior pole length change
over time as well.
OUTCOME
Meta-analysis by Khavanin et al. (3) demonstrated a pooled total
complication rate of 13.12% (range 6.7% to 21.3%), among 15 large studies.
Tissue-related complications were the most common—recurrent ptosis
(5.2%), poor or hypertrophic scarring (3.74%), and postoperative asymmetry
of breast or nipple areolar complex (2.7%). Implant-related complications
included capsular contracture (3.0%), hematoma/seroma (2.8%), and
infection (0.93%). Among 13 studies, reoperation rate was found to be
10.65% (range 6.7% to 15.4%). The most common indications for
reoperation were tissue related, specifically recurrent ptosis and poor
scarring.
In our own study cohort of 171 patients, the most common reason for
reoperation was implant size exchange (4.7%), followed by scar revision
(2.9%) and capsular contracture (2.3%). There was no case of recurrent
ptosis. This is most likely attributable to the technique, focused upon
optimizing mastopexy first, then using a conservative implant to create
superior pole fullness.
In 62 patients, we assessed the postoperative distance from nipple to the
inframammary fold over time (mean follow-up of 15 months), and found that
this distance elongates by an average of 1.3 cm (range 1 to 2.3 cm). To
accommodate for this change, the new nipple position should take into
consideration this expected change (Fig. 107-3). As previously mentioned,
knowing that larger implants place more pressure on the skin, implant
selection should be less than 300 cc to avoid accentuating this elongation.
POSTOPERATIVE CARE
One-stage augmentation mastopexy is performed usually as an outpatient
procedure, but patients may stay overnight if other procedures are performed
concurrently. Drains are removed after output is less than 30 cc over a 24-
hour period, usually during the first postoperative visit. A supportive surgical
bra should be worn after surgery for approximately 6 weeks, after which
patients can transition to underwire bra provided healing is appropriate. There
are no restrictions to light activities, but strenuous activities and exercises are
avoided until 3 weeks after surgery.

CASES

CASE 1

A 48-year-old woman presented with deflated ptotic breasts, desiring


restoration of youthful breasts. She is a healthy, active individual, no
smoking history. She underwent one-stage augmentation mastopexy.
Central pedicle was utilized with Wise-pattern skin resection. Total of
112 g of breast tissue was resected from the right breast and 125 g from
the left. Smooth round 275-cc implants were placed in the subpectoral
plane for superior pole fullness. An abdominoplasty was performed
concurrently. Procedure was uncomplicated and she was discharged on
postoperative day 1 in excellent condition. Recovery was uneventful
(Fig. 107-4).
FIGURE 107-4 A–C: Patient is a 48-year-old woman presented with deflated ptotic breasts,
desiring restoration of youthful breasts. She underwent Wise-pattern augmentation mastopexy
with resection of 112 g and 125 g of breast tissue, and placement of 275-cc subpectoral implants
for superior pole fullness. Anterior, oblique, and lateral views are shown preoperative (left)
and 6 months postoperatively (right).
CONCLUSION
One-stage augmentation mastopexy can be reliable and safe when careful
preoperative planning is combined with conservative technique. Performing
mastopexy prior to placement of implant can optimize surgical outcome.

REFERENCES

1. Gonzalez-Ulloa M. Correction of hypotrophy of the breast by means of


exogenous material. Plast Reconstr Surg Transplant Bull 1960;25:15–
26.
2. Regnault P. The hypoplastic and ptotic breast: a combined operation
with prosthetic augmentation. Plast Reconstr Surg 1966;37(1):31–37.
3. Khavanin N, Jordan SW, Rambachan A, et al. A systematic review of
single-stage augmentation-mastopexy. Plast Reconstr Surg
2014;134(5):922–931.
4. Spear S. Augmentation/mastopexy: “surgeon, beware.” Plast Reconstr
Surg 2003;112(3):905–906.
5. Spear SL, Boehmler JH 4th, Clemens MW. Augmentation/mastopexy: a
3-year review of a single surgeon’s practice. Plast Reconstr Surg
2006;118(7 Suppl):136S–147S; discussion 148S–149S, 150S–151S.
6. Beale EW, Ramanadham S, Harrison B, et al. Achieving predictability
in augmentation mastopexy. Plast Reconstr Surg 2014;133(3):284e–
292e.
7. Spear SL, Dayan JH, Clemens MW. Augmentation mastopexy. Clin
Plast Surg 2009;36(1):105–115, vii; discussion 117.
8. Adams WP Jr, Spear SL. Augmentation mammaplasty. Plast Reconstr
Surg 2006;118(7 Suppl):5S–6S.
9. Davison SP, Spear SL. Simultaneous breast augmentation with
periareolar mastopexy. Semin Plast Surg 2004;18(3):189–201.
CHAPTER 108

Augmentation-Mastopexy With
Shaped or Round Implants, Is There a
Difference?
ROY DE VITA | ERNESTO MARIA BUCCHERI | AMEDEO VILLANUCCI
HISTORY
Since its introduction in 1960 by Gonzalez-Ulloa (1), augmentation-
mastopexy still remains a widely debated surgical procedure among plastic
surgeons worldwide. Despite the evolution of surgical techniques, it offers
different controversial aspects in which the decisional process needs to
balance the best possible aesthetic results with the least number of
complications. Augmentation-mastopexy is the procedure of choice in
presence of breast ptosis associated with parenchyma hypotrophy. At the
same time, it can refresh a beautiful breast shape and restore or, eventually,
increase breast volume. Usually, patients who request an augmentation-
mastopexy procedure are older patients, in whom the physiologic aging
process, multiple pregnancies, lactation, and weight fluctuations have led
simultaneously to loss of volume and breast shape. This procedure is still
considered difficult, due to the several potential complications and the
patients’ dissatisfaction in the postoperative period. One of the most disputed
issues relates to the use of round or shaped implants. Despite the large
amount of published data on their use in primary augmentation (2–6),
specific literature about the difference between round and shaped implants in
augmentation-mastopexy is lacking. Furthermore, a standardized decisional
algorithm does not exist. The surgeon often finds himself having to choose
the type of implant to use by relying only on his/her personal experience and
the patients’ preferences. This chapter describes our choice in the implant
decision-making process in order to address the patient’s wishes and to
reduce complications and revision surgeries. Our 10-year experience on the
“balcony technique” of breast augmentation and inverted T mastopexy and
the positive results (7) allow us to declare that the use of round high-
projection textured implant is our preferred choice.
PREOPERATIVE EVALUATION AND PLANNING
The first essential step to a correct planning of the procedure is a preoperative
consultation conducted by the plastic surgeon combined with the patients’
clinical examinations. The anamnestic data are recorded and the patients
should be asked for general health status, smoking habits, pregnancies and
lactations, weight history including fluctuation, major changes, and surgical
weight loss. Breast health evaluation should include past history of breast
cancer, abnormal mammograms, as well as a summary of previous surgeries,
if any. Surgeon should also ask the patient for self-awareness of any pre-
existing breast asymmetry and assess asymmetry grade by clinical
examination and preoperative photo documentation. All these assessments
will help in achieving the desired aesthetic goals and avoiding patient’s
dissatisfaction.
Preoperative markings are made with the patient in the upright position.
Firstly, the surgeon should outline the standard breast landmarks: sternal
notch, chest midline from sternal notch to xyphoid apophysis, breast
midlines, and inframammary folds (IMFs). A modified Wise keyhole pattern
customized for each patient is drawn on the skin. The distance from the
nipple to the sternal notch is measured and the postoperative position of the
nipple is determined by palpating the tissue from the middle of IMF and by
Pitanguy maneuver. The postoperative position of the nipple areolar complex
(NAC) is established at approximately 1 cm cranially to the anterior
projection of the IMF on the mammary meridian. The postoperative position
of the areola is marked as a circle (diameter of 45 mm) in which the center
corresponds to the new nipple position. Afterward, two vertical lines are
outlined from the ends of the neoareola to the convergence point between the
breast midline and the IMF, with the breast respectively displaced medially
and laterally. Pillars’ length for the vertical mastopexy component is set at
6.5 to 7.5 cm. The more the breast is pushed medially and laterally, the wider
the distance between the pillars will result and the greater the skin amount
removed. These vertical limbs are linked inferiorly to the IMF markings by
horizontal branches. Implant volume is determined for each patient in
accordance with the desired cup size and the breast/thoracic measurements
(width and height of breast base, thoracic circumference, jugular-to-nipple
distance, nipple-to-nipple distance, and nipple-to-IMF distance).
OPERATIVE TECHNIQUE
Procedure is performed under general anesthesia, with the patient in a semi-
seated position and abducted arms. The skin incisions are conducted by
retracing the preoperative design. The NAC is marked with a 45-mm–
diameter circle and then incised along this marking. The modified Wise
pattern is deepithelialized, with attention to avoid the NAC. The apex of the
inferior flap is incised at the base of the medial and lateral pillars of the Wise
pattern and below the NAC pedicle. Subsequently, a thin dermoglandular flap
is raised up to reach the pectoralis fascia plane. The inferior flap comprising
breast parenchyma of the lower pole is supplied by the fifth and sixth
intercostal perforators. Then, a subglandular pocket is created to contain the
high-projection textured round implant. Concerning this surgical step, we
stress the recommendation of leading dissection along the correct suprafascial
plane, in order to reduce post-operative bleeding and the likely formation of
seromas. We also recommend using long and narrow retractors equipped with
a cold light source to easily conduct dissection at the upper pole. The width
of the implant pocket is a critical aspect since it has an important impact on
the esthetic outcome: A pocket too narrow will not allow a correct
remodeling of the mammary tissues and will not comfortably accommodate
the implant while on the other hand, a pocket too wide exposes to the risk of
implant malposition and displacement difficult to correct, even by using the
appropriate dressings.
The NAC is mobilized and repositioned as a superolateral or superomedial
pedicle and medial and lateral pillars are sutured on the vertical line to
provide breast parenchyma reshaping and to create the definitive implant
pocket. Once the implant is inserted into the pocket, the inferior flap is
sutured laterally and medially to the pectoralis major fascia with absorbable
2-0 undyed poliglecaprone-25 sutures in a balcony fashion to provide implant
support and lower pole coverage; the pectoralis major muscle remains
therefore untouched. When necessary, in the event of too long inferior flap, it
could be resected at the upper edge to a length of 4 to 7 cm. In all patients
suction drains were routinely positioned into the implant pocket that emerged
from the skin 2 cm laterally to the lateral end of the horizontal component of
inverted T mastopexy. The vertical and horizontal incisions are closed with
absorbable 3-0 undyed poliglecaprone-25 sutures as single intradermal
stitches while the NAC incision is closed with nylon 4-0 sutures as single
dermal–epidermal stitches.
POSTOPERATIVE CARE
A compression dressing with gauze and cotton is applied immediately after
the surgery. Then, within 24 hours postoperatively, the dressing is replaced
with a sports bra which the patients are advised to continue wearing for 6
weeks. Patients are discharged with a prescription for oral analgesics and a
full course of oral antibiotic prophylaxis after 1 or 2 nights of hospital stay.
Drains are left in place until the first follow-up visit, usually scheduled 3 to 5
days after the surgery. Antibiotic prophylaxis is discontinued after the drain
removal at the first follow-up visit if the amount of fluid collected is <50 mL
within the 24 hours. Further follow-up visits and photograph are scheduled at
1, 3, 6 months, and 1 year postoperatively. A complete case is reported as
shown in Figure 108-1A–I.

CASES

CASE 1

In Figure 108-1, a 32-year-old woman is shown a second degree of


ptosis and hypotrophic breasts post breastfeeding preoperative (Fig. 108-
1A–C) and postoperatively (Fig. 108-1D–I).
FIGURE 108-1 A: Preoperative frontal view, a 32-year-old woman with a second degree of
ptosis and hypotrophic breasts post breastfeeding. B: Preoperative three-quarter right side
(same patient). C: Preoperative lateral right side (same patient). D: Six months postoperatively
frontal view, the balcony technique was used with high-projection round implant in a
subglandular positioning. E: Six months postoperatively three-quarter right side. F: Six
months postoperatively lateral right side. G: Two years postoperatively frontal view. H: Two
years postoperatively three-quarter right side. I: Two years postoperatively lateral right side.
OUTCOMES
Breast augmentation with mastopexy is a combination of two surgical
procedures seemingly antithetic: breast volume expansion by means of
implant placement and reduction of the soft tissue envelope by the excision
and redraping of skin and parenchyma. It can restore a youthful, naturally
shaped breast in case of moderate to severe breast ptosis with hypotrophy
when preoperative planning and intraoperative techniques are appropriate.
Conversely, surgeon’s inaccuracy could be paid with a considerable increase
in complications and unpleasant aesthetic results. Breast augmentation alone
is a relatively simple operation that involves placement of an implant beneath
breast tissues. Relatively few short-term complications are associated with
breast augmentation. Likewise, mastopexy alone is an equally linear
procedure and involves reshaping the breast, repositioning the nipple
superiorly, and redraping, repositioning, and/or removing the excess skin.
Complications associated with mastopexy are also uncommon and include
undesirable or unattractive scarring, nipple malposition, and recurrent ptosis.
Augmentation and mastopexy each render the other procedure more difficult
and together increase the likelihood of complications beyond that of either
procedure alone (8). An error in the preoperative decision-making process
can lead to a high rate of postoperative complications, greater patient
dissatisfaction, and consequent increased number of secondary correction
procedures. Given its dichotomy, that is, increasing volume and reducing and
redraping breast tissues, when performed as single-stage procedure, the
pivotal issue becomes controlling both implant- and tissue-related
complications in a single operation (9).
Undoubtedly, a key point in the decision-making process during the
preoperative planning concerns the implant choice and its plane location.
Modern fifth-generation devices are the result of several innovations which
have helped to optimize performance. They relate to implant filler material
(form-stable gels), surface structure (various forms of texturization), and
shape (including both round and anatomical implants). These three key
properties should always be considered during the implant selection process
for breast aesthetic surgery, in addition to the specific dimensions of the
implant, as the goals of breast aesthetic surgery should be more about
proportion and shape than merely volume (10). Choosing implant shape,
round or anatomical, is one of the most essential and yet controversial
decisions in cosmetic breast augmentation-mastopexy. Many surgeons
choose implant shape based on their personal experience or expert opinion
(11). Although several experiences reported implant choice in breast
augmentation, literature lack publications specifically looking at shaped
versus round implants in augmentation-mastopexy patients (12). We believe
that good aesthetic outcomes and high patients’ satisfaction from our
“balcony technique” of breast augmentation and inverted T mastopexy are
determined mainly by the standardization of the surgical technique combined
with the systematic use of round implants. Firstly, the advantage of using
round implants in this operation relates to the type of patients that require this
procedure. Usually these are patients who previously had primarily
medium/large and tonic breasts before their ptotic and hypoplastic evolution.
Therefore, in these cases adequate implant coverage provided by breast
tissues is guaranteed to the point of making the use of shaped implant useless.
Moreover, such patients usually request for greater upper pole fullness to
restore youthful and well-contoured breasts. As stated in literature (10),
patient’s desire is one of the key factors in the decision-making process about
implant choice in breast augmentation. Patients may require a natural
appearance but have very different ideas about what that actually means and
some of them request for an “augmented” appearance or oversized breast
with accentuated upper pole. According to our experience, patients with
hypotrophic and ptotic breast who are candidates for “balcony technique”
expressly ask the surgeon for greater upper pole fullness and we believe that
this goal is always guaranteed by the use of round implants. Although there is
lack of literature concerning the use of round versus anatomical implant in
the setting of augmentation-mastopexy, the same literature is full of studies
about the advantages of round versus anatomical implants in primary breast
augmentation to achieve greater upper pole fullness. Therefore, from the
experience reported in literature about augmentation, we can state that the
same principles are applicable to augmentation-mastopexy. Moreover, with
regard to the exclusive use of round implants in augmentation with inverted T
mastopexy, we must say that the relationship between implant and implant
pocket provides a further argument in favor. In this case, the implant pocket
has to be necessarily wider than the real needs with respect to the real size of
the preoperatively designed implant. This is because we need to provide a
remodeling of the glandular flaps that will be placed above the implant.
Reshaped flaps must fall softly on the implant surface and it must fit a little
more comfortable into the pocket. Therefore, the surgeon needs to provide a
greater opening and a wider pocket. This will result in a pocket larger than
necessary accordingly to the real implant volume and in a greater tissue
dissection and dead spaces with possible and potential formation of serum.
Moreover, without any doubts, achieving pocket control for the surgeon is
not simply with dead and wider spaces. In this setting, round implants
guarantee us that we will have no problems, even in the long-term follow-up,
with regard to possible rotations since periprosthetic fluid collection is well
documented in relation to implant rotation (13–16). Just as we have no doubts
about round implants’ use in augmentation-mastopexy we are equally
confident in stating that subglandular positioning is to be preferred over the
submuscular techniques. In fact, consequences of submuscular positioning
are well-described entities: animation deformity, waterfall effect, implant
malposition, and muscle strength reduction (17–20). All of these above-
mentioned occurrences cause frequent patient dissatisfaction and high rates of
reintervention. Furthermore, patients who undergo augmentation-mastopexy
usually have a pinch test appropriate at the upper pole and consequently no
need for further implant coverage.
Since the interaction between the patient’s tissues and the implant
placement is not completely predictable preoperatively, there is another main
challenging step for the surgeon in the procedure planning: calculate the
proper amount of excess skin to be removed. Excessive skin removal can
result in a tensioned suture that leads to a considerable increase in
complications due to reduced blood supply. These complications include skin
and/or NAC necrosis, surgical dehiscence, and the formation of unsightly
scars and unpleasing results. On the other hand, a hypocorrection can lead to
unsatisfactory esthetic results such as bottoming out of the implant and ptosis
recurrence. In our experience, we did not encounter serious complications:
the low complication rate from our highly standardized balcony technique
proves that augmentation and mastopexy can be performed safely. All
patients underwent reduction of the skin envelope by a customized, modified
Wise keyhole pattern and received high-projection textured round implants in
the subglandular plane. This technique sets a standard for the maximum
amount of tissue to be resected in simultaneous augmentation-mastopexy of
severely hypotrophic ptotic breasts. A chief complication of the Wise keyhole
pattern of skin resection is the dehiscence at the union of the vertical and
horizontal incisions. This point is even more vulnerable when this lift
technique is combined with augmentation because the presence of the
implant and the subsequent stress affecting the breast tissues reduce the blood
supply to breast tissues and increase the risk of dehiscence, fat necrosis, or
even extrusion. In our balcony technique, the inferior dermoglandular flap
increases lower pole coverage, providing two tissue layers of protection at the
weakest point of the incision. Any dehiscence at the inverted T junction, even
if simply caused by excessive manipulation of thin skin flaps, would not
hesitate in exposure or extrusion of the implant. Recurrent ptosis is also a
common complication of augmentation-mastopexy. While persistent ptosis is
defined as ptosis in the early postoperative period and it is a condition
attributable essentially to an improper surgical technique, breasts with
recurrent ptosis are well contoured in the early postoperative period but they
bottom out 6 or more months after surgery. In our experience we reported
long-lasting result and a very few cases of implant bottoming out. This is
mainly due to the features of the inferior dermoglandular flap. It not only
provides implant coverage and protection but also enables suspension and
stability of the implant against gravity. One of the most common concerns
regarding any inverted T mastopexy relates to the greater number of scars it
produces. Many authors have described procedures for short-scar mastopexy
plus implantation to treat patients with mild to moderate breast ptosis and
hypoplasia. These mastopexy techniques involve a round block scar, an
inverted teardrop scar, or a J scar plus implantation to lift the NAC. The so-
called “scar wars” debate has led some investigators to conclude that an
inverted T incision and implantation allow for appropriate skin redraping and
yield upper pole fullness, thus constituting the best treatment for grade II or
III ptosis and glandular hypotrophy. Furthermore, the Wise incision pattern in
a customized fashion allows for a symmetric postoperative contour for
patients with preoperative breast asymmetry and this ensures a good control
of the breast volume and shape.
CONCLUSION
Augmentation-mastopexy with shaped or round implants, is there a
difference? The question remains unanswered, therefore further comparative
studies are required. As mentioned above, the implant choice to use in this
type of procedure still lies on surgeon’s personal experience and in patient’s
preference. According to our experience, in order to avoid complications
from the use of shaped implant, especially implant rotation, and to provide
the best upper pole fullness, we suggest the use of high-projection round
implants and we do not consider at all shaped implants useful regarding
augmentation-mastopexy. Moreover, we undermine that achieving pocket
control for the surgeon is not really simple in mastopexy with consequent
dead and wider spaces. We also advocate using a round implant with
mastopexy because when compared to anatomic implants, the results are
superimposable when the skin pinch test is greater than 2 cm.

REFERENCES

1. Gonzalez-Ulloa M. Correction of hypotrophy of the breast by means of


exogenous material. Plast Reconstr Surg Transplant Bull 1960;25:15–
26.
2. Hidalgo DA, Weinstein AL. Intraoperative comparison of anatomical
versus round implants in breast augmentation: a randomized controlled
trial. Plast Reconstr Surg 2017;139:587–596.
3. Montemurro P, Cheema M, Hedén P, et al. Do not fear an implant’s
shape: a single surgeon’s experience of over 1200 round and shaped
textured implants in primary breast augmentation. Aesthet Surg J
2018;38(3):254–261.
4. Al-Ajam Y, Marsh DJ, Mohan AT, et al. Assessing the augmented
breast: a blinded study comparing round and anatomical form-stable
implants. Aesthet Surg J 2015;35(3):273–278.
5. Friedman T, Davidovitch N, Scheflan M. Comparative double blind
clinical study on round versus shaped cohesive gel implants. Aesthet
Surg J 2006;26(5):530–536.
6. Bengtson BP, Van Natta BW, Murphy DK, et al; Style 410 U.S. Core
Clinical Study Group. Style 410 highly cohesive silicone breast implant
core study results at 3 years. Plast Reconstr Surg 2007;120(7 Suppl
1):40S–48S.
7. de Vita R, Zoccali G, Buccheri EM. The balcony technique of breast
augmentation and inverted-T mastopexy with an inferior
dermoglandular flap. Aesthet Surg J 2017;37(10):1114–1123.
8. Spear SL. Augmentation/mastopexy: “Surgeon, beware.” Plast Reconstr
Surg 2006;118(Suppl):133S–134S; discussion 135S.
9. Doshier LJ, Eagan SL, Shock LA, et al. The subtleties of success in
simultaneous augmentation-mastopexy. Plast Reconstr Surg
2016;138(3):585–592.
10. Hedén P, Montemurro P, Adams WP Jr, et al. Anatomical and round
breast implants: how to select and indications for use. Plast Reconstr
Surg 2015;136(2):263–272.
11. Cheng F, Cen Y, Liu C, et al. Round versus anatomical implants in
primary cosmetic breast augmentation: a meta-analysis and systematic
review. Plast Reconstr Surg 2019;143(3):711–721.
12. Sarosiek K, Maxwell GP, Unger JG. Getting the most out of
augmentation-mastopexy. Plast Reconstr Surg 2018;142(5):742e–759e.
13. Montemurro P, Papas A, Hedén P. Is rotation a concern with anatomical
breast implants? A statistical analysis of factors predisposing to rotation.
Plast Reconstr Surg 2017;139(6):1367–1378.
14. Maxwell GP, Scheflan M, Spear S, et al. Benefits and limitations of
macrotextured breast implants and consensus recommendations for
optimizing their effectiveness. Aesthet Surg J 2014;34:876–881.
15. Brink RR. Sequestered fluid and breast implant malposition. Plast
Reconstr Surg 1996;98:679–684.
16. Sieber DA, Stark RY, Chase S, et al. Clinical evaluation of shaped gel
breast implant rotation using high-resolution ultrasound. Aesthet Surg J
2017;37(3):290–296.
17. Dyrberg DL, Bille C, Gunnarsson GL, et al. Breast animation deformity.
Arch Plast Surg 2019;46(1):7–15.
18. Frame J. The waterfall effect in breast augmentation. Gland Surg
2017;6(2):193–202.
19. Roxo AC, Nahas FX, Pinheiro Rodrigues NC, et al. Functional and
volumetric analysis of the pectoralis major muscle after submuscular
breast augmentation. Aesthet Surg J 2017;37(6):654–661.
20. Moliver CL, Sanchez ER, Kaltwasser K, et al. A muscular etiology for
medial implant malposition following subpectoral augmentation. Aesthet
Surg J 2015;35(7):NP203–NP210.
CHAPTER 109

Avoiding Pitfalls With Mastopexy–


Augmentation
ALI A. QURESHI | W. GRANT STEVENS
HISTORY
Despite publications dating back to the late 1970s about mastopexy–
augmentation, in 2003, Spear published “Augmentation/Mastopexy:
‘Surgeon, Beware’” reminding plastic surgeons of the challenges and risk of
a simultaneous procedure. Mastopexy seeks to rejuvenate the ptotic breast by
reducing the skin envelope and raising the nipple areola complex (NAC) into
a more youthful position (1). Augmentation with an implant volumizes the
deflated breast and can provide structure to an amorphous breast. The
procedures, when performed simultaneously, are riskier because the skin
envelope is being reduced while the breast is being made larger. Without
careful attention, there can be devastating consequences for NAC survival
and the overall aesthetics of the breast. The convention had been and remains
for some, to stage all cases of the ptotic, volume depleted breast, performing
the mastopexy separate from the augmentation in no particular order.
Since that time, we and others have published a series of single stage
mastopexy–augmentation demonstrating safety and predictability of results
with careful planning and patient selection. In a two-stage procedure, there
are by definition two separate operations: the mastopexy and the
augmentation. Either one of these can have revisions, leading to potentially
more revisionary surgery. In the series published by Stevens et al., the
revision rates were between 8.6% and 16.9% (2–4). Calobrace et al. also
published a series with a revision rate of 23.2% (5).
Only recently, a meta-analysis of 23 studies found an overall complication
rate of 13.1% for mastopexy–augmentation and a 10.65% reoperation rate
(6,7). Complications assessed included: recurrent ptosis (5.2%), poor scarring
(3.74%), capsular contracture (2.97%), asymmetry (2.94%), seroma (1.42%),
hematoma (1.37%), and infection (0.93%) (6,7). Proponents of single stage
mastopexy–augmentation argue that the rates of reoperation and revision are
less than the guaranteed 100% two-surgery rate for a two stage mastopexy–
augmentation.
Secondary mastopexy–augmentation is a mastopexy–augmentation that is
performed after a prior breast augmentation, mastopexy, breast reduction,
mastopexy–augmentation, and mastectomy/lumpectomy (8).
With the paradigm shift toward single-stage mastopexy–augmentation, we
review our experience, tips, and insights to help plastic surgeons achieve
consistent, safe results with breast rejuvenation and deal with common
pitfalls of this procedure. We also review pearls of secondary mastopexy–
augmentation.
INDICATIONS
Mastopexy–augmentation is most commonly used to rejuvenate the volume
depleted and ptotic breast. It can also be used in cases of tuberous breast
deformity, which is beyond the scope of the present chapter and may be done
in stages.
Revisions of a mastopexy–augmentation can be due to “tissue-related” or
“implant-related” issues (Fig. 109-1) (3,4,8). Tissue-related issues include
recurrent ptosis, pseudoptosis, and unacceptable scarring. Implant-related
issues include capsular contracture and implant malposition.
Indications for revision in our experience have included saline implant
deflation, desired change in implant size, recurrent ptosis, poor scarring,
areolar asymmetry, implant malposition, capsular contracture (grade III/IV),
implant infection, and implant rippling. We review here some of the more
challenging complications and revisions to deal with in mastopexy–
augmentation.
CONTRAINDICATIONS
Revisionary mastopexy–augmentation is offered to patients who understand
that these procedures often require maintenance as the operated breast ages
and the implant undergoes changes as well. Relative contraindications would
be if patients are unwilling to accept the risks inherent to a revisionary
procedure like this. It is our practice to obtain a mammogram within 1 year of
the surgical date. Imaging including MRI can be helpful in identifying a
possible implant rupture.

FIGURE 109- Pitfalls of mastopexy–augmentation include “tissue related” and/or


“implant-related” issues including capsular contracture (A), bottoming out (B), and
poor scaring (C).
PREOPERATIVE PLANNING
As with any surgery, it is important for the surgeon to understand the goals of
the patient and how the patient defines a successful outcome. This involves
all aspects of surgery including pain, downtime, resuming work and activities
like when patients can pick up their kids and go to the gym, scar burden, size,
and shape. It is always important to clarify questions like which plane of
implantation is acceptable and what would be too big/too small for the
patient, as patients’ thoughts may have changed from the time of initial
consultation. This is especially important in patients who are undergoing
revisionary or secondary mastopexy–augmentation because they may have
positive or negative experiences in the past that have led the patient to you as
their surgeon.
Tissue-based planning is important and can help lead to predictable
outcomes with natural results, even in secondary mastopexy–augmentation.
Standard measurements include: sternal notch to nipple (S-N), nipple to IMF
(N-IMF), internipple distance, and base width. We also measure sternal notch
to IMF (S-IMF) distance, which others may not be accustomed to measuring.
The difference between S-N and S-IMF determines how much the nipple
elevation is required. For example, a woman with grade III ptosis who has an
S-N distance of 32 and an S-IMF distance of 26 needs 6 cm of nipple
elevation. In general, the more the nipple needs to be elevated the greater the
lower pole of the breast will be reduced in its horizontal and vertical
dimensions and the greater the scar burden overall. Even in revisionary
procedures, we most commonly use the dual-plane technique for
augmentation, though subfascial augmentations will be performed in patients
unwilling to have the implant behind their muscle.
When marking, we place the nipple position at the level of the IMF and no
higher than this landmark. A “mosque” design or circumvertical pattern is
drawn. The vertical limbs are drawn with a width commensurate with the
expected amount of skin removal, though this is often a conservative width
since more skin can always be excised after the augmentation step. In
general, the vertical limbs are drawn with a goal length of 7 to 9 cm from N-
IMF. Expected dog ear excisions are then drawn out at the base in which the
vertical length is reduced with a horizontal skin excision between the new
and old IMF.
OPERATIVE TECHNIQUE
All our mastopexy–augmentations are done using a tumescent technique that
has been described previously. We inject 250 cc of normal saline solution
containing 1 mg of epinephrine and 30 cc of 2% lidocaine. The tumescent is
injected in the intradermal plane of the planned incisions and beneath the
areola. Most commonly a circumvertical pattern is used with a superior
pedicle for the NAC regardless of whether the previous pedicle is known or
unknown. It is important to leave a wide enough dermoglandular pedicle to
ensure both adequate arterial inflow and venous outflow. In general,
dissection is carried out sharply with a blade and electrocautery is used for
hemostasis and subpectoral dissection, when necessary. When possible, we
leave a cuff of breast tissue where the “T” junction will be for wound healing
purposes and to reduce the likelihood of exposed implant if there is delayed
healing there.
CAPSULAR CONTRACTURE
The management of capsular contracture is beyond the scope of the present
chapter and is not unique to mastopexy–augmentation. A controversial topic,
the management of grades III and IV capsular contracture includes open
capsulotomy, partial to total capsulectomy, and creation of neo-subpectoral
pockets. Some advocate the use of acellular dermal matrices as well.
However, regardless of management of the capsule, the literature supports
exchanging an old for a new implant has lower rates of recurrent capsular
contracture. Many times capsular contracture is associated with a known or
silent rupture.
In our experience, grade IV capsular contracture with rupture may benefit
from partial or total capsulectomy. However, an alternative in grades III and
IV capsular contracture without rupture is open capsulotomies and implant
replacement with new implants. Usually this involves superomedial
capsulotomy and inferior capsulotomy with radial scores of the lower pole
which can become constricted and push the implant upward. Maintaining the
capsule may help maintain blood supply to the tissues and NAC, which is
critical in a secondary mastopexy–augmentation. With less dissection and
raw surface of tissues, there is often less bleeding which is thought to
increase risk of recurrent capsular contracture. Regardless of technique,
drains are not standardly used in revisionary mastopexy–augmentation.
IMPLANT MALPOSITION
Most commonly superior implant malposition is because of a grade III/IV
capsular contracture that can be improved with capsular management at the
discretion of the surgeon. However, inferior implant malposition may be a
more involved operation. Often inferior malposition happens from the weight
of the implant and attenuation of the inframammary fold.
Several techniques have been described for inferior im-plant malposition.
In a revisionary mastopexy–augmentation, tissue support devices like
acellular dermal matrices and mesh can be used to address inferior implant
malposition (9,10). In general, these repairs appear to have more durability
than suture repair and capsular manipulation, likely because they provide
greater counter tension to the gravity of the implant and native breast tissue
weight.
In our experience, symmastia is not an issue when a dual-plane technique
is used at the time of a primary mastopexy–augmentation. However, lateral
malposition may occur in larger implants or attenuated tissues. We most
commonly use a lateral capsulorrhaphy or “popcorn” technique to reduce the
size of the lateral pocket with good outcomes. Tissue support devices have
been rarely necessary for lateral implant migration in our experience but can
be sewn to the free edge of the pectoralis muscle and then tacked down
laterally to create a smaller pocket. Alternatively, a neo-subpectoral pocket
can be developed which would create a smaller pocket for a new implant in
revisionary mastopexy–augmentation.
RECURRENT PTOSIS
The most common long-term sequelae after mastopexy–augmentation is
recurrent ptosis. The rate at which ptosis can recur depends on the size of the
implant, fluctuations in body weight, and normal aging. If a patient has
breastfed after a mastopexy–augmentation, this may accelerate the aging
process of the operated breast.
In general, the ptosis needs to be evaluated carefully and differentiated
from pseudoptosis and implant malposition. Accurate diagnosis will guide
the operative plan and lead to better outcomes and results.
When there is pseudoptosis, the gland and the implant may be mostly
below the IMF and typically the N-IMF distance is greater than the 7 to 9 cm
set at the time of surgery. In such a situation, we perform a “smile
mastopexy” in which a horizontal elliptical excision is performed to reduce
the vertical height of the N-IMF distance.
Commonly, the pseudoptotic breast has expanded in the horizontal
dimension as well. The breast may benefit from a vertical elliptical excision
of skin as well. This can also be used to revise the vertical scar which may
have widened with time. When both a vertical and horizontal skin excision is
performed without an incision around the areola, we call this a “sailboat
mastopexy.”
UNACCEPTABLE SCARRING
Many patients who have poor scarring or contour irregularities previously
had a periareolar or circumareolar approach for a previous augmentation or
mastopexy–augmentation. In our experience, these scars are why a
periareolar or circumareolar approach is rarely our first choice for a primary
mastopexy–augmentation.
Revision mastopexy–augmentation in patients who have unacceptable
scarring should also be inquired about their previous healing. Commonly,
patients will report suture reaction, sensitivity to tape and glue or wound or
previous permanent suture that extruded.
To reduce unacceptable scarring, the basic principles of plastic surgery
must be adhered to. A layered, tension-free closure cannot be
overemphasized. The surgeon must understand the soft tissue dynamics as
well as the weight and size of the implant when assessing tension at the time
of closure. This may necessitate downsizing the implant if the soft tissue
envelope is too tight. Careful and thoughtful preoperative counseling with the
patient is critical to ensuring a good outcome and a size the patient still finds
acceptable.
INTRAOPERATIVE CARE
Routine perioperative antibiotics are administered. Meticulous, blood-free
dissection is the goal for augmentation. Lap pads are also not placed into the
pocket to minimize debris in the pocket. These precautions are taken to
reduce the risk of capsular contracture. Tension in the closure should be
addressed in the deep layers of breast parenchymal closure and not at the
level of the dermis or subcuticular closure. We do not use permanent sutures
in our closure.
POSTOPERATIVE CARE
Patients are placed in a lightly compressive wrap immediately after surgery
and transitioned into a surgical bra on postoperative day 1. Overly aggressive
compression can impede venous outflow to the NAC, the same way a
compressive dressing would to a fresh free flap.
Patients are to avoid heavy lifting for about 2 weeks after surgery and
gradually resume their normal activities of daily living. Vigorous exercise
and upper body weightlifting are discouraged until the first month after
surgery. Patients’ transition into an underwire bra depends on their healing
between weeks 2 and 4.

CASES
CASE 1

This 36-year-old woman (Fig. 109-2) previously had circumareolar


mastopexy–augmentation with subglandular saline implants. At the time
of presentation, she had two implant-related issues. On the left she had a
spontaneous deflation and on the right she had a grade IV capsular
contracture. To manage these complications, she had a secondary
mastopexy–augmentation. A circumvertical technique was used and a
pocket change was performed from subglandular to dual plane. Implants
were changed to 350 cc round, smooth highly cohesive silicone implants.
FIGURE 109-2 Circumvertical mastopexy with removal and replacement of implants.

CASE 2

This 40-year-old woman (Fig. 109-3) previously had a primary breast


augmentation through a periareolar approach in a dual plane by another
provider. She presented with dissatisfaction of the contour of her scar and
lower pole of the breast and ptosis. She underwent a circumvertical
mastopexy with removal and replacement of her implants to address these
tissue-related issues.
FIGURE 109-3 Patient with a third mastopexy–augmentation with a sailboat mastopexy, in
which the vertical and horizontal dimensions of the lower pole were reduced without a new
incision around the areola.

CASE 3

This 32-year-old woman (Fig. 109-4) previously had a breast


augmentation and a secondary mastopexy–augmentation developed right-
sided capsular contracture along with pseudoptosis and stretching of the
lower pole of the breast. She underwent a third mastopexy–augmentation
with a sailboat mastopexy, in which the vertical and horizontal
dimensions of the lower pole were reduced without a new incision around
the areola. She also had capsulotomies and implant removal and
replacement with new but same sized implants.

FIGURE 109-4 Breast augmentation and a secondary mastopexy–augmentation developed


right-sided capsular contracture along with pseudoptosis and stretching of the lower pole of the
breast.

CASE 4

This 63-year-old woman (Fig. 109-5) previously had a mastopexy–


augmentation with silicone implants in a subglandular plane. She
developed capsular contracture and pseudoptosis bilaterally. She
underwent a circumvertical mastopexy–augmentation with capsulotomies
and implant removal and replacement.

FIGURE 109-5 Mastopexy–augmentation with silicone implants in a subglandular plane.


GENERIC RISKS
The most feared complication after revisionary mastopexy–augmentation is
NAC necrosis, partial or complete. Careful dissection and leaving an
adequate dermoglandular pedicle for the NAC is critical, regardless of
whether the previous pedicle is known or unknown. In our experience, using
a superior pedicle and the technique described has never led to a case of
complete NAC necrosis. Occasionally, venous congestion can occur and
there may be partial areolar skin loss. When this happens, proper wound care
and patient counseling is critical. While the temptation may be to surgically
debride the marginalized areola, we have found better long-term
pigmentation and outcomes with secondary wound healing. If the circular
contour of the areola becomes compromised after wound healing occurs, then
a small revisionary procedure under local to restore the circular areola can be
performed.
OUTCOMES
The literature, including reports by Stevens et al. and Calobrace et al.,
demonstrate revision rates were between 8.6% and 23.2% for single-stage
mastopexy–augmentation (2,3,5). Tissue-related revisions in combined
mastopexy–augmentation versus mastopexy alone were 5.4% versus 8.6%.
Implant-related revisions in combined mastopexy–augmentation versus
augmentation alone were 11.2% versus 13%. Circumareolar mastopexies
accounted for 24% of cases in our series but 39% of revisions, making this a
less favorable operation (8).
A review of 100 consecutive outpatient secondary mastopexy–
augmentations with average 3.5-year follow-up was performed by Stevens et
al. (8). Patients previously had a breast augmentation (70%), biopsy or
lumpectomy (15%), augmentation-mastopexy (13%), reduction (5%),
mastopexy (3%), or reconstruction (2%). Thirty-six percent had two or more
previous breast surgeries. The indications for secondary mastopexy–
augmentation were capsular contracture (33%), asymmetry (22%), implant
deflation or rupture (11%), implant size change (6%), implant rippling (3%),
or poor scarring (3%). All patients had ptosis.
CONCLUSION
Secondary mastopexy–augmentation is a challenging and rewarding
operation. Accurate diagnosis of “tissue-related” versus “implant-related”
issues will dictate an operative plan that will lead to durable long-term
results. The most feared complication of complete NAC necrosis can be
avoided with careful dissection and planning.

REFERENCES

1. Qureshi AA, Myckatyn TM, Tenenbaum MM. Mastopexy and


mastopexy-augmentation. Aesthet Surg J 2018;38(4):374–384.
2. Stevens WG, Freeman ME, Stoker DA, et al. One-stage mastopexy with
breast augmentation: a review of 321 patients. Plast Reconstr Surg
2007;120(6):1674–1679.
3. Stevens WG, Macias LH, Spring M, et al. One-stage augmentation
mastopexy: a review of 1192 simultaneous breast augmentation and
mastopexy procedures in 615 consecutive patients. Aesthet Surg J
2014;34(5):723–732.
4. Stevens WG, Stoker DA, Freeman ME, et al. Is one-stage breast
augmentation with mastopexy safe and effective? A review of 186
primary cases. Aesthet Surg J 2006;26(6):674–681.
5. Calobrace MB, Herdt DR, Cothron KJ. Simultaneous
augmentation/mastopexy: a retrospective 5-year review of 332
consecutive cases. Plast Reconstr Surg 2013;131(1):145–156.
6. Khavanin N, Jordan SW, Rambachan A, et al. A systematic review of
single-stage augmentation-mastopexy. Plast Reconstr Surg
2014;134(5):922–931.
7. Gupta V, Yeslev M, Winocour J, et al. Aesthetic breast surgery and
concomitant procedures: incidence and risk factors for major
complications in 73,608 cases. Aesthet Surg J 2017;37(5):515–527.
8. Stevens WG, Stoker DA, Freeman ME, et al. Mastopexy revisited: a
review of 150 cases for complications and revision rates. Aesthetic Surg
J 2007;27(2):150–154.
9. Maxwell GP, Gabriel A. Acellular dermal matrix for reoperative breast
augmentation. Plast Reconstr Surg 2014;134(5):932–938.
10. Adams WP Jr, Moses AC. Use of poly-4-hydroxybutyrate mesh to
optimize soft-tissue support in mastopexy: a single-site study. Plast
Reconstr Surg 2017;139(1):67–75.
CHAPTER 110

Management of Recurrent Ptosis


Following Augmentation Mastopexy
M. BRADLEY CALOBRACE | CHET MAYS
HISTORY
The treatment of the ptotic breast can be complex with the technique and
ultimate result dependent on a variety of factors. When a mastopexy is
deemed necessary, this can be performed alone or in conjunction with
placement of a breast implant. Mastopexies alone are often inadequate to
achieve the aesthetic goals of the patients, both in terms of volume and
fullness in the upper pole. The addition of an implant in an augmentation
mastopexy can provide stability of the results over time compared to a
mastopexy alone.
It cannot be overstated that appropriate patient selection and perioperative
planning along with optimal surgical technique contributes significantly to
the long-term success of the procedure. Much attention is often given to the
mastopexy approach, whether it is periareolar, vertical, or inverted T.
However, potentially even more impactful in the results is consideration for
the type of implant to be placed and the pocket selected to optimize long-term
success. It is likewise these decisions and operative techniques that often lead
to an unsatisfactory outcome in augmentation mastopexy. It is also not
surprising in light of the challenge inherent in incorporating the competing
surgical goals of adding volume while at the same time tightening the skin
envelope. It is this inherent challenge in simultaneous augmentation
mastopexy that has led to reoperation rates being reported as high as 20% to
50% (1,2).
One such outcome leading to the need for revisional surgery is recurrent
ptosis after an augmentation mastopexy (1,3,4). The ptosis that develops
could be pseudoptosis with stretching of the lower pole or may actually be
descent of the breast tissue off of the implant, known as a waterfall or snoopy
deformity. Understanding the etiology of these deformities provide the
framework for not only managing these complications but also minimizing
the occurrence through preemptive perioperative decision making and
optimal surgical technique.
ETIOLOGY
The development of ptosis after an augmentation mastopexy comes in many
forms and from many contributing causes. The correction of recurrent ptosis,
and more importantly the avoidance of such complications, requires a
thorough understanding of the problem. It is important to classify the type of
recurrent ptosis present; pseudoptosis or waterfall deformity. Pseudoptosis, or
bottoming out, can be defined as the stretching or descent of the lower pole of
the breast postoperatively. This can often be with normal NAC positioning,
but also may include inadequate positioning of the NAC as well. This
generally involves stretching of the lower pole with an increase in the nipple-
to-fold distance and loss of upper pole volume. The waterfall deformity
presents as descent of the breast tissue off the implant resulting in ptosis of
the breast and NAC without elongation of the nipple-to-fold distance and
often with maintenance of upper pole volume. The cause of each type of
ptosis is often multifactorial, but understanding the contributing factors
provides a framework for prevention and correction (Tables 110-1 and 110-
2) (1,3–8).
Etiology of Recurrent Ptosis
Pseudoptosis
Relaxation of the breast envelope with change in shape of the breast is one of
the most common developments postoperatively. This change in shape,
which is almost universal, can be mild and a part of normal healing or may
become excessive requiring treatment. This lower pole “bottoming out” may
result from either excessive stretch of the skin envelope with inferior descent
of the NAC or stretch of the lower pole with a normal NAC position (9). This
may also involve loss of the fold position creating an appearance of the NAC
being too high on the breast mound. These patients usually have descent of
the implant with the stretched lower pole leading to loss of upper pole
volume (Fig. 110-1).

TABLE 110-1 Etiology of Recurrent Ptosis


Pseudoptosis (Bottoming out)
Inappropriate/inadequate mastopexy
Inadequate shortening of vertical limb
Implant selection—oversized, smooth, high profile
Inadequate debulking of the lower pole during mastopexy
Skin and soft tissue laxity

TABLE 110-2 Etiology of Waterfall Deformity


Waterfall Deformity
Inadequate mastopexy
Capsular contracture/tight capsule
Implant selection—textured, highly cohesive
Pocket selection—submuscular, inadequate dual plane
Skin and soft tissue laxity

Patients with excessive elasticity to the skin, such as those whom have
experienced significant deflation after pregnancy and breast feeding, and in
particular, those patients who have undergone significant weight loss are
particularly prone to this complication. These patients are also often observed
to have poor capsule formation with very thin capsules providing minimal
support for the implant (Fig. 110-2).
Patients whom have undergone a vertical-only augmentation mastopexy
can also develop pseudoptosis postoperatively with bottoming out due to
excess vertical length being left at the time of the initial operation (Fig. 110-
3).

Waterfall Deformity
The development of this postoperative sequelae results from the descent of
the breast off the otherwise stable breast implant (Fig. 110-4).
These patients often are noted to have good implant position with
maintenance of upper pole volume. Similarly, to the development of
bottoming out, the patients with significant skin laxity and a poor soft tissue
envelope preoperatively are more prone to the development of the waterfall
deformity. However, it is often the disharmony between the stability of the
breast implant and the instability of the overlying lax breast tissue that leads
to its development. The stability of the implant may be due to implant factors,
such as a textured or more highly cohesive device. The stability may also be
due to the implant placement in the submuscular pocket, preventing
expansion of the lower pole to assist in keeping the breast “lifted” (10). A
capsule that forms with more stability, such as a grade 2 capsular contracture,
can lead to a disconnect between the implant and overlying breast. Patients
who had an initial augmentation mastopexy with inadequate mastopexy, such
as a periareolar approach when a vertical approach would have been more
optimal, are likely to develop a waterfall deformity as well (Fig. 110-5).

FIGURE 110- Anterior view of pseudoptosis with a stretched lower pole and loss of
upper pole volume.
FIGURE 110-2 Grasping of a thin capsule to demonstrate the minimal support that
is provided to the implant.
FIGURE 110-3 Pseudoptosis is present after vertical augmentation mastopexy due to
excess vertical length being left at the time of the mastopexy.

FIGURE 110-4 Waterfall deformity showing the descent of the breast off the stable
implant.

FIGURE 110-5 Waterfall deformity after periareolar augmentation mastopexy. This


patient would have benefited from adding a vertical component to the mastopexy to
lift the breast tissue over the most projecting point of the implant.
MANAGEMENT

Recurrent Ptosis
The operative strategy for correction requires establishing an accurate
diagnosis and developing an operative plan for correction that addresses not
only the anatomic problem but also the contributing factors responsible for
the pseudoptosis or waterfall deformity development postoperatively. The
timing of operative intervention can affect the ultimate success as capsular
development requires time and variable amounts swelling develop within the
soft tissue postoperatively. The operative goal is to give the best chance for
correction with one operation and thus delaying an adequate amount of time
to allow for capsular formation, resolution of edema, and stability of the
operative result. Surgical intervention should be delayed at least 6 months to
allow for demonstration of the final outcome. The surgical planning and
operative intervention can be accomplished more accurately and with the best
chance for success.
The operative strategy in correction is based on the type of ptosis present,
the primary cause of the recurrent ptosis, and any additional contributing
factors. Often, a combination of factors has led to the unsatisfactory result,
and the operative approach may include addressing some or all of these
factors. Common to all types of recurrent ptosis and at the root of the
problem is the issue of skin and soft tissue laxity. As one cannot alter the
quality of the soft tissue envelope, all aspects of surgical intervention in
primary or secondary breast surgery is to correct the position of the unstable,
lax breast tissue and to create an environment that maintains that correction
over time. The strategies outlined provide a framework for decision making
to optimize the correction and long-term stability of the results.
Pseudoptosis (Bottoming Out)
The mastopexy itself with incisions through the breast disrupts the natural
architecture of the breast with division of the Cooper ligaments which act to
maintain the native breast shape. The breast structure is potentially already
weakened from pregnancy, weight loss, and aging and the added weight of
the implants is more than the skin envelope can support, leading to recurrent
ptosis.
Relifting the Breast With Low Breast and NAC
The recurrent ptosis after an augmentation mastopexy results from expansion
of the overlying skin envelope, loss of breast shape, and potential lowering of
the inframammary fold (IMF) position with or without descent of the NAC.
Thus, surgical correction must include recorrection of the ptosis with a
revisional mastopexy (1,11). This often requires reelevation of the NAC
along with tightening of the lower pole of the breast. The NAC may we
widened or misshapen and necessitates correction as well. Fortunately, the
initial skin tightening improved the conditions as the skin has somewhat of a
finite ability to stretch, and thus the relift often is much more successful at
restoring and maintaining the shape of the breast than the original mastopexy.
The design of the mastopexy would be a typical design with the objective to
not focus on short scars, but rather ensure adequate skin removal and NAC
repositioning is accomplished. This often involves an inverted-T type of skin
resection. The design of the skin resection should not be confused with the
pedicle blood supply (Fig. 110-6) (12).
FIGURE 110-6 The black lines represent the typical markings for pseudoptosis
treatment with a vertical and horizontal skin resection “sailboat mastopexy.” No
incisions were made around the NAC which helps preserve blood supply.

The pedicle blood supply is always based superiorly regardless of the


initial pedicle design, most often a superior but occasionally a superomedial
pedicle. It is important to understand that often augmentation mastopexy, the
implant placement sacrifices the central pedicle supplied by the deep fourth
branch of the intermammary artery and thus superiorly based flaps are more
reliable and preferred (Fig. 110-7).

FIGURE 110-7 Blood supply to the nipple areolar complex (NAC). The second
branch of the internal mammary artery (IMA) supplies the superior pedicle. The
third branch of the IMA supplies the medial pedicle. The fourth branch of the IMA
running in the deeper plane of the inferior breast is shown with the dotted lines and
represents the inferior pedicle.

The areola is repositioned in the paramedian of the breast above the IMF
centralized on the new elevated breast mound. Marking for the planned NAC
position and mastopexy resection should be estimated and then finalized with
tailor tacking prior to committing to the proposed mastopexy markings (Fig.
110-8).
Slightly overtightening the vertical segment can be strategically performed
to allow for a small degree of postoperative settling to occur. The shape of
the breast is assessed with the patient in the upright position and
modifications in the degree of lift of the NAC or tightening of the skin
envelope are made as needed. Using this strategy, an aesthetic and long-term
correction of the problem can be achieved (Fig. 110-9).

Relifting the Low Breast and Normal NAC Position


The approach is identical to what has been described, except in planning the
mastopexy, there is no need to reposition the NAC. This is a true isolated
lower pole stretch deformity often secondary to inadequate lower pole
debulking, underresection of lower pole vertical excess skin, or from over-
sized implants stretching the lower pole over time (5).

FIGURE 110-8 Tailor-tacking of the left breast to confirm shape and estimate skin
and breast tissue resection.

It is important to evaluate the root causes in an effort to prevent the same


outcome after correction. Not resecting the lower pole breast volume during a
vertical mastopexy and simply closing the skin during the mastopexy over the
lower pole volume is one of the most common causes of lower pole failure
with bottoming out postoperatively resulting in recurrent ptosis. Thus, in
every bottomed-out breast, it is important to evaluate for residual lower pole
parenchyma as a possible cause and address it through resection if necessary.
Of course, some cases are simply due to a stretch deformity with poor tissue
quality, and the lower pole is actually thinned, and no residual parenchymal
fullness is present. These cases are more likely to benefit also from pocket
control procedures, the potential addition of a soft tissue support structure,
and/or alterations in the breast implant choice (Fig. 110-10).

Relifting the Breast With a Lowered IMF


Another variation in a bottomed-out breast is the descent of the breast
implant below the level of the IMF. Clinically, the NAC often looks
especially high as the implant has not only lengthened the lower pole skin
down to the fold, it has also descended below the level of the fold further
exaggerating the bottomed-out appearance. In these cases, part of the
abdominal skin below the native IMF inadvertently has become a part of the
lower pole breast skin. In these cases, not only does the lower pole skin need
to be addressed through a revisional mastopexy, but also the skin below the
native IMF needs to be reincorporated back onto the abdomen, reestablishing
the IMF position to its appropriate location. In planning this revision, the
IMF must first be determined and reset prior to deciding what additional skin
tightening might be necessary. It is critically important to resist the
temptation to incorporate this abdominal skin into the mastopexy design. This
step requires management of the breast pocket and capsule to accomplish the
repair, not skin resection. By gently repositioning the implant superiorly, the
position of the native fold can be determined, and the breast footprint
reestablished. Once the correct IMF position is determined, the capsule
inferior to this new position needs to be obliterated to prevent implant
descent into the pocket below the correct IMF position. Some surgeons prefer
to resect this portion of capsule and suture the two edges together for
obliteration of the space. A neosubpectoral pocket is sometimes employed
with the creation of a completely new subpectoral pocket and obliteration of
the underlying old pocket including the malpositioned IMF (11,13). More
commonly, a suture capsulorrhaphy has been utilized and is extremely
effective in obliterating the lower pole pocket (14,15). More recently, the
thermal (popcorn) capsulorrhaphy technique has been employed successfully
for obliteration of the malpositioned IMF (16,17). This can be accomplished
alone, with suture reinforcement, or with the addition of a soft tissue support
structure such as a mesh scaffolding (Figs. 110-11 and 110-12) (17,18).
FIGURE 110-9 A: Before and after photo of correction of the low breast and low
NAC with revision mastopexy, implant exchange, fat grafting, and acellular dermal
matrix (ADM) insertion on the left side. B: Reveals the markings and preoperative
plan with ADM insertion and fat grafting to the left breast.
FIGURE 110-10 Relifting a low breast of a 47-year-old female with a secondary
mastopexy, implant exchange with textured round 440-cc high-profile silicone
implants and popcorn capsulorrhaphy.

Whereas the repair of the IMF can prove technically demanding, the
popcorn technique has dramatically and effectively simplified the repair with
good long-term success. The IMF should be reset with redraping of adequate
skin back onto the abdomen. If it is determined there remains excess skin
stretch in the lower pole, an IMF resection of an ellipse of skin at the fold
may prove beneficial (Fig. 110-13).
FIGURE 110-1 A 35-year-old female with bottomed-out breast and inferior
malposition of the implants with a low IMF. She underwent implant exchange with a
440-cc high-profile smooth silicone on the right and a 415-cc high-profile smooth
silicone on the left with popcorn capsulorrhaphy and bilateral vertical horizontal
(sailboat) mastopexy with GalaFORM (Galatea Surgical) insertion.

FIGURE 110-12 Popcorn capsulorrhaphy being performed with insulated forceps


and electrocautery. The full-thickness thermal injury to the capsule is key to the
technique to allow appropriate tightening or shrinkage of the capsule.

Pocket Control
As has been described for the correction of the malpositioned IMF associated
with recurrent ptosis, it has been extremely helpful to consider “pocket
control” in all revisional augmentation mastopexy cases. Unlike a mastopexy
revision without implants, the success of augmentation mastopexy revision is
in part secondary to the ability of the skin envelope to support the position of
the underlying breast implant. Thus, in nearly all cases of mastopexy revision
involving an implant, the breast pocket is tightened and repositioned to
optimize the results and minimize the need for the skin envelope to support
the optimal implant position. This is accomplished most often through the
popcorn capsulorrhaphy technique as described above. Important in all
capsulorrhaphy pocket tightening procedures, mirror capsulotomies should be
performed on the opposite side of the repair to reduce the tension on the
repair and improve the long-term success (14). The addition of sutures or
mesh is determined based on the need for pocket optimization and the status
of the capsule. Patients with stretch deformities often are poor capsule
formers and present with very thin, filmy capsules that provide very little
support for the breast implant. Repair of these types of capsules is less
reliable and the addition of additional support is recommended (Fig. 110-14)
(17–19).
Additionally, in submuscular implants, if the bottomed-out breast also has
a significant animation deformity or downward force secondary to muscle
contraction, addressing this can provide improved long-term results. This can
be accomplished by simply performing a dual plane conversion which simply
creates a more extensive dual plane in the same pocket. The muscle is
identified on the lower pole of the breast and released from the overlying
parenchyma creating a more extensive subglandular pocket in the lower pole
(Fig. 110-15).
By getting the muscle moved up and out of the lower pole of the breast, the
effect of muscle contraction and subsequent animation of the breast is greatly
reduced or eliminated. However, the coverage provided by the muscle can
still enhance the coverage of the implant in the upper pole and cleavage
region. By maintaining the thickness of the soft tissue cover in this area, any
chance of implant or wrinkle visibility is eliminated. If the animation is more
extensive, an exchange to a subglandular or subfascial pocket may be
warranted (20).
FIGURE 110-13 A 29-year-old female with a stretched lowered pole after saline
implant augmentation. She underwent bilateral implant exchange from a 400-cc
overfilled saline to a 565-cc high-profile textured round silicone implant with
bilateral IMF resections.

FIGURE 110-14 Insertion of GalaFORM 3D (Galatea Surgical) into the lower pole
of the breast to provide additional lower pole support and reinforcement of the IMF.

Implant Decision
Finally, when planning a corrective surgery for a bottomed-out breast, the
impact the breast implant may have played on the development of the
deformity must be considered. Most of the time, the implant is not changed
and the pocket control and remastopexy sufficiently addresses the deformity.
However, when oversized or large high-profile implants have been used,
downsizing the implant may help provide improved long-term success of the
revision (5).
Likewise, if a smooth implant is in place, the exchange to a textured device
can provide improved stability of the implant in the breast pocket and
potentially less stretch of the skin after relifting the breast. Of course, large
saline implants can create a significant stretch deformity in the lower pole
and exchange to a silicone implant is often warranted to improve the chances
of long-term success. With the recent issues related to the use of textured
implants, an excellent alternative is to utilize a smooth implant and
incorporate a supportive scaffolding/mesh into the lower pole to add support
to the implant pocket and overlying skin envelope.

FIGURE 110-15 Release of the breast tissue from the underlying pectoralis major
muscle to create a more extensive dual plane.

Waterfall Deformity (Snoopy Deformity)


The etiology of the recurrent ptosis of the waterfall deformity type likewise is
often secondary to the inherit instability and poor tissue quality of the ptotic
breast. The additional defining feature is the stability of the breast implant
compared to the unstable overlying breast tissue, creating a situation where
the breast descends off of the underlying breast implant resulting in ptosis.
One of the hallmarks which distinguishes this condition from the previously
described bottomed-out breast is the maintenance of upper pole volume in the
face of recurrent breast ptosis. Correction can be accomplished through
addressing the overlying ptotic breast, the underlying stable implant and
capsule, or often both.

Relifting the Breast


Often, simply performing a mastopexy to reestablish the position of the
breast over the implant is adequate to correct the ptosis. Fortunately, there is
generally no associated stretch deformity; the breast tissue and skin are rather
normal and unaffected by the deleterious effects of the implant. The
mastopexy is almost always based on the superior or superiomedial pedicle
and performed as a vertical mastopexy with resection of a lower pole
elliptical wedge with or without resection of skin at the fold as a horizontal
wedge. Insufficient debulking of the lower pole at the time of the initial
augmentation mastopexy is one of the contributing causes. During a revision,
special attention should be given to debulking this lower pole of breast tissue
to minimize recurrent failure in the lower pole (Fig. 110-16).
FIGURE 110-16 Insufficient debulking of the lower pole at time of original
augmentation mastopexy led to a waterfall deformity that required relifting of the
breast tissue back on top of the implant.

Managing the Pocket


Unlike pseudoptosis and bottoming out where the pocket is often loose and
stretched, in this deformity the pocket is generally stable. In fact, it is often
more stable than the overlying breast tissue, leading to descent of the breast
off the implant within the stable pocket. One of the most common causes is
an early capsular contracture, such as a grade 2 contracture. The firm capsule
holds the implant in place and its firmness restricts the implant from
expanding the lower pole to support the overlying breast tissue. This type of
ptosis is often seen in subpectoral breast augmentations as the muscle
stabilizes the implant and restricts expansion of the lower pole leading to
ptosis. Correction requires an assessment of the etiology and balancing the
benefit and risk of the options.
The most common correction is to simply perform a secondary mastopexy,
lifting the breast back up onto the underlying implant to create harmony
between the two. This deformity can be seen in submuscular or subglandular
augmentations as the capsule may prevent implant descent and expansion of
the lower pole leading to the ptosis. If the capsule is too restrictive, a lower
pole capsulotomy, partial capsulectomy, or neosubpectoral pocket may be
performed to allow improved expansion of the lower pole. If the implant is
submuscular and the muscle is preventing expansion of the lower pole, a dual
plane conversion may be performed. This requires cutting through the
capsule to expose the caudal edge of the pectoralis muscle in the lower pole
of the breast and dissecting cranially to create a large subglandular pocket
inferiorly. The release of the caudal edge of the muscle is performed
incrementally, creating the least amount of release that will adequately
address the lower pole (Fig. 110-17).
Placement of a retractor into the breast pocket and elevating superiorly
while rocking the breast tissue over the retractor will assist in assessing the
effects of the implant on the overlying skin and breast tissue that has been
tailor tacked for the revisional mastopexy once placed in the pocket. This
dual plane conversion maintains the submuscular coverage of the implant in
the upper pole and medially while allowing improved expansion and effect
on the overlying implant.
FIGURE 110-17 A 43-year-old female with waterfall deformity. She underwent
implant exchange, creation of a neosubpectoral pocket, and a periareolar vertical
short horizontal mastopexy to relift the breast.

In more severe cases, especially if the submuscular pocket has created


associated animation deformity, a pocket exchange from the submuscular to
the subglandular pocket can correct the animation and allow harmony
between the implant and the overlying breast tissue (20). This is especially
helpful as well when the overlying breast tissue is extremely lax, as no matter
how much dual plane is created, the tissue will often once again descend off
the submuscular implant. Of course, a sufficient amount of soft tissue
coverage must be present to reduce the likelihood of implant visibility or
wrinkling postoperatively. A pinch test of at least 2 cm in the upper and
medial borders of the breast is a good guideline for the consideration of a
subglandular pocket (Fig. 110-18).
To accomplish this, the capsule is entered on the undersurface of the breast
to gain access to the pectoralis muscle. Traction is then applied to the inferior
margin of the muscle and a new pocket is dissected between the muscle and
overlying breast tissue creating a new subglandular or subfascial pocket.
Once the appropriately sized pocket has been developed, the muscle is
stabilized to the chest wall. Gentle traction is applied to the newly released
pectoralis major muscle and the edge is sutured down to the chest wall with
numerous interrupted figure-of-eight 2-0 Vicryl sutures. If the muscle cannot
be pulled all the way down into an anatomic position along the IMF, its edge
is simply sutured down on the chest wall wherever it can comfortably reach
without undue tension.

FIGURE 110-18 Upper pole pinch test of at least 2 cm or greater will provide soft
tissue coverage for the subglandular pocket.

Implant Decision
When dealing with a waterfall deformity, some consideration should be given
to what impact the implant selection may have played in the development of
the deformity. Textured implants are much more likely to stay positioned in
the breast pocket and not settled with the overlying breast. The frictional
forces or adherence of these implants creates a more stable environment
compared to the overlying breast tissue. When relifting the breast with or
without management of the pocket and capsule, an exchange to a more
mobile smooth implant may assist in keeping the implant in the lower pole of
the breast. The smooth implant is more likely to create some additional
stretching and expansion of the lower pole over time, thus reducing the
likelihood of a future waterfall deformity. One must be careful, though, as too
much expansion and stretching of the lower pole through implant and pocket
exchange can inadvertently result in pseudoptosis with bottoming out of the
breast. It is this judgment and the necessary balancing act between under- and
overcorrection that makes these procedures so challenging.
CONCLUSION
The correction of the ptotic breast can be challenging, especially when
combining an augmentation and mastopexy in one operation. The reoperation
rates are often high due to the complexity of expanding a breast through the
augmentation while simultaneously reducing and lifting the skin envelope.
One of the most common sequelae is recurrent ptosis of the breast, either as
pseudoptosis with bottoming out or through the development of a waterfall
deformity. Correction is best accomplished only after determining the most
significant causes, which include an inadequate mastopexy as well as the
effects of the breast pocket, pectoralis muscle, capsule, and/or implant.
Although all recurrent ptotic breasts need relifting, the additional cause and
techniques required for correction are quite different between the bottomed-
out breast and waterfall deformity. The best outcome is often only possible
when correction addresses these contributing factors. Minimizing this
complication in augmentation mastopexy will likewise be best accomplished
by proactively developing strategies to minimize these confounding issues in
preoperative planning and then performing the operation with precise
technical execution.
DISCLOSURE
Dr. Calobrace has been a speaker for Sientra and has been on their Medical
Advisory Board. He has no financial disclosures. Dr. Mays is a speaker and
consultant for Sientra and has no financial disclosures.

REFERENCES

1. Spear SL, Low M, Ducic I. Revision augmentation mastopexy:


indications, operations, and outcomes. Ann Plast Surg 2003;51:540–546.
2. Friedman RM. Augmentation/mastopexy: ‘surgeon beware’. Plast
Reconstr Surg 2004;113:2230–2231.
3. Stevens WG, Macias LH, Spring M, et al. One-stage augmentation
mastopexy: a review of 1192 simultaneous augmentation and mastopexy
procedures in 615 consecutive cases. Aesthet Surg J 2014;34:723–732.
4. Calobrace MB, Herdt DR, Cothron KJ. Simultaneous
augmentation/mastopexy: a retrospective 5-year review of 332
consecutive cases. Plast Reconstr Surg 2013;131:145–156.
5. Tebbetts JB, Teitelbaum S. High- and extra-high-projection breast
implants: potential consequences for patients. Plast Reconstr Surg
2010;126:2150–2159.
6. Calobrace MB, Kaufman DL, Gordon AE, et al. Evolving practices in
augmentation operative techniques with Sientra HSC round implants.
Plast Reconstr Surg 2014;134(Suppl 1):57S–67S.
7. Tessone A, Millet E, Weissman O, et al. Evading a surgical pitfall:
mastopexy-augmentation made simple. Aesthetic Plast Surg
2011;35:1073–1078.
8. Lee MR, Unger JG, Adams WP. The tissue-based triad: a process
approach to augmentation mastopexy. Plast Reconstr Surg
2014;134:215–225.
9. Handel N. The double-bubble deformity: cause, prevention, and
treatment. Plast Reconstr Surg 2013;132(6):1434–1443.
10. Tebbetts JB. Dual plane breast augmentation: optimizing implant-soft-
tissue relationships in a wide range of breast types. Plast Reconstr Surg
2001;107(5):1255–1272.
11. Spring MA, Macias LH, Nadeau M, et al. Secondary augmentation-
mastopexy: indications, preferred practices and the treatment of
complications. Aesthet Surg J 2014;34(7):1018–1040.
12. Hall-Findlay EJ. Pedicles in vertical breast reduction and mastopexy.
Clin Plast Surg 2002;29:379–391.
13. Maxwell GP, Birchenough SA, Gabriel A. Efficacy of neopectoral
pocket in revisionary breast surgery. Aesthet Surg J 2009;29(5):379–
385.
14. Chasen PE. Breast capsulorrhaphy revisited: a simple technique for
complex problems. Plast Reconstr Surg 2005;115(1):296–301.
15. Tebbetts JB. Discussion: breast capsulorrhaphy revisited: a simple
technique for complex problems. Plast Reconstr Surg 2005;115(1):296–
301; discussion 302–303.
16. Harris R, Raphael P, Harris SW. Thermal capsulorrhaphy: a modified
technique for breast pocket revision. Aesthet Surg J 2014;34(7):1041–
1049.
17. Calobrace MB, Mays C, Wilson R, et al. Popcorn capsulorraphy in
revison aesthetic breast surgery. Aesthet Surg J 2020;40(1):63–74.
18. Nair NM, Mills DC. Poly-4-hydroxybutyrate (P4HB) scaffold internal
support: preliminary experience with direct implant opposition during
complex breast revisions. Aesthet Surg J 2019;39(11):1203–1213.
19. Maxwell GP, Gabriel A. Efficacy of acellular dermal matrices in
revisionary aesthetic breast surgery: a 6-year experience. Aesthet Surg J
2013;33:389–399.
20. Hammond DC, Schmitt WP, O’Connor EA. Treatment of breast
animation deformity in implant-based reconstruction with pocket change
to the subcutaneous position. Plast Reconst Surg 2015;135(6):1540–
1544.
CHAPTER 111

Liposuction Mastopexy
JAIME S. SCHWARTZ
HISTORY
Mastopexy is one of the most commonly performed breast surgeries. The
goal of the procedure is to reshape and reposition the breast, as well as the
nipple areolar complex (NAC) on the chest wall. Most cases where there is
an imbalance of more skin than internal volume (consisting of subcutaneous
tissue, breast tissue, and/or implants) require a mastopexy. This is most often
seen after changes in breast size due to puberty, pregnancy and weight loss,
natural aging, and skin laxity.
In order to create better symmetry and shape, oftentimes tissue needs to be
removed. This is accomplished by creating a pedicle to maintain
neurovascular supply. The concern with pedicle creation is that some of
the removed tissues contribute to the overall viability and sensation of the
NAC. The most robust blood supply comes from the superior and superior
medial aspects. The best nerve supply comes from the lateral portion of the
breast. The most common pedicle used in mastopexy is an inferior pedicle
due to its ease. This removes some portions of the best nerve and blood
supply. Superior and superior medial pedicles have been developed to
counteract this, but these are technically harder to relocate the NAC and also
have the disadvantage of removing the dermis from the T-junction, which is
best for any delayed healing. Furthermore, studies have shown that even
though the locations of the main sources of blood supply are constant, partial
or complete absence of branches from the main sources does occur (1). This
makes the blood supply to the NAC unpredictable.
Liposuction mastopexy was first performed in the 1980s when liposuction
became a popular surgical procedure (2). It was seen as a way to reduce the
volume of the breast while avoiding direct parenchymal resection which can
reduce the blood and nerve supply to the NAC. It has been advocated as a
modality for women who may be averse to scars but would like to reduce the
size of their breasts in order to reduce the symptoms of macromastia (3). It
has always been considered one of the better options for breast rereduction as
part of or the total procedure whether or not the previous pedicle is known
(4,5). Studies have shown that an enlarged breast of macromastia consists
primarily of fat and that the glandular element is rather small. Fat comprises
61% in the central region to 74% in the lateral region of the breast (6).
My personal experience with liposuction mastopexy began with a 32-year-
old nulliparous female with a mild form of Ehlers–Danlos who desired a
breast lift. She had grade 2 ptosis on the right and grade 1 on the left which
would require the NAC to be moved 4 to 5 cm. The procedure would require
some volume reduction to correct for asymmetry, with the right breast larger
by approximately 50 cc. Knowing the added risks with Ehlers-Danlos, we
discussed removing the volume discrepancy through liposuction only and
relocation of the NAC via deepithelialization and minimal flap release to
close the skin without tension (Fig. 111-1). 3D imaging enabled a more
precise volume discrepancy of tissue removal for symmetry. The procedure
and postoperative period were uneventful. No drains were used, and she only
required acetaminophen for 24 hours.
INDICATIONS
Liposuction mastopexy can be used for any patient regardless of prior surgery
or not. It’s especially indicated for women that have subcutaneous tissue
volume asymmetry. Due to the fact that blunt liposuction cannulas will not
remove breast tissue, this procedure can be used prior to pregnancy in
patients worried about breastfeeding.
CONTRAINDICATIONS
Any patient that is not healthy enough to undergo surgery should not be
scheduled for an elective procedure. If there is not enough subcutaneous
tissue for removal and the breast is largely parenchyma. Any concern for
breast cancer on previous screening.
PREOPERATIVE PLANNING
All patients undergo medical clearance from their primary physician. If there
are more physicians involved in the patients care due to other medical
problems, a clearance is also obtained from each one of these doctors, and
most of the time a telephone correspondence with myself and/or my
anesthesiologist.
Women should be at a stable weight that is regarded as safe for surgery for
at least 6 months prior. If they consider this their normal weight, I ask them
not to try to lose weight prior to the procedure. I have found when patients try
to “make weight” for a procedure, it is often done by severely decreasing
caloric intake in a short time frame which can result in greater chance of
complications such as, but not limited to, delayed healing. If they are heavier
than normal, such as their weight 1 year ago, I will ask them to try weight
loss prior to the procedure.

FIGURE 111- Before and after of a patient who underwent mastopexy and
liposuction.

It is very important to document the breast in as much detail as possible. I


typically use ptosis, degree of constriction, total volume (TV), volume
difference (VD), sternal notch to nipple (SN-N), nipple to inframammary fold
on stretch (N-IMF), base diameter (BD), breast height (BH), top of breast to
nipple (TB-N), sternal notch to top of the breast (SN-TB), midline to nipple
(MD-N), midline to meridian at the IMF (MD-M), and nipple to navel (N-N).
I also document nipple sensation, skin quality, contour deformities, any
lesions, rashes, excoriations, and previous scars as well their scar quality. It is
also important to assess the local area such as axillary tissue or skin excess,
chest wall deformities or asymmetries, and clavicle height differences
(scoliosis). In patients that have lost a lot weight or who have a history of
massive weight fluctuations, it’s important to assess where the breast sits in
relation to the chest wall. In many of these patients, the breast is sitting below
the 6th rib and may be more part of the upper abdomen. This is important to
point out and document because no lift is going to relocate the entire breast
back onto the chest wall.
Patients are seen 2 weeks prior to surgery to review the surgical plan, sign
consent forms, and review postoperative medications and instructions. They
are given Hibiclens to be used for 1 week daily prior to surgery. Medications
consist of gabapentin, antibiotics for 5 days, ibuprofen, and Tylenol. The
gabapentin is started 24 hours prior to surgery with a 5-day total course (Fig.
111-1).
OPERATIVE TECHNIQUE
It may be performed awake with local, monitored anesthesia care (MAC),
total intravenous anesthesia (TIVA) (author’s choice), or general anesthesia.
Patients are marked the day of surgery. Marks begin with the sternal notch
connecting the navel. A tape measure is then placed around the patient’s neck
and the meridian of each breast is marked. This is transposed below the
breast onto the chest or abdominal wall. The breast is then lifted, and
the meridian is elongated to the IMF and the IMF is also marked. I allow the
breast to fall onto the meridian line which places this mark on the inferior
portion of the breast as a point of reference. The midline to meridian (MD-M)
is checked at the IMF bilaterally (Figs. 111-2 and 111-3A–E).

FIGURE 111-2 From right to left across the top TB-N, SN-TB, SN-N. From right to
left across bottom N-N, N-IMF, MD-M.
FIGURE 111-3 A: Skin removal markings. B: Liposuction tissue removal areas. C:
Liposuction tissue removal areas (side view) D: Same patient 3D imaging. E: Same
patient 3D imaging measurements.

The new nipple position is placed by pressing a finger into and through the
IMF (which gives a point slightly higher than
IMF transposition). Symmetry is checked using the sternal notch (SN-N) and
the midline (MD-N). The NAC is then centered on the chest wall (by lifting
and pressing gently to the chest) and the top of the breast is marked out. The
tops of the breasts are connected horizontally. All measurements are then
checked, photographed, and documented (SN-TB, TB-N, N-IMF, MD-N,
actual N-N) (Fig. 111-4).
The breast is then displaced medially and laterally to assess skin laxity and
excess. This is marked from the new nipple position to the meridian on the
chest wall.
The liposuction volume reduction areas are marked by lifting the NAC to
its new position. A vertical mark is then placed following the anterior axillary
line to delineate the excess breast laterally. The IMF is then transposed
horizontally to show the excess breast inferiorly.
The rest of the marks are done with the patient asleep supine. The marks
are then photographed and reviewed with the patient and the OR nurse.
The patient is placed supine with sequential compression devices (SCDs)
and thromboembolic deterrent (TED) hose. The arms are attached to an
armboard with appropriate padding, and the patient is likewise secured to the
bed. The patient is then raised with back up to check for positioning. Once
confirmed, the patient is then prepped and draped.

FIGURE 111-4 Same patient after liposuction tissue removal. Note the symmetry.

The marking of the vertical limb length is achieved by stretching the skin
along the nipple and vertical line. It is typically set at 10 cm (which will leave
an 8-cm areola-to-IMF distance).
TIP: It is also important to correlate the vertical limb length with the
TB-N. For mastopexy, they should be roughly the same in order to
correctly center the nipple as well as achieve appropriate cosmesis. If the
TB-N is much larger than N-IMF, the nipple position should be checked
for being too low and vice versa. If unsure, it is best to sit the patient up,
recheck, and reposition the measurements if needed. Holding a single-
prong skin hook upward in the proposed nipple will give the most
accurate vertical measurements (TB-N and vertical limbs).
To create the horizontal limbs, a mark is then placed along the medial IMF
at a point where the breast begins to curve vertically (upward). The most
important part of this mark is to make sure it is not readily visible if wearing
a low-cut top. The distal lateral vertical limb mark is then pulled toward the
breast meridian point at the IMF. The furthest point that folds over is then
marked. The IMF incision is marked 1 cm above the true IMF. In the midline
of this incision, a 1-cm inferiorly based, equilateral triangle is incorporated.
TIP: The vertical excision length is based on the native IMF, whereas
the actual incision is 1 cm higher. This leaves an extra 1 cm as a safety
measure for closure and tension.
The breast is then tumesced (1 L with 20-cc 1% lidocaine plain, 20-cc
0.25% Marcaine with epinephrine, and 1 amp = [Epinephrine] 1 mg/mL
[1:1000] solution for injection) with a standard infiltration cannula through
small stab incisions medial and lateral inside the horizontal ellipse (not on the
incision marks). The tumescent is started deep to the breast and placed
beyond the breast borders especially superior/superior medial and lateral
(axilla). Approximately half of the tumescent is placed deep and the other
half is then placed superficially to hydrodissect the flaps.
If performing a mastopexy with volume reduction for symmetry and breast
shaping, I use half the volume of breast tissue (500-g breast = 250-cc fluid).
If a larger reduction is planned and liposuction may need to be performed
throughout the entire breast, a one-to-one volume of breast to tumescent is
used (500 g = 500-cc fluid).
TIP: It’s very important to make sure that equal volumes are placed
into each breast as to not cause false asymmetry.
I am right handed, so I typically begin on the patient’s left side and access
the medial incision of the right breast first. I use a 4-mm blunt TriPort
attached to power-assisted liposuction. This incision allows me to contour the
entire inferior and lateral portion of the breast. I then move to the patient’s
right side where I finish the right breast through the lateral incision. I then
repeat for the left breast, starting on the patient’s right side and then moving
to the left. The amount of aspirate is checked and when the numbers match
my preoperative plan, the patient is then sat up.
A single-prong skin hook is placed into the new nipple position and the
breast is tailor tacked bilaterally. A 38-mm cookie cutter is then placed to
mark out the new areola position. All measurements are checked for
symmetry (SN-N, TB-N, N-IMF, MD-N). A 3-0 silk suture is also used to
check the height and position of the areola from the SN and the midline.
All marks are reinforced as well as realignment markings placed.
TIP: With the patient’s back up, this is a good time to recheck all
measurements—particularly vertical limb lengths. I will typically
shorten them at this time if needed (Figs. 111-5 and 111-6).
The patient is placed supine and staples removed. The incisions are
injected with local anesthesia (50/50 0.25% Marcaine and 0.5% Lidocaine).
A 42-mm cookie cutter is used to mark out the areola on stretch. The pattern
is then deepithelialized with a 10 blade.
An electrocautery is used to incise the dermis along the horizontal and
vertical limbs (leaving a 1-cm cuff). This is extended into the areola for only
about 1 cm following the curve. Double-prong skin hooks are placed along
the vertical limbs and the tissue is released only enough to get the medial and
lateral limbs to the midline without tension. The double-prong skin hooks are
then placed on either side of the areola dermal incision. Gentle blunt
dissection with a finger is performed superiorly to “separate” the tissues. This
allows for movement of the NAC superiorly without cutting.
Hemostasis is checked and achieved. Sutures (3-0 Monocryl) are placed at
the two T-junctions to begin and at the realignment marks.
TIP: At the inferior T-junction the vertical limbs are sutured to the
top of the equilateral triangle, leaving 1 cm of excess skin. The excess
skin at the triangle can be used in many ways. Most commonly, I trim
these skin edges (which are the most compromised) to fit the lateral
borders of the triangle.
FIGURE 111-5 A: Tailor tacking and rechecking all measurements for symmetry. B:
New NAC placement with all measurements checked for symmetry.

The NAC is closed with 4-0 Monocryl deep dermal sutures at eight major
points. A 38-mm cookie cutter is then used to recheck that the new areola is
perfectly round. Any excess skin is deepithelialized, and the NAC is closed
with more interrupted 4-0 Monocryl if needed and a 4-0 Monocryl running
subcuticular suture. No drains are used.
TIP: When suturing dermis to dermis that has not been cut, or only
one side had been cut, place the sutures parallel to the skin.
The patient is then cleansed with alcohol to remove markings and then
with triple-antibiotic solution. Dermabond, Telfa, and Tegaderm are placed
sterile. The back of the OR table is raised, and two assistants stabilize the
elbows and shoulders while the anesthesiologist stabilizes the airway. The
patient is leaned slightly forward and is wrapped with thick cotton and two
ACE wraps lightly.
INTRAOPERATIVE CARE
Throughout the surgery the patient is kept normotensive. I prefer to see and
control any bleeding sources during the procedure.
POSTOPERATIVE CARE
All patients are seen the next day and the compression dressing is taken
down. Nipple viability is assessed. The next appointment is at 1 week when
the Tegaderm is removed, a regular sports bra is placed, and the patient may
shower. They are then seen at 3 weeks and are given ointment to place on the
glue to facilitate removal. The next appointments are at 6 weeks, 3 months, 6
months, and 1 year.
Most patients can return to work within a week or less depending upon
their job.
From the time they are discharged after surgery for the first 2 weeks
patients are told to walk as much as possible. From week 2 to week 4, they
can start to increase their blood pressure a bit by walking on an incline
treadmill or riding a stationary bike. At weeks 4 to 6, they can increase their
blood pressure even more by hiking or doing lower body exercise. At 6
weeks, if everything appears healed, they are released to full working out
activity as long as they are wearing a sports bra.

FIGURE 111-6 A: Flaps released just enough to allow for tension-free closure. B:
Blunt superior dissection to allow for NAC movement with cutting.

CASES
CASE 1

See Figure 111-7 for case example.


FIGURE 111-7 Case 1: same patient from Figure 111-4, pre- and 3 months postop.

CASE 2

See Figure 111-8 for case example.


FIGURE 111-8 Case 2: Pre- and postoperative images at 6 months.

CASE 3

See Figure 111-9 for case example.


FIGURE 111-9 Case 3: Pre- and postoperative images at 6 months.
GENERAL RISKS
The risks of liposuction mastopexy are similar to either of the procedures
individually, however, they seem to be less when combined, comparatively.
The risks of liposuction include perforation and overresection. The risks of
mastopexy include loss of NAC, delayed healing, skin necrosis, asymmetry,
poor scarring, bleeding, as well as the other general risks for all procedures.
OUTCOMES
Overall complication rate was 6.4% and was all due to delayed healing at the
inferior T-junction of less than 2 cm. There was no nipple necrosis (0%). A
few women had long-standing hyperemia of the bilateral inferior breast that
resolved within 2 to 6 weeks without any consequences.
Subjectively, at 6 months after the procedure there was no loss of nipple
sensation if they were sensate prior to the procedure (0%). In women that
were insensate or had decreased sensation prior, 35.5% stated they gained
nipple sensitivity with 13% partial sensation and 22.5% hypersensitive or full
sensation. The most common complaint was nipple hypersensitivity.
CONCLUSION
As long as the breast is, to a large extent, subcutaneous tissue, this procedure
can be applied to mastopexy as well as breast reduction. I have not had a
limitation to the amount of NAC movement that can be achieved. By
removing subcutaneous tissues from the areas “weighing” the breast down
such as inferiorly and laterally, the NAC moves superiorly on its own. If a
larger reduction is needed, further debulking and “separation” with
liposuction superiorly also allows for the NAC to transpose more easily
without compromising blood supply.
Another advantage of liposuction mastopexy is that if not enough tissue is
able to be removed via liposuction alone, conversion to a traditional open
procedure is easily performed.
Furthermore, subcutaneous tissues are metabolically active and will change
the most with weight gain or loss. By removing fat only, the breast volume is
not subject to change as much with weight fluctuations in the future.
Performing liposuction mastopexy has allowed for better control of
asymmetries via targeted and concise volume reduction with less risk to
neurovascular structures. Rather than cutting, by using the method of
weighing and sitting the patient up to see if the breasts looked or “felt” equal
it is possible to remove an exact quantity.

REFERENCES

1. van Deventer PV, Graewe FR. The blood supply of the breast revisited.
Plast Reconstr Surg 2016;137(5):1388–1397.
2. Matarasso A, Courtiss EH. Suction mammaplasty: the use of suction
lipectomy to reduce large breasts. Plast Reconstr Surg 1991;87:709–
717.
3. Moskovitz MJ, Baxt SA, Jain AK, et al. Liposuction breast reduction: a
prospective trial in African American women. Plast Reconstr Surg
2007;119(2):718–726.
4. Hammond DC, Loffredo M. Breast reduction. Plast Reconstr Surg
2012;129(5):829e–839e.
5. Mistry RM, MacLennan SE, Hall-Findlay EJ. Principles of breast re-
reduction: a reappraisal. Plast Reconstr Surg 2017;139(6):1313–1322.
6. Cruz-Korchin N, Korchin L, González-Keelan C. Macromastia: how
much of it is fat? Plast Reconstr Surg 2002;109(1):64–68.
CHAPTER 112

Neopectoral Technique for Implant


Malposition
ALLEN GABRIEL | MAURICE Y. NAHABEDIAN |

G. PATRICK MAXWELL
HISTORY
Implant malposition is one of the most common reasons for revision surgery
after breast augmentation mammoplasty. Core clinical studies of implant
manufacturers indicate a revision rate of 10% to 25% within 10 years after
primary augmentation that is due to malposition or capsular contracture
(1–3). Capsular tissue attenuation and contracture, together with inadequate
pocket dissection and inadequate management of the pectoralis major muscle
(in subpectoral augmentations), are the most important factors contributing to
malposition. The correction of malposition is a more complex procedure than
primary augmentation and can be particularly challenging in the context of
thinned tissues and atrophied capsules. Several techniques have been
described for the correction of malposition (4,5); each has its strengths and
shortcomings. The neopectoral technique has few limitations and offers a
powerful method of correcting malposition or capsular contracture associated
with subpectorally placed implants (6,7).
CORRECTIVE TECHNIQUES FOR IMPLANT MALPOSITION
Implant malposition is typically corrected using one of two approaches—the
revision of the existing implant pocket or the creation of a new implant
pocket in a different plane.
Revision of Existing Pocket
The revision of an existing pocket is the simplest approach to correcting
implant malposition and continues to be the mainstay approach, especially
with submuscularly placed implants. The approach involves tightening or
releasing the existent capsule by performing a capsulotomy or
capsulorrhaphy or both, to reposition the implant into the new desired
position. Successful repair has been reported with this approach (4,8), but
failure to adequately address the deforming forces that caused the original
malposition can compromise durability of the repair in the long term (5,9).
The persistence of deforming forces within the pocket may eventually cause
the sutures to fail, leading to pocket enlargement and the recurrence of
malposition. Various techniques have been used to reinforce the repair to
reduce the risk of suture failure, including mirror image capsulotomy,
implant downsizing, and/or tissue reinforcement with capsular flaps or
acellular dermal matrices. Capsular flaps have been successfully used to
correct inferior malposition and symmastia (5,10–12), but the strength and
longevity of capsular tissue can be inconsistent and flaps can relax over time,
resulting in recurrence of malposition. Importantly, capsular flaps cannot be
created with thin capsules.
Creation of a New Pocket
Creation of a new pocket in a different plane completely eliminates the
original deforming forces contributing to the malposition and provides an
opportunity to recreate the soft tissue/implant dynamics and redefine the
anatomical landmarks of a primary augmentation. A more precise pocket
creation is also achievable within a new plane than revising an already
distorted pocket within an existing plane. In patients with subpectorally
placed implants, a new pocket can be created in the subglandular plane or in a
neopectoral plane (i.e., a new plane under the subpectoral muscle).
Subpectoral to Subglandular Pocket Conversion
The subglandular pocket conversion is ideal when the cause of the
malposition is muscle related. Improper pectoralis major muscle dissection
and release are important sources of implant malposition. Superior implant
malposition can arise from the incomplete release of the lower attachments of
the pectoralis major. Inferior and lateral malposition can occur with lateral
overdissection of the pectoralis major and medial malposition from extensive
medial release of the muscle.
Subpectoral to subglandular pocket conversion technique essentially
entails the removal of the posterior capsule, retaining the anterior capsule,
and reattaching the pectoralis muscle back to its origins. Muscle reattachment
recreates the native muscle anatomy and addresses muscle contraction–
induced deformities such as animation deformity. Subglandular site change is
limited by the availability of adequate soft tissue coverage for the implant.
Inadequate soft tissue coverage and support can lead to undesirable
consequences such as rippling, implant visibility, and implant palpability and
increase the risk of inferior malposition and capsular contracture. Autologous
fat grafting and the use of acellular dermal matrices can help improve tissue
thickness and volume, allowing for the feasibility of subglandular pocket
conversion in the absence of adequate soft tissue coverage. Costs and the
need for additional surgeries may, however, limit these options.

Subpectoral to Neopectoral Pocket Conversion


In patients with subpectoral implants who have inadequate soft tissue
coverage, an alternate option is to move the implant to a neopectoral location.
The authors developed this site change procedure and defined the neopectoral
as the pocket deep to the pectoralis major but superficial to the anterior
capsule, which is left intact (6). Removing the anterior capsule is not
advisable as it would cause further tissue damage and would lead to a larger
pocket than the original pocket, necessitating the use of larger-than-desired
implants.
The creation of a neopocket has several advantages over performing a total
capsulectomy. Firstly, it is an easier and less traumatic dissection. Secondly,
it is a more precise dissection. With a precise dissection and definition of the
inferior, medial, and lateral borders of the pocket, effective correction of a
double-bubble deformity or inferior malposition, symmastia, or lateral
malposition, respectively, are achievable. A precise pocket is particularly
important if using an anatomic implant for a snug fit of the implant within the
pocket is critical to prevent anterior–posterior malposition. Thirdly, the
creation of a new vascularized pocket may also help in preventing the
development of capsular contracture in the absence of any clinically evident
infectious cause. Failure to eliminate the infectious cause, if present, may
lead to a recurrence of capsular contracture.
The neopectoral pocket technique is limited by the need for thick capsular
tissue. Pocket creation can be challenging when capsular tissue is thin and
atrophied. In addition, muscle-related malposition may not be fully addressed
by a neopectoral pocket and concurrent adjustment of the subpectoral muscle
may be necessary.
OPERATIVE TECHNIQUE
NEOPECTORAL TECHNIQUE

Preoperative Planning
Preoperative planning begins with a thorough evaluation of the patient while
in an upright position (sitting or standing) to identify the underlying etiology
of malposition and understand the anatomic limitations and the desired
outcome. The desired boundaries of the new breast implant position, as well
as the ideal IMF position, are carefully marked.
Capsule Dissection
Dissection begins via an inframammary skin incision (Fig. 112-1), unless a
concurrent mastopexy is also needed, which is carried to the level of the
capsule without entering it. Using electrocautery, the dissection is continued
in a supracapsular plane immediately superficial to the anterior capsule until
the pectoralis muscle edge is identified (Fig. 112-2). Leaving the implant in
place facilitates the dissection. At this point, a retractor is inserted between
the pectoralis major and the underlying anterior capsule to ease their
separation and dissection is continued in the same plane (Fig. 112-3). When
the intended limits of the preoperatively marked borders of the neopectoral
pocket are reached, dissection is stopped. An incision is made into the
anterior capsule and the implant is removed. If additional dissection is
necessary, this is facilitated by elevating the pectoralis muscle with insertion
of a retractor between the muscle and the collapsed capsule. Elevation of the
muscle causes taut caudal retraction of the anterior capsule, allowing
visualization of the plane of dissection (Fig. 112-4).
FIGURE 112- Capsule is accessed via an inframammary fold incision.
FIGURE 112-2 Dissection begins in a supracapsular plane, initiated immediately
superficial to the anterior capsule until the pectoralis muscle edge is identified.

FIGURE 112-3 Once the edge of the pectoralis major is identified, a retractor is
placed to ease the separation between the pectoralis major and the underlying
anterior capsule. It is easier to initiate this plane with the implant in place.
FIGURE 112-4 When satisfactory dissection of the neopectoral pocket is achieved,
the implant is removed through an incision into the anterior capsule. If additional
dissection is necessary, taut caudal retraction of the anterior capsule with retractor
elevation of the overlying pectoral muscle facilitates it.

Neopectoral Pocket Creation


Once dissection is completed, the capsule is carefully examined for
calcifications and its degree of thickness assessed to determine whether it can
be used for the creation of the neopectoral pocket (Fig. 112-5A). In cases of a
calcified capsule or highly thinned capsule or evidence of heavy silicone
leakage into the pocket, neopectoral pocket creation is abandoned and a
capsulectomy is performed to completely remove the capsule. Ideally for
neopectoral pocket creation, the capsule needs to be uncalcified and have
sufficient thickness to be able to support and hold the implant in place. A
capsule that is taut is usually not problematic and can be retained.
Next, the capsular (old pocket) space is obliterated. This is achieved by
suturing the two edges of the capsule down to the chest wall with 2-0 Vicryl
sutures (Fig. 112-5B). Any excess capsule is trimmed. Obliterating the
capsular space serves to stabilize the capsule and prevent the implant from
migrating back into it and keeps the anterior surface of the capsule from
sliding on the chest wall. It does not serve to correct the malposition, which is
achieved with the creation of the neopectoral pocket.
Following creation of the neopectoral pocket, sizers are placed and the
patient is placed in a 90-degree position and contour and pocket irregularities
are addressed. A drain is placed in the neopectoral space, the implant is
inserted, and the incision is closed (Fig. 112-5C). Although the procedure is
referred to as neopectoral, the implant will not be completely subpectoral.
Only the superomedial aspects of the implant will be covered by the
pectoralis muscle while the inferolateral aspects will be covered by glandular
tissue as in the initial augmentation. Following incision closure, the patient is
again placed in a 90-degree position and final adjustments are completed.
Acellular Dermal Matrix/Mesh Support
As an adjunct to the neopectoral technique, acellular dermal matrices or
bioabsorbable meshes can be used to reinforce the neopectoral pocket and
enhance soft tissue thickness, especially in patients with thinned soft tissues
or thinned capsule. The acellular dermal matrix or mesh is typically sutured
to the inframammary fold and/or to the medial border to prevent downward
or medial migration of the implant, respectively.
FIGURE 112-5 A and B: The capsule is examined and the old pocket is sutured using
interrupted Vicryl sutures. C and D: The drain and implant are placed and the
incision is closed.

CASES

The authors have successfully utilized the neopectoral approach for the
correction of malposition and capsular contracture in a series of 198
patients (7). Over an average follow-up period of 26 months (at least 12
months for all patients), there was one case of recurrence of malposition.
Representative cases of successful repair from the authors’ practice are
presented in Figures 112-6 to 112-8.

CASE 1

FIGURE 112-6 A–C: Preoperative views of a 49-year-old woman who had undergone
augmentation mastopexy. D–F: Thirty months after revision augmentation mastopexy
(inverted T) which included the development of neopectoral pocket, lower pole coverage, and
reinforcement of inferior and lateral walls with ADM and replacement of round implants with
form stable, highly cohesive gel anatomic implants. Successful correction of inferior and lateral
malposition was achieved.

CASE 2
FIGURE 112-7 A–C: Preoperative views of a 38-year-old woman who had undergone multiple
previous revision augmentations. D–F: Twenty-six months after revision augmentation
through IMF incision which included the development of neopectoral pocket, lamellar
separation, lower pole coverage with ADM, and replacement of implants with textured gel
implants.

CASE 3

FIGURE 112-8 Patient as seen in Case 2 demonstrates the softness (A) of implants 26 months
following the treatment of her implant malposition, lamellar scarring (B), and tissue thinning.
CONCLUSION
The neopectoral technique is applicable in most situations in which a
subpectoral implant is malpositioned. It allows for the precise control of
pocket dimension for optimal implant positioning and stability, thus,
effectively correcting and preventing implant malposition. Continued
superomedial coverage of the implant by the pectoralis muscle in the
neopectoral pocket provides the necessary tissue coverage needed to mask
implant-related contour deformities that may otherwise be visible through
attenuated overlying breast tissues.

REFERENCES

1. Spear SL, Murphy DK; Allergan Silicone Breast Implant U.S. Core
Clinical Study Group. Natrelle round silicone breast implants: core
study results at 10 years. Plast Reconstr Surg 2014;133(6):1354–1361.
2. Maxwell GP, Van Natta BW, Bengtson BP, et al. Ten-year results from
the Natrelle 410 anatomical form-stable silicone breast implant core
study. Aesthet Surg J 2015;35(2):145–155.
3. Stevens WG, Calobrace MB, Alizadeh K, et al. Ten-year core study data
for Sientra’s food and drug administration-approved round and shaped
breast implants with cohesive silicone gel. Plast Reconstr Surg
2018;141(4S):7S–19S.
4. Haiavy J, Frenzel CA. Correction of implant malposition with
capsulorrhaphy: a retrospective review and implementation of patient
survey. Am J Cosmetic Surg 2011;28(2):75–83.
5. Voice SD, Carlsen LN. Using a capsular flap to correct breast implant
malposition. Aesthet Surg J 2001;21(5):441–444.
6. Maxwell GP, Gabriel A. The neopectoral pocket in revisionary breast
surgery. Aesthet Surg J 2008;28(4):463–467.
7. Maxwell GP, Birchenough SA, Gabriel A. Efficacy of neopectoral
pocket in revisionary breast surgery. Aesthet Surg J 2009;29(5):379–
385.
8. Harris R, Raphael P, Harris SW. Thermal capsulorrhaphy: a modified
technique for breast pocket revision. Aesthet Surg J 2014;34(7):1041–
1049.
9. Kaufman D. Pocket reinforcement using acellular dermal matrices in
revisionary breast augmentation. Clin Plast Surg 2012;39(2):137–148.
10. Yoo G, Lee PK. Capsular flaps for the management of malpositioned
implants after augmentation mammoplasty. Aesthetic Plast Surg
2010;34(1):111–115.
11. Parsa FD, Parsa AA, Koehler SM, et al. Surgical correction of
symmastia. Plast Reconstr Surg 2010;125(5):1577–1579.
12. Wessels L, Murphy S, Merten S. The capsular hammock flap for
correction of breast implant ptosis. Aesthetic Plast Surg
2014;38(2):354–357.
CHAPTER 113

Subpectoral “Dual-plane” Conversion


for Treating Aesthetic Concerns After
Breast Augmentation
JONATHAN COOK | JASON N. POZNER
HISTORY
Subglandular (prepectoral) breast implants have been linked to many breast
implant–related issues including rippling, implant palpability, and an
increased risk of capsular contracture. Conversion to a previously unused
subpectoral pocket is a powerful technique for treating these issues.
Subpectoral conversion is also effective for treating aesthetic concerns that
arise following dual-plane breast augmentation. By placing the new implant
within a freshly dissected site, it is possible to achieve similar aesthetic
results to primary submuscular augmentation (1) with an acceptably low risk
of complications. What follows is an overview of our approach to various
situations in which we utilize subpectoral dual-plane conversion (Fig. 113-1).
APPLICATIONS
Rippling and Implant Palpability
Subglandular implant placement often leads to implant rippling and
palpability. Conversion to a partial submuscular plane provides an extra layer
of coverage in the superior and medial area and may lead to decreased
rippling and palpability.
Loss of Upper Pole Fullness
Subglandular breast augmentation can lead to loss of superior fullness as the
implants migrate inferiorly on the chest wall. Subpectoral conversion enables
treatment of the inferiorly malpositioned implant by shifting its pocket
superiorly on the chest wall, while the pectoralis muscle provides an
anatomic guideline for defining the lateral and medial borders of the breast
footprint. A mesh is often used to enhance support (see section that follows).
Capsular Contracture
The patient with capsular contracture requires consideration of the underlying
cause (e.g., bacterial contamination, a break in sterile technique, hematoma or
seroma, tissue trauma, or implant rupture) when planning corrective surgery.
Patients undergoing capsulectomy will often require additional soft tissue
support and soft tissue coverage. Subpectoral conversion presents an
effective way to address these concerns, especially when combined with the
adjunct techniques discussed below. It is our preference to perform en bloc
capsulectomy whenever safely possible for patients presenting with Baker
grade III or IV capsular contracture.
FIGURE 113- Treatment algorithm for treating aesthetic concerns after primary
breast augmentation.

Implant Malposition
For patients with implant malposition following previous dual-plane
augmentation, a similar approach may be used to create a “neosubpectoral”
pocket (2). This space is developed by dissecting a fresh pocket beneath the
pectoralis major muscle, between the pectoralis and the underlying capsule.
As originally described by Maxwell, the previous capsule may then be closed
off and tacked down to the chest wall posteriorly (Fig. 113-2), to prevent
migration of the implant back into the previous space. In practice, the
decision to leave a contracted capsule in place is one that should be made
using clinical judgment; one must take into account the degree of contracture
(e.g., Baker grade), the thickness of the capsule and its adherence to
surrounding tissue, the presence of seroma fluid, and whether there is any
evidence of bacterial contamination. For patients with subglandular implants,
we believe that the previous capsule should be completely removed via total
capsulectomy.
ADJUNCT TECHNIQUES
When primary augmentation results in a thin, scarred tissue envelope or
insufficient tissue support, reoperation may translate into further technical
difficulties. To address the findings of attenuated capsular tissue, poor soft
tissue coverage, or insufficient tissue support, we frequently utilize porcine-
derived acellular dermal matrix (ADM) (“Strattice,” LifeCell Corporation,
Branchburg, NJ) or bioresorbable surgical mesh (“GalaFLEX,” Galatea
Surgical, Lexington, MA) as part of our approach.
We find ADM to be beneficial when addressing concerns of implant
rippling, implant malposition, and capsular contracture. When placed above
the subglandular portion of the implant in the dual-plane position, ADM
functions to mask surface irregularities by supplementing the soft tissue
envelope. This is useful for patients with a paucity of soft tissue (such as
those who present with implant rippling or visible implant edges) or
following total capsulectomy. ADM also enables more precise control of the
position of the implant on the chest wall, by serving as an interposition graft
between the elevated pectoralis major muscle and the inframammary fold
(IMF). There is also ample evidence from the reconstructive literature (3–13)
that the use of ADM decreases the incidence of capsular contracture.
Although the mechanism is unknown, we routinely use ADM when operating
for the correction of capsular contracture. Our clinical experience with a
bioresorbable surgical mesh has shown that the material quickly incorporates
and provides additional structural strength for patients whose soft tissue
envelope lacks adequate support.
FIGURE 113-2 Neosubpectoral pocket.
OPERATIVE TECHNIQUE
When converting a patient from a subglandular implant position to the
subpectoral dual-plane site, we start by accessing the breast through the old
incision, unless they require concurrent mastopexy. The old incisions may be
excised at this time if they are hypertrophic, reddened, tethered, or otherwise
healing poorly. For patients undergoing concurrent mastopexy, we will open
the breast with a circumvertical or circumvertical-plus-horizontal incision to
provide wide access.
It is necessary to first address the capsule and then create the new pocket.
Depending upon the thickness of the capsule, a partial or complete
capsulectomy is performed. The posterior capsule (i.e., on the anterior surface
of the pectoralis major muscle) is always removed. Failure to remove this
capsule portion results in incomplete muscle expansion and banding. In
patients presenting with Baker grade III or IV capsular contracture, a
complete capsulectomy is performed. Our capsulectomy technique is to
expose the capsule through the previous incision, then dissect it free from the
surrounding tissue using electrocautery on both cut and coagulation modes
(Fig. 113-3). Blunt dissection is avoided to prevent bleeding. Following
capsulectomy, for patients with capsular contracture, we first irrigate the
pocket with hypochlorous acid solution and then irrigate using triple
antibiotic betadine solution.
The inferior edge of the pectoralis muscle is then elevated using
electrocautery as in a primary dual-plane augmentation (Fig. 113-4). We
recommend exercising caution when approaching the medial edge of the
pectoralis muscle to avoid overdissection of its sternal attachments. Unless it
is obvious that the pocket would not extend far enough medially, we typically
release only a few fibers of the medial-most sternal pectoral attachments.
Overdissection in this area may result in symmastia, medial malposition,
excessive medial fullness, or laterally oriented nipples.
FIGURE 113-3 Breast implant within capsule in preparation for en bloc
capsulectomy.
FIGURE 113-4 Cut inferior edge of pectoralis major muscle, prior to creation of
subpectoral pocket.

Working from medial to lateral, the pectoralis major muscle is then


released from its costal attachments inferiorly, and the serratus anterior and
pectoralis minor muscles laterally. The subpectoral space is developed under
direct vision using a lighted retractor, through careful use of blunt dissection
and electrocautery (Fig. 113-5). One or two vessels are commonly
encountered, and these are anticipated and controlled. We are careful to avoid
overdissection laterally past the anterior axillary line to prevent excessive
lateralization of the implant. One method to estimate the extent of this
dissection is to use the width of the previous capsule as an approximation for
the necessary width of the new subpectoral space unless the subglandular
pocket has been overdissected. Any excess pocket space must be closed prior
to final implant placement. Our preference is to use interrupted 2-0 Vicryl
(Ethicon, Inc, Somerville, New Jersey) suture for this purpose. After the
pectoralis muscle has been elevated in patients with previous subglandular
implants, we employ Marionette sutures to close off the subglandular space
and prevent the implant from returning to the previous pocket (Fig. 113-6).
These are 3 to 5 half mattress or simple sutures of 2-0 Vicryl, placed through
the underside of the inferior edge of the pectoralis muscle and passed through
the breast tissue (Fig. 113-7).

FIGURE 113-5 Subpectoral space defined.

Once the pocket has been adequately dissected and tailored, we place an
implant sizer in the pocket and temporarily close the skin with staples. The
patient is then sat up to evaluate the position of the implant and the need for
further refinement. Additional procedures may be performed at this time if
necessary, including the placement of internal sutures to adjust the shape of
the implant pocket, or any external procedures to adjust the skin envelope
(such as a mastopexy). Once we are satisfied with the position of the implant
within the new breast pocket and skin envelope, the implant sizer is removed.
The breast pocket is irrigated using triple antibiotic betadine solution and a
permanent implant is placed using “no touch” technique.
FIGURE 113-6 “Marionette suture,” anchoring the overlying breast parenchyma to
the elevated pectoralis major muscle.
FIGURE 113-7 Marionette sutures schematic. A: Frontal view. B: Lateral view. C:
Lateral view showing approximate position of sutures. Sutures may either be placed
within breast tissue, or transcutaneously as shown, to anchor pectoralis muscle.

For patients with capsular contracture or a paucity of soft tissue coverage,


we utilize ADM to reinforce the inferolateral aspect of the new implant
pocket. This serves to both disguise the inferolateral subglandular pole of the
implant and prevent inferolateral implant migration over time. We currently
use a single piece of ADM and size this according to the breast dimensions.
We secure the ADM to the chest wall and IMF inferolaterally using simple
interrupted 2-0 Vicryl sutures, and to the inferior edge of the pectoralis
muscle superiorly using modified mattress sutures. Any excess ADM is
trimmed, so the final closure lays flat without ridges or ripples. The rare
patient with extremely thin tissue may have an additional piece of ADM
placed superiorly between the elevated muscle and the breast skin/tissue. This
is sewn into place with 2-0 Vicryl sutures. A drain is placed after all full
capsulectomies, and after all ADM placements.
Finally, for patients with inadequate inferior soft tissue support, we utilize
a bioresorbable surgical mesh to reinforce a portion of the new implant
pocket. We determine the location for the bioresorbable mesh after assessing
the skin laxity and soft tissue quality, and often place the mesh in the
inferolateral or inferior positions within the pocket. A single rectangular
mesh (10 cm × 20 cm) is cut diagonally along its longest dimension and then
shaped using Mayo scissors, or alternatively, we use two preformed mesh
pieces. We secure the bioresorbable mesh to the surrounding tissue using
interrupted 2-0 Vicryl sutures and make every effort to limit the amount of
rippling or pleating so that the mesh lies flat between the implant and the soft
tissue pocket (Fig. 113-8).
DISCUSSION
Patients who present for revisionary procedures to address secondary
concerns after breast augmentation have already endured the physical and
emotional stress of the initial surgery, and often have extremely high
expectations. For this reason, it is of primary importance to address their
aesthetic concerns with a focus on providing reproducible results in the safest
way possible.
The technique of subpectoral dual-plane conversion creates a fresh, well-
vascularized, scar-free environment for the placement of a breast implant, and
the pectoralis major muscle camouflages its superior edge—augmenting soft
tissue coverage (14).
ADM is especially helpful as an adjunct for patients who have undergone
total capsulectomy, and in patients with inadequate soft tissue coverage—in
whom their native tissue may attenuate over time if not adequately
reinforced. Similarly, bioresorbable surgical mesh can be used as a scaffold
for native tissue ingrowth, reinforcing the native soft tissue support and
providing a more durable structural element to assist with implant
positioning. Whether using ADM or a bioresorbable mesh, we believe that
these materials further enhance the benefits of dual-plane positioning in
appropriately selected patients.
FIGURE 113-8 Bioresorbable mesh sutured in place at inferior pole (anchored to
pectoralis major, above and IMF, below).
CONCLUSIONS
Through adequate planning and meticulous surgical technique, many of the
complications of primary breast augmentation can be avoided and treated. By
converting to the subpectoral pocket, in combination with ADM or
bioresorbable mesh placement, it is possible to successfully treat a range of
concerns arising from primary breast augmentation.

REFERENCES

1. Chopra K, Gowda AU, Kwon E, et al. Techniques to repair implant


malposition after breast augmentation: a review. Aesthetic Surg J
2016;36(6):660–671.
2. Maxwell GP, Birchenough SA, Gabriel A. Efficacy of neopectoral
pocket in revisionary breast surgery. Aesthetic Surg J 2009;29(5):379–
385.
3. Maxwell GP, Gabriel A. Acellular dermal matrix for reoperative breast
augmentation. Plast Reconstr Surg 2014;134(5):932–938.
4. Breuing KH, Colwell AS. Inferolateral AlloDerm hammock for implant
coverage in breast reconstruction. Ann Plast Surg 2007;59(3):250–255.
5. Salzberg CA, Dunavant C, Nocera N. Immediate breast reconstruction
using porcine acellular dermal matrix (StratticeTM): Long-term
outcomes and complications. J Plast Reconstr Aesthetic Surg
2013;66(3):323–328.
6. Zienowicz RJ, Karacaoglu E. Implant-based breast reconstruction with
allograft. PlastReconstr Surg 2007;120(2):373–381.
7. Spear SL, Parikh PM, Reisin E, et al. Acellular dermis-assisted breast
reconstruction. Aesthetic Plast Surg 2008;32(3):418–425.
8. Namnoum JD. Expander/implant reconstruction with AlloDerm: Recent
experience. Plast Reconstr Surg 2009;124(2):387–394.
9. Lanier ST, Wang ED, Chen JJ, et al. The effect of acellular dermal
matrix use on complication rates in tissue expander/implant breast
reconstruction. Ann Plast Surg 2010;64(5):674–678.
10. Israeli R, Feingold RS. Acellular dermal matrix in breast reconstruction
in the setting of radiotherapy. Aesthetic Surg J 2011;31(7 Suppl):51S–
64S.
11. Cassileth L, Kohanzadeh S, Amersi F. One-stage immediate breast
reconstruction with implants: a new option for immediate
reconstruction. Ann Plast Surg 2012;69(2):134–138.
12. Glasberg SB, Light D. AlloDerm and Strattice in breast reconstruction: a
comparison and techniques for optimizing outcomes. Plast Reconstr
Surg 2012;129(6):1223–1233.
13. Hanna KR, DeGeorge BR, Mericli AF, et al. Comparison study of two
types of expander-based breast reconstruction: acellular dermal matrix-
assisted versus total submuscular placement. Ann Plast Surg
2013;70(1):10–15.
14. Tebbetts JB. Dual plane breast augmentation: optimizing implant-soft-
tissue relationships in a wide range of breast types. Plast Reconstr Surg
2006;118(Supplement):81S–98S; discussion 99S–102S.
CHAPTER 114

Secondary Revision of the Augmented


Breast
DAVID A. SIEBER
HISTORY
Secondary breast revision can be one of the most challenging procedures for
even the most experienced surgeon. Oftentimes patients have had a bad
experience with a previous surgeon and come to you hoping for a solution.
Just like all things in surgery, it is best to approach the breast in an organized
manner evaluating and addressing each layer from the skin down to the chest
wall. There have been many advances made over the last 20 years regarding
secondary revision of the augmented breast from implementation of three-
dimensional (3D) imaging to the use of acellular dermal matrix (ADM)
and/or mesh for soft tissue support.
INDICATIONS

Patient Assessment
During the initial consultation it is helpful to hear in the patient’s own words
what they are hoping to address. Are they happy with their current size or
would they prefer to be larger or smaller? Patients frequently do not
remember much about their past surgeries. It is important to ask about
incision location and submuscular versus subglandular pocket. Ask whether
they had breast asymmetries prior to their original procedure. What, if
anything, was done to address these asymmetries? Have they had mesh or
ADM placed? If this is a tertiary or quaternary procedure, what was done
before? What worked and what didn’t work? Patients should have a recent
mammogram within the last year if over the age of 40. A focused medical
history should also be taken to elicit for any other conditions that may
preclude surgery. The patient should request all of their old medical records,
operative reports, and implant cards to be sent to your office. Revision cases
are like a puzzle so all the pieces must be obtained to ensure an optimal
outcome.
A focused physical examination is then performed. All examinations start
with breast measurements using a plastic tape measure and calipers. These
measurements include sternal notch to nipple (SN) distance, nipple to
inframammary fold (N-IMF) (Fig. 114-1), base width (BW) (Fig. 114-2),
skin pinch thickness (Fig. 114-3), and maximal skin stretch (SS) (Fig. 114-4).
These measurements are critical because oftentimes a unilateral malposition
or capsular contracture will present as an obvious asymmetry, however the
breast measurements may be very similar on both sides. Next a global
assessment of the breasts is obtained. Take note of the location of the
incisions as well as the quality of the scars. Any asymmetries should also be
appreciated. Is the asymmetry due to nipple position or due to variation in
pockets?
Next assess the quality of the skin over the entire skin envelope. Stretch
marks in the skin indicate poor skin elasticity and may suggest the need for
soft tissue support. When looking at the skin, also assess the soft tissue
coverage. This assessment should take into consideration all four quadrants
of the breast. This soft tissue coverage is important as it helps to conceal the
implant and masks any rippling. Patients with extensive rippling usually have
poor soft tissue coverage resulting in a visible and palpable implant. The
most common area for a soft tissue deficit is in the lower poles of the breast.
In patients who have had multiple capsulectomies in the past, the lower pole
will be even more thin and attenuated. This is also seen in patients with long
standing subglandular augmentations as the skin and soft tissue thins out with
implant descent over time.

FIGURE 114- Nipple to inframammary fold (N-IMF).


FIGURE 114-2 Base width (BW).
FIGURE 114-3 Skin pinch thickness.
FIGURE 114-4 Maximal skin stretch (SS).

Identify the location of the implant in the subglandular or submuscular


plane. A simple technique for determining this is to have the patient place
their hands on their hips and push in. This will activate the pectoralis muscle
resulting in the implants being pulled up and out. If there is no movement
with muscular activation, then the implant is most likely in a subglandular
plane. If there is still a question about location, then a simple ultrasound can
be performed to determine the correct plane.
Total assessment of the implant pocket needs to be performed. Is there
inferior or lateral malposition? Oftentimes asking the patient if the implants
fall out into the axilla when laying down is helpful. It’s a good idea to
examine the patient both standing and supine as the implant position may
change with differences in patient position. Assess for symmastia by
displacing the implants medially to see where the medial edge of the pocket
lays. Lastly, displace the implant superiorly to see if the pocket was
overdissected superiorly. This may be difficult to determine during the
examination but is readily evident at the time of surgery. This superiorly
dissected pocket is very difficult to close during revisional surgery and is
better addressed with a neosubpectoral pocket instead of simple
capsulorrhaphy.
Most patients do not remember the size, style, projection, and shape of
their current implants. If the patients have their original implant cards, you
should ask for a copy of them to confirm the size, style, shape, and fill
volume. Previous operative reports should also be obtained to confirm
implant size and to correlate with findings on physical examination. If the
patient is unable to obtain their old operative records, all FDA implant
manufacturers have been performing implant tracking on silicone gel
implants. Mentor and Allergan began tracking in 2006 with the reapproval of
silicone breast implants. Sientra began tracking in 2012 when their implants
first came to market. Saline implant tracking started in 2019, making location
of saline implant information very difficult for many patients. Ideally the
information obtained should include implant size, projection, style, round
versus shaped, and smooth versus textured. For saline implants it is also
important to find out what fill volumes were used. If despite your best efforts,
no additional information can be obtained, then taking a BW measurement
will help give an approximation of volume whereas a BW of 12 cm equates
to 300 cc in a moderate-profile implant.
CONTRAINDICATIONS
Once you have completed the physical examination, educate the patient on
expected outcomes. Are you able to tackle the issue in a single surgery or will
it need to be staged? Expectation management is one of the most important
components of revision surgery. Patients do not like surprises and may
already feel as though plastic surgeons are not trustworthy due to past
experiences with other surgeons. In my hands, I can rarely hit a home run
with a single procedure. It’s always best to inform the patient that they may
require multiple procedures and pull it off in a single stage versus telling the
patient that they will only need a single surgery when in actuality, they
needed additional procedures. Any patient with unrealistic expectations
should not be operated on.
PREOPERATIVE PLANNING

Use of 3D Imaging
3D imaging is an integral part of any breast practice. Vectra 3D imaging
(Canfield Scientific, Parssipany, NJ) takes a 3D photograph of the patient
which is then manipulated to simulate a surgical result. The software is also
able to evaluate breast volumes as well as differences between each breast. It
is an invaluable tool for patient education as it allows the patient to see size
differences between breasts, asymmetry, and malposition with a high degree
of accuracy (1). It allows you to describe to the patient in detail what you will
and will not be able to address with each surgery. There currently is a
“revision” module on Vectra which allows for increasing implant sizes in
those women who desire larger implants at the time of revision surgery. You
are also able to simulate all types of mastopexies so that the patient can
visually see what their breasts may look like after surgery as well as incision
placement, a common concern for many patients.
Formulating a Surgical Plan
The first step is to assimilate all of the data and variables from your history
and physical examination. During revision surgery patients commonly
present with breasts requiring two different treatments (e.g., a capsule on one
side and a malposition on the contralateral side). This should be pointed out
to the patient at the time of consultation and care must be taken to explain to
the patient that there may be differences in healing timelines between the two
breasts because of this. There are multiple factors to consider in revision
breast surgery which will be explained in more detail below.
OPERATIVE TECHNIQUE/INTRAOPERATIVE CARE
CHOOSING A NEW IMPLANT
New implant selection can be very straight forward if the patient desires to
have a similar size and style implant placed. Almost uniformly, if patients
present with saline implants, these are replaced with silicone implants. The
benefits of silicone implant especially those related to overall feel and
decreased incidence of rippling are important in revisions. Breast BW
parameters should always be respected, and implants should remain within +/
− 1 cm of the measured BW. Saline implants are traditionally overfilled so as
to produce less rippling. However, these high fill volumes result in implants
which actually behave as higher-profile devices. A moderate projection 300-
cc saline implant filled to 350 cc may actually behave more like a 350- to
400-cc moderate plus silicone implant. If patients desire larger implants but
are limited by their BW, then a higher-projection implant may be utilized to
accommodate these higher volumes.
When choosing incisions, it is my preference to use an inframammary
approach. There are many benefits to this approach including reduced
incidence of capsular contracture as well as better control of the final
inframammary fold (IMF) position and nipple to fold distance (2–5). Most
revision surgery can be performed through a 4- to 4.5-cm incision. The
medial portion of the incision should be placed 1 cm medial to the papule of
the nipple (Fig. 114-5) and extend laterally in the marked IMF. If lowering
the fold, a new N-IMF distance is measured and the incision should lie
parallel to the original IMF. Once opening the skin, initial dissection should
be nearly parallel to the chest wall then changed to a 45-degree angle once
past the fibers composing the IMF. This ensures that fibers comprising the
IMF are maintained.
FIGURE 114-5 Location of IMF incision.

Once the old implant has been removed a new pocket needs to be created
to the precise dimensions of the new implant. My preferred method is to
create a neosubpectoral pocket or perform a site change from subglandular to
submuscular (6). Ideally, all implants should be in a new submuscular pocket
when possible. The neosubpectoral pocket is able to address all types of
implant malposition (medial, lateral, superior, and inferior). Due to the need
for creating a new pocket between the capsule and skin, this technique should
not be used in patients lacking adequate soft tissue coverage as this may
devascularize the skin flap leading to skin necrosis. In cases of malposition,
the skin and soft tissue has already demonstrated that it is unable to provide
lasting support of the implant and breast tissue. For this reason, soft tissue
support is commonly placed to reinforce the area of previous malposition.
There are currently a variety of products on the market available for soft
tissue support. The most prevalent are derived from either human or porcine
cells. Although commonly used in reconstruction, these products carry a high
expense for patients undergoing cosmetic surgery. GalaFLEX (Galatea
Surgical, Lexington, MA) was introduced in 2014 and is composed of poly-4-
hydroxybutarate. It is a bioresorbable scaffold which is broken down over the
course of 18 months through hydrolysis and is replaced by collagen (7). This
product is available in both flat sheets as well as 3D shapes to emulate the
lower pole of the breast.
In cases where a neosubpectoral pocket cannot be created, then
capsulorrhaphies should be placed in order to recreate a tight pocket to the
precise dimensions of the implant being used. For very minor adjustments a
popcorn capsulorrhaphy may be performed (8). This thermal damage
contracts and tightens the existing capsule. For larger pocket adjustments a
popcorn capsulorrhaphy is performed first and then is oversewn to reduce the
pocket dimensions. The thermal damage will help the two edges of capsule to
scar together, creating a more durable result. Using capsulorrhaphy sutures
may cause indents along the path of placement, these typically resolve over 2
to 3 months after surgery. After tightening the pocket and suture placement,
Galaflex can be placed to further support the repair (9). It’s important to note
that all ADMs and mesh require a vascular supply in order to function as
desired. For this reason, a strip of capsule may need to be removed in certain
areas so that some or all of the ADM or mesh is in contact with a raw,
vascular surface.
With proper preoperative planning, sizers are not commonly needed in
primary augmentation. Using sizers in most instances increases case time as
well as has the potential to introduce bacteria into the pocket. However, in
revision cases sizes are sometimes needed to fine-tune breast size for better
symmetry. This is more common in cases where saline implants are used with
unknown fill volumes or the preoperative sizes were not able to be located.
Sizers are also helpful in patients who had significant asymmetry prior to
their initial augmentation, resulting in the use of two different-sized implants.
There are a variety of ways to address volume differences between breasts.
The easiest is of course to use two different-sized implants to help achieve
greater symmetry. If a lift is being performed to address excess skin, then
some tissue may be removed from the larger breast as a part of this
procedure. Tissue removal is usually helpful to correct differences of about
50 to 100 cc, before a formal reduction needs to be performed. One additional
option is to fat graft the smaller breast for symmetry. This technique is not as
precise due to the variable resorption of the transferred fat. In my experience,
fat transfer to the breast does not have as high a survival rate as when it is
transferred to the buttocks or other areas of the body.
TREATING EXCESS SKIN
Once the correct implant has been placed, and the pocket has been closed,
skin excess should now be addressed. The type of mastopexy performed
should be dictated by preoperative measurements. It is very common for
secondary cases to have excess lower pole skin which presents as
pseudoptosis and results in a nipple to fold measurement typically greater
than 10 cm but a sternal notch to nipple distance which is normal. The
patients who present with this most commonly are those who have long-
standing subglandular saline implants which tend to stretch the lower pole
skin with time. The treatment for these patients is to perform site change
along with a wedge excision of the lower pole of the breast. This also gives
you an opportunity to create a correct nipple to fold distance based on the
volume of the implant and BW (Table 114-1). The general rule of thumb is
that the N-IMF length should increase by 1 mm for each increase of 10 cc in
the implant above 300, with a 300-cc implant having an N-IMF length of 12
cm. This of course reaches a limit when using larger implants, but acts as a
simple starting point to estimate correct N-IMF length.
In patients with a nipple to fold distance greater than 10 cm and a skin
stretch greater than 4 cm these patients have both a need for nipple elevation
as well as removal of lower pole excess skin and will require a full
mastopexy. Patients with a vertical excess of greater than 6 cm as well as the
above parameters may require a two-stage approach for optimal results and to
minimize the possibility for postoperative complications (10,11)—
performing the mastopexy first followed by a dual plane breast augmentation
6 months later.
Patients may present with a history of augmentation and periareolar
mastopexy as the initial surgeon was trying to prevent the patient from
having “too much” scarring. In reality however, these patients should have
been treated initially with an augmentation mastopexy. In cases where the
patient has had a previous mastopexy which needs to be performed again for
additional skin tightening, it is imperative to acquire old operative reports so
as to determine the blood supply to the nipple areolar complex (NAC). If the
blood supply from previous surgeries cannot be determined, then it is best to
proceed with caution and only perform limited undermining of the skin flaps.
With proper surgical planning, repeat mastopexy or augmentation mastopexy
can be performed safely while minimizing risk of complications (12).
In those patients who have subglandular implants with very thin soft tissue
coverage yet also require a mastopexy, then it is my preference to stage the
procedure. During the first stage the implant is moved from a subglandular to
a submuscular plane. During this initial procedure lower pole skin may be
removed if pseudoptosis is present. At the second stage a formal mastopexy
may be performed. Depending on the amount of soft tissue present, caution
should again be taken as many women have thin skin flaps from multiple
prior procedures. At the second-stage mastopexy, fat grafting may also be
performed. Doing this in a stage approached also allows for fine-tuning of the
skin and pocket at the second procedure.
POOR SOFT TISSUE COVERAGE
In those women with poor soft tissue coverage, the gold standard is fat
grafting. These patients typically present after having multiple revision
surgeries in the past leaving them with a thin and attenuated lower pole of the
breast. The key to fat grafting is to make sure there is a posterior wall to
support and retain the fat beneath the skin flap. This is especially true in those
patients with very little soft tissue to begin with. This posterior wall is best
composed of capsule and acts as a rigid structure, preventing grafted fat from
seeping into the implant pocket. If performing a capsulectomy and
simultaneous fat grafting, some graft may stay, but it is dependent on having
pre-existing soft tissue into which to transfer the fat. As long as there is a
capsule and intact skin there is both a deep and superficial buttress between
which the fat may be transferred.

TABLE 114-1 Correlation Between Implant Volume, Base Width, and


Predicted N-IMF Length

Additional methods which may be employed are the use of soft tissue
scaffolds. Both porcine and human ADMs can be used to create an increase
of 3- to 5-mm thickness to the soft tissue. These materials are typically placed
along the lower pole of the breast, but Maxwell has described a parachuting
technique to place materials such as Strattice (Allergan, Branchburg) into the
upper pole of the breast as well (13,14). Full coverage of implants with ADM
is being used commonly today in breast reconstruction but is being not used
as commonly in aesthetic patients due to the cost associated with full
coverage of an implant (15–18).
ANIMATION DEFORMITY
Animation deformity can be caused by both over- and underrelease of the
pectoralis muscle. When the muscle is underreleased, the implant will sit high
and results in a dramatic deformity due to the large number of pectoralis
fibers pulling against the implant. This is because the implant lies in an
almost entirely submuscular pocket. Activation of the pectoralis muscle
causes compression and displacement of the implant which is translated
through the skin. In patients with an underreleased muscle, additional muscle
fibers need to be released off of the 6th rib up to the sternal boarder. This
accomplishes two things. It will almost completely resolve the
hyperanimation and will also cause the implant to drop into a more natural
location within the breast parenchyma and on the chest wall.
Overrelease of the pectoralis muscle can also cause another set of
deformities. Overrelease commonly occurs when surgeons attempt to create
more cleavage through release of the muscle superiorly along the sternal
border. This maneuver not only causes an animation deformity but is also
accompanied by banding across the implant along the lower pole of the breast
where the muscle fibers compress the implant. Repairing muscles which have
been overreleased tend to be more difficult and should be explained to the
patient pre-operatively.
There are three possible options which may improve this deformity. The
first is to attempt to fat graft the lower pole of the breast where the banding
occurs. This addition of soft tissue may make the deformity slightly less
visible with animation. A second option is to use a piece of ADM to try and
reestablish the insertion of the muscle along the sternum. This repair can be
difficult as there is often very poor tissue medially to which to sew the ADM.
A last resort is to move the implant from a submuscular to a subglandular
plane. This of course will resolve all issues of banding and hyperanimation
but will result in a more visible implant both medially and superiorly (19). In
some reconstructive patients with animation deformities, Gabriel et al. have
had good success in full implant coverage with ADM to provide better
implant coverage resulting in less visibility and rippling (20).
CAPSULAR CONTRACTURE
Capsular contracture can be a troublesome issue for both the patient and the
surgeon. My usual protocol is to give the patient another attempt at treating
their capsular contracture before condemning them to abandon implants
entirely. I’ve developed a simple algorithm based on available data to help
simplify the decision-making process. All patients with recurrent capsular
contractures are started on Singular 10 mg daily 1 month prior to surgery and
continued for 3 months postoperatively (21). Accolate, another leukotriene
inhibitor, has been shown to be more effective but at the potential risk of
causing liver enzyme dysfunction (22–24).
Many patients seen in my office had their original and sometimes
revisional surgery performed through a periareolar incision which has been
shown to have a higher incidence of capsular contracture due to the implants
contact with bacteria found within the milk ducts (2–5). In all patients
presenting with capsular contracture and a periareolar incision, they are
advised to convert to an inframammary incision (IMF) due to the reduced
risk of capsular contracture formation with an IMF incision. Any time a
patient is being treated for capsular contracture new implants are also placed
at the time of surgery due to possible biofilm formation on the implant shell.
Patients with subglandular implants are counseled to undergo a site change
to a submuscular location which also has been shown to have a lower
incidence of capsular contracture (2,5). The intricacies of performing a site
change with and without soft tissue support are detailed in the section titled
“Choosing a New Implant.” There has been some science supporting the use
of ADM for patients with capsular contracture as the ADM disrupts the
activity of the myofibroblasts (25,26). It is not my normal practice to use
ADM or other soft tissue support unless there is another indication for use
(27). Sewing in a soft tissue support product increases the risk of adverse
events such as hematoma formation as well as increased costs to the patient
and time in the operating room for the surgeon. Many patients presenting
with capsular contracture do have other simultaneous issues such as implant
malposition which would dictate the use of some type of soft tissue support.
These factors always need to be weighed against the possible risks.
Although removing the entire capsule, is oftentimes tedious and difficult,
attempts should be made to remove the capsule entirely. When evaluating
recurrence of capsular contracture with implant exchange alone, partial, or
total capsulectomy, total capsulectomy has the lowest rates of capsule
recurrence (28,29). For this reason, the entire capsule should be removed
when possible.
Patients will often present with a higher Baker grade capsule on one side
compared to the other, creating a unique problem. In my experience when
only treating the side with a grade 3 or 4 capsule, it becomes apparent that
there was a Baker grade 2 or 3 capsule on the contralateral side which is very
noticeable in the postoperative period. For this reason, it is best to treat both
breasts with similar techniques, total capsulectomies, in order for the breasts
to have similar long term outcomes.
There are certain instances where performing bilateral total capsulectomy
may not be possible in both breasts. There are patients who will present with
a hard, painful Baker grade 4 capsule on one side, where the implant is
malpositioned superiorly, yet the contralateral side has a soft Baker grade 1
or 2 capsule and significant inferior, medial, or lateral malposition. In patients
such as these a total capsulectomy is performed on the appropriate side while
a procedure such as creation of a neosubpectoral pocket is performed on the
contralateral side to address the implant malposition. Patients are advised
during the consultation that they may require two procedures in order to
achieve the outcome they desire. It is seldom possible to get everything
perfect with a single procedure. Patients with unrealistic expectations should
not be operated on!
The last and possibly most important technique used to combat capsular
contracture is use of the 14-point plan (Table 114-2) which includes pocket
irrigation with a triple antibiotic (TAB) solution containing betadine (30–34).
There is often a lot of confusion regarding the correct formulation of the
antibiotic solution. The original TAB solution as described by Adams
contained betadine, cefazolin, and gentamycin in 500 ml of sterile saline (31).
In 2000 when implant manufacturers warned against using betadine with
implants Adams published an updated TAB solution which did not contain
betadine (32). In 2017 the FDA approved a request by one implant
manufacturer for use of betadine with breast implants; this led to new
recommendations for antibiotic irrigation to either use TAB with betadine or
half-strength betadine (10% povidone-iodine) for all pocket irrigation (35).
NIPPLE POSITION
It is my opinion that nipple position is something that should be addressed as
a final step. It is more important to achieve a desirable breast shape first,
which may take multiple procedures to achieve. That being said, there are
some patients who will clearly need a mastopexy as a part of their secondary
surgery. Many patients who have had previous mastopexies may have an
inferiorly, superiorly, laterally, or medially positioned NAC. As a basic rule,
periareolar repositioning is only able to move an areola approximately 2 cm
in any direction. Any further than this causes excessive pleating and will
distortion the round shape of the areolar skin. It is my practice to determine
the location of the NAC based off of the distance from the IMF. The IMF is a
relatively fixed location which acts as the base of the breast footplate. A
breast with a BW of 12 cm should have a nipple to IMF of 8 cm. As the
breast BW increases by 0.5 cm so does the N-IMF measurement (Table 114-
1). Measuring from the IMF ensures that the nipple is in a correct location
over the breast mound, but does not necessarily ensure that it will match the
contralateral breast. It is more important that the NAC be centered over the
breast mound itself. Measuring nipple position from the sternal notch can
create too much variability in the final nipple position as the breast implant
settles.
Inferiorly positioned nipples can be raised using a multitude of techniques,
the most common being a full or periareolar mastopexy. For nipples which
need to be raised >2 cm a vertical or Wise-pattern mastopexy is utilized, as
this is at the limit of what is generally achievable with a periareolar
repositioning alone. This provides optimal nipple position as well as an ideal
breast shape.

TABLE 114-2 14-Point Plan for Reduction of Bacterial Contact With


Breast Implants
1. Use intravenous antibiotic prophylaxis at the time of aesthetic induction
2. Use an inframammary incision
3. Use nipple shields to prevent bacterial spillage from breast ducts
4. Perform atraumatic dissection of tissue planes using electrocautery
5. Perform careful prospective hemostasis
6. Avoid dissection into the breast parenchyma
7. Use a submuscular and/or dual plane pocket
8. Perform pocket irrigation with triple antibiotic solution containing
betadine (50,000 U bacitracin, 1 g cefazolin, 80 mg gentamycin, 50 cc
betadine in 500 cc normal saline) or at least half-strength betadine (1:1
normal saline to povidone-iodine solution)
9. Take steps to minimize implant-to-skin contact (adequate incision size,
reprep skin, use of sleeve)
10. Minimize time of implant opening and avoid using sizers when possible
11. Change surgical gloves and clean instruments prior to handling implant
or instrumentation of pocket after irrigation
12. Avoid use of drainage tube postoperatively
13. Use a layered closure
14. Recommend postoperative antibiotic prophylaxis for patients
undergoing invasive procedures (tattoos, piercings, deep dental
procedures)
Derived from Deva AK, Adams WP Jr, Vickery K. The role of bacterial biofilms in device-associated
infection. Plast Reconstr Surg 2013;132(5):1319–1328.

Medially and laterally displaced nipples can be slightly more problematic


but oftentimes need a small adjustment for proper positioning. If the patient
requires a traditional mastopexy, then it is easy to move the nipple to its
correct location. It’s important to keep in mind that the nipple should be
positioned in the meridian of the breasts not necessarily at the center of the
vertical limbs or directly through the pre-existing nipple position. Small
adjustments to nipple position are made by performing a periareolar
mastopexy with more skin excision on the side to which the nipple needs to
move. It is always better to incise completely around the areola so as to retain
the circular shape of the NAC. Performing crescent excisions tend to distort
the areolar shape from a circle to more of an oval.
Superiorly displaced areolas are more problematic as it’s unacceptable to
have a vertical incision above the areola. Although there are some described
techniques for moving the areola inferiorly, these usually result in a scar
above or even the need for free nipple grafting (36–38). An alternative is to
perform a wedge excision of lower pole breast skin. This is best used in
patients with some soft tissue laxity, as placing too much tension on the
incision will cause both poor scarring as well as a flattening of the breast.
Using this technique, the ideal nipple to fold distance should be measured
under maximal tension. This location is marked and any tissue between the
mark and the IMF is excised as a wedge to eliminate any dog-ears.
Expectation Management
One of the most important aspects of breast revision procedures is
management of patient expectations. Depending on the complexity of the
presenting issue, many patients will require at least two procedures to
accomplish the results they desire. Other patients may never be able to
achieve what they desire. It is better to say no to a patient then to be the
surgeon responsible for their dissatisfaction. I am always very clear with
patients regarding outcomes, downtime, as well as limitations of what is
possible. Many revision patients have already had a bad, oftentimes traumatic
experience previously and this should be kept in mind at all times.
POSTOPERATIVE CARE
At the completion of surgery, Mastisol and Steri-Strips are applied over the
incisions. Incisions are then covered with Telfa and Tegaderm. The
Telfa/Tegaderm is removed on the third postoperative day. Patients may
begin showering immediately after surgery. The Steri-Strips are left in place
until they begin to fall off (typically 1 to 2 weeks). Scar therapy is begun
using a silicone-based gel once the Steri-Strips fall off and is continued for 1
year postoperatively.
Patients are placed in a soft cotton sports bra after surgery. This is more or
less worn for comfort. These are used instead of surgical bra because they are
more comfortable for the patient and the patients like having them for future
use more than traditional surgical bras. Many patients come in for follow-up
months later still wearing the bra they were placed in after surgery. They
should not wear any bras with underwires for a total of 6 weeks after surgery.
Patients should refrain from elevating their heart rate about 100 bpm for
the first 2 weeks after surgery. Aerobic activity may be resumed at 2 weeks
post op, nonchest weight training may be resumed at 4 weeks, and
chest/abdominal exercises resumed at 6 weeks.
CONCLUSION
Secondary revision of the augmented breast can be a very challenging issue
to address. Patients should always be managed in an organized and stepwise
approach. Once deficits and issues have been identified during a detailed
physical examination, a structured plan should be created to address each
issue. Adjuncts to traditional breast revision such as 3D imaging and soft
tissue support should be implemented when necessary to mitigate the need to
future revisions. Possibly more important than surgical technique is
expectation management. Utilizing the techniques in this chapter should
provide consistent and reliable outcomes.

REFERENCES

1. Roostaeian J, Adams WP Jr. Three-dimensional imaging for breast


augmentation: is this technology providing accurate simulations?
Aesthet Surg J 2014;34(6):857–875.
2. Calobrace MB, Stevens WG, Capizzi PJ, et al. Risk factor analysis for
capsular contracture: a 10-year Sientra study using round, smooth, and
textured implants for breast augmentation. Plast Reconstr Surg
2018;141(4S Sientra Shaped and Round Cohesive Gel Implants):20S–
28S.
3. Li S, Chen L, Liu W, et al. Capsular contracture rate after breast
augmentation with periareolar versus other two (inframammary and
transaxillary) incisions: a meta-analysis. Aesthetic Plast Surg
2018;42(1):32–37.
4. McGuire P, Reisman NR, Murphy DK. Risk factor analysis for capsular
contracture, malposition, and late seroma in subjects receiving Natrelle
410 form-stable silicone breast implants. Plast Reconstr Surg
2017;139(1):1–9.
5. Namnoum JD, Largent J, Kaplan HM, et al. Primary breast
augmentation clinical trial outcomes stratified by surgical incision,
anatomical placement and implant device type. J Plast Reconstr Aesthet
Surg 2013;66(9):1165–1172.
6. Spear SL, Dayan JH, Bogue D, et al. The “neosubpectoral” pocket for
the correction of symmastia. Plast Reconstr Surg 2009;124(3):695–703.
7. Williams SF, Martin DP, Moses AC. The history of GalaFLEX P4HB
scaffold. Aesthet Surg J 2016;36(suppl 2):S33–S42.
8. Calobrace MB, Mays C, Wilson R, et al. Popcorn capsulorrhaphy in
revision aesthetic breast surgery. Aesthet Surg J 2020;40(1):63–74.
9. Adams WP Jr, Toriumi DM, Van Natta BW. Clinical use of GalaFLEX
in facial and breast cosmetic plastic surgery. Aesthet Surg J
2016;36(suppl 2):S23–S32.
10. Lee MR, Unger JG, Adams WP Jr. The tissue-based triad: a process
approach to augmentation mastopexy. Plast Reconstr Surg
2014;134(2):215–225.
11. Sanniec K, Adams WP Jr. The tissue-based triad in augmentation
mastopexy: single-stage technical refinements. Aesthet Surg J
2019;39(12):1331–1341.
12. Dickinson BP, Handel N. Approaching revisional surgery in
augmentation and mastopexy/augmentation patients. Ann Plast Surg
2012;68(1):12–16.
13. Maxwell GP, Gabriel A. Acellular dermal matrix for reoperative breast
augmentation. Plast Reconstr Surg 2014;134(5):932–938.
14. Maxwell GP, Gabriel A. Non-cross-linked porcine acellular dermal
matrix in revision breast surgery: long-term outcomes and safety with
neopectoral pockets. Aesthet Surg J 2014;34(4):551–559.
15. Sigalove S, Maxwell GP, Sigalove NM, et al. Prepectoral implant-based
breast reconstruction: rationale, indications, and preliminary results.
Plast Reconstr Surg 2017;139(2):287–294.
16. Gabriel A, Maxwell GP. Prepectoral breast reconstruction in challenging
patients. Plast Reconstr Surg 2017;140(6S Prepectoral Breast
Reconstruction):14S–21S.
17. Gabriel A, Maxwell GP. Implant selection in the setting of prepectoral
breast reconstruction. Gland Surg 2019;8(1):36–42.
18. Gabriel A, Sigalove S, Sigalove NM, et al. Effect of body mass index on
outcomes after prepectoral breast reconstruction. Plast Reconstr Surg
2019;144(3):550–558.
19. Hammond DC, Schmitt WP, O’Connor EA. Treatment of breast
animation deformity in implant-based reconstruction with pocket change
to the subcutaneous position. Plast Reconstr Surg 2015;135(6):1540–
1544.
20. Gabriel A, Sigalove S, Sigalove NM, et al. Prepectoral revision breast
reconstruction for treatment of implant-associated animation deformity:
a review of 102 reconstructions. Aesthet Surg J 2018;38(5):519–526.
21. Huang CK, Handel N. Effects of Singulair (montelukast) treatment for
capsular contracture. Aesthet Surg J 2010;30(3):404–408.
22. Scuderi N, Mazzocchi M, Fioramonti P, et al. The effects of zafirlukast
on capsular contracture: preliminary report. Aesthetic Plast Surg
2006;30(5):513–520.
23. Schlesinger SL, Ellenbogen R, Desvigne MN, et al. Zafirlukast
(Accolate): a new treatment for capsular contracture. Aesthet Surg J
2002;22(4):329–336.
24. Gryskiewicz JM. Investigation of accolate and singulair for treatment of
capsular contracture yields safety concerns. Aesthet Surg J
2003;23(2):98–101.
25. Cheng A, Lakhiani C, Saint-Cyr M. Treatment of capsular contracture
using complete implant coverage by acellular dermal matrix: a novel
technique. Plast Reconstr Surg 2013;132(3):519–529.
26. Stump A, Holton LH 3rd, Connor J, et al. The use of acellular dermal
matrix to prevent capsule formation around implants in a primate model.
Plast Reconstr Surg 2009;124(1):82–91.
27. Namnoum JD, Moyer HR. The role of acellular dermal matrix in the
treatment of capsular contracture. Clin Plast Surg 2012;39(2):127–136.
28. Collis N, Sharpe DT. Recurrence of subglandular breast implant
capsular contracture: anterior versus total capsulectomy. Plast Reconstr
Surg 2000;106(4):792–797.
29. Adams WP Jr. Capsular contracture: what is it? What causes it? How
can it be prevented and managed? Clin Plast Surg 2009;36(1):119–126,
vii.
30. Deva AK, Adams WP Jr, Vickery K. The role of bacterial biofilms in
device-associated infection. Plast Reconstr Surg 2013;132(5):1319–
1328.
31. Adams WP Jr, Conner WC, Barton FE Jr, et al. Optimizing breast
pocket irrigation: an in vitro study and clinical implications. Plast
Reconstr Surg 2000;105(1):334–338; discussion 339–343.
32. Adams WP Jr, Conner WC, Barton FE Jr, et al. Optimizing breast-
pocket irrigation: the post-betadine era. Plast Reconstr Surg
2001;107(6):1596–1601.
33. Adams WP Jr, Rios JL, Smith SJ. Enhancing patient outcomes in
aesthetic and reconstructive breast surgery using triple antibiotic breast
irrigation: six-year prospective clinical study. Plast Reconstr Surg
2006;117(1):30–36.
34. Culbertson EJ, Felder-Scott C, Deva AK, et al. Optimizing breast pocket
irrigation: the breast implant-associated anaplastic large cell lymphoma
(BIA-ALCL) era. Aesthet Surg J 2019:sjz246.
35. Jewell ML, Adams WP Jr. Betadine and breast implants. Aesthet Surg J
2018;38(6):623–626.
36. Spear SL, Albino FP, Al-Attar A. Classification and management of the
postoperative, high-riding nipple. Plast Reconstr Surg
2013;131(6):1413–1421.
37. Spear SL, Albino FP. Management of the high-riding nipple after breast
reduction. Clin Plast Surg 2016;43(2):395–401.
38. Rietjens M, De Lorenzi F, Andrea M, et al. Free nipple graft technique
to correct nipple and areola malposition after breast procedures. Plast
Reconstr Surg Glob Open 2013;1(8):e69.
CHAPTER 115

Combining Lipofill and Small Implants


for Breast Augmentation
OBAID CHAUDHRY | DANIEL DEL VECCHIO
HISTORY
Breast augmentation utilizing fat has advanced over the past decade. Fat
transfer to the breast has increased 41% over 2016, and this trend does not
appear to be subsiding (1). The idea of core volume augmentation with fat
had significant promise, but there is lack of acceptance among patients and
physicians due to opposition of BRAVA pre-expansion as well as limitations
of augmenting breasts in a single session as a result of graft to capacity
restrictions (2–6).
In order to solve the above issues, an alternative solution was devised. The
composite breast augmentation utilizes the core volume projection of an
implant and surrounds this with fat to attain the best of both worlds (3,7,8).
Although popular, the use of prosthetic implants in isolation have largely
been fraught with high revision rates and failure of a successful aesthetic
outcome. A common misconception is that device failure is the leading cause
of these problems, however, it is most likely soft tissue failure and an absence
of ample breast tissue leading to unpleasant visibility. After a significant
interest arose in fat grafting, core volume augmentation to the breast became
a potential solution to avoiding complications associated with implants.
However, limitations of fat only are comparable to the “mountains of sand”
phenomenon, where core volume augmentation is limited in exchange for a
wide breast base. These restraints led to the path of utilizing an implant to
provide the core volume and projection of the breast coupled with fat to
provide the natural look and feel as a means of delivering a perfect solution
to the world of breast augmentation.
Since the development of the composite breast augmentation by the senior
author, it has garnered significant interest as a solution for reconstructive and
cosmetic patients. This chapter will emphasize the evolution of the composite
breast augmentation with regards to fat: implant ratios, and clinical cases
where the ratios are presented.
Fat Grafting to the Breast
Fat grafting to the breast can be categorized in three groups, all of which have
specific indications. These include core volume fat transplantation with
BRAVA pre-expansion, simultaneous implant exchange with fat (SIEF), and
the composite breast augmentation (3–6,9,10). For patients requesting fat
transfer to the breast, the composite breast augmentation remains the most
popular technique (Fig. 115-1).
Core volume fat transplantation for primary breast augmentation is a
dependable technique for <1% of patients (Fig. 115-1). Fat, similar to the
“mountains of sand” analogy, does not provide core volume projection. As
more fat is transferred (even with BRAVA pre-expansion), the breast base
becomes unusually wide without a significant centrally projected mound
(Fig. 115-2). Nonetheless, core volume fat transplantation to the breast is still
a viable option in constricted breasts, severe congenital asymmetries, or with
a mastopexy in order to restore lost volume without a prosthetic device (Figs.
115-3 to 115-7) (3). Focused fat transplantation allows preferential fill of the
lower breast pole to obtain Mallucci’s 45:55 ideal breast ratio (Fig. 115-8)
(11).
In certain scenarios, breast deformities may develop after implant
placement secondary to soft tissue failure rather than device failure. For these
complications, modification of the soft tissue envelope over the implant,
rather than replacement, will provide a significant improvement (Fig. 115-9).
In these cases, removal of the breast implant is recommended with SIEF.
First described in 2012 by the senior author, SIEF provides a viable option
for patients requiring breast implant removal. In these cases, pre-expansion of
the breast mound is undertaken prior to removal of the implant, and fat
grafting is performed in the “third space” of the breast (9). This concept
provides a separate plane for fat transfer to help improve breast deformities
and significant asymmetries related to capsular contracture or implant
malposition (Fig. 115-10).
FIGURE 115-1 As one can see from the graph, fat for core volume is rare. Implant-
only augmentation is only suitable for a quarter of patients. The remaining majority
are candidates for the composite breast augmentation.
FIGURE 115-2 Fat for core volume is reliable, but not robust. An analogy provided
here compares fat to “mountains of sand.” A significant limitation of fat is its
inability to provide core volume projection.

The use of breast implants in isolation will deliver adequate results for
patients with ideal soft tissue shape and characteristics, which comprise
approximately 25% of all patients desiring augmentation. The majority,
however, will require a composite technique in order to achieve the best
results. First published in 2013, the composite breast augmentation is
considered the best of both worlds: the core volume projection of a breast
implant combined with the natural look and feel of autologous fat. Since
2013, this technique has been adopted by many for both reconstructive and
cosmetic breast functions (3,6–8,10,12–15). This chapter will focus on the
spectrum of fat to implant ratios ideal for a composite breast augmentation
and the decision making process behind selecting the correct ratios.
INDICATIONS
The ideal composite patient has small breasts with insufficient breast tissue to
cover her desired implants. If an implant is used in isolation, and one follows
the Tebbetts/Adams “high five” principles, the surgeons’ options include
placing an inadequately small implant or one that disrupts the soft tissue
mound of the breast in order to achieve a narrow cleavage gap (16). In the
composite technique, one does not violate the native breast footprint, and the
“high five” principles are preserved. The composite breast implant prevents
the surgeon from this dilemma by inserting a smaller implant with a narrow
diameter and utilizing fat for transitional filling of the medial cleavage gap.

FIGURE 115-3 Severe congenital asymmetry treated with core volume fat
transplantation only. One year postoperative.
FIGURE 115-4 Severe congenital asymmetry treated with core volume fat
transplantation only. Six months postoperative.

FIGURE 115-5 Severe constricted breast treated with 600-cc total fat.
Postoperatively, the lower pole shows significant expansion.
FIGURE 115-6 Mastopexy combined with 400-cc fat shown at 3 years postoperative.
In order to avoid ptosis, one may avoid an implant and use fat.

FIGURE 115-7 Mastopexy combined with fat shown at 1 year postoperative. One
must recognize that a breast lift is more than just nipple repositioning, but also
entails volume restoration. When fat is used, the complications associated with a
mastopexy augmentation are not present.
FIGURE 115-8 Core volume fat transplantation only utilized to obtain the ideal
45:55 upper to lower pole aesthetics, as described by Patrick Mallucci. Here, the
lower pole has been expanded.

FIGURE 115-9 An obvious lower pole deformity is seen on the left breast. This is not
due to implant malposition, and rather than removing the device, the soft tissue can
be modified over the implant to create a natural, aesthetically pleasing lower pole.
This is one of the basic tenants of the composite procedure.

FIGURE 115-10 Simultaneous implant exchange with fat (SIEF). The process may
require BRAVA pre-expansion, and shown here is injection of fat in the third space
of the breast in two stages, with simultaneous removal of the implant.
CONTRAINDICATIONS
Contraindications for the composite breast augmentation are comparable to
those for liposuction. Furthermore, patients with a strong family history of
breast cancer, unreasonable expectations with respect to size and shape, and
those unwilling to undertake secondary “touch-up” procedures to provide
further volume and modification of the cleavage gap may not be ideal
candidates for composite breast augmentation. Lastly, patients with implants
desiring prosthesis removal secondary to capsular contracture or other
implant-related issues are better suited for SIEF.
PREOPERATIVE PLANNING
Most patients presenting for primary breast augmentation are composite
candidates (see Fig. 115-1). The breast implant delivers the core volume
projection, whereas the fat supplies the width and transition, especially the
cleavage gap, and equalizes any asymmetries. In this scenario, the breast
implants and fat are codependent entities. The ideal candidate is one with
insufficient soft tissue and a thin body frame. One may address the abrupt
transition zones with fat in order to produce the ideal 45/55 rule without the
need of an anatomic, textured implant. Certain patients with ideal soft tissue
characteristics and breast aesthetics are eligible for breast implants alone,
however this cohort does not embody all patients and is highly variable
among practices. Another group of patients, who desire an increase in breast
size, but are not in favor of prosthetic devices, comprise the “padded bra”
cohort. These women request larger breasts but do not want a breast
augmentation with implants. These are the patients that may pursue core
volume augmentation with fat.
A significant part of the preoperative preparation includes quantifying the
amount of fat needed to produce an excellent result. The original composite
breast augmentation paper by Auclair et al. provided a wide array of case
scenarios by all the authors (3). A common combination utilized by Auclair
included a 300-cc implant with approximately 80 to 100 cc of fat placed in
the upper inner quadrant to produce a soft, full cleavage gap. In contrast, Del
Vecchio’s technique utilized an implant and fat of equivalent volumes. After
reviewing these two methods, one can visualize two ratios: a 1:3 fat to
implant ratio, and a 1:1 ratio, respectively. A third option includes a 2:1 fat to
implant ratio, where the implant provides the necessary core volume
projection, while the fat produces the width and transition. In all scenarios,
the fat and implant are codependent entities, and the volume maintenance of
fat is key for a successful outcome. In any case, the surgeon is able to provide
the patient with the best of both worlds with these ratios: the core volume
projection of an implant with the natural look and feel of fat (Fig. 115-11).
Based on the above concept, one can see that an endless number of fat to
implant ratios exist in any given breast procedure. The senior author prefers a
2:1 ratio and usually does not recommend anything below a 1:2 ratio.
Nevertheless, a wide spectrum of ratios are present with the propensity for fat
survival and ideal aesthetics. Anything below or above a 1:3 or 2:1 ratio of
fat to implant would be fat insufficient or excessive, respectively (Fig. 115-
12A,B).

FIGURE 115-11 Composite breast augmentation may also be utilized in revision


cases. Shown here is an example of inadequate soft tissue coverage, rippling, and a
wide cleavage gap. A 1:1 fat to implant ratio was utilized with a 6-month
postoperative result showing significant improvement. Notice the improved cleavage
gap and lack of rippling postoperatively.

As the surgeon prepares preoperatively for each case, a question arises:


How much fat should one place to achieve the best aesthetic result with
maintenance of the volume transferred? As shown in Figure 115-12A,B, the
wide array of fat to implant ratios ranges from 1:3 to 2:1, with implant or fat-
only techniques being at the extreme ends of the curve. Nevertheless, it must
be highlighted that ratios are the derivatives, and the end result is dictated by
the aesthetics of the breast mound. It must be stressed that the ratio is not
what derives the surgical strategy. A simple comparison is that of filling a
tank of gas in a car. The driver does not preemptively decide on the amount
of gas needed to fill the car. Instead, they will fill the gas tank until it is
complete, and will assess the amount of gallons and cost at the end. The same
concept is true for the composite approach: the aesthetics is key when
analyzing the end result, while the ratio is the derivative. The main takeaway
point is to keep the prosthetic within the soft tissue footprint, and add fat to
enhance the cleavage gap.
FIGURE 115-12 A, B: The spectrum of fat to implant ratios is shown. Although a
wide range of rations can be utilized, the realistic limits for composite breast
augmentation is 1:3 to 2:1. The extreme ends of the spectrum are core volume fat
only, where a range of fat excess ratios’ exists, to implant only, which is in the realm
of fat insufficient volumes. One must recognize the ratio is a derivative, whereas
aesthetics drives the end result. The ratio should not define the surgical strategy by
the plastic surgeon.

TABLE 115-1 Three Different Methods for Composite Breast


Augmentation Based on Implant Location

Another factor to assess within the composite continuum is the plane of


dissection and fat placement. Three different scenarios to consider include:
type 1: subglandular or subfascial primary breast augmentation and fat
overlay, type 2: submuscular primary breast augmentation with implants and
fat, and type 3: revision breast augmentation using implants and fat (Table
115-1). The senior author favors a subfascial approach with fat overlay as this
avoids animation deformities and lateral drift of the prosthesis. In type 3
patients, BRAVA pre-expansion is necessary in order to considerably
increase the third space of the recipient mound, which is generally two to
three times the volume of the subcutaneous space.
The location of fat placement can vary depending on location of the
implant. In a submuscular placement of the implant, a higher volume of fat
can be placed for a larger overlay. If the implant is placed in the subfascial or
subglandular place, there is a progressively smaller volume of total fat that
may be used for footprint coverage.
The approximate volume of fat that is needed can be estimated
preoperatively based on not only tissue characteristics, but for a wide variety
of implant volumes. Assuming the geometry of an implant to be that of a
sphere, one can calculate the amount of fat needed based on a variety of
radius measurements for a range of implant volumes (Fig. 115-13). One may
be able to quantitatively measure the residual volume postoperatively if a
preoperative and postoperative three-dimensional image is obtained, which is
based on the following equation:

(Total Breast Volume Postop) – (Total Breast Volume Preop) – (Implant


Volume) = Retained Volume

Percent Volume Maintenance = Retained Volume/Total Volume of Grafted


Material
FIGURE 115-13 Spectrum of fat needed for coverage of implant, with different
thickness, based on implant size. This does not take into account the amount of
volume that diminishes over time. (From Auclair E, Blondeel P, Del Vecchio DA.
Composite breast augmentation: soft-tissue planning using implants and fat. Plast
Reconstr Surg 2013;132[3]:558–568.[Figure 7, p. 567].)
OPERATIVE TECHNIQUE
Preoperative markings and technique are shown in Videos 115-1 and 115-2.
A comprehensive history and physical examination must include: nipple
height evaluation, volume, inframammary fold level, chest wall asymmetry,
and rotation. The sizes of the implants are selected based on the base
diameter or the “High Five” technique. The surgeon must remember to not
disrupt the breast mound, as any disturbance of the footprint will inevitably
lead to complications of the prosthesis and/or breast itself.
General or local anesthesia (breast augmentation under local anesthesia, or
BALA) may be administered. The tumescent solution is prepared based on
surgeon preference, however, the senior author only uses epinephrine in the
solution of crystalloid if the patients are undergoing general anesthesia. This
prevents any concerns for lidocaine toxicity, and based on previous studies,
lidocaine does not offer any long-term postoperative analgesic effect (17).
Simultaneous separation tumescence (SST) is utilized to infiltrate the
abdomen or other donor sites based on the amount of fat that is required
(18–20). This technique offers a bloodless lipoaspirate with a much quicker
means of infiltrating relative to a standard Klein needle. After infiltrating the
donor sites, the tumescent should be placed in the subglandular plane of the
breasts as this will provide a bloodless dissection.
A high-definition approach to the donor site(s) is generally preferred, as
this complements the aesthetic results of a composite breast augmentation.
The author prefers a suction-assisted approach for collecting the fat. Incisions
are placed in the groin creases bilaterally, and one in the supraumbilical
region for access to the breasts. Donor-site deformities will detract away from
the results of the breast, and thus care must be taken to minimize these
complications. One such way is to utilize SAFELipo, as described by Wall
(19,20). Equalization with a basket cannula that is off suction on the power-
assisted device, will aid in diminishing contour irregularities of the donor
site, similar to a rake flattening and “equalizing” a mound of sand.
The fat is collected in a sterile 3-L canister, and is separated from the
tumescent via gravity. The senior author prefers a multiple canister method,
which assists in keeping track of the amount of fat taken from each area. No
separate washing or centrifuging system is utilized. After the fat taken from
the donor areas is performed, and the quality and quantity appear suitable, the
abdomen and other sites are once again visualized and palpated to assess any
irregularities. These must be corrected intraoperatively, usually with
equalization or further suctioning, in order to produce an aesthetically
appealing donor site. After this is performed, the surgeon then proceeds to
focus on the breasts.
A 4-cm inframammary incision is placed within each fold, and the surgeon
proceeds with a subfascial approach. The amount of dissection is based on
preoperative markings and breast implant shape and base diameter. This
plane should be bloodless secondary to the tumescent fluid infiltrated. After
both breasts are dissected, the fat is injected prior to placement of the implant
in order to prevent any accidental implant penetration. The fat is placed based
on the preoperative markings, which is most commonly in the superiomedial
transition zones in the subcutaneous place to enhance cleavage gap. The
senior author utilizes a roller pump to directly inject the fat through a power-
assisted device with an exploded-tip cannula instead of traditional injection
cannulas on syringes.
After the fat has been placed in the breasts, the pockets are irrigated with
triple-antibiotic solution. The implants are opened and placed in triple-
antibiotic solution, and the 14-point plan, as outlined previously, is followed
(21). A true “no-touch” technique has been adopted and a Keller funnel is
used for this purpose. Generally, the implant size ranges from 200 to 300 cc,
however this can vary based on the soft tissue mound of the breast. Sizers are
not utilized, and implants are the same size on each side, even in cases of
asymmetry, as the fat provides a means to concealing these differences. Once
the implants are placed in the breast pockets, the wounds are closed with
absorbable sutures in a layered fashion, with a 3-0 Vicryl for the fascia, and a
3-0 Monocryl for the deep dermis and subcuticular skin. Donor sites are
closed with 3-0 chromic sutures. Donor sites are dressed with compression
garments, and the breasts are left without any garments or bras to avoid
pressure on the grafts.
POSTOPERATIVE CARE
Composite breast augmentation is a same-day surgery, and patients are
discharged within a few hours postoperatively. No compression or bra is
worn for 3 weeks to maximize fat graft survival. Since the authors prefer a
subglandular approach, patients generally have a quicker recovery and may
return to exercise and heavy lifting after 7 to 10 days. No drains are placed in
either the breasts or the donor site. Pain control postoperatively may be with
either narcotics or NSAIDs. The pain in the breasts is negligible as the
prosthesis does not violate the breast mound and a subglandular dissection is
completed. Donor-site dressings are placed, and include an abdominal binder,
and compression to any other areas where fat was harvested.
Patient satisfaction is high secondary to the quick, painless recovery with a
subglandular breast augmentation combined with the natural look and feel of
fat, which delivers them the best of both worlds.

CASES

The Figures 115-14 to 115-16 are case examples of different ratios.

FIGURE 115-14 A, B: A 1:2 composite ratio is shown with preoperative and


immediate on table results. Silicone gel implants placed were 375 cc, with 210
cc of fat on the left, and 275 cc on the right.
FIGURE 115-15 A 1:1 composite ratio is shown, with preoperative, on table,
and 3-year postoperative results. The long-term results show significant
maintenance of the fat with improvement of the cleavage gap. The natural
look and feel of a breast with the core volume projection of an implant is
obtained.

FIGURE 115-16 Pre- and postoperative results showing a 2:1 fat to implant
ratio. A 180-cc implant in the subfascial plane was utilized with 350 cc of fat.
RISKS AND COMPLICATIONS
Though infrequent, complications are similar to any breast augmentation, and
may include hematoma, seroma, malposition of the implants, and capsular
contracture. Implant malposition can be treated with external massage,
however if there is no improvement then reoperation will be required.
Capsular contracture will require an open capsulotomy versus full
capsulectomy. The best treatment for capsular contracture is prevention,
which includes following the 14-point plan, practicing prospective
hemostasis, and adhering to a no-touch technique with minimal to no
contamination. To our knowledge, there is no difference in capsular
contracture rates in the literature between a standard breast augmentation and
the composite breast augmentation.
Common donor-site issues include seroma and contour irregularities.
Seromas are drained with needle aspiration, and small contour distortions can
be treated with aggressive massage. However, if these abnormalities remain
greater than 6 months or are substantial, reoperation may be required with the
equalization technique.
OUTCOMES AND SECONDARY PROCEDURES
At times, a “round 2” may be necessary in order to fill deficient areas as a
result of fat atrophy. This can be performed based on surgeon evaluation and
patient preference. Commonly, these patients may be thin with scarce fat
supply, and obtaining fat from previously harvested donor sites may be
significantly more challenging, and thus other areas, such as the extremities
may be utilized. To avoid this, overgrafting the recipient site during the initial
operation is recommended, however one must keep in the mind the graft to
capacity ratio. The clinical endpoint should be the aesthetics, rather than the
amount placed.
Donor-site irregularities can be treated conservatively with aggressive
massage. However, equalization of the sites may be necessary if these areas
are significantly displeasing and present greater than 6 months
postoperatively.
The survival of the grafted fat is superior in the composite breast
augmentation rather than core volume, based on the graft to capacity ratio
(2,3). There are lower volumetric stresses on the recipient site, which in turn
delivers an ideal environment in the composite breast augmentation. The
volume of fat does not violate the concept of the graft to capacity ratio, and is
similar to a two-dimensional skin graft model (3). The different yet
complementary volumetric spacers of both fat and implants allow the surgeon
to size and shape breast in a customized fashion that typically is addressed
with either excision of breast tissue or use of differential implant sizes. One
can achieve core volume augmentation with an implant and overlay this with
the natural fill of fat.
Drawbacks of the composite procedure include a variable learning curve.
Unlike implants, fat grafting in the breast is technique dependent, and rates of
survival are likely to vary depending on the skill level and technique utilized
by the plastic surgeon. Another fear among the patients and surgeon are the
development of benign calcifications, which may raise suspicion on imaging.
Nonetheless, Cameron et al. had shown that composite breast augmentation is
safe and does not interfere with interpretation on mammography, and
additional studies were not necessary in their average follow-up period of 29
months (7,22).
Finally, although satisfaction rates are high among patients and surgeons,
there have been no objective studies to quantify this assertion, and thus this
would be direction for further studies.
CONCLUSION
The composite breast augmentation is not just implants with fat. It represents
a solution for patients desiring a natural look and feel of their breasts, but
without the loss of core volume projection. The concept embodies, at the very
least, three major ratio subsets of a 1:2, 1:1, and 2:1 fat to implant ratio, all of
which seek to achieve different solutions for patients with unique breast
characteristics. The concept will continue to advance in the future and solve a
variety of breast implant complications.

REFERENCES

1. American Society of Aesthetic Plastic Surgeons. 2016 Cosmetic Surgery


National Data Bank Statistics, March 2017. Available online at
https://www.surgery.org/sites/default/files/ASAPS-Stats2016.pdf.
Accessed February 20, 2019.
2. Del Vecchio DA, Del Vecchio SJ. The graft-to-capacity ratio:
volumetric planning in large-volume fat transplantation. Plast Reconstr
Surg 2014;133(3):561–569.
3. Auclair E, Blondeel P, Del Vecchio DA. Composite breast
augmentation: soft-tissue planning using implants and fat. Plast
Reconstr Surg 2013;132(3):558–568.
4. Khouri RK, Rigotti G, Cardoso E, et al. Megavolume autologous fat
transfer: part I. Theory and principles. Plast Reconstr Surg
2014;133(3):550–557.
5. Khouri RK, Rigotti G, Cardoso E, et al. Megavolume autologous fat
transfer: part II. Practice and techniques. Plast Reconstr Surg
2014;133(6):1369–1377.
6. Del Vecchio DA, Bucky LP. Breast augmentation using preexpansion
and autologous fat transplantation: a clinical radiographic study. Plast
Reconstr Surg 2011;127(6):2441–2450.
7. Auclair E, Anavekar N. Combined use of implant and fat grafting for
breast augmentation. Clin Plast Surg 2015;42(3):307–314.
8. Kerfant N, Henry AS, Hu W, et al. Subfascial primary breast
augmentation with fat grafting: a review of 156 cases. Plast Reconstr
Surg 2017;139(5):1080e–1085e.
9. Del Vecchio DA. “SIEF”—simultaneous implant exchange with fat: a
new option in revision breast implant surgery. Plast Reconstr Surg
2012;130(6):1187–1196.
10. Katzel EB, Bucky LP. Fat grafting to the breast: clinical applications
and outcomes for reconstructive surgery. Plast Reconstr Surg
2017;140(5S Advances in Breast Reconstruction):69S–76S.
11. Mallucci P, Branford OA. Shapes, proportions, and variations in breast
aesthetic ideals: the definition of breast beauty, analysis, and surgical
practice. Clin Plast Surg 2015;42(4):451–464.
12. Bravo FG. Parasternal infiltration composite breast augmentation. Plast
Reconstr Surg 2015;135(4):1010–1018.
13. Maione L, Caviggioli F, Vinci V, et al. Fat graft in composite breast
augmentation with round implants: a new concept for breast reshaping.
Aesthetic Plast Surg 2018;42(6):1465–1471.
14. Maione L, Caviggioli F, Vinci V, et al. Fat graft in composite breast
augmentation with round implants: a new concept for breast reshaping.
Aesthetic Plast Surg 2018; Letter to the Editor. 2019;43(2):552–553.
15. Kerfant N, Marchac A, Auclair E. Fat grafting in composite breast
augmentation with round implants: a new concept for breast reshaping.
Aesthetic Plast Surg 2018; Letter to the Editor. 2019;43(2):550–551.
16. Tebbetts JB, Adams WP. Five critical decisions in breast augmentation
using five measurements in 5 minutes: the high five decision support
process. Plast Reconstr Surg 2005;116:2005–2016.
17. Danilla S, Fontbona M, de Valdés VD, et al. Analgesic efficacy of
lidocaine for suction-assisted lipectomy with tumescent technique under
general anesthesia: a randomized, double-masked, controlled trial. Plast
Reconstr Surg 2013;132(2):327–332.
18. Del Vecchio D, Wall S Jr. Expansion vibration lipofilling: a new
technique in large-volume fat transplantation. Plast Reconstr Surg
2018;141(5):639e–649e.
19. Wall SW. SAFE circumferential liposuction with abdominoplasty. Clin
Plast Surg 2010;37:485–501.
20. Wall SH Jr, Lee MR. Separation, aspiration, and fat equalization: SAFE
liposuction concepts for comprehensive body contouring. Plast Reconstr
Surg 2016;138:1192–1201.
21. Deva AK, Adams WP Jr, Vickery K. The role of bacterial biofilms in
device-associated infection. Plast Reconstr Surg 2013; 132(5):1319–
1328.
22. Cameron JA, Auclair E, Nelson M, et al. Radiologic evaluation of
women following cosmetic breast augmentation with silicone implants
and fat grafting. Plast Reconstr Surg 2014;134 (4 Suppl 1):91–92.
CHAPTER 116

Breast Revisionary Surgery and the


Role of Acellular Dermal Matrix and
Bioabsorbable Mesh
ALLEN GABRIEL | MAURICE Y. NAHABEDIAN | G. PATRICK MAXWELL | STEVEN R.
SIGALOVE
HISTORY
Approximately 400,000 implant-based breast procedures are performed in the
United States each year, including over 300,000 augmentation mammaplasty
procedures and over 80,000 reconstructive procedures (1). A substantial
percentage of these patients are likely to undergo revisionary surgery. Data
from Core Clinical Studies of implant manufacturers indicate that about a
third of women who had augmentation mammaplasty and between a third and
half of women who had breast reconstructive surgery undergo a reoperation
within 5 to 6 years of their initial procedure (2–6). In addition, a similar
percentage of women who have had a previous history of breast revisionary
surgery after augmentation or reconstruction undergo further revisionary
surgeries. Capsular contracture and implant malposition/asymmetry/ptosis
were reported to be the primary reasons for revisionary surgery. Other less
frequently reported reasons included wrinkling/rippling, palpability, and
visibility.
Breast revisionary surgery has traditionally involved implant pocket site
change, in conjunction with capsulotomy or capsulectomy, implant
replacement, and the use of capsular flaps for creation and reinforcement of
the breast pocket (7). In the current era, acellular dermal matrices (ADMs)
have become an integral part of revisionary surgery (8–12), as they have been
for primary breast reconstruction (1,13). More recently, the use of
bioabsorbable meshes is emerging as an alternative to ADMs or to
complement ADMs (12,14).
INDICATIONS FOR ADM USE
Depending on the reason for revisionary surgery, ADM use is categorized
into four distinct indications—pocket stabilizer for the correction of implant
malposition, correction of capsular contracture, lower pole implant coverage
for the correction of ptosis or stretch deformity, and soft tissue thickener for
masking implant wrinkling/rippling, palpability, and visibility. It should be
noted that ADM use in breast surgery is now considered an OFF-LABEL use
since the FDA’s decision in March 2019 (15).
Pocket Stabilizer
Implant malposition, manifesting as inferior, lateral, or medial malposition, is
primarily related to pocket overdissection and periprosthetic tissue atrophy.
Corrective surgery involves one of two approaches—revision of the existing
pocket or creating a new pocket in a different plane. An existing pocket is
typically modified by performing a capsulorrhaphy and/or capsulotomy
followed by implant exchange. Although successful repair has been reported
with this approach (16,17), it is often difficult to adequately address the
deforming forces within an existing pocket, leading to recurrence in the long
term (18,19). Capsular flaps or ADM may be used to help reinforce the repair
but these supportive tissues do not necessarily address the deforming forces
within the pocket.
The revisionary approach of pocket site change, in contrast, completely
eliminates the original deforming forces and recreates the primary
augmentation or reconstruction environment, allowing the redefinition of the
breast footprint and pocket boundaries. The old capsule is extirpated and a
new pocket is created in the subglandular plane1 (augmentation patients) or
the prepectoral plane (reconstruction patients) if the original implant was in
the subpectoral plane. If the original implant was in the subglandular or
prepectoral plane, a new pocket is created in the subpectoral plane. In cases
where the implant is already in the subpectoral plane, an additional option is
a pocket change to the neopectoral pocket. The neopectoral pocket is
developed deep to the pectoralis major but superficial to the anterior capsule
(20). Although the neopectoral pocket is technically not in a different plane
(as it is still in the subpectoral plane), by suturing down the old pocket, it
eliminates the original deforming forces of the old pocket. For more details
on the neopectoral pocket, see Chapter 112.
In pocket change to the subpectoral plane, the inferior attachments of the
pectoralis major muscle are elevated and a new implant is introduced into the
newly created subpectoral pocket. The superior two-thirds of the implant are
typically covered by the muscle. The ADM is placed at the lower pole of the
breast. The superior border of the ADM or mesh is sutured to the lower
border of the muscle. The inferior border of the ADM or mesh is secured at
the inferolateral or inferomedial pocket, depending on the type of
malposition. This application of the ADM is similar to the now well
established “pectoral muscle extension” technique performed in breast
reconstruction. As the lower third of the implant in reconstructive patients is
covered only by thinned mastectomy skin, the ADM is imperative as it
provides additional coverage, thus diminishing thinned tissue–related
complications. In addition, the ADM reinforces the pocket. In reinforcing the
pocket, the ADM strengthens, tightens, and stabilizes the pocket, thereby
keeping the implant in its intended location and minimizing implant
excursions and thus preventing the recurrence of implant malposition. The
ADM also helps to define the inframammary and lateral mammary folds and
provide better control of implant pocket and position. In augmentation
patients, although there is often ample soft tissue coverage at the lower pole,
the ADM serves to prevent “window-shading” of the pectoralis muscle as
well as prevent inferior malposition from laxity of the overlying soft tissue
with time. The ADM or mesh sutured at the lower pole provides the needed
lower pole support in this case.
In the creation of the neopectoral pocket, the ADM is used in a similar
fashion as in the subglandular or subpectoral site change technique to fortify
the pocket. When there is sufficiently thick old capsular tissue and adequate
local tissue integrity, the neopectoral dissection will often hold the implant in
position without the need for buttressing the repair with ADM.
The prepectoral site conversion in reconstructive patients involves the
complete wrapping of the implant with ADM before its placement under the
skin envelope. The ADM is secured to the chest wall tissues and the
pectoralis muscle as well as to the overlying subcutaneous tissues. As
reconstructive patients often lack subcutaneous tissue due to mastectomy,
complete ADM coverage of the implant helps to prevent complications
associated with lack of tissue, such as skin necrosis; implant exposure;
implant palpability, visibility, wrinkling, and rippling; and capsular
contracture. The ADM in this application not only provides soft tissue
coverage and cushions the implant from direct contact with the skin envelope
but it also serves to stabilize the entire pocket.
Correction of Capsular Contracture
The etiology of capsular contracture remains to be elucidated but microbial
biofilms have been implicated as a potential inciting event that drives the
uncontrolled inflammatory response that culminates in capsular contracture
(21–23). Corrective surgery for capsular contracture has traditionally
involved capsulotomy or capsulectomy with or without site change and
implant exchange (24). However, this approach has not been reliable in
correcting the contracture and is associated with a high recurrence rate (25).
The addition of ADM to the repair has dramatically reduced the risk of
recurrence, as demonstrated in numerous publications (8,9,11,12,25,26).
The ADM for this indication is sutured at the inferolateral or inferomedial
borders, as in the correction of implant malposition for subglandularly or
subpectorally placed implants, or is completely wrapped around the implant
for prepectorally placed implants. The ADM is believed to act as a barrier
between the new implant and the host tissue, thus diminishing the host
immune response, capsule reformation, and capsular contracture (27–29). In
addition to diminishing the host immune response, the ADM also serves to
reinforce and stabilize the pocket. Given the extensive clinical data that
suggest that ADM, particularly AlloDerm, mitigates the risk of capsular
contracture, it would be judicious to use this matrix when contracture is the
main presenting reason for revision surgery, especially in patients with a
history of recurrent contracture.
Lower Pole Coverage
Augmentation and reconstructive patients often have thinned breast tissue. In
augmentation patients, tissue thinning is due to the downward pull of the
weight of the implant as well as to age-related natural changes in breast
volume over time. Reconstructive patients have thinned subcutaneous tissue
due to mastectomy, which is compounded by the weight of the implant. In
both types of patients, the lack of adequate lower pole support eventually
results in tissue stretching and ptosis. Ptosis is a reason for revision surgery in
about 10% of augmentation patients and in about 5% of reconstruction
patients, 5 to 6 years after breast surgery (2,5).
The conventional approach for the correction of ptosis involves mastopexy
in conjunction with site change and implant exchange, but ptosis can recur in
the absence of adequate lower pole support. ADM can be used to provide the
required lower pole support. If the new implant is in the subpectoral or
neopectoral pocket, the ADM is sutured to the pectoralis muscle border
superiorly and to the lower pole inferiorly as in the correction of implant
malposition. If the new implant is placed subglandularly, the lower pole is
again supported by a layer of ADM. In prepectorally placed implants, extra
lower-pole support is not necessary as the implant is completely wrapped
with ADM. The support and coverage provided by the ADM also allows
mastopexy to be safely performed over the implant.
Soft Tissue Thickener
In patients with thinned, stretched breast tissue, surface irregularities, such as
rippling, and wrinkling, of the underlying implant as well as the implant
edges can be visible. The problem is often exaggerated in thin women and in
those with overly large implants. Surface irregularities are most often noted
superomedially but can also occur laterally or inferolaterally.
Conventional revision surgery to correct implant surface irregularities
include exchanging the existing implant for a smooth implant, subpectoral
site change, and/or capsule modifications to decrease the pocket size for the
placement of a smaller implant. Placement of a smooth implant or a smaller
implant may ameliorate visibility of surface irregularities but it does not
address the thinned tissue, which is the cause of the problem. An extra-thick
ADM can be used to reinforce thinned tissue and augment the soft tissue
coverage in these instances.
After site change and/or capsule modification, the extra-thick ADM is
placed over the implant under the area of thinned tissue. The ADM is
anchored by suturing its corners to the overlying existing capsule or new
pocket. The sutures are tied to themselves externally, under no tension.
Intimate contact with the overlying capsule or pocket is critical to allow for
rapid revascularization and cellular repopulation of the ADM. For this
application, the use of an ADM is preferable to a bioabsorbable mesh as
ADMs have a softer feel and have greater pliability.
WHICH ADM TO USE?
Several acellular matrix products are currently available for use in breast
surgery, including human-derived (FlexHD [Ethicon, Somerville, NJ];
AlloDerm Regenerative Tissue Matrix [Allergan, Branchburg, NJ], AlloDerm
RTM Ready To Use [Allergan], and DermACELL [NOVADAQ, Bonita
Springs, FL]); porcine-derived (Permacol [Covidien, Boulder, CO], Strattice
[Allergan], and Artia [Allergan]); and bovine-derived (SurgiMend [Integra,
Plainsboro, NJ]) matrices. In addition to the variability in the source of tissue
they are derived from and in the processing method, these products also vary
with respect to their biomechanical properties. In general, the porcine-derived
matrices appear to be stronger and stiffer than human-derived matrices (30);
while the latter are more pliable and softer. The difference in biomechanical
properties among the ADMs is an important factor to consider when selecting
an ADM for an intended application in breast revisionary surgery.
For the indication of pocket stabilizer, a sturdier and tauter matrix (such as
Strattice or Artia) is preferable so as to restrict implant displacement within
the pocket. Similarly, for the indication of lower pole coverage for the
correction of ptosis, a tauter matrix is preferable to mitigate stretch deformity.
For the correction of capsular contracture, a more pliable matrix (such as
AlloDerm) is preferable so as not to cause too much lower pole constriction.
In addition, the ability of the ADM to mitigate the development of capsule
contracture, particularly AlloDerm, is an important consideration. For the
indication of tissue thickener, matrix pliability and thickness are important
criteria for ADM selection.

CASES
USE OF ADMS
Representative case examples highlighting the indications for ADM use
in breast revisionary surgery from the author’s practice are presented in
the Cases 1 to 3.

CASE 1

Figure 116-1A–C shows preoperative views of a 37-year-old woman


who had undergone breast augmentation and presented with bilateral
capsular contractures. Figure 116-1D–F shows the patient 32 months
after revision augmentation mastopexy (inverted T) which included the
development of neopectoral pocket, lower pole coverage with ADM, and
replacement of implants with form-stable implants.
FIGURE 116-1 A 37-year-old patient is shown preop (A–C) and postop at 32
months (D–F) in Case 1.

In Figure 116-2, the patient as seen in Figure 116-1 demonstrating the


softness of implants 32 months following the treatment of her capsular
contracture and ptosis.
FIGURE 116-2 Patient as shown in Case 1, Figure 116-1 demonstrating
softness of implants.

CASE 2

Figure 116-3A–C shows preoperative views of a 45-year-old woman


who had undergone multiple previous attempts at correction of capsular
contracture; Figure 116-3D–F shows the patient 22 months after
revision augmentation through IMF incision which included the
development of neopectoral pocket, lower pole coverage with ADM, and
replacement of implants with higher-profile silicone implants.
FIGURE 116-3 A 45-year-old patient is shown preop (A–C) and postop at 22
months (D–F) in Case 2.

In Figure 116-4, the patient as seen in Figure 116-3 demonstrating the


softness of implants 22 months following the treatment of her capsular
contracture.
FIGURE 116-4 Patient as shown in Case 2, Figure 116-3 demonstrating
softness of implants.

CASE 3

Figure 116-5A–C shows preoperative views of a 43-year-old woman


who had undergone prior augmentation with overfilled saline implants
and now with bottoming out. In Figure 116-5D–F, the patient is shown
12 months after revision augmentation through IMF incision which
included the development of neopectoral pocket, lower pole coverage
with ADM, and replacement of implants with higher-profile silicone
implants.
FIGURE 116-5 A 43-year-old patient is shown preop (A–C) and postop at 12
months (D–F) in Case 3.
INDICATIONS FOR BIOABSORBABLE MESH USE
The indications for bioabsorbable mesh use in breast revision surgery are
similar to those of ADMs, including as a pocket stabilizer for the correction
of implant malposition, correction of capsular contracture, and lower pole
implant coverage for the correction of ptosis or stretch deformity. In all of
these indications bioabsorbable meshes are used as soft tissue support to
reinforce the repair and the newly created implant pocket. Bioabsorbable
meshes are less desirable as a soft tissue thickener as they are not pliable.
The authors have had some experience with the use of bioabsorbable mesh
in the correction of implant malposition and capsular contracture. In a small
cohort of reconstructive patients (24 breasts) who had site change to the
prepectoral position, bioabsorbable mesh (GalaFlex) was used to fully wrap
the implant. (This is an OFF-LABEL use as the FDA has not cleared or
approved any surgical mesh for use in breast surgery/reconstruction
[15].) Preliminary data from a mean follow-up of 10 months show no
complications, including malposition recurrence and capsular contracture.
The authors have also used bioabsorbable mesh (GalaFlex) in conjunction
with ADM in prepectoral revision cases (64 patients, 124 breasts). In this
technique, the mesh is wrapped around the lower portion of the implant while
the rest of the implant is wrapped with ADM. At a mean follow-up of 18
months, complications were low (3.2%) and there was no incidence of
recurrence of malposition or capsular contracture (12).
The authors have a preference for mesh use at the lower pole because
compared with ADMs, mesh is sturdier and it does not stretch. Mesh, thus,
provides better lower pole support and pocket stability. A caveat though is
the lack of long-term data on mesh use. In particular, there is a need to
understand the long-term host inflammatory response to the mesh, although
short-term data seem promising. As bioabsorbable meshes are still synthetic
in nature, foreign body reaction with these meshes is a valid concern.

CASES
USE OF BIOABSORBABLE MESH
Representative case examples of bioabsorbable mesh use in breast
revisionary surgery from the author’s practice are presented in Cases 4 to
6.

CASE 4

Figure 116-6A–C preoperative views of a 64-year-old woman who had


undergone multiple previous attempts at correction of malposition are
shown. In Figure 116-6D–F the patient is shown 24 months after
revision augmentation through IMF incision which included the
development of neopectoral pocket, lower pole coverage with
bioabsorbable mesh, and replacement of implants with low-profile
silicone implants.
FIGURE 116-6 A 64-year-old patient is shown preop (A–C) and postop at 24
months (D–F) in Case 4.

CASE 5

Figure 116-7A–D preoperative views of a 41-year-old woman who had


undergone prior saline augmentation presenting with snoopy breast are
shown. In Figure 116-7E–H the patient is shown 24 months after
revision augmentation through IMF incision which included release of
muscle to dual plane 2 and lower pole support with bioabsorbable mesh
and replacement of implants with high-profile silicone implants.
FIGURE 116-7 A 41-year-old patient is shown preop (A–D) and postop at 24
months (E–H) in Case 5.
CASE 6

Figure 116-8A–C shows preoperative views of a 31-year-old woman


who had undergone prior breast augmentation and decided 1 year after
placement of implants to have them removed. She is now presenting with
a desire to have implants placed again. In Figure 116-8D–F 20 months
after revision augmentation through IMF incision which included
identifying the muscle and for the dual plane pocket which was retracted.
Lamellar release was performed to release the pec major muscle and both
muscle and lower pole were supported with bioabsorbable mesh and
replacement of implants with high-profile silicone implants.
FIGURE 116-8 A 31-year-old patient is shown preop (A–C) and postop at 24
months (D–F) in Case 6.
CONCLUSION
Revisionary breast surgery is common among patients who have previously
undergone augmentation mammaplasty or reconstructive surgery. Implant
malposition, capsular contracture, ptosis, and wrinkling/rippling are some of
the most frequent reasons for reoperation. Repair techniques generally
involve a combination of capsule modification, site change, and implant
exchange. ADMs have proved to be integrable to the repair as they support
and reinforce the repair, enhance soft tissue thickness, and prevent capsular
contracture. More recently, bioabsorbable meshes have been introduced into
revision surgery, primarily to reinforce the implant pocket. The future of
mesh use in revisionary surgery will be dependent on long-term data and the
host response to the mesh.

REFERENCES

1. American Society of Plastic Surgeons. 2018 Plastic surgery statistics


report. Available online at
https://www.plasticsurgery.org/documents/News/Statistics/2018/plastic-
surgery-statistics-full-report-2018.pdf. Accessed September 10, 2019.
2. Spear SL, Murphy DK, Slicton A, et al. Inamed silicone breast implant
U.S. Study Group. Inamed silicone breast implant core study results at 6
years. Plast Reconstr Surg 2007;120(7 Suppl 1):8S–16S.
3. Cunningham B, McCue J. Safety and effectiveness of Mentor’s
MemoryGel implants at 6 years. Aesthetic Plast Surg 2009;33:440–444.
4. Stevens WG, Harrington J, Alizadeh K, et al. Five-year follow-up data
from the U.S. clinical trial for Sientra’s U.S. Food and Drug
Administration-approved Silimed® brand round and shaped implants
with high-strength silicone gel. Plast Reconstr Surg 2012;130:973–981.
5. Maxwell GP, Van Natta BW, Murphy DK, et al. Natrelle style 410
form-stable silicone breast implants: core study results at 6 years.
Aesthet Surg J 2012;32:709–717.
6. Hammond DC, Migliori MM, Caplin DA, et al. Mentor contour profile
gel implants: clinical outcomes at 6 years. Plast Reconstr Surg
2012;129:1381–1391.
7. Baxter RA. Intracapsular allogenic dermal grafts for breast implant-
related problems. Plast Reconstr Surg 2003;112:1692–1696; discussion
1697–1698.
8. Maxwell GP, Gabriel A. Efficacy of acellular dermal matrices in
revisionary aesthetic breast surgery: a 6-year experience. Aesthet Surg J
2013;33:389–399.
9. Maxwell GP, Gabriel A. Non-cross-linked porcine acellular dermal
matrix in revision breast surgery: long-term outcomes and safety with
neopectoral pockets. Aesthet Surg J 2014;34:551–559.
10. Spear SL, Sher SR, Al-Attar A, et al. Applications of acellular dermal
matrix in revision breast reconstruction surgery. Plast Reconstr Surg
2014;133:1–10.
11. Spear SL, Seruya M, Clemens MW, et al. Acellular dermal matrix for
the treatment and prevention of implant-associated breast deformities.
Plast Surg Nurs 2017;37:76–87.
12. Sigalove S, Maxwell GP, Gabriel A. Outcomes utilizing Inspira
implants in revisionary reconstructive surgery. Plast Reconstr Surg
2019;144(1S Utilizing a Spectrum of Cohesive Implants in Aesthetic
and Reconstructive Breast Surgery):66S–72S.
13. Margulies IG, Salzberg CA. The use of acellular dermal matrix in breast
reconstruction: evolution of techniques over 2 decades. Gland Surg
2019;8:3–10.
14. Becker H, Lind JG 2nd. The use of synthetic mesh in reconstructive,
revision, and cosmetic breast surgery. Aesthetic Plast Surg
2013;37:914–921.
15. U.S. Food and Drug Administration. General and Plastic Surgery
Devices Panel of the Medical Devices Advisory Committee. Benefits
and Risks of Breast Implants. March 25–26, 2019.
16. Haiavy J, Frenzel CA. Correction of implant malposition with
capsulorrhaphy: a retrospective review and implementation of patient
survey. Am J Cosmetic Surg 2011;28:75–83.
17. Harris R, Raphael P, Harris SW. Thermal capsulorrhaphy: a modified
technique for breast pocket revision. Aesthet Surg J 2014;34:1041–1049.
18. Voice SD, Carlsen LN. Using a capsular flap to correct breast implant
malposition. Aesthet Surg J 2001;21:441–444.
19. Kaufman D. Pocket reinforcement using acellular dermal matrices in
revisionary breast augmentation. Clin Plast Surg 2012;39:137–148.
20. Maxwell GP, Gabriel A. The neopectoral pocket in revisionary breast
surgery. Aesthet Surg J 2008;28:463–467.
21. Rieger UM, Mesina J, Kalbermatten DF, et al. Bacterial biofilms and
capsular contracture in patients with breast implants. Br J Surg
2013;100:768–774.
22. Rieger UM, Raschke GF, Frei R, et al. Role of bacterial biofilms in
patients after reconstructive and aesthetic breast implant surgery. J Long
Term Eff Med Implants 2014;24:131–138.
23. Ajdic D, Zoghbi Y, Gerth D, et al. The relationship of bacterial biofilms
and capsular contracture in breast implants. Aesthet Surg J
2016;36:297–309.
24. Wan D, Rohrich RJ. Revisiting the management of capsular contracture
in breast augmentation: a systematic review. Plast Reconstr Surg
2016;137:826–841.
25. Hester TR, Ghazi BH, Moyer HR, et al. Use of dermal matrix to prevent
capsular contracture in aesthetic breast surgery. Plast Reconstr Surg
2012;130(5S-2):126S–136S.
26. Spear SL, Sinkin JC, Al-Attar A. Porcine acellular dermal matrix
(Strattice) in primary and revision cosmetic breast surgery. Plast
Reconstr Surg 2013;131:1140–1148.
27. Basu CB, Leong M, Hicks MJ. Acellular cadaveric dermis decreases the
inflammatory response in capsule formation in reconstructive breast
surgery. Plast Reconstr Surg 2010;126:1842–1847.
28. Leong M, Basu CB, Hicks MJ. Further evidence that human acellular
dermal matrix decreases inflammatory markers of capsule formation in
implant-based breast reconstruction. Aesthet Surg J 2015;35:40–47.
29. Chopra K, Buckingham B, Matthews J, et al. Acellular dermal matrix
reduces capsule formation in two-stage breast reconstruction. Int Wound
J 2017;14:414–419.
30. Ibrahim AM, Ayeni OA, Hughes KB, et al. Acellular dermal matrices in
breast surgery: a comprehensive review. Ann Plast Surg 2013;70:732–
738.

1Note: Although the subglan dular plane and the prepectoral plane are the same plane located under the
skin envelope, the difference in terminology is to highlight the presence or absence of glandular tissue,
respectively.
SECTION VIII

General Considerations in Aesthetic and


Reconstructive Surgery
117 Chest Masculinization for the Transmasculine Individual
118 Aesthetic Breast Surgery in Transgender Patients: Feminization
119 Tuberous Breast: Correction With and Without Implants
120 Effect of Smoking on Breast Plastic Surgery
121 Should elective Surgery Be Offered to High BMI Patients?
122 Breast Implant–Associated Anaplastic Large Cell Lymphoma
123 Proactive Approach to Capsular Contracture Prevention
124 Diagnosing, Treating, and Preventing Biofilms in Implant-based Breast
Surgery
125 Breast Implant Illness: What We Know Now?
126 Avoiding and Managing Patient Dissatisfaction
CHAPTER 117

Chest Masculinization for the


Transmasculine Individual
ARA A. SALIBIAN | RACHEL BLUEBOND-LANGNER
BACKGROUND

Gender Identity
A person’s gender identity refers to one’s core sense of being male, female,
parts of both, or neither. This identity does not always align with the sex
assigned at birth, which is typically based on natal genitalia. Transmasculine
individuals are assigned female at birth, but identify with masculinity,
whereas transfeminine individuals, are assigned a male sex at birth, but
identify with femininity. Gender nonbinary individuals do not identify
exclusively as either female or male.
According to the Williams Institute survey from 2016, approximately 1.4
million people, or 0.6% of adults in the United States, identify as transgender
(1). The incidence of gender dysphoria, a strong discordance between one’s
assigned and identified gender that causes significant distress, is estimated to
be 4.6 in 100,000 individuals (2). Gender dysphoria has an International
Classification of Disease (ICD-10) code under gender identity disorders
(F64.0-9) and is therefore considered a treatable medical condition that can
be covered by insurance.
For the transmasculine individual, the presence of breasts causes
significant distress and dysphoria (3). Chest wall masculinization,
colloquially referred to as masculinizing “top surgery,” has been
demonstrated to significantly improve quality of life, well-being, mental
health, sexual confidence, and body image in transmasculine individuals
(4–6). With increased access to care and increased coverage by insurance, the
number of transmasculine individuals seeking chest wall masculinization has
increased.
History
The surgical techniques utilized in chest masculinization evolved from
surgical treatments for gynecomastia, described by Davidson in 1979 (7).
Around the same time, Lindsay described the C, J, and inverted-T incision for
gender-affirming mastectomy (8). Periareolar techniques were later adapted
to masculinizing top surgery by Hage and Bloem, who also described
fusiform incisions and free nipple grafting in 1995 (9). Later in 2008,
Monstrey proposed a classification system based on bra size, ptosis grade,
and skin elasticity that directs decision making among five different
techniques including circumareolar variations, extended concentric
techniques, and free nipple grafting (10).
We prefer a simplified approach that utilizes two different techniques,
either the circumareolar technique or the double-incision free nipple graft
technique, based on the amount of glandular tissue, skin laxity, and ptosis
(11). Our approach still aims to fulfill the objectives proposed by Hage et al.
in 1995: 1) removal of breast tissue, 2) aesthetic contouring of the chest wall,
3) appropriate sizing and positioning of the nipple areolar complex (NAC), 4)
obliteration of the inframammary fold (IMF), and 5) minimization of scars
(9,12).
PREOPERATIVE CONSIDERATIONS

Preoperative Evaluation
General Considerations
As with any gender-affirming surgery, chest wall masculinization requires a
comprehensive approach to the healthcare needs of transgender and gender
nonbinary patients. Foremost, patients’ chosen names, gender identity, and
preferred pronouns should be elicited and documented appropriately.
Additional history relevant to gender-affirming surgery includes the date of
social transition and initiation of hormone therapy, if applicable. An “organ
inventory” is a useful means of documenting what organs have been removed
to guide future preventative care.
World Professional Association for Transgender Health (WPATH)
standards of care (SOC) should be followed for all patients undergoing
gender-affirmation surgery (13). Patients undergoing chest wall
masculinization require one referral letter from a qualified mental health
professional. Hormone therapy is not a prerequisite for chest wall
masculinization, though many transmasculine individuals are on testosterone.
Patients under the age of 18 may be candidates for chest wall masculinization
if a consensus is reached by the parents, the patient, the pediatrician, and the
mental health provider that delaying the patient’s surgery until after the age
of 18 will be harmful.

TABLE 117-1 Fisher Grading Systema


Grade Glandular Tissue Skin Laxity NAC Positionb
Grade 1 Minimal None Above
Grade 2a Moderate None/Little Above
Grade 2b Moderate Increased At/below
Grade 3 Significant None/little/increased Below
Grade 4 Deflated Significant Below
aBluebond-Langner R, Berli JU, Sabino J, et al. Top surgery in transgender men: how far can you push
the envelope? Plast Reconstr Surg 2017;139:873e–882e.
bIn
relation to inframammary fold.
NAC, nipple areolar complex.

Focused Assessment
Specific history pertinent to chest wall masculinization includes family
history of breast cancer and prior breast surgeries including biopsies, partial
mastectomies, mastopexy, augmentation, or reduction (14). Many transmale
patients bind the chest wall to conceal breasts. Binding history, including
length and frequency of binding should be documented. Binding can have a
negative effect on skin quality and elasticity (9), and can also worsen ptosis
which may influence the choice of operative technique. Smoking history is
also obtained and patients are advised to stop smoking at least 8 weeks prior
to surgery. Finally, patients’ desires with regard to surgical outcomes are an
important aspect of the preoperative evaluation. Preferences for incision
location, contour, and nipple position should be reviewed with the patient and
used to arrive at the most appropriate surgical technique jointly.
We find the Fischer scale (Table 117-1) (11), a grading system modified
from the Simon classification of gynecomastia, useful in determining the
optimal technique (periareolar or double incision) based on the amount of
glandular tissue, skin laxity, and degree of NAC ptosis (15). A Fischer grade
I patient has minimal breast tissue, no skin laxity, and a NAC above the IMF
(Fig. 117-1). Patients with Fischer grade 2 breasts have moderate glandular
tissue (Fig. 117-2) and are divided in 2a and 2b categories based on the
amount of skin laxity and the position of the NAC. A grade 2a breast has
minimal skin laxity and a NAC above the IMF whereas a 2b breast has
increased skin laxity and a NAC at or below the IMF. Fischer grade 3 breasts
have significant glandular tissue and a NAC below the IMF, with variable
amounts of skin laxity (Fig. 117-3). Fischer grade 4 breasts are deflated with
significant skin laxity and a NAC below the IMF (Fig. 117-3).

TABLE 117-2 Key Surgical Points in Double-Incision, Free Nipple Graft


Chest Wall Masculinization
Place incision in pectoral shadow, not the IMF
Incision should follow the pectoral shadow laterally
Obliterate the IMF during mastectomy
Place the nipple at the lower lateral aspect of the pectoralis major
Resize the NAC (2.2 cm)
Removal all glandular tissue so the chest is flat
Address the axillary roll if present
IMF, Inframammary fold; NAC, nipple areolar complex.

A standard breast examination should also be performed to identify any


palpable masses, skin changes, or nipple retraction or discharge. Routine
breast measurements including sternal notch-to-nipple, nipple-to-IMF,
internipple distance, areolar diameter and base diameter are recorded. Any
breast and/or chest wall asymmetry such as pectus deformity is documented
and discussed with the patient.

FIGURE 117-1 Fischer grade I breast: minimal glandular tissue, no skin laxity, and
NAC above the IMF. (From Bluebond-Langner R, Berli JU, Sabino J, et al. Top surgery
in transgender men: how far can you push the envelope? Plast Reconstr Surg
2017;139:873e–882e.)

FIGURE 117-2 Fischer grade 2 breasts have moderate glandular tissue. Left: Fischer
grade 2a breast with minimal skin laxity and NAC above the level of the IMF. Right:
Fischer grade 2b breast with increased skin laxity and NAC at or below the level of
the IMF. (From Bluebond-Langner R, Berli JU, Sabino J, et al. Top surgery in
transgender men: how far can you push the envelope? Plast Reconstr Surg
2017;139:873e–882e.)

Indications and Contraindications


The Fischer scale is utilized to determine the optimal mastectomy technique
that additionally best aligns with the patient’s desires. Typically, most
Fischer 1 and 2a patients are treated using a circumareolar technique which
offers enough access to resect all of the breast tissue as well as some skin.
Grade 3 and 4 patients are usually treated using a double-incision free nipple
graft technique given the large amount of glandular tissue or skin,
respectively, to be excised. Decision making for grade 2b patients is more
challenging (11). Grade 2b patients that are interested in the circumareolar
technique should be counseled on the increased likelihood of needing a
revision to address excess skin and the NAC. If a 2b patient elects a
periareolar approach, a larger concentric circle is utilized in order to resect
skin and resize the areola (10). Generally we wait 9 months prior to offering a
revision and encourage massage. The most common indication for revision is
either excess skin in the inferolateral aspect of the chest or widening of the
areola. We do not advise concomitant nipple reduction.
An extensive discussion should be had with the patient regarding risks and
expected outcomes that are individualized to each patient. Aside from the
general risks of surgery, the potential for loss of nipple sensation, asymmetry,
nipple and/or areolar necrosis, contour deformities, visible scarring, and the
need for revisionary surgery must be explained to, and understood by the
patient. Preoperative education and shared decision making are critical
aspects of gender-affirming procedures (16).

FIGURE 117-3 Left: Fischer grade 3 breast with significant glandular tissue and
NAC position below the IMF. Skin laxity can be variable. Right: Fischer grade 4
patient with deflated breasts, significant skin laxity, and NAC below the IMF. (From
Bluebond-Langner R, Berli JU, Sabino J, et al. Top surgery in transgender men: how far
can you push the envelope? Plast Reconstr Surg 2017;139:873e–882e.)

While absolute contraindications for chest masculinization are rare,


patients must be optimized prior to surgery in order to minimize relative
contraindications. Weight loss can be difficult due to inability to exercise
while wearing a binder or anxiety about going to a gym, but should be
encouraged to achieve the best outcome. Smoking cessation is particularly
important to ensure nipple survival. Systemic diseases, such as diabetes or
HIV, should be managed prior to surgery to ensure optimal healing. Mental
health must also be optimized and patients should have the appropriate
external support and access to follow up to streamline the recovery process.
Cancer Screening
Transmasculine individuals remain at risk for developing breast cancer but
are less likely to undergo regular preventative care for cancer screening (17).
Aside from eliciting a thorough history of risk factors for breast cancer,
patients should have screening mammography prior to surgery according to
the criteria for cisgender women (18). We require screening mammography
within 1 year prior to chest wall masculinization in patients over the age of
40 or those with family history and associated risk factors. Patients must be
counseled that despite the goal of removing the entire breast, some breast
tissue may be left behind and clinical examination is still recommended
postoperatively. We do suggest that all breast tissue regardless of age be
submitted to pathology. Surgeons should strive to remove all breast tissue
keeping in mind the footprint of the breast.
Hormone Therapy
Patients’ hormone therapy regime and provider should be queried and
documented. The appropriate management of hormones in the perioperative
period is still debated. In our practice, we have moved away from stopping
testosterone therapy prior to surgery. However, we do check a hemoglobin as
testosterone can increase hemoglobin leading to a hyperviscous state. Any
changes in hormone therapy should be made in coordination with the
patient’s hormone therapy provider.
INTRAOPERATIVE CARE

Circumareolar Technique
The midline IMF and outline of the breast are marked. The areola is then
resized to 1.8 cm. A second circle 1 cm beyond or to the edge of the areola is
then marked (Fig. 117-4). The superior half of the semicircle is
deepithelialized from the 9 o’clock to the 3 o’clock position in order to
preserve subdermal perfusion to the nipple. The inferior half of the semicircle
is also deepithelialized and then a full-thickness incision is made from the 3
o’clock to the 9 o’clock position and carried down through the subcutaneous
fat to the breast capsule with electrocautery. Inferiorly the plane between the
breast capsule and subcutaneous tissue is dissected past the IMF and care is
taken to obliterate the IMF. A lighted retractor is useful in this dissection.
Superiorly, 1 to 1.5 cm of breast tissue is maintained behind the nipple to
preserve the blood supply and prevent formation of a saucer deformity. The
superior breast flap is then elevated in the plane between the breast capsule
and the subcutaneous tissue to the upper and lateral borders of the breast. The
glandular tissue is the elevated off of the chest wall and the pocket is
inspected for hemostasis as well as to ensure that all glandular tissue has been
removed.
FIGURE 117-4 Markings for circumareolar mastectomy. The nipple is resized to 22
mm and a second, larger concentric circle is marked around the areola. The superior
semicircle is deepithelialized to preserve subdermal perfusion and the inferior
semicircle is utilized for access. (From Bluebond-Langner R, Berli JU, Sabino J, et al.
Top surgery in transgender men: how far can you push the envelope? Plast Reconstr Surg
2017;139:873e–882e.)

The procedure is the performed in the same fashion on the contralateral


side. The pocket is then thoroughly irrigated and hemostasis is confirmed.
One round fluted drain is placed in the subcutaneous pocket on either side.
The incisions are closed in a layered fashion with 3-0 deep dermal sutures,
followed by a 2-0 barbed purse-string suture and a 5-0 fast-absorbing gut
suture. The incisions are dressed with petroleum-based gauze, dry gauze, and
contouring foam. Finally, a binder or compression vest is placed over the
chest wall.
Double-Incision Free Nipple Graft Technique
Markings for the double-incision free nipple graft technique are performed
with the patient standing in the preoperative area. The horizontal incision is
marked at the inferior boarder of the pectoralis muscle not the IMF (Figs.
117-5 and 117-6). The lateral boarder of the pectoralis muscle is marked and
the lateral tail of the incision is then angled up toward the axilla to follow the
lateral edge of the pectoralis muscle. The IMF and midline are also marked. It
is ideal to keep the incision 2 cm off the midline. The incisions sometimes
must meet in the center to avoid a central dog-ear. In this case the incisions
are angled slightly superiorly (Fig. 117-7).
FIGURE 117-5 Markings for double-incision free nipple graft technique. The
incision is placed at the inferior boarder of the pectoralis, not necessarily the IMF,
and is carried laterally along the lateral border of the pectoralis. (Adapted from
Bluebond-Langner R, Berli JU, Sabino J, et al. Top surgery in transgender men: how far
can you push the envelope? Plast Reconstr Surg 2017;139:873e–882e.)
FIGURE 117-6 Placement of the incision along the pectoral shadow and not the IMF
in the free nipple graft technique is critical in obtaining appropriate masculine
aesthetic outcomes. Above: Incisions are concealed in the pectoral shadow inferiorly
and laterally and subsequently emphasize the pectoralis muscle. Below: The outcome
could have been improved by carrying the incisions up laterally along the border of
the pectoralis muscle.
FIGURE 117-7 In the double-incision technique, it may be necessary to have the
incisions meet in the midline to avoid dog-ears. A gentle inverted V recapitulates the
gull wing of the pectoralis muscles.

FIGURE 117-8 The nipple areolar complex should be resided to be smaller, around
2.2 × 2.2 cm, to more closely resemble the male nipple and areola phenotype.

In the operating room, the NACs are marked as 2.2 × 2.2 cm circles (Fig.
117-8) and are sharply removed as full-thickness skin grafts and preserved on
the back table. A full-thickness incision is then made in the superior mark
and the dissection is carried down to the level of the breast capsule using
electrocautery. This dissection is carried superiorly and laterally in the plane
between the capsule and the subcutaneous fat to develop the superior
mastectomy flap. It is important to follow the breast capsule. Care is taken to
include all breast parenchyma in the axillary tail and the dissection is carried
laterally to the edge of the latissimus dorsi muscle. The breast tissue is
subsequently elevated off of the pectoralis muscle. The superior flap is then
pulled down inferiorly and the position of the inferior transverse incision is
marked. This is often above the IMF. The inferior incision is made and the
mastectomy is completed inferiorly. Care is taken to dissect beyond and
obliterate the IMF. The pocket is inspected to ensure that all glandular tissue
has been removed and hemostasis is obtained. The mastectomy is then
repeated in the same fashion on the contralateral side.
The incisions are temporarily tacked closed with staples and the patient is
sat upright with their arms to the side. The new nipple position is marked in
the lower outer corner of the pectoralis, generally 2 cm above the incision and
2 to 2.5 cm medial to the lateral pectoral border. Measurements are taken to
ensure symmetry and small adjustments are made to optimize nipple position
according to individual chest wall contour and symmetry. A 2.2 × 2.2 cm
circle is then deepithelialized in the appropriate position bilaterally. The
nipples are thinned on the back table, placed back on the chest wall, and
sutured into place with a running 5-0 fast-absorbing gut suture. A fluted
circular drain is placed in the subcutaneous pocket on either side and
transverse incisions are closed with a dermal stapler, followed by a running
intradermal barbed suture.
The incisions are dressed with adhesive tape and the nipples are secured
with cotton, mineral oil, and petroleum gauze bolsters. Dry gauze dressings
are subsequently placed over the incisions and soft foam is contoured to the
chest. Finally, the patient is placed in a binder or a compression vest.
POSTOPERATIVE CARE
Patients should be checked the next morning for a hematoma. Drains are
stripped three times a day. If a free nipple graft was performed the bolsters
are taken down at 5 to 7 days. Antibiotic ointment and nonadhesive dressings
are subsequently applied to the nipples twice daily. Drains are removed after
output is less than 30 cc over a 24-hour period and binders are discontinued 1
week after the drain is removed. Patients are then allowed to shower and
strenuous activity, exercise, or heavy lifting are limited for 4 to 6 weeks after
surgery. Patients are instructed to take acetaminophen and ibuprofen for pain
and are given a very limited prescription of narcotic medication for
breakthrough pain.

CASES

CASE 1

A Fisher grade 2b transmale patient desiring chest wall masculinization


planned for a circumareolar technique is shown in Case 1, Figure 117-9.
Figure 117-9A shows the patient (preoperative) demonstrating moderate
breast size with skin redundancy. Figure 117-9B shows the patient
postoperative demonstrating flat chest wall contour, well-hidden
periareolar scars, and appropriate NAC positioning.
FIGURE 117-9 Fisher grade 2b transmale patient. A: Preoperative
photograph demonstrating moderate breast size with skin redundancy. B:
Postoperative photograph after periareolar mastectomy with flat chest wall
contour, well-hidden periareolar scars, and appropriate NAC positioning.

CASE 2

A Fisher grade 2b transmale patient desiring chest wall masculinization


planned for double-incision free nipple graft technique is shown in Case
2, Figure 117-10. Figure 117-10A shows the patient preoperatively
demonstrating moderate breast size with skin redundancy. Figure 117-
10B shows the patient postoperative with the incision hidden in pectoral
shadow, appropriate contour, and placement of NAC just medial to lateral
pectoral border.

FIGURE 117-10 Fisher grade 2b transmale. A: Preoperative photograph


demonstrating moderate breast size with skin redundancy. B: Postoperative
photograph after double-incision mastectomy with free nipple grafts
demonstrating incisions hidden in pectoral shadow, appropriate contour, and
placement of NAC just medial to lateral pectoral border.

CASE 3
A Fisher grade 3 transmale patient desiring chest wall masculinization
planned for double-incision free nipple graft technique is shown in Case
3, Figure 117-11. In Figure 117-11A, the patient is shown preoperative
demonstrating significant glandular tissue with increase skin laxity and
NAC position below the IMF. In Figure 117-11B, the patient is shown
postoperative with incisions following pectoral shadow laterally and
slanted slightly superiorly medially.

FIGURE 117-11 Fisher grade 3 transmale patient. A: Preoperative


photograph demonstrating significant glandular tissue with increase skin
laxity and NAC position below the IMF. B: Postoperative photograph after
double-incision free nipple graft technique with incisions following pectoral
shadow laterally and angled slightly superiorly medially. (From Bluebond-
Langner R, Berli JU, Sabino J, et al. Top surgery in transgender men: how
far can you push the envelope? Plast Reconstr Surg 2017;139:873e–882e.)
GENERIC RISKS
Chest masculinization is a safe operation however there are certain
complications which should be highlighted. Hematoma rates range from 6%
to 15% (11,19–22). Smaller hematomas can sometimes be milked out
through drains; however larger collections should be evacuated in the
operating room to prevent fibrosis that leads to contour deformity,
compromise of the NAC, and infection. Seromas should also be aggressively
drained to avoid fibrosis and contour deformity (Fig. 117-12). Infection and
wound dehiscence are exceptionally rare (11,23–25), though these
complications may be higher in patients with comorbidities predisposing to
poor wound healing such as obesity and in smokers.

FIGURE 117-12 A: Bilateral postoperative seromas, larger on the right, after


circumareolar technique. B: Flat chest wall contour restored after aggressive serial
aspirations.

NAC necrosis can occur secondary to poor skin graft take or a poorly
vascularized subareolar pedicle, and is reported in 1.2% to 5.8% of cases
(11,23,26). Contributing factors include pressure from a subcutaneous
collection such as a hematoma, as well as predisposition to poor vascularity
in active smokers. After healing with local wound care, secondary
reconstruction and tattooing can be performed. Nipple hypopigmentation
often occurs in darker-skinned patients. Thinning the graft helps preserve
pigment. The pigment often returns but can also be tattooed at 6 to 9 months.
Minor revisions may be necessary but can often be done in the office (27).
Common reasons for revision in the circumareolar technique include resizing
of the NAC due to spreading, nipple reduction, and excision of excess skin in
the inferolateral aspect of the chest through a circumareolar incision. For the
double-incision technique a standing cone deformity centrally or laterally, a
wide or hypertrophic scar or incision that does not follow the pectoralis
boarder may need to be addressed.
OUTCOMES
Chest wall masculinization has been shown to improve many quality-of-life
measures as well as mental health in transgender and gender nonbinary
patients (4,5). This can be a life-saving measure in individuals with gender
dysphoria. The safety of chest wall masculinization has been well
demonstrated. While rates of overall complications range from around 7.7%
to 27% (11,20,22,26,28), the majority of these are minor complications that
do not require significant interventions. Acute reoperation occurs most
commonly for hematoma, and has been found to be significantly higher in
techniques that do not excise skin (29), possibly due to poorer visualization
with these techniques.
The need for secondary revision procedures should be discussed with
patients preoperatively. Chest wall revision can be indicated for a number of
reasons including contour deformities, scar widening or hypertrophy, residual
axillary fullness, and NAC widening. The need for revision can be higher
with particular techniques and patient phenotypes, such as the Fisher grade
2b patient who elects for a periareolar or a patient with a higher BMI. This is
consistent with other studies that have shown overall lower rates of revision
with double-incision free nipple graft techniques (29). While selection of the
appropriate technique and precise execution of the procedure minimizes the
need for revision, secondary operations are sometimes necessary regardless
in order to achieve the best aesthetic outcome.
CONCLUSION
Chest wall masculinization has increased with the expansion of insurance
coverage to include gender-affirming procedures, the standardization of
surgical techniques, and the ability to provide reproducible surgical
outcomes. The preoperative workup is critical for the success of these
procedures, and requires a multidisciplinary approach. Breast size, skin
laxity, and degree of ptosis together with patient desires dictate the technique
selected. Successful chest wall masculinization requires removal of all
glandular tissue, obliteration of the IMF, resizing of the NAC, and
appropriate placement of incisions. Attention to details and adherence to
principles will minimize postoperative complications and the need for
secondary procedures while optimizing the ability to create an aesthetic,
masculine chest.

REFERENCES

1. Flores AR, Herman JL, Gates GJ, et al. How many adults identify as
transgender in the United States. 2016.
https://williamsinstitute.law.ucla.edu/wp-content/uploads/How-Many-
Adults-Identify-as-Transgender-in-the-United-States.pdf. Accessed
December 25.
2. Arcelus J, Bouman WP, Van Den Noortgate W, et al. Systematic review
and meta-analysis of prevalence studies in transsexualism. Eur
Psychiatry 2015;30:807–815.
3. van de Grift TC, Cohen-Kettenis PT, Steensma TD, et al. Body
satisfaction and physical appearance in gender dysphoria. Arch Sex
Behav 2016;45:575–585.
4. Agarwal CA, Scheefer MF, Wright LN, et al. Quality of life
improvement after chest wall masculinization in female-to-male
transgender patients: a prospective study using the BREAST-Q and
body uneasiness test. J Plast Reconstr Aesthet Surg 2018;71:651–657.
5. Poudrier G, Nolan IT, Cook TE, et al. Assessing quality of life and
patient-reported satisfaction with masculinizing top surgery: a mixed-
methods descriptive survey study. Plast Reconstr Surg 2019;143:272–
279.
6. Canner JK, Harfouch O, Kodadek LM, et al. Temporal trends in gender-
affirming surgery among transgender patients in the United States.
JAMA Surg 2018;153(7):609–616.
7. Davidson BA. Concentric circle operation for massive gynecomastia to
excise the redundant skin. Plast Reconstr Surg 1979;63:350–354.
8. Lindsay WR. Creation of a male chest in female transsexuals. Ann Plast
Surg 1979;3:39–46.
9. Hage JJ, Bloem JJ. Chest wall contouring for female-to-male
transsexuals: Amsterdam experience. Ann Plast Surg 1995;34:59–66.
10. Monstrey S, Selvaggi G, Ceulemans P, et al. Chest-wall contouring
surgery in female-to-male transsexuals: a new algorithm. Plast Reconstr
Surg 2008;121:849–859.
11. Bluebond-Langner R, Berli JU, Sabino J, et al. Top surgery in
transgender men: how far can you push the envelope? Plast Reconstr
Surg 2017;139:873e–882e.
12. Hage JJ, van Kesteren PJ. Chest-wall contouring in female-to-male
transsexuals: basic considerations and review of the literature. Plast
Reconstr Surg 1995;96:386–391.
13. The World Professional Association for Transgender Health. Standards
of Care for the Health of Transsexual, Transgender, and Gender
Nonconforming People. 7th Version. 2011;
https://www.wpath.org/media/cms/Documents/Web
Transfer/SOC/Standards of Care V7 – 2011 WPATH.pdf. Accessed
April 10, 2018.
14. Salim A, Metz E, Constant JS, et al. Does previous breast reduction
affect the outcome of gender-affirming subcutaneous mastectomy? Ann
Plast Surg 2018;80:S279–S284.
15. Simon BE, Hoffman S, Kahn S. Classification and surgical correction of
gynecomastia. Plast Reconstr Surg 1973;51:48–52.
16. Smith YL, Van Goozen SH, Kuiper AJ, et al. Sex reassignment:
outcomes and predictors of treatment for adolescent and adult
transsexuals. Psychol Med 2005;35:89–99.
17. Bazzi AR, Whorms DS, King DS, et al. Adherence to mammography
screening guidelines among transgender persons and sexual minority
women. Am J Public Health 2015;105:2356–2358.
18. American Cancer Society. American Cancer Society Guidelines for the
Early Detection of Cancer. 2018; https://www.cancer.org/healthy/find-
cancer-early/cancer-screening-guidelines/american-cancer-society-
guidelines-for-the-early-detection-of-cancer.html. Accessed January 2,
2019.
19. Cregten-Escobar P, Bouman MB, Buncamper ME, et al. Subcutaneous
mastectomy in female-to-male transsexuals: a retrospective cohort-
analysis of 202 patients. J Sex Med 2012;9:3148–3153.
20. McEvenue G, Xu FZ, Cai R, et al. Female-to-male gender affirming top
surgery: a single surgeon’s 15-year retrospective review and treatment
algorithm. Aesthet Surg J 2017;38:49–57.
21. Frederick MJ, Berhanu AE, Bartlett R. Chest surgery in female to male
transgender individuals. Ann Plast Surg 2017;78:249–253.
22. Donato DP, Walzer NK, Rivera A, et al. Female-to-male chest
reconstruction: a review of technique and outcomes. Ann Plast Surg
2017;79:259–263.
23. van de Grift TC, Elfering L, Bouman MB, et al. Surgical indications and
outcomes of mastectomy in transmen: a prospective study of technical
and self-reported measures. Plast Reconstr Surg 2017;140:415e–424e.
24. Bjerrome Ahlin H, Kolby L, Elander A, et al. Improved results after
implementation of the Ghent algorithm for subcutaneous mastectomy in
female-to-male transsexuals. J Plast Surg Hand Surg 2014;48:362–367.
25. Berry MG, Curtis R, Davies D. Female-to-male transgender chest
reconstruction: a large consecutive, single-surgeon experience. J Plast
Reconstr Aesthet Surg 2012;65:711–719.
26. Wolter A, Diedrichson J, Scholz T, et al. Sexual reassignment surgery in
female-to-male transsexuals: an algorithm for subcutaneous
mastectomy. J Plast Reconstr Aesthet Surg 2015;68:184–191.
27. Ammari T, Sluiter EC, Gast K, et al. Female-to-male gender-affirming
chest reconstruction surgery. Aesthet Surg J 2019;39(2):150–163.
28. Takayanagi S, Nakagawa C. Chest wall contouring for female-to-male
transsexuals. Aesthetic Plast Surg 2006;30:206–212; discussion 213–
214.
29. Wilson SC, Morrison SD, Anzai L, et al. Masculinizing top surgery: a
systematic review of techniques and outcomes. Ann Plast Surg
2018;80:679–683.
CHAPTER 118

Aesthetic Breast Surgery in


Transgender Patients: Feminization
LOREN S. SCHECHTER | ALEXANDER FACQUE

Population estimates of the prevalence and incidence of transgender and


gender diverse communities vary by location, time period, and methodology
used to collect data. Due to structural and methodologic limitations of data
collection, the true size of these communities is likely underestimated. In the
United States, population estimates have been reported at 22.9 per 100,000
(1) or, in other estimations, 0.6% of the population (2), approximately 1.4
million adults (3). Gender diversity represents the collective experience of
many individuals’ gender identity, role, or expression that differ from cultural
norms or expectations (4). Gender dysphoria is a diagnosis that refers to the
discomfort or distress that is caused by a discrepancy between a person’s
gender identity and that person’s sex assigned at birth (5). An effort has been
made to distinguish the many manifestations of gender diversity found within
our society from the diagnosis of gender dysphoria, in order to depathologize
the former.
Chest feminization (breast augmentation) for the treatment of gender
dysphoria is considered a reconstructive, rather than a cosmetic procedure. In
fact, The World Professional Association for Transgender Health (WPATH),
in the seventh version of the Standards of Care for the Health of Transsexual,
Transgender, and Gender Nonconforming People (SOC) emphasizes that
breast augmentation can be medically necessary, depending on the clinical
situation of a given patient’s condition and life situation (4). For those
individuals seeking surgical intervention, chest feminization is one of the
more commonly requested surgical procedures (6). In one report, 67% of
patients undergoing vaginoplasty for gender confirmation also underwent
breast augmentation (7). Many of the principles of breast augmentation in
cisgender women are applicable in chest feminization for transgender
women; however, anatomic differences and the effects of hormone treatment
(HT) require technical modifications and other specific considerations when
selecting breast implants.
TRANSFEMININE MAMMOGENESIS
Many gender diverse individuals seek medical management with hormone
therapy. Hormone treatments for transgender women include various
combinations of estrogen, progestin, and antiandrogen medications. The most
common form of exogenous estrogen, ethinyl-estradiol (EE), can be
administered through oral, transdermal, or intramuscular routes. HT produces
feminizing physical changes through induction of breast development, altered
fat distribution, and softening of skin. It also downregulates gonadotropin
levels in order to lower circulating testosterone levels (8,9). Mammogenesis
in transfeminine individuals receiving estrogen follows a pattern similar to
cisgender female puberty (10); however, for some individuals, the result of
hormone therapy alone will be inadequate to create a sufficiently feminine
breast form (11–15). Breast growth in response to exogenous hormones may
be independent of hormone dose, type, or mode of delivery (16,17). There
appears to be no difference in the final breast size of transgender women who
received combination therapy with progestin and estrogen when compared to
those individuals who received estrogen alone or in those individuals taking
gonadotropin releasing hormone (GnRH) analogs (7,13,18,19). Wierck et al.
in 2014 observed that breast growth usually begins within 2 to 3 months
following initiation of HT and continues to progress over 2 years (13). This
finding is consistent with Meyer et al., who found that the duration of
hormone therapy influences final breast size (17). As such, many surgeons,
and the WPATH SOC, recommend a 12-month period of feminizing
hormone therapy prior to breast augmentation. Some surgeons report that
preoperative hormone therapy optimizes surgical results by allowing breast
growth and promoting skin expansion (4,12). The senior author does not
require 1 year of preoperative hormone therapy. It is not uncommon for
patients to describe breast pain and tenderness during the proliferative phase.
It is the author’s experience that once breast pain and tenderness have
resolved, no significant additional breast growth will be achieved.
PREOPERATIVE CONSIDERATIONS
Effective communication is important in building trust between patients and
physicians. Language used in the gender diverse community, including
pronoun selection, continues to evolve. Individuals may identify as male,
female, both, or neither, and may consider themselves as gender diverse,
nonbinary, genderqueer, or gender expansive. A person’s pronouns (he/his,
she/her, or the gender neutral they/their) cannot be assumed based on the
physician’s interpretation of the patient’s appearance. Asking and correctly
using a patient’s pronouns will convey respect for gender diversity and foster
an environment of trust.
In the preoperative evaluation, a medical history including hormone use,
usage of illicit drugs and tobacco, and history of injections (i.e., silicone) to
the breast is obtained. Silicone injections may have adverse effects, including
granulomas and draining sinus tracts. These issues may preclude breast
augmentation. Breast cancer screening guidelines follow those of cisgender
women. Currently, the U.S. Preventive Services Task Force (USPSTF)
recommends screening mammography every other year from age 50 to 74
(20). The American College of Radiology recommends mammograms yearly,
starting at age 40 (21). Knowledge of a patient’s family and personal history
of breast malignancy guides the need for imaging studies and/or genetic
testing. A genetic predisposition (such as BRCA mutations) should be
considered in patients with multiple breast and/or ovarian cancers within their
family (often diagnosed at an early age); 2 or more primary breast and/or
ovarian cancers in a single family member, and/or cases of male breast cancer
within their family (22).
As per the SOC, preoperative guidelines for breast augmentation and
creation of a feminine chest include: persistent, well-documented gender
dysphoria (one referral letter from a mental health professional), capacity to
make a fully informed decision and to consent for treatment, age of majority
in a given country (although surgical treatment of adolescents is permitted),
and, if significant medical or mental health concerns are present, they must be
reasonably well controlled. While hormone therapy is not a prerequisite to
surgery, many surgeons recommend a minimum of 12 months of hormone
therapy in order to optimize results (4). In the senior author’s practice,
estrogen (and progesterone) are discontinued 2 weeks prior to and following
surgery, in order to reduce the risk of venous thromboembolism (VTE).
TRANSFEMININE BREAST ANATOMY
Transgender women have a wider chest with lateralized nipples (increased
distance between breast meridians), a shorter nipple to inframammary fold
(IMF) length, a smaller nipple areolar complex (NAC) which is often ovoid
or elliptical in shape, a tighter skin envelope, and a larger pectoralis major
muscle (e-Fig. 118-1) (14,23). These anatomic differences influence implant
selection and surgical planning including pocket location and incision choice.

E-FIGURE 118-1 Transfeminine breast anatomy: wide chest wall, lateralized NAC,
tight skin envelope with constricted lower pole, limited breast volume, small NAC
diameter, broad and thick pectoralis major muscle, and an indistinct IMF. Each of
these features impacts the technique, choice of incision, pocket location, and choice of
implant. (With permission and © of Drs. Loren Schecter and Alexander Facque.)
SURGICAL CONSIDERATIONS
Extrapolating from the cisgender population, the “ideal” breast has: (1) 55%
of the implant located in the lower pole (below the NAC), (2) an NAC with
an upward cant of 20 degrees, (3) an upper pole which slopes with a straight
or mildly concave shape, and (4) a lower pole which has a tight, convex
curve (24). Creation of both medial and lateral cleavage is important, as a
breast that does not extend past the chest wall typically confers a more
masculine or prepubertal appearance (e-Fig. 118-2).

E-FIGURE 118-2 A. Preoperative transfeminine patient demonstrating a wide chest


wall, lateralized NAC, minimal breast development, and lower pole skin deficiency.
B. Post-operative result following subpectoral breast augmentation via an
inframammary approach, mini abdominoplasty, and liposuction. (With permission
and © of Drs. Loren Schecter and Alexander Facque.)

Options for breast augmentation include both implant-based and lipofilling


techniques. Lipofilling is generally reserved as an adjunct maneuver for
camouflaging wide medial cleavage that may occur following breast
augmentation (12). On occasion, preliminary tissue expansion may be
required for individuals with a tight skin envelope. In the author’s practice,
this is not commonly performed.
Incision
Incision options include periareolar, inframammary fold (IMF), and
transaxillary. Due to the smaller NAC (and often larger implant selection), a
periareolar incision is not often recommended. In addition, periareolar and
transaxillary incisions may place the patient at a higher risk of capsular
contracture (25,26). While some patients prefer to avoid incisions on the
breast, the transaxillary approach may limit the ability to control medial and
inferior dissection of the pocket. Accurate inferior and medial pocket
dissection is important. Due to the wider chest and more prominent pectoralis
major muscle, the medial pectoralis major is typically released. It is important
to leave the overlying fascial connections intact so as to prevent symmastia.
For these reasons, the author prefers an IMF incision. An IMF incision
facilitates placement of large implants and allows for visualization of the
entire breast pocket. The IMF incision is also associated with a lower rate of
capsular contracture (25–27). The IMF incision is typically placed 1.5 to 2
cm below the existing IMF depending upon the preoperative nipple to fold
distance and the implant size and profile (e-Fig. 118-3). In 2016, Mallucci
and Branford created a formula for IMF incision placement to assist with
positioning of the final scar at the new IMF. Termed the ICE method, the
formula is as follows: I (implant dimensions, in cm) − C (capacity of the
breast, in cm) = E (excess tissue required, in cm) (i.e., I − C = E). The excess
tissue required is the distance between the existing IMF and the
recommended IMF. This formula also allows precise determination of the
implant distribution between the upper and lower poles; however, it is
required that the exact characteristics of the implant is known before the
initial incision is made (24).

E-FIGURE 118-3 Pre-operative, intra-operative, and post-operative views of a


patient undergoing chest feminization. A: Pre-operative image demonstrating a wide
chest with lateralized NAC. Also of note are minimal breast development, an
indistinct IMF, and a short IMF to NAC length. Pre-operative markings
demonstrating anticipated lowered IMF. B: Intra-operative photo with implant
placed and IMF lowered. The author recommends undermining, but maintaining the
inferomedial attachments of the pectoralis muscle. The parasternal pectoralis is
released maintaining the integrity of the overlying fascia. The implant is centered
under the NAC. C: Post-operative result with placement of a 530cc subpectoral
implant. (With permission and © of Drs. Loren Schecter and Alexander Facque.)

Implant Fill
The choice between saline and silicone implants is primarily based on patient
preference. Patients are counseled that saline implants may be associated with
a higher degree of skin irregularity, or “rippling,” especially in thin patients
(27,28). The potential benefits of saline implants include the ability to place
the implant through a smaller incision, adjustability of size (within
manufacturers’ guidelines), and the early recognition of implant deflation. In
the senior author’s experience, while silicone implants typically require a
longer incision for placement, they are typically preferred by patients due to a
more “natural” feel. Implant manufacturers and the FDA recommend an MRI
periodically in order to assess for implant rupture (29,30).
Implant Shape and Texturization
In the author’s practice, the choice between smooth and textured devices has
evolved based on concerns related to the increase in cases of Breast Implant
Associated Anaplastic Large Cell Lymphoma (BIA-ALCL) with textured
implants. Texturization is designed to reduce the risk of malposition with
shaped implants and has demonstrated a decreased incidence of capsular
contracture (25,26). The incidence of BIA-ALCL is recorded at between 1 in
3,817 and 1 in 30,000 individuals and has only been found in people with
exposure to textured breast implants (31–33). While the purported aesthetic
benefit of shaped implants includes a more natural breast contour, this
theoretical advantage has been called into question. In postoperative
cisgender breast augmentation patients, a majority of both patients and
surgeons are unable to distinguish whether round or shaped implants were
placed (34). The disadvantages of shaped implants (less natural feel, risk of
rotation, and increased incision length), without a clear aesthetic benefit have
resulted in their decreased use compared to smooth, round implants (35).
Implant Size
In the author’s chest feminization practice, larger (most often between 375 cc
and 500 cc) implants are typically chosen as compared to implant choice in
cisgender women (e-Fig. 118-4). Not only does the wider chest require a
wider base width implant, many transgender women also request large
implants (7).
E-FIGURE 118-4 Pre and post operative chest feminization. A 425cc moderate plus
profile silicone implant placed via an IMF incision. (With permission and © of Drs.
Loren Schecter and Alexander Facque.)

Pocket Selection
The subpectoral pocket allows greater soft tissue coverage of the implant and
possibly less risk of capsular contracture (25,26,36). However, due to the
thicker and broader pectoralis major muscle, animation deformities may be
more obvious. In patients with sufficient breast development, a subglandular
pocket may be an option. While the subglandular position is associated with
less postoperative pain, it is also associated with a higher rate of capsular
contracture. Also, less implant “support” in the lower pole raises concerns
regarding “bottoming out” of the implant. When a subglandular pocket is
chosen, Scarpa fascia is secured to the chest wall during closure. The dual
plane technique (partial muscle coverage, partial glandular coverage) offers
the advantage of increased soft tissue coverage in the upper pole (more
natural appearance, less rippling) and the benefit of recruiting breast tissue to
cover the lower pole (37). The dual-plane technique is also useful with a
constricted lower pole (quite common in transgender women), or a when a
small degree of breast ptosis is present.
SPECIAL CONSIDERATIONS IN CHEST FEMINIZATION
The author’s preference is to center the implant beneath the NAC. As a result
of the wider chest and lateralized NAC in transgender women, an increased
space between the midline cleavage may result. A wide base width implant
and adjunct lipofilling may ameliorate this (12). Transgender women also
tend to have smaller, more elliptically shaped NAC. While the NAC tends to
enlarge following breast augmentation, tattoo can be used to augment NAC
size if desired. In some patients with an insufficient skin envelope
(particularly in the vertical dimension of the lower pole), tissue expansion
may be helpful. In the author’s opinion, tissue can typically be recruited with
medial pectoralis fiber release, lateral pocket dissection, and lowering the
IMF, thereby precluding the need for tissue expanders (38,39). On occasion,
scoring of the lower pole of the breast may be performed to release a
constricted lower breast.
POSTOPERATIVE CARE
Following surgery, patients are placed in a soft, supportive garment and are
instructed to avoid lifting over 10 to 15 pounds for 3 weeks. Patients may
resume unrestricted activity 6 weeks after surgery. Breast massage begins 2
to 3 weeks following surgery.
COMPLICATIONS
Complications following chest surgery are similar to those seen in cisgender
breast augmentation, with an incidence ranging from 0% to 10.9% (40,41).
Kanhai and colleagues reported 22 complications occurring in the 201
patients in their series. These “ranged from hematoma to symmastia,” with
capsular contracture the most frequently occurring, recorded in 11 of the 22
complications or 5.4% of cases (40). Additional possible complications
include alterations in nipple and/or breast sensation, implant palpability, skin
rippling, implant rupture, and implant malposition (12).
Postoperative breast surveillance is consistent with protocols for cisgender
women (22). Gooren and colleagues performed a cohort study in 2,307
transgender individuals with an exposure to HT between 5 years and 30
years. They reported 10 cases of breast cancer in transgender women. Three
of the 10 cases were not estrogen-dependent breast carcinomas. This study
suggests that HT does not increase the risk of breast cancer development in
transgender women; the incidence of breast carcinoma was comparable to
cisgender male breast cancer, but lower than in the cisgender female
population (42).
OUTCOMES
The majority of patients undergoing chest feminization are satisfied with the
outcome following surgery. In one report, 107 subjects were followed for 5.5
years after breast augmentation. Of these, 80 respondents (75%) reported
satisfaction with the outcome. Of the 27 that were dissatisfied, 18 believed
that their breasts were too small (7). In a prospective, noncomparative cohort
study, Weigert et al. reported that the improvements in breast satisfaction,
psychosocial well-being, and sexual well-being are statistically significant
and clinically meaningful to the patient with average increases in each
category of 40 to 57 points (41). Improvement in sexual well-being should be
considered in conjunction with outcomes of genital confirmation surgery,
which at times occurred in tandem with chest feminization in this study and
could have influenced the result. Another important consideration to the
findings of this study was that the gains in well-being were measured using
the BREAST-Q. This study tool is not validated in the gender diverse
population.
SUMMARY
As societal acceptance of gender diversity continues to improve, surgeons
will likely encounter more requests for chest feminization. Plastic surgeons
are well equipped to transfer their skills from cisgender breast augmentation
to transfeminine chest surgery. The WPATH SOC are designed to assist the
surgeon in preoperative selection of patients. Knowledge of the specific
anatomic considerations and technical modifications in gender diverse
patients is required to optimize surgical results and achieve a safe and
aesthetically pleasing result.

REFERENCES

1. Blosnich JR, Brown GR, Shipherd JC, et al. Prevalence of gender


identity disorder and suicide risk among transgender veterans utilizing
Veterans Health Administration care. Am J Public Health
2013;103:e27–e32.
2. Flores AR, Herman JL, Gates GJ, et al. How many adults identify as
transgender in the United States? Los Angeles: UCLA, Williams
Institute; 2016.
3. Deutsch MB. Making it count: improving estimates of the size of
transgender and gender nonconforming populations. LGTB Health
2016;3(3):181–185.
4. Coleman E, Bockting W, Botzer M, et al. Standards of care for the
health of transsexual, transgender, and gender-nonconforming people,
version 7. Int J Trans 2012:13(4);165–232.
5. Fisk NM. Editorial: gender dysphoria syndrome—the conceptualization
that liberalizes indications for total gender reorientation and implies a
broadly based multi-dimensional rehabilitative regimen. West J Med
1974;120(5):386–391.
6. Grant et al., 2010:
http://transequality.org/PDFs/NTDSReportonHealth_final.pdf
7. Kanhai R, Hage J, Karim R. Augmentation mammaplasty in male-to-
female trans-sexuals: facts and figures from Amsterdam. Scand J Plast
Reconstr Surg Hand Surg 2001;35:203–206.
8. Spack NP. Management of transgenderism. JAMA 2013;309:478–484.
9. Elbers J, Asscheman H, Seidell J, et al. Effects of sex steroid hormones
on regional fat depots as assessed by magnetic resonance imaging in
transsexuals. Am J Physiol 1999;276:E317–E325.
10. Marshall WA, Tanner JM. Variations in pattern of pubertal changes in
girls. Arch Dis Child 1969;44(235):291–303.
11. Orentreich N, Durr NP. Proceedings: mammogenesis in transsexuals. J
Invest Dermatol 1974;63:142–146.
12. Claes KEY, D’Arpa S, Monstrey SJ. Chest surgery for transgender and
gender nonconforming individuals. Clin Plast Surg 2018;45(3):369–
380.
13. Wierck K, Gooren L, T’Sjoen G. Clinical review: breast development in
trans women receiving cross-sex hormones. J Sex Med
2014;11(5):1240–1247.
14. Morrison SD, Wilson SC, Mosser SW. Breast and body contouring for
transgender and gender nonconforming individuals. Clin Plast Surg
2018;45(3):333–342.
15. Gooren LJ. Clinical practice. Care of transsexual persons. N Engl J Med
2011;364:1251–1257.
16. Meyer WJ 3rd, Finkelstein JW, Stuart CA, et al. Physical and hormonal
evaluation of transsexual patients during hormonal therapy. Arch Sex
Behav 1981;10:347–356.
17. Meyer WJ 3rd, Webb A, Stuart CA, et al. Physical and hormonal
evaluation of transsexual patients: a longitudinal study. Arch Sex Behav
1986;15:121–138.
18. Dittrich R, Binder H, Cupisti S, et al. Endocrine treatment of male-to-
female transsexuals using Gonadotropin-Releasing Hormone agonist.
Exp Clin Endocrinol Diabetes 2005;113:586–592.
19. De Cuypere G, T’Sjoen G, Beerten R, et al. Sexual and physical health
after sex reassignment surgery. Arch Sex Behav 2005;34:679–690.
20. Siu AL. Screening for breast cancer: U.S. Preventive Services Task
Force recommendation statement. Ann Intern Med 2016;164(4):279–
296.
21. Lee CH, Dershaw DD, Kopans D, et al. Breast cancer screening with
imaging: recommendations from the Society of Breast Imaging and the
ACR on the use of mammography, breast mri, breast ultrasound, and
other technologies for the detection of clinically occult breast cancer. J
Am Col Rad 2010;7(1):18–27.
22. Colebunders B, T’Sjoen G, Weyers S, et al. Hormonal and surgical
treatment in trans-women with BRCA1 mutations: a controversial topic.
J Sex Med 2014;11(10):2496–2499.
23. Beer GM, Budi S, Seifert B, et al. Configuration and localization of the
nipple-areola complex in men. Plast Reconstr Surg 2001;108(7):1947–
1952; discussion 1953.
24. Mallucci P, Branford OA. Design for natural breast augmentation: the
ICE principle. Plast Reconstr Surg 2016;137(6):1728–1737.
25. Li S, Chen L, Liu W, et al. Capsular contracture rate after breast
augmentation with periareolar versus other two (inframammary and
transaxillary) incisions: a meta-analysis. Aesthetic Plast Surg
2018;42(1):32–37.
26. Namnoum JD, Largent J, Kaplan HM, et al. Primary breast
augmentation clinical trial outcomes stratified by surgical incision,
anatomical placement and implant device type. J Plast Reconstr Aesthet
Surg 2013;66(9):1165–1172.
27. Hidalgo DA. Breast augmentation: choosing the optimal incision,
implant, and pocket plane. Plast Reconstr Surg 2000;105:2202–2216;
discussion 2217–2218.
28. Codner MA, Mejia JD, Locke MB, et al. A 15-year experience with
primary breast augmentation. Plast Reconstr Surg 2011;127(3):1300–
1310.
29. FDA Update on the Safety of Silicone Gel-Filled Breast Implants.
Center for Devices and Radiological Health: U.S. Food and Drug
Administration. https://www.fda.gov/media/80685/download. Accessed
May 16, 2019.
30. Important Information for Augmentation Patients About Mentor
MemoryGel® Silicone Gel-Filled Breast Implants. Mentor Corporation.
https://www.fda.gov/media/80187/download. Accessed May 16, 2019.
31. Clemens MW, Nava MB, Rocco N, et al. Understanding rare adverse
sequelae of breast implants: anaplastic large-cell lymphoma, late
seromas, and double capsules. Gland Surg 2017;6:169–184.
32. Loch-Wilkinson A, Beath KJ, Knight RJW, et al. Breast implant-
associated anaplastic large cell lymphoma in Australia and New
Zealand: high-surface-area textured implants are associated with
increased risk. Plast Reconstr Surg 2017;140:645–654.
33. de Boer M, van Leeuwen FE, Hauptmann M, et al. Breast implants and
the risk of anaplastic large-cell lymphoma in the breast. JAMA Oncol
2018;4:335–341.
34. Hidalgo DA, Weinstein AL. Intraoperative comparison of anatomical
versus round implants in breast augmentation: a randomized controlled
trial. Plast Reconstr Surg 2017;139(3):587–596.
35. Hidalgo DA, Sinno S. Current trends and controversies in breast
augmentation. Plast Reconstr Surg 2016;137:1142–1150.
36. Calobrace MB, Stevens WG, Capizzi PJ, et al. Risk factor analysis for
capsular contracture: a 10-year Sientra study using round, smooth, and
textured implants for breast augmentation. Plast Reconstr Surg
2018;141(4S Sientra Shaped and Round Cohesive Gel Implants):20S–
28S.
37. Tebbetts JB. Dual plane breast augmentation: optimizing implant-soft-
tissue relationships in a wide range of breast types. Plast Reconstr Surg
2006;118:81S–98S; discussion 99S–102S.
38. Schusterman MA. Lowering the inframammary fold. Aesthet Surg J
2004;24:482–485.
39. Kim YJ, Kim YW, Cheon YW. Prevention of implant malposition in
inframammary augmentation mammoplasty. Arch Plast Surg
2014;41:407–413.
40. Kanhai RC, Hage JJ, Asscheman H, et al. Augmentation mammaplasty
in male-to-female transsexuals. Plast Reconstr Surg 1999;104(2):542–
549; discussion 550–551.
41. Weigert R, Frison E, Sessiecq Q, et al. Patient satisfaction with breasts
and psychosocial, sexual, and physical well-being after breast
augmentation in male-to-female transsexuals. Plast Reconstr Surg
2013;132(6):1421–1429.
42. Gooren LJ, van Trotsenburg MA, Giltay EJ, et al. Breast cancer
development in transsexual subjects receiving cross-sex hormone
treatment. J Sex Med 2013;10(12):3129–3134.
CHAPTER 119

Tuberous Breast: Correction With and


Without Implants
NIMA KHAVANIN | MAURICE Y. NAHABEDIAN
HISTORY
Since the tuberous breast was first described by Rees and Aston in 1976,
there have been considerable advances in our understanding of the deformity
and the options for surgical correction (1). As defined by Mandrekas (2–5),
the tuberous breast is constricted, both in length and width, often with
herniation of breast tissue into a hypertrophied areola. Other common clinical
features include a deficiency of skin, particularly in the lower pole, regional
or generalized breast hypoplasia, a high-riding, constricted inframammary
fold, ptosis, and contralateral asymmetry.
During puberty, the mammary tissues begin to grow along with
enlargement of the areola until they reach their final shape around the age of
15 to 16 (6). The breast tissue grows within the confines of a fascial
envelope, the superficial fascia of the breast. This fascia includes two layers:
a superficial layer, which forms the outer covering the breast parenchyma,
and a deep layer, which forms its posterior boarder and lies on top of the deep
fascia of the pectoralis major and serratus anterior (6). This fascia is
continuous except for the area underlying the areola due to the breasts’
embryologic origin as an invagination of ectoderm; this discontinuity allows
for communication between the nipple and the underlying breast
parenchyma. In the case of the tuberous breast, a constricting ring of
unknown origin at the periphery of the nipple areolar complex prevents the
natural expansion of the breast tissues during puberty. Instead, the growing
tissues are forced down the path of least resistance beneath the areola, where
there is no superficial layer of the superficial fascia (Fig. 119-1) (3,7–9).
Several classification schemes have been described to capture the severity
of the malformation and the quadrants of the breast involved. The initial
system described by von Heimburg et al. (10) in 1996 included four types of
tuberous breasts based on the quadrants of the breast involved (lower medial,
lower medial and lateral, or circumferential) and the presence or deficiency of
skin in the subareolar region. This classification was subsequently modified
by Grolleau et al. (7) in 1999 and has become widely adopted by the plastic
surgery community (2,3). This Grolleau classification describes three types of
tuberous breasts: type I (minor form) in which only the lower medial
quadrant is deficient (over 50% of cases), type II in which both lower
quadrants are deficient (26%), and type III (20%) in which all four quadrants
are deficient with constriction of the breast base horizontally and vertically
(Fig. 119-1) (7).
Treatment of the tuberous breast has evolved along with our knowledge of
the pathoanatomy, implant technology, and surgical technique. Regardless of
the approach, however, several principles have been described as the
cornerstone of an aesthetic reconstruction (11):

1. The constricted base should be released in both the vertical and


horizontal place and old inframammary fold obliterated
2. Nipple position should be corrected using a combination of mastopexy
and lowering of the inframammary fold
3. Correction of areolar hypertrophy and reduction of herniated tissues
4. Restoration of breast volume
5. Restoration of breast symmetry

FIGURE 119-1 Preoperative view of a patient with constriction of the inferomedial


pole of the left breast with hypertrophy of the nipple areolar complex and herniation
of the breast tissues.

More specifically, Rees and Aston first described a technique in which the
base diameter of the breast was expanded using radial scoring (1). Dinner and
Dowden believed the deformity was due to a cutaneous band and advocated
for a skin incision (12), whereas Ribeiro identified a constrictive fascial ring
and suggested dividing it horizontally (8,13). More recently, Mandrekas
described a procedure similar to Ribeiro, but with vertical division of the
band (5), and Pacifico and Kang described a technique that combined areola
reduction, subglandular implant placement, and subdermal undermining (14).
The advent of form-stable, anatomically shaped implants allowed for a
natural upper pole contour while maximizing stretch on the constricted lower
pole tissues (15). Finally, since autologous fat grafting gained popularity in
the realm of breast reconstruction (16), several authors have reported
successful correction of the tuberous breast deformity with a combination of
fat grafting and percutaneous constriction bad release with or without
external tissue expansion (11,17).
INDICATIONS
One or more surgical procedures are often necessary to adequately
reconstruct the tuberous breast deformity. The specific procedure(s) indicated
is/are contingent on patient presentation, including the classification of the
tuberous breast as well as the appearance of the contralateral breast. The
surgeon’s armamentarium includes the full host of techniques including a
combination of mastopexy and/or augmentation techniques using either
prosthetic breast implants, autologous lipofilling (2,15,17), tissue expansion
(18,19), or breast parenchymal rearrangement (7).
Specific examination findings to consider when deciding on the optimal
surgical approach include:

1. Grolleau classification
2. Areolar hypertrophy and nipple position
3. Regional or generalized parenchymal hypoplasia
4. Degree of skin deficiency
5. Contralateral breast
6. Presence or absence of donor fat
CONTRAINDICATIONS
Contraindications to surgical repair of the tuberous breast include active
infection of the breast, active cancer, pregnancy, current radiation therapy,
known sensitivity to silicone, and other unstable and/or active medical
conditions. Patients with unrealistic postoperative expectations may also not
benefit from reconstruction.
PREOPERATIVE PLANNING
Preoperative planning for tuberous breast reconstruction begins with a
focused patient history and physical examination. Most tuberous breasts are
hypoplastic and require some form of volume augmentation—typically with
an implant. These cases require a methodologic approach toward incision
location, pocket selection, implant selection, adjunct procedures such as fat
grafting, or even the need for prior tissue expansion.
Most commonly a periareolar approach is used to place an implant while
controlling areola hypertrophy and nipple position. In cases where there is
limited areolar hypertrophy or soft tissue herniation, an inframammary fold
approach may also be utilized. This approach however requires precise
planning in order to determine the location of the inframammary fold in order
to camouflage the incision within the crease.
Regarding implant selection, saline-filled devices are typically not
preferred because the lack of soft tissue coverage may result in rippling and
palpable edges. Many authors advocate for the use of form-stable anatomic or
round cohesive gel implants in these cases (11,15). These implants are able to
resist the deformation of the tight envelope, maintaining their shape and
resulting in a superior aesthetic result. Shaped devices also more closely
resemble the dimensions of a natural breast.
OPERATIVE TECHNIQUE
The surgical management of the tuberous breast is contingent upon the
severity of the deformity. Specific details of techniques useful in several
different presentations are presented below.
GROLLEAU TYPE I OR II (MILD CONSTRICTION)
Very mild forms of the tuberous breast abnormality may present with limited
constriction and hypoplasia of the lower medial or both lower medial and
lateral breast. If such a patient desires an augmentation, the constricting
bands need to be released via radial incisions through the parenchyma to the
level of the dermis. Failure to recognize the abnormality will result in flatness
of the affected area and a poor aesthetic result.
Alternatively, in the absence of glandular hypoplasia, the breast tissues can
be rearranged so that the existing tissues fill the pocket created after release
of the affected areas. Grolleau et al. (7) describe mammaplasty with a
superiorly based pedicle while rotating a deepithelialized, inferolaterally
based dermatoglandular flap into the lower medial quadrant for the type I
breasts. Flaps can also be fashioned from the subareolar parenchyma, either
based anteriorly on the subareolar tissue (11) or posteriorly on the chest wall
(8), and folded down into the affected lower quadrants. More recently,
autologous fat grafting, typically in one or two sessions, has been described
as an efficacious modality to correct minor presentations of the tuberous
breast deformity (20).
GROLLEAU TYPE II OR III WITH HYPOPLASIA
A circumareolar pattern skin excision around the perimeter of the desired
nipple areolar complex is often indicated in order to address areolar
hypertrophy. This donut-type or Wise-pattern mastopexy also allows the
surgeon to address nipple mispositioning and achieve symmetry with the
contralateral breast. After the initial skin incision, dissection proceeds either
directly through the breast parenchyma down to the pectoralis fascia in a
breast-splitting approach, or skin flaps can be elevated by traveling in a
subcutaneous place down to the inframammary fold. Undermining continues
to the level of the new inframammary fold creating a pocket of adequate
height and weight for the selected implant.
Dissection then proceeds upward behind the breast above the plane of the
pectoralis fascia. The inferior part of the breast parenchyma is dissected off
the muscle, leaving only the upper pole attached. The flap is then externalized
through the periareolar opening for further manipulation. Since the initial
description of the tuberous breast, authors have proposed several methods for
the release and redraping of the constricted breast parenchyma. Rees and
Aston (1) were the first to discuss radial scoring of the constricting bands that
tether the parenchyma and prevent normal expansion. More recently,
alternative techniques for internal glandular reshaping have been proposed
that correct the deformity without significant morbidity or contour
irregularities. Mandrekas and Zambacos (3) describe vertically transecting
the breast parenchyma along the middle, freeing up the constricting band and
creating two pillars. This releases the narrow breast and allows the tissues to
redrape in a flatter but wider configuration. The pillars are then loosely
approximated with absorbable sutures to avoid the formation of a gap
inferiorly.
In most cases, some form of additional volume is necessary in order to
achieve a normal breast shape or symmetry. If necessary, the implant can be
inserted at this time into either a subglandular or dual plane position
depending on the degree of overlying soft tissue support.
In cases of extreme asymmetry or when pocket dissection does not
procedure enough release of the constricted breast base, a two-stage approach
to reconstruction may be warranted. A tissue expander can be placed during
the initial operation and exchanged for a permanent implant once the desired
breast size and shape has been achieved. This can often be combined with
contralateral symmetry procedures during the second stage in order to
maximize the aesthetic outcome.
Once the implant has been inserted and the released breast parenchyma has
been reduced, the areolar diameter is controlled with the use of a wagon-
wheel permanent suture (typically Gore-Tex) (21). In most cases, it is safest
to not commit to the skin excision for the mastopexy/areolar reduction until
after the implant has been inserted. While the hypertrophied areola may give
the impression that there is excess skin, tuberous breasts are often deficient in
tissues, and the appropriate amount to excise may not be apparent
preoperatively (11).
More recently, autologous fat has been described as a method for
increasing volume in the tuberous breast. This technique provides the added
benefit of giving the surgeon control over the precise distribution of the
volume throughout the breast. Percutaneous needle release of the constricting
bands (also known as rigottomies) (22) are combined with the injections in
order to restore the contour of the inferior pole and lower the inframammary
fold to the desired level. This technique can be combined with external tissue
expansion using the BRAVA device in order to improve fat graft retention by
increasing the graft capacity ratio and improving recipient site perfusion (11).
Some authors have noted softening of the tuberous breast following serial fat
injection (17). Injectors must be careful, however, to avoid depositing fat
directly beneath the nipple areolar complex as this may result in herniation of
the grafted tissues and worsening of the abnormality.
POSTOPERATIVE CARE
Following correction of the tuberous breast deformity, patients are instructed
to minimize strenuous activity for 6 weeks. A postsurgical support bra is
applied and worn continuously for 2 weeks. Drain use is unlikely except in
some situations where a reduction of a tuberous breast is necessary. Incision
care is variable but typically includes adhesive Steri-Strips and Xeroform
gauze. Skin glue can also be considered.
For patients who receive silicone-based breast implants, the U.S. Food and
Drug Administration recommends magnetic resonance imaging to screen for
silent rupture. Imaging should be first considered at 3 years following
placement of the implant and every 2 years thereafter. Other complications,
including anaplastic large cell lymphoma, are rare. There are currently no
recommendations for any screening beyond routine follow-up for these
conditions.

CASES

CASE 1

Figure 119-2A illustrates a patient with tuberous breast deformity and


breast asymmetry illustrating correction with mastopexy techniques and
areolar reduction without the use of prosthetic devices.
FIGURE 119-2 A–C: Preoperative view of a 24-year-old female with severe
constriction of the lower pole of the right breast with herniation of the breast
parenchyma through the nipple areolar complex in addition to minor
constriction of the inferomedial pole of the left breast. D: A 42-mm cookie
cutter was used to mark out the nipple areolar complex and the central
breast mounds of the breast were deepithelialized. Skin flaps ever elevated
superomedially and superolaterally. The constricted base of the breast was
managed by scoring the undersurface of the parenchyma while taking care to
not violate the central parenchymal perfusion. The parenchymal herniation
was controlled with imbricating sutures placed along the herniated dermis
surrounding the periareolar region. The contralateral breast was reduced for
symmetry. E–G: Postoperative photograph at 1.5-year follow-up.
RISKS
Many of the risks of tuberous breast reconstruction are similar to those
encountered with standard breast mastopexy, implant placement, and fat
grafting and include: hematoma, seroma, infection, poor wound healing, flap
necrosis, poor aesthetic outcome, breast asymmetry, loss of sensation,
implant migration, implant rupture, capsular contracture, fat necrosis, oil
cysts, and the need for reoperation.
There are, however, several potential complications more specific to the
tuberous breast. These include a double-bubble deformity, implant rippling or
palpability in the setting of hypoplastic breasts, widening of the periareolar
scar, and recurrence of the tuberous breast.
OUTCOMES
General complications rates following implant-based tuberous breast
correction are similar overall to general breast augmentation and range
between 7% and 10% (23,24). Aesthetic outcomes have ranged from good to
excellent with satisfaction ratings generally over 90% (3,11,25). Tenna et al.
(26) recently surveyed patients undergoing tuberous breast correction with
implants using the BREAST-Q and reported a mean satisfaction with breasts
of 78 +/− 22 and satisfaction with outcome of 78 +/− 17.
Autologous fat grafting is well tolerated in this patient population and
generally achieves good aesthetic results. In the first reported use for this
indication, Coleman and Saboeiro (16) injected fat into the subcutaneous
tissues and pectoralis muscle in two sessions. The first included 370 cc on the
right and 380 cc on the left, the second, 4 years later, 340 cc on the right and
300 cc on the left. The vast majority of patients requires one or two sessions
of lipotransfer (20). Injection into muscle combined with percutaneous
rigottomies and in some cases external tissue expansion have been
hypothesized to vastly improve graft retention (11). Nearly a quarter of
patients will develop oil cysts (20) and other may develop liponecrosis,
however these are rarely symptomatic and easily identified as benign findings
by trained radiologists (17). Studies have noted over 90% satisfaction with
this technique (20). However, a retrospective comparison of fat grafting and
implants using the Breast-Q demonstrated significantly greater satisfaction
with breasts and outcomes when using an implant (27).
CONCLUSION
The aesthetic reconstruction of the tuberous breast poses a considerable
challenge to plastic surgeons. The ideal surgical approach should be
individualized to a patient’s presentation and the specific findings on physical
examination. In general, there are several salient points to consider during
surgical planning. A circumareolar-pattern skin excision allows for control of
areolar width and nipple positioning. Pocket dissection widens the breast
footprint and lowers the inframammary fold to a more appropriate level. The
inferior breast parenchyma should be undermined, and the constricted tissues
are released through radial scoring and/or full-thickness incisions. A breast
implant in a single stage, or in two combined with a tissue expander, can
provide additional volume if necessary. Together, combined with new
treatments such as fat grafting, these techniques can be leveraged to safely
and effectively reshape the breast in a majority of patients.

REFERENCES

1. Rees TD, Aston SJ. The tuberous breast. Clin Plast Surg 1976;3(2):339–
347.
2. Mandrekas AD, Zambacos GJ. Tuberous breast deformity: classification
and treatment strategy for improving consistency in aesthetic correction.
Plast Reconstr Surg 2015;136(2):269e–270e.
3. Mandrekas AD, Zambacos GJ. Aesthetic reconstruction of the tuberous
breast deformity: a 10-year experience. Aesthet Surg J 2010;30(5):680–
692.
4. Zambacos GJ, Mandrekas AD. The incidence of tuberous breast
deformity in asymmetric and symmetric mammaplasty patients. Plast
Reconstr Surg 2006;118(7):1667.
5. Mandrekas AD, Zambacos GJ, Anastasopoulos A, et al. Aesthetic
reconstruction of the tuberous breast deformity. Plast Reconstr Surg
2003;112(4):1099–1108; discussion 1109.
6. Osborne MP. Breast development and anatomy. In: Harris JR, Hellman
S, Henderson IC, et al., eds. Breast Diseases. 2nd ed. Philadelphia, PA:
Lippincott; 1991:1–13.
7. Grolleau JL, Lanfrey E, Lavigne B, et al. Breast base anomalies:
treatment strategy for tuberous breasts, minor deformities, and
asymmetry. Plast Reconstr Surg 1999;104(7):2040–2048.
8. Ribeiro L, Canzi W, Buss A Jr, et al. Tuberous breast: a new approach.
Plast Reconstr Surg 1998;101(1):42–50; discussion 51–52.
9. Atiyeh BS, Hashim HA, El-Douaihy Y, et al. Perinipple round-block
technique for correction of tuberous/tubular breast deformity. Aesthet
Plast Surg 1998;22(4):284–288.
10. von Heimburg D, Exner K, Kruft S, et al. The tuberous breast deformity:
classification and treatment. Br J Plast Surg 1996;49(6):339–345.
11. Brown MH, Somogyi RB. Surgical strategies in the correction of the
tuberous breast. Clin Plastic Surg 2015;42(4):531–549.
12. Dinner MI, Dowden RV. The tubular/tuberous breast syndrome. Ann
Plast Surg 1987;19(5):414–420.
13. Ribeiro L, Accorsi A Jr, Buss A, et al. Short scar correction of the
tuberous breast. Clin Plast Surg 2002;29(3):423–431, vii.
14. Pacifico MD, Kang NV. The tuberous breast revisited. J Plast Reconstr
Aesthet Surg 2007;60(5):455–464.
15. Panchapakesan V, Brown MH. Management of tuberous breast
deformity with anatomic cohesive silicone gel breast implants. Aesthet
Plast Surg 2009;33(1):49–53.
16. Coleman SR, Saboeiro AP. Fat grafting to the breast revisited: safety
and efficacy. Plast Reconstr Surg 2007;119(3):775–785; discussion
786–787.
17. Claudio Silva-Vergara C, Fontdevila J, Weshahy O. Fat grafting
technique, a paradigm shift in the treatment of tuberous breast. World J
Plast Surg 2018;7(1):72–77.
18. Kolker AR, Collins MS. Tuberous breast deformity: classification and
treatment strategy for improving consistency in aesthetic correction.
Plast Reconstr Surg 2015;135(1):73–86.
19. Versaci AD, Rozzelle AA. Treatment of tuberous breasts utilizing tissue
expansion. Aesthet Plast Surg 1991;15(4):307–312.
20. Delay E, Sinna R, Ho Quoc C. Tuberous breast correction by fat
grafting. Aesthet Surg J 2013;33(4):522–528.
21. Hammond DC, Khuthaila DK, Kim J. The interlocking Gore-Tex suture
for control of areolar diameter and shape. Plast Reconstr Surg
2007;119(3):804–809.
22. Khouri RK, Rigotti G, Cardoso E, et al. Megavolume autologous fat
transfer: part II. Practice and techniques. Plast Reconstr Surg
2014;133(6):1369–1377.
23. Innocenti A, Innocenti M, Mori F, et al. Tuberous breast: past, present,
and future: personal classification, treatment, and surgical outcomes.
Ann Plast Surg 2018;80(2):104–108.
24. Zholtikov V, Korableva N, Lebedeva J. Tuberous breast deformity
correction: 12-year experience. Aesthet Plast Surg 2019;43(1):16–26.
25. Nahabedian MY. Breast deformities and mastopexy. Plast Reconstr
Surg 2011;127(4):91e–102e.
26. Tenna S, Cagli B, Brunetti B, et al. Management of tuberous breast
deformities: review of long-term outcomes and patient satisfaction with
BREAST-Q. Aesthet Plast Surg 2017;41(6):1249–1258.
27. Brault N, Stivala A, Guillier D, et al. Correction of tuberous breast
deformity: a retrospective study comparing lipofilling versus breast
implant augmentation. J Plast Reconstr Aesthet Surg 2017;70(5):585–
595.
CHAPTER 120

Effect of Smoking on Breast Plastic


Surgery
BRIAN BIGGERSTAFF | LAUREN PATTY | GREGORY R. D. EVANS
HISTORY
The effects of smoking on wound healing are well established. Smoking is
known to have detrimental effects on healing potential via multiple
mechanisms. These deleterious effects of smoking become more pronounced
following certain breast surgeries where vascular compromise of tissue
secondary to surgery places patients at higher risk of postoperative
complications. Knowledge of these risks enable plastic surgeons to make
more informed decisions regarding surgical management of patients who
smoke.
PATHOPHYSIOLOGY OF SMOKING
Once inhaled, tobacco is degraded into numerous toxic metabolites which
then circulate in the blood, producing various pathophysiologic effects
downstream which ultimately diminish tissue perfusion, limit peripheral
oxygen delivery, and compromise wound healing.
Smoking produces vasoconstriction, which consequently compromises
cutaneous capillary blood flow (1), by disrupting the homeostatic balance of
local vasoactive mediators. Nicotine impairs physiologic vasodilation by
indirectly inhibiting the production of prostacyclin and nitric oxide. Reduced
levels of prostacyclin and nitric oxide allow for vasoconstriction and
thrombus formation (2–6). Toxic tobacco metabolites directly damage
endothelial cells lining small vessels resulting in their detachment from the
basement membrane and loss of release of endothelial-derived relaxation
factor, thus further impairing vasorelaxation (2). Additionally, nicotine
directly and indirectly induces peripheral vasoconstriction by stimulating
increased production of thromboxane A2 and systemic catecholamine release
(2–4).
Smoking promotes thrombotic microvascular occlusion by disrupting the
physiologic balance of pro- and antithrombogenic factors, which ultimately
contributes to decreased peripheral perfusion. Vascular endothelium damaged
by toxic tobacco metabolites stimulate thrombus formation by both extrinsic
and intrinsic coagulation pathways, ultimately resulting in platelet adhesion,
aggregation, and propagation (2,7). Additionally, the loss of nitric oxide and
prostacyclin-mediated inhibition of platelet adhesion creates an environment
prone to thrombogenesis.
In addition to diminishing perfusion, smoking also impairs oxygen
delivery and utilization at peripheral tissues and inhibits normal wound
healing mechanisms. Increased production of methemoglobin in response to
tobacco byproduct carbon monoxide causes a left shift in the oxyhemoglobin
curve, thus reducing oxygen availability for tissue delivery. Nicotine also
directly reduces proliferation of cells involved in wound healing (i.e.,
fibroblasts, macrophages, red blood cells), further diminishing tissue
oxygenation and limiting healing potential. At a cellular level, hydrogen
cyanide in tobacco smoke inhibits key enzymes crucial to the inflammatory
phase of wound healing. These combined effects of tobacco serve to
significantly diminish perfusion and reduce wound healing capability in
peripheral tissues (Fig. 120-1).
IMPACT ON BREAST SURGERY
The aforementioned deleterious effects of smoking on tissue perfusion are
more pronounced in tissues with tenuous or compromised vascular supply
secondary to surgery. This is particularly evident following certain breast
surgeries, such as reduction mammaplasty or immediate reconstruction
following mastectomy, resulting in complications such as delayed wound
healing, skin flap necrosis, epidermolysis, and surgical site infections (8).
The physiologic effects of smoking which cause poor cutaneous perfusion,
microvascular vasoconstriction and thrombi, and decreased oxygen delivery
to tissue provide a reasonable theoretical explanation for increased rates of
skin flap necrosis, infection, and delayed wound healing seen in patients who
smoke perioperatively.
Accurate quantification of complications specifically attributable to
perioperative smoking can be somewhat challenging for several reasons.
Even before considering the effects of smoking, reported complication rates
in general vary widely among various breast surgeries. For example, reported
overall complication rates for reduction mammoplasty range from 6% to 53%
among various series. Second, there is a large degree of heterogeneity among
studies. Definitions of what represent complications are not coherent across
various series. While a spitting suture may be considered a complication in
one series, it may not be in another. Moreover, as one would reasonably
expect, the available studies are largely unrandomized and unblinded, often
are retrospective, and are thus subject to various biases to some degree.
Further sources of heterogeneity include differences in perioperative
management of smoking, differences in surgical technique, and differences in
patient’s previous history of breast surgeries. In spite of these challenges,
several studies have elegantly shown clinical associations between smoking
and wound healing complications in breast surgery.
FIGURE 120-1 Smoking leads to wound healing problems via multiple
pathophysiologic mechanisms. (Adapted from Krueger JK, Rohrich RJ. Clearing the
smoke: the scientific rationale for tobacco abstention with plastic surgery. Plast Reconstr
Surg 2001;108[4]:1063–1073; discussion 1074–1077.)

Mastopexy, Augmentation, and Combined Mastopexy-


Augmentation
Interestingly, there are much more data evaluating smoking complications for
combined mastopexy-augmentation than either stand-alone procedure
(augmentation or mastopexy alone), likely due to the fact that the combined
procedure outcomes and results are more frequently evaluated than either of
the individual procedures (Fig. 120-2). As for stand-alone augmentation
mammoplasty, one series found increased rate of complications for primary
augmentation in smokers versus nonsmokers (9), but did not show increased
risk in secondary augmentation.
The same series also found increased complications in primary vertical
mastopexy in smokers versus nonsmokers, but no increased risk in secondary
vertical mastopexy or combined mastopexy-augmentation (9). However, in
both cases the study did not clearly specify which type of complications
occurred more often in smokers. Another series found no correlation between
smoking and increase rate of complications in primary or secondary
combined mastopexy-augmentation (10). However, in this case smokers were
asked to abstain for 2 or more weeks prior to surgery, and those unable or
unwilling to abstain were converted to staged procedure (10).
The largest series to date on combined mastopexy-augmentation was
recently reported by Messa and Messa, a retrospective review of 1,131
patients (11). Roughly 10% of patients in their series were smokers. Overall
complication rate for augmentation-mastopexy was reported as 15.3%. Their
reoperative rate was 14.7%, which included recurrent ptosis as the most
common indication. They found increased rate of complications in smokers
(35.1% vs. 13.1%), as well as increased rate of reoperation (31.5% vs.
12.8%) in smokers.

FIGURE 120-2 A 45-year-old female patient at her 4-week postop visit; photos show
her right (A) and left (B) breasts. She underwent bilateral augmentation and
mastopexy, which was complicated by wound breakdown at the inferior T-incision
with eventual exposure of her implant.

Of note, all patients in the series consented to cease smoking at least 2


weeks prior to and following surgery, however the authors point out that they
did not check physiologic levels prior to proceeding with surgery.
In the series, the authors separated complications into soft tissue related
(included hypertrophic scarring, delayed wound healing, partial skin flap or
areolar necrosis, recurrent or persistent ptosis, pseudoptosis, areolar and
breast asymmetry, and loss of nipple or areolar sensation; major skin flap or
nipple areolar loss was defined as ≥2 cm) and implant related (included
capsular contracture [Baker III or IV], implant palpability, implant
malposition, implant infection, deflation or rupture, and hematoma). While
increased implant-related complications trended toward significance (9% vs.
4.1%, p = 0.062) in smokers, the more significant difference, as may be
expected in smokers, was with increase in tissue-related complications
(26.1% vs. 9.0%, p < 0.00001). This difference was most impacted by wound
healing issues. Tissue-related reoperations were required in 22.5% of
smokers (as compared to 6.2% in nonsmokers). Implant-related
complications occurred in 9% of smokers and required reoperation in 9% (as
compared to 4.1% in nonsmokers and reoperation rate of 6.7%).
Reduction Mammaplasty
Complication rates in smokers versus nonsmokers in the context of reduction
mammoplasty has been reported in several studies, from which several
inferences can be made. Overall complications are increased in reduction
mammoplasty in smokers versus nonsmokers, with an estimated relative risk
of 1.4 to 3.4 (12–14). As mentioned previously, the reported overall
complication rates (6% to 53%) vary widely for reduction mammoplasty, as
do definitions of complications. While the prospective multicenter BRAVO
study did not report a significant increase in overall complications in
smokers, they did find a significant difference in delayed wound healing with
relative risk (RR) similar to those reported in other studies. However, after
performing logistic regression analysis their finding no longer achieved
significance. Their study was, however, somewhat limited by small number
of patients (15).
In several other series, complications are reported to be increased in
patients who smoke. As may be expected—and as is seen with mastopexy-
augmentation—the most significant increase in complications occurs with
wound healing problems and delayed wound healing. Increased necrosis at
the T-incision (RR = 3.1) (12), surgical site infection (RR = 1.7 to 3)
(12,13,16), wound dehiscence (RR = 1.7) (13,16), and delayed wound
healing (RR = 2.3 to 2.8) (12,15) have all been shown to occur with increased
incidence.
For patients who are smokers, it does not appear that the number of
cigarettes per day is directly related to complication rates (12). The threshold
of nicotine levels to cause physiologic changes that lead to development of
wound healing issues is low enough that even light smoking is sufficient to
cause increased complications. Timing however, does play a significant role.
For those patients who are able to cease smoking prior to the operative
period, there is a reduction of smoking-related complications inversely
proportional to the amount of time the patient is nicotine free. Those patients
able to abstain for at least 4 weeks have the same rate of wound healing
complications as nonsmokers (14).
Breast Reconstruction
Whereas mastopexy, augmentation, and even reduction mammoplasty to
some degree are typically done as cosmetic procedures on a totally elective
basis, surgical treatment for cancer carries a more urgent timing component.
In the context of breast cancer, appropriate oncologic treatment cannot be
significantly delayed for smoking cessation. While delayed breast
reconstruction remains a viable option, and may be the preferred route of
some surgeons with postmastectomy reconstruction, knowing the effects that
smoking has on reconstruction possibilities may help guide these decisions
more accurately.
Regardless of the reconstruction method planned, it is worth mentioning
that mastectomy, when considered even as its own entity, is known to have
increased complications in patients who smoke. Increased rates of skin
necrosis in the mastectomy skin flaps are seen at a rate of seven to nine times
as likely as in nonsmokers (8). Additionally, epidermolysis of the skin flaps
and surgical site infections are more common in smokers than in nonsmokers
(8). Thus, regardless of the reconstruction modality chosen, immediate
reconstruction is likely to have increased complications.
Indeed, immediate reconstruction of any type has been shown to have
increased skin necrosis in smokers (17). This includes subpectoral implant,
latissimus flap with implant, latissimus flap alone, or tissue expander
placement (17). Smoking was found to be the only risk factor associated with
reconstruction failures in immediate reconstruction in one retrospective series
consisting of 266 patients with an average follow-up of 7 years postop (17).
Implant-Based Reconstructions
Implant-based reconstruction is the most common method of breast
reconstruction utilized after mastectomy. In general, there are two major
approaches to immediate, implant-based reconstruction: direct implantation
of the permanent implant, or placement of a tissue expander with planned
exchange for the permanent implant in a second-stage surgery. With tissue
expanders, any amount of air or saline can be left in the expander at the time
of initial placement from zero to fully expanded. The primary advantage of
immediate implant placement is possibility of single-stage reconstruction,
while the primary advantage of tissue expansion is less stress immediately
placed on the mastectomy skin flaps, with theoretical decreased risk of flap
complications and implant loss.
Smoking has indeed been shown to be a risk factor for complications in
immediate implant placement (18), with overall complication rates of 39%, as
compared to 26% in nonsmokers (19). For direct-to-implant reconstructions,
there is increased rate of implant loss in smokers with prepectoral implant
placement (18). However, in one series, when compared to nonsmokers there
was not an increased risk of implant loss when the implant was placed in a
subpectoral plane (18).
Free Flap
Several clinical studies have shown correlations between smoking and
complications in free TRAM breast reconstruction (20,21). Smoking is
associated with increased frequency of mastectomy skin flap necrosis in the
context of free TRAM flap breast reconstruction. Additionally, there are
increased smoking-related complications seen at the donor site in this
population. Abdominal skin flap necrosis occurs at an increased rate as
compared to nonsmokers (19,22,23). Smokers also have increased incidence
of abdominal wall hernia formation at the free TRAM donor site (22), fat
necrosis of the TRAM flap (19,23), and surgical site infection (23) as
compared to nonsmokers. Delayed wound healing at the flap inset site is also
more frequent (20,21), and more often requires a secondary procedure for
wound closure (20).
Flap survival, however, does not appear to be impacted as strongly. Early
laboratory studies in animals have demonstrated variable smoking-related
outcomes on microvascular anastomotic patency (22). However, in human
studies, no clinical difference has been appreciated between flap loss or
anastomotic complications between smokers and nonsmokers (20,22,23).
In fact, free tissue transfer is often considered one of the most reasonable
breast reconstruction options for smokers, as long as the patient is otherwise a
good candidate. While the patient and surgeon must be willing to accept the
increased wound complications at both the mastectomy and donor site, as
well as hernia risk at donor site, risk of flap loss is not increased, and risk of
implant loss is not an issue with this type of reconstruction.
Free tissue transfer reconstruction is typically a longer operation and
generally requires more physiologic reserve than implant-based
reconstructions. Given the well-known detrimental effects that long-term
smoking has on overall health (especially cardiopulmonary function), when
considering free TRAM flap for a long-term smoker, appropriate
cardiopulmonary work-up should be sought to make sure the patient is
medically fit to undergo such an operation. Likewise, long-term smoking is
known to worsen peripheral vascular disease (PVD), and the possibility of
calcified vessels should be considered, as severe PVD may also make
patients medically unfit, and/or calcified vessels may significantly increase
technical difficulty.
LABORATORY TESTING
Given the clear effect that perioperative smoking has on breast surgery
complications, some surgeons advocate testing for presence of nicotine in the
perioperative period. While various methods exist to determine whether a
patient has been directly exposed, measurement of cotinine (a metabolite of
nicotine) level is the most common. Cotinine has a longer half-life than
nicotine (17 hours vs. 2 hours, respectively) (24), can be detected for up to 4
days after consumption of tobacco products, and levels are directly
proportional to the quantity of nicotine absorbed. These characteristics make
cotinine a good short-term marker of nicotine exposure, and more likely to
detect tobacco use in the previous several days than measurement of nicotine
levels. Cotinine levels can be measured from saliva, blood, and urine. Saliva
and blood concentrations are somewhat similar, whereas urine cotinine levels
tend to be four to six times higher, allowing for more reliable and valid
detection when using quantitative analysis methods (25).
Urine cotinine tests utilizing enzyme-linked immunosorbent assay
(ELISA) are a simple and cheap (<$2.50) way to detect if a patient has
smoked in the past 2 to 4 days with good sensitivity (96% to 97%) and
excellent specificity (99% to 100%) (14).
The role this laboratory test plays in clinical decision making varies widely
according to surgeon preference. One group advocates compulsory urine
cotinine testing in the immediate preoperative period to verify patients’
nonsmoking status, and will definitively cancel the procedure if cotinine
detected. They argue that the cost of performing the test on all patients is
justified in order to reduce postoperative morbidity, complication-related
added costs, and patient dissatisfaction (14). On the other hand, many
surgeons do not incorporate this test into their work-up at all, taking patients
at their word, and/or accepting higher risk of complications in patients who
do smoke. Others may use the test selectively, on patients with smoking
history for instance, or perhaps to check in a patient who has agreed to stop
smoking prior to a procedure. Regardless of how it is used, the urine cotinine
test provides a cost-effective method of verifying patients’ nonsmoking
status, which enables surgeons and patient to make any changes to the
surgical plan deemed necessary.
FIGURE 120-3 Percentage of patients with wound healing complications based on
preoperative timing of smoking cessation. The relationship shows a stepwise increase
in complications as the length time of cessation until surgery decreases. (Adapted
from Chan LK, Withey S, Butler PE. Smoking and wound healing problems in reduction
mammaplasty: is the introduction of urine nicotine testing justified? Ann Plast Surg
2006;56[2]:111–115.)
PERIOPERATIVE MANAGEMENT OF SMOKING
Currently, no definitive or formal guidelines exist regarding the management
of smoking perioperatively. Based on retrospective reviews of postoperative
patient outcomes, general recommendations regarding perioperative smoking
have been made. One study which evaluated outcomes in breast
reconstruction patients found that overall complication rates were similar
between smokers who were able to cease smoking 3 weeks prior to their
operation and nonsmokers (25% and 26% complication rate, respectively)
(19). Several other series (covering a broad range of breast procedures) have
found that cessation at least 4 weeks prior to surgery to be most effective in
reducing complications (2,14,15).
Chan et al. showed that rates of wound healing complications after breast
reduction in smokers who abstained for at least 4 weeks preoperatively were
similar to those of nonsmokers (33.7% and 33.3%, respectively). Those
smokers who abstained for less than 4 weeks before surgery and those who
continued to smoke demonstrated stepwise, proportionally higher rates of
wound healing problems (53% and 68%, respectively) (Fig. 120-3) (14).
Another group showed similar reductions with smoking cessation 4 weeks
pre- and postoperatively (2).
These findings are also mirrored in free tissue transfer reconstructions.
Chang et al. found reduced smoking-related complication rates in autologous
free flap–based breast reconstruction when patients discontinued smoking 4
weeks prior to surgery (22). This included TRAM donor sites as well, such
that no appreciable difference in free TRAM donor sites exist between
nonsmokers and those who were able to abstain for at least 4 weeks preop
(22).
In an attempt to minimize smoking-related complications, it appears that
the optimal timing for perioperative smoking cessation be at least 4 weeks
prior to surgery and 6 weeks postoperatively if possible. Adherence to these
recommendations offers the potential to reduce the number and/or frequency
of postoperative complications after breast surgery. This means fewer postop
visits and less resource utilization required to manage complications, as well
as improved overall patient satisfaction.
When considering the cost-benefit relationship of postoperative smoking-
related morbidity (i.e., wound healing issues, dehiscence, surgical site
infection, return to operating room, and potential for unfavorable scarring as
a result of the aforementioned), aftercare resources utilized, and overall
patient dissatisfaction attributed to smoking-related complications, it may be
in the surgeon’s best interest to require perioperative smoking cessation and
ensure patients are in fact adhering to this requirement before proceeding
with breast surgery.
The vast majority of surgeons will have patients attempt to discontinue
smoking perioperatively (which can hopefully be parleyed into quitting
permanently). It would seem clear that patients would choose to adhere to
these recommendations in order to improve their outcome, however in
practice we know that patients often have a very difficult time with cessation.
Roughly 40% to 50% of smokers attempting to abstain in the perioperative
are successful at the time of surgery (26). To make matters even more
challenging, we are often asking them to quit their addiction shortly after a
recent cancer diagnosis, an extremely stressful time for most people.
Furthermore, when considering methods of smoking cessation, it is worth
mentioning that existing date support complete nicotine abstention as the
most effective method in reducing postoperative complications (2). As such,
cessation aids, such as nicotine patch or nicotine gum should not be a part of
the ideal perioperative cessation protocol.
AUTHORS’ RECOMMENDATIONS
While evidence clearly shows that perioperative smoking increases
complications in breast surgery, implementing this knowledge into a
consistent surgeon-specific or practice-specific policy is not quite as clear-
cut. There are multiple factors that make the decision more complicated.
With the vast amount of information available to everybody, patients often
come to the consultation with more education than in the previous decades,
and can have strong feelings about how they want to proceed with their
reconstruction. Discussions with breast surgeons prior to consultation with
the reconstructive surgeon can also be a source of preconceived ideas about
what they want for reconstruction. Breast surgery is often emotional for
patients in general, and in the face of a cancer diagnosis, this can become
even more of a factor. As compassionate physicians we strive to provide the
most comprehensive, best overall care for our patients. This, of course,
includes the usual medical and surgical risk-benefit analysis, but must also
consider the patient’s psychological and emotional wellness.
Surgeons use many different strategies for management of perioperative
smoking. While some surgeons are willing to proceed with surgery as long as
patients are willing to accept increased risk, others have strict policy to not
operate unless patients are fully abstinent for at least 4 to 6 weeks, while
following multiple cotinine levels in the preop period. Empirically, most
surgeons fall somewhere between these two ends of the spectrum.
When developing one’s stance regarding operating on patients who smoke,
at very minimum patients who smoke must be aggressively educated about
their increased risk of complications and possible consequences. The surgeon
must also be willing to accept the increased risk, as increased complications
will lead to increase stress and utilization of time and resources (including
numerous postop visits, extended wound care, or additional operations). Use
of the cotinine test is individualized according to surgeon preference.
OUR STRATEGY
In our practice, for breast reconstruction we prefer patients to be nicotine free
for at least 2 weeks prior and 6 weeks post surgery. At the initial consultation
patients who smoke are educated about the increased risks and discuss
cessation. We typically check one cotinine level in the immediate
preoperative period.
In our experience, even the most well-intentioned and motivated patients
often have a difficult time with discontinuation of tobacco. For this reason,
we are more likely to recommend delayed reconstruction. If the patient
strongly wishes to proceed with immediate reconstruction, we are more likely
to offer a reconstructive option that maximizes soft tissue coverage and/or
minimize stress on flaps. As such we will often steer reconstruction toward
latissimus flap (usually with implant) or free tissue transfer if the patient is
otherwise a good candidate. Latissimus and free tissue transfer
reconstructions offer additional soft tissue coverage immediately deep to
mastectomy flaps. Thus, while we do see occasional postop wound
complications in these patients, the stakes are often not as high. Specifically,
in these cases the main goal is to avoid removal of the implant if possible.
If the patient insists on implant-based reconstruction we will proceed with
staged reconstruction with placement of tissue expander, but with minimal
initial fill of the expanders to minimize any stress on the mastectomy flaps.
We evaluate the mastectomy flaps intraoperatively for color, warmth,
perfusion, bleeding status, thickness, etc., frequently utilizing SPY
fluorescence imaging. If flaps do not look healthy at the time of surgery, we
will delay reconstruction. All of this is discussed with the patient prior to the
operation. We are less enthusiastic about offering direct-to-implant
reconstruction to smoking patients.
CONCLUSION
It is well known that smoking has numerous detrimental effects on overall
health, and it has been proven that nicotine and tobacco impede wound
healing via multiple pathophysiologic mechanisms. Wound healing is further
challenged in breast surgery, where blood supply to the tissues is already
attenuated, and there is increased reliance on microvasculature and the small-
caliber subdermal plexus. Multiple studies confirm increased complication
rates in smokers undergoing multiple types of breast surgery. As would be
expected, the increased complications are largely related to issues with
wound healing.
The ideal perioperative management of patients who smoke is abstinence 4
weeks prior to and 4 to 6 weeks post surgery, which, if successful reduces
smoking-related complications to the level of nonsmokers. Unfortunately,
this strategy is frequently unsuccessful, forcing the patient and surgeon to
either accept increased risk of morbidity or change the surgical plan. Options
include delaying surgery/reconstruction altogether or altering the surgical
plan to mitigate the increased risk. Surgeons may want to consider
autologous reconstruction in smokers, or if proceeding with implant-based
reconstruction may want to maximize soft tissue coverage of the implant
and/or minimize the stress on the breast flaps. Additional soft tissue coverage
may help prevent implant exposure in some cases of wound breakdown,
which may help avoid implant loss in some cases, one of the most dreaded
complications of breast surgery. There are multiple approaches to
perioperative management of smoking, and each surgeon should develop his
or her own approach based on their own reasoning, comfort level, and
philosophy. Treatment plans can also be individualized for patients on a case-
by-case basis.

REFERENCES

1. Reus WF, Robson MC, Zachary L, et al. Acute effects of tobacco


smoking on blood flow in the cutaneous micro-circulation. Br J Plast
Surg 1984;37(2):213–215.
2. Krueger JK, Rohrich RJ. Clearing the smoke: the scientific rationale for
tobacco abstention with plastic surgery. Plast Reconstr Surg
2001;108(4):1063–1073; discussion 1074–1077.
3. Bartsch RH, Weiss G, Kastenbauer T, et al. Crucial aspects of smoking
in wound healing after breast reduction surgery. J Plast Reconstr Aesthet
Surg 2007;60(9):1045–1049.
4. Silverstein P. Smoking and wound healing. Am J Med
1992;93(1A):22S–24S.
5. Nadler JL, Velasco JS, Horton R. Cigarette smoking inhibits
prostacyclin formation. Lancet 1983;1(8336):1248–1250.
6. Mitchell JA, Ali F, Bailey L, et al. Role of nitric oxide and prostacyclin
as vasoactive hormones released by the endothelium. Exp Physiol
2008;93(1):141–147.
7. Yau JW, Teoh H, Verma S. Endothelial cell control of thrombosis. BMC
Cardiovasc Disord 2015;15:130.
8. Sorensen LT, Horby J, Friis E, et al. Smoking as a risk factor for wound
healing and infection in breast cancer surgery. Eur J Surg Oncol
2002;28(8):815–820.
9. Swanson E. All seasons vertical augmentation mastopexy: a simple
algorithm, clinical experience, and patient-reported outcomes. Plast
Reconstr Surg Glob Open 2016;4(12):e1170.
10. Calobrace MB, Herdt DR, Cothron KJ. Simultaneous
augmentation/mastopexy: a retrospective 5-year review of 332
consecutive cases. Plast Reconstr Surg 2013;131(1):145–156.
11. Messa CA, Messa CA. One-stage augmentation mastopexy: a
retrospective ten-year review of 2,183 consecutive procedures. Aesthet
Surg J 2019;39(12):1352–1367.
12. Bikhchandani J, Varma SK, Henderson HP. Is it justified to refuse
breast reduction to smokers? J Plast Reconstr Aesthet Surg
2007;60(9):1050–1054.
13. Hillam JS, Borsting EA, Chim JH, et al. Smoking as a risk factor for
breast reduction: an analysis of 13,503 cases. J Plast Reconstr Aesthet
Surg 2017;70(6):734–740.
14. Chan LK, Withey S, Butler PE. Smoking and wound healing problems
in reduction mammaplasty: is the introduction of urine nicotine testing
justified? Ann Plast Surg 2006;56(2):111–115.
15. Cunningham BL, Gear AJ, Kerrigan CL, et al. Analysis of breast
reduction complications derived from the BRAVO study. Plast Reconstr
Surg 2005;115(6):1597–1604.
16. Fischer JP, Cleveland EC, Shang EK, et al. Complications following
reduction mammaplasty: a review of 3538 cases from the 2005–2010
NSQIP data sets. Aesthet Surg J 2014;34(1):66–73.
17. Pinsolle V, Grinfeder C, Mathoulin-Pelissier S, et al. Complications
analysis of 266 immediate breast reconstructions. J Plast Reconstr
Aesthet Surg 2006;59(10):1017–1024.
18. Bailey MH, Smith JW, Casas L, et al. Immediate breast reconstruction:
reducing the risks. Plast Reconstr Surg 1989;83(5):845–851.
19. Padubidri AN, Yetman R, Browne E, et al. Complications of
postmastectomy breast reconstructions in smokers, ex-smokers, and
nonsmokers. Plast Reconstr Surg 2001;107(2):342–349; discussion
350–351.
20. Reus WF 3rd, Colen LB, Straker DJ. Tobacco smoking and
complications in elective microsurgery. Plast Reconstr Surg
1992;89(3):490–494.
21. Chang LD, Buncke G, Slezak S, et al. Cigarette smoking, plastic
surgery, and microsurgery. J Reconstr Microsurg 1996;12(7):467–474.
22. Chang DW, Reece GP, Wang B, et al. Effect of smoking on
complications in patients undergoing free TRAM flap breast
reconstruction. Plast Reconstr Surg 2000;105(7):2374–2380.
23. Selber JC, Kurichi JE, Vega SJ, et al. Risk factors and complications in
free TRAM flap breast reconstruction. Ann Plast Surg 2006;56(5):492–
497.
24. Benowitz NL, Hukkanen J, Jacob P 3rd. Nicotine chemistry,
metabolism, kinetics and biomarkers. Handb Exp Pharmacol 2009;
(192):29–60.
25. Raja M, Garg A, Yadav P, et al. Diagnostic methods for detection of
cotinine level in tobacco users: a review. J Clin Diagn Res
2016;10(3):ZE04–ZE06.
26. Thomsen T, Villebro N, Moller AM. Interventions for preoperative
smoking cessation. Cochrane Database Syst Rev 2014;(3):CD002294.
CHAPTER 121

Should Elective Surgery Be Offered to


High-BMI Patients?
OMAR ELFANAGELY | JOHN P. FISCHER
HISTORY
Our society is in the midst of an obesity epidemic. According to the Centers
for Disease Control, which defines obesity as having a body mass index
(BMI) of greater than 30 kg/m2, 39% of the U.S. population is affected. This
amounts to over 93 million adults (1). Obesity is not only a concern at the
national level, but is in fact a global pandemic with the rates of obesity
having nearly tripled since 1975 (2).
The medical community has known the morbidity associated with an
elevated BMI for more than 2,000 years (3). The disease burden associated
with this cohort spans across multiple organ systems (4). In particular, the
high-BMI woman is at risk to multiple pathologies of the breast, manifesting
in the form of higher rates of breast cancer and both physical and
psychological symptoms associated with macromastia (5). In fact, the
incidence of breast cancer mirrors the trend in obesity with a steady increase,
accounting for the largest of all newly reported cancer cases in women (6,7).
Of those women diagnosed, approximately 40% will subsequently receive
postmastectomy reconstruction surgery (8). Not surprisingly, this health state
places patients at higher risk when it comes to breast surgery and ultimately
presents a challenge to the surgeon. In the perioperative period, patients with
higher BMIs when compared to normal-weight patients are at an increased
risk for complications with anesthesia (9). Pre- and postoperatively, patients
with elevated BMIs face both medical and surgical complications as depicted
in Figure 121-1.
The epidemiology of obesity shows a clear gender disparity. The
prevalence of overweight and obese men and women varies greatly between
countries, but overall more women are afflicted than men with 15%
belonging to the former and 40% belonging to the latter (2,10). Subsequently,
surgeons are increasingly encountering patients with elevated BMIs. In the
elective setting, surgeons are ethically obligated to give special consideration
to these higher-risk patients and the ultimate decision to proceed with
surgery. As such, it is the purpose of the authors of this chapter to bring
awareness to the reader, evaluate the efficacy of available techniques, and
provide recommendations to avoid potential pitfalls.
FIGURE 121-1 Outlines the challenges of operating on the obese patient, categorized
into medical risks (left) and surgical risks and complications (right).
TECHNICAL APPROACH

Reconstruction
Autologous Tissue
Autologous breast reconstruction accounts for approximately 25% to 30% of
all reconstructive surgeries (11). Breast reconstruction with autologous tissue
is reliable and provides excellent long-term aesthetic results with acceptable
postoperative morbidity (12). One common technique is the abdominal flap,
which is frequently utilized with satisfactory outcomes in selected patients
(6,13). Common examples of abdominal flaps include the pedicled transverse
rectus abdominis myocutaneous (TRAM) flap, free TRAM flap, and muscle-
sparing flaps such as the free muscle-sparing TRAM flap, superior inferior
epigastric artery (SIEP) flap, and deep inferior epigastric perforator (DIEP)
flap. The overweight and obese population, however, poses a unique
challenge (14,15).
Obese women undergoing a pedicled TRAM flap have significantly higher
flap complications; including flap loss, hematoma, seroma, and skin necrosis.
They are also at risk for donor-site complications such as infection, delayed
wound healing, dehiscence, seroma, bulge, and hernia (16). Given the
independent risk factors associated with obesity, some clinicians have
suggested a BMI more than 25 kg/m2 as a relative contraindication to TRAM
flap breast reconstruction (17–19). Despite the increase in flap loss, our
institution was able to show a 98% success rate with tissue transfer (20). One
common alternative to the TRAM flap is the latissimus dorsi flap (LDF),
which has been shown to carry the lowest 30-day morbidity when compared
to traditional reconstruction methods (21,22).
The general consensus reports increased incidence of perioperative
complications following autologous breast reconstructive surgery, though a
more recent study noted a relative risk of donor-site complications within the
obese population. Specifically, obese patients can undergo autologous
abdominal free flaps safely without increased risk for donor-site hernia or
flap loss compared to nonobese patients; however, they should be counseled
regarding the potential risk of complications. (23). Autologous breast
reconstruction in the elevated BMI patient is directly associated with flap loss
and donor-site morbidity. Despite this, at times this approach may represent
the best option for these patients with cited higher patient satisfaction and
durable results (21,24–27).

Alloplastic
Although autologous reconstruction offers a more natural-appearing breast,
implant-based breast reconstructions are shorter operations, have faster
recoveries, and are without donor-site morbidity (28). These benefits have
solidified implant-based breast reconstruction as a standard in the United
States. According to published statistics by the American Society of Plastic
Surgeons (ASPS), 101,657 women underwent breast reconstruction in 2018
(8). Of these, approximately 68% were tissue expander to implant based.
With the growing trend for implant-based reconstruction, complications
associated with the higher-BMI group have increasingly been reported.
According to the literature (29,30), complications after alloplastic breast
reconstruction occur in about one-third of cases. In one study, high-BMI
patients had almost 10 times higher risk of developing severe complications
(31).
Aesthetic
Cosmetic and Curative
Given the rise in the elevated BMI population, overweight and obese patients
are increasingly seeking cosmetic surgeons for symptomatic relief. Reduction
mammoplasty is a proven treatment for macromastia, with benefits shown to
effectively relieve physical and psychological ailments associated with these
conditions (32).
The overweight and obese population undergoing reduction mammoplasty,
similar to that receiving breast reconstruction, is associated with increased
early postoperative complications (33). Studies have furthermore shown that
the risk gradually increases with an increase in the obesity severity (34).
Consequently, morbidly obese patients are at the highest risk, with
complications occurring in nearly 12% of this cohort.
The risk of surgical complications after cosmetic or curative breast surgery
is higher in the obese patient. However, to consider an elevated BMI an
exclusion criterion would be inappropriate. Based on the literature,
mammoplasty can be performed safely, even in the morbidly obese patient,
but requires appropriate planning and careful patient selection (35).
CHALLENGES
The national trend in rising BMI constitutes a new challenge to the modern
plastic surgeon. Special considerations must be taken along each aspect of the
patient’s journey in order to maximize outcome and ensure reproducible
results.
Preoperative Considerations
Focus should start with the first patient visit. As in all cases, a thorough
history and physical examination should be performed. Scrutiny should be
placed on comorbidities and toxic social habits, as this provides the necessary
foundation for appropriate patient selection. Likewise, during the consent,
attention on concisely distilling the increased risks this population faces is
paramount to achieving satisfactory results and avoiding disappointment. In
situations where immediate surgical intervention is deemed unsafe,
consideration for postponing with plans for weight loss is necessary. Though
weight loss is beneficial for ease of procedure and quality of life, patients
should be made aware it does not decrease risk of postoperative
complications (36).
Once the decision to proceed with surgery has been made there are a few
points, which can ease potential difficulties. First and foremost, the surgeon
must decide what type of procedure to perform. In the realm of
reconstruction, conflicting data exist regarding the ideal method. Obese
patients, particularly class II and III, have been found to experience higher
failure rates with implant-based and immediate breast reconstruction (27),
suggesting consideration for free flap technique or delayed approach. The
latissimus flap was noted to carry the lowest morbidity compared to other
autologous flaps (21). However one study, which examined immediate 30-
day complications, found increased BMI was associated with higher
morbidity in autologous reconstruction compared to tissue expander
reconstruction (21), though it should be noted that by focusing on the
immediate 30-day postoperative period, the study ignored long-term
complications associated with implant-based reconstruction.
The morbidly obese patient deserves special deliberation, separate from the
overweight or obese patient. While at significantly increased risk for
perioperative complications, no significant difference was seen in 30-day
surgical complication rates between implant and autologous reconstruction
(37). More so, the use of the latissimus flap plus tissue expander in the
morbidly obese patient may serve as a better method, as it is associated with a
lower incidence of infection and expander loss when compared to tissue
expander reconstruction alone (18,38).
Perioperative and Postoperative Considerations
As with any surgery, the key to success begins with preparation. In the case
of the elevated BMI patient, this starts by alerting everyone involved in the
care of the patient of the added challenges associated and making the
necessary adjustments. This may entail different instruments, a bariatric table,
and/or extra personnel.
Intraoperatively, there are many maneuvers and techniques that should be
considered in order to minimize the risks of complications associated with
this cohort. When considering the autologous reconstruction, one potential
aid is the use of laser-assisted indocyanine green (ICG) angiography to
accurately detect mastectomy skin flap necrosis and prevent postoperative
complications (39,40). To minimize the risks of donor-site morbidity, the
literature suggests having a low threshold for placing mesh in obese patients
(41,42). Use of mesh should be considered, particularly if performing a
muscle-harvesting flap. Another consideration is the placement of incisional
negative-pressure dressing, with promising, though preliminary data from
one author who noted a decrease in wound healing complications (23).
Lastly, some general consideration should include limiting the abdominal
dissection, avoiding tension at closure, being aggressive in removing skin
from the mastectomy flaps, and completely removing all of Hartrampf zone
4. When undergoing implant reconstruction we suggest consideration of a
larger implant and performing a balancing reduction procedure, such as a
mastopexy or reduction mammoplasty. When the above suggestions are
employed the authors have produced consistent and aesthetically satisfying
results as depicted in Figure 121-2.
FIGURE 121-2 A: Depicts a delayed breast reconstruction patient following left
modified radical mastectomy. B: Postoperative view of the same patient following a
left DIEP flap and right prophylactic mastopexy and reduction mammoplasty.
(Courtesy of Dr. Joseph M. Serletti, MD, FACS, Division of Plastic Surgery,
University of Pennsylvania.)

As with all surgical cases, DVT prophylaxis should be given with key
focus on appropriate dosage. In particular, the morbidly obese patient
benefits from weight-based DVT prophylaxis in comparison to standard
doses (43). Postoperatively, patients should follow routine postoperative care
with particular attention on early mobilization.
CONCLUSION
Obesity is a global crisis with no signs of tapering off. Some forecasts predict
obesity rates to exceed 50% by 2030 (44). Despite evidence showing an
increased risk of postoperative complications in the obese population (14),
elective breast surgery can be successfully performed with reliable functional
and aesthetic results. This can be accomplished through proper patient
selection, careful preoperative planning, thorough surgical technique, and
careful postoperative management. Ultimately, BMI is merely a surrogate for
adipose burden and may not depict a patient’s true risk. The decision to
proceed and which procedure to perform should be made on a case-by-case
basis after careful counseling about the risks (45–47).

REFERENCES

1. National Center for Health Statistics. National Health and Nutrition


Examination Survey. www.cdc.gov/obesity/data/adults.html. Accessed
2019.
2. W. H. Organization. “Obesity and Overweight.” World Health
Organization. https://www.who.int/news-room/fact-
sheets/detail/obesity-and-overweight. Accessed June 16, 2019.
3. Bray GA. The Battle Of The Bulge. Pittsburg, PA: Dorrance; 2007.
4. Kanker W, Fonds O. Food, Nutrition, Physical Activity, and the
Prevention of Cancer: A Global Perspective. www.wcrf-nl.org.
Accessed 2019.
5. Carmichael AR, Bates T. Obesity and breast cancer: a review of the
literature. Breast 2004;13(2):85–92.
6. Crisera CA, Chang EI, Da Lio AL, et al. Immediate free flap
reconstruction for advanced-stage breast cancer: is it safe? Plast
Reconstr Surg 2011;128(1):32–41.
7. Cancer Facts & Figures 2019. American Cancer Society.
https://www.cancer.org/content/dam/cancer-org/research/cancer-facts-
and-statistics/annual-cancer-facts-and-figures/2019/cancer-facts-and-
figures-2019.pdf. Accessed July 10, 2019.
8. ASPS. Plastic Surgery Statistics Report: 2018. American Society of
Plastic Surgeons.
https://www.plasticsurgery.org/documents/News/Statistics/2018/plastic-
surgery-statistics-full-report-2018.pdf. Accessed July 16, 2019.
9. Shearer ES. Obesity anaesthesia: the dangers of being an apple. Br J
Anaesth 2013;110(2):172–174.
10. Kanter R, Caballero B. Global gender disparities in obesity: a review.
Adv Nutr 2012;3(4):491–498.
11. Panchal H, Matros E. Current trends in postmastectomy breast
reconstruction. Plast Reconstr Surg 2017;140(5S Advances in Breast
Reconstruction):7s–13s.
12. Sternberg EG, Perdikis G, McLaughlin SA, et al. Latissimus dorsi flap
remains an excellent choice for breast reconstruction. Ann Plast Surg
2006;56(1):31–35.
13. Ross AC, Rusnak CH, Hill MK, et al. An analysis of breast cancer
surgery after free transverse rectus abdominis myocutaneous (TRAM)
flap reconstruction. Am J Surg 2000;179(5):412–416.
14. Panayi AC, Agha RA, Sieber BA, et al. Impact of obesity on outcomes
in breast reconstruction: a systematic review and meta-analysis. J
Reconstr Microsurg 2018;34(5):363–375.
15. Selber JC, Kurichi JE, Vega SJ, et al. Risk factors and complications in
free TRAM flap breast reconstruction. Ann Plast Surg 2006;56(5):492–
497.
16. Spear SL, Ducic I, Cuoco F, et al. Effect of obesity on flap and donor-
site complications in pedicled TRAM flap breast reconstruction. Plast
Reconstr Surg 2007;119(3):788–795.
17. Fischer JP, Nelson JA, Kovach SJ, et al. Impact of obesity on outcomes
in breast reconstruction: analysis of 15,937 patients from the ACS-
NSQIP datasets. J Am Coll Surg 2013;217(4):656–664.
18. Jandali S, Nelson JA, Sonnad SS, et al. Breast reconstruction with free
tissue transfer from the abdomen in the morbidly obese. Plast Reconstr
Surg 2011;127(6):2206–2213.
19. Chang DW, Wang B, Robb GL, et al. Effect of obesity on flap and
donor-site complications in free transverse rectus abdominis
myocutaneous flap breast reconstruction. Plast Reconstr Surg
2000;105(5):1640–1648.
20. Fischer JP, Nelson JA, Sieber B, et al. Free tissue transfer in the obese
patient: an outcome and cost analysis in 1258 consecutive abdominally
based reconstructions. Plast Reconstr Surg 2013;131(5):681e–692e.
21. Hanwright PJ, Davila AA, Hirsch EM, et al. The differential effect of
BMI on prosthetic versus autogenous breast reconstruction: a
multivariate analysis of 12,986 patients. Breast 2013;22(5):938–945.
22. Yezhelyev M, Duggal CS, Carlson GW, et al. Complications of
latissimus dorsi flap breast reconstruction in overweight and obese
patients. Ann Plast Surg 2013;70(5):557–562.
23. Chang EI, Liu J. Prospective evaluation of obese patients undergoing
autologous abdominal free flap breast reconstruction. Plast Reconstr
Surg 2018;142(2):120e–125e.
24. Atisha DM, Alderman AK, Kuhn LE, et al. The impact of obesity on
patient satisfaction with breast reconstruction. Plast Reconstr Surg
2008;121(6):1893–1899.
25. Sinha S, Ruskin O, D’Angelo A, et al. Are overweight and obese
patients who receive autologous free-flap breast reconstruction satisfied
with their postoperative outcome? A single-centre study. J Plast
Reconstr Aesthet Surg 2016;69(1):30–36.
26. Larson KE, Ozturk CN, Kundu N, et al. Achieving patient satisfaction in
abdominally based free flap breast reconstruction: correlation with body
mass index subgroups and weight loss. Plast Reconstr Surg
2014;133(4):763–773.
27. Garvey PB, Villa MT, Rozanski AT, et al. The advantages of free
abdominal-based flaps over implants for breast reconstruction in obese
patients. Plast Reconstr Surg 2012;130(5):991–1000.
28. Fischer JP, Wes AM, Tuggle CT 3rd, et al. Risk analysis of early
implant loss after immediate breast reconstruction: a review of 14,585
patients. J Am Coll Surg 2013;217(6):983–990.
29. Yoon AP, Qi J, Brown DL, et al. Outcomes of immediate versus delayed
breast reconstruction: results of a multicenter prospective study. Breast
2018;37:72–79.
30. Thorarinsson A, Fröjd V, Kölby L, et al. A retrospective review of the
incidence of various complications in different delayed breast
reconstruction methods. J Plast Surg Hand Surg 2016;50(1):25–34.
31. Sadok N, Krabbe-Timmerman IS, de Bock GH, et al. The effect of
smoking and body mass index on the complication rate of alloplastic
breast reconstruction. Scand J Surg 2019;1457496919826711.
doi:10.1177/1457496919826711
32. Chadbourne EB, Zhang S, Gordon MJ, et al. Clinical outcomes in
reduction mammaplasty: a systematic review and meta-analysis of
published studies. Mayo Clin Proc 2001;76(5):503–510.
33. Nelson JA, Fischer JP, Chung CU, et al. Obesity and early
complications following reduction mammaplasty: an analysis of 4545
patients from the 2005–2011 NSQIP datasets. J Plast Surg Hand Surg
2014;48(5):334–339.
34. Myung Y, Heo CY. Relationship between obesity and surgical
complications after reduction mammaplasty: a systematic literature
review and meta-analysis. Aesthet Surg J 2017;37(3):308–315.
35. Roehl K, Craig ES, Gomez V, et al. Breast reduction: safe in the
morbidly obese? Plast Reconstr Surg 2008;122(2):370–378.
36. Ozturk CN, Kundu N, Bernard S, et al. Breast reconstruction with
abdominal-based free flaps in high body mass index population:
postoperative complications and impact of weight loss. Ann Plast Surg
2014;72(1):13–22.
37. Fischer JP, Cleveland EC, Nelson JA, et al. Breast reconstruction in the
morbidly obese patient: assessment of 30-day complications using the
2005 to 2010 National Surgical Quality Improvement Program data sets.
Plast Reconstr Surg 2013;132(4):750–761.
38. Luce EA, Adams RL, Chandler RG, et al. Tissue expander versus tissue
expander and latissimus flap in morbidly obese breast reconstruction
patients. Plast Reconstr Surg Glob Open 2015;3(3):e323.
39. Li K, Zhang Z, Nicoli F, et al. Application of indocyanine green in flap
surgery: a systematic review. J Reconstr Microsurg 2018;34(2):77–86.
40. Burnier P, Niddam J, Bosc R, et al. Indocyanine green applications in
plastic surgery: a review of the literature. J Plast Reconstr Aesthet Surg
2017;70(6):814–827.
41. Mirzabeigi MN, Wilson AJ, Fischer JP, et al. Predicting and managing
donor-site wound complications in abdominally based free flap breast
reconstruction: improved outcomes with early reoperative closure. Plast
Reconstr Surg 2015;135(1):14–23.
42. Wan DC, Tseng CY, Anderson-Dam J, et al. Inclusion of mesh in
donor-site repair of free TRAM and muscle-sparing free TRAM flaps
yields rates of abdominal complications comparable to those of DIEP
flap reconstruction. Plast Reconstr Surg 2010;126(2):367–374.
43. Rondina MT, Wheeler M, Rodgers GM, et al. Weight-based dosing of
enoxaparin for VTE prophylaxis in morbidly obese, medically-ill
patients. Thromb Res 2010;125(3):220–223.
44. Finkelstein EA, Khavjou OA, Thompson H, et al. Obesity and severe
obesity forecasts through 2030. Am J Prev Med 2012;42(6):563–570.
45. Meijs AP, Koek MBG, Vos MC, et al. The effect of body mass index on
the risk of surgical site infection. Infect Control Hosp Epidemiol
2019;40(9):991–996.
46. Freckelton L, Lambert K, Smith NA, et al. Impact of body mass index
on utilization of selected hospital resources for four common surgical
procedures. ANZ J Surg 2019;89(7–8):842–847.
47. Choban PS, Flancbaum L. The impact of obesity on surgical outcomes:
a review. J Am Coll Surg 1997;185(6):593–603.
CHAPTER 122

Breast Implant–Associated Anaplastic


Large Cell Lymphoma
MARK W. CLEMENS
HISTORY
Breast implant–associated anaplastic large cell lymphoma (BIA-ALCL) is an
uncommon T cell lymphoma that develops on an average a decade after
implantation of a textured breast implant (1–5). BIA-ALCL was first
described by Keech and Kreech in 1997 (6), though the first case is now
attributed to a case report from 1996 (7). BIA-ALCL received only limited
national attention until a U.S. Food and Drug Administration (FDA) safety
communication in 2011 (8,9). Awareness has exponentially grown following
provisional classification by the World Health Organization (10,11), National
Cancer Institute (12), annual advisory updates from the U.S. Food and Drug
Administration (13), numerous government agencies worldwide (14–16), and
media coverage (17). While the exact mechanism of pathogenesis remains
elusive, clear data has now been reported on the histopathology (18–26),
epidemiology (27–31), imaging (32,33), treatment outcomes (34,35), and
practice guidance (36). This chapter will review the current risk of disease
development, theories on pathogenesis, and the diagnosis and treatment of
BIA-ALCL.
EPIDEMIOLOGY
Lymphomas involving the breast account for ∼2% of all extranodal
lymphomas and less than 1% of all non-Hodgkin lymphomas (NHLs) (37).
Most lymphomas that involve the breasts are of B cell lineage, with diffuse
large cell B cell lymphoma and extranodal marginal zone lymphoma of
mucosa-associated lymphoid tissue being most common. ALCL is an
uncommon T cell neoplasm that accounts for ∼3% of NHLs. In a series of
106 cases, Talwalkar et al. reported that cases of ALCL accounted for 6% of
all lymphomas involving the breast, and two cases in that study were
associated with breast implants (36). These data suggested that ALCL and
breast implants were associated.
De Jong et al. (27) conducted a case control study in the Netherlands that
included 389 women with NHL in the breast over a 16-year span; 5 cases of
ALCL were identified in patients with breast implants, and 6 other patients
with ALCL lacked implants. For each of these 11 patients, the authors
selected one to five controls with other lymphomas of the breast, matched to
age and year of diagnosis. The calculated odds ratio was 18.2 (95%
confidence interval, 2.1 to 156.8) indicating that patients with breast ALCL
are significantly more likely to have breast implants. De Jong et al. in 2008
estimated that the incidence of breast implant ALCL in the Netherlands was
approximately 1 to 3 per million per year.
Lipworth et al. examined five long-term studies with clinical follow-up as
long as 37 years. A total of 48 lymphomas in 43,000 women with implants
were found compared to an expected 54 lymphoma cases (38). More recently,
Largent et al. reviewed prospectively six clinical studies sponsored by a
breast implant manufacturer and they reported 28 lymphomas in 89,382
women with implants, compared to 43 expected lymphomas over a median
follow-up of only 2.7 years (39). Both reports concluded that the incidence of
ALCL was not increased in patients with implants; however, these studies
had significant limitations. The first study included a relatively small number
of women and none of the lymphomas were in the breast. The second study
had a short period of observation at 2.7 years, inadequate when one considers
that the mean time from implantation to the diagnosis of breast implant
ALCL is 9 years.
Wang et al. (40) utilized a database of 123,392 women from the California
Teacher Study cohort to identify 2,990 women with breast implants. They
conducted a prospective study to evaluate the association between breast
implants and T cell lymphoma. Of 89 women who developed T cell
lymphoma, only two who had breast implants developed ALCL. Although
their hazard ratio calculation showed no association between breast implants
and T cell lymphoma overall, a statistically significant association was seen
for breast implants and ALCL. Furthermore, they found a 10.9 times
increased risk specific for ALCL in patients who reported a history of breast
implants at the study baseline. With this growing epidemiologic data, as well
as strong clinical and pathologic evidence, there is substantial support for a
pathogenic relationship. This epidemiologic data is likely hampered by
underdiagnosis and misdiagnosis of BIA-ALCL by imaging and/or
histopathology (41). De Boer et al. in 2018 estimated that the lifetime risk of
BIA-ALCL was 1 in 6,920 patients with a breast implant (42). It’s important
to note that this was a study of women in the Netherlands which is a 99%
textured implant market essentially making this the risk of BIA-ALCL in
textured implants.
Doren et al. (28) estimated that the prevalence of breast implant ALCL
among patients is 1 in 30,000 women averaged across different textured
surface implants, and the risk of breast implant ALCL is increased by nearly
70-fold in patients with textured implants when compared with all women in
the general population and with smooth implants. Of note, this study was a
U.S. population-based study with an approximate manufacturer mix of 50:50
Allergan to Mentor during the study time period. Allergan Biocell to Mentor
Siltex was noted to have an 8:1 ratio, or a risk of 1:6,600 Allergan compared
to a risk of 1:56,000 Mentor. Importantly, there has been no case report, case
series, or prospective registry to date recording a clinical history of only
smooth implants leading to the development of BIA-ALCL. If these findings
are confirmed, there is hope that reimplantation with smooth implants may be
an alternative for women with BIA-ALCL wishing to continue to have breast
implants (43). The U.S. FDA has reported that a few cases (<7%) reported to
the adverse events database have included a smooth implant at time of
explantation, however all cases either involved a clinical history of a textured
implant or no clinical history available for review. Magnusson et al. (44)
reported the risk assessment of BIA-ALCL in Australia and based upon 81
BIA-ALCL patients and breast implant sales data, the authors report updated
manufacturer-specific disease risks as follows: Silimed polyurethane, 1 in
2,832 (95% CI, 1,582 to 5,673); Allergan Biocell, 1 in 3,345 (95% CI, 2,475
to 4,642), and Mentor Siltex, 1 in 86,029 (95% CI, 15,440 to 1,301,759).
Pertinent to the U.S. market was the reporting of a 25.7 to 1 ratio of Biocell
to Siltex BIA-ALCL risk. These findings demonstrate that risk of BIA-ALCL
is not only associated with a textured surface, but varies by type of texturing.
Because of this, a number of different classifications of surface texturing
were described in 2018 and summarized in Table 122-1 (45–51).
The largest series ever reported on textured implants, the Continued
Access/Continued Access Reconstruction/Revision Expansion (CA/CARE)
clinical trial, which was a 10-year, multicenter study of Allergan Biocell
textured implants initially identified 4 cases of BIA-ALCL out of 17,656
patients. Since publication, the lead author further identified a total of 8
patients bringing the risk estimate in their large prospective multicenter
cohort to 1:2,207 (52,53). A recent study conducted at Memorial Sloan-
Kettering Cancer Center reported a single-surgeon experience of 6,023
Allergan Biocell breast reconstructions and having a risk of 1:443 (54). On
July 23, 2019, the FDA called for a class I device recall of Allergan Biocell
tissue expanders and implants due to an overrepresentation of Biocell cases
when market share was taken into account (55). The FDA reported that when
manufacturer was known, Allergan Biocell was associated in approximately
91% of world cases of BIA-ALCL. The device recall was followed
immediately with a worldwide voluntary recall of Biocell products by
Allergan.
The PROFILE registry now recognizes 288 confirmed or suspected cases
in the United States bringing the total worldwide cases to 871 as of December
6th, 2019 (e-Fig. 122-1A) (56). The majority of BIA-ALCL cases come from
North America, Europe, and Australia, however cases overall are likely
underreported worldwide. (e-Fig. 122-1B).
E-FIGURE 122-1 Geographic distribution of patients diagnosed with BIA-ALCL. A
worldwide distribution of over 800 cases reported (A) and United States distribution
of 288 cases reported in 31 states (B). The range of reported cases per country or
state is shown in the insets.

Pathogenesis
Research efforts have focused on several theories of lymphomagenesis with
most in agreement of an inciting multifactorial chronic inflammatory
stimulus leading to T cell dysplasia in a genetically susceptible patient
(57–63). As breast implant ALCL has arisen in patients with either silicone-
or saline-filled implants and not in smooth implants, textured shell surface
rather than the implant contents appears to be the essential driver in
pathogenesis. Chronic antigenic stimulation may lead to recruitment,
proliferation, and expansion of T cells, prolonging T cell lifespan, and
leading to clonal expansion and eventually to malignant transformation. The
shedding of silicone particles is more pronounced with textured implants
(19). In a study by Meza Britez et al., inflammation predominantly with a T
cell phenotype around breast implants was statistically more common in
patients with textured breast implants as compared to smooth implants (64).
Hu et al. based on microbiome studies of textured implants in patients with
breast implant ALCL have proposed that the trigger for chronic inflammation
lies in the presence of high bacterial loads and biofilms, however Ralstonia
bacteria are no longer suspected to be a causative factor (65). Perhaps gram-
negative bacteria could produce a lipopolysaccharide antigen that may
stimulate cytokine production resulting in chronic Th1 cell stimulation,
however these findings require peer review publication and further
confirmation.
NCCN CONSENSUS GUIDELINES FOR DIAGNOSIS AND DISEASE
MANAGEMENT
In 2016, the National Comprehensive Cancer Network (NCCN) established
widely accepted consensus guidelines for the diagnosis and management of
BIA-ALCL within their Clinical Practice Guidelines for NHLs, now adopted
by the American Society of Plastic Surgeons (ASPS) and the American
Society for Aesthetic Plastic Surgery (ASAPS) (66,67). NCCN guidelines
represent the authoritative oncology standards utilized worldwide, and are
also important in coverage justification by insurance providers. The
guidelines are available for free from www.nccn.org, and the essential
elements are summarized in Figure 122-1. While NCCN guidelines represent
the most up to date evidence-based approach to this disease, many treating
physicians may never have encountered the variable disease stages, and
therefore individual treatment plans are best formulated in a multidisciplinary
fashion.

TABLE 122-1 Summary of Smooth and Texture Surface Classifications


FIGURE 122-1 Diagnosis and treatment follows National Comprehensive Cancer
Network (NCCN) Guidelines which are available for free download from
www.nccn.org. (Reprinted with permission from Clemens MW, Jacobsen ED, Horwitz
SM. 2019 NCCN consensus guidelines on the diagnosis and treatment of breast implant
associated ALCL. Aesthet Surg J 2019;39:S3–S13.)
APPROACH TO SUSPECTED PATIENT
Delayed seromas greater than 1 year after implantation occur in
approximately 0.1% to 0.2% of patients following implantation of textured
implants (52). In prospective studies, BIA-ALCL has been estimated to occur
in 9% to 15% of delayed seroma presentations (43,68). Any seroma occurring
greater than 1 year after implantation not readily explainable by infection or
trauma should be considered suspicious for disease. An otherwise normal
seroma is not part of the disease spectrum of BIA-ALCL. Patients most
commonly presents with the rapid onset of a spontaneous fluid collection
(60%) or capsular mass (10% to 40%) at an average of 8 to 10 years
following implantation with a textured breast implant, and are distributed
roughly equally between cosmetic and reconstructive indications (38). All
reported cases to date where a detailed implant history was available involved
a textured surface breast implant (35). Other more rare described symptoms
have included skin rash (69), capsular contracture (70), and lymphadenopathy
(38). However, capsular contracture in isolation as the only disease
manifestation has not been described and therefore, its reliability as a
symptom of the disease is questionable and may be coincidental. Disease is
not isolated to female patients as three transsexual patients with textured
implants have been confirmed (71). Following NCCN guidelines, initial
workup of an enlarged breast should include ultrasound evaluation
specifically for a fluid collection, breast mass, or enlarged regional lymph
nodes (axillary, supraclavicular, and internal mammary). For cases where
ultrasound is indeterminate or requires further confirmation, physicians may
also utilize magnetic resonance imaging (MRI). Adrada et al. reviewed 44
breast implant ALCL patients with imaging studies and reported on the
sensitivity/specificity for detecting an effusion using ultrasound (84%/75%),
computerized tomography (55%/83%), MRI (82%/33%), and PET/CT
(38%/83%) (32). Additionally, the sensitivity/specificity to detect a mass was
reported for ultrasound (46%/100%), computerized tomography
(50%/100%), MRI (82%/33%), and PET/CT (64%/88%). The sensitivity of
mammography was found to be inferior for both effusion and mass and
therefore is not considered an acceptable imaging modality for BIA-ALCL.
Based on these findings, ultrasound evaluation is used as a screening tool
while PET/CT scan is utilized after an established diagnosis for oncologic
workup prior to surgery (Fig. 122-2).

FIGURE 122-2 A patient with effusion-limited (Stage 1A) left-sided BIA-ALCL is


shown on an Axial 18F-fluorodeoxyglucose positron emission tomography (PET)-CT
image with increased metabolic activity of right capsule. A: Note an paratracheal
lymph node with small cell lung cancer was incidentally found as a second primary
cancer. Both diseases were treated and patient achieved complete remission. B and
C: Demonstrate PET-CT images of invasive BIA-ALCL masses (Stage IIA) growing
radially out from the surface of a textured implant. D: Demonstrates the same
invasive masses upon surgical resection with the associated implant. (Reprinted with
permission from Clemens MW, Brody GS,Mahabir RC, et al. How to diagnose and treat
breast implant associated anaplastic large cell lymphoma. Plast Reconstr Surg
2018;141[4]:586e–599e.)

Periprosthetic fluid collections should undergo fine-needle aspiration. At


time of aspiration, ultrasound guidance may aid in implant protection and
displacement, and can be performed either in a clinic setting or by
interventional radiology. A suspicious mass requires tissue biopsy and
evaluation by an oncologist to rule out breast cancer. Specimens should be
sent for cell block cytology and CD30 immunohistochemistry. Pathologists
will require a clinical history and directions to “rule out BIA-ALCL.” Fluid
specimens do not require storage in any specialized media, and should be
transported to a pathology lab within a reasonable amount of time (48 hours).
While cells may lyse if left for a prolonged time period, diagnostic protein
markers do not degrade and diagnosis is possible on fixed cell blocks years
later. Fluid collections may be centrifuged down to a supernatant to
concentrate cells for pathology evaluation. If after evaluation, diagnosis of
lymphoma is indeterminate, secondary hematopathology consultation is
recommended at a tertiary cancer center with disease experience.
Best practice guidelines for the pathologic diagnosis of BIA-ALCL were
released in February 2020 as part of a collaboration between the FDA, the
NIH, and MD Anderson Cancer Center (72). Percutaneous aspiration alone is
not therapeutic and is only considered to be a diagnostic option. Note that a
small incidental volume of periprosthetic fluid may be normal and common
around breast implants. A larger volume of fluid yields a more accurate
diagnosis, but a minimum of 10 to 50 mL is appropriate to provide enough
material for preparation of cytopathology smears, cell block with
immunohistochemistry for CD30, and other lineage-associated markers, and,
when possible, flow cytometry and molecular genetic studies.
DIAGNOSTIC CRITERIA
BIA-ALCL diagnosis requires a monoclonal T cell expansion of large
anaplastic (Reed–Sternberg) cells that express CD30, within a periprosthetic
effusion or mass aggregate (Fig. 122-3) (5,73). CD30 refers to a cell
membrane protein that serves as a lymphoma tumor marker, although CD30
can occur normally on activated T cell lymphocytes. A background of
CD30+ T cells are estimated to occur between 0.1% and 5% of circulating T
cells, and note a higher concentration may exist in inflammatory states.
Increased CD30 expression can be induced on both T cells and B cells as a
result of viral infection (74). CD30+ lymphocytes have been described
temporarily increasing from a background of 0.1% to as high as 95%
transiently (50). Immunoblastic proliferation that occurs in infectious
mononucleosis can develop Reed–Sternberg-like cells temporarily making
differentiation from Hodgkin lymphoma difficult. BIA-ALCL, as well as the
entire family of ALCL, displays diffuse CD30 expression on their cell
surface. Morphologic evaluation by a pathologist and determination of clonal
expansion on flow cytometry are critical to diagnosis (Fig. 122-3, Inset). If
the pathology is negative for ALCL, the patient can be referred to a plastic
surgeon for management of a benign seroma. In accordance with the U.S.
FDA’s recommendation, histologic confirmation of BIA-ALCL should be
reported to the ASPS BIA-ALCL PROFILE registry
(www.thepsf.org/PROFILE). The purpose of this important registry is to
increase scientific data on breast implant–associated ALCL in women with
breast implants as well as to support research to characterize the disease.
FIGURE 122-3 A malignant effusion in a BIA-ALCL patient demonstrates large
pleomorphic anaplastic cells with prominent horseshoe-shaped nuclei, and nuclear
folding and strong diffuse CD30 reactivity by immunohistochemistry (CD30
immunohistochemistry with hematoxylin counterstain, 1000X magnification). Inset
demonstrates a single T cell clone on flow cytometry. Positive cytology, CD30
expression, and clonality demonstrated here are required for diagnosis. (Reprinted
with permission from Clemens MW, Brody GS, Mahabir RC, et al. How to diagnose and
treat breast implant associated anaplastic large cell lymphoma. Plast Reconstr Surg
2018;141[4]:586e–599e.)
PREOPERATIVE ONCOLOGIC WORKUP
Following confirmation of BIA-ALCL diagnosis, preoperative consultation
with a lymphoma oncologist and consideration of a surgical oncologist are
recommended. Oncologic workup should proceed prior to any operative
intervention. A bone marrow biopsy may be indicated, but is only performed
in rare select cases at the oncologist’s discretion to differentiate from other
peripheral T cell lymphomas. Testing for anaplastic lymphoma kinase (ALK)
translocation status also differentiates from ALK+ systemic ALCL, a much
more aggressive disease with poor prognosis. Note that BIA-ALCL is always
ALK negative, and therefore ALK is not a screening tool, but a descriptive
tool for established disease. For confirmed cases, a PET/CT scan is beneficial
for demonstrating associated capsular masses, chest wall involvement,
regional lymphadenopathy, and/or distant organ metastasis (9). A PET scan
can act as a roadmap for surgical planning, resection strategy, and timing of
surgery. For instance, unresectable chest wall invasion may become
resectable following neoadjuvant chemotherapy.
SOLID TUMOR STAGING
BIA-ALCL was formally staged as a liquid tumor, however tumor biology
has preferentially supported staging as a solid tumor. The Lugano revision to
the Ann Arbor Staging System is a liquid tumor staging with stage IE disease
limited to breast involvement only, and stage IIE disease limited to the breast
and ipsilateral axillary lymph nodes (75). Using this system, nearly all BIA-
ALCL patients have low-stage disease, either stage 1E (83% to 96%) or stage
IIE (3.6% to 18.8%) (Table 122-2) (38). An MD Anderson solid tumor TNM
staging system is modeled after the American Joint Committee on Cancer
(AJCC) TNM (Tumor, lymph Node, Metastasis) (Figs. 122-4 and 122-5).
Using this system, BIA-ALCL is a spectrum of disease from IA (35.6%), IB
(11.5%), IC (13.8%), IIA (25.3%), IIB (4.6%), III (9.2%), to stage IV (0% to
9%) (Table 122-2) (5). The World Health Organization currently classifies
BIA-ALCL as a lymphoma at all stages (7). Clinical observation of effusion-
limited (IA) disease demonstrates a typically indolent course, and therefore
this stage may be more akin to a lymphoproliferative disorder. However,
BIA-ALCL can become an invasive lymphoma and metastasize at more
advanced stages. Other malignant lymphoproliferative disorders include
lymphomatoid papulosis and primary cutaneous ALCL. Both can
spontaneously regress, and have an observed progression rate to invasive
lymphoma of 5.6% to 9% and 10% to 27%, respectively (76,77). It is not yet
possible to determine the progression rate of effusion-only (IA) BIA-ALCL
to invasive lymphoma as the staging requires pathologic examination of the
resected capsule, in essence treating the disease. Therefore, how indolent the
disease is or quantifying what amount of delay in treatment will lead to
progression of disease is not yet possible. It is important to note that all of
these designations and nomenclatures are still referring to a cancer. To date,
spontaneous resolution of disease without any treatment intervention has not
been reported. Patients with BIA-ALCL can have progression of their
disease, lymph node involvement, and death of disease, particularly with
significant delay in diagnosis or suboptimal treatment (78). These patients are
described as having local or regional extension of their disease or very rare
distant organ metastasis, which is more similar to solid tumors. This
emphasizes the solid tumor classification and that this is a distinct entity that
progresses locally.
TABLE 122-2 MD Anderson Solid Tumor TNM Staging for Breast Implant
Associated With ALCL
MD Anderson Solid Tumor TNM Staging for Breast Implant–Associated
ALCL
TNM or Stage Description
Designation
T: Tumor Extent
T1 Confined to effusion or a layer on luminal side of
capsule
T2 Early capsule infiltration
T3 Cell aggregates or sheets infiltrating the capsule
T4 Lymphoma infiltrates beyond the capsule
N: Lymph Node
N0 No lymph node involvement
N1 One regional lymph node (+)
N2 Multiple regional lymph nodes (+)
M: Metastasis
M0 No distant spread
M1 Spread to other organs/distant sites
Stage
IA T1N0M0
IB T2N0M0
IC T3N0M0
IIA T4N0M0
IIB T1-3N1M0
III T4N1-2M0
IV TanyNanyM1
Reprinted with permission from Clemens MW, Medeiros LJ, Butler CE, et al. Complete surgical
excision is essential for patients with breast implant-associated anaplastic large cell lymphoma. J Clin
Oncology 2016;34(2):160–168.
SURGICAL TREATMENT
Timely diagnosis and complete surgical excision of disease, implants, and the
surrounding fibrous capsule is the optimal approach for the management
breast implant ALCL in the majority of patients. Disease localized to the
capsule (Lugano IE, MDA IA-IIA) may be treated with surgery alone in the
majority of cases (Fig. 122-6). Surgical goals are a total capsulectomy with
removal of the breast implant, excision of any associated capsular mass, and
excisional biopsy of suspicious lymph node(s). In retropectoral or dual plane
implants, adherence to the ribcage may make resection difficult and
tumescence of the anatomical plane can facilitate capsulectomy (79). Care
should be taken when dissecting capsule off of intercostal muscles to avoid a
pneumothorax. It remains unclear what effect inadvertent spillage of the
seroma during capsulectomy has on local seeding of disease, however
clinically, this has not been observed to influence recurrence rates. Complete
mass excision with negative margins is essential as retained disease likely
will subject the patient to otherwise unnecessary adjuvant chemotherapy. At
present, there is no role for radical mastectomy, sentinel lymph node biopsy,
or full axillary dissection. Per NCCN guidelines, surgeons may consider
removal of the contralateral implant as approximately 4.6% of cases to date
have demonstrated incidental ALCL in the contralateral breast implant (5).
Consultation with a surgical oncologist may be beneficial for plastic surgeons
unaccustomed to oncologic ablation and lymph node excisional biopsies.
FIGURE 122-4 Clinical and pathologic staging of BIA-ALCL follows the MD
Anderson Solid Tumor Staging System modeled after the American Joint Committee
on Cancer (AJCC) TNM (Tumor, lymph Node, Metastasis) stages. (Reprinted with
permission from Clemens MW, Medeiros LJ, Butler CE, et al. Complete surgical excision
is essential for patients with breast implant-associated anaplastic large cell lymphoma. J
Clin Oncology 2016;34[2]:160–168.)

Pathologic evaluation of both the periprosthetic fluid and the capsule are
important for staging of the disease. Evaluation of the capsule may be
performed by either widely sampling the internal lining with multiple punch
biopsies, or alternatively, the capsule may be opened and set out flat, and the
sphere-shaped capsule can be thought of as a cube with each of the six faces
of the cube requiring two biopsies, for a total of 12 biopsy specimens per
capsule to reliably detect tumor in a specimen.

FIGURE 122-5 Pathologic T staging. (A and B) T1: lymphoma cells confined to the
effusion or a layer on the luminal side of the capsule; (C and D) T2: lymphoma cells
superficially infiltrate the luminal side of the capsule. Arrows indicate the areas of
invasion; (E and F) T3: clusters or sheets of lymphoma cells infiltrate into the
thickness of the capsule; and (G and H) T4: lymphoma cells infiltrating beyond the
capsule, into the adjacent soft tissue or breast parenchyma. Left column,
hematoxylin and eosin stain; right column, CD30 immunohistochemistry;
magnification, 3100. (Reprinted with permission from Clemens MW, Medeiros LJ,
Butler CE, et al. Complete Surgical Excision is Essential for Patients with Breast Implant-
associated Anaplastic Large Cell Lymphoma. J Clin Oncology 2016;34(2):160–168.)
FIGURE 122-6 A 77-year-old woman underwent postmastectomy prosthetic
reconstruction for breast cancer in 2003. Eleven years after implantation, she
developed rapid swelling of the right breast manifested as marked breast asymmetry (A).
BIA-ALCL was diagnosed on fine-needle aspiration. Patient then received a total
capsulectomy and implant removal (B). (Reprinted with permission from Clemens MW,
Brody GS, Mahabir RC, et al. How to diagnose and treat breast implant associated
anaplastic large cell lymphoma. Plast Reconstr Surg 2018;141(4):586e–599e.)

Lamaris et al. recently described a novel, algorithmic approach to


reconstructing the breast following BIA-ALCL based on their own
experience with 18 consecutive reconstructions (43). In their case series,
immediate reconstruction (smooth implant or autologous tissue) was reserved
for patients with surgically resectable disease (Stage IA–IC). Alternatively,
stage IA–IC patients also had the option of delaying reconstruction (smooth
implant or autologous tissue or autologous fat grafting) until repeat PET
imaging had been completed 3 to 6 months following oncologic resection.
Advanced disease (Stage IIA–IV) was considered as a relative
contraindication to immediate reconstruction. Patients with advanced disease
typically undergo repeat imaging at 6 to 12 months following oncologic
resection. If no evidence of residual or recurrent disease is found, delayed
reconstruction using the same reconstructive adjuncts for immediate
reconstruction may be undertaken. Overall, 96% of patients were either
satisfied or highly satisfied with their reconstruction and no surgical
complications were observed at long-term follow-up (42 months). As such,
breast reconstruction remains a viable option in select cases following
definitive treatment (61).
INDICATIONS FOR ADJUVANT TREATMENTS
Patients with advanced disease (2% to 8%) such as lymph node metastasis
will frequently warrant adjuvant chemotherapy (Lugano II–IV, MDA IIB–
IV) (Table 122-1). Systemic ALCL is treated with an anthracycline-based
regimen (cyclophosphamide, vincristine, doxorubicin, and prednisone:
CHOP) for first-line therapy. Anthracycline-based multiagent chemotherapy
with or without radiation therapy followed by autologous stem cell rescue is
the standard approach for most patients with newly diagnosed peripheral T
cell lymphomas (80). However, NCCN guidelines allow physicians to
consider following either systemic ALCL chemotherapy regimens with
CHOP or preferably brentuximab vedotin as a first-line agent. Brentuximab
vedotin is a toxin–antibody conjugate to CD30. Pro et al. reported 4-year
survival data from an ongoing Phase 2 study of brentuximab vedotin in
patients with refractory systemic ALCL which demonstrated an objective
response rate (ORR) of 83% and complete remission rate of 62% (81,82). A
randomized phase 3 study is evaluating brentuximab vedotin in combination
with cyclophosphamide, doxorubicin, and prednisone for front-line treatment
of CD30+ mature T cell lymphomas, including systemic ALCL. Outcomes of
chemotherapeutic regimens in BIA-ALCL are from case reports, however
complete remissions have been achieved in patients with organ metastasis
when treated with brentuximab vedotin (83). The drug may also have a role
as a neoadjuvant targeted agent for downgrading chest wall invasion (84).
Stem cell transplant and external beam radiation therapy are only reserved for
unresectable disease in a salvage setting.
FIGURE 122-7 Treatment of BIA-ALCL includes total capsulectomy with excision
of any associated masses as residual disease left on the chest wall may continue to
progress and require further treatment such as chemotherapy. With subpectoral
implants, elevation of the posterior capsular wall off of the rib cage may be difficult,
but is still essential. Pictured is standard tumescence being infiltrated by angiocath
into the posterior capsule of a BIA-ALCL patient to facilitate complete removal of
the capsule. Inframammary approach was utilized to allow for immediate
reconstruction. (Reprinted with permission from Clemens MW, Brody GS, Mahabir RC,
et al. How to diagnose and treat breast implant associated anaplastic large cell lymphoma.
Plast Reconstr Surg 2018;141[4]:586e–599e.)
FOLLOW-UP AND DISEASE SURVEILLANCE
Patients are best followed by an oncologist that may monitor for disease
recurrence and evaluate for adjunctive therapy (Fig. 122-7). Treated patients
with no evidence of disease are evaluated every 3 to 6 months for 2 years,
and then as clinically indicated. Physicians may include CT or PET/CT scans
every 6 months for 2 years then only as clinically indicated.
TREATMENT OUTCOMES
BIA-ALCL generally appears to be a biologically indolent disease with an
excellent prognosis when confined to the capsule and treated with complete
surgical resection. No known cases of confirmed disease regression or
complete spontaneous resolution without treatment have been reported to
date. Statistically worse prognosis has been identified in patients with mass
formation and extracapsular extension (23). Miranda et al. reported on the
long-term outcomes of 60 patients and found more patients without a mass
achieved complete remission compared with those with a mass (93% of 42
patients compared with 72% of 18 patients) (18). The median overall survival
for patients with a discrete breast mass was 12 years, whereas the median
overall survival had not been reached for patients who did not have a discrete
breast mass. It remains unclear whether the worse prognosis associated with a
mass is due to a more aggressive variant, more progressed disease, or perhaps
a consequence of inadequate surgical ablation of tumor infiltration.
Clemens et al. reported on the outcomes of 87 patients treated with surgery
alone (40%); surgery and radiation (9%); surgery and chemotherapy (19%);
surgery, chemotherapy, and radiation (30%); or with chemotherapy alone
(2%) (34). Both the presence of a mass at the time of diagnosis and
extracapsular disease extension were associated with an increased risk for
recurrence and patient death. At a median follow-up of 45 months, 28% had
recurrent disease, of whom 73% were treated with salvage chemotherapy.
Complete surgical excision of the disease had the lowest recurrence rate of
4% at 1, 3, and 5 years. Kaplan Meier survival curves by treatment modality
are displayed in Figure 122-8. At present, a total of 34 patients have been
reported dead from BIA-ALCL disease in Australia, Brazil, France, Italy, the
Netherlands, New Zealand, Sweden, Argentina, and the United States
(11–13,35,53,85,86). A recurring theme in these tragic outcomes is
significant delay in diagnosis, and/or chemotherapeutic treatment of the
disease with limited or no surgical resection.
FIGURE 122-8 Survival curves according to treatment approaches (A) and TNM
solid tumor staging (B). Event-free survival (left), overall survival (right). (Reprinted
with permission from Clemens MW, Medeiros LJ, Butler CE, et al. Complete surgical
excision is essential for patients with breast implant-associated anaplastic large cell
lymphoma. J Clin Oncology 2015.)
CONCLUSION
BIA-ALCL appears to begin as an indolent effusion-limited disease with
excellent prognosis in the majority of patients. NCCN consensus guidelines
have been established and widely adopted for the diagnosis and management
of breast implant ALCL. Surgical ablation with explantation and
capsulectomy is frequently curative with disease confined to the capsule.
Understanding and implementation of a standardized approach is critical to
prevent delays in diagnosis, disease progression, and avoidable adverse
sequelae.

REFERENCES

1. Food and Drug Administration website on breast implant associated


ALCL.
www.fda.gov/MedicalDevices/ProductsandMedicalProcedures/ImplantsandProsthetic
Accessed March 2017.
2. Clemens MW, Miranda RN. Coming of age: breast implant-associated
anaplastic large cell lymphoma after 18 years of investigation. Clin Plast
Surg 2015;42(4):605–613.
3. Ramos-Gallardo G, Cuenca-Pardo J, Rodríguez-Olivares E, et al. Breast
implant and anaplastic large cell lymphoma meta-analysis. J Invest Surg
2017;30:56–65.
4. Gidengil CA, Predmore Z, Mattke S, et al. Breast implant associated
anaplastic large cell lymphoma: a systematic review. Plast Reconstr
Surg 2015;135(3):713–720.
5. Clemens MW, Nava MB, Rocco N, et al. Understanding rare adverse
sequelae of breast implants: anaplastic large-cell lymphoma, late
seromas, and double capsules. Gland Surg 2017;6(2):169–184.
6. Keech JA Jr, Creech BJ. Anaplastic T-cell lymphoma in proximity to a
saline-filled breast implant. Plast Reconstr Surg 1997;100:554–555.
7. Lyapichev K, Medeiros LJ, Clemens MW, et al. Reconsideration of the
first recognition of breast implant-associated anaplastic large cell
lymphoma: a critical review of the literature. Ann Diagn Pathol
2020;45:151474.
8. U.S. Food and Drug Administration. Anaplastic large cell lymphoma
(ALCL) in women with breast implants: Preliminary FDA findings and
analyses. Available at:
http://www.fda.gov/MedicalDevices/ProductsandMedicalProcedures/ImplantsandPro
Accessed November 20, 2014.
9. Miranda RN, Medeiros LJ, Ferrufino-Schmidt MC, et al. Pioneers of
breast implant–associated anaplastic large cell lymphoma: history from
case report to global recognition. Plast Reconstr Surg 2019;143(3S):1S–
7S.
10. Swerdlow SH, Campo E, Pileri SA, et al. The 2016 revision of the
World Health Organization (WHO) classification of lymphoid
neoplasms. Blood 2016;127(20):2375–2390.
11. World Health Organization International Agency for Research on
Cancer. IARC monographs on the evaluation of carcinogenic risks to
humans: Report of the advisory group to recommend priorities for IARC
monographs during 2015–2019. Available at:
http://monographs.iarc.fr/ENG/Publications/internrep/14-002.pdf.
Accessed August 1, 2017.
12. U.S. National Cancer Institute. Treatment for health professionals.
Available at: http://www.cancer.gov/types/lymphoma/hp/adult-nhl-
treatment-pdq#link/_100_toc. Accessed August 1, 2017.
13. U.S. Food and Drug Administration. Anaplastic Large cell Lymphoma
(ALCL) In Women with Breast Implants: Medical Device Reports of
Breast Implants in Women with ALCL. 2017. www.fda.gov. March
2017.
14. Institut National du Cancer. Agence Nationale de Sécurité du
Médicament. Breast implant associated anaplastic large cell lymphoma:
Expert opinion. Available at: http://www.e-
cancer.fr/content/download/119635/1429833/file/Breast%20implant-
associated%20anaplastic%20large%20cell%20lymphomas.pdf.
Accessed February 1, 2017.
15. Australian Therapeutic Goods Administration. Breast implants: Update
on TGA monitoring of anaplastic large cell lymphoma. Available at:
https://www.tga.gov.au/alert/ breast-implants. Accessed December 20,
2016.
16. Medicines and Healthcare products Regulatory Agency. Breast implants
and Anaplastic Large Cell Lymphoma (ALCL). Available at:
https://www.gov.uk/guidance/breast-implants-and-anaplastic-large-cell-
lymphoma-alcl. Accessed July 26, 2017.
17. Grady D. A Shocking Diagnosis: Breast Implants ‘Gave Me Cancer’.
New York: The New York Times; 2017:1–2.
18. Miranda RN, Aladily TN, Prince HM, et al. Breast implant-associated
anaplastic large-cell lymphoma: long-term follow-up of 60 patients. J
Clin Oncol 2014;32(2):114–120.
19. Lechner MG, Megiel C, Church CH, et al. Survival signals and targets
for therapy in breast implant associated ALK–anaplastic large cell
lymphoma. Clin Cancer Res 2012;18(17):4549–4559.
20. Montgomery-Goecker C, Fuda F, Krueger JE, et al. Immunophenotypic
characteristics of breast implant-associated anaplastic large-cell
lymphoma by flow cytometry. Cytometry B Clin Cytom
2015;88(5):291–293.
21. Kuehlmann B, Prantl L. Breast implants and possible association with
ALCL: a retrospective study including a histological analysis of 296
explanted breast tissues and current literature. Clin Hemorheol
Microcirc 2016;63(4):439–449.
22. Taylor CR, Siddiqi IN, Brody GS. Anaplastic large cell lymphoma
occurring in association with breast implants: review of pathologic and
immunohistochemical features in 103 cases. Appl Immunohistochem
Mol Morphol 2013;21(1):13–20.
23. Xu J, Wei S. Breast implant-associated anaplastic large cell lymphoma:
review of a distinct clinicopathologic entity. Arch Pathol Lab Med
2014;138(6):842–846.
24. Miranda RN, Lin L, Talwalkar SS, et al. Anaplastic large cell lymphoma
involving the breast: a clinicopathologic study of 6 cases and review of
the literature. Arch Pathol Lab Med 2009;133(9):1383–1390.
25. Aladily TN, Medeiros LJ, Alayed K, et al. Breast implant-associated
anaplastic large cell lymphoma: a newly recognized entity that needs
further refinement of its definition. Leuk Lymphoma 2012;53(4):749–
750.
26. Aladily TN, Medeiros LJ, Amin MB, et al. Anaplastic large cell
lymphoma associated with breast implants: a report of 13 cases. Am J
Surg Pathol 2012;36(7):1000–1008.
27. de Jong D, Vasmel WL, de Boer JP, et al. Anaplastic large-cell
lymphoma in women with breast implants. JAMA 2008;300(17):2030–
2035.
28. Doren EL, Miranda RN, Selber JC, et al. U.S. epidemiology of breast
implant-associated anaplastic large cell lymphoma. Plast Reconstr Surg
2017;139(5):1042–1050.
29. Srinivasa DR, Miranda RN, Kaura A, et al. Global adverse event reports
of breast implant-associated ALCL: an international review of 40
government authority databases. Plast Reconstr Surg 2017;139(5):1029–
1039.
30. Loch-Wilkinson A, Beath K, Knight RJW, et al. Breast implant
associated Anaplastic Large Cell Lymphoma in Australia and New
Zealand—high surface area textured implants are associated with
increased risk. Plast Reconstr Surg 2017;140(4):645–654.
31. Campanale A, Boldrini R, Marletta M. BIA-ALCL vigilance and
surveillance by the Italian Ministry of Health. Plast Reconstr Surg
2017;141(1):11e–19e.
32. Adrada BE, Miranda RN, Rauch GM, et al. Breast implant-associated
anaplastic large cell lymphoma: sensitivity, specificity, and findings of
imaging studies in 44 patients. Breast Cancer Res Treat 2014;147:1–14.
33. Acevedo-Báñez I, García-Gomez FJ, Jiménez-Granero P, et al. 18F-
FDG-PET/CT in implant-associated anaplastic large cell lymphoma of
the breast. Br J Haematol 2015;169(1):1.
34. Clemens MW, Medeiros LJ, Butler CE, et al. Complete surgical
excision is essential for the management of patients with breast implant-
associated anaplastic large-cell lymphoma. J Clin Oncol
2016;34(2):160–168.
35. Brody GS, Deapen D, Taylor CR, et al. Anaplastic large cell lymphoma
occurring in women with breast implants: analysis of 173 cases. Plast
Reconstr Surg 2015;135(3):695–705.
36. Clemens MW, Miranda RN, Butler CE. Breast implant informed
consent should include the risk of anaplastic large cell lymphoma. Plast
Reconstr Surg 2016;137(4):1117–1122.
37. Talwalkar SS, Miranda RN, Valbuena JR, et al. Lymphomas involving
the breast: a study of 106 cases comparing localized and disseminated
neoplasms. Am J Surg Pathol 2008;32:1299–1309.
38. Lipworth L, Tarone RE, McLaughlin JK. Breast implants and
lymphoma risk: a review of the epidemiologic evidence through 2008.
Plast Reconstr Surg 2009;123:790–793.
39. Largent J, Oefelein M, Kaplan HM, et al. Risk of lymphoma in women
with breast implants: analysis of clinical studies. Eur J Cancer Prev
2012;21:274–280.
40. Wang SS, Deapen D, Voutsinas J, et al. Breast implants and anaplastic
large cell lymphomas among females in the California Teachers Study
cohort. Br J Haematol 2016;174:480–483.
41. Thompson PA, Lade S, Webster H, et al. Effusion-associated anaplastic
large cell lymphoma of the breast: time for it to be defined as a distinct
clinico-pathological entity. Haematologica 2010;95:1977–1979.
42. de Boer M, van Leeuwen FE, Hauptmann M, et al. Breast implants and
the risk of anaplastic large-cell lymphoma in the breast. JAMA Oncol
2018;4(3):335–341.
43. Lamaris GA, Butler CE, Deva AK, et al. Reconstruction following
breast implant associated anaplastic large cell lymphoma. Plast Reconstr
Surg 2019;143(3S):51S–58S.
44. Magnusson M, Beath K, Cooter R, et al. The epidemiology of breast
implant–associated anaplastic large cell lymphoma in Australia and New
Zealand confirms the highest risk for grade 4 surface breast implants.
Plast Reconstr Surg 2019;143(5):1285–1292.
45. Barr S, Hill EW, Bayat A. Functional biocompatibility testing of
silicone breast implants and a novel classification system based on
surface roughness. J Mech Behav Biomed Mater 2017;75:75–81.
46. Valencia-Lazcano AA, Alonso-Rasgado T, Bayat A. Characterisation of
breast implant surfaces and correlation with fibroblast adhesion. J Mech
Behav Biomed Mater 2013;21:133–148.
47. Non-Active Surgical Implants, Mammary implants, Particular
requirements. The International Organization for Standardization (ISO)
14607. 3rd ed. Vernier, Geneva: 2018.
48. Rebiere B, Petit E, Cot D. Definition D’Une Gamme De Texturation
Pour Les Implants Mammaires. Instiut Europeen des Membranes.
Published online at www.iemm.univ-montp2.fr. July 2, 2018.
49. Jones P, Mempin M, Hu H, et al. The functional influence of breast
implant outer shell morphology on bacterial attachment and growth.
Plast Reconstr Surg 2018;142(4):837–849.
50. Atlan M, Nutib G, Wangb H, et al. Breast implant surface texture
impacts host tissue response. J Mech Behav Biomed Mater
2018;88:377–385.
51. James GA, Boegli L, Hancock J, et al. Bacterial adhesion and biofilm
formation on textured breast implant shell materials. Aesth Plast Surg
2019;43(2):490–497.
52. McGuire P, Reisman NR, Murphy DK. Risk factor analysis for capsular
contracture, malposition, and late seroma in subjects receiving Natrelle
410 form-stable silicone breast implant. Plast Reconstr Surg
2017;139(1):1–9.
53. Clemens MW, McGuire P. Discussion: a prospective approach to inform
and treat 1340 patients at risk for BIA-ALCL. Plast Reconstr Surg
2019;144(1):57–59.
54. Cordeiro PG, Ghione P, Ni A, et al. Risk of breast implant associated
anaplastic large cell lymphoma (BIA-ALCL) in a cohort of 3546 women
prospectively followed long term after reconstruction with textured
breast implants. J Plast Reconstr Aesthet Surg 2020;73(5):841–846.
55. U.S. Food and Drug Administration. The FDA requests Allergan
voluntarily recall Natrelle Biocell textured breast implants and tissue
expanders from the market to protect patients: FDA safety
communication. Available at: https://www.fda.gov/medical-
devices/safety-communications/fda-requests-allergan-voluntarily-recall-
natrelle-biocell-textured-breast-implants-and-tissue. Accessed
November 10, 2019.
56. PSF PROFILE Registry Statistics. Available at:
http://www.thepsf.org/PROFILE. Accessed August November 11, 2019.
57. Jacombs A, Tahir S, Hu H, et al. In vitro and in vivo investigation of the
influence of implant surface on the formation of bacterial biofilm in
mammary implants. Plast Reconstr Surg 2014;133(4):471e–480e.
58. Hammond DC. Reply: Chronic Biofilm Infection in Breast Implants Is
Associated with an Increased T-Cell Lymphocytic Infiltrate:
Implications for Breast Implant–Associated Lymphoma. Plast Reconstr
Surg 2015;135(6):1057e–1059e.
59. Prince HM, Johnstone R. Commentary on: biomarkers provide clues to
early events in the pathogenesis of breast implant-associated anaplastic
large cell lymphoma. Aesthet Surg J 2016;36(7):782–783.
60. Kadin ME, Deva A, Xu H, et al. Biomarkers provide clues to early
events in the pathogenesis of breast implant-associated anaplastic large
cell lymphoma. Aesthet Surg J 2016;36(7):773–781.
61. Brody GS. The case against biofilm as the primary initiator of
breastimplant-associated anaplastic large cell lymphoma. Plast Reconstr
Surg 2016;137(4):766e–767e.
62. Bizjak M, Selmi C, Praprotnik S, et al. Silicone implants and lymphoma:
the role of inflammation. J Autoimmun 2015;65:64–73.
63. Orciani M, Sorgentoni G, Torresetti M, et al. MSCs and inflammation:
new insights into the potential association between ALCL and breast
implants. Breast Cancer Res Treat 2016;156(1):65–72.
64. Meza Britez ME, Caballero Llano C, Chaux A. Periprosthetic breast
capsules and immunophenotypes of inflammatory cells. Eur J Plast
Surg 2012;35:647–651.
65. Hu H, Jacombs A, Vickery K, et al. Chronic biofilm infection in breast
implants is associated with an increased T-cell lymphocytic infiltrate:
implications for breast implant-associated lymphoma. Plast Reconstr
Surg 2015;135(2):319–329.
66. Clemens MW, Horwitz SM. NCCN consensus guidelines for the
diagnosis and management of breast implant-associated anaplastic large
cell lymphoma. Aesthet Surg J 2017;37(3):285–289.
67. National Comprehensive Cancer Network. www.nccn.org/about.
Accessed November 2016.
68. Di Napoli A, Pepe G, Giarnieri E, et al. Cytological diagnostic features
of late breast implant seromas: from reactive to anaplastic large cell
lymphoma. PLoS ONE 2017;12(7):e0181097.
69. Alcalá R, Llombart B, Lavernia J, et al. Skin involvement as the first
manifestation of breast implant-associated anaplastic large cell
lymphoma. J Cutan Pathol 2016;43(7):602–608.
70. Lazzeri D, Zhang YX, Huemer GM, et al. Capsular contracture as a
further presenting symptom of implant-related anaplastic large cell
lymphoma. Am J Surg Pathol 2012;36(11):1735–1736; author reply
1736–1738.
71. de Boer M, van der Sluis WB, de Boer JP, et al. Breast implant-
associated anaplastic large-cell lymphoma in a transgender woman.
Aesthet Surg J 2017;37(8):NP83–NP87.
72. Jaffe ES, Ashar BS, Clemens MW, et al. Best practices guideline for the
pathologic diagnosis of breast implant-associated anaplastic large-cell
lymphoma. J Clin Oncol 2020;38(10):1102–1111.
73. Clemens MW, Miranda RN. Commentary: lymphomas associated with
breast implants: a review of the literature. Aesthet Surg J
2015;35(5):545–547.
74. Falini B, Pileri S, Pizzolo G, et al. CD30 (Ki-1) molecule: a new
cytokine receptor of the tumor necrosis factor receptor superfamily as a
tool for diagnosis and immunotherapy. Blood 1995;85(1):1–14.
75. Cheson BD, Fisher RI, Barrington SF, et al. Recommendations for
initial evaluation, staging, and response assessment of Hodgkin and non-
Hodgkin lymphoma: the Lugano classification. J Clin Oncol
2014;32:3059–3068.
76. Paulli M, Berti E, Rosso R, et al. CD30/Ki-1-positive
lymphoproliferative disorders of the skin—clinicopathologic correlation
and statistical analysis of 86 cases: a multicentric study from the
European Organization for Research and Treatment of Cancer
Cutaneous Lymphoma Project Group. J Clin Oncol 1995;13(6):1343–
1354.
77. Wieser I, Wohlmuth C, Nunez CA, et al. Lymphomatoid papulosis in
children and adolescents: a systematic review. Am J Clin Dermatol
2016;17:319–327.
78. Clemens MW, Collins MS, Butler CE, et al. Characteristics and
treatment of patients with breast implant-associated anaplastic large cell
lymphoma presenting with aggressive features. Plast Reconstr Surg
2015;136(4 Suppl):119–120.
79. Brody GS. Brief recommendations for dealing with a new case of
anaplastic large T-cell lymphoma. Plast Reconstr Surg
2012;129(5):871e–872e.
80. Horwitz SM, Zelenetz AD, Gordon LI, et al. NCCN guidelines insights:
non-Hodgkin’s Lymphomas, Version 3.2016. J Natl Compr Canc Netw
2016;14(9):1067–1079.
81. Pro B, Advani R, Brice P, et al. Four-year survival data from an ongoing
pivotal phase 2 study of brentuximab vedotin in patients with relapsed or
refractory systemic anaplastic large cell lymphoma [abstract]. Blood
2014;124: Abstract 3095.
82. Pro B, Advani R, Brice P, et al. Brentuximab vedotin (SGN-35) in
patients with relapsed or refractory systemic anaplastic large-cell
lymphoma: results of a phase II study. J Clin Oncol 2012;30:2190–
2196.
83. Zimmerman A, Locke FL, Emole J, et al. Recurrent systemic anaplastic
lymphoma kinase–negative anaplastic large cell lymphoma presenting as
a breast implant–associated lesion. Cancer Control 2015;22(3):369–373.
84. Johnson L, O’Donoghue J, Stark H, et al. Abstract P5-03-02: breast
implant associated anaplastic large cell lymphoma (BIA-ALCL)— The
UK experience and first reported case of neoadjuvant brentuximab.
Cancer Res 2017;77(4 Supplement):P5-03-02.
85. Carty MJ, Pribaz JJ, Antin JH, et al. A patient death attributable to
implant-related primary anaplastic large cell lymphoma of the breast.
Plast Reconstr Surg 2011;128(3):112e–118e.
86. Ivaldi C, Perchenet AS, Jallut Y, et al. Two cases of lymphoma in an
implant capsule: a difficult diagnosis, an unknown pathology [in
French]. Ann Chir Plast Esthet 2013;58:688–693.
CHAPTER 123

Proactive Approach to Capsular


Contracture Prevention
MICHAEL DELONG | JASON ROOSTAEIAN | WILLIAM P. ADAMS JR
HISTORY
Implant-based breast augmentation is consistently the most common
operative cosmetic procedure in the United States with roughly 300,000 cases
every year; however, like all medical devices, breast implants are prone to
device failures or associated complications. The human body naturally
responds to the presence of a breast implant by developing a surrounding
vascularized scar tissue capsule. This complication, referred to as capsular
contracture, is considered the most common long-term complication of
implant augmentation, and can result in significant hardening, visible
distortion, and physical pain. Once symptoms occur, surgical capsulectomy
and implant removal or replacement is the “gold standard” of treatment, and
capsular contracture is cited as the most common reason for reoperation in
patients with breast implants. Unfortunately, surgical intervention may only
provide temporary relief, with up to 40% of patients experiencing recurrent
capsular contracture, especially with specific corrective procedures. Given
the patient expense and morbidity of reoperation, and the significant
recurrence risk, ideal management is prevention.
BACKGROUND/ETIOLOGY
Twenty-five years ago, the etiology of capsular contracture remained
incompletely understood; significant progress in reducing the incidence rate
has been achieved over the past several decades by identifying and
addressing contributing factors. Generally, subclinical infection theory of
capsular contracture is now widely accepted as the causative and preventable
contributor to the development of contracture. Other etiologies that are
speculated to be involved in disease pathogenesis include hypertrophic scar
hypothesis, idiopathic myofibroblast activation, silicone gel bleed,
hematoma, or infection-related inflammation. The issue with the other
theories is they don’t have supportive clinical data, and stack up weakly to
the subclinical infection theory.
The connection between capsular contracture and bacterial contamination
of the implant was first postulated in the early 1980s. Shah et al. (1) reported
significant capsular contracture development in rabbit implant pockets
prospectively inoculated with the Staphylococcus epidermidis bacteria
compared to sterile controls. Similarly, Burkhardt helped define the bacterial
role in capsular contracture by demonstrating an association between
subacute periprosthetic infection and capsular contracture by culturing
pockets of open capsulotomy patients, and also showed a benefit in a level 1
study (2–5). These cultures revealed that a high proportion of contracted
patient capsules were contaminated with S. epidermidis despite no signs or
symptoms of clinical infection. Although S. epidermidis was specifically
implicated in these initial studies, further research has suggested that other
bacterial species may also be involved, including Propionibacterium acnes,
Escherichia coli, and others (6,7).
Theorizing that microbial contamination was causing capsular contracture,
these investigators then studied the effects of antimicrobial treatment of
implant pockets on contracture rates. They achieved significant mitigation of
capsular contracture development using antimicrobial pocket irrigation or
intraluminal antibiotic solution in the implants in a prospective, randomized,
and double-blind study (4). These high-level data provided initial evidence
that capsular contracture could be effectively prevented by advancements in
surgical technique. Adams reported and reviewed 30 studies, all of which
support the use of antimicrobial breast pocket irrigation (8,9).
However, not all studies have reproducibly demonstrated an association
between bacterial contamination and contracture formation, which may
partially be the result of differing methodologies. In 1983 Gayou et al.
reported visible bacterial contamination in only 4% of pathologic capsules
using electron microscopy (10). While interesting, these results have been
questioned due to the predilection for bacteria to form fastidious biofilms that
may limit detection without appropriate methodology. Similarly, with both
supporting and more perplexing findings, Netscher et al. reference the
relative difficulty of obtaining a “standard culture” of breast implant pockets
due to biofilm formation. They used standard cell culture to retrospectively
evaluate 389 implants without clinical signs of infection. In regression
analysis they demonstrated the only finding that correlated with grade III/IV
contracture was a positive culture. While they demonstrated a significant
correlation between contamination with various organisms and grade III/IV
capsular contractures, they only detected bacteria in 24% of all capsules, and
more contaminated capsules were Baker grade I than IV (7). The likely
explanation is that culturing bacteria require specialized techniques (Table
123-1) (11).
Subsequent study and evolving techniques for bacterial detection have
further advanced the understanding of capsular contracture and generally
supported the subclinical infection hypothesis. Pajkos et al. examined 48
implant/capsule samples during explantation in 27 breasts with capsular
contracture by routine culture methods as well as by maceration with
sonication. Routine culture was negative for all samples, yet 17 of 19 samples
taken from patients with significant contracture were positive for bacteria
using maceration and sonication (11). These same general results have been
reproducibly demonstrated by other investigators using sonication methods
(12,13).
Further prospective preclinical in vivo experiments have corroborated the
subclinical infection hypothesis. The best cause–effect proof of bacteria as
the etiology of capsular contracture was reported by Tamboto et al. who
performed submammary breast augmentations in a porcine model and
inoculated some of these pockets with S. epidermidis (14). Inoculated pockets
were strongly associated with biofilm formation on the implant, which was
significantly associated with the development of capsular contracture.
Interestingly, the uninoculated pockets that ultimately developed biofilm and
capsular contracture were found to be “self-inoculated” by native porcine S.
epidermidis. These investigators further demonstrated that antibiotic-eluting
films and mesh inserted into inoculated pockets around breast implants could
effectively eliminate capsular contracture (0%) in their porcine model
compared to 100% rate in inoculated pockets without antibacterial device
(15). Again, these data demonstrate that capsular contracture rates can be
affected by modifications to surgical technique.

TABLE 123-1 Baker Grading System for Capsular Contracture


Baker Grade Clinical Evaluation
I Soft capsule, no visible distortion
II Hardened capsule on palpation, no visible distortion
III Hardened capsule on palpation with visible distortion
IV Hardened capsule on palpation with visible distortion and
patient discomfort

The subclinical infection hypothesis has gained further support by


observed associations between surgical factors and the development of
capsular contracture. For primary augmentation patients, investigators have
reproducibly reported a higher rate of capsular contracture for implants
placed in the subglandular plane compared to the submuscular pocket. While
there may be multiple reasons for this association, it is theorized that
placement of the implant immediately adjacent to breast tissue, which is
known to often contain bacterial contaminants, results in a higher rate of
implant inoculation, biofilm formation, and ultimately, capsular contracture.
Additionally, the use of a periareolar incision with direct dissection and
implant insertion through breast tissue is known to increase the likelihood of
capsular contracture (16,17). Again, it is theorized that contamination of the
implant during insertion through contaminated breast tissues is responsible
for these findings.
The mechanistic process connecting subclinical infection to the
development of capsular contracture has been extensively studied since the
preliminary reports. The presence of subclinical infection, or other
inflammatory process, is thought to promote increased expression of
inflammatory mediators with increased CD4+ cell concentration (18,19) and
elevated interleukin-8 levels (20). Ultimately this localized inflammatory
response leads to a fibrotic host response with increased fibroblast density
surrounding the implant with deposition of a disoriented thicker collagen
architecture within the contracted capsule (21). By understanding the
pathophysiology of capsular contracture, investigators may eventually have
success developing local or systemic medications or technologies that impede
these mechanistic steps.
Implant surface texturing has been introduced in an effort to disrupt the
dense collagen deposition around breast implants and ultimately prevent
capsular contracture. Initial texturization of breasts implants occurred early
with the “natural Y” polyurethane (PU) foam-coated implant in 1968. It was
believed that this coating would prevent the contraction of capsular
myofibroblasts thereby disrupting progressive contracture of the capsular
tissues (22). PU implants were universally associated with low early capsular
contracture rates; however, the potential carcinogen, 2,4-toluenediamine, was
discovered in the urine of patients with these PU implants and these implants
were subsequently voluntarily removed from the market. Retrospectively
many associated the low capsular contracture with PU with the rough surface
texturing. Based on this misnomer, manufacturers pursued different surface
textures to replace the PU foam implants. Currently manufacturers have each
developed their own proprietary method for texturing implant surfaces, which
are generally classified by three different techniques: salt loss, vulcanization,
imprinting.
The clinical data related to implant texturing and associated rates of
capsular contracture have been relatively inconsistent. Early studies
suggested that device texturing could significantly reduce contracture rates, a
hypothesis that has been supported by several original studies and meta-
analyses. However, these studies were all flawed and the best level 1
prospective split breast studies failed to show consistent benefit of surface
texture in reducing capsular contracture (23–27). Furthermore during the
same period the significant reduction of capsular contracture using high-level
surgical technique was demonstrated. Many physicians believed that
texturing may selectively reduce contracture rates most effectively for
augmentation patients based on the PU experience. In theory, the benefits of
disrupted collagen architecture may be counterbalanced by increased
bacterial biofilm formation and subclinical infection related to the increased
surface area for bacterial adherence and shielding from the host immune
system; however this has never been proven in any clinical model. Studies
have demonstrated that textured implants are contaminated with higher
bacterial quantities compared to smooth counterparts. Manufacturers have not
made marketing claims in the United States about reduced contracture rates
for textured devices based on their clinical data. There was much marketing
for textured devices with regard to contracture and the “Velcro” effect both of
which had little or no data to back up the claims, yet the majority of textured
proponents do so based on these marketing misnomers.
Nevertheless, in the past decade, texturing has become more controversial
due to an association with the development of Breast implant–associated
anaplastic large cell lymphoma (BIA-ACLC), a novel World Health
Organization–recognized entity (28). The estimated incidence rates for BIA-
ALCL are varied and are generally considered to be significantly different for
each manufacturer and specific texturing process (29). The data currently
support a correlation between higher surface area and roughness devices
(macrotextured) and higher incidence rates compared to microtextured
alternatives. These findings have resulted in a recent recall of Allergan’s
Biocell macrotextured devices in the United States by the Food and Drug
Administration, following removal of these devices from the market in
France and Canada (30). Interestingly, data also indicates bacteria play a
primary role in the pathogenesis of BIA-ALCL (31–37).
Studies have rarely been able to detect bacteria in all contracted capsule or
implant samples; however, this is likely due to culture technique and
sampling error. Other factors that have been potentially implicated in the
development of capsular contracture include implant rupture, hematoma,
idiopathic myofibroblast activation, and other inflammatory conditions. A
coagulated hematoma in the periprosthetic space is a perfect culture medium
for bacteria and also thought to recruit and activate a host inflammatory
response to clear the debris and blood products, ultimately resulting in a
similar inflammatory process and pathway as a subclinical infection (38).
Hematomas are therefore generally considered a contributor, but far less
frequent or important risk factor than bacterial load. Implant rupture or gel
leak is similarly referenced as a potential partial cause of capsular
contracture.
Another factor that is heavily associated with the development of capsular
contracture is therapeutic irradiation. While this is most often seen in
reconstructive patients, augmentation patients undergoing breast conservation
therapy coupled with radiation are also susceptible to the adverse fibrotic
sequelae of radiation to their implants (39). The exact mechanism is
unknown, but research suggests that the radiation may only mildly alter the
implant itself and the likely cause is fibrosis from damage to the surrounding
cellular tissues. In particular, radiation therapy likely inhibits the immune
system’s ability to control bacterial load around the implant.
PROACTIVE APPROACH FOR PREVENTION
The best data point to the net bacterial load being critical in the formation of
capsular contracture, and furthermore it is dynamic situation that is mediated
by the threshold mechanics, where the host defenses and bacteria are in an
ongoing equilibrium to increase the load (bacteria) versus decrease the load
(host). The reader should understand this threshold phenomenon. As long as
the load is below the threshold there is no clinical issue, but once the bacterial
load rises above the threshold the host response is the formulation of capsular
contracture (40). Fortunately, refinements and advances in surgical technique
have resulted in reliable significant reduction in capsular contracture rates
over the past several decades. Most of the potential causes discussed above
can be controlled or mitigated with a thoughtful and strategic approach to
breast surgery.
The subclinical infection hypothesis remains the most studied, and likely
most important, of the risk factors for the development of capsular
contracture. While all surgical technique is intended to be sterile with
complete absence of bacterial contamination, this is realistically impossible.
By recognizing the paramount importance of minimizing the bacterial load
during breast implant procedures can significantly impact capsular
contracture. All potential sources of contamination or portions of the case
with increased risk of contamination are identified and acknowledged. The
sources of contamination include the patient’s skin flora, the inevitable
bacterial contamination in the breast tissue itself, and the possible impending
contamination of the surgical field from the surrounding nonsterile equipment
or personnel as the case proceeds. Specific best practice surgical techniques
to minimize capsular contracture have been recommended for over 20 years
(8,41–49).
Meticulous antisepsis and adherence to proper technique is important
during surgical prep and draping. Some data have suggested that the specific
use of chlorhexidine during surgical prep may reduce capsular contracture
rates, although this was demonstrated in a small population of patients (50).
Chlorhexidine has been shown in recent studies to immediately kill many of
the common bacteria in breast implants’ procedures (9,51). Surgical draping
should ensure that appropriate barriers are in place to prevent contamination
of the surgical field by surrounding unprepped tissues or equipment. One
common site for potential contamination is the nipple, which effectively
exposes the surgical field to ductal bacteria during the operation. The use of
barrier dressings as nipple shields has been proposed as a method to combat
this source of intraoperative contamination. Culture swabs from nipple
shields have demonstrated that they are effectively able to prevent bacterial
migration into the surgical field during breast augmentation surgery, and
some evidence exists to suggest that the use of nipple shields reduces clinical
capsular contracture rates (52–54). In addition to standard surgical
preparation, prophylactic systemic antibiotics given immediately
preoperatively are recommended to reduce the bacterial bioburden during
surgery and minimize the likelihood of implant contamination. While the use
of preoperative antibiotics has not been reliably correlated to reduced
capsular contracture rates in studies (55,56), the scientific principles are
logical and most think the downsides of antimicrobial prophylaxis are
relatively minimal. In a randomized clinical trial a single dose of preoperative
antibiotics was equivalent to extended use with regard to surgical site
infection in tissue expander breast reconstruction patients (57).
The avoidance of breast flora is also an important consideration when
selecting the surgical incision and approach. The use of a periareolar incision,
requiring dissection directly through potentially contaminated breast tissues,
has been reproducibly associated with higher capsular contracture rates
compared to other choices (17,41).
The inframammary technique is often cited as the most reliable and
consistent surgical incision and allows a controlled approach with excellent
visualization and limited exposure to breast parenchyma. The best data on
capsular contracture rates all comes from the inframammary (58–60).
The principles of careful surgical dissection are similarly important to
ensure a good outcome and reduce capsular contracture rates. Because
hematomas are generally considered a risk factor for capsular contracture,
minimally traumatic technique is recommended with meticulous attention to
hemostasis. Specifically, blunt dissection is generally discouraged because of
the risk for bleeding with uncontrolled avulsion of tissues. By limiting
bleeding and tissue damage, inflammation can theoretically be minimized
with a resulting reduction in fibrotic capsular response.
The next decision is the pocket plane. The breast implant can be positioned
subglandular (or subfascial) or retropectoral (traditional without any inferior
pectoral origin release or dual plane with division of the inferior origins of
the pectoralis major muscle). The placement of the breast implant below the
pectoralis in either a traditional subpectoral or dual plane position provides a
vascular muscle tissue barrier between the implant and the breast
parenchyma, which is a potential source of bacterial contamination. By
limiting contamination, it would be expected that capsular contracture rates
can be mitigated with subpectoral pocket selection, and this theory has been
robustly supported by numerous studies (61). While a comprehensive
discussion of the many advantages and shortcomings of the different surgical
pockets is beyond the scope of this chapter, the subpectoral pocket is
recommended for surgeons prioritizing the reduction of capsular contracture.
The specific breast implant characteristics are also important to the risk of
capsular contracture Many surgeons particularly internationally prefer
texture. Most surgeons who prefer texture when asked state that they believe
it to have less capsular contracture and hold the implant in place. This is an
example of propagation of urban legend in the specialty as the data simply
does not support these misnomers. Nevertheless, this choice must be
carefully balanced against many other considerations including the emerging
concern for association between textured devices and BIA-ALCL. Some prior
studies have also suggested that capsular contracture rates may be higher in
patients with silicone gel–filled implants compared to saline implants (62).
This finding appears reasonable based on mechanistic studies suggesting that
silicone gel bleed and particulates can induce inflammation near an implant’s
surface. However, the recent data on the topic have failed to reliably confirm
any association between implant fill and capsular contracture rates (63).
Ultimately, the selection of a specific breast implant device relies on many
parameters and should be individualized based on each surgeon’s experience
and the patient’s preferences.
Once the pocket has been dissected and the breast implant has been
chosen, the surgical site is then prepared for implantation. Again, the priority
is to ensure appropriate hemostasis and eliminate or reduce potential bacterial
contaminants. Antimicrobial breast pocket irrigation is recommended to
reduce bacterial load around the implant. A robust compilation of literature
supports this technique with well-demonstrated reduction in capsular
contracture rates (8,64). Different irrigation fluids have been studied, and
three current proven irrigations currently exist: Betadine triple, non-Betadine
triple antibiotic, and 50% Betadine (44–46,48,64).
Before handling the implant, surgical gloves should be exchanged for new
sterile gloves. Similarly, cleaned or unused surgical instruments should be
reserved for portions of the case involving the breast implant itself. The
breast implant must then be introduced into the prepared pocket without
contaminating the shell during insertion through the surgical incision.
Multiple methods of reducing skin contamination exist including reprepping
skin with chlorhexidine (our preferred method, sleeves or other Tegaderm
barriers).
After the implant has been successfully positioned with acceptable
appearance, it may be tempting to leave a closed suction drain to reduce
blood products and serous fluid that may incite an inflammatory process
around the implant. However, percutaneous drains also serve as a potential
source for bacterial introduction and are generally discouraged in primary
breast augmentation; however, they may be required in more complex
revision or reconstructive cases. In a study of over 3,000 augmentation
patients, the use of closed suction drains was found to increase capsular
contracture rates by nearly fivefold (65). The incision is then ideally closed in
multiple layers to provide the most durable and impenetrable coverage of the
implant as possible.
After surgery, the use of postoperative systemic antibiotics is considered
controversial due to limited data to support a strong correlation with capsular
contracture rates, although most data favor only one perioperative dose of
antibiotics and this was supported by a level 1 study (57). However, a course
of systemic antibiotics for any future procedure that will breach the skin or
mucosa is recommended due to the risk of hematogenous spread to the
implant surface.
These well-established practices originally recommended in 2000 (44,46)
have been codified into a the 14-point plan (49) that is recommended for
every surgeon performing breast implant procedures (Table 123-2).
Adams et al. have reported on a series of over 42,000 patients undergoing
breast augmentation with macrotextured breast implants with nearly
ubiquitous adherence to these 14 recommendations (34). Their patient cohort
was followed by a mean of 11.7 years with an impressive 2.2% capsular
contracture rate. These data demonstrate that a methodical and practical
proactive approach to breast augmentation surgery can successfully minimize
capsular contracture rates and optimize safety outcomes for patients.
Interestingly, the expected number of BIA-ALCL cases should have been 15;
however, there were no cases in the series. Given the known role of bacteria
in BIA-ALCL it is no surprise that risk reduction is significant using proven
techniques known for capsular contracture.

TABLE 123-2 The 14-Point Plan to Minimize Rate of Capsular Contracture


Formation
1. Use intravenous antibiotic prophylaxis at the time of anesthetic induction.
2. Avoid periareolar/ transaxillary incisions; these have been shown in both
laboratory and clinical studies to lead to a higher rate of contracture.
3. Use nipple shields to prevent spillage of bacteria into the pocket.
4. Perform careful atraumatic dissection to minimize devascularized tissue.
5. Perform careful hemostasis.
6. Avoid dissection into the breast parenchyma.
7. The use of a dual plane pocket has anatomic advantages.
8. Perform pocket irrigation with correct proven triple antibiotic solution or
50% (1:1 dilution) or stronger Betadine.
9. Steps to minimize skin contamination.
10. Minimize implant open time and replacement of implant or sizers.
11. Change surgical gloves prior to handling and use new or cleaned
instruments and drapes.
12. Avoid using a drainage tube, which can be a potential site of entry for
bacteria.
13. Use a layered closure
14. Use antibiotic prophylaxis to cover subsequent procedures that breach
skin or mucosa.

From Deva AK, Adams WP Jr, Vickery K, et al. The role of bacterial biofilms in device-associated
infection. Plast Reconstr Surg 2013;132(5):1319–1328.
EXPERIMENTAL PREVENTION METHODS
Other, more experimental preventive strategies and therapies have been
proposed and reported, but have not reached routine clinical implementation.
Investigators have previously attempted to reduce capsular contracture by
preventing fibrosis around the implant using locally acting scar-mitigating
agents. In particular, steroids have been studied as an intracapsular injection
with promising results in preclinical models. However, the use of steroid
medications has largely been abandoned due to concerns related to
deterioration of the implant shell integrity and more importantly negative
effect on local tissue due to steroids.
Some investigators have attempted to chemically modify the surface of the
implant itself to mitigate the host immune response and prevent capsular
contracture. Materials that have been used include spider silk proteins and
poly (2-methacryloyloxyethyl phosphorylcholine), a common moiety that
mimics mammalian cells (66,67). This approach has demonstrated success in
preclinical studies but currently remains experimental.
Systemic inflammatory and fibrosis modulators have also been
investigated in capsular contracture patients. Specifically, postoperative
leukotriene inhibitors have been theorized to attenuate the development of
dense fibrotic capsules. With systemic oral postoperative administration,
leukotriene antagonists have been shown to improve capsule compliance and
reduce capsular contracture rates in breast augmentation patients (68).
Clinical experience has been mixed, some data suggested that leukotriene
antagonists may have efficacy at reversing capsular contracture after it
occurs; however, the benefits only delayed the ultimate surgical intervention,
not prevented it. Additionally, leukotriene antagonists are associated with
occasional liver damage, and patients on these medications should be
periodically monitored with liver function panels.
FIGURE 123-1 A–C: Clinical example of a 39-year-old female with history of prior
mastopexy and augmentation using submuscular 275-cc silicone implants 2 years
prior who demonstrates bilateral Baker grade III capsular contracture. D–F: Three-
month postoperative result after bilateral complete capsulectomy, revision
mastopexy, and submuscular implant replacement.

Similarly, the antifibrotic transforming growth factor-β modulator,


pirfenidone, has been studied as a preventive or curative therapy for capsular
contracture (69). Preliminary clinical data has demonstrated success
alleviating capsular contracture after it develops in patients, however this
medication has not been widely studied or adopted.
CONCLUSION
Capsular contracture remains the most frequent complication after implant-
based breast augmentation and affects a large number of women due to the
substantial demand for breast augmentation surgeries. While historical
capsular contracture rates were unacceptably high, progressive advancement
in surgical techniques and technologies have resulted in a significant
demonstrable reduction. A strategic and proactive approach to breast
augmentation utilizing the 14-point plan can successfully prevent capsular
contracture in the majority of patients and should be routinely implemented
for all cases (see Fig. 123-1). While ongoing research continue, the proven
surgical technique is felt by most to reduce the risk of capsular contracture to
less than 2%.

REFERENCES

1. Shah Z, Lehman JA Jr, Tan J. Does infection play a role in breast


capsular contracture? Plast Reconstr Surg 1981;68(1):34–42.
2. Burkhardt BR. Capsular contracture: hard breasts, soft data. Clin Plast
Surg 1988;15(4):521–532.
3. Burkhardt BR, Demas CP. The effect of Siltex texturing and povidone-
iodine irrigation on capsular contracture around saline inflatable breast
implants. Plast Reconstr Surg 1994;93(1):123–128; discussion 129–130.
4. Burkhardt BR, Dempsey PD, Schnur PL, et al. Capsular contracture: a
prospective study of the effect of local antibacterial agents. Plast
Reconstr Surg 1986;77(6):919–932.
5. Burkhardt BR, Eades E. The effect of Biocell texturing and povidone-
iodine irrigation on capsular contracture around saline-inflatable breast
implants. Plast Reconstr Surg 1995;96(6):1317–1325.
6. Virden CP, Dobke MK, Stein P, et al. Subclinical infection of the
silicone breast implant surface as a possible cause of capsular
contracture. Aesthetic Plast Surg 1992;16(2):173–179.
7. Netscher DT, Walker LE, Weizer G, et al. A review of 198 patients (389
implants) who had breast implants removed. J Long Term Eff Med
Implants 1995;5(1):11–18.
8. Adams WP Jr, Calobrace MB. Discussion: the questionable role of
antibiotic irrigation in breast augmentation. Plast Reconstr Surg
2019;144(1):253–257.
9. Adams WP Jr. Commentary on: surgical site irrigation in plastic
surgery: what is essential? Aesthet Surg J 2018;38(3):276–278.
10. Gayou R, Rudolph R. Capsular contraction around silicone mammary
prostheses. Ann Plast Surg 1979;2(1):62–71.
11. Pajkos A, Deva AK, Vickery K, et al. Detection of subclinical infection
in significant breast implant capsules. Plast Reconstr Surg
2003;111(5):1605–1611.
12. Rieger UM, Mesina J, Kalbermatten DF, et al. Bacterial biofilms and
capsular contracture in patients with breast implants. Br J Surg
2013;100(6):768–774.
13. Del Pozo JL, Tran NV, Petty PM, et al. Pilot study of association of
bacteria on breast implants with capsular contracture. J Clin Microbiol
2009;47(5):1333–1337.
14. Tamboto H, Vickery K, Deva AK. Subclinical (biofilm) infection causes
capsular contracture in a porcine model following augmentation
mammaplasty. Plast Reconstr Surg 2010;126(3):835–842.
15. Jacombs A, Allan J, Hu H, et al. Prevention of biofilm-induced capsular
contracture with antibiotic-impregnated mesh in a porcine model.
Aesthet Surg J 2012;32(7):886–891.
16. Wiener TC. The role of betadine irrigation in breast augmentation. Plast
Reconstr Surg 2007;119(1):12–15; discussion 16–17.
17. Wiener TC. Relationship of incision choice to capsular contracture.
Aesthetic Plast Surg 2008;32(2):303–306.
18. Steiert AE, Boyce M, Sorg H. Capsular contracture by silicone breast
implants: possible causes, biocompatibility, and prophylactic strategies.
Med Devices (Auckl) 2013;6:211–218.
19. Wolfram D, Rabensteiner E, Grundtman C, et al. T regulatory cells and
TH17 cells in peri-silicone implant capsular fibrosis. Plast Reconstr
Surg 2012;129(2):327e–337e.
20. Kyle DJ, Harvey AG, Shih B, et al. Identification of molecular
phenotypic descriptors of breast capsular contracture formation using
informatics analysis of the whole genome transcriptome. Wound Repair
Regen 2013;21(5):762–769.
21. Moyer KE, Ehrlich HP. Capsular contracture after breast reconstruction:
collagen fiber orientation and organization. Plast Reconstr Surg
2013;131(4):680–685.
22. Ashley FL. Further studies on the natural-Y breast prosthesis. Plast
Reconstr Surg 1972;49(4):414–419.
23. Asplund O, Gylbert L, Jurell G, et al. Textured or smooth implants for
submuscular breast augmentation: a controlled study. Plast Reconstr
Surg 1996;97(6):1200–1206.
24. Fagrell D, Berggren A, Tarpila E. Capsular contracture around saline-
filled fine textured and smooth mammary implants: a prospective 7.5-
year follow-up. Plast Reconstr Surg 2001;108(7):2108–2112; discussion
2113.
25. Hakelius L, Ohlsen L. Tendency to capsular contracture around smooth
and textured gel-filled silicone mammary implants: a five-year follow-
up. Plast Reconstr Surg 1997;100(6):1566–1569.
26. Poeppl N, Schreml S, Lichtenegger F, et al. Does the surface structure of
implants have an impact on the formation of a capsular contracture?
Aesthetic Plast Surg 2007;31(2):133–139.
27. Tarpila E, Ghassemifar R, Fagrell D, et al. Capsular contracture with
textured versus smooth saline-filled implants for breast augmentation: a
prospective clinical study. Plast Reconstr Surg 1997;99(7):1934–1939.
28. Brody GS, Deapen D, Taylor CR, et al. Anaplastic large cell lymphoma
occurring in women with breast implants: analysis of 173 cases. Plast
Reconstr Surg 2015;135(3):695–705.
29. Collett DJ, Rakhorst H, Lennox P, et al. Current risk estimate of breast
implant-associated anaplastic large cell lymphoma in textured breast
implants. Plast Reconstr Surg 2019;143(3S A Review of Breast
Implant-Associated Anaplastic Large Cell Lymphoma):30S–40S.
30. 7-24-19 F-AR. The FDA Requests Allergan Voluntarily Recall Natrelle
BIOCELL Textured Breast Implants and Tissue Expanders from the
Market to Protect Patients: FDA Safety Communication. 2019.
31. Loch-Wilkinson A, Beath KJ, Knight RJW, et al. Breast implant
associated Anaplastic Large Cell Lymphoma in Australia and New
Zealand – higher risk for macrotextured implants supports a bacterial
etiology. Australian Society for Aesthetic Plastic Surgery; 2016.
32. Adams WP Jr. Discussion: anaplastic large cell lymphoma occurring in
women with breast implants: analysis of 173 cases. Plast Reconstr Surg
2015;135(3):709–712.
33. Adams WP Jr. Discussion: bacterial biofilm infection detected in breast
implant-associated anaplastic large-cell lymphoma. Plast Reconstr Surg
2016;137(6):1670–1672.
34. Adams WP Jr., Culbertson EJ, Deva AK, et al. Macrotextured breast
implants with defined steps to minimize bacterial contamination around
the device: experience in 42,000 implants. Plast Reconstr Surg
2017;140(3):427–431.
35. Adams WPJ. Discussion: the epidemiology of breast implant–associated
anaplastic large cell lymphoma in Australia and New Zealand confirms
the highest risk for grade 4 surface breast implants. Plast Reconstr Surg
2019;143(5):1293–1294.
36. Deva AK. Reply: Chronic biofilm infection in breast implants is
associated with an increased T-cell lymphocytic infiltrate: implications
for breast implant-associated lymphoma. Plast Reconstr Surg
2015;135(6):1059e–1060e.
37. Deva AK. Commentary on: breast erythema in a patient with breast
implant-associated anaplastic large cell lymphoma: a case report
discussing cutaneous manifestations. Aesthet Surg J 2018;38(3):NP53–
NP55.
38. Dancey A, Nassimizadeh A, Levick P. Capsular contracture—What are
the risk factors? A 14 year series of 1400 consecutive augmentations. J
Plast Reconstr Aesthet Surg 2012;65(2):213–218.
39. Mark RJ, Zimmerman RP, Greif JM. Capsular contracture after
lumpectomy and radiation therapy in patients who have undergone
uncomplicated bilateral augmentation mammoplasty. Radiology
1996;200(3):621–625.
40. Jacombs A, Tahir S, Hu H, et al. In vitro and in vivo investigation of the
influence of implant surface on the formation of bacterial biofilm in
mammary implants. Plast Reconstr Surg 2014;133(4):471e–480e.
41. Adams WP Jr. Capsular contracture: what is it? What causes it? How
can it be prevented and managed? Clin Plast Surg 2009;36(1):119–126,
vii.
42. Adams WP Jr. Discussion: Subclinical (biofilm) infection causes
capsular contracture in a porcine model following augmentation
mammaplasty. Plast Reconstr Surg 2010;126(3):843–844.
43. Adams WP Jr. Commentary on: effect of incision choice on outcomes in
primary breast augmentation. Aesthet Surg J 2012;32(4):463–464.
44. Adams WP Jr, Conner WC, Barton FE Jr, et al. Optimizing breast
pocket irrigation: an in vitro study and clinical implications. Plast
Reconstr Surg 2000;105(1):334–338; discussion 339–343.
45. Adams WP Jr, Conner WC, Barton FE Jr, et al. Optimizing breast-
pocket irrigation: the post-betadine era. Plast Reconstr Surg
2001;107(6):1596–1601.
46. Adams WP Jr, Rios JL, Smith SJ. Enhancing patient outcomes in
aesthetic and reconstructive breast surgery using triple antibiotic breast
irrigation: six-year prospective clinical study. Plast Reconstr Surg
2006;117(1):30–36.
47. Blount AL, Martin MD, Lineberry KD, et al. Capsular contracture rate
in a low-risk population after primary augmentation mammaplasty.
Aesthet Surg J 2013;33(4):516–521.
48. Giordano S, Peltoniemi H, Lilius P, et al. Povidone-iodine combined
with antibiotic topical irrigation to reduce capsular contracture in
cosmetic breast augmentation: a comparative study. Aesthet Surg J
2013;33(5):675–680.
49. Deva AK, Adams WP Jr, Vickery K. The role of bacterial biofilms in
device-associated infection. Plast Reconstr Surg 2013;132(5):1319–
1328.
50. Carvajal J, Carvajal M, Hernández G. Back to basics: could the
preoperative skin antiseptic agent help prevent biofilm-related capsular
contracture? Aesthetic Surg J 2018;39(8):848–859.
51. Zhadan O, Becker H. Surgical site irrigation in plastic surgery. Aesthet
Surg J 2018;38(3):265–273.
52. Collis N, Mirza S, Stanley PRW, et al. Reduction of potential
contamination of breast implants by the use of ‘nipple shields’. Br J
Plast Surg 1999;52(6):445–447.
53. Horsnell JD, Searle AE, Harris PA. Intra-operative techniques to reduce
the risk of capsular contracture in patients undergoing aesthetic breast
augmentation—A review. Surgeon 2017;15(5):282–289.
54. Wixtrom RN, Stutman RL, Burke RM, et al. Risk of breast implant
bacterial contamination from endogenous breast flora, prevention with
nipple shields, and implications for biofilm formation. Aesthet Surg J
2012;32(8):956–963.
55. Gylbert L, Asplund O, Berggren A, et al. Preoperative antibiotics and
capsular contracture in augmentation mammaplasty. Plast Reconstr Surg
1990;86(2):260–267; discussion 268–269.
56. Keramidas E, Lymperopoulos N, Rodopoulou S. Is antibiotic
prophylaxis in breast augmentation necessary? A prospective study.
Plastic Surg (Oakv) 2016;24(3):195–198.
57. Phillips BT, Fourman MS, Bishawi M, et al. Are prophylactic
postoperative antibiotics necessary for immediate breast reconstruction?
Results of a prospective randomized clinical trial. J Am Coll Surg
2016;222(6):1116–1124.
58. Adams WP Jr. The process of breast augmentation: four sequential steps
for optimizing outcomes for patients. Plast Reconstr Surg
2008;122(6):1892–1900.
59. Tebbetts JB. Achieving a zero percent reoperation rate at 3 years in a 50-
consecutive-case augmentation mammaplasty premarket approval study.
Plast Reconstr Surg 2006;118(6):1453–1457.
60. Tebbetts JB, Adams WP. Five critical decisions in breast augmentation
using five measurements in 5 minutes: the high five decision support
process. Plast Reconstr Surg 2005;116(7):2005–2016.
61. Puckett CL, Croll GH, Reichel CA, et al. A critical look at capsule
contracture in subglandular versus subpectoral mammary augmentation.
Aesthetic Plast Surg 1987;11(1):23–28.
62. Asplund O. Capsular contracture in silicone gel and saline-filled breast
implants after reconstruction. Plast Reconstr Surg 1984;73(2):270–275.
63. Liu X, Zhou L, Pan F, et al. Comparison of the postoperative incidence
rate of capsular contracture among different breast implants: a
cumulative meta-analysis. PLoS One 2015;10(2):e0116071.
64. Jewell ML, Adams JWP. Betadine and breast implants. Aesthet Surg J
2018;38(6):623–626.
65. Araco A, Gravante G, Araco F, et al. Infections of breast implants in
aesthetic breast augmentations: a single-center review of 3,002 patients.
Aesthetic Plast Surg 2007;31(4):325–329.
66. Zeplin PH, Berninger AK, Maksimovikj NC, et al. [Improving the
biocompatibility of silicone implants using spider silk coatings:
immunohistochemical analysis of capsule formation]. Handchir
Mikrochir Plast Chir 2014;46(6):336–341.
67. Park JU, Ham J, Kim S, et al. Alleviation of capsular formations on
silicone implants in rats using biomembrane-mimicking coatings. Acta
Biomater 2014;10(10):4217–4225.
68. Scuderi N, Mazzocchi M, Rubino C. Effects of zafirlukast on capsular
contracture: controlled study measuring the mammary compliance. Int J
Immunopathol Pharmacol 2007;20(3):577–585.
69. Veras-Castillo ER, Cardenas-Camarena L, Lyra-Gonzalez I, et al.
Controlled clinical trial with pirfenidone in the treatment of breast
capsular contracture: association of TGF-beta polymorphisms. Ann Plast
Surg 2013;70(1):16–22.
CHAPTER 124

Diagnosing, Treating, and Preventing


Biofilms in Implant-based Breast
Surgery
SUBHAS C. GUPTA | CASSANDRA DREW | CHARLES DEGUZMAN | CHANEL LEE
HISTORY
Capsular contracture is the only significant long-term complication of breast
implant placement for which limited strategies exist for prevention. While
many etiologic surgical parameters have been proposed as causative reasons
for capsular contracture, biofilm presence on medical implants have been
demonstrated as the primary confirmed etiology of capsular contracture in
breast implants (1). The study of biofilms extends well beyond plastic
surgery and even beyond medicine, and much of our understanding comes
from industrial sources who have examined these microbial communities in
diverse environments such as swimming pools, plumbing fixtures, and dental
appliances.
Costerton et al. have demonstrated that bacteria would prefer to live as a
biofilm rather than in a planktonic, free swimming, state when sufficient
nutrients are present in the environment (2). This concept predicts that
implants in nutrient-rich environments, such as the body, would be
predisposed to the accumulation of biofilms. This aligns with the findings in
modern medicine that biofilms predominate over their planktonic
counterparts and account for 60% to 80% of microbial infections (3).
The extracellular matrix and close contact of different species of bacteria
produce a unique microenvironment that can affect the growth patterns and
structure of the biofilm. Altogether, these changes contribute to a stable
community that is more efficient than the same mix of the planktonic
counterparts of these microbes (4).
DEFINITION
Biofilms, by definition, are an adherent community of microbes within a self-
made extracellular matrix (5). This definition underplays the vast difference
between planktonic microbes and the sessile microbes that compose biofilms.
A majority of biofilms are composed of several species of bacteria, whereas
even biofilms of a single species compared to their planktonic counterpart
have profound differences (4). One of the most apparent differences is the
presence of extracellular matrix. In many cases, the extracellular matrix is a
hydrated polyanionic complex of polysaccharides. The extracellular matrix is
usually hydrophilic and contains inorganic ions, amino acids, and
extracellular DNA.
GROWTH
The first step in biofilm creation is the adherence of sessile bacteria to a
surface. This adhesion is broken down into two stages: primary adhesion,
which is usually relatively loose and irreversible, and secondary adhesion,
which is often oxidation/hydration and creates strong bonds between the
microbes and the target surface.
Primary adhesion is dependent upon many things, namely hydrophobic
interactions, van der Waals forces, steric interactions, electrostatic
interactions, hydrodynamic forces, Brownian motion, convection, and surface
area and texture. The innate characteristics of the bacteria and surface greatly
determine primary adhesion. It ordinarily takes anywhere from a minute to
ten minutes for microbes to transition from primary adhesion to secondary
adhesion.
Often attachment can be aided by priming surfaces for biofilm formation.
This is achieved through the accumulation of molecules that can increase the
probability of bacterial adherence. For example, breast implants are
commonly conditioned with the accumulation of acute phase proteins or lipid
droplets. These can easily interact with the Microbial Surface Component
Recognizing Matrix Molecules possessed by many Gram-positive bacteria,
which in turn increases the probability of adhesion (6).
Secondary adhesion creates stronger, more stable binding by the
interaction of adhesins and the given surface. At the end of this stage, the
cells will be irreversibly bound to the surface. It is during this phase that cells
may bind to each other and aggregate on the substratum (6).
Once cells attach to a surface, biofilm-specific genes are upregulated, and a
distinct biofilm phenotype emerges. Although at present, the particular
mechanism of how the genes are upregulated is unknown, it is hypothesized
to be a combination of nutrient limitation, stress, relatively high cell density,
and the interaction of metabolic products. At some point, the biofilm reaches
its optimal growth and its growth plateaus or regresses. It is then when the
outermost surface of the biofilm can begin to generate planktonic cells that
are released into the environment in search of new homes (6).
RESISTANCE
Once established, the biofilm can survive far longer than planktonic
organisms due to its resistance to surfactants, phagocytosis, and antibiotics.
This resistance is due to several different mechanisms (6). One such
mechanism is that biofilms can produce cells in a dormant stage that can
survive until the environment has become more hospitable. This is made
possible since these cells, aptly called persister cells, have reduced
metabolism, which enables them to survive for long periods with a low intake
of possibly threatened resources (7).
In addition, decreased metabolism can shield microbes from certain types
of antibiotics that rely on rapidly dividing microbes as their mode of action.
This means that after the active planktonic bacteria have been annihilated, the
biofilm may persist and can reproduce undetected months or even years later
(8).
Interestingly, these microbes form a small fraction (5–35%) of what is
considered the entire biofilm (8). The bulk of the biofilm is, in fact,
composed of the extracellular matrix. The extracellular matrix acts as a
nutrient reservoir during stressful conditions. It also acts as a secure anchor to
the substratum. One common misconception is that the resistance to
antibiotics is solely due to the inability of antibiotics to penetrate the
extracellular matrix. Although some antibiotics can be consumed or bind with
elements within the matrix, this does not fully explain biofilm resistance (7).
Anderl et al. performed a study that compared Klebsiella pneumoniae
biofilms with and without Beta-lactamase, and ampicillin was able to
penetrate through the K. pneumoniae mutant biofilm but not through the wild
type K. pneumoniae biofilm. However, even the K. pneumonia biofilm that
was penetrated with ampicillin was still resistant to ampicillin, suggesting
other mechanisms for resistance must be in place (9).
One possible explanation for this increased resistance is the proximity of
the individual cells within the biofilm. Close proximity provides a
community that is thought to have a synergistic effect on the individual
microbes within the film, for example, by increasing the potential for
horizontal exchange of genes and by creating products and metabolites that
can be used by other species within the biofilm. This can lead to individual
microbes communicating to coordinate activities that may contribute to the
survival of the community in less hospitable environments (7).
In addition, the relatively concentrated density of microbes within the
biofilm can alter the immediate environment. The change of pH, reservoirs of
metabolites, and other cellular products can interact with offending
mechanisms of destruction and is thought to contribute significantly to the
decreased antimicrobial effects of otherwise potent antibiotics (8).
BIOFILM PATHOLOGIES
The extracellular matrix of biofilms is an essential part of bacterial adherence
and, therefore, also plays a vital role in many medical pathologies. The
unique and large amount of variance seen in the structure of biofilms make
them very resilient and allow them to survive in different environments,
making biofilms responsible for many infections in the hospital setting.
Without the proper sanitation precautions, biofilms of bacteria can be
responsible for infections that develop from nonbiologic foreign materials
like dirty needles, catheters, prosthetic devices, or implants (10). Even when
all sanitation precautions are met, local complications of breast implant
surgery like capsular contraction or infection are responsible for a large
portion of the reoperation rate of patients receiving breast implants.
CAPSULAR CONTRACTURE
One of the most common complications after breast implant placement is the
development of capsular contracture. Capsular contracture is characterized by
the body creating scar tissue that thickens and tightens around the implant,
causing the breast to feel firmer and causing physical pain along with many
aesthetic changes. The phenotype of capsular contracture can vary wildly
between patients and the severity of the case, but generally, breasts will often
become more spherical in shape. The implants will typically migrate
cephalad, resulting in noticeable asymmetry between the two breasts (Fig.
124-1).

FIGURE 124-1 Left capsular contracture.

One study of this group of patients had capsular contracture being the most
common complication at 11.4% with hematoma (2.3%) and infection (2%)
far behind in second and third place (11). Evidence suggests that a significant
cause of capsular contracture is the inflammation that develops due to the
presence of biofilms, specifically Staphylococcus epidermidis; even
subclinical contamination can induce the development of capsular contracture
(12,13). This means that no planktonic free-floating bacteria itself can be
detected, as the presence of just the biofilm alone can cause the development
of capsular contracture.
Patients with capsular contracture often describe that their breasts or
implants feel harder due to the tightening of the scar tissue. The scarring of
capsular contracture may even be seen on mammography and may interfere
and be a challenge for breast cancer patients or those undergoing frequent
mammography (14). The severity of capsular contracture can be described as
one of four different Baker grades:
Grade I: the breast is normally soft and looks natural
Grade II: the breast is a little firm but looks normal
Grade III: the breast is firm and looks abnormal (visible distortion)
Grade IV: the breast is hard, painful, and looks abnormal (greater
distortion)
Patients should be educated on how a normal capsule around a breast and
implant should look and feel to monitor for any signs of developing capsular
contracture on themselves. After surgery, breasts should be Baker grade I,
while surgical revision and removal of the fibrous capsule should be
considered for patients with Baker grade III or Baker grade IV (15). When
assessing for the firmness of the implanted breast via touch, it should be
noted that textured implants, in general, feel firmer than smooth-walled.
Though breast procedures, in general, have some of the highest rates of
complications in plastic surgery, capsular contracture is the leading cause of
revisions in breast augmentation patients and can occur weeks to even years
after the implant is first placed. Though the further the patient is postsurgery,
the less likely one is to develop capsular contracture; the potential of a
delayed onset makes it essential for patients and physicians to regularly
monitor and check for signs of capsular contracture development (16).
PROPHYLACTIC SURGICAL TECHNIQUES
Because Staphylococcus epidermidis is a common bacterium seen in healthy
skin flora and its biofilms constitute a significant cause of capsular
contracture (17), a proper surgical sterile technique must be followed during
implantation to prevent capsular contracture.
Though incisions are often determined based on where the scar is placed,
each incision location harbors different levels of bacteria and are predisposed
to certain types of bacteria. The area of the periareolar incision has relatively
high concentrations of bacteria, causing a statistically significant increase in
capsular contraction if that approach is made (18). The use of an insertion
funnel intraoperatively can help mitigate this risk (19).
Any increase of tension on the surrounding muscles or tissue can also lead
to a rise in capsular contracture. Breast implants should not be over
expanded, have an ample amount of soft tissue coverage, and preferably be
placed in a submuscular pocket to minimize disruption of the pectoralis
musculocutaneous perforators (15). The use of an acellular dermal matrix
provides an additional layer of tissue between the skin and the implant to
reduce the risk of capsular contracture from a structural perspective but the
presence of another foreign object also increases the risk of infection and
other complications (20). Surgeons must weigh the risks and benefits
accordingly.
BREAST IMPLANT COATINGS
Studies have been done analyzing the material, texture, and coatings of breast
implants to see how changes to the implant itself can affect rates of infection
and capsular contracture (21). Some surgeons opt for textured implants
believing that they have lower rates of capsular contracture, but the current
literature does not seem to show any clear evidence supporting this.
Specialized coatings, dressings, and sponges have also been developed to
tackle biofilm development with promising results that can either have
antiadhesive or antimicrobial properties. Research on these methods is
relatively new, with many studies being proof of concepts limited to in vitro
or animal models (22,23).
ANTIBIOTIC AND ANTISEPTIC USE
The most common approach in preventing biofilm development is some sort
of chemoprophylaxis, often the use of antibiotics to destroy the
microorganism creating the biofilm. Though antibiotics are the most popular
form of biofilm treatment and prevention, biofilms are notoriously resistant to
them. In general, due to the complex nature of biofilms, the concentration of
antibiotics needed to kill a mature biofilm is often hundreds of times the
concentration required to kill the same quantity of bacteria in a planktonic
phase (23).
The CDC recommends first-generation cephalosporin for systemic
perioperative prophylaxis in breast surgery involving implants (24), but not
all surgeons use antibiotics in breast surgery due to concerns of excessive
antibiotic use. Despite extensive data in the literature, the consensus is still
mixed. Many studies of breast augmentation have shown no efficacy in
prophylactic antibiotics in preventing wound infection or delayed healing
(25) while a Cochrane meta-analysis analyzing eleven studies found
prophylactic antibiotics administered preoperatively reduces the risk of
surgical site infection in patients undergoing surgery for breast cancer (26).
The inconclusive results of antibiotics may be due to the unique structure of
biofilms and bacterial genetic diversity that they promote (27). Though there
is no consensus on the choice of antibiotics for antibiotic prophylaxis, some
have shown certain antibiotics, fluoroquinolones, in particular, as being better
at penetrating biofilms than other antibiotics. If antibiotics are administered,
antimicrobial prophylaxis should be discontinued as soon as possible and
delivered in a single dose as there were no significant differences found in
extended protocols (28).
Despite the concerns of some physicians, a recent meta-analysis suggests
that perioperative povidone–iodine irrigation is not associated with implant
rupture and reduces rates of Baker classes III and IV capsular contracture
(29). The use of antibiotic rinses, as well as topical antibiotics, also seem to
prevent infections in breast augmentation (30). Current antibiotics may also
be more effective if given through a slow-release medium, like a hydrogel,
especially when preventing the often-delayed onset of capsular contracture
(31).
ALTERNATIVE FORMS OF CHEMOPROPHYLAXIS
Outside of antibiotics, some other forms of chemoprophylaxis can be
implemented. The literature on the efficacy of many of these techniques is
lacking, and many more studies should be done to explore their viability (32).
Though antibiotics work on killing the bacteria that create the biofilm,
there have been recent efforts to develop pharmacologic strategies that
specifically target biofilms. Breaking down the structural integrity of biofilms
prevents the development of infection or capsular contracture without the risk
of developing antibiotic resistance. Some have levied the effects of enzymes
and products created by other microbes to directly break up the structure of
biofilms in both in vitro and in vivo settings (33). Many materials also work
as surfactants, breaking up the fabric of biofilms by disrupting the
hydrophobic and electrostatic bonds used for biofilm and bacterial attachment
to tissue. Though the use of detergents like castile soap has been studied and
proven to be efficient for treating orthopedic implants, little to no research
has been done on its use with breast implants (34). Metal and metal
nanoparticles have also been used extensively in the field of orthopedic
surgery to break up biofilm structures with little application in breast surgery
as of yet (34).
As a response to the increasingly popular trend of more “natural” treatment
options wanted by many patients, studies have also analyzed the effects of
products like honey and turmeric on biofilms. Both honey and turmeric have
demonstrated reduction and total inhibition of biofilm development
laboratory models, but no study has been done to analyze this effect in
patients (35).
Because of the complex nature of biofilms, more research should be done
on nontraditional forms of biofilm, for example, some nonantibiotic drugs
have also shown promising results in reversing and preventing capsular
contracture, like leukotriene receptor antagonists, but the mechanism behind
this phenomenon is unknown (36).
MECHANICAL PROPHYLAXIS
Though less common in plastic surgery, many fields use mechanical
modalities to prevent and destroy biofilms. Due to the wide chemical
variance in biofilms, physically breaking up the biofilm with noninvasive
techniques may be another viable treatment option. It should be noted that
certain forms of physical manipulations can negatively affect patient
outcomes as radiating a permanent implant increases the risk of capsular
contracture in patients receiving postoperative radiation therapy for cancer
(37). Changes to the frequency, rate, or amplitude of electromagnetic
radiation, though, can enhance antibiotic efficacy against biofilms and reduce
rates of capsular contracture (38).
High-frequency ultrasound devices closed capsulotomy techniques have
also been used to treat capsular contraction via controlled agitation. This
agitation creates enough force to break down fibrotic tissue of capsular
contracture, promote blood flow to the region, and even break down the
molecular bonds of underlying biofilms (39).
Mechanical stimuli can also be used in conjunction with chemical
techniques to make a treatment that is greater than the sum of its parts. For
example, the implementation of weak electrical currents has been shown to
increase the efficacy of antibiotics on biofilms, producing a phenomenon
termed the “bioelectric effect” (38). The electrical currents alter the
extracellular matrix of biofilms and are thought to enhance the penetration of
antimicrobial agents and change the surrounding pH of the environment (40).
INTRAOPERATIVE DETECTION
Recent work has found that intraoperative disclosing agents such as
Methylene blue may assist in the identification of biofilm-associated capsular
contracture and identify the portion of the implant capsule that needs to be
removed. A comparison of intraoperative Methylene blue stained implant
pockets in a patient with only left-sided capsular contracture is seen in Figure
124-2. Clearly, the blue is adherent to a much larger region of the left breast,
and this capsule was excised in its entirety.

FIGURE 124-2 Intraoperative disclosure of biofilm with Methylene blue stain. The
right breast was a Baker grade II and the left breast was a Baker grade IV.
CONCLUSION
In conclusion, biofilms pose a significant threat to plastic surgeons. The
extracellular matrix and community interactions create an altogether different
foe to combat contrasted with the well-studied planktonic counterparts. The
high rate of infection and emerging evidence on its causation of capsular
contracture make biofilms remarkable. However, new modes of prophylaxis
against biofilms are emerging as researchers and clinicians better learn to
study and combat biofilms. Though the literature of biofilm often does not
provide enough definitive evidence to create sweeping guidelines on what
prophylaxis methods to use, the field is filled with many potential treatment
options. As we learn more about the mechanisms behind biofilm
development, more processes can be developed to tackle biofilm
development systematically. This chapter outlined a wide breadth of
prevention that has currently been studied and potential options. Good
clinical judgment should be implemented when deciding what preventative
techniques to use.

REFERENCES

1. Virden CP, Dobke MK, Stein P, et al. Subclinical infection of the


silicone breast implant surface as a possible cause of capsular
contracture. Aesthetic Plast Surg 1992;16(2):173–179.
2. Costerton JW, Lewandowski Z, Caldwell DE, et al. Microbial biofilms.
Annu Rev Microbiol 1995;49(1):711–745.
3. Omar A, Wright JB, Schultz G, et al. Microbial biofilms and chronic
wounds. Microorganisms 2017;5(1):E9.
4. Resch A, Leicht S, Saric M, et al. Comparative proteome analysis of
Staphylococcus aureus biofilm and planktonic cells and correlation with
transcriptome profiling. Proteomics 2006;6(6):1867–1877.
5. Costerton JW, Stewart PS, Greenberg EP. Bacterial biofilms: a common
cause of persistent infections. Science 1999;284:1318–1322.
6. Dunne WM. Bacterial adhesion: seen any good biofilms lately?. Clin
Microbiol Rev 2002;15(2):155–166.
7. O’Toole AM. (2015). Thermal Deactivation of Pseudomonas
Aeruginosa Biofilms (Doctoral dissertation, University of Iowa).
8. Del Pozo JL, Patel R. The challenge of treating biofilm-associated
bacterial infections. Clin Pharmacol Ther 2007;82(2):204–209.
9. Anderl JN, Franklin MJ, Stewart PS. Role of antibiotic penetration
limitation in Klebsiella pneumoniae biofilm resistance to ampicillin and
ciprofloxacin. Antimicrob Agents Chemother 2000;44(7):1818–1824.
10. Uckay I, Pittet D, Vaudaux P, et al. Foreign body infections due to
Staphylococcus epidermidis. Ann Med 2009;41(2):109–119.
11. Kjoller K, Holmich LR, Jacobsen PH, et al. Epidemiologic investigation
of local complications after cosmetic breast implant surgery in Denmark.
Ann Plast Surg 2002;48(3):229–237.
12. Persichetti P, Giovanni Lombardo GA, Marangi GF, et al. Capsular
contracture and genetic profile of ica genes among Staphylococcus
epidermidis isolates from subclinical periprosthetic infections. Plast
Reconstr Surg 2011;127(4):1747–1748.
13. Virden CP, Dobke MK, Stein P, et al. Subclinical infection of the
silicone breast implant surface as a possible cause of capsular
contracture. Aesthetic Plast Surg 1992;16:173–179.
14. Tang SS, Gui GP. A review of the oncologic and surgical management
of breast cancer in the augmented breast: diagnostic, surgical and
surveillance challenges. Ann Surg Oncol 2011;18(8):2173–2181.
15. Thorne CH, Chung KC, Gosain AK, et al. Grabb and Smith’s Plastic
Surgery. 7th ed. Wolters Kluwer Health Adis (ESP); 2013.
16. Dancey A, Nassimizadeh A, Levick P. Capsular contracture—what are
the risk factors? A 14 year series of 1400 consecutive augmentations. J
Plast Reconstr Aesthet Surg 2012;65(2):213–218.
17. Oliveira WF, Silva PMS, Silva RCS, et al. Staphylococcus aureus and
Staphylococcus epidermidis infections on implants. J Hosp Infect
2018;98(2):111–117.
18. Bartsich S, Asherman J, Whittier S, et al. The breast: a clean-
contaminated surgical site. Aesthet Surg J 2011;31(7):802–806.
19. Flugstad NA, Pozner JN, Baxter RA, et al. Does implant insertion with a
funnel decrease capsular contracture? A preliminary report. Aesthet Surg
J 2015;36(5):550–556.
20. Antony AK, McCarthy CM, Cordeiro PG, et al. Acellular human dermis
implantation in 153 immediate two-stage tissue expander breast
reconstructions: determining the incidence and significant predictors of
complications. Plast Reconstr Surg 2010;125(6):1606–1614.
21. Barnsley GP, Sigurdson LJ, Barnsley SE. Textured surface breast
implants in the prevention of capsular contracture among breast
augmentation patients: a meta-analysis of randomized controlled trials.
Plast Reconstr Surg 2006;117(7):2182–2190.
22. Secinti KD, Özalp H, Attar A, et al. Nanoparticle silver ion coatings
inhibit biofilm formation on titanium implants. J Clin Neurosci
2011;18(3):391–395.
23. Caubet R, Pedarros-Caubet F, Chu M, et al. A radio frequency electric
current enhances antibiotic efficacy against bacterial biofilms.
Antimicrob Agents Chemother 2004;48(12):4662–4664.
24. Mangram AJ, Horan TC, Pearson ML, et al. Guideline for prevention of
surgical site infection, 1999. Hospital Infection Control Practices
Advisory Committee. Infect Control Hosp Epidemiol 1999;20(4):247–
278; quiz 279–280.
25. LeRoy J, Given KS. Wound infection in breast augmentation: the role of
prophylactic perioperative antibiotics. Aesthetic Plast Surg
1991;15(4):303–305.
26. Gallagher M, Jones DJ, Bell-Syer SV. Prophylactic antibiotics to
prevent surgical site infection after breast cancer surgery. Cochrane
Database Syst Rev 2019;9:CD005360.
27. del Pozo JL, Patel R. The challenge of treating biofilm-associated
bacterial infections. Clin Pharmacol Ther 2007;82(2):204–209.
28. Khan UD. Breast augmentation, antibiotic prophylaxis, and infection:
comparative analysis of 1,628 primary augmentation mammoplasties
assessing the role and efficacy of antibiotics prophylaxis duration.
Aesthetic Plast Surg 2010;34(1):42–47.
29. Yalanis GC, Liu EW, Cheng HT. Efficacy and safety of povidone-iodine
irrigation in reducing the risk of capsular contracture in aesthetic breast
augmentation: a systematic review and meta-analysis. Plast Reconstr
Surg 2015;136(4):687–698.
30. Hughes G, Webber MA. Novel approaches to the treatment of bacterial
biofilm infections. Br J Pharmacol 2017;174(14):2237–2246.
31. Gupta P, Vermani K, Garg S. Hydrogels: from controlled release to pH-
responsive drug delivery. Drug Discov Today 2002;7(10):569–579.
32. LeRoy J, Given KS. Wound infection in breast augmentation: The role
of prophylactic perioperative antibiotics. Aesthetic Plast Surg
1991;15(1):303–305.
33. Kaplan JB. Therapeutic potential of biofilm-dispersing enzymes. Int J
Artif Organs 2009;32(9):545–554.
34. Huyette DR, Simpson WA, Walsh R, et al. Eradication by surfactant
irrigation of Staphylococcus aureus from infected complex wounds. Clin
Orthop Relat Res 2004;427:28–36.
35. Lu J, Turnbull L, Burke CM, et al. Manuka-type honeys can eradicate
biofilms produced by Staphylococcus aureus strains with different
biofilm-forming abilities. PeerJ 2014;2:e326.
36. Graf R, Ascenço ASK, Freitas R da S, et al. Prevention of Capsular
Contracture Using Leukotriene Antagonists: Plast Reconstr Surg
2015;136(5):592e–596e.
37. Whitfield GA, Horan G, Irwin MS, et al. Incidence of severe capsular
contracture following implant-based immediate breast reconstruction
with or without postoperative chest wall radiotherapy using 40 Gray in
15 fractions. Radiother Oncol 2009;90(1):141–147.
38. Caubet R, Pedarros-Caubet F, Chu M, et al. A radio frequency electric
current enhances antibiotic efficacy against bacterial biofilms.
Antimicrob Agents Chemother 2004;48(12):4662–4664.
39. Planas J, Migliano E, Wagenfuhr J, et al. External ultrasonic treatment
of capsular contractures in breast implants. Aesthetic Plast Surg
1997;21(6):395–397.
40. Stoodley P, deBeer D, Lappin-Scott HM. Influence of electric fields and
pH on biofilm structure as related to the bioelectric effect. Antimicrob
Agents Chemother 1997;41(9):1876–1879.
CHAPTER 125

Breast Implant Illness: What We


Know Now?
STEVEN TEITELBAUM | PATRICIA MCGUIRE | ALLEN GABRIEL
HISTORY
Silicone breast implants have been in use for over half a century. At present,
95% of breast implants placed in breast reconstruction and 88% of breast
implants placed in augmentation mammaplasty are silicone implants, based
on most recent data from the American Society of Plastic Surgeons (1). The
safety of silicone implants has been well established through rigorous patient
follow-up in postmarketing approval studies (2–5). Nonetheless, the
controversy regarding a possible link between silicone implants and systemic
diseases, which originated in the 1960s, persists to this day. Currently
referred to as breast implant illness (BII), breast implant–related systemic
diseases are increasingly reported by patients and are fueled by social media.
Plastic and reconstructive surgeons must be prepared to discuss BII with their
patients. Our current understanding and knowledge of BII, clinical evidence
for BII (or lack of it), and management of patients seeking treatment for BII
are discussed and reviewed in this chapter.
WHAT IS BII?
The term BII refers to a myriad of symptoms experienced by women with
breast implants and which they believe are related to their implants. While
other medical diseases have had published descriptions in the medical
literature which detail signs and symptoms, laboratory abnormalities, and
diagnostic criteria, BII consists of 50 to 75 general somatic complaints. These
complaints are neither generated from medical publications that examined the
incidence of these entities in women with breast implants as compared with a
control population nor have they been shown to consistently improve after
implant removal. Rather the complaints appear to be generated without
scientific study and posted at the whims of the webmasters of various
websites. Figure 125-1 is an example of several lists of symptoms from
patient-run websites. It is notable that (a) the list of symptoms is different on
different web sites; (b) the symptoms are common maladies experienced by
all individuals—by women with and without implants as well as by males
and females; (c) the list includes opposite symptoms—for example, hyper-
and hypothyroid symptoms; (d) there are no subjective or objective testing
criteria for BII; and (e) no difference in the symptom complex is proposed
whether the implant is saline or silicone filled, smooth, textured, or
polyurethane. In essence, a patient has BII if they have any somatic issue that
they believe is due to their breast implants. There is/are no known
pathophysiologic explanation/s for these somatic symptoms.
It is extremely important to understand that breast implant–associated
anaplastic large cell lymphoma (BIA-ALCL) is not BII and BII is not ALCL.
The latter is a rare form of non-Hodgkin lymphoma that has been associated
specifically with the textured surface of breast implants (6), but not with the
breast implants per se. BIA-ALCL is a well-described entity and its existence
is not in question. It is also important to understand that BII does not include
rheumatologic/autoimmune disorders such as Sjögren syndrome, rheumatoid
arthritis, scleroderma, etc. These are diseases with established diagnostic
criteria, specific signs and symptoms, and a pathophysiologic mechanism. In
contrast, BII is a list of symptoms.
SILICONE IMPLANT AND SYSTEMIC DISEASE—IS THERE A LINK?

Early History
Although BII does not include rheumatologic/autoimmune disorders, the
notion for BII probably stems from the potential link between silicone and
autoimmune disease, which was first reported in 1964, soon after the
introduction of silicone implants into the market in 1962. Miyoshi et al.
reported connective tissue–like disease in two patients after exposure to
silicone-related substances during augmentation mammoplasty, which they
referred to as human adjuvant disease (7). An adjuvant is an agent that
stimulates the immune system in a nonspecific manner. Silicon dioxide
(silica; SiO2) is a known, potent adjuvant. Autoimmune-type syndromes have
been observed with silica; for example, the development of systemic sclerosis
in stone masons. The silicone in implants, however, is not the same
compound as silica.
FIGURE 125-1 BII symptoms reported on patient-run websites.

Silica is a naturally occurring mineral while silicone does not exist


naturally. Silicone is synthesized from silica. The latter is reduced with
methyl chloride and then hydroxylated producing polydimethylsiloxane
(PDMS; (CH3)2-SiO). Impurities such as antioxidants, dyes, accelerators,
and plasticizers are removed during processing of medical-grade silicone (8).
Silicone gel in implants is composed of cross-linked, polymeric chains of
PDMS monomers of varying lengths. Small amounts of impurities are known
to be present in silicone gel from the implant manufacturing process. The
clinical significance of these impurities is not known and whether they have
the potential to cause systemic diseases remains to be seen.
Since the first case report of Miyoshi et al. describing a possible link
between silicone implant and systemic disease, there are now more than 400
reports of various health conditions in association with breast implants (9).
Expert evidence reviews, including a 1998 National Science Panel Report
(10), the 1999 Institute of Medicine report (11), a 2001 U.S. Federal Court-
appointed National Science Panel Review (12), and a 2011 U.S. Food and
Drug Administration Review (13), as well as other reviews (14,15) have all
found no evidence to link silicone breast implants with an increased
incidence of systemic disorders. Of note, the most recent systematic review
by Balk et al. conducted in 2016, concluded that there is inconclusive
evidence for any association between silicone gel implants and long-term
health outcomes (16).
Recent Studies
Two recent studies, however, have now reportedly shown a potential
association between silicone implants and systemic disease. Watad et al.
performed a cross-sectional analysis of 24,651 silicone breast implant
recipients from an electronic healthcare database in Israel in 2018 and
compared this cohort with 98,604 age-matched controls without breast
implants (17). The database included up to 20 years of data on 2 million
members, representing 25% of the Israeli population. Compared to women
without breast implants, women with breast implants had a higher relative
risk for any autoimmune/rheumatic disorder. The risk was highest for Sjögren
syndrome, systemic sclerosis, and sarcoidosis. The authors concluded that
silicone breast implants seem to be associated with a higher likelihood of
autoimmune/rheumatic disorder diagnosis. However, no evidence of causal
effect was demonstrated in this study; this study also included women with
“known or suspected implants” in the implant cohort and the timing of
implant placement, whether before or after the patient developed symptoms is
also unknown.
In 2019, Coroneos et al. performed a retrospective cohort analysis of the
prospectively collected safety data from the FDA-mandated postapproval
studies of implant manufacturers (Allergan Inc. and Mentor Corp.) (18). Data
of almost 100,000 women followed over a 7-year period were reportedly
analyzed and compared with normative data. The analysis found silicone
implants to be associated with higher rates of connective tissue diseases,
including Sjögren syndrome, scleroderma, and rheumatoid arthritis.
This Coroneos et al. analysis, however, had major methodologic
shortcomings (19). The analysis was not based on raw data from the implant
manufacturers but rather on summarized data. There was protocol variation in
data collection between the manufacturers’ studies, which was not accounted
for. Moreover, data analysis was actually based on less than 34,000 patients
(8,437 Mentor patients and 25,219 Allergan patients) as opposed to the
almost 100,000 reported in the study as there was significant loss to follow-
up from both manufacturers’ studies. This limits the interpretation of the
study results. In addition, the Mentor data were patient reported while the
Allergan data were physician reported. The increased incidence of connective
tissue disorders was seen only in the Mentor study and not in the Allergan
study but the analysis tended to emphasize the smaller Mentor patient-
reported data, which is misleading. Further, the analysis failed to use a
matched-cohort design to control for confounding variables in the two study
cohorts as well as in the normative population cohort. Lastly, a 2017 report of
an interim analysis covering 5 years follow-up of the same datasets found no
increased risk of any connective tissue disease compared with national norms
or those with saline implants (20), which is inconsistent with the 7-year
analysis. The significant methodologic flaws, potential bias, and
inconsistencies in the Coroneos et al. analysis prompted the FDA to release a
statement urging the public and healthcare community to view the
conclusions from the analysis with caution (21).
SOCIAL MEDIA AND THE SPREAD OF MISINFORMATION
The lack of convincing scientific evidence has not deterred social media
groups from continuing to propagate a link between breast implants and
systemic diseases. The largest of these groups has over 100,000 members. A
review of posts from this group found that almost 50% of posts described a
symptom of BII (22). Further, in the setting of breast reconstruction, 81% of
posts mentioned dissatisfaction with their breast implants; of which 66%
were attributed to unexpected illness after implant placement and 58% to a
general feeling of being unwell. Another analysis of social media platforms
reported an alarming trend of including cancer or BIA-ALCL under the term
BII (23). Although spreading misinformation is not a crime but it is a
disservice to the public as it leads to undue stress and unwarranted
treatments. To abate the spread of misinformation, the scientific community
could start by educating patients who undergo breast procedures.
HOW TO MANAGE PATIENTS WITH BII?

Physical Examination
Patients with BII are genuinely distressed by their symptoms, which affect
their psychological and physical well-being. The approach to these patients
should, thus, be to first acknowledge their symptoms and offer guidance and
care. A physical examination should be performed to evaluate for capsular
contracture, infection, or other potential causes for breast issues. Medical
evaluation should be directed by patients’ symptoms, with breast imaging as
indicated. For example, serologic testing should be performed in those
presenting with symptoms suggestive of rheumatic or autoimmune diseases.
Many disorders can have similar symptoms to BII, such as vitamin D
deficiency and thyroid disorders. An effort should, thus, be made to
identifying underlying medical comorbidities and treating them, if possible.
Some patients, however, will have no underlying medical comorbidities or
risk factors.
Surgery
Patients with BII often present to plastic surgeons requesting implant removal
as well as removal of the surrounding capsule. They have concerns that the
surrounding capsule contains toxins, mold, or bacteria which contribute to
their symptoms. The so-called toxic substances that patients are concerned
about are the degradation products from implants subjected to extreme heat
or chemical dissolution that are posted on the FDA site by implant
manufacturers (Table 125-1) (24). BII advocates refer to this list of
byproducts as proof that implants contain toxic substances such as arsenic
and toluene. Patients should be educated about the origin of these substances.
Importantly, patients should be made aware that these substances are present
in minute amounts, that is, at undetectable levels or at levels less than those
found in drinking water (Table 125-2) (25,26). The concern regarding mold
appears to have originated from images of explanted implants that have been
left in a drawer where over time bacteria or mold present in the environment
have colonized the implants. Patients should also be educated that there is no
scientific evidence for the need for capsulectomy in the absence of
malignancy, although capsulectomy can be preferable in the case of a
ruptured gel implant.

TABLE 125-1 Heavy Metal Concentrations in Silicone Gel Implants


Patients have a right to have their implants removed and surgeons should
respect their wish. However, patients should be advised of the risks of
surgery and the possibility that their symptoms may not be resolved
following explantation or if they are resolved, it may be temporary. A
Canadian study has reported differing outcomes following explantation
depending on pre-existing disease (27). Patients with proven autoimmune
disease showed no improvement of physical symptoms or autoantibody levels
and went on to have a clinical deterioration following explantation. Patients
with documented rheumatic disease but no autoimmune disease were found
to have transient symptom improvement with a recurrence of symptoms at 6
to 12 months. Patients who did not meet diagnostic criteria for rheumatic or
autoimmune disease had a greater than 80% improvement in physical
symptoms and greater than 90% improvement in psychological well-being.
There are limited data as to whether symptom improvement in patients with
no documented autoimmune disease is temporary or permanent. A
prospective analysis of patients undergoing silicone breast implant
explantation showed a decrease in musculoskeletal symptoms and bodily
pain, as well as an increase in vitality, mental health, and body area
satisfaction in these patients compared with control patients (28). However, 2
years later, 50% of the patients who had silicone gel implants removed
underwent implant replacement with saline or silicone implants, suggesting
that symptom improvement was subjective at least in half of the patients.

TABLE 125-2 Permissible Limits for Metals in Drinking Water


The concerns about toxins being present in the capsules has led to the
widespread belief among BII patients that the capsule and implant must be
removed “en bloc.” These patients believe that leaving any amount of capsule
behind, leaves the toxins from the implant behind and therefore their
symptoms will not improve. There is no indication for en bloc removal of an
implant capsule in the absence of malignancy, such as with BIA-ALCL.
There are plastic surgeons who are capitalizing on these fears and promoting
themselves as “en bloc experts” having special surgical skills that other
highly trained plastic surgeons do not have. These surgeons are promoted
within the BII community and they often post photographs of implants and
capsules that they have removed. This may represent a dangerous precedent
as patients come to plastic surgeons as a result of seeing these advertisements
and demand a specific operative procedure that may or may not be in their
best interest. Patients need to be educated on the potential risks of
capsulectomy, including a higher risk of hematoma and the potential for
pneumothorax in the case of a submuscular implant. Data from MD
Anderson Cancer Center indicate a 4% risk of pneumothorax with en bloc
resection for BIA-ALCL (29). This risk is justified in the presence of a
malignancy, but is it justified for a thin capsule from a smooth saline device?
Surgeons have to ask themselves this question and educate patients on the
risks and benefits of capsulectomy.
It is the authors’ belief that surgical decision making must be based upon
verifiable, empirical, peer-reviewed data. To be valid a scientific hypothesis
must be falsifiable. The philosophical grounding of classic logic theory
demands that the burden of proof in proposing BII as a new disease rests with
those proposing this new disease, not upon the “BII-skeptics” to prove that it
does not exist. Indeed, surgeons have been criticized on patient forums for
being skeptical about BII. This is anathema to good medicine because a
physician can be no greater than the suspicion with which they evaluate
diseases, drugs, and treatments. The Latin proverb “quod gratis asseritur,
gratis negatur” means “what can be asserted gratuitously can be denied
gratuitously” and the paltry of evidence supporting the existence of BII does
not need to be refuted through a vigorous challenge. Mathematics states that
if you multiple any number by zero that the sum is zero; the scientific validity
of a single anecdote is zero and even if there are a thousand anecdotes the
value remains zero. Nor does the number of “likes” on a social media post or
number of members of an online community lend any credibility to the
existence of an entity, as evidence by the hundreds of thousands of people on
a Facebook flat earth page and the countless “anti-vax” websites.

Insurance Coverage
There is ongoing debate about whether BII should be assigned a Current
Procedural Terminology (CPT) code. Women with implants who are
chronically ill believe that implants are causing their symptoms, that the only
cure is explantation, and that as a medically necessary procedure insurers
should pay for their explantation. But an ICD-10 code has never been given
to a disease that has not been proven to be a disease. Furthermore, surgeries
that have not been proven to cure a disease, are considered experimental and
usually not covered by insurance.
MOVING FORWARD
There are currently ongoing studies that are attempting to decipher the
possible causes for the systemic symptoms reported by patients. Immune
response to bacterial biofilms, an allergic reaction to a component of
implants, or an immune hyperreactivity inherent to the patient are some of the
possibilities that are being investigated. There is research that suggests that in
some cases BII may be a somatoform disorder.
Despite research efforts, it should be acknowledged that proving a
nonexistent disease is difficult. It is even more difficult in the case of BII
because there are so many and varied symptoms. Further, prospective studies
need to be performed with age-matched controls as the symptoms reported by
women with silicone breast implants also occur in women who have never
had implants. It is hoped that the ongoing studies will provide some answers
or at least guide further research. Convincing BII social media groups to
follow the science might be hard as it is not their preferred narrative; but,
properly performed scientific studies and patient education are the only way
to move the narrative forward.
CONCLUSION
The authors acknowledge that the symptoms reported by patients are real, but
a direct scientific link between the symptoms and breast implants is lacking.
There is, thus, a need for more scientific studies, but proving a negative is an
arduous task that will take a lot of time and resources.

REFERENCES

1. American Society of Plastic Surgeons. 2018 Plastic Surgery Statistics


Report. Available at:
https://www.plasticsurgery.org/documents/News/Statistics/2018/plastic-
surgery-statistics-full-report-2018.pdf. Accessed January 28, 2020.
2. Spear SL, Murphy DK; Allergan Silicone Breast Implant U.S. Core
Clinical Study Group. Natrelle round silicone breast implants: Core
Study results at 10 years. Plast Reconstr Surg 2014;133(6):1354–1361.
3. Maxwell GP, Van Natta BW, Bengtson BP, et al. Ten-year results from
the Natrelle 410 anatomical form-stable silicone breast implant core
study. Aesthet Surg J 2015;35(2):145–155.
4. Hammond DC, Canady JW, Love TR, et al. Mentor contour profile gel
implants: clinical outcomes at 10 years. Plast Reconstr Surg
2017;140(6):1142–1150.
5. Stevens WG, Calobrace MB, Alizadeh K, et al. Ten-year core study data
for Sientra’s Food and Drug Administration-approved round and shaped
breast implants with cohesive silicone gel. Plast Reconstr Surg
2018;141(4S):7S–19S.
6. K Groth A, Graf R. Breast implant-associated anaplastic large cell
lymphoma (BIA-ALCL) and the textured breast implant crisis. Aesthetic
Plast Surg 2020;44(1):1–12.
7. Miyoshi K, Miyamura T, Kobayashi Y. Hypergammaglobulinemia by
prolonged adjuvancity in man. Disorders developed after augmentation
mammaplasty. Jap Med J 1964;2122:9–14.
8. Luria LW. The role of medical grade silicones in surgery and its topical
applications. Operative Techniques in Plastic and Reconstructive
Surgery 2002;9(2):67–74.
9. Nanayakkara PW, de Blok CJ. Silicone gel breast implants: What we
know about safety after all these years. Ann Intern Med
2016;164(3):199–200.
10. Diamond B, Hulka BS, Kerkvliet N, et al. Silicone breast implants in
relation to connective tissue diseases and immunologic dysfunction: a
report by a National Science Panel to the Honorable Sam C. Pointer Jr.
coordinating judge for the Federal Breast Implant Multi-District
Litigation. Fed J Sci 1998.
11. Bondurant S, Ernster V, Herdman R; Institute of Medicine (US)
Committee on the Safety of Silicone Breast Implants. Safety of Silicone
Breast Implants. Washington, DC: National Academies Press; 1999.
12. Tugwell P, Wells G, Peterson J, et al. Do silicone breast implants cause
rheumatologic disorders? A systematic review for a court-appointed
national science panel. Arthritis Rheum 2001;44(11):2477–2484.
13. Center for Devices and Radiological Health, U.S. Food and Drug
Administration. FDA update on the safety of silicone gel-filled breast
implants—June 2011. Available at:
https://www.fda.gov/downloads/medicaldevices/productsandmedicalprocedures/impl
Accessed February 05, 2020.
14. Janowsky EC, Kupper LL, Hulka BS. Meta-analyses of the relation
between silicone breast implants and the risk of connective-tissue
diseases. N Engl J Med 2000;342(11):781–790.
15. Lipworth L, Holmich LR, McLaughlin JK. Silicone breast implants and
connective tissue disease: no association. Semin Immunopathol
2011;33(3):287–294.
16. Balk EM, Earley A, Avendano EA, et al. Long-term health outcomes in
women with silicone gel breast implants: a systematic review. Ann
Intern Med 2016;164(3):164–175.
17. Watad A, Rosenberg V, Tiosano S, et al. Silicone breast implants and
the risk of autoimmune/rheumatic disorders: a real-world analysis. Int J
Epidemiol 2018;47(6):1846–1854.
18. Coroneos CJ, Selber JC, Offodile AC 2nd, et al. US FDA breast implant
postapproval studies: long-term outcomes in 99,993 patients. Ann Surg
2019;269(1):30–36.
19. Colwell AS, Mehrara B. Editorial: US FDA breast implant postapproval
studies-long-term outcomes in 99,993 patients. Ann Surg
2019;269(1):39–40.
20. Singh N, Picha GJ, Hardas B, et al. Five-year safety data for more than
55,000 subjects following breast implantation: comparison of rare
adverse event rates with silicone implants versus national norms and
saline implants. Plast Reconstr Surg 2017;140(4):666–679.
21. Ashar B. Statement from the FDA Center for Devices and Radiological
Health on agency’s commitment to studying breast implant safety.
Available at:
https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm620589.htm
Accessed February 05, 2020.
22. Tang SY, Israel JS, Afifi AM. Breast implant illness: symptoms, patient
concerns, and the power of social media. Plast Reconstr Surg
2017;140(5):765e–766e.
23. Adidharma W, Latack KR, Colohan SM, et al. Breast implant illness:
are social media and the internet worrying patients sick? Plast Reconstr
Surg 2020;145(1):225e–227e.
24. U.S. Food and Drug Administration. Summary of safety and
effectiveness data. Available at:
https://www.accessdata.fda.gov/cdrh_docs/pdf2/P020056b.pdf.
Accessed February 16, 2020.
25. Wixtrom RN. Silicone breast implants and platinum. Plast Reconstr
Surg 2007;120(7 Suppl 1):118S–122S.
26. U.S. Environmental Protection Agency. 2018 Edition of the Drinking
Water Standards & Health Advisory Tables. Available at:
https://www.epa.gov/dwstandardsregulations/2018-drinking-water-
standards-and-advisory-tables. Updated January 27, 2020. Accessed
February 03, 2020.
27. Peters W, Smith D, Fornasier V, et al. An outcome analysis of 100
women after explantation of silicone gel breast implants. Ann Plast Surg
1997;39(1):9–19.
28. Rohrich RJ, Kenkel JM, Adams WP, et al. A prospective analysis of
patients undergoing silicone breast implant explantation. Plast Reconstr
Surg 2000;105(7):2529–2537.
29. Tevis SE, Hunt KK, Clemens MW. Stepwise en bloc resection of breast
implant-associated anaplastic large cell lymphoma with oncologic
considerations. Aesthet Surg J Open Forum 2019;1(1):1–12.
CHAPTER 126

Avoiding and Managing Patient


Dissatisfaction
CHRISTOPHER HOMSY | JOSHUA A. BLOOM | ABHISHEK CHATTERJEE
HISTORY
Restorative breast surgery, whether for cosmetic purposes or reconstruction,
can be a very challenging endeavor. Understanding a woman’s own image of
her breasts cannot be overemphasized. Plastic surgeons are trained to provide
patients with excellent patient care based on fundamental scientific
knowledge and evidence-based medicine, together coupled with sophisticated
technical skills acquired from many years of surgical training. One must
always remember there is never a “one size fits all” approach. At times, a
woman’s view of her breasts may not conform to the surgeon’s intricate
geometric analysis of dimensions and ratios. Patients’ expectations should be
recognized and noted preoperatively. Navigating these expectations will
dictate the postoperative level of satisfaction and avoid surgeon
disappointment, patient distress, and potential risk of litigation. This chapter
aims to provide plastic surgeons with a guide on how to manage the
dissatisfied “breast patient,” but more importantly, how to prevent it.
DEFINING A “SUCCESSFUL” OUTCOME
In short, a successful outcome should result in a satisfied, happy patient. The
surgical literature is abundant with evidence-based “outcomes papers.” These
studies usually compare different techniques or approaches of a surgical
problem and focus on the success of the procedure, mostly from a surgeon’s
standpoint. In breast surgery for instance, a “successful” outcome could be
defined as a healthy and viable autologous flap or reasonably symmetric and
soft breast mounds in implant-based reconstruction. Usually, these clinical
outcomes tend to be associated with a highly reproducible surgical technique,
as well as low complication rates, but do not thoroughly address the
outcomes from a patient’s perspective. More recently, there has been a shift
in outcomes reporting with the addition of “patient-based” parameters that
fall under the umbrella of what is now widely known as Patient-Reported
Outcomes Measures (PROMs). PROMs are defined as “any report of the
status of a patient’s health condition that comes directly from the patient,
without interpretation of the patient’s response by a clinician or anyone else”
(1).
PROMs add new variables to the equation of what constitutes a successful
outcome, such as body image, cosmetic satisfaction, decisional satisfaction,
and physical, psychological and sexual well-being, to name a few. A detailed
discussion of PROMs is beyond the scope of this chapter. However, plastic
surgeons are invited to be familiar with this fairly new concept, in order to
better assess their outcomes more accurately and improve overall patient
experience and outcomes.
BREAST SURGERY EFFECT ON BODY IMAGE
Women’s breasts play a central role in body ideals and self-esteem.
Worldwide, breast aesthetics have trended toward objectification of medium
to large breasts. Breast size–related dissatisfaction is found more commonly
in nations with smaller reported breast sizes. A recent survey of women from
40 different countries showed that only 29.3% were satisfied with their
current breast size. Several risk factors of greater breast size–related
dissatisfaction have been described: (1) body weight and appearance
discontent, (2) negative overall body image, (3) lower self-esteem, and (4)
poor breast awareness (lower breast self-examination frequency and
confidence in detecting breast change). Conversely, women with greater
breast satisfaction have increased breast cancer detection and early diagnosis
(2).
Breast reconstruction is an integral part of breast cancer treatment in
restoring quality of life. Reconstruction must result in satisfactory cosmetic
and psychological outcomes. Unfortunately, up to 40% of patients are
dissatisfied with the surgical reconstruction decision making (3). In oncologic
breast surgery, the “Breast-Q” is a tool used to assess patient perceptions
before and after breast reconstruction through quality-of-life measures
(psychosocial, physical, and sexual well-being) and satisfaction. With regard
to autologous postmastectomy breast reconstruction, Breast-Q scores are
highest with immediate breast reconstruction, while delayed reconstruction,
surgery failure, and conversion to another reconstruction technique all result
in lower scores (3). Pedicled or free abdominal flap reconstruction is
associated with the highest levels of cosmetic satisfaction and higher quality
of life (OR 1.1, p < 0.001) (4). In patient follow-up at 3 years after breast
reconstruction followed by radiotherapy, 8% are dissatisfied with their
cosmetic outcome. Not surprisingly, their dissatisfaction is independently
associated with decreased quality of life and body image. Moreover, these
dissatisfied patients scored higher on depression score questionnaires,
indicating the need for preoperative counseling and close psychosocial
follow-up (5). In patients undergoing oncoplastic surgery, which is defined as
a form of breast conservation where a large partial mastectomy defect is
reconstructed using volume displacement or volume replacement techniques
(6), PROMs have shown excellent results. Specifically, validated tools such
as Breast-Q (7) and the Nottingham Score (8) have demonstrated superior
patient-reported outcomes when oncoplastic surgery using volume
displacement reduction mammoplasty or mastopexy techniques were
compared to mastectomy and immediate reconstruction.
In the realm of cosmetic breast surgery, similar factors play into patient
satisfaction. Online reviews and word of mouth play an important role in the
selection of cosmetic breast surgeons. Per patient-reported online reviews of
breast augmentation procedures, good aesthetic outcome was the most
important for patient satisfaction, but intangible factors including good
bedside manner, friendly/helpful office staff, listening, and answering
questions were also integral to patient satisfaction (9). Poor aesthetic outcome
for breast augmentation was related to asymmetry (60.9%) and malposition
(41.3%) in a majority of responses. Protective traits against patient
dissatisfaction also include setting realistic expectations, being proactive, and
accessibility of follow-up care (9).
UNDERSTANDING THE RISK FACTORS

Patient Expectations
Interviews of patients undergoing implant-based breast reconstruction have
identified that these patients may have inaccurate expectations despite
seemingly adequate preoperative teaching. Patients have poor understanding
of the postoperative appearance and physical outcome of reconstructed
breasts. Patients report that they are not prepared for the “unnatural”
appearance, loss of sensation, firmness, and the lack of breast movement of
the reconstructed breast. Inaccurate expectations can be corrected by realizing
that these are commonly reported areas of dissatisfaction and providing
preoperative education and taking care to fully explore patient expectations
(10).
Patient expectations have been recognized as an important predictor of
health outcomes. There is an intimate relationship between patient
expectations, satisfaction, and health-related quality of life. Women
underestimate their expected health-related quality of life and overestimate
the stigma of surgery (11). Research has identified four major themes that
form the basis of patient expectations in breast reconstruction and the Breast-
Q Expectations module. The first is women’s expectations about their
appearance and outcome of breast reconstruction surgery vary from realistic
and understanding that “your breasts aren’t going to be exactly the same
anymore,” to unrealistic as she expected her breasts to “actually look better.”
The authors often go to operative detail with the patient while stressing
realistic expectations by showing patients pre- and postoperative photos of
past patients undergoing breast reconstruction. These photos include not only
uncomplicated outcomes but also ones that needed revision so that patients
understand the risks involved in the surgical journey. The photos should also
include long-term follow-up images of the patient so that potential long-term
complications such as high-grade capsular contracture can be visually
understood by the present patient. The second theme is the psychosocial
impact of reconstruction, and within it there are three important subthemes:
coping, feelings about oneself, and sexuality. The third theme is the physical
impact of reconstruction, which included issues such as sensation in the
breasts and reconstructed nipples following surgery. Women were surprised
to have no feeling in their breasts, even if they were told in advance. The
final theme involved the process of care and recovery, including
complications, postoperative pain, and support from the medical team. Many
women were surprised how little time it seemed the medical team had
available to spend with them and listen to their concerns (11). Through
identification of these major themes influencing patient expectations, the
plastic surgeon can more readily counsel the preoperative breast
reconstruction patient and help them better understand what to expect and
guide them through the reconstructive process.
A large proportion of breast cancer survivors have unmet expectations,
primarily relating to their appearance. Forty percent of women who
underwent postmastectomy breast reconstruction reported their reconstruction
as worse than expected as compared to 25% who reported their
reconstruction as better than expected. Many women report that they did not
fully understand how the reconstructed breast might feel or look different
from their natural breast. Secondary to appearance-related concerns include
pain, discomfort, and unanticipated longer recovery time that contribute to
reconstruction dissatisfaction. Implant-based reconstruction patients reported
unanticipated pain and discomfort, primarily related to tissue expansion. As
discussed above, women’s overall knowledge related to breast reconstruction
is low highlighting a need for improved education and informed decision
making with postmastectomy breast reconstruction (12).
Breast augmentation continues to be one the most performed cosmetic
procedures with more than 300,000 surgeries according to the American
Society of Plastic Surgeons statistics report in 2018. The choice of implant
depends on many variables in order to achieve the desired size, shape, and
feel. The available implant options are almost innumerable. Breast
augmentation sizing is a key component in the preoperative patient
evaluation, and is directly proportional to patient satisfaction. Sizing
techniques have traditionally relied on simple methods such as placing
implant sizers into bras. More recently, the use of three-dimensional (3D)
technology has allowed for a more accurate planning and simulation of what
an augmented breast would look like postoperatively. Plastic surgeons
typically take a middle-of-the-road approach relying partially on a
measurement system and partially on the patient’s request. The most common
expressed fear by patients is that they will appear too big, but the most
common cause of dissatisfaction is that the patient believes the size of the
implant has not produced a full enough breast. 19.4% of patients wished to
have larger implants and 3.7% desired smaller implants at 12 weeks
postoperatively (13). Recent studies have shown that the use of 3D imaging
for breast augmentation was associated with an increase in accuracy in
predicting postoperative breast volume. The use of this technology, however,
is limited by cost and inaccurate measurements in ptotic breasts (14).
Alternative modalities that have been used to align patient expectations to
what the surgeon can offer have included requesting patients to bring in
photographs of breast forms that they would like to be similar to during the
preoperative visit (15) or the use of external sizers in the preoperative setting
(16) to have a reasonable idea of how much volume expansion is needed for
the augmentation.
The Impact of Social Media
Social media has become an outlet for patients to seek and share their
healthcare experience. Through an understanding of patient preferences, there
is an opportunity to improve healthcare delivery. Fifty-four percent of
patients on social media shared an experience. In one study, breast cancer
patients were much more satisfied with free flap reconstruction (satisfaction
with surgery, recovery, or outcome) than with implant-based reconstruction
(52% vs. 20%). Those who posted about free flaps (deep inferior epigastric
perforator, [DIEP]) reported a higher rate of side effects and numbness, while
those who underwent implant-based reconstruction reported higher rates of
infection, contracture, and implant failure, as main factors leading to
dissatisfaction. Social media posts and discussion pages allow plastic
surgeons to better understand patient expectations and experiences and guide
education, management, and support to enhance the patient relationship (17).
The role of social media is even more pronounced in the cosmetic world.
Plastic and cosmetic surgeons increasingly use platforms such as Facebook,
Instagram, SnapChat, and Twitter to publish their “before and after”
photographs to attract more audience and clientele. Commonly, the pictures
posted on social media tend to include the best possible results, and are at
times digitally edited or altered. This may lead to unreasonable expectations
and could result in an unhappy patient. The surgeon should make every effort
to educate women seeking cosmetic breast surgery that what they see on
social media is merely a representation and would not necessarily apply to
them. It is nonetheless helpful for the plastic surgeon to use photographs
provided by the patient of what they might consider an “ideal result,” as a
guide to optimize preoperative assessment and planning.
Lack of Informed Consent
With any surgical procedure, it is imperative to be able to adequately discuss
the risks, benefits, and alternatives with the patient. While we as surgeons are
able to very readily discuss these aspects of the procedure, we are less adept
at discussing the true meaning of these postoperative outcomes. What a
“complication” means to the surgeon may be very different to what the
patient considers as good or bad result. To the surgeon, a wound
complication may seem a “nuisance” that would “only” require dressing
changes, but to the patient, daily dressing changes or a wound VAC may be
quite distressing, not to mention expensive as it may take away from their
daily occupation. As such, the informed consent is not the act of signing the
document itself, but the actual process of education and understanding
documented by the consent. During the preoperative visit, it is the
responsibility of the surgeon to provide patients with an in-depth explanation
of the surgical procedure, alternatives, and risks associated with it.
Sometimes, this may require multiple visits and discussions to allow
appropriate time for questions to be answered before proceeding with an
elective procedure.
While there is no difference in aesthetic satisfaction when comparing
paternalistic and shared decision–making physician styles, general
satisfaction varies greatly. Compared to the paternalistic style, shared
decision making results in a much higher general satisfaction (69.3% vs.
38.9%). Therefore, communication style plays an integral role and has a
direct impact on patient experience, satisfaction, and quality of life. When
patients take an active role in their care using an informed or shared
approach, their overall satisfaction is much greater (18).
Recognizing the Psychological Factor
As mentioned above, many women are dissatisfied with their breasts at
baseline, and those who seek aesthetic breast surgery are no exception. To
make matters worse, breast cancer and breast reconstruction is a very
stressful life event and psychiatric disorders, including depression and
anxiety, are likely underrecognized and underestimated in this population.
Women undergoing breast reconstruction should have adequate family/social
support and coping mechanisms. Data has identified that 15.3% of
autologous breast reconstruction patients are diagnosed with a psychiatric
disorder preoperatively and 20.5% postoperatively. Trauma/stressor-related
disorders accounted for the majority of psychiatric disorders before
reconstruction, compared to depressive and anxiety disorders after breast
reconstruction (19).
Postmastectomy breast reconstruction results in better sexual function,
better body image, and less depressive symptoms as compared to mastectomy
alone. Among patients undergoing mastectomy alone, a higher frequency of
sexual dysfunction was correlated with higher education and lack of a marital
partner (20). However, other studies have demonstrated no difference
between total mastectomy, breast-conserving surgery, and breast
reconstruction in regard to depressive symptoms 1 year postoperatively. It
may be that the true benefit of breast reconstruction lies in the physical and
cosmetic realm rather than psychological, or that the full effects are not seen
until later in the postoperative period (21). Nevertheless, comorbid
depression in patients undergoing breast reconstruction was associated with a
higher incidence of pulmonary, hematologic, gastrointestinal, infectious,
wound, and venous thromboembolic complications. Thus, depression must be
effectively treated and optimized prior to breast reconstruction to ensure safe
and favorable outcomes (22). Quite often, social workers are part of the
breast cancer treatment team and they can also be leaned upon to help guide
patients through these stressful times that may exacerbate or create
depression and anxiety. Often, breast cancer support groups are available at
breast cancer centers, and these forms of group therapy help patients in their
journey. These resources are indispensable and should be used by the
reconstructive surgeon as part of the team approach for breast cancer
treatment.
One particularly important entity worth mentioning when discussing the
psychology of patients seeking aesthetic breast surgery is body dysmorphic
disorder (BDD). BDD is a psychiatric condition that presents as an impairing
preoccupation with a slight or imagined defect in one’s physical appearance.
Unlike normal appearance-related concerns, BDD preoccupations are
experienced as intrusive, difficult to resist, and hard to control (23). In the
general population, prevalence rates for BDD range from 0.7% to 2.4%.
These rates may underestimate the actual prevalence in the plastic surgery
population. For instance, 15.04% of cosmetic plastic surgery patients carry a
diagnosis of BDD (24). Psychiatric screening of this patient population may
be useful for improving overall patient satisfaction.

TABLE 126-1 Risk Factors for a Dissatisfied Patient


Patient Factors Surgeon Factors
Mental illness Poor communication
Personality disorders Unrecognized Body dysmorphic disorder
Low-self esteem Arrogance/overconfidence
Negative body image Lack of Informed consent
Unrealistic expectations False or unrealistic promises
MANAGING THE DISSATISFIED PATIENT
An unhappy patient should always be approached with empathy, honesty, and
patience. As discussed earlier, dissatisfaction can stem from one or more
factors, and it is the surgeon’s role to identify the source of this
dissatisfaction in order to handle it properly (Table 126-1). Every effort
should be made to listen carefully to the complaint(s) without interruption, no
matter how “minor” they would appear to be. Sitting down may be perceived
by the patients as a longer-lasting encounter. Removing distractions shows
that the surgeon acknowledges the patient’s concerns. An apology does not
imply an acceptance of any legal responsibility but can have a therapeutic
calming effect and may diffuse much of the patient’s negative emotions.
When medically indicated, offering a solution will facilitate the resolution of
the problem. For instance, if a patient requires a revision due to a
complication or a suboptimal surgical result, the surgeon’s fee may be
waived, with the understanding that there may be other fees including
anesthesia and facility fees that would still apply. Finally, if the patient is still
not satisfied or if the surgeon deems that the problem is beyond their surgical
expertise, it is then reasonable to offer and arrange for a second opinion. By
doing so, the surgeon is by no means abandoning their patient, but will still
strive to provide the best possible care and guidance.
CONCLUSION
Satisfaction is measured by the surgical result and its alignment to the
patient’s expectations. Whether for oncologic or cosmetic indications, it is
crucial to fully understand and document the expectations and concerns of the
breast surgery patient in order to minimize misinformation, misguidance, and
dissatisfaction. Plastic surgeons must also take into account the constraints
imposed by social media and the patients’ ease of access to information. An
ounce of prevention is worth many pounds of cure. The astute plastic surgeon
should be able to identify underlying pathologic psychosocial behaviors and
disorders that, if missed or overlooked, may lead to unfortunate
consequences.

REFERENCES

1. Sharma R, Shulman LN, James T. The future of quality improvement in


breast cancer: patient-reported outcomes. Am J Med Qual 2017;32:469–
471.
2. Swami V, Tran US, Barron D, et al. The Breast Size Satisfaction Survey
(BSSS): breast size dissatisfaction and its antecedents and outcomes in
women from 40 nations. Body Image 2020;32:199–217.
3. Ménez T, Michot A, Tamburino S, et al. Multicenter evaluation of
quality of life and patient satisfaction after breast reconstruction, a long-
term retrospective study. Ann Chir Plast Esthét 2018;63:126–133.
4. Juhl AA, Christensen S, Zachariae R, et al. Unilateral breast
reconstruction after mastectomy—patient satisfaction, aesthetic
outcome, and quality of life. Acta Oncol 2017;56(2):225–231.
5. Batenburg CT, Gregorowitsch ML, Maarse W, et al. Patient-reported
cosmetic satisfaction and the long-term association with quality of life in
irradiated breast cancer patients. Breast Cancer Res Treat
2020;179:479–489.
6. Chatterjee A, Gass J, Patel K, et al. A consensus definition and
classification system of oncoplastic surgery developed by the American
Society of Breast Surgeons. Ann Surg Oncol 2019;26(11):3436–3444.
7. Chand ND, Browne V, Paramanathan N, et al. Patient-reported
outcomes are better after oncoplastic breast conservation than after
mastectomy and autologous reconstruction. Plast Reconstr Surg Glob
Open 2017;5(7):e1419.
8. Kelsall JE, McCulley SJ, Brock L, et al. Comparing oncoplastic breast
conserving surgery with mastectomy and immediate breast
reconstruction: case-matched patient reported outcomes. J Plast
Reconstr Aesthet Surg 2017;70(10):1377–1385.
9. Dorfman RG, Purnell C, Qiu C, et al. Happy and unhappy patients: a
quantitative analysis of online plastic surgeon reviews for breast
augmentation. Plast Reconstr Surg 2018;141(5):663e–673e.
10. Sneil L, McCarthy C, Klassen A, et al. Clarifying the expectations of
patients undergoing implant breast reconstruction: a qualitative study.
Plast Reconstr Surg 2010;126(6):1825–1830.
11. Pusic AL, Klassen AF, Snell L, et al. Measuring and managing patient
expectations for breast reconstruction: impact on quality of life and
patient satisfaction. Expert Rev Pharmacoecon Outcomes Res
2012;12(2):149–158.
12. Steffen LE, Johnson A, Levine BJ, et al. Met and unmet expectations for
breast reconstruction in early post-treatment breast cancer survivors.
Plast Surg Nurs 2017;37(4):146–153.
13. Brown T. Patient expectations after breast augmentation: the imperative
to audit your sizing system. Aesth Plast Surg 2013;37:1134–1139.
14. Roostaeian J, Adams WP. Three-dimensional imaging for breast
augmentation: is this technology providing accurate simulations?
Aesthet Surg J 2014;34(6):857–875.
15. Pruzinsky T. Cosmetic plastic surgery and body image: Critical factors
in patient assessment. In: Thompson JK, ed. 2001.
16. Nava MB, Catanuto G, Rocco N. A decision-making method for breast
augmentation based on 25 years of practice. Arch Plast Surg
2018;45(2):196–203.
17. Ashraf AA, Colakoglu S, Nguyen JT, et al. Patient involvement in the
decision-making process improves satisfaction and quality of life in
postmastectomy breast reconstruction. J Surg Res 2013;184:665–670.
18. Tang SYQ, Israel JS, Poore SO, et al. Facebook facts: breast
reconstruction patient-reported outcomes using social media. Plast
Reconstr Surg 2018;141(5):1106–1113.
19. Becherer BE, Kamali P, Paul MA, et al. Prevalence of psychiatric
comorbidities among women undergoing free tissue autologous breast
reconstruction. J Surg Oncol 2017;116:803–810.
20. Archangelo SCV, Sabino Neto M, Veiga DF, et al. Sexuality, depression
and body image after breast reconstruction. Clinics (Sao Paulo)
2019;74:e883.
21. Zhang C, Hu G, Biskup E, et al. Depression induced by total
mastectomy, breast conserving surgery and breast reconstruction: a
systematic review and meta-analysis. World J Surg 2018;42:2076–2085.
22. Drinane JJ, Pham TH, Schalet G, et al. Depression is associated with
worse outcomes among women undergoing breast reconstruction
following mastectomy. J Plast Reconstr Aesthet Surg 2019;72:1292–
1298.
23. Phillips KA, Dufresne RG. Body dysmorphic disorder: a guide for
dermatologists and cosmetic surgeons. Am J Clin Dermatol
2000;1(4):235–243.
24. Ribeiro RVE. Prevalence of body dysmorphic disorder in plastic surgery
and dermatology patients: a systematic review with meta-analysis.
Aesthetic Plast Surg 2017;41(4):964–970.
SECTION IX

Final Considerations
127 Informed Consent: Medicolegal Considerations in Breast Surgery
128 Social Media for the Aesthetic and Reconstructive Breast Surgeon
129 Integrating High-Resolution Ultrasound Into Your Practice Including
Background, Ultrasound Basics, Current Studies, and Clinical
Applications
130 Perioperative Principles in Breast Surgery
CHAPTER 127

Informed Consent: Medicolegal


Considerations in Breast Surgery
NEAL R. REISMAN

Surgery of the female breast remains a high-risk area for medical malpractice.
While augmentation mammoplasty remains an increasingly popular surgical
procedure, the risk of malpractice liability appears to be increasing, with
complaints of scarring, capsular contracture, and improper size implants,
breast implant–associated ALCL, and breast implant illness, to name a few.
Although there are many methods to help reduce medical liability, patient
selection and the informed-consent process remain the best. In addition,
practice trends demonstrate failing loyalty and patient movement from
surgeon to surgeon. Risk management need not be a negative impact on the
practice. In fact, I believe that a well-presented and informative informed-
consent process is a good way to build and maintain a practice, create patient
loyalty, better understand patient expectations and recognize the
unreasonable patient, and fulfill legal requirements.
A medical malpractice lawsuit may arise from a variety of factors,
including failed expectations, negligence, warranty issues, and failure to
provide informed consent. Informed consent is not the patient-signed piece of
paper, but rather a process during which there is interchange between the
physician and his or her staff, the patient, and often her significant other. This
chapter addresses this process.
Informed consent is the process during which risks, hazards, alternatives,
and more information about a procedure are presented to the patient sufficient
to allow the patient to make an informed decision about proceeding with
surgery. The issues that require discussion in this chapter include the
standards for informed consent, what parties may participate in the informed-
consent process, methods to increase retention and understanding of this
process, sample inclusions in the informed-consent process, necessary
documentation in the medical record for informed consent, and the impact in
a medical negligence lawsuit.
STANDARDS FOR INFORMED CONSENT
What is required to achieve informed consent? There are two main national
legal standards for informed consent: the Reasonable Patient Standard and
the Reasonable Physician Standard. In addition, certain states have specific
added requirements, achieved through tort reform efforts, that must be
presented, understood, and agreed by the patient to protect the surgeon
against an informed-consent claim. The standards for informed consent
depend on the resident state. The majority of states require a Reasonable
Patient Standard. This standard establishes that sufficient information be
presented such that a reasonable patient can make an informed decision about
the procedure. A few states may still require the Reasonable Physician
Standard, in which information must be presented based on what a reasonable
physician would discuss, enabling the patient to make an informed decision.
The burden for informed consent will be one of these, following the practice
state.
The majority of states using the Reasonable Patient Standard permit the
patient to be interactive in the discussion process; however, the final
acceptance level is whether all necessary information has been presented to
the hypothetical reasonable patient sufficient to make a decision for surgery.
This should not be interpreted as all-available information required about the
procedure, but as necessary information for this hypothetical reasonable
patient to make an informed decision. One can rest assured that if a critical
fact is omitted from discussion and the patient develops that complication,
the patient will claim she never would have accepted the surgery had she
known that critical information. Many surgeons and risk managers suggest a
laundry list of complications and facts to cover during the informed-consent
process. My only concern is that such a list must be periodically updated to
avoid leaving out one additional necessary complication, because an
argument might be made that the surgeon intended to omit the added
complication: The physician was so complete in developing the list, he or she
must have intended to leave that one additional problem out for patient
discussion for fear she would never have consented to the procedure had that
fact been disclosed.
The Reasonable Physician Standard is somewhat easier to interpret. All
necessary information that a reasonable physician would discuss concerning
risks, hazards, alternatives, and no treatments concerning the procedure in
question must be presented. The argument with this standard may include
what has been described as “the battle of the experts.” One expert will state
he or she would have included more than what was provided, whereas the
other side supports what was done. It is important to understand what
standard applies to a given practice area(s) and that the physician develops a
system for informed consent to comply.
Last, some states, such as Texas, have legislated panel lists of procedures
that require specific state-approved consents. Texas, for example, has two
panels: Panel A, requiring specific informed consents, and Panel B, not
requiring specific disclosures. It is important to comply with these state
requirements because compliance may bar or prevent a claim for failure to
provide informed consent if documentation is provided that the specific
procedure and its risks were discussed and acknowledged following
legislative rules. These state-specific lists are intended to assist with tort
reform by preventing claims for lack of informed consent if panel lists are
acknowledged and required disclosures made.
WHO MAY PROVIDE INFORMED CONSENT?
The main responsibility for informed consent rests with those performing the
proposed procedures. The surgeon has the ultimate responsibility of
explaining to the patient the necessary ingredients of informed consent.
However, it is acceptable to develop a team approach to cover, explain,
demonstrate, or discuss aspects of informed consent. Often a nurse, patient
coordinator, or similar employee will add to and provide additional
information to the patient after the physician has discussed the surgery and
addressed the patient’s concerns. This approach may be established by a
variety of combinations. I am aware of practices that start with the nurse or
patient counselor providing the necessary information to educate the patient.
If the patient then chooses to proceed, the surgeon then has the responsibility
to discuss further detail and address expectations. I caution against relying
only on the office staff and personnel to provide all information. An
argument may be made that these office-based staff do not have privileges to
perform the surgery, have not been trained to perform these procedures, and,
in fact, have never done so. It ultimately falls on the surgeon to specifically
address what he or she will be performing on the patient. There are many
components in the informed-consent process that should be discussed. The
surgeon need not, and does not, have the duty to explain all to the patient.
The patient’s partner, boyfriend, spouse, or other is an integral part of the
informed-consent process. The partner may have ideas and goals different
from those of the patient. It is important to ascertain his or her views and how
the patient interacts with him or her. Critical issues include size, shape,
implant choices, and reasonable expectations. The patient will be influenced
by her partner, and all opinions are important as they relate to expectations.
Failed expectations are a major reason for medical malpractice lawsuits.
False or unreasonable expectations must be dispelled prior to surgery,
whether the opinions are held by the patient or her partner. Conflicts in
choices of the patient and her partner must be resolved. I am aware of
instances of the patient choosing too large an implant size solely based on
pressure from a boyfriend. The boyfriend leaves, and now the patient is very
unhappy about her result. It may be wise, with patient’s approval and
permission, to also involve the partner in the document signing. The team
approach will aid in an open discussion from all. Many partners will make
comments to the staff and not to the surgeon. Good communication among
the team members and alerting of the surgeon to suspected problems are
critical. The team approach assumes that someone will discuss and explain
necessary information as one’s state dictates. This team presentation lends
itself to the different learning styles necessary for patient education and
retention, as I now discuss.
COMPONENTS OF LEARNING INFORMED CONSENT
It has commonly been believed that only 35% of information actually
discussed is retained in the patient’s memory. Past cardiovascular video
recordings of informed consents demonstrated that less than 50% of what was
actually presented was retained by the listening patient. This may be old data
and not applicable today. Learning is a complex function based on many
factors, including visual effects, auditory input, and personalized information,
all brought together into some memory pattern. There are nine learning styles
that may be used to help people learn and retain more. The three main
learning styles are visual, auditory, and kinesthetic.
All three basic learning styles should be used when an informed-consent
program is developed. The visual learner requires some schematic or actual
photograph to process information. This fact may explain the lower retention
statistics of the past when only auditory learning was considered. Visual
learners require information that either verbally paints a picture or uses actual
drawings and other visual aids. The only concern is not to guarantee that the
patient will obtain the same result as shown. The photographic and visual aid
information may use patient pictures, sample implants, anatomy pictures, and
sizing charts as examples of visual aids.
The auditory learner requires the listened word for processing. Such
learners may not relate to a picture but listen intently to information
presented. The office should develop a good system to cover the necessary
information via this method of learning. If the surgeon, although a wonderful
technician, has difficulty communicating, another member of the team should
provide this important information. There should be a fluid discussion
allowing interaction and questions as the information is presented, processed,
and discussed.
The third learning style is that of the kinesthetic learner. Kinesthetic
learning requires some personal interaction and relationship between
information presented and the patient’s past or current experiences. This
learning style is the most difficult to develop and present. An example might
be for the multiparous patient seeking breast augmentation to remember
when her breasts were engorged during and after pregnancy. The size and
shape at that point may help her understand swelling and size issues with
breast augmentation. This information is something she can personally relate
to, and combined with visual aids and auditory information, her retention
should be much better than 35% to 50%.
The goal of informed consent is to enhance patient information and permit
the patient to make an informed decision once the necessary information is
presented. It is helpful to present information, often through a team approach,
that can be remembered and used in the decision process. In addition, the
practice will be enhanced by providing the patient an appropriate amount of
information presented in a concise fashion. The more all three learning styles
are used, the better informed and prepared the patient will be. An old adage
is, “If you tell something in advance that occurs, you are smart; if you tell
them the same thing after the event, you are making excuses.” It may be
important to develop a team to present information in all the three learning
styles. Not only is the patient’s retention improved, but also she will enjoy
the information being presented and it will increase her ability to make an
informed decision.
INCLUSIONS OF INFORMED CONSENT
The materials presented in informed consent for breast augmentation include
a variety of discussion points. This chapter is not intended to be a standard of
what exactly should be discussed. Rather, it should serve as a guideline for
topics that either a reasonable patient requires or a reasonable physician
deems necessary. There are patients who would rather not listen to all the
“bad” information, and they have that right. This, as well as the patient’s
acknowledgment, should be documented. However, most patients want to
have as much information as they can. The list that appears later in this
section may serve as a guide for the practitioner’s development in the
informed-consent process, with further in-depth discussions as needed. It
must be remembered that no warranties should be given, expressly or even
implied, that would increase liability and risk. The surgeon, patient, and
partner should all have realistic expectations. If the expectations cannot be
determined, it may be recommended to continue with the informed-consent
process until that goal is reached. Unfortunately, there are patients who never
reach the goal of an informed-consent process, and it is best to decline their
surgery demands.
Discussions initially focus on the patient’s history; general health; family
history, especially that of breast cancer; presence of breast disease; recent
mammogram; and any abnormal results. The history should elicit information
of connective tissue disease, psychological issues, psychiatric treatments, or
any other significant disease, either in the patient or in the family. There
should have been a complete breast examination noting breast masses, nipple
discharge, and other findings such as asymmetry and axillary pathology. My
discussions then are divided into general surgical risks and inherent risks of
any procedure. These include, but are not limited to, bleeding, infection,
incision and scar issues, anesthesia requirements, perioperative experience
such as lab tests, intravenous insertion, dressings, and the immediate recovery
period. Smoking should be discussed as general acceptance of potential
interference with healing and blood supply especially when mastopexy or
breast reduction is being considered. There may not be consensus about how
long to avoid nicotine (including patches and other nicotine reduction
devices), but it is relevant. A urine cotinine test can confirm the presence of
this breakdown nicotine product indicating recent nicotine use. The challenge
is there is now documentation against smoking in the medical record and it is
discovered either by cotinine test or other means the patient is continuing to
smoke. I would recommend delaying or canceling the surgery until such a
safe avoidance is reached. Further, documenting a higher complication risk
and then proceeding establishes your knowledge of the dangers of smoking.
Proceeding with surgery may further expose the practice as most believe
there is a fundamental duty of a physician to “protect” the patient. Arguably a
patient cannot consent to a negligent procedure, as the physician has that duty
to protect the patient. The combined surgery of implantation and mastopexy
continues to exhibit a higher complication rate. The more factors that affect
the outcome, should raise red flags to the physician about timing, procedures,
and patient preparation along with patient expectations. Such factors would
include smoking, prior breast reduction surgery, and massive weight loss, to
name a few.
The inherent risks of any surgical procedure should be presented as just
that, not specific to breast augmentation. There will be a scar with the
potential for nonhealing or bad scarring from any surgical procedure.
Bleeding can occur such that additional surgery may be required. Many
drugs, nutraceuticals, herbs, age management supplements, and aspects of
diet can affect bleeding. I give my patients a list of what to specifically avoid,
and they sign that they have received it. Infection can also occur. It may help
to further explain how to recognize infection and how it may be treated, as
well as the possibility of implant removal. Remote infection is also important
to discuss, and the patient should be requested to inform the physician of any
distant-area concerns. Some level of anesthesia is required. I usually discuss
anesthesia risks minimally and rely on the anesthesia department to fulfill
their legal obligations of informed consent. I do not want to become an agent
for the anesthesiologist. If anesthesia is chosen without an anesthesiologist,
the duty falls on the physician caring for the patient, namely the surgeon. The
experience of the surgery day is outlined, attempting to avoid surprises by
explaining what the patient will experience.
Financial issues should be fully explained and documented with the
patient’s acknowledgment. There should be a full disclosure of the future and
probably implant replacement costs, both within the first year and later. The
financial responsibility, as well as additional charges for pathology,
anesthesia, and facility fees, in addition to any surgical fees, should be
presented to and accepted by the patient. One should ask further about travel
plans, lifestyle habits, or work responsibilities that require an interruption in
care with the patient assuming too much activity too early. I believe this is
very important to ask about, and instructions about aftercare should be
indicated with specific avoidances that the patient accepts and acknowledges.
The next group of discussion issues consists of breast implant–related issues.
These include, but are not limited to, the following:
Choices and types of implants: saline, silicone, U.S. Food and Drug
Administration (FDA)-approved gel, and form-stable silicone when
approved by the FDA. There are specific risks associated with each
implant type
Surgical choices of implant position: submuscular, dual plane, subfascial,
and subglandular, each with specific risk and result issues
Incision choices, size determination, and patient dimensional
considerations: inframammary, areolar, transaxillary, and others, each
with specific risks and results. A discussion about sentinel node
evaluation possibly being affected by transaxillary incisions should occur.
The size of the incision used with silicone gel implants may be associated
with a higher rupture rate if difficult placement occurs
Capsular contracture: There is some evidence that preventive antibiotic
treatment for dental care and treatment of allergies that masquerade a
sinus infection or urinary tract infection theoretically lower the incidence
of capsular contracture
Implant deflation and rupture
Follow-up and mammography: magnetic resonance imaging issues
Pain and sensory changes
Fluid collection: seroma formation
Implant infection
Necessary future surgery
Silicone-related issues and the media
FDA guidelines
Future effects on breast tissue
Removal and the effect on breast shape and skin draping
Specific avoidances such as nipple piercing
A less than desirable result
Implants should be discussed referring to generations of implants, not a
generality about all implants. The implants of the 1960s and 1970s are quite
different than those available today either through adjunct FDA-approved
studies or manufacturer premarket approval application studies. An analogy
of cars may help the patient understand that problems during the 1980s do not
equate to problems in the 21st century. Most patients own a newer model car
and can imagine there is no relationship between their car and a 1978 car.
Implants are similar because the implant cover or shell is comprised of a
thicker material and a barrier shield has been placed to diminish implant
material leakage through the capsule.
Implant size issues are always a potential problem. Even using the three
learning styles noted earlier, patient interpretation may still prevent a clear
understanding of goals and expectations. The patient’s dimensions as to chest
width, breast tissue and skin thickness, chest height, and degree of ptosis may
be important to implant choice. The patient should be presented with
information that permits an understanding of why certain size selections are
appropriate and also why certain implant choices may not be appropriate.
Medical decisions, physician choices, and patient expectations usually lead to
implant choices. The choices available to the patient should be presented with
a discussion about the benefits and risks specific to each. Appropriate implant
choices can be discussed and shown, with selection assisted by the patient’s
goals and expectations. Examples include filling her bra with implant sizers
in an attempt to simulate her desired result or prompting her to remember her
shape during pregnancy. The dimensional measurements of the patient’s
breast width and thickness should have a great bearing on size choices.
Implant widths are accurate today, and the patient implant choices should
closely reflect the patient’s chest width. One must overcome the widely held
view that implant size is related to volume alone (i.e., cubic centimeters). It is
important to demonstrate the different implants and implant width compared
with the patient’s own measurements showing different volumes specific to
that breast width. Therefore, the patient should understand that volume (or
cubic centimeters) is not the only answer, especially when comparing present
and desired size, as well as results, to her friends.
Displacement of implants, nipple displacement, and the potential for future
surgery should be discussed. The patient should understand that certain bras
that specifically create cleavage by pushing the implants toward the midline
may permanently displace the implant, nipple, and pocket, requiring surgical
correction. It may help to use an image of a pyramid. When the base of the
pyramid moves in one direction, the tip or top moves in the opposite
direction. The implant base moves medially, and the top or nipple moves
laterally. Patients should understand their involvement in this and can
possibly avoid this complication.
Another patient concern group is those patients with a tall chest height and
breast position lower on the chest wall. It can be fraught with problems
attempting to “raise” the breast mound position higher on the chest. Some
surgeons believe they can accomplish this feat with skin-tightening
procedures, but skin stretches and the goal often fail; only now there are
evident scars that may or may not be in the correct place. Some surgeons
believe they can utilize acellular dermal matrices (ADMs) to create a sling to
hold the implant in position. While this may achieve the desired goal, there is
an added expense and such surgeries are not without additional complications
and recovery. A solution to help the patient’s desires might be the use of fat
grafting to create a smoother angle just above the breast and the appearance
of a higher contour. Be aware of this issue as it can lead to significant legal
issues. A further trap is the patient with a capsule contracture that has brought
the implant higher on the chest. Revisionary surgery is to treat the capsule
contracture (an inherent risk and not a complication). The result of effective
treatment usually allows the new implant to now be in the appropriate
position on the patient’s chest, which is often lower than it was
preoperatively and may cause patient complaints. The preop discussions
should make the patient aware of this issue and be well documented in the
record.
DISSATISFACTION WITH COSMETIC RESULTS
Dissatisfying results such as wrinkling, uneven sizes, implant shifting,
incorrect size, unanticipated shape, ability to feel implant, scar deformity,
irregular or raised scarring, and/or sloshing may occur. Careful surgical
planning and technique can reduce but not always prevent such results. For
saline-filled implants with valves, one might be able to feel the valves.
Repeated surgeries to improve the appearance of the breasts and/or remove
ruptured or deflated prostheses may result in an unsatisfactory cosmetic
outcome.
“THE $75,000 BREAST”
A new phenomenon is creating added risks for plastic surgeons. There are
patients who have had complicated results from breast augmentation. These
problems arise from improper size demands, repetitive capsular contractures,
or displacement reoccurrences, often leading to an excess of 10 surgeries to
“fix,” as the patient views her breast(s). These problematic patients frequently
have spent in excess of $50,000 to $75,000 over a number of years in an
attempt to reach “their” goals.
The surgeon who accepts the care of such patients without discussing their
prior problems and difficulty in complete repair faces added risks. Many
patients are still unrealistic about their goals. Many of these complicated
patients, despite having multiple failed attempts at correction, believe or are
led to believe “this” surgery will work. Possibly, the ego believes that “this”
surgery, as a new surgical approach, will be the answer. Imagine when yet
another failed attempt occurs, with added costs and resentment. The lesson to
be learned is to carefully assess what brought the patient to this level of
failure. Is it choice of implant, pocket dissection, thin skin and cover,
inadequate discussions and asymmetry, or combinations of these problems?
The surgeon and staff should be very careful to listen, discuss the difficulty
of complete repair, avoid the suggestion of a guarantee, and avoid becoming
yet another statistic in this patient’s issues. Attempts to divide the patient’s
presentation into components may help the patient understand how difficult
her goal may be. Possibly, the use of ADM materials may help with refining
the pocket to a more controllable one, as well as providing additional
thickness and contour. This will add additional expense, furthering the
patient’s frustration. Photographs and a discussion with the patient and family
are critical in advance of surgery to point out specific difficulties such as
wrinkling, asymmetries, and displacements. It also may be wise to outline the
need for yet another revision or second stage if necessary. The surgeon
should avoid any comments that create a warranty or imply that he or she has
all the answers and that obtaining the desired goal is reachable and can be
done with ease. This has become more important, as lawsuits are being filed
after an inherent risk such as capsular contracture or displacement such as a
double-bubble deformity. It appears that patient responsibility has taken a
smaller role than surgeon ability in the expectation of hitting a “home run”
every time. This has been seen even with well-documented informed-consent
documents.
FUTURE CARE
There should be discussion about future care that may be required or
suggested. This includes follow-up with the plastic surgeon, mammograms
when indicated, possible magnetic resonance imaging in the future to assess
the implant integrity, and the need for implant change. A strong case should
be made for breast self-examination, as well as an awareness of nipple
discharge and changes in feel and shape of the breast. There may be no
consensus, but many believe that dental prophylaxis with antibiotics may
help to reduce capsule contracture incidence. Future care discussions should
include follow-up appointments. The plastic surgeon is the proper physician
to inspect the breast and specifically be able to evaluate for breast implant-
associated anaplastic large cell lymphoma (BIA-ALCL), contractures,
displacement, additional tests such as ultrasound and aspiration of seroma
fluid if necessary. The added costs of such additional tests should be
discussed in advance. This surgery is seldom a “once and done” type of
procedure.
This list is not intended to be a standard that must be included in every
discussion with patients. The standards of informed consent are described
previously. The surgeon, patient, and partner should enter discussions
applicable to their state law. The patient usually dictates interaction and
understanding, and this is important before proceeding with surgery and
surgical choices.
DOCUMENTATION
The informed-consent paper is usually worthless other than to prove the
patient actually signed a piece of paper. The signature does not prove she
understands the information. It is necessary, however, in the present medical
malpractice climate to document what was discussed and, more important, to
document that the patient’s questions were answered and that she elects to
proceed as understanding what was presented. The medical practice must
comply with state law if it addresses informed consents and possible lists of
risks that require discussion and signature. There is no need to document the
entire consultation, because informed consent is the process of information
and understanding. The medical record is present to assist physicians in
caring for the patient, not as a legal proceeding. This is a major difference
between medicine and the law. There is often an argument that if an act is not
documented, it did not occur; however, we all know that many acts are
performed in the routine course of treatment that are not recorded. It is not
required to have that complete of a record. It is helpful for the medical
practice to have examples of what was shown to the patient, as well as her
signature on information acknowledging her understanding. It is also helpful
to include acknowledgment from her significant other. The spouse or
boyfriend may add many demands to the patient’s expectations. He is usually
involved at some level, certainly at home, if not in the medical office. It is
wise to encourage his presence during the consultation, and it may be
suggested to add a place for his signature so he also understands the risks and
elects to proceed.
IMPACT IN A LAWSUIT
Informed-consent issues have a definite impact in a medical malpractice
lawsuit. The defense of such a lawsuit may depend on what was told to the
patient-plaintiff and whether the surgeon acted within a standard of care. Too
often, a well-known and somewhat expected complication results in a
lawsuit. The main issues become whether the surgeon caused the
complication by substandard care and if the patient was informed of the
potential risks of such a problem. The informed-consent process can help the
defense by demonstrating to the jury that the complication was discussed and
understood by the patient. Therefore, documentation that this was discussed
and understood should exist. The mere signature on the informed-consent
paper may not be adequate to prove the patient understood the information.
The patient-plaintiff usually states that she would never have proceeded with
surgery if she had only known the possibility of the complication occurring.
The defense will usually present to the jury a highly magnified copy of the
patient-plaintiff paper acknowledging and accepting even the possibility of
death as an accepted complication, trying to show how unbelievable the
argument is that she would not have proceeded had she been aware of the
actual complication.
Informed consent is usually made an issue by the plaintiff, often to add
another allegation of substandard activity. Many medical malpractice suits
allege multiple complaints in addition to negligence. These additional
allegations include a lack of informed consent, privacy issues, breach of
warranty, and product liability, if a product is involved. A plaintiff strategy
may be to place significant pressure on the defendant for him or her to
request the insurance liability carrier to settle the suit up to the limits of the
malpractice policy. If that letter is sent, and there is a subsequent judgment
against the defendant surgeon in excess of the policy limits, the liability
carrier must pay the difference. This is called the Stowers doctrine. The
defense will receive allegations that are not covered by the doctor’s liability
policies, in addition to negligence and informed-consent issues, often solely
to create pressure for the doctor to settle. If there is truly a lack of
documented informed consent, an expert is not required. The patient acts as
an expert to express how she was never made aware of critical issues
necessary for her to make her decision. The defendant doctor must then refute
this allegation by testimony and the medical record. It does become a “she
said, he said” conflict. The more the doctor can present evidence and
testimony that these issues were covered, the better his or her defense will be
able to refute such allegations.
THE MEDICOLEGAL CONSIDERATIONS OF BREAST SURGERY
There is significant liability to all medical specialties from treating women of
breast cancer age. The alleged failure to diagnose or treat breast cancer
creates this problem. There is no difficulty in finding a plaintiff’s expert to
state that the breast cancer was present for years and missed on an
examination or on a mammogram. All involved may be culpable. The plastic
surgeon is in a unique position in this cause. Plastic surgery treats many
diseases and aspects of the female breast. Plastic surgeons often order
mammograms and routinely examine our patients. A legal duty is established
when we order a diagnostic test to ensure we refer the patient to a reputable
center. The second part of this duty is to check the result and follow-up with
the patient. There can be no miscommunication among patient, results, and
any specialists the patient may see.
A good method of protecting oneself when treating, consulting, or
examining a breast care–related patient is to document a number of important
facts. These may include the following:
A family history of breast disease
History of breast problems, biopsy, nipple discharge, and/or pain
Recent and past mammograms (if appropriate)
Self-examination techniques, with their importance taught and
emphasized
Examination documentation of skin, breast, nipple, and axilla
A log of diagnostic tests—when ordered, results, and patient notification
A log and collection of referrals, correspondence, and patient
correspondence
I have always given patients a copy of their lab, pathology, and radiology
results. There is a duty to provide acceptable care when treating patients.
Once you order something or comment on an issue, you should follow up and
complete what was started. In other words, if a mammogram is ordered,
obtain the results, give a copy to the patient, and comment on the result and
document follow-up. If you refer the patient to another specialist, send a letter
or document the telephone call, as well as follow up with documented
responses and treatment decisions. You can never eliminate liability, but you
can certainly diminish your exposure, especially in this high-risk arena.
Breast Implant–Associated ALCL: A rare observed cancer associated to
breast implants of a type of T-cell lymphoma. The FDA report of BI-ALCL
lists breast implant–associated lymphoma (BI-ALCL) is not breast cancer—it
is a type of non-Hodgkin lymphoma (cancer of the immune system). In most
cases, BI-ALCL is found in the scar tissue and fluid near the implant, but in
some cases, it can spread throughout the body. An individual’s risk of
developing BI-ALCL is considered to be low; however, this cancer is serious
and can lead to death, especially if not treated promptly. In most patients, it is
treated successfully with surgery to remove the implant and surrounding scar
tissue, and in some patients, also treatment with chemotherapy and radiation
therapy. Symptoms can be a mass within the breast pocket, capsular
contracture, and seroma formation around the implant. Early treatment of a
diagnostic evaluation of the fluid and removal of the implant and capsule
have resulted in resolution of this scenario. A major reason to encourage
patients for follow-up is to be able to recognize findings and procedure
appropriately. The discussion with patients about the association with
textured implants should be documented and the FDA has not recommended
removing textured implants in an asymptomatic patient. The financial issues
of such a workup should be discussed including ultrasound, cytology, and
other lab tests and consultations.
Breast Implant Illness: A poorly understood group of symptoms such as
fatigue, memory loss, rash, “brain fog,” and joint pain that can be associated
with breast implants has been reported. Investigations are ongoing to evaluate
these symptoms. This is listed in the FDA Systemic Symptoms of breast
implants article and is little understood. In 1999, the Institute of Medicine
cited that there was not sufficient evidence to implicate silicone implants with
systemic illness. Additional studies confirmed this but yet there are many
women believing such vague symptoms are directly caused by breast
implants. I would suggest listening to patients who believe this and not
attempt to dissuade them from their strongly held position despite the lack of
evidence. Some of these patients desire to remove their breast implants and
that is their right. There should be a careful and complete discussion with the
patient what they might look like if their goal is met. Perhaps extra skin,
additional scarring, lack of projection, and no resolution to their symptoms
can be some of what to expect. There should be a dialogue about the capsule
in the absence of an implant rupture. Should the capsule be removed or kept
to facilitate fat grafting in the future? Some patients are grateful you have
listened to them and have taken them seriously. Others are resentful when
their symptoms persist and now they have in addition lost their shape.
In summary, this chapter presents a discussion of informed consent for
breast augmentation and breast-related surgery. Informed consent, a process
and not the signed document, is an important component of patient care and
legal protection. It is complex, and there is no specific requirement that all
should abide by, but rather a lengthy discussion of the required components
to enable the patient and the surgeon to make an informed choice about her
proposed care. Surgery of the breast remains a high-risk medicolegal
exposure. There are safeguards outlined in this chapter that may help
practitioners deal with this added risk. Liability will never be eliminated, but
it may be reduced. A long-standing tongue-in-cheek comment is that if the
practitioner has no patients, office, or employees, they may be able to avoid
legal exposure.
CHAPTER 128

Social Media for the Aesthetic and


Reconstructive Breast Surgeon
SUBHAS C. GUPTA | SABA MOTAKEF | JEREMY CHIDESTER | SEEMA SUGANDH |
CASSANDRA DREW | CHANEL LEE | STACEY RODDICK | LAURA TOBING
HISTORY
Social media consists of internet-based applications that allow individual
users to create and share audiovisual content through online communities
known as social networks. The first social networks emerged in the form of
websites, such as GeoCities and Classmates.com, in the 1990s with broader
access to the internet. Over the years, social media has created dramatic new
ways by which we interact and engage with one another over the internet.
This social media phenomenon continues to grow dramatically. At the time
of this writing, there are 4.4 billion active internet users, and it is estimated
that the number of users increases by an average one million new users a day.
Today, the number of active social media users is estimated at 3.5 billion
users around the world, up 9% from 2018 (1).
By virtue of their ability to facilitate the dispersion of text, images, audio,
and videos while connecting individuals with similar interests, social media
applications have proven extraordinarily useful for reconstructive and
aesthetic plastic surgeons practicing in both academic and private practice
settings (2,3). Plastic surgeons were quick to incorporate social media into
their marketing practices; in 2011, our group reported that as many as 50% of
plastic surgeons in some markets regularly used social media to engage with
patients and promote themselves and their practices (4). Today, social media
use has become even more prevalent among plastic surgeons as these
applications have proven invaluable for: networking with colleagues;
educating and informing patients and the general public; disseminating
research; presenting novel surgical and nonsurgical techniques; and
marketing aesthetic and reconstructive plastic surgery practices (5).
While these applications have proven very useful, they also present unique
challenges to plastic surgeons. These applications are rife with potential
ethical, legal, and professional drawbacks (6). Despite these challenges, when
correctly executed, the opportunities for networking, sharing techniques and
ideas, and potential marketing return on investment (ROI) are second to none
(7). In a rapidly changing social climate, it is now virtually mandatory for
both academic and private practice reconstructive and aesthetic plastic
surgeons to embrace social media and routinely engage with patients and
colleagues on these platforms.
SOCIAL MEDIA PLATFORMS
A variety of different social media platforms exist today. Broadly, 13
different categories of social media have been described (8). These platforms
primarily differ in terms of the type of content they allow users to share and
the demographic that composes their user base. The social media platforms
most frequently used by plastic surgeons can be categorized as social
networks (Facebook, Linked In, Twitter), photo-sharing applications
(Instagram), video-sharing applications (YouTube, Snapchat), enterprise
social networks (RealSelf), and products/services review networks (RealSelf,
Yelp, Google). Many of the platforms frequented by plastic surgeons and
their clientele are consistently found among the most popular social
networks, by monthly active users (9). Each of these individual social media
networks can offer various advantages and disadvantages for plastic surgeons
practicing in different environments. These are summarized below.
Facebook
With over 2.2 billion monthly active users, Facebook (Menlo Park, CA) has
rapidly become the most popular social network in the world since it was first
established in 2005 (9). This application allows users to make a professional
profile or page for a plastic surgery practice through which photos, videos,
educational articles, news, and upcoming events and specials can be shared
with Facebook users who follow this page. Targeted advertisements can also
be generated to reach potential patients based on parameters such as age,
gender, location, education, and interests. As this platform has been online
for well over a decade, its user base has begun to age. According to 2018
data, only 27.2% of Facebook users were from the 25- to 34-year-old
demographic (10).
Instagram
Boasting 1 billion monthly active users, Instagram, a subsidiary of Facebook,
is an increasingly popular social network, especially among younger internet
users. According to 2019 data, 24.2% of Instagram users were from the 18- to
24-year-old demographic while 33.8% of users were from the 25- to 34-year-
old demographic (11). Data from May 2019 demonstrates that 56% of
Instagram users are female (12). This social media application is primarily
geared toward sharing photos and videos, making this application useful for
sharing before and after photos, advertisements, and video clips. Up to 10
photos can be shared in a single post. Videos are limited to 60 seconds;
however, videos can be up to 10 minutes long using Instagram’s IGTV
feature. Photos and videos can also be shared through Instagram’s “Stories”
feature. These videos become inaccessible after 24 hours. Like Facebook,
Instagram provides advertisers the opportunity to create targeted
advertisements (“wall photos” or “Stories”) based on location, interests, and
demographic data. Because of its heavy emphasis on photography and other
visual content and its popularity with a lucrative, youthful demographic,
Instagram has become an especially important social media application for
branding and advertising.
Twitter
Twitter (San Francisco, CA) is an online social network that allows users to
share photos, videos, and text known as “tweets.” Text posts must be under a
280-character limit while videos must be less than 140 seconds long. The
limits placed on character counts and video length make tweets a form of
“microblogging” by forcing users to make shorter, blog-type posts known as
“microposts” (13). While not as popular as Facebook or Instagram, this social
network still has over 300 million monthly active users. Twitter’s unique
format makes this application especially useful for sharing information real
time during live events. Because of this, this social media network has proven
popular for updates during medical conferences and meetings.
Although the vast majority of posts on Twitter regarding plastic surgery
are made by the general public (5), Twitter has proven especially useful for
plastic surgeons networking with fellow colleagues in plastic surgery and for
sharing research and educating and engaging with patients around the world.
For this reason, Twitter use has become especially popular with plastic
surgery journals seeking to share and publicize research and disseminate
publications (14). Not surprisingly, a recent study demonstrated a direct
correlation between the size of journals’ audiences on Twitter and article
Altmetric scores (15).
RealSelf
RealSelf (Seattle, WA) serves as both an enterprise social network for
aesthetic providers and patients and a product/services review platform for
patients that boasts 9.9 million monthly active users (16). Patients can visit
this website to research surgical and nonsurgical aesthetic treatments, find
aesthetic providers, ask questions, or read or leave reviews for their
providers. Participation in this website is free for patients. Aesthetic providers
can also participate on RealSelf through a free or paid profile. Basic
information about the aesthetic provider can be shared with patients, in
addition to before and after photos and other content. Providers can upgrade
their profiles by actively participating on this website (e.g., answering patient
questions or updating information on their profiles). Providers can also
increase their profile’s visibility and gain access to various profile metrics
with a paid membership. One major advantage of the RealSelf social network
is that it verifies the credentials of its providers. Providers on this page must
be board certified or board eligible. Providers can pay for “spotlights” that
can provide a significant boost to plastic surgeons’ search engine
optimization by using RealSelf’s page to boost providers’ profiles to the top
of search engine results. There appears to be more direct communication as
patients ask questions that receive detailed answers from multiple surgeons.
This communication is predicated on the advice to see a board-certified
plastic surgeon in person, and that the information presented is general, and
not specific, advice.
Snapchat
Snapchat (Santa Monica, CA) is a social media application that allows users
to share photo or short video messages known as “snaps.” Snaps can be
shared with contacts or can be shared publicly as a “story.” This application
has 49 million monthly active users (17). A fundamental feature of this
application is that photos and videos that are shared are only available for a
short period of time before they can no longer be viewed or accessed by the
recipient. As such, this app has limited use for plastic surgeons other than
short-term promotion. Snaps can be edited and personalized with a variety of
filters, virtual stickers, and even augmented reality objects. This application
is especially popular among a younger demographic and is currently listed as
the most popular social network among teenagers (18). As many as 78% of
U.S. internet users in the 18- to 24-year-old demographic reported using
Snapchat in a 2018 survey (19).
YouTube
YouTube (San Bruno, CA) is a primarily video-sharing social media
application that allows users to upload and share videos with the general
public. This application is useful for plastic surgeons sharing videos with
patients, colleagues, and plastic surgery trainees. Because of this, YouTube
videos tend to be more educationally oriented. A recent study suggested that
YouTube is the preferred source of educational videos among surgical
trainees preparing for cases (20); however, given the nonstandardized nature
of videos on this platform, discretion is advised (21). Although YouTube
does allow some opportunities for practice promotion, social media networks
like Instagram, RealSelf, and Facebook are better suited for these strategies.
PATIENT CONSENT
One of the most important elements of an ethical, professional, and
medicolegally sound social media strategy is informed consent. Posting
patient photographs on social media can present potential challenges with
regard to patient confidentiality and has the potential to violate the statutes of
the Health Insurance Portability and Accountability Act of 1996 if not
performed with appropriate informed consent. Ownership of patient
photographs is also a concern—once photographs are posted on social media
platforms, the physician (and patient) effectively lose exclusive copyright
ownership of these photographs (22). Explicit, written and verbal consent
should be obtained from patients before photographs with any identifying
imagery are taken and posted on social media (23). Patients should be fully
informed that their photographs will be posted on social media platforms.
Patients should have the ability to withdraw consent at any time (24).
Schoenbrunner et al. proposed an informed consent that allows patients the
ability to opt in or out of different uses of their photographs (6). This can also
be specifically adjusted to become an “opt in” style where patients are
required to specifically provide consent for each of the various social media
outlets/platforms according to the individual practice’s needs.
PROFESSIONALISM
Care should be taken to adhere to the professional standards set forth by the
American Society of Plastic Surgeons Code of Ethics when posting content
on social media (6). Sensationalism should be avoided in posts, and separate
personal and professional accounts should be maintained (25). Social media
should remain “expert driven and educationally based” (26). Posts should
present the surgeon and our specialty in a tasteful and professional manner.
Posts should be censored appropriately and care should be taken to follow
specific guidelines for nudity and other content for respective social media
networks. If graphic content is to be presented in an educational manner, it
should be preceded by a warning. As always, patient privacy and informed
consent remain a top priority. Any identifying piercings, jewelry, birthmarks,
or tattoos should be blurred appropriately. Any patient incentives to obtain
consent to share content on social media, monetary or otherwise, are
prohibited by the American Society of Plastic Surgeons Code of Ethics.
Buying followers on social media platforms or utilizing bots can be viewed
as false advertising and a breach of ethics (26). Patient care should never be
compromised in order to obtain or share content on social media.
GENERAL GUIDELINES FOR A SOCIAL MEDIA CONTENT MARKETING
STRATEGY
Broadly, we propose that posts on social media networks such as Facebook,
Twitter, and Instagram, which remain the most popular social media
networks utilized by plastic surgeons, should fall into several key categories
to create an organized and comprehensive social media strategy.
Patient Education
These posts include content that educates patients about specific procedures,
postprocedure care, or patient safety concerns. While self-promotion remains
a fundamental goal of plastic surgeons posting on social media, an emphasis
should be placed on educational content. Plastic surgeons can share content
on social media that can illustrate different surgical options for various
aesthetic or reconstructive problems, surgical and nonsurgical techniques, or
share information with patients and colleagues about different products and
devices. For example, many patients have connected with each other on
social media to discuss concerns regarding systemic symptoms that they feel
are related to breast implants in what is now known as “breast implant
illness.” Similarly, many plastic surgeons have turned to social media to
educate and inform patients about recent controversies surrounding breast
implant illness.
Research
Social media presents an important opportunity for plastic surgeons to share
research with colleagues. This may include plastic surgeons’ own research or
new, trending, or other pertinent research that patients may find useful in
understanding various surgical options or making informed decisions about
surgery. Research should ideally be presented in lay terms so that it is more
accessible to the general public. As an example, many plastic surgeons have
recently turned to social media to answer questions, share research, and
alleviate patient fears after the recent FDA black box warning on textured
implants.
Before and After Photos
Before and after photographs on social media allow plastic surgeons to share
cases representative of their own work and also provide the unique
opportunity to educate patients about outcomes that can be expected with
different aesthetic and reconstructive procedures. Care should be taken to
ensure that posts do not create unrealistic expectations for outcomes of
different procedures (27).
Specials
Plastic surgeons practicing in an aesthetic practice setting can utilize social
media to educate patients about specials for surgical and nonsurgical
procedures or products.
Events
Plastic surgeons can utilize social media to inform patients about practice
events such as an open house, educational events for patients, and online
question and answer sessions. In a more academic environment, plastic
surgeons can share content to promote upcoming meetings, courses, or other
academic events.
Practice Updates
Social media can be used to provide updates with patients about new staff,
changes to the practice location, and changes in the types of surgeries or
procedures offered. For example, posts might inform patients about a new
energy-based device for nonsurgical body contouring or skin tightening.
Evolus (Newport Beach, CA) has used social media effectively to engage
with potential patients and encourage conversion to its Jeuveau
(prabotulinumtoxinA-xvfs) neurotoxin through its #NEWTOX NOW
campaign by encouraging plastic surgeons to “Be social, unbox and share”
using the hashtag #newtox (28).
Personal
Although caution is advised when sharing personal posts on social media, if
performed in a tasteful and professional manner, these posts are a useful way
to familiarize patients with their surgeon, and can also be used as an avenue
for plastic surgeons to share unique or interesting skills or interests. A 2019
study suggested that “private” posts led to higher levels of engagement than
other categories of posts (29). Special care should be taken to maintain
professionalism when sharing personal content.
Patient Testimonials
This category of posts allows plastic surgeons to share testimonials from
previous patients with their followers on social media. These posts allow
plastic surgeons to promote themselves and their practice. Plastic surgeons
can repost content from product/services review platforms such as RealSelf,
Yelp, and Google onto social media platforms, such as Instagram and
Facebook, to reach a broader audience.
ETHICAL CONCERNS FROM SOCIAL MEDIA CONTENT

Patient “Ratings”
Social media has become a growing and vital resource used a business
directory service with crowd-sourced reviews for nearly all businesses and
healthcare professionals. Sites such as Yelp, Google reviews, Health Grades,
and WebMD allow patients and customers to search, rate, and read reviews
on businesses including plastic surgeons and medical practices.
Content found on these platforms may cloud patient perceptions. This
ability to create and share ratings online has immensely changed evaluative
judgments about medicine and its influence among the populace. Information
disperses rapidly on social media and can be valuable in making a plastic
surgery clinic’s brand or treatments well known. Patients can post their
excitement about their treatment, which can then generate favorable celebrity
status and interest. Moreover, it increases the likelihood that the patient
would be willing to continue with the same practice over comparable
practices with less desirable reviews. Conversely, negative reviews can
spread equally as fast because of the growing significance that consumers
have placed on online reviews over the last few years. By searching past
reviews from other consumers on popular forums such as Google or Yelp,
poor reviews can affect the reputation of a medical clinic. It can detract and
instill distrust in future patients. Therefore, negative reviews must be handled
in a delicate and constructive manner. The goal should be to use a negative
review as an educational tool and a display of compassion with a patient-
centered approach to medicine. For example, if a breast surgery patient posts
a negative review 5 weeks postop because of dissatisfaction with the results,
this grants the plastic surgery staff and/or surgeon an opportunity to turn this
into a positive learning experience by personally responding with helpful
information or reassurance regarding the healing process and timeline of
outcomes after the breast surgery. The providers’ response can also showcase
the plastic surgery community’s character and develop trust with their future
patients.
Ethical Boundaries
The context, content, intent, and presentation of social media posts should be
considered before publishing online. Acceptable publicity is usually centered
around medical and academic achievements, education, patient satisfaction,
and the specialty’s brand. However, social media can not only be a source of
advertisement and networking, but also a source of entertainment for the
viewers and followers. Because of the drive to be informative and endorse
one’s brand are some of the motivating factors to post more and gain more
followers, physicians may feel compelled to post or authorize posts that may
be conceivable violations of ethics. Generally, posts that demean the practice,
or show inappropriately graphic or unprofessional images should be avoided.
A common post seen on surgical social media such as the team photo at the
end of a case while the patient is still under anesthesia, or a video of a
surgeon dancing and appearing comedic while scrubbed in may not be
unethical, but do not reflect the profession favorably nor foster trust of the
patient.
Chandawarkar et al. break down the violations of social media use in
medicine into four categories: legal violations, professional violations, ethical
violations, and gray zone violations (30). Legal violations of social media
include postings on social media that violate HIPAA laws, breach patient
consent, infringe local laws and ordinances, or encroach federal trade
commission rules. Professional violations are posts displaying unprofessional
behavior, consumption of alcohol or drugs, breach in hospital policies,
offensive material, or poor training situations and outcomes. These types of
violations may result in disciplinary action. Ethical violations, on the other
hand, are not normally monitored or governed by policy or clear guidelines.
For example, most plastic surgeons consider it unethical if the medical office,
physician, or staff member is making the post gain notoriety at the expense of
the patient. These are posts that potentially increase the risk of the patient’s
life, such as prolonging anesthesia for filming or photographing pictures of
the team after the surgery. This is a violation because the focus is on the team
rather than proper care of the patient still under anesthesia. Hence, if social
media is inappropriately used, the consequences can produce an unfavorable
image against the medical practice and the medical community.
Personal Versus Professional Posting
There should be a clear separation between personal and professional social
media accounts. It is recommended that friends and followers of these
accounts should not overlap and the intent behind what is published on these
accounts should be scrutinized. If the purpose of a post is to advertise and
promote the medical office and encourage patient education, then it is
appropriate for a medical practice social media page. However, if the intent is
self-driven, then it should be on a private, personal account.
Risk of Unrealistic Expectations
Social media can also promote unachievable levels of beauty because of the
plethora of appealing, yet altered, imagery on television, movies, and in
advertisements. Models can be altered by filters and other software, but
people, under increased pressure and expectations, are encouraged to change
their bodies to look more like the idealized images portrayed. Platforms such
as Facebook, Instagram, and Twitter allow users to choose what content they
are “following” or “like.” Subsequently, the platform’s algorithm calculates
that content and constantly advertises it on the user’s feeds, which then subtly
influences the user’s perception of what is normal. Accordingly, social media
can act as a catalyst for body dissatisfaction.
Another feature of social media that helps to popularize unrealistic
expectations is anonymity. Anonymity allows comments and the sharing of
opinions that are normally deemed inappropriate, rude, or hurtful and are
usually withheld in public spaces without the barrier of a computer screen. As
there is no longer any fear of repercussion, judgment is easily expressed and
people become more aware of perceived physical flaws that may have not
been a concern prior to the post. The concern and intrusive thoughts of
perceived defects or flaws in one’s appearance due to comparison of oneself
to others on social media or the dissatisfaction with not appearing in real life
as one does using the filters of social media imaging may lead to body
dysmorphia and dissatisfied patients if not properly identified and educated
prior to surgery.
Conversely, enhancing one’s physical attributes and enhancing physical
attractiveness has been shown to have beneficial effects on personality and
interpersonal relationships. When patient’s receive positive feedback, and
social media has become in increasing steady source of this positive
feedback, the results of the feedback are internalized and produce beneficial
enhancements to self-esteem. The improvement in self-esteem occur when
the patient and those with whom the patient is sharing this experience, have
realistic expectations for the alterations achieved by surgery.
One of the most challenging tasks for a plastic surgeon is to correctly
interpret the patient’s expectations. These postoperative expectations have
historically been implicit and were rarely explicitly articulated by the patient.
Today’s patients commonly present for consultation with a series of social
media images of the outcome they desire. The benefit of clinical before and
after photos, is that of a standardized photo with the same angles, lighting,
and background to make before and after images a reasonable comparison.
When a patient comes in with a nonstandard Instagram image of a model and
requests a body shape like the person in the photo, factors unknown to the
patient are influencing the aesthetic of the model including the camera angle,
lighting, and software photo enhancements. Education around interpretation
of nonstandard images is of great importance in this setting to ensure
reasonable expectations.
CONCLUSION
The social media phenomenon has fundamentally changed the way plastic
surgeons engage with patients and each other, market their practices to
prospective patients, educate the general public about the specialty, and share
and disseminate research. Ethical and professional concerns will always exist
in this space, and it is crucial that plastic surgeons strictly adhere to a high
ethical standard when sharing content and connecting with patients on these
platforms. Despite these drawbacks, these social media platforms are now a
helpful platform to plastic surgeons. The social media landscape is changing
constantly and dramatically, and plastic surgeons should remain current with
these rapidly changing trends to continue to engage with social media safely
and effectively.

REFERENCES

1. https://datareportal.com/reports/digital-2019-global-digital-overview
2. Humphries LS, Curl B, Song DH. #SocialMedia for the academic plastic
surgeon-elevating the brand. Plast Reconstr Surg Glob Open
2016;4(1):e599.
3. Kuechel MC. Showcase your service: social media and marketing basics
in a dynamic, over-populated, mixed-message, and highly competitive
world. Facial Plast Surg Clin North Am 2010;18(4):533–536.
4. Wong WW, Gupta SC. Plastic surgery marketing in a generation of
“tweeting.” Aesthet Surg J 2011;31(8):972–976.
5. Branford OA, Kamali P, Rohrich RJ, et al. #PlasticSurgery. Plast
Reconstr Surg 2016;138(6):1354–1365.
6. Schoenbrunner A, Gosman A, Bajaj AK. Framework for the creation of
ethical and professional social media content. Plast Reconstr Surg
2019;144(1):118e–125e.
7. Gould DJ, Nazarian S. Social media return on investment: how much is
it worth to my practice? Aesthet Surg J 2018;38(5):565–574.
8. Aichner T, Jacob F. Measuring the degree of corporate social media use.
Int J Mark Res 2015;57(2):257–275.
9. https://buffer.com/library/social-media-sites
10. https://www.statista.com/statistics/398136/us-facebook-user-age-groups/
11. https://www.statista.com/statistics/248769/age-distribution-of-
worldwide-instagram-users/
12. https://www.statista.com/statistics/530498/instagram-users-in-the-us-by-
gender/
13. Kaplan Andreas M, Haenlein Michael. “The early bird catches the news:
nine things you should know about micro-blogging” (PDF). Business
Horizons 2011;54(2):105–113.
https://www.sciencedirect.com/science/article/pii/S0007681310001254
14. Asyyed Z, McGuire C, Samargandi O, et al. The use of twitter by plastic
surgery journals. Plast Reconstr Surg 2019;143(5):1092e–1098e.
15. Zhou JZ, Lemelman BT, Done N, et al. Social media and the
dissemination of research: insights from the most widely circulated
articles in plastic surgery. Plast Reconstr Surg 2018;142(2):555–561.
16. https://www.realself.com/dr/claimprofile
17. https://www.statista.com/statistics/545967/snapchat-app-dau/
18. https://www.statista.com/statistics/250172/social-network-usage-of-us-
teens-and-young-adults/
19. https://weareflint.co.uk/main-findings-social-media-demographics-uk-
usa-2018
20. Rapp AK, Healy MG, Charlton ME, et al. YouTube is the most
frequently used educational video source for surgical preparation. J Surg
Educ 2016;73(6):1072–1076.
21. Derakhshan A, Lee L, Bhama P, et al. Assessing the educational quality
of ‘YouTube’ videos for facelifts. Am J Otolaryngol 2019;40(2):156–
159.
22. Teven CM, Park JE, Song DH. Social media and consent: are patients
adequately informed? Plast Reconstr Surg 2017;140(5):770e–771e.
23. Rohrich RJ. So, do you want to be Facebook friends? How social media
have changed plastic surgery and medicine forever. Plast Reconstr Surg
2017;139(4):1021–1026.
24. Satyanarayana Rao KH. Informed consent: an ethical obligation or legal
compulsion? J Cutan Aesthet Surg 2008;1:3335.
25. Bennett KG, Berlin NL, et al. The ethical and professional use of social
media in surgery: a systematic review of the literature. Plast Reconstr
Surg 2018;142(3):388e–398e.
26. Ghavami A. Discussion: the ethical and professional use of social media
in surgery: a systematic review of the literature. Plast Reconstr Surg
2018;142(3):401e–402e.
27. Gutierrez PL, Johnson DJ. Can plastic surgeons maintain
professionalism within social media? AMA J Ethics 2018;20(4):379–
383.
28. https://www.marketwatch.com/press-release/evolus-accelerates-next-
phase-of-us-launch-of-jeuveautm-with-newtox-now-consumer-
conversion-program-2019-06-05
29. Klietz ML, Kaiser HW, Machens HG, et al. Social media marketing:
what do prospective patients want to see? Aesthet Surg J
2020;40(5):577–583.
30. Chandawarkar AA, Gould DJ, Stevens G. Insta-grated plastic surgery
residencies: the rise of social media use by trainees and responsible
guidelines for use. Aesthet Surg J 2018;38(10);1145–1152.
CHAPTER 129

Integrating High-Resolution
Ultrasound Into Your Practice
Including Background, Ultrasound
Basics, Current Studies, and Clinical
Applications
BRADLEY BENGTSON | MARK SCHAFER | SERENA CHASE | PATRICIA MCGUIRE
HISTORY
Recently, the U.S. Food and Drug Administration (FDA) issued a draft
Guidance Document (October 2019) with new recommendations on
screening patients for silicone gel breast implant rupture. Notably, the FDA
has accepted ultrasound as an alternative for screening asymptomatic patients
based on multiple studies and numerous plastic surgeon cited experiences.
The Guidance replaces the current FDA magnetic resonance imaging (MRI)
screening recommendations with a new protocol requiring that, for
asymptomatic patients, the first ultrasound or MRI should be performed at 5
to 6 years postoperatively, then every 2 years thereafter. For symptomatic
patients or patients with equivocal ultrasound results for rupture at any time
postoperatively, an MRI is recommended (1). These recommendations are to
be incorporated into both the physician labeling and the patient labeling for
silicone implants (Table 129-1).
BACKGROUND
Historically, MRI has been the radiologic “gold standard” for monitoring
silicone gel breast implants with 80% to 90% reported accuracy (2), but from
a practical standpoint, MRI is expensive, rarely covered by insurance,
cumbersome, inconvenient, and excludes patients secondary to retained metal
or severe claustrophobia. Additionally, published studies on MRI sensitivity
and specificity reveal significant variability with several studies challenging
the role of MRI as an effective screening tool in asymptomatic patients (3–7).
The majority of MRI studies have been in symptomatic patients versus
asymptomatic patients confirmed in surgery which may not correlate to the
asymptomatic cohort. As stated, “given these concerns, extrapolating the
existing MRI literature for screening asymptomatic women implanted with
newer devices (fourth and fifth generation) is problematic” (8). The true
incidence of silent rupture itself is unknown. To date, there is not a
standardized method of reporting verified rupture rates without implant
retrieval (3). Further, reported rupture rates vary significantly between
manufacturers, implant types, type of procedure, and method of patient
evaluation and actual patient follow-up in published studies is extremely
variable. New generation devices tend to be over 90% filled, have higher
cohesive fillers, and more uniform shells. El-Haddad et al. identified a 3.4%
(7/205 pts) rupture rate at 10 years in round silicone Sebbin implants (9).
Huemer et al. identified one implant rupture in 100 primary augmentation
patients in a 3-year study of Motiva Ergonomic devices (10). In a 10-year
study by Stevens et al., of 1,788 patients, the rupture rate of Sientra cohesive
implants was 8.6% across all cohorts, both round and shaped (11). Seigle-
Murandi, in a retrospective 12-year study of primarily Allergan devices,
reported a 3.3% rupture rate on MRI or other testing (27/809 patients),
however only 27/225 were confirmed by surgery with round textured
showing a higher rupture rate than shaped textured devices (12). Spear,
reporting on round smooth and textured Allergan implants, revealed a 13.0%
rupture rate in the MRI patient cohort although not all were confirmed by
surgery (13). Studying Style 410 shaped gel implants, Bengtson found a 1%
rupture rate 3 years in the implant core study which increased to 5.7% by
year 10 (14).
TABLE 129-1 Current Physician and Patient Silicone Breast Implant FDA
Labeling
Physician Labeling For asymptomatic patients, the first ultrasound or
MRI should be performed at 5–6 yrs
postoperatively, then every 2 yrs thereafter. For
symptomatic patients or patients with equivocal
ultrasound results for rupture at any time
postoperatively, an MRI is recommended.
Patient Labeling It is recommended that you have periodic imaging of
your silicone gel–filled breast implants to screen
for implant rupture regardless of whether your
implants are for cosmetic augmentation or
reconstruction. These recommendations do not
replace other additional imaging that may be
required depending on your medical history or
circumstances (i.e., screening mammography for
breast cancer). Even if you have no symptoms,
you should have your first ultrasound or MRI at
5–6 yrs after your initial implant surgery and then
every 2 yrs thereafter. If you have symptoms at
any time or uncertain ultrasound results for breast
implant rupture, an MRI is recommended.

As with other medical devices, silicone gel breast implants have a finite
life span. In general, rupture rates increase after 6 to 8 years of implantation.
Based on data from the FDA clinical trials of these implants, the 10-year
failure rate in primary augmentation for the MRI cohort is between 8.7% and
24.2% (15). Hillard, in a general implant review, found rupture rates from
1.1% to 35.4% looking at Allergan, Mentor, and Sientra devices at 6 years,
however the FDA and others have noted very low follow-up rates in some of
these studies. Hillard also reported an increase in implants less than 20 years
old beginning at 6 years with increases to 15% by year 10 after augmentation
giving many surgeons their foundation for reporting a lower rupture rate to 6
years and then increasing to about 1%/yr by 10 yearsX. Clinically apparent
implant rupture is reported in published literature to occur at rates up to 35%
or as low as 2% (16). However, since asymptomatic, the silent rupture rate in
the general population is unknown but suspected to be considerably higher
than the clinically apparent rupture rate. A 2018 postimplantation study of
nearly 100,000 patients found that such MRI surveillance occurs at a rate of
less than 5%, likely due to the prohibitive costs associated with MRI scans,
although much of this data was self-reported by the patient (17). While all
ruptures are silent, over time a rupture may result in secondary symptoms
including capsular contracture, deformity, pain, and nodularity if the silicone
spreads extracapsularly. Whether symptomatic or not, the FDA and the vast
majority of plastic surgeons recommend the surgical removal of the ruptured
implants.
Initial ultrasound studies in the 1980’s and 1990’s revealed less accuracy
but were limited by antiquated technology combined with early-generation
implant technology having less shell fill, thinner shells, and higher degrees of
implant wrinkling, capsular contracture, and shell failure (15,18–24).
Both high-resolution ultrasound (HRUS) technology advancements and
implant technology are now merging with more standardized stronger shell
thickness, increase implant fill volumes, and more cohesive fillers make for a
dramatic increase in the accuracy of HRUS technology decreasing both false
positives and false negatives. New higher-frequency ultrasound systems in
the 12 MHz to 18 MHz range are resulting in significantly higher accuracy
rates in many published studies and emerging plastic surgery experiences.
MRI and CT scans are a static snapshot in time, whereas ultrasound (or
HRUS) is a dynamic examination. HRUS has minimal to no cost to the
patient, is mobile, safe, painless, efficient, highly accurate, and may be
performed in a plastic surgeon’s office. In addition, suspected areas of shell
failure can be maneuvered to further elucidate and demonstrate any
suspicious areas. HRUS is also gaining data to show accuracy similar or
surpassing MRI scanning for silent rupture of silicone gel implants in the
office setting. In 2012, Bengtson and Eaves showed that surgeon performed
HRUS and radiologist-confirmed scans were 100% accurate in predicting
implant shell integrity in 29 of 29 imaged breasts confirmed at the time of
surgery in both symptomatic and asymptomatic patients (14).
Additionally, in a 2018 study, Bogetti found the sensitivity and specificity
of ultrasound were 90% and 80%, respectively while the MRI sensitivity and
specificity were 87% and 85%, respectively. The authors of this study
concluded that ultrasound evaluation may be the first-level examination in
case of suspicious symptomatic breast implant rupture (25). Further, Sieber
identified all raised anterior silicone breast implant reference marks in their
study of 69 patients (26). Finally, Rietjens in 2014 showed that the negative
predictive value of ultrasound when evaluating breast implants for ruptures
was 85%, meaning that in the case of negative ultrasound findings, MRI may
be avoided (27).
Brown has correctly noted, “the gold standard for finding out whether an
implant has ruptured is removal and examination of the implant” (3).
Recently, Salzman reported his experience with HRUS at ASAPS 2019
collected from May 2012 until November 10, 2019. He identified 82 patients
with fractured implants with 54 patients taken to surgery. He found 47
ruptured implants with 7 false positives. In addition, 62 patients read as intact
were intact with no false negatives. Sensitivity was 100%; specificity was
89%. Two false-positive implants were flipped upside down, 2 had gel
fracture with internal bubbles but intact shells were intact (false positive), and
the other 3 patients had grade 3–4 capsules with deep folds (28).
Also reporting at the American Society for Aesthetic Plastic Surgery in
2019, Bengtson presented his retrospective series determining the accuracy of
new HRUS systems on a variety of breast implant styles and shell types.
Over the past 16 years, consecutive patients were scanned with HRUS and
subsequently confirmed in surgery in 680 intraoperative patients looking at
shell failure. He reported 5 false positives and no false negatives found all in
first 300 patients, with no false positives or negatives in the last 380 patients
(Fig. 129-1A,B). In the work reported at ASAPS 2019, there were 5 false
positives, in patients with double-lumen implants, severe capsular contracture
or very old, underfilled highly wrinkled shells that are challenging to image
with any diagnostic method. An additional retrospective trial and a
nationwide prospective trial with a new HRUS system in over 40 sites
documenting shell surface, peri-implant fluid, and accuracy of shell rupture is
being initiated (29).
FIGURE 129-1 A: Study outcome terminology. B: HRUS—first 680 patients.
ULTRASOUND BASICS
For millennia, animals such as bats, dolphins, and whales have used sound to
avoid obstacles and detect prey. They make sounds that bounce off of targets
they are interested in, such as food, and they listen for the echoes. Based on
the direction of the echo and the time taken for its return, they can estimate
how to turn and how far to go. Scientists and biologists have only recently
begun to appreciate the sophistication of their techniques for creating,
focusing, receiving, and processing sound.
Medical ultrasound systems work on this same basic principle. An
electronic system generates a focused, pulsed sound wave, transmits it into a
patient, and then waits for the echoes to return. Since sound travels at a
known speed in tissue, the time between sending out the sound and receiving
it back can be converted into a distance. Based on the direction and depth of
the echo, the system converts the information into an image representing the
sound reflection pattern. Specifically, the system determines the time to a
specific received echo, and puts a corresponding bright spot on the image at a
depth corresponding to that time. The brightness of the spot matches the
strength of the received echo, so stronger echoes (from larger or more
prominent tissue structures) are brighter. The longer the time between
sending out the pulse and receiving the echo, the deeper the spot appears on
the image.
The specific components of the ultrasound system (see Fig. 129-2)
include: the imaging display and control console; the ultrasound unit itself
containing the electronics to generate and process the ultrasound signals; and
a transducer that converts electrical signals into sound energy and back
again. Depending upon the clinical requirements, ultrasound systems can be
as large as several hundred pounds, with multiple displays and transducers, or
small enough that the entire system is handheld. The basic ultrasound
imaging technology is called “B-mode,” and the image itself is called a B-
scan. More sophisticated systems not only produce images of tissue structures
but can also detect blood flow (30) or tissue stiffness (31) or provide three-
dimensional images (32). Irrespective of their specific design, all these
systems rely on some fundamental principles of ultrasound.
FIGURE 129-2 Components of an ultrasound system.

Ultrasound, or sound above the range of human hearing, is a vibration or


pressure wave, traveling through media. It is comprised of higher pressure
(compression) and lower pressure (rarefaction) regions that alternate as the
wave travels. The wave is therefore a form of mechanical energy. In order to
travel properly, there needs to be a continuous mechanical connection
between the source of the ultrasound (the transducer) and the imaging target
(tissue structures). Thus, ultrasound will not travel through air, and all
medical ultrasound scanning requires coupling gel in order to maintain good
mechanical connection.
Ultrasound is characterized by the frequency of the wave, that is, the
number pressure variations per unit of time. Diagnostic medical ultrasound
operates in the frequency range of 2 to 30 MHz, where Hz is cycles per
second. Ultrasound transducers are usually referred to by their operating
frequency, that is, “a 12-MHz transducer.” The choice of the transducer
frequency is critically important in ultrasound imaging, since the higher the
frequency, the better the resolution. This is because the frequency determines
the wavelength, which is the volume of space occupied by one wave. The
smaller this volume, the better the resolution, as the imaging system cannot
distinguish among targets that are closer together than the wavelength. Put
more formally, the frequency and the wavelength are related by the speed of
sound in tissue:

λ = c/f

where λ is the wavelength, c is the speed of sound as it travels, and f is the


frequency. As an example, at 1 MHz, the wavelength in tissue is about 1.5
mm, and at 10 MHz, the wavelength is 10 times smaller, or 0.15 mm. The
smaller the object to be detected or resolved, the higher the frequency
required. Thus, the tendency is to use higher frequency transducers to obtain
the best imaging performance.
However, higher resolution comes at a cost: the higher the frequency, the
greater the attenuation (loss of energy) in the wave. Energy loss can be
extremely high (bone) or low (amniotic fluid). For example, when imaging
through 2 cm of breast tissue, the attenuation is over 60× greater at 10 MHz
than at 1 MHz. So, the higher the frequency, the shorter the range of tissue
depth that can be imaged successfully. HRUS is generally classified as
having a frequency of 10 MHz or higher. This provides very high resolution,
but at the same time, only a limited maximum “penetration depth” in tissue of
5 to 6 cm, making it perfectly suited for imaging of breast implants, but not
for deep abdominal regions.
Another important concept for ultrasound imaging is reflection, since
images are formed from the echoes reflected back from tissue structures.
Reflection depends upon the difference in acoustical properties between
adjacent tissue regions. Specifically, the ultrasound energy reflected at an
interface between two tissues, for instance, between fascia and muscle layers,
depends upon the acoustic impedances of the two tissues. Acoustic
impedance, Z, is the product of the density (ρ) and the sound speed (c), which
in turn relates to the stiffness of the tissue. Most soft tissues only vary in
acoustic impedance by a few percent, so just a small amount of ultrasound is
reflected back and most travels through to deeper depths. Adjacent tissues
with larger differences in material properties will produce larger echoes, for
example, skin and air, or muscle and bone. The more ultrasound energy that
is reflected back, the less there is available to continue on to image deeper
tissue. A strongly reflective surface, such as bone, prevents sound from
passing more deeply, creating an “acoustic shadow” behind it. Because air
has an extremely low acoustic impedance, air gaps and bubbles essentially
block all ultrasound from passing through, so coupling gel is key to proper
imaging.
Conversely, because the interior of a breast implant is all a single,
homogenous material, there are no internal differences in acoustic impedance
and thus no reflections. Since there are no reflections, there are no echo
signals to process and display, and the interior of a normal breast implant will
appear completely dark or anechoic (literally, “no echoes”).
There is a relatively large difference in acoustic impedance between the
internal implant material and the implant shell, so the shell appears as a
distinct bright echo on the ultrasound image. The same is true for the
interface between tissue and the outside surface of the implant, again,
generally producing a distinct echo. The shell also provides a smooth,
relatively flat reflective surface, which further increases its reflectivity, much
like a mirror. This is called a “specular reflection.” Specular reflection from
the implant shell makes it distinctive and easy to find on an image, since it is
generally unlike any other structure in the body. However, the strong
reflections can cause spurious images, called image artifacts, to appear. In
addition, if the specular reflector is at an angle to the ultrasound beam, the
energy reflects off and away rather than back to the transducer, like looking
at a mirror that is angled. This causes the reflector to disappear from the
image, which is another type of artifact.
FIGURE 129-3 Schematic of linear array transducer, comprised of multiple
individual transducer elements. A group of array elements are fired together to
create a single ultrasound beam transmission, or “scan line.” Using different element
groups, lines are then scanned sequentially along the length of the array. This type of
scan produces a rectangular image on the screen.

With the basic concepts of frequency, wavelength, resolution, attenuation,


penetration depth, impedance, and reflection established, the next section will
describe the ultrasound transducer in more detail, since it is the direct
interface between the patient and the imaging system. After that, several
example images of intact and ruptured breast implants will be presented.
The ultrasound transducer is the vital link between the patient and the
ultrasound imaging system. It first converts electrical signals into vibrations
that create the ultrasound waves, and then does the reverse in order to capture
echoes from tissue interfaces. While there are several types of transducers
and scanning patterns, the most appropriate one for use in breast implant
scanning is the “linear array.”
As the name implies, this type of transducer is comprised of an array of
individual transducer elements, each acting independently, organized in a
linear fashion. Figure 129-3 is a schematic cross-section of the transducer,
showing the individual transducer elements within. By electronically
transmitting with and receiving from a group of elements, the transducer
creates an individual ultrasound “beam,” launched perpendicularly from the
transducer surface (see Fig. 129-3). By sequentially using adjacent groups of
elements, the beam can be swept or “scanned” from one end of the transducer
to the other. The full set of beams comprises a “scan” or image. With a linear
array, the beam scanning process produces a rectangular cross-sectional
image of tissue.
Timing patterns on transmission and delay patterns on reception can focus
the ultrasound beams at different depths. This is shown schematically in
Figure 129-4. The ultrasound beam is the narrowest at the focal location,
which provides the best discrimination of close targets and the best image
quality. Because of the wave nature of ultrasound, the closer the focus is to
the transducer, the tighter the focus, but the more rapidly the beam expands
beyond the focus.
The operator can adjust the depth of the focal location to get the best
possible image. It is also possible to have more than one focal point by
scanning once with one transmit focal depth, and then scanning again with a
second transmit focal depth. The two successive images are then combined
through image processing to produce a composite with optimal focusing over
a larger depth. The trade-off is that since two scans are required to produce a
single image, the number of images displayed per second (the “frame rate”) is
reduced by half.
FIGURE 129-4 Schematic representation of electronic focusing at different depths.
Focusing close to the transducer face produces a narrower beam in the focal region,
but the beam expands rapidly beyond that point. Focusing further away produces a
wider beam, but one that maintains focus over a longer depth.

A similar approach is used to receive the returning echoes, and the receive
focal location can be rapidly changed to match the progress of the ultrasound
wave as it reflects from deeper and deeper points in tissue. This is called
“dynamic receive focusing” and is generally standard with any current
ultrasound system.
The operator has several other imaging controls available to enhance the
resolution of an image, create a more uniform looking appearance, or reduce
the effects of artifacts.
In addition to setting the electronic focusing (to the position of the implant
shell, for instance), the user can set the transmit frequency. Higher
frequencies afford better resolution, but at the cost of less penetration into
tissue. The frequency control should, therefore, be as high as possible given
the depth to the target of greatest interest.
To compensate for the attenuation of the ultrasound through tissue, the
operator can increase the overall gain. Increasing the gain generally brings
out the appearance of the smaller, less reflective or more attenuating tissue
structures. This is different than the brightness control, which increases the
brightness of everything in the image.
Since the ultrasound beam is attenuated as it travels through tissue, echoes
from deeper tissue structures are naturally weaker than those from closer
structure. This would make the image appear brighter near the transducer (the
top of the image) than further away (the bottom of the image). To compensate
and make the image uniform throughout, the gain is increased as a function
of time. This is called “time gain compensation (TGC),” since time and depth
are related by the speed of sound. Because not all tissues have the same
attenuation, the user can adjust the TGC to produce a more uniform
appearance.
When there is a strong specular reflector in the image, as is the case with
the shell of an implant, there is possibility of a false image or artifact, caused
by reverberation or multiple echoes. This happens often while scanning
breast implants. Compounding the issue, the anechoic region below the shell
accentuates the appearance of the artifact. Figure 129-5 illustrates the source
of the problem. The ultrasound beam from the transducer passes through
tissue, creating echoes, until it hits the specular reflector (the shell) and a
strong echo is returned. This echo actually reflects off of the front surface of
the transducer and begins to travel back down from the transducer, again
producing echoes of the tissue between the transducer and the shell.
Most current systems optimize the imaging controls automatically
depending upon the application: implant, seroma or fluid, nerve blocks, etc.
So, let’s put all this science into action and look at some basic images of
breast implants and some common images encountered in silicone breast
implant imaging.
Figure 129-6 shows the general appearance of a normal, intact implant.
The top of the image corresponds to the skin surface where the transducer is
located. The total depth into tissue in this image is 30 mm. Just below the
skin line and above the implant is normal breast tissue. Depending upon the
location and the implant position, the overlying tissue is comprised of
glandular, connective, or muscle tissues. The brighter horizontal lines are
internal fascia and connective tissue layers. Muscles are easily distinguished
from glandular tissue due to their internal structure. Below the breast tissue is
the implant shell, which appears as a thin, double-line “railroad track.”
Different shell types, such as smooth or textured, present with slightly
different appearances. Smooth shells are visualized as a very smooth uniform
image while heavily textured shell surfaces show a more indistinct reflection.
In many instances, the capsule or acellular dermis or scaffold if present,
appears directly above the shell as a thicker bright line. The interior of the
implant presents no echoes and appears completely dark.
FIGURE 129-5 Illustration of source of reverberation artifact. Ultrasound from the
transducer (in blue) strikes and reflects from a specular reflecting surface back to
the transducer, where it reflects back down again (in green) and echoes back at a
later time. Because the system uses time to correlate to distance, these spurious
echoes appear deeper in the image. Note that the colors are for illustration only to
help match the reflected waves to the corresponding image.

FIGURE 129-6 Typical image of intact implant. Breast parenchyma tissue overlying
implant. Implant shell has “railroad track” (thin double line) appearance. Internal
region of implant completely dark (anechoic).

FIGURE 129-7 Example of acoustic shadowing artifact. Because of a lack of gel on


transducer at one location, a linear region below that spot is distorted and less bright
than the surrounding areas.

Figure 129-7 is an example of an acoustic shadow artifact, caused by a


region with insufficient coupling gel on the transducer. The artifact appears
as a vertical darkened band within the image. It is easily noticed and
corrected by applying more gel and continuing the examination with better
contact along with altering the angle of the transducer on the skin.
CASE STUDIES
Now that the basic concepts of ultrasound image generation have been
presented, the next section reviews some clinical applications. Along with
breast implant evaluation to determine intact verses ruptured devices, HRUS
is transformational in many aspects of plastic surgery practices including
ultrasound-guided seroma management, identification of deep fill ports, fat
transfer guidance, and many others (Fig. 129-8).
Surgeons that incorporate ultrasound effectively in their practices often
comment that they have difficulty remembering what their practice was like
without it. Ultrasound examination becomes an extension of the physical
examination and allows surgeons to: visualize deeper tissue planes; determine
if any fluid is present; better plan for surgery knowing if an implant is
textured or smooth; and most importantly, whether the implant shell is
ruptured or intact. It allows for better billing practices and time management
for plastic surgeons knowing what to expect in surgery. Surgeons are advised
to conduct an ultrasound examination of their revision patients directly prior
to surgery to better visualize and compare the ultrasound findings to the
clinical scenario. This is a distinct advantage that plastic surgeons have over
radiologists or technicians that do not have the benefit of breast implants in
situ.
FIGURE 129-8 HRUS plastic surgery applications.

One concern that surgeons have about bringing on ultrasound is their fear
that they may miss a rupture or misdiagnose an intact implant. There are
many reasons patients come to revision including size change, capsular
contracture, malposition repair, concurrent ptosis operation, or older implants
that patients want to have exchanged. A surgeon new to ultrasound should get
a confirmatory MRI before basing their decision about whether to take a
patient to surgery solely upon their reading of ruptured implant. It does take
time for surgeons to develop confidence in imaging with this technology.
There is a definite learning curve integrating HRUS into a practice, however
the majority of false positives and negatives will be early in the surgeon’s
experience, and will decrease as improved higher fill and more cohesive
implants are used.
Next are a number of patient presentations and case studies with
representative ultrasounds and their clinical correlation.

CASES
CASE 1

These HRUS images show 7-year-old round textured implants in a 45-


year-old female. Both her implants were scanned as intact which was
confirmed at surgery along with their associated capsules (Fig. 129-9).

FIGURE 129-9 Intact textured implants with thick capsules.

CASE 2

Bilateral ruptured 22-year-old smooth silicone implants on ultrasound


showing layered collapsed shell on ultrasound and during retrieval
method with bulb suction and adjacent capsules (Fig. 129-10).
FIGURE 129-10 Extracting a ruptured smooth walled implant.

CASE 3

This patient is a 38-year-old, 6 years postoperative from augmentation


with textured gel implants. She presented with 1 week of progressive
swelling of her right breast. Ultrasound-guided seroma aspiration was
performed in the office with removal of ∼60 cc of bloody fluid. All fluid
was negative for cytology and BIA-ALCL markers. Her HRUS is also
shown with 6-week clinical image following her initial aspiration with no
new or residual fluid (Fig. 129-11).
FIGURE 129-11 Fluid collection surrounding textured implant.

CASE 4

A 42-year-old 10 years status post augmentation with textured smooth


implants presented with swelling and pain in her right breast. Her
preoperative mammogram was normal. Her left breast was normal on her
preop HRUS and intraoperatively. Her right breast showed a ruptured
implant with extensive gel outside the shell but contained within the
implant capsule (Fig. 129-12).
FIGURE 129-12 Ruptured right and intact left textured implants.

CASE 5

This patient is a 39-year-old status post augmentation with shaped


cohesive gel implants who noticed increased softness of her right breast 8
years following surgery. She had an MRI and then presented where a
HRUS confirmed a probable rupture of her right breast implant
confirmed at surgery. Her left breast implant was intact on MRI and
confirmed on HRUS and at surgery (Fig. 129-13).
FIGURE 129-13 Ruptured right (A–E) and intact left (F–H) textured
implants.

CASE 6

This is a 54-year-old presenting 6 years following breast revision for


capsular contracture. Strattice ADM was placed following capsulectomy
on the right side along with bilateral implant exchange with high-profile
silicone implants. She presented just prior to this second revision surgery
with her left breast “just not feeling the same.” Both of her implants were
flipped and it was difficult to confirm that the abnormality in the shell
was the patch. Her ultrasound images and intraoperative findings are
shown (Fig. 129-14).

FIGURE 129-14 Intact smooth implant with acellular dermis.

CASE 7
A 42-year-old 15 years after breast augmentation with an intact textured
double-lumen gel implant. This is a real challenge and looks like a
collapsed implant shell into the internal implant cavity. It is very
important to visualize the implant shell at the surface to avoid reading as
a false positive. The patient also had a deep fold that can be smoothed out
easily with gentle compression, one of the major advantages of having a
dynamic verses a static test such as MRI or CT (Fig. 129-15).

FIGURE 129-15 Intentionally cut open internal double-lumen implant.

CASE 8

HRUS is also extremely effective to visualize and treat seroma and fluid
collections throughout the body such as this large abdominal seroma
following a standard lipoabdominoplasty versus what true internal
closure of tissue looks like on ultrasound following the use of a new
internal closure device with multiprong manifold (Fig. 129-16).
FIGURE 129-16
CONCLUSION
Now is the time for the plastic surgeon community to embrace and integrate
ultrasound technology into their practices, and learn how this technology may
be utilized to screen for breast implant issues for the benefit of their patients
and practices. Ultrasound screening for breast implant rupture does not
require a radiologist’s interpretation, just basic familiarity with ultrasound
concepts, sufficient hands-on training on the part of the surgeon or their staff,
and repetitive clinical use. Many surgeons have found that it quickly becomes
a part of their extended physical examination. Since plastic surgeons are
intimately familiar with the specific anatomy of the breast, the physical
construction of breast implants, and the nature of implant ruptures and
clinical complications, they are uniquely qualified to leverage basic
ultrasound capabilities for screening purposes. Learning to image shallow,
well-defined targets such as breast implants is rapid because the relationship
between the ultrasound image and the implant is very intuitive, and a routine
screening examination can be done in just a few minutes and incorporated
into your routine postoperative visits. Breast implants present a relatively
straightforward ultrasound imaging situation: (1) they are very distinct from
the surrounding tissue; (2) their general appearance is consistent in terms of
depth, location, brightness, and imaging characteristics; (3) ruptured implants
can be differentiated from intact ones because of the unique “image
signatures” of the shell and implant material; (4) unlike static MRI images,
ultrasound examinations are dynamic, and specific physical manipulations
may be done during the examination to confirm questionable findings such as
folds and creases. Everyone needs a new reliable screening tool for implant
screening for asymptomatic patients: the FDA needs it, implant
manufacturers need it, plastic surgeons need it, but most importantly our
patients need it. By far and away the best technology that is up to the task is
high-resolution ultrasound.

REFERENCES

1. US Food and Drug Administration. Notice by the FDA Guidance


Document October 2019. Document citation 84 FR 57029; docket
number FDA-2019-D-4467; document number 2019–23197. Available
online at: https://www.federalregister.gov/documents/2019/10/24/2019-
23197/breast-implants-certain-labeling-recommendations-to-improve-
patient-communication-draft-guidance-for
2. Gorczyca DP, Gorczyca SM, Gorczyca KL. The diagnosis of silicone
gel breast implant rupture. Plast Reconstr Surg 2007;120(7 Suppl
1):49S–61S.
3. Brown SL, Silverman BG, Berg WA. Rupture of silicone gel breast
implants: causes, sequelae, and diagnosis. Lancet 1997;350:1531–1537.
4. Cher DJ, Conwell JA, Mandel JS. MRI for detecting silicone gel breast
implant rupture: meta-analysis and implications. Ann Plast Surg
2001;47:367–380.
5. Song JW, Kim HM, Bellfi LT, et al. The effect of study design biases on
the diagnostic accuracy of magnetic resonance imaging for detecting
silicone gel implant ruptures: a meta-analysis. Plast Reconstr Surg
2011;127:1029–1044.
6. Paetau AA, McLaughlin SA, McNeil RB, et al. Capsular contracture and
possible implant rupture: is magnetic resonance imaging useful? Plast
Reconstr Surg 2010;125:830–855.
7. Collis N, Litherland J, Enion D, et al. Magnetic resonance imaging and
explanation investigation of long-term silicone implant integrity. Plast
Reconstr Surg 2007;120:1401–1406.
8. Bengtson BP, Eaves FF. High-resolution ultrasound in the detection of
silicone breast implant shell failure: background, in vitro studies, and
early clinical results. Aesthetic Surg J 2012;32(2):157–174.
9. El-Haddad R, Lafarge-Claoue B, Garabedian C, et al. A 10-year
prospective study of implant-based breast augmentation and
reconstruction. Eplasty 2018;18:e7.
10. Huemer GM, Wenny R, Aitzetmüller MM, et al. Motiva ergonomix
round silk surface silicone breast implants: outcome analysis of 100
primary breast augmentations over 3 years and technical considerations.
Plast Reconstr Surg 2018:141(6);831e–842e.
11. Stevens WG, Calobrace MB, Alizadeh K, et al. Ten-year core study data
for Sientra’s Food and Drug Administration-Approved round and
shaped breast implants with cohesive silicone gel. Plast Reconstr Surg
2018;141(4S);7S–19S.
12. Seigle-Murandi F, Lefebvre F, Bruant-Rodier C, et al. Incidence of
breast implant rupture in a 12-year retrospective cohort: evidence of
quality discrepancy depending on the range. J Plast Reconstr Aesthet
Surg 2017;70(1):42–46.
13. Spear SL, Murphy DK. On behalf of the Allergan silicone breast implant
U.S. core clinical study group. Natrelle round silicone breast implants:
core study results at 10 years. Plast Reconstr Surg 2014;133(6):1354–
1361.
14. Bengtson BP, Van Natta BW, Murphy DK, et al. Style 410 highly
cohesive silicone breast implant core study results at 3 years. Plast
Reconstr Surg 2007;120(7 suppl 1):40S–48S.
15. Rohrich RL, Adams WP, Beran SJ, et al. An analysis of silicone gel
breast implants: diagnosis and failure rates. Plast Reconstr Surg
1998;102:2304–2308.
16. Hillard C, Fowler JD, Barta R, et al. Silicone breast implant rupture: a
review. Gland Surg 2017;6(2):162–168.
17. Coroneos CJ, Selber JC, Offodile AC 2nd, et al. US FDA breast implant
post-approval studies: long-term outcomes in 99,993 patients. Ann Surg
2019;269(1):30–36.
18. Ahn CY. Comparative silicone gel breast implant evaluation using
mammography, sonography, and magnetic resonance imaging:
Experience with 59 implants. Plast Reconstr Surg 1994;94:620–627.
19. Di Benedetto G, Cecchini S, Crassetti L, et al. Comparative study of
breast implant rupture using mammography, sonography, and magnetic
resonance imaging: correlation with surgical findings. Breast J
2008;14:532–537.
20. Goodman CM, Cohen V, Thornby J, et al. The lifespan of silicone gel
breast implants and a comparison of mammography, ultrasonography,
and magnetic resonance imaging in detecting implant rupture: a meta-
analysis. Ann Plast Surg 1998;41:577–585.
21. Ikeda DM, Borofsky HB, Herfkens RJ, et al. Silicone breast implant
rupture: pitfalls of magnetic resonance imaging and relative efficacies of
magnetic resonance, mammography and ultrasound. Plast Reconstr Surg
199;104:2054–2062.
22. Chung KC, Wilkins EC, Bell RJ Jr, et al. Diagnosis of silicone gel breast
implant rupture by ultrasonography. Plast Reconstr Surg 1996;97:104–
109.
23. Caskey CI, Berg WA, Anderson ND, et al. Breast implant rupture:
Diagnosis with US. Radiology 1994;190:819–823.
24. Venta LA, Salomon CG, Flisak ME, et al. Sonographic signs of breast
implant rupture. AJR Am J Roentgenol 1996;166:1413–1419.
25. Bogetti P, Fraccalvieri M, Cappello F, et al. Novel decision algorithm
for the diagnosis of silicone gel breast implant ruptures. Eur J Plast Surg
2018;41:677–684.
26. Sieber DA, Stark RY, Chase S, et al. Clinical evaluation of shaped gel
breast implant rotation using high-resolution ultrasound. Aesthet Surg J
2017;37(3):290–296.
27. Rietjens M, Villa G, Toesca A, et al. Appropriate use of magnetic
resonance imaging and ultrasound to detect early silicone gel breast
implant rupture in postmastectomy reconstruction. Plastic Reconstr Surg
2014;134(1):13e–20e.
28. Salzman MJ. Update on high resolution ultrasound. Hot Topics and
Instructional Course. San Diego, CA: American Society of Plastic
Surgeons; 2019.
29. Bengtson BP, McGuire PA, Glicksman CA. Integrating High Resolution
Ultrasound into your practice. Hot Topics and Instructional Courses on
HRUS. New Orleans, LA: American Society for Aesthetic Plastic
Surgery; 2019.
30. Allan P, Baxter G, Weston M, eds. Clinical Ultrasound. 3rd ed. United
Kingdom: Elsevier Health Sciences; 2011. doi:10.1016/C2010-1-66391-
2.
31. Sigrist R, Liau J, El Kaffas A, et al. Ultrasound elastography: review of
techniques and clinical applications. Theranostics 2017;7(5):1303–1329.
32. Lutz HT, Buscarini E, eds. Manual of Diagnostic Ultrasound. 2nd ed.
World Health Organization; 2011. ISBN 978-9241547451.
CHAPTER 130

Perioperative Principles in Breast


Surgery
JOHN G. APOSTOLIDES
HISTORY
Perioperative management of the surgical patient is an essential component of
successful surgical and patient outcomes. The surgical result consists of more
than the operative procedure. In order to achieve safe, effective, and
successful surgical treatment, we must understand and implement the
appropriate perioperative management of each patient. The perioperative
period spans four time periods (preoperative period, intraoperative period,
immediate postoperative period, late postoperative period). The first time
period is the preoperative period which spans from the beginning of the
patient encounter to the time of anesthetic induction. Preoperative assessment
and optimization aims to determine appropriate surgical candidates and to
optimize patients who will be undergoing a surgical procedure. Risk
reduction begins in this preoperative period. Additionally, pain management
of the surgical patient can begin in this preoperative period with the goal of
minimizing inflammation and postoperative pain and reducing postoperative
opioid use. Intraoperative management aims to maintain the safe and optimal
surgical conditions and to complement the non–opioid-based pain
management. The immediate postoperative period consists of the period of
time from the completion of surgery and the application of the dressings, to
the sixth postoperative week when the patient no longer has physical
restrictions to their postoperative activity. This is a crucial time period which
starts with optimizing the healing and recovery, and continues with
restrictions and management to limit complications. The late postoperative
period begins after the sixth postoperative week, when patients begin to
resume normal activity. It is at this point in the surgical process where the
patient will begin to regain normal strength, range of motion, and function.
In this chapter we will break down the perioperative management of the
surgical patient into its various components (risk management, pain
management, incisional and soft tissue management, drain management,
antibiotic protocols, and recovery and restrictions). Understanding the
management of each component allows the surgeon and surgical team to
optimize the surgical and patient outcomes and maintain the highest levels of
patient safety.
THE SCIENCE OF POSTOPERATIVE WOUND HEALING
The specialty of plastic surgery is rooted in the fundamental understanding of
wound healing. Every surgical patient will undergo the various phases of the
healing process. By definition, the act of surgery creates controlled wounds.
Surgical management aims to allow for successful and optimal wound
healing. An understanding of basic wound healing principles and
fundamentals is essential to proper perioperative management. Wound
healing has been categorized into four phases, each an essential component of
successful healing. These four phases, 1) hemostasis, 2) inflammation, 3)
proliferation, 4) maturation occur and overlap along a time continuum. Any
deviation from the norm in any of these phases can result in delayed wound
healing and surgical complications. These complications can lead to
reoperation or failed surgical outcomes. Perioperative management of the
surgical patient is focused on optimizing, modulating, and controlling these
phases of the healing process (Fig. 130-1).
Hemostasis is the first phase of wound healing and is initiated at the time
of trauma, or surgically at the time of incision. This process is initiated by the
outpouring of blood and lymphatic fluid, triggering the extrinsic and intrinsic
coagulation pathways through activation of platelets (1). In addition to
clotting, aggregation of these blood products results in subsequent release of
growth factors and deposition of extracellular matrix. Platelet aggregation
leads to a releasing of adenosine 5′ diphosphate (ADP) resulting in a
clumping of platelets and initiation of thrombosis. This pathway is associated
with short-lived vasoconstriction. Vasodilation soon follows as the
inflammatory phase begins (2).
The inflammatory phase typically begins when the hemostasis process
takes place and last 3 to 6 days. Influx of white blood cells and thrombocytes
(polymorphonuclear leukocytes, neutrophils, monocytes, fibroblasts, and
endothelial cells) release mediators and cytokines which amplify the
inflammatory response. The purpose of this inflammatory phase is to build
off of hemostasis through chemotaxis and increased vascular permeability in
order to limit further damage, remove cellular debris and bacteria, and
stimulate cell migration. A significant component of this cell migration is
stem cell trafficking of mesenchymal stem cells (MSCs) to the site of trauma
or injury (3). Within this inflammatory phase, cell migration and activation,
when successful also lead to self-initiated termination of the inflammatory
process. Otherwise a prolonged inflammatory phase can lead to abnormal and
delayed wound healing (4).

FIGURE 130-1 Diagrammatic time table of wound healing.

The proliferation phase soon follows the beginning of the inflammatory


phase. At approximately 48 hours after initial trauma/injury, the proliferative
phase begins the process of tissue regeneration. Collectively, proliferation is
characterized by epithelialization, angiogenesis, granulation tissue formation,
collagen synthesis, and deposition. Fibroblasts begin to synthesize new
collagen and glycosaminoglycan. Wound stabilization begins with this newly
developed core of proteoglycans. Within 1 week of injury, this collagen
synthesis allows wound breaking strength to reach approximately 3% to 5%
of uninjured strength. Fibroblasts are dependent on adequate oxygen supply
for proper hydroxylation of proline and lysine residues to achieve normal
collagen production. Collagen, elastin, and the extracellular matrix are
dependent on these fibroblasts. Reepithelialization begins with keratinocyte
migration from the wound periphery and adjacent wound edges.
Neovascularization occurs through angiogenesis (formation of new vessels
from pre-existing vessels) and vasculogenesis (de novo vessel formation) (5).
Proliferation can continue for approximately 6 weeks and sets the stage for
the maturation process.
The maturation phase is the final stage in wound healing, it begins around
the third week, and can last up to 18 months. During this process, wound
tensile strength increases as initial type III collagen decreases from
approximately 30% to between 10% and 20% and type I collagen levels
increase. Wound contraction occurs due to myofibroblasts. Appropriate
wound healing during the maturation phase should result in quick healing and
minimally visible scars. The resulting strength of the healed wound should
attain 80% tensile strength at approximately 3 months (6).
This wound healing process, when successful and normal, should lead to
healed surgical wounds in approximately 6 weeks. This 6-week period in the
wound healing process directly correlates to postoperative management and
recovery time periods.
SURGICAL RISK REDUCTION
The process of surgical risk reduction begins in the preoperative period when
the surgeon determines a patient’s suitability and candidacy for surgery. The
most significant factor in ensuring successful outcomes and patient safety is
avoiding surgery on patients who are unsuitable for surgery due to risk
factors that cannot be, or have not been, reduced and eliminated. Surgical risk
reduction is achieved through management of surgical risk factors which
contribute to poor wound healing and or high surgical morbidity.
Perioperative risk reduction relies on cardiac management, smoking
cessation, diabetic/hyperglycemic control, nutritional management, and
venous thromboembolism (VTE) prophylaxis.
The importance of perioperative cardiac management in noncardiac
surgical procedures lies in the high number of surgical procedures performed
and associated cardiac complications. In these procedures, cardiac
complications account for half of all perioperative morbidity (7). Breast
surgery and reconstructive surgery are considered low-risk procedures
regarding cardiac risk. These types of procedures have less than 1% 30-day
cardiac event rates. Nevertheless, evaluation of patient-related risk factors is
essential. Thorough history taking and assessment of functional capacity will
commonly indicate patients that are at a higher risk. The inability to climb
two flights of stairs or run short distances indicates low functional capacity
and therefore higher cardiac risk. When functional capacity is high, surgical
prognosis is very good. Low–perioperative cardiac risk patients can undergo
low-risk surgical procedures such as breast surgery without further cardiac
workup (8). Intermediate- and higher-risk patients can have their surgical risk
factors evaluated using a validated risk prediction tool such as the American
College of Surgeons (ACS) NSQIP surgical risk calculator. This preventive
approach is pivotal and if warranted, risk-reduction strategies such as drugs
and/or surgery should be implemented.
Surgical risk reduction includes smoking and nicotine cessation. Nicotine
use has resulted in statistically significant increases in surgical risk. This
relates to both wound healing complications as well as surgical morbidity.
Cigarette smoke contains greater than 4,000 components, of which nicotine,
hydrogen cyanide, and carbon monoxide are the most damaging. The
vasoconstrictive effect of nicotine from a single cigarette has been shown to
decrease the blood flow velocity in a digital vessel by 42% (9). In addition,
nicotine increases platelet binding thereby increasing risk of thrombus.
Carbon monoxide has a 200-times greater binding affinity than oxygen
thereby decreasing oxygen delivery to the surgical wound and affecting
proper collagen synthesis. When compared to nonsmoking, smoking is
significantly associated with increased postoperative infection rates in all
types of surgery. Additionally in the setting of mastectomy, smoking is
associated with significantly higher risk of skin flap necrosis and
epidermolysis (10). Additionally, smokers and recent smokers have a
significant association with higher rates of postoperative pneumonia,
infections, and death in comparison to nonsmokers (11). Nicotine and
smoking cessation should occur prior to surgery. The longer the period of
cessation, the more significant the risk reduction, although there is no clear
recommended duration of cessation. Current plastic surgery
recommendations are for greater than 4 weeks of cessation pre- and
postoperatively.
Diabetic and hyperglycemic management in the perioperative period is a
significant factor in risk reduction and achieving successful surgical results.
Diabetes and associated hyperglycemia have deleterious effects on the entire
body and specifically wound healing. Hyperglycemia can result in protein
and enzyme dysfunction. Chronic diabetes is associated with macrovascular
and microvascular disease, which can result in decreased oxygen levels and
decreased blood flow (12). The results are impaired wound healing.
Additionally, the effect of surgical procedures, anesthesia, and postoperative
healing can affect glycemic levels in the body and make glycemic control
more challenging and even more crucial. Surgical stressors can result in
increased cortisol and catecholamine levels which decrease insulin
sensitivity. In addition, the sympathetic response can decrease insulin
secretion (13). These effects make tight glycemic control more challenging.
Anesthetic agents can also affect glycemic levels, commonly by causing
hyperglycemia. In the diabetic patient, perioperative management of glucose
levels revolves around: 1) reduction of overall morbidity and mortality, 2)
avoidance of hyper and hypoglycemia, 3) maintenance of fluid and
electrolyte balances, 4) prevention of ketoacidosis, and 5) maintaining target
glucose levels below 140 mg/dL. In elective breast surgery, patient glycemic
requirements should be glucose levels less than 200 mg/dL and HbA1C <7%.
Similar to glycemic management, nutritional status and optimization plays
a significant role in wound healing and surgical success. Malnourished
patients undergoing plastic surgery procedures will have abnormal wound
healing function. Macronutrients are essential to all phases of wound healing.
Protein depletion will prolong the inflammatory phase, decrease fibroblast
function, and inhibit successful proliferative phase function (14). Wound
healing also increases baseline protein and caloric demands. Nutritional
replacement in the postoperative period should meet these demands.
Micronutrients such as vitamin C and A, zinc, and magnesium are also
essential to proper wound healing. Malnutrition and deficits in these macro
and micronutrients will increase risk of postoperative infection and delayed
wound healing. Nutritional status assessment and optimization should take
place prior to the surgical procedure and continue in the postoperative period.
VTE prophylaxis is standard of care in the surgical setting. VTE remains
the most common preventable cause of death in the surgical patient. Proper
risk assessment and thromboprophylaxis is required for patient safety and
risk reduction. Mechanical thromboprophylaxis, such as intermittent
pneumatic compression devices, should be placed on the lower extremities
and therapy initiated prior to anesthetic induction. Combined with early
ambulation in low-risk patients and procedures, no further chemical
prophylaxis is required in breast surgery. In higher-risk patients and certain
surgical criteria, the surgeon should consider postoperative
chemoprophylaxis. In breast surgery with the following criteria,
chemoprophylaxis should be considered:
1. Expectation of general anesthesia >3 hours,
2. Patients with risk factors:
1. age >65
2. obesity
3. increased length of hospital stay
4. recent surgery within 30 days
5. cancer
6. use of hormonal therapy
7. biochemical abnormalities: deficiencies of Antithrombin, protein C,
protein S, Factor V Leiden
3. Patients undergoing immediate autologous breast reconstruction
In these cases, chemoprophylaxis with unfractionated heparin (UFH) or
low–molecular-weight heparin (LMWH) such as enoxaparin can be
combined with mechanical prophylaxis to reduce thromboembolism risk (15).
The surgeon must weigh the morbidity and risk of VTE with bleeding
potential. The patient risk factors, surgical details, and postoperative
expectations are factors in this decision process.
PAIN MANAGEMENT
Current trends in pain management are focused on non–opioid-based
practices to control surgical and postoperative pain and reduce opioid
requirements. Optimal pain management begins in the preoperative period,
continues during the intraoperative period, and is then managed appropriately
during the postoperative recovery. Prior to the surgical procedure, non–
opioid-based pharmaceutical therapy can be initiated to reduce intraoperative
and postoperative inflammation and pain. Systemic administration of 1,000
mg of acetaminophen, celecoxib 400 mg, and gabapentin 300 mg 30 to 60
minutes prior to surgical start time can significantly reduce postoperative
opioid requirements (16). At the initiation of the surgical procedure, local
anesthetic administration can also lead to decreased nociceptor activation and
decreased opiate requirements during the anesthetic period.
Intraoperative regional anesthesia can also provide significant pain
management during the surgical procedure that extends into the immediate
postoperative period. Long-acting local anesthetic agents can reduce
intraoperative and postoperative opioid usage and their associated negative
side effects. Regional blocks for the breast include paravertebral blocks
(PVBs), pectoral nerve blocks (PECs), epidural anesthesia, or a local block at
the surgical site. Liposomal bupivacaine (Exparel) is an extended release
form of bupivacaine that may last as long as 72 hours. This long-acting
anesthetic can decrease opioid requirements in the postoperative period. In
cases where liposomal bupivacaine is not available, Dexmedetomidine
(Precedex) combined with bupivacaine can prolong the duration of the
anesthetic result (17). Dexmedetomidine is a highly specific and selective
alpha-2 adrenoceptor agonist. The alpha 2-: alpha 1-binding selectivity of
Dexmedetomidine is eight times greater than Clonidine thereby decreasing
the unwanted side effects of alpha 1 receptor. Combining 1 mL of
Dexmedetomidine (100 mcg) with 0.25% bupivacaine with 1/200,000
epinephrine can safely be used to provide prolonged local or regional
anesthesia to the surgical site. In breast surgery, localized anesthesia is highly
effective and safe.
Following the surgical procedure, multimodal postoperative pain
management continues. Cold therapy and elevation can contribute to the pain
management plan by limiting edema and inflammation. Opioid-sparing
techniques remain an important component strategy for postoperative pain
management. Nonsteroidal anti-inflammatory drugs (NSAIDs) have become
a viable option in postoperative pain control. Cox-1 inhibitors such as oral
ibuprofen or intravenous ketorolac can provide significant analgesia and
reduce opioid requirements. There is, however, an increased bleeding risk
with these COX-1 inhibitors. Additionally, COX-2 inhibitors such as
celecoxib are an alternative as they do not increase bleeding. Oral and
intravenous acetaminophen has also proven to be effective in reducing
surgical pain. Maximum daily dosage must remain below 4,000 mg. Finally,
opioid-based medications can be utilized on a prn (as needed) basis in either
oral or intravenous form. Intravenous patient-controlled anesthesia with
opioid medications has been shown to be a safe and effective method for pain
control during the hospital course (18).
Effective and well-planned pain management is essential to minimizing
opioid-associated side effects and complications, as well as facilitating better
and smoother recovery. An adjunct to pain management in the postoperative
period is the postoperative dressing or garment which can provide comfort
and maintain the optimal environment for surgical healing.
INCISION AND SOFT TISSUE MANAGEMENT
Breast surgery encompasses both functional and aesthetic restoration of the
breast. In these cases, the plastic surgeon utilizes incisions and soft tissue
rearrangement and manipulation to achieve the desired surgical result. In
many cases, the surgeon is pushing the boundaries of soft tissue and
incisional healing and vascularity. When addressing reconstructive breast
procedures, acellular dermal matrix (ADM) incorporation and nipple and skin
viability are of the essence. For example, in prepectoral reconstruction, the
mastectomy skin flaps are self-reliant and isolated from the underlying
pectoralis muscle and chest wall. It is this fact that makes tissue perfusion
and skin flap viability essential to success. In the operating room, the surgical
dressing has the vital function of maintaining and optimizing this vascular
and viable environment. Additionally, it is important to safely immobilize
these skin flaps, incisions, and soft tissue to allow for tissue ingrowth,
healing, and incorporation. Closed incision and soft tissue negative pressure
therapy and complete breast coverage with transparent film occlusive
dressing allow for a vascular and safe environment while simultaneously
immobilizing the mastectomy skin flaps and preventing shearing forces. This
negative pressure therapy (Prevena Restor Bella Form) is applied to the
incisions, nipple areolar complex, and affected soft tissues. The benefit of
this therapy includes protection from contamination, minimizing tissue
edema, promoting vascular flow, and minimizing skin tension (19). These
benefits are achieved without compression of the underlying breast. Negative
pressure therapy creates a reduction in underlying compression, while
immobilizing and supporting the surgical site. Much like the physiologic
results of cupping therapy, negative pressure therapy lifts the soft tissues
rather than compress them. The result is an environment which is optimal for
soft tissue healing, vascular recovery, wound healing, ADM incorporation,
tissue ingrowth, and incisional healing. Understanding the role of MSCs in
wound healing and their selective trafficking to the surgical site, one can
postulate that negative pressure soft tissue therapy will optimize and
modulate this stem cell trafficking in the wound healing process. These
negative pressure therapy devices in the setting of breast surgery and other
surgical procedures have shown significant reduction in surgical site infection
(SSI), decreased seroma rates, decreased postoperative complications, and
reoperation rates (20,21). In addition, increased patient comfort and
decreased opioid requirements have been demonstrated (22). Incisional and
soft tissue negative pressure therapy and management represents the ability to
modulate and complement the wound healing process. Improved vascular
perfusion coupled with noncompressive splinting and improved lymphatic
outflow will minimize persistent edema (Figs. 130-2 to 130-4).

FIGURE 130-2 Image of closed incision negative pressure therapy (Prevena Restor
Bellaform & Prevena Customizable) applied at the end of an aesthetic breast
mastopexy and abdominoplasty surgical procedure.

Complementing the negative pressure therapy is a drain site dressing


utilizing chlorhexidine gluconate disks and occlusive dressings to create an
aseptic environment at the skin drain site. Proper drain dressings are
important, especially in the setting of prolonged drain placement. Drains are
commonly in place for 2 weeks and minimizing infection potential is
essential.
After postoperative day 7, closed incision negative pressure therapy is
commonly removed, at which point the occlusive transparent film dressing
can be reapplied, or soft compressive bras can be worn to continue the
“immobilizing” effect. Current incisional and soft tissue therapy devices can
now deliver therapy for up to 14 days, extending the physiologic period of
optimal wound healing. This allows the surgeon to maintain the optimized
surgical site until the inflammatory phase has passed and the proliferation
phase of wound healing is well underway. Negative pressure therapy
provides noncompressive complete breast support and immobilization. This
time period allows for the surgical site to be supported and optimal
physiology to be maintained until reliable neovascularization and collagen
production. Following removal of the negative pressure therapy, supportive
garments are placed. The goal of these garments and dressings is to prevent
shearing, decrease incisional tension, and preserve the surgical healing that
has occurred as the patient’s activity begins to increase. This supportive
garment or bra is encouraged for 4 to 6 weeks following surgery (Figs. 130-5
to 130-7).
FIGURE 130-3 Image of closed incision and soft tissue negative pressure therapy
(Prevena Restor Bellaform) applied at the end of unilateral surgical procedure.
FIGURE 130-4 Image of closed incision and soft tissue negative pressure therapy
(Prevena Restor Bellaform) applied at the end of bilateral surgical procedure.
FIGURE 130-5 Image of post prepectoral reconstruction breast at day 7 removal of
closed incision negative pressure therapy.
FIGURE 130-6 Image of postreduction mammaplasty breast at day 14 removal of
closed incision and soft tissue negative pressure therapy.
FIGURE 130-7 Image of post prepectoral reconstruction breasts at day 14 removal
of closed incision and soft tissue negative pressure therapy.
DRAIN MANAGEMENT AND ANTIBIOTIC PROTOCOL
Closed suction drains are widely used in reconstructive and aesthetic breast
surgery. Elimination of dead space, prevention of seroma, and optimizing
apposition of soft tissues, skin flaps, and ADMs are all essential to surgical
success. Drain placement, as previously discussed, is a significant component
to the postoperative management (23). Surgical procedures with large areas
of undermining or dead space, or use of ADM often benefit from surgical
drains. Depending on the type of surgery, average drain duration is 1 to 2
weeks, based on drain output. When drain output levels reach 25 cc per 24-
hour period or less, they are removed. In the setting of implants, antibiotics
are administered during the postoperative period until all drains have been
removed (24). In nonimplant breast surgery, perioperative antibiotics are
administered, typically for 24 hours, and then discontinued (25).
Postoperative practices vary among physicians, but showering is typically
restricted until the closed incision negative pressure therapy is removed. At
that point, after postoperative day 7, patients are permitted to shower.
Soaking, bathing, and swimming are restricted for the first 6 weeks.
RECOVERY AND REHABILITATION
The late postoperative period begins at the 6-week time period. It is at this
point in wound healing that the surgical sight has sufficient tensile strength
and vascular stability. At this point, postoperative management transitions
from surgical site support, stabilization and protection to patient recovery and
rehabilitation in function. Postbreast surgery recovery is focused on regaining
arm and shoulder mobility, restoring back posture, and regaining strength and
stamina. These processes can often take 12 to 24 months for near-full
recovery. In addition, scar massage and maturation will take a minimum of
18 to 24 months. Patient restrictions vary depending on surgeon preference
and surgical procedure. Commonly, at the 6-week postoperative mark,
patients receive clearance to resume strenuous activity, exercise, and
swimming or soaking in water. This is dependent on normal and successful
wound healing. Delayed healing will lead to prolonged postoperative
restrictions.
CONCLUSION
Proper perioperative management of the breast surgery patient is focused on
optimizing the patient’s status prior to surgery, ensuring intraoperative and
postoperative success, and modulating and controlling various aspects in
wound healing to benefit outcomes. This management must complement our
surgical procedures, and maintain the intraoperative results until the patient
has attained sufficient healing.

REFERENCES

1. Witte MB, Barbul A. General principles of wound healing. Surg Clin


North Am 1997;77:509–528.
2. Martin P, Leibovich SJ. Inflammatory cells during wound repair. Trends
Cell Biol 2005;15:599–607.
3. Abbott JD, Huang Y, Liu D, et al. Stromal cell-derived factor-1 alpha
plays a critical role in stem cell recruitment to the heart after myocardial
infarction but is not sufficient to induce homing in the absence of injury.
Circulation 2004;110:3300–3305.
4. Adamson R. Role of macrophages in normal wound healing. J Wound
Care 2009;18:349–351.
5. Ross R, Benditt EP. Wound healing and collagen formation. I.
Sequential changes in components of guinea pig skin wounds observed
in the electron microscope. J Biophys Biochem Cytol 1961;11:677–700.
6. Bowden LG, Byrne HM, Maini PK, et al. A morphoelastic model for
dermal wound closure. Biomech Model Mechanobiol 2016;15(3):663–
681.
7. Kristensen SD, Knuuti J, Saraste A, et al. 2014 ESC/ESA Guidelines on
non-cardiac surgery: cardiovascular assessment and management: The
Joint Task Force on non-cardiac surgery: cardiovascular assessment and
management of the European Society of Cardiology (ESC) and the
European Society of Anaesthesiology (ESA). Eur Heart J
2104;35(35):2383–2431.
8. Glance LG, Lustik SJ, Hannan EL, et al. The surgical mortality
probability model: derivation and validation of a simple risk prediction
rule for noncardiac surgery. Ann Surg 2012;255(4):696–702.
9. Sarin CL, Austin JC, Nickel WO. Effects of smoking on digital blood
flow velocity. JAMA 1974;229:1327–1328.
10. Sorensen LT, Hørby J, Friis E, et al. Smoking as a risk factor for wound
healing and infection in breast cancer surgery. Eur J Surg Oncol
2002;28(8):815–820.
11. Hawn MT, Houston TK, Campagna EJ, et al. The attributable risk of
smoking on surgical complications. Ann Surg 2011;254(6):914–920.
12. Greenhalgh DG. Wound healing and diabetes mellitus. Clin Plast Surg
2003;30:37–45.
13. Zaloga GP. Catecholamines in anesthetic and surgical stress. Int
Anesthesiol Clin 1988;26(3):187–198.
14. Campos AC, Groth AK, Branco AB. Assessment and nutritional aspects
of wound healing. Curr Opin Clin Nutr Metab Care 2008;11:281–288.
15. Geerts W, Heit JA, Clagett GP, et al. Prevention of venous
thromboembolism. Chest 2001;119:132S–175S.
16. Parsa A, Sprouse-Blum AS, Jackowe DJ, et al. Combined preoperative
use of celecoxib and gabapentin in management of postoperative pain.
Aesthetic Plast Surg 2009;33(1):98–103.
17. Agarwal S, Aggarwal R, Gupta P. Dexmedetomidine prolongs the
effects of bupivacaine in supraclavicular brachial plexus block. J
Anaesthesiol Clin Pharmacol 2014;30(1):36–40.
18. Hudcova l, McNicol E, Quah C, et al. Patient controlled opioid analgesia
versus conventional opioid anesthesia for postoperative pain. Cochrane
Database Syst Rev 2006;(4):CD003348.
19. Semsardzadeh NN, Tadisina KK, Maddox J, et al. Closed incision
negative pressure therapy is associated with decreased surgical-site
infections: a meta-analysis. Plast Reconstr Surg 2015;136(3):592–602.
20. Gabriel A, Sigalove S, Sigalove N, et al. The impact of closed incision
negative pressure therapy on postoperative breast reconstruction
outcomes. Plast Reconstr Surg Glob Open 2018;6(8):e1880.
21. Ferrando PM, Ala A, Bussone R, et al. Closed incision negative pressure
therapy in oncological breast surgery: comparison with standard care
dressings. Plast Reconstr Surg Glob Open 2018;6:e1732.
22. Gunatilake RP, Swamy GK, Brancazio LR, et al. Closed-incision
negative-pressure therapy in obese patients undergoing cesarean
delivery: a randomized controlled trial. AJP Rep 2017;7(3):e151–e157.
23. Unalp HR, Onal MA. Analysis of risk factors affecting the development
of seromas following breast cancer surgeries. Breast J 2007;13:588–
592.
24. Avashia YJ, Mohan R, Berhane C, et al. Postoperative antibiotic
prophylaxis for implant based breast reconstruction with acellular
dermal matrix. Plast Reconstr Surg 2013;131(3):453–461.
25. Phillips BT, Bishawi M, Dagum AB, et al. A systematic review of
antibiotic use and infection in breast reconstruction. Plast Reconstr Surg
2013;131(1):1–13.
Index
NOTE: Page numbers followed by the letter f refer to figures; those followed
by the letter t refer to tables.

A
Abdominal fascia
access to, 782
donor site bulging, 779
incisions over, 871
Abdominal flaps. See also Specific flaps
aesthetic concerns, 867–868
reconstruction using, 1186
Abdominal hernias
flap reconstruction and, 762, 768
prevention of, 1162
Abdominal tissue, free autologous, 867–872
Abdominal wall
bulging of, 762, 763, 767–768, 786, 844
closure of, 234, 765, 871
desmoid tumor of, 197
DIEP flap reconstruction and, 778–783
hernia, 762, 1181
lymph nodes, 287
neuronal density of, 779
previous surgery to, 770
strength of, 768
TAP blocks to, 720
TRAM flap reconstruction and, 1186
vascular imaging of perforators, 836
vasculature of, 843
Abdominoplasty
case studies, 363f–365f, 1067f, 1075f
flap harvest, 288, 868
high BMI and, 302
incidental, 843
prior, 763, 770, 780, 812, 844
RAFT procedure, 915–916
scars, 327, 786, 814f, 818f
seroma following, 1260f
SSO, 844–847
Ablation therapy
cryoablation, 66–67, 66t, 68
laser, 66t
microwave, 66t, 68
ovarian, 126, 128–129
radiofrequency, 66t, 67–68
in situ, 65–66, 65–68, 68–69
in situ, for breast cancer, 65–69
thermoablation, 65–68
Abortions
breast cancer risk and, 5
trauma related, 49
Abscesses
mastitis and, 197
AC regimens
neoadjuvant chemotherapy and, 119
nodal positivity rates after, 249
Accelerated partial breast irradiation (APBI)
benefits of, 97
description of, 97
external beam, 99
intracavitary therapy, 97–98, 98f
intraoperative, 99
patient selection guidelines, 100t
Accolate (zafirlukast), 667, 939, 1128
Acellular dermal matrix (ADM)
addition of
nipple positioning and, 656–657
adherence of, 579f
adjunctive use of
revision surgery and, 621–622
alternatives to, 1144
around implants, 565
assembly, 451f
bioabsorbable meshes and, 1144
bovine-derived, 1146
in breast reconstruction, 449, 573–581, 649, 706
for capsular contractures, 575–576, 577f, 939
PMRT considerations, 709
case studies, 1146f–1149f
categories of, 1144
description of, 573–574
for direct-to-implant reconstruction, 473
for dual plane reconstruction, 444, 533, 574–575, 574f
elasticity of, 573f, 576
EndoMT and, 667
expander/implants and, 597–598
fibroblasts and, 667
flaps lined with, 551f
handline of, 574
history of, 573, 706
HRUS image, 1259f
human, 573f
human-derived, 1146
implant coverage and, 639
indications for use of, 1144–1146
infections and, 566–567
integration of, 640
introduction of, 444
list of, 565t
lower pole coverage, 1145–1146, 1149f, 1151f, 1152f
macrophages and, 667
meshed, 582–589, 584f
complications, 588
operative technique, 583–587
risks of, 588
tissue expanders with, 585f–587
wrap-around technique, 584f
myofibroblasts and, 667
neopectoral technique and, 1113
nonperforated, 574f
no-touch technique and, 583
off-label use of, 1144
outcomes, 579f
placement, 730f
porcine-derived, 1118, 1146
positioning of, 580f
postoperative care, 584–587
premeshed, 583–584
prepectoral reconstruction with, 666–667, 668f
prepectoral space, 625
in radiated breast, 525
radiation therapy and, 576–577
reconstructions using, 515f
reinforcement with, 1120
in revisionary surgery, 1144
rinsing of, 535
selection of, 1146–1149
seromas and, 566–567
soft tissue management and, 1266–1267
soft tissue support and, 837
soft tissue thickening, 1146
subpectoral reconstruction using, 462f
support by, 459
suturing of, 536f
technical aspects of, 574–575
use for expander coverage, 512
use of, 642, 642f
in contralateral breasts, 679
varieties of, 573f
vascularity and, 667
wound dehiscence and, 566–567
Acetaminophen
liver damage and, 716
pain management using, 1266
postoperative, 352, 717, 720, 1162
presurgical, 780
Acoustic impedance, ultrasound, 1250
Acoustic shadowing artifacts, ultrasound, 1253f
ACR. See American College of Radiologists (ACR)
Acroval, 832
ACS. See American Cancer Society (ACS)
Acute leukemia, chemotherapy-related, 124–125
Acute pain, breast surgery and, 712
Adductor longus tendon
location of, 794
palpation of, 802
Adenomas
excision of, 197
lactational, 195
nipple, 196–197
Adenosis
breast cancer risk and, 8, 8t
sclerosing, 193–195, 193f
ADH. See Atypical ductal hyperplasia (ADH)
Adipocutaneous layer
elasticity of, 837
prosthetic reconstruction and, 837
Adipocytes
adipokine secretion by, 888
adipose-derived stem cells and, 893
aromatase expression in, 896
fat transfer and, 352
harvest of, 852
hypoxia of, 910
hypoxic, 910
suction pressure on, 899–900
trauma to, 352, 910
Adipose stem cells (ASCs)
isolation of, 888
Adipose tissue, autologous, 882
Adipose-derived stem cells (ADSCs)
breast cancer cell growth and, 901
hypoxia-resistant, 910
transfer of, 893
Adjuvant chemotherapy
breast reconstruction after, 527f
decision-making, 128–129, 858
efficacy of, 123
fertility preservation during, 124
history of, 122–123
indications for, 28, 118, 248, 1198–1199
in male breast cancer, 180
opioid dependency and, 712–713
in recurrent breast cancer, 62
risk of chronic pain and, 712–713
timing of, 188, 320, 499, 523, 640
tissue expanders and, 670, 863
trastuzumab for, 125–126
unnecessary, 29, 117, 1197
wound dehiscence and, 847
Adjuvant endocrine therapy. See also Endocrine therapy
adjuvant chemotherapy and, 122
cancer recurrence risk and, 199
indications for, 28
radiation therapy versus, 94–95
tamoxifen in, 112, 126–127
Adjuvant hormone therapy
indications, 28
Adjuvant systemic therapy, 115–134
ADM. See Acellular dermal matrix (ADM)
Ado-trastuzumab emtansine (T-DM1), 119t, 122
trastusumab versus, 122
Adriamycin, CAF therapy and, 111
Adriamycin/cyclophosphamide (AC). See AC regimens
ADSCs. See Adipose-derived stem cells (ADSCs)
Adult height
breast cancer risk and, 7–9
time of menarche and, 5
Advertising
Facebook, 1241–1242
false, 1243
Instagram, 1242
AeroForm Tissue Expander, 538
Aesthetic breast surgery
breast symmetry and, 758
history of, 758
implant selection, 1039–1051
polyurethane implants
operative technique, 1040–1050
outcomes, 1041f–1050f, 1051
postoperative care, 1040–1041
subglandular augmentation, 1048f–1049f
transgender patients, 1167–1171
Aesthetic subunits, breast, 414
AFG. See Autologous fat grafting (AFG)
Africa, breast cancer incidence in, 3
African Americans
breast cancer incidence, 4
age and, 5
stage IV cancers, 107
breast cancer mortality rates, 4
inflammatory breast cancer in, 109
metastatic illness in, 5-year survival, 107
AFT. See Autologous fat transfer (AFT)
Age/aging
axillary nodal recurrence rates, 61
at breast cancer diagnosis, 15–18
breast cancer imaging and, 15–18
breast cancer mortality rates and, 3
breast cancer risk and, 3–6, 10t
breast cancer risk factors for, 10t
breast imaging after 70, 19
decision-making process and, 209
mammography screening and, 15–18
of menarche, 5
of menopause, 5
necrosis rates and, 606
nipple-sparing mastectomy and
NAC malposition in, 651
women with breast cancer
omission of RT and, 93–95
AICAP flap. See Anterior intercostal artery perforator (AICAP) flap
AJCC. See American Joint Commission on Cancer (AJCC)
AK method. See “Akademikliniken Method” (AK method)
“Akademikliniken Method” (AK method), 1013–1018
preoperative marking, 1017t
ALCL. See Anaplastic large cell lymphoma (ALCL)
Alcohol, breast cancer risk and, 6–7, 7t, 35, 40
ALH. See Atypical lobular hyperplasia (ALH)
Allergan implants, 922
BIOCELL recall, 922
disease risk associated with, 1191
rupture rates, 1248
SSF, 560f
Style 15, 541f
Style 410
AK preoperative marking, 1017t
BIA-ALCL and, 1006
Style 410 MX, 479f, 485f–486f
Style 457, 548f
Style SCF 325 cc, 995f
Style SCF 335 cc, 994f
Allis clamps, 533
use of, 977
AlloDerm
ADM, 450, 490f, 519f, 566
available types of, 565t
capsular contracture risk and, 1145, 1146
case studies, 628f, 629f, 634f, 678f–679f
choice of, 1146
expanders covered wtih, 667
prepectoral reconstructions, 566
ALND. See Axillary lymph node dissection (ALND)
Alopecia
chemotherapy-related, 124–125
ALT flap. See Anterolateral thigh (ALT) flap
Alvimopan, bowel prep using, 232
Ambulation
early, 721, 845, 1068, 1265–1266
patient education on, 756
postoperative, 760
wound healing and, 721, 845, 1068, 1265–1266
Amenorrhea
breastfeeding and, 6
chemotherapy-related, 124–125
secondary infertility and, 124–125
American Cancer Society (ACS)
guidelines for breast cancer screening, 21t
American College of Medical Genetics, 33t
American College of Obsteticians and Gynecologists, 33t
American College of Radiologists (ACR), 21t
American Joint Commission on Cancer (AJCC)
Cancer Staging Manual, 28
TNM classification
inflammatory breast cancer, 110
American Society for Aesthetic Plastic Surgery (ASAPS), 1025
guidelines for BIA-ALCL, 1193
American Society for Testing Methodology, 923
American Society of Breast Surgeons
breast cancer screening guidelines, 22t
recommendations, 33t
American Society of Clinical Oncology (ASCO)
breast cancer risk stratification, 31
guidelines for testing, 24
posttreatment mammograms, 20
recommendations, 33t
American Society of Plastic Surgeons (ASPS)
guidelines for BIA-ALCL, 1193
professional standards, 1243
Ampicillin, biofilm sensitivity to, 1213
Analgesia, postoperative, 720. See also Specific drugs
Anaplastic large cell lymphoma (ALCL). See also Breast implant-
associated anaplastic large cell lymphoma (BIA-ALCL)
breast, incidence of, 1190
breast cancer and, 961
early diagnosis of, 1006
implant-related, 675
solid tumor staging, 1196f
Anastomosis
DIEP flaps, 832f
efficiency in, 756
microvascular, 756
microvascular failure, 835–836
nerve coaptation and, 779, 832f
Anastrozole
breast cancer risk reduction and, 36
mechanism of action by, 36, 127
restrictions on use of, 34–36, 200
studies on, 121, 129
“Anchor scar” mastopexy, 1059
Anchoring sutures
flaps, 728–729, 728f
Anesthesia
fat donor sites, 904
local
epinephrine-containing, 977
liposomal infiltration, 718, 718t
regional
intraoperative, 1266
standardization of
surgical efficiency and, 753
topical
tranexamic acid, 569
Anesthesiologists, 753
Angiogenesis. See also Neoangiogenesis
ADM and, 582
external vacuum expansion and, 911
fat grafting and, 888, 896
graft immobilization and, 912
induction of, 115, 837, 896
negative pressure wound therapy and, 610
neovascularization and, 1264
Angiography. See also Indocyanine green (ICG)
fluorescent, 452
flap perfusion testing, 172
indocyanine green, 783, 1187
intraoperative, 153f, 523f, 707
intra-operative after mastectomy, 523f
lymphangiography, 230f
magnetic resonance
preoperative, 836
preoperative planning, 232
operative assessment using, 608, 609
predictive accuracy of, 608
preoperative CT, 836
skin flap viability assessed bu, 608
tissue perfusion assessed by, 706
Animation deformity, 624f, 838f
breast augmentation and, 993
causes of, 1128
description of, 621
example of, 994f
implant-based reconstruction and
management of, 621–626
submuscular positioning and, 1080
treatment of, 621–622
Anterior cutaneous intercostal sensory nerve exposure of, 781
Anterior intercostal artery perforator (AICAP) flap, 326–327
breast reconstruction and, 311
defect filled with, 340f
description of, 337
in reconstructed breast, 854
reconstructive plan, 328
sites for, 338f
Anterior lamella annulus, anatomy of, 996f
Anterolateral thigh (ALT) flap
operative technique, 874
Anthracyclines
administration of, 119
cardiotoxicity associated with, 123
chemotherapy based on
for BIA-ALCL, 1198–1199
myelodysplastic syndrome and, 124
taxanes with
in inflammatory breast cancer, 111
trastuzumab combined therapy with, 126
Antiandrogen medications
transfeminine mammogenesis and, 1167
Antibiotics. See also Specific antibiotics
biofilm prophylaxis with, 1214–1215
biofilm resistance to, 1213
dressings impregnated with, 977
implant washes, 1057
intraoperative
during flap harvest, 774
oral
postoperative, 997–998
perioperative, 977
mastopexy-augmentation, 1086
preoperative, 450
prophylactic
intraoperative, 938
postoperative, 997–998
protocol for
drain management and, 1269
triple (TAB) solutions, 583, 1129
bacterial exposure reduced by, 996
irrigation of wounds with, 980, 1119
pocket irrigation, 569
Anticardiolipin antibody syndrome
thrombosis and, 839
Anticoagulants
prophylactic presurgical, 293–294
Antiphospholipid antibody syndrome, 839
Antisepsis, technique and, 1207
Antiseptics, biofilm prophylaxis with, 1214–1215
APBI. See Accelerated partial breast irradiation (APBI)
Apologies, value of, 1228
Aponeurectomy, percutaneous, 894
Apopotic injuries, cryoablation and, 66
Areola
breast deformities, 944
cinching, 735
herniation, 945
micropigmentation, 790f
necrosis after breast reduction, 383–384
positioning, 373–375
skin resection pattern, 373–375
Areola, size variability of, 1052
Army/Navy retractors, 977
Aromatase inhibitors
adjuvant therapy with, 127–128
development of, 127
Aromatases, function of, 127
Arterial stiffness, after radiation therapy, 859
Arterial thrombosis, flap failure and, 836
Arthralgias, chemotherapy-related, 124–125
Arthroscopic shavers, 422
ASAPS. See American Society for Aesthetic Plastic Surgery (ASAPS)
ASCO. See American Society of Clinical Oncology (ASCO)
ASCs. See Adipose stem cells (ASCs)
Aseptic maneuvers, capsular contracture prevention and, 996–997
Ashkenazi Jewish populations
BRCA genes and, 9–10
BRCA1 mutation in, 45t
Asia, breast cancer incidence in, 3
Asian Pacific Islanders, breast cancer incidence, 4
ASPS. See American Society of Plastic Surgeons (ASPS)
Asymmetry
after breast reduction, 385–386
augmentation mammaplasty for, 937f
breast surgery complication of, 385–386
inframammary fold
preoperative appearance, 1003f–1004f
natural breast
preoperative planning and, 325–326
nipple
preoperative, 653, 656
notch-to-nipple measurements, 937f
rates of
mastopexy-augmentation and, 1083
Ataxia telangiectasia mutated (ATM) gene
breast cancer risk and, 10, 19–20
breast cancer screening guidelines, 47t, 51
cancer risk and, 46t
ATM gene. See Ataxia telangiectasia mutated (ATM) gene
Atrophic vaginitis, tamoxifen and, 127
Atrophy, radiation therapy and, 893
Atypical ductal hyperplasia (ADH)
breast cancer risk and, 8
description of, 194
histology of, 194f
Atypical hyperplasias, 194
recommendations, 197t
Atypical lobular hyperplasia (ALH)
breast cancer risk and, 8
description of, 194
Auditory learners, informed consent and, 1235
Audretsch, Werner, 308
Augmentation mammaplasty. See also Breast augmentation
for asymmetry, 937f
athletic patients
needs of, 936f
delayed complications of, 938–940
BIA-ALCL, 940
implant deflation, 939–940
implant rupture, 939–940
periprosthetic capsular contractures, 938–939
dimensional analysis, 927t
effect of smoking on, 1179–1180
implant position in, 928–929
incisions, 933, 934, 934t, 996–997
inframammary approach, 1000–1005
operative technique, 1004–1005
operative planning, 928–929
operative technique
implant pocket in, 934–935
inframammary approach, 933
periareolar approach, 933–934
postoperative care, 935–936
transaxillary approach, 934
outcomes, 979f, 980f
patient management, 936–940
periareolar approach to, 976–981
history of, 976
technique, 976–981
perioperative complications, 936–938
capsular contractures, 936
changes in nipple sensitivity, 936
disfigurement, 936
excessive postoperative bleeding, 936
hematomas, 936
Mondor disease, 938
pain, 936
postoperative wound infections, 938
seromas, 936
preoperative assessments, 928f
preoperative planning, 927t
subfascial
implant selection, 997
postoperative care, 997
transaxillary
endoscope use in, 996
Augmentation mastopexy. See also Mastopexy-augmentation
anatomical assessment for, 1054–1056
candidates for, 1052
circumareolar pattern
operative technique, 1062–1065
complications of, 1070, 1080
considerations, 1052–1071
crescent lift, 1061–1062
decision-making process, 1080
fat grafting, 1066–1067
history of, 1052, 1077
inverted nipple correction, 1068
inverted T scar pattern, 1063f
marking, 1066f
liposuction, 1068
maintenance over time, 1053–1054
nipple reduction, 1068
operative technique, 1060–1061, 1078
single-stage, 1060–1061
outcomes, 1070, 1079–1081
patient expectations, 1052–1054
patient selection, 1052
planning for, 1077–1078
polyurethane implants, 1041f
postoperative care, 1068–1070, 1078
preoperative evaluation, 1052–1054, 1077–1078
reinforcement materials, 1068
scars, 1081
shapes of, 1077–1082
surgical planning, 1056
choosing pattern for, 1057–1059
implant selection, 1056–1057
incisions, 1057
plane selection, 1057
universal markings, 1059–1060, 1064f
vertical pattern
marking, 1066f
operative technique, 1065–1066
Augmented breasts
breast cancer treatment in, 144–146
breast carcinoma in, 135–149
rates of, 135t
breast conservation therapy in, 145–146
cancer recurrence rates, 143t, 144f
capsular firmness of
Baker Classification of, 938t
contralateral breasts
reconstruction of, 641–642, 678–679
general considerations, 921–942
implant-based reconstruction options, 675–682
mastectomy in, 676f
physical examination of, 136–138
prepectoral mastopexy, 643f
radiologic imaging of, 138–142
risk of breast cancer in, 136
subglandular
mastectomy in, 676, 676f
reconstruction in patients with, 640–641, 641f, 678, 681f
subpectoral
reconstruction in patients with, 640, 677, 678f
tissue quality in, 676
Australia, breast cancer survival and, 3
Autism, PTEN mutations and, 45
Autoimmune diseases, breast implant illness and, 1218–1221
Autologous breast reconstruction
abdominal based
fat grafting in, 906
adjunct fat grafting in, 901–902
adjunctive procedures, 875
basic principles of, 725–726
case studies, 875f, 876f
contraindications, 873
delayed
indications, 525
efficiency in, 751–757
enhancing volume in, 879–884
flaps used in, 879
history of, 879
operative techniques, 880–883
timing of, 879–880
in high-BMI patients, 1186
immediate abdominal-based
steps in, 754t
immediate versus delayed
complication rates and, 861
indications, 873
intraoperative care, 875
nipple-sparing mastectomy and
NAC malposition in, 651
outcomes assessment, 856–857
postoperative care, 856, 875
preoperative planning, 725
in thin patients, 873
secondary procedures, 850–857
breast mound revision, 851–852
planning for, 850–851
stage II
timing of, 863
technical approach
aesthetic, 1186
reconstruction, 1186
thin patients, 873–878
operative technique, 873–876
Autologous fat breast reconstruction
fat grafting in, 903–907
Autologous fat grafting (AFG). See also Fat grafting
cell-enriched, 891
contour remodeling, 852–853
contraindications, 903–904
history of, 887, 903
hybrid breast reconstruction and, 484–487
indications, 902, 903, 903f
operative technique, 904f–905f
fat harvest, 904
fat processing, 904
fat transfer, 905
outcomes, 905–906, 906f
postoperative care, 905
preoperative planning, 904
prepectoral breast reconstruction and, 899
in prepectoral implant placement, 625–626
salvage use of
for irradiated tissue, 671–672
tissue expansion with
breast reconstructive surgery, 908–917
total breast reconstruction and, 908–917
tuberous breast correction and, 1177
utility of, 902
Autologous fat transfer (AFT)
ancillary procedures, 914
benefits of
in radiated breast, 525
delivery of, 911–912
donor site marking, 913–916
external vacuum expansion and
generic risks of, 916
operative technique, 909–912
grafting technique, 914
megavolume, 908
postgraft care, 912
radiation change and, 893
recipient site marking, 914
recipient site preparation, 911
for RT damages, 473
in total breast reconstruction, 908, 909–912
Autologous flaps
neurotization of, 831–834
Autologous reconstruction
fat grafting after, 897
Autologous tissue, shaping of, 725–750
Autologous tissue transfer, reconstruction using, 850
Autologous tissue-based reconstructive surgery
post-mastectomy radiation therapy and, 860
Autologous-based free tissue transfer
in irradiated prostheses, 669–670
Avascular grafts, 915
Avelumab, NAT and, 121
AWS. See Axillary web syndrome (AWS)
Axilla
clinically positive, 239–240
adjuvant chemotherapy patients, 240
management in IBTR, 88–89
preparation of
for vascular lymphatic transplant, 233–234
Axillary dissection
axillary radiotherapy versus, 161
completion of, 243
radiation versus
risks in, 268
Axillary lymph node dissection (ALND)
after NAC
indications for, 252
alternative methods for, 255–259
alternatives to, 252–253
avoiding
strategies for, 249–250
BCT and, 62
case selection for, 239–240
complications of, 244–245
axillary web syndrome, 244–245
infection, 245
lymphedema, 244
sensory morbidity, 245
shoulder dysfunction, 245
in early breast cancer
risks of, 249–250
history of, 157, 237–238
in IBTR, 88–89
indications for, 240t
lymphedema after, 273
outcomes
extensive surgery and, 260
pathology, 239
positive nodes
PMRT and, 160
postoperative care, 244f
prior inadequate, 240
regional nodal RT, 100–102–11
SNLB and
prognostic value of, 106
technique of, 240–244
anatomic boundaries of, 241f
closing, 244f
extent of, 241, 241f
flap elevation, 242
incisions, 241–242, 242f
operative field, 244f
Axillary nodal recurrence
breast cancer, 60–63
diagnosis, 61
prognosis in, 61–62
radiotherapy after, 62
risk factors for, 61
salvage surgical therapy after, 62
time to, 61
treatment of, 61–62
Axillary nodes
postneoadjuvant assessment, 248–254
status of
breast cancer recurrence and, 115–116
Axillary sentinel lymph node biopsy
in invasive lobular carcinoma (ILC), 83f
Axillary vein, identification of, 243–244
Axillary vein stenosis, MRA diagnosis of, 232
Axillary web syndrome (AWS), 244–245
Axillary webbing, Poland syndrome and, 949

B
Bacitracin
triple antibiotics with, 450, 583, 938, 971, 996, 1129t
Bair-Hugger machine, heating of, 752
Baker Classification, 1209f
BCT and, 146t
at breast cancer diagnosis, 146, 146t
breast firmness scale, 146
capsular contractures and, 556, 571, 576, 671, 702, 1205t
of capsular firmness
in augmented breasts, 938t, 1008
Balcony technique
breast augmentation, 1077, 1079f, 1080
complication rates, 1081
patent satisfaction and, 1079
patent selection, 1080
Balfour retractors, placement of, 232
Bandaging
breast reduction surgery, 380–382
compression therapy and, 277, 279, 281
for lymphedema, 244
padding in, 277
taping and, 380, 382
Bannayan-Riley-Ruvalcaba syndrome, 45
Barbed sutures, 847, 856, 1022
BARD 1 gene
breast cancer risk and, 10
cancer risk and, 46t
TNBC risk and, 46
Base width (BW) distance
assessment of, 1123
measurement of, 1123, 1124f
“Batwing” modifications
mastopexy, 310t
case study, 526f
“Batwing” resections
incisions, 74, 75f
BCI. See Breast Cancer Index (BCI)
BCRAT (National Cancer Institute Breast Cancer Risk Assessment Tool),
31
BCS. See Breast conservation surgery (BCS)
BCT. See Breast conservation therapy (BCT)
BDDs. See Body dysmorphic disorders (BDDs)
Best Practice Standardization, 751–757
Betadine
dilute solution of, 980
irrigation using, 459, 948, 971, 996
TAB solutions and, 583, 1119, 1129
BIA-ALCL. See Breast implant-associated anaplastic large cell lymphoma
(BIA-ALCL)
BII. See Breast implant illness (BII)
Bilateral prophylactic mastectomy
decision making process, 209
reconstructive surgery after, 701f
Bilateral wire-localized lumpectomy
for invasive lobular carcinoma, 83f
Bioabsorbable meshes
case studies, 1150–1153, 1151f–1153f
indications for use of, 1150
lower pole support, 1153f
off-label use of, 1150
BIOCELL
recall, 922
structure of, 925f
textured surface
creation of, 931
Siltex-textured surface vs., 932
textured surface of, 1024
BIOCELL textured implants (Allergan)
BIA-ALCL and, 940
withdrawal of, 940
BioDimensional Planning System, 923–924, 927
development of, 932
implant shape and, 932
Bioelectric effects, biofilm prophylaxis and, 1215
Bioengineered breast concept
prepectoral reconstruction and, 445–447
principles of, 446f
Biofilms
bulk of, 1213
capsular contracture and, 1204–1205, 1213–1214
history of, 1212
chemoprophylaxis for, 1214–1215
contamination by
capsular contractures and, 996
definition of, 1212
growth of, 1212–1213
implants and, 1191, 1212–1217
intraoperative detection of, 1215–1216
mechanical prophylaxis, 1215
pathologies of, 1213
phenotypes of, 1213
primary adhesion of
factors in, 1212
resistance of, 1213
secondary adhesion of
factors in, 1212–1213
structural integrity of, 1215
Bioimpedance spectroscopy (BIS), 230, 266
Biomaterials, evolution of, 472
Bioplasty Corporation, 926
Biopsies. See also Sentinel lymph node biopsies (SLNB)
core needle
in augmented patients, 138
breast cancer diagnosis and, 105
inflammatory breast cancer, 110–111
core needle biopsies
in augmented patients, 138
DCIS confirmation by, 199
excisional, lymph nodes, 1197
fine-needle aspiration, 1198f
cystic breast masses, 192–193
in inflammatory breast cancer, 110
needle biopsies, implants and, 137–138
open, in augmented patients, 138
periprosthetic fluid, 1194, 1197
prostate gland, 49
sentinel node, 237–247
in ductal carcinoma in situ, 238
stereotactic core needle, 199
vacuum-assisted
in augmented patients, 138
devices for, 422
procedure, 139f
BI-RADS. See Breast Imaging Reporting and Data System (BI-RADS)
Birth weights, breast cancer risk and, 5, 8
BIS. See Bioimpedance spectroscopy (BIS)
Bisphosphonates
bone-modifying therapy and, 129
Blake drains, 533, 535, 536f, 537f, 707
Bleeding. See also Hemostasis
breast reduction
superomedial pedicle vertical, 368
control of, 1000
flap harvest sites, 776
Blogging, 1241–1243
BMD. See Bone mineral density (BMD)
BMI. See Body mass index (BMI)
BOADICEA model, 42t, 43
Body dysmorphic disorders (BDDs), 1228, 1228t
Body image
anxiety and, 212
breast and, 831–832
breast surgery and, 638, 1225–1226
femininity and, 831
lymphedema and, 273, 292
mastectomy and, 215, 850
negative impact of, 37, 921
nipple-sparing mastectomy and, 650
patient satisfaction and, 56, 154, 210, 279, 321
prophylactic mastectomy and, 211
quality of life and, 1157
self-confidence and, 831
self-esteem and, 850, 867
Body mass index (BMI)
breast cancer risk and, 7, 35
breast conservation surgery and, 350
breast reconstruction and
prepectoral, 450
flap failure and, 835
flap necrosis and, 605–606
flap thickness and, 218, 607
high
breast pathologies and, 1185
case studies, 516–518, 516f–520f
comorbid conditions, 516
cosmetic surgery in, 1186
definition of, 510
disease burden in patients with, 1185
elective surgeries in, 1185–1189
implant-based reconstruction in, 510–521
improving outcomes, 516–520, 516t
medical risks of surgery, 1185f
perioperative considerations, 1187–1188
postoperative considerations, 1187–1188
preoperative considerations, 1186–1187
surgical risks, 1185f
hybrid breast reconstruction and, 484
lymphovenous bypass and, 231–232
mastectomy flap thickness and, 169
mastectomy specimen size and, 731f
nipple-sparing mastectomy and, 217
complications and, 650
NAC malposition in, 651
outcomes and, 302
risk factors, 300
surgical outcomes and
PMRT and, 163
thin patients
autogenous breast surgery in, 873–878
donor sites, 873
BodyLogic implant sizing tool, 927
Bone metastases, 107–108
Bone mineral density (BMD)
aromatase inhibitor therapy and, 35–37
loss of, 127
Bone-modifying therapies, 129
Bottoming out. See Pseudoptosis
Bovie electrocautery device, 934. See also Electrocautery
Bowel screening
endoscopic, 51
Bra sizes
correct, 962
preoperative, 394, 411f
transmasculine individuals, 1157
Brachytherapy, 590
limitations in, 99
multicatheter
APBI and, 97, 98f
Brain, plasticity of
reproductive life stages and, 831
BRAND4P procedure, 466–467
operative technique, 467–469
postoperative care, 467–468, 468f–470f
BRAVA device, 1174
core volume fat transplants and, 1132
opposition to, 1132
Brazil, breast cancer mortality rates and, 3
BRCA 1/2 gene mutations
breast cancer risk and, 9–10, 19–20, 45t, 177, 522
breast cancer screening guidelines, 47t
cancer risk and, 38
cancers related to
interventions, 44
prognosis, 50
treatment strategies, 49–50
contralateral carcinomas and, 758
family clusters of, 44–46
function of, 45t
male carriers of
screening of, 48–49
nipple-sparing mastectomy in, 215
risk reduction mastectomy and, 37t
variants
breast cancer and, 47–49
BRCA mutation carriers
breast cancer risk and, 9
nipple-sparing mastectomy in, 188
BRCA1-associated RING domain protein-1 (BARD1). See BARD1 gene
BRCAPRO model, 42t, 43
Breast, 192–193. See also Breast tissue; Specific procedures
3-D imaging of, 1011
aesthetic form of, 927f, 1007
aesthetic subunits of, 326t, 414
anatomy of, 167–176, 369–371, 393
blood supply, 369f
cross view of, 1057f
transgender, 1168
vascularity of, 393f, 607
asymmetries
anatomical implants in, 1011
augmented, secondary revision of, 1123–1131
benign disorders of, 192
atypical hyperplasias, 194
imaging of, 198–199
body image and, 831–832
calcifications
benign, 20
characteristics of
contralateral implants, 632f
reconstructed, 632f
shape of, 631
size, 630
contour remodeling
flap rearrangement and, 855
contralateral matching procedures, 758
contralateral symmetrization, 472
cysts, 192–193, 193t
density of
breast cancer risk and, 8, 40–41
diseases of, 192–203
elasticity of, 1027f
fascial system, 995–996, 996f
footprint of
measures taken for, 726
variability of, 372f
form, determinates of, 446f
imaging after 70, 19
imaging of (See also Mammography)
calcifications on, 896
cancer screening, 961
improvements in, 19
performance in, 1035
inflammatory conditions
fat necrosis, 197
granulomatous mastitis, 197
mammary duct ectasia, 197
inframammary folds, 373
initial measurements, 1054
kinetics of, 1035–1037
“lazy-S” shape borders of, 729
life-time changes, 1025
meridian, marking of, 373
molecular pathology of, 24–30
morphology categories, 474–475
natural asymmetries, 1026f
natural asymmetry of, 325–326
natural shape of, 932–933
nerve supply to, 831f
nonproliferative lesions, 192
preoperative form of, 933f
proliferative lesions without atypia, 193–194
ptosis, 501f
repositioning of, 1102
reshaping of, 1102
self-examination of, 49
sensation and, 831f
shapes of, flow chart for reconstruction, 642f
size of, 926–927
complication rates and, 604
flow chart for reconstruction, 642f
necrosis rates and, 606
nipple-sparing mastectomy and, 217
patient satisfaction and, 1225
stretching of, 1027f
surgical anatomy of, 326–327
surgical removal of, 638
surgically altered
breast cancer diagnosis, 15–23
breast cancer screening, 15–23
imaging of, 20–21
symmetry of, 758–761
tight envelope, 1019f
tissue quality
reconstruction outcomes and, 676
subdermal blood supply and, 676
tuberous development, 1054f
types, 475–478
large, 476f, 477–478, 480–484, 497–503
medium-sized, 475–477, 476f, 480, 482–483
ptotic, 477–478, 480–484, 497–503
small, 475, 476f, 478–480, 482
types of, 475–484
ultrasonography, 168f
upper border, marking of, 373, 374f
volume correction, 945–947
weight of
sag and, 1025
width measurement, 1016
Breast augmentation. See also Augmentation mammaplasty
alloplastic materials and, 921
complicated results
informed consent and, 1237–1238
complication prevention in, 952
composite, 1132–1143
complications, 1142
contraindications for, 1137
fat for core volume, 1132f
history of, 1132–1133
implant location and, 1139t
indications for, 1133–1137
operative technique, 1140
outcomes, 1142
postoperative care, 1140
preoperative planning, 1137–1139
risks, 1142
secondary procedures, 1142
contralateral, 479f
definition of, 950
glandular reshaping, 945
history of, 921, 965, 993, 1006
implant reconstruction in, 351
implant-based
history of, 1204
incision choices, 976, 977f
incisions, 996–997
inframammary approach to, 965–975
case studies, 973f–974f
lifelong risk in, 959–960
light-weight implants in, 1025–1038
case studies, 1031f–1034f
recovery after, 1030f, 1037
mastopexy, 1072–1076
case studies, 1075f, 1115f
cooperative details, 1072t
history of, 1072
implant placement, 1073f
implant selection, 1073
marking, 1073, 1073f
outcomes, 1074
patient expectations, 1073
patient outcomes, 1073
postoperative care, 1074–1076
reliability, 1072–1073
safety, 1072–1073
operative technique, 1020–1022, 1021f, 1022f
closure, 971–972
dual plane submuscular pocket, 969–971
implant pockets, 968–969
incision, 968
local anesthesia, 966, 966f, 966t
patient positioning, 966, 966f
postoperative management, 972
sterile draping, 966
surgical prep, 966
outcomes, 956f
patient assessments, 926–928
patient education on, 950–964
patient expectations, 1227
patient positioning, 977
postoperative care, 1022–1023
exercise during healing, 1009–1010
postoperative follow-up, 1012f
preference-sensitive decisions, 952
preoperative appearance, 1001f, 1002f
preoperative markings, 1018–1020
preoperative planning, 965, 1001f
decision making, 1000
incision planning, 1000–1004
preoperative marking, 965f
procedure of, 1011–1020
recovery process
patient education about, 954t
revision, 957f
case studies, 1115f
risks of
patient education about, 953t, 956
saline implants, 985f
semisolid materials, 921
shaped implants in, 1006–1024
sizer systems, 1011–1012
sizing, 1227
subfascial, 993–999
animation deformity and, 994f
aseptic maneuvers and, 996
bilateral, 995f
history of, 993
implant selection, 997
indications for, 993–995
postoperative care, 997–998
recovery period, 993
silicone implants in, 997
subpectoral
technique, 978f
surgical goals, 926–933
transaxillary approach, 982–992
endoscopic, 982, 984f
equipment, 983
history of, 982, 993
implant placement, 988, 989f, 990f, 991f
incisions, 983–985, 984f
initial dissection, 985
markings, 982–983, 983f
nonendoscopic approach, 989
operative technique, 988–989
outcomes, 991f
pocket creation, 985–988
positioning, 983, 983f
postoperative care, 988, 988f
transgender patients
complications, 1169–1170
incision options, 1168
outcomes, 1170
postoperative care, 1169
preoperative considerations, 1167–1168
surgical considerations, 1168–1169
treatment algorithm
for aesthetic concerns, 1117f
in tuberous breast deformities, 943–949
Breast base width variability, 1052
Breast borders, “lazy-S” shape, 729
Breast cancer
5-year survival rates, 15
age at diagnosis
imaging and, 15–18
age-specific rates of, 17f
in augmented patients
mammogram of, 138f
axillary nodal recurrence, 60–63
rates of, 60–61
basal-like subtype, 26–27
bilateral, risk of, 758
central tumors, management of, 85
characteristics of, 300–301
chemoprevention of, 35–37, 47–48
death rate trends in, 17f
decision making in, 522
diagnosis
in augmented women, 135–149
surgically altered breast, 15–23
diagnostic failures, liability issues, 1239
early
aromatase inhibitors in, 128t
prognostic factors in, 115–118
trastuzumab-containing chemotherapy and, 125t
elderly women, 64–65
ER status, 116–117
ER-negative
breastfeeding and, 6
ER-positive
risk factors for, 9
treating residual disease in, 122
genes associated with susceptibility, 177
high-penetrance genes, 44–46, 45t
genetic counseling, 32
HER-2 expression, 116
systemic therapy and, 107
high-risk patients, 31–39
management of, 32–38
risk reduction strategies, 33t
screening, 33t
history, 183
in-breast recurrence
mechanisms of, 183
incidence of, 3, 15, 638, 850
race and, 4f
trends in, 3
inflammatory
diagnosis, 109–111
epidemiology, 109
NSM contraindication by, 216
intact primaries in
systemic therapy for, 108
intrinsic subtypes of, 26, 28
invasive disease
mastectomy in, 91–93
lifetime risk of, 15–16, 19–20, 522
local recurrence
presentation of, 183–185
locally advanced, 105f
5-year survival, 105
bleeding mass in, 107f
diagnosis of, 105–106
epidemiology of, 105
surgical management of, 105–114
systemic treatment of, 106
locoregional recurrences, 184f
PMRT and, 706
lymph node negative
PMRT and, 158
male
screening of BRCA carriers, 48–49
management of
nonsurgical, 64–69
metastatic
non-breast sites of, 107
removal of primary tumor in, 108
tamoxifen-resistant, 127
treatment of, 49–50
molecular subtypes
locoregional recurrences, 184f
mortality rates of, 3
age and, 3
augmented breasts, 144t, 145f
geography and, 3
race and, 4f
nutritional factors in
calcum, 6
carotenoids, 6
dairy items, 6
nonstarchy vegetables, 6
obesity and, 1185
oncologic parameters, 488
oncoplastic surgery
decision making in, 299–307
oncoplasty surgery, 70–77
palpability
at time of diagnosis, 143t
pathologic features of, 57
personal history of
breast cancer risk and, 20
postmenopausal risk of, 5
alcohol and, 6–7, 7t
premenopausal risk of, 5
alcohol and, 6–7
physical activity and, 7–8
preoperative photos, 531f
prognostic factors
effects of implants on, 142–144
histopathic features, 116
hormone receptor expression, 116
tumor stages, 115–116
radiation therapy for
history of, 665
recurrence of, 185f
after BCT, 54
BCT with/without RT, 55t
fat grafting and, 888, 901
locoregional, 20
risk, 186f
risk reduction strategies, 183–191
second BCT for, 88t
risk assessment models, 31–32, 41–43, 42t
risk factors
BRCA mutation carriers and, 9
contralateral breast, 356
fat grafting and, 887–892
risk factors for, 3–6, 8t, 32t, 40–41
adult height, 8–9
age and, 10t
age of menarche, 5
age of menopause, 5
alcohol and, 6–7
benign breast disease and, 8
breast density and, 8, 40–41
breast feeding, 6
family history, 9–10, 40
genetics, 9–10
growth factors and, 8–9
healthy lifesyle and, –35
hormone replacement therapy and, 9
oral contraception (OCP) and, 9
parity, 5
physical activity and, 7–8
pregnancy and, 5
reproductive history, 5
smoking, 7
risk reduction, 35–37
risk stratification, 31
Oncotype DX and, 123
screening for
breast imaging, 961
high-risk, keys for, 20
NCCN guidelines for, 47t
surgically altered breast, 15–23
transfemales and, 204–205
in situ ablation therapy
cryoablation, 66–67
radiofrequency ablation, 67–68
social media impact and, 1227
stage IV
clinical trials, 107–109
incidence of, 107
race/ethnicity and, 107
with single metastasis, 107
surgical management of, 105–114
systemic therapy, 107–109
stages of
effects of implants on, 142–144
survival rates and, 3
tests in, 105
at time of diagnosis, 143t, 183
surgical management of, 105–114
surgical prevention, 47–48
survival rates, stages and, 3
survivors of
patient expectations and, 1226–1227
treatment of
in augmented patients, 144–146
decision making, 299
history, 299
triple-negative
breastfeeding and, 6
residual disease in, 121–122
tumor microenvironments, 888
Breast cancer, types of
outcomes and, 890–891
Breast Cancer Index (BCI)
description of, 29
in early-stage breast cancer, 117t
function of, 118
Breast conservation surgery (BCS)
case studies, 311f–320f
complications, surgeon’s perspective on, 320
contraindications, 350
contralateral breast, 351–352
margins, 320–321
nipple-sparing mastectomy and, 498f
outcomes, 320
patient satisfaction, 321
plastic surgeon’s perspective, 311f–320f
postoperative care, 311
preoperative planning, 351–352
recurrences and, 321–322
sentinel node biopsies and, 239
symmetry procedures
case studies, 352f–355f
fat transfer, 352, 355f
intraoperative care, 352
outcomes, 355–356
postoperative care, 352
volume displacement techniques, 310–311
volume replacement techniques, 311
Breast conservation therapy (BCT)
5-year survival, 62
in augmented patients, 145–146
Baker grade changes after, 146t
BCT versus MST, 890
cancer recurrences after, 54
complication rates, 336
contraindications, 56–57, 56t, 88
corrections
case studies, 595f–597f, 599f–602f
implants in, 598–599
operative technique, 599
outcomes, 602
in DCIS patients, 199–200
definition of, 893–894
failures, 87–90
history of, 308, 590
IBTR and post-IBTR survival rates, 87t
for invasive breast cancer, 92t
radiation therapy after, 92t
lipofilling after, 901
local recurrence after, 183
mastectomy versus
in invasive breast cancer, 55t
locoregional recurrences, 87
patient preferences, 55–56
oncoplastic techniques
plastic surgeon perspective, 308–323
patient selection for, 54–59
history and physical, 54–55
patient preferences, 55–56
radiologic evaluation, 55
post-BCT surveillance, 57
preoperative planning, 598–599
radiation therapy after, 91–104
long-term survival rates, 54
radical mastectomy versus, 54
radiotherapy after
recurrence risk and, 189f, 190f
regional recurrence after, 60
shared decision making in, 208
Breast deformities. See also Ptosis
animation, 624f, 838f
breast augmentation and, 993
causes of, 1128
description of, 621
example of, 994f
implant-based reconstruction and, 621–626
submuscular positioning and, 1080
treatment of, 621–622
classification of, 944
areolar, 944
base, 944
breast volume and, 944
inframammary fold, 944
ptosis and, 944
skin envelope, 944
congenital
augmentation in patient with, 943–949
anatomic basis of deformities, 943–944
core volume fat transplantation for, 1133f
dog-ear
flap harvest sites, 776
double-bubble, 1007
tuberous breast correction and, 1176
ptosis, 944
skin envelopes, 944
skin stretch deformity, 957f
Snoopy, 1152f (See also Waterfall deformity)
Snoopy-nose, 929
surgical management, 944–945
tuberous, 943f, 1172f
anatomic basis of, 943–944
anatomical implants in, 1009f, 1010f
augmentation in patients with, 943–949
base, 944f
characteristics of, 1172
classification of, 1172
correction of, 1172–1177
contraindications, 1173
first description of, 1172
postoperative appearance, 1176f
preoperative appearance, 946f, 947f, 1175f
presentation of, 943
release of, 944–945
surgical outcomes, 946f, 947f
type 1, surgical management of, 944
waterfall deformity, 1066 (See also Snoopy-nose deformities)
anterior view of, 1092f
etiology of, 1090–1092, 1091t, 1099f
implant decisions, 1101
implant exchange
utcomes of, 1100f
lateral view of, 1092f
management of, 1098–1101
outcomes, 1099f
Breast diseases, benign, 8, 8t
Breast ducts
diameter of, 220
microvasculature of, 220
Breast footprint, definition of, 756
Breast height (BH)
measurement of, 1103–1105
preoperative assessment, 928, 928f
preoperative planning and, 1103–1105
Breast hyperplasia, DCIS and, 192–203
Breast Imaging Reporting and Data System (BI-RADS), 192–193, 896
on breast cancer risk, 41
Breast implant illness (BII), 1218–1224
CPT codes for
insurance coverage and, 1223
description of, 1218, 1239
history of, 1218
informed consent and, 1239
patient management
physical examination, 1220
surgery, 1220–1223
recent studies of, 1219–1220
symptoms of, 1218, 1219f
worries about, 675
Breast implant-associated anaplastic large cell lymphoma (BIA-ALCL),
1190–1203. See also Anaplastic large cell lymphoma (ALCL); Implants; T
cell lymphomas
adjuvant treatments
indications for, 1198–1199
augmentation mammaplasty and, 940
breast cancer and, 961
diagnostic criteria, 1195, 1198f
disease surveillance, 1199
early diagnosis of, 1006
effusion-limited
imaging of, 1194f
epidemiology of, 1190–1191
etiology of, 1006
follow-up, 1199
histopathology, 1190
malignant effusion, 1195f
history of, 1190
implant texture and, 1006, 1206
incidence of, 961, 1206, 1239
invasive, imaging of, 1194f
lifetime risk of, 1191
NCCN guidelines, 1191–1193, 1193f
pathogenesis of, 1190, 1191, 1206
preoperative oncologic workup, 1195
Ralstonia pickettii linked to, 996
saline implants and, 922
shaped implants and, 1011
solid tumor staging, 1195–1196, 1197f, 1198f
survival curves and, 1200f
surgical treatment of, 1196–1198
suspected patients, 1193–1195
textured implants and, 1056–1057
textured implants linked to, 997
treatment outcomes, 1199–1200
Breast implants. See Implants
Breast lift procedure
contralateral breast, 350
operative technique, 351–352
Breast mound
aesthetics of, 1139
augmentation, 853, 913
fat injections, 909
fat placement, 852, 945
firmness of, 599
flap selection and, 756, 805, 837, 854
goals of revisions, 843, 851
Goldilocks, 826
meridian of, 359
mushrooming of, 914
NAC position on, 399, 406–408, 1004, 1058–1062, 1066, 1091
case study, 401f, 403f
nipple position, 373, 1129
patient expectations, 1052
periareolar incisions, 599
postoperative care, 452, 1140
radiation effects on, 590
recreation of, 443, 683, 690, 824, 824f, 827
reshaping, 70
case study, 76f
goals of, 310
projection of, 328
revision of, 851–852
tissue fixation, 827f
size reduction of, 728
skin over, 368
subpectoral recreation of, 458
teardrop-shaped, 805f
Tegaderm over, 452
tissue deficiency, 846
Wise-type skin excision, 405
Breast parenchyma
anatomy of, 995–996
density of
variability, 1052
retraction of, 995f
skin and, 188f
volume of
variability, 1052
Breast pockets. See Pockets
Breast reconstruction. See also Reconstructive breast surgery
abdominal-based
aesthetic results, 867–872
closure, 871
contraindications, 868–869
history of, 867
incisions, 870–871
indications, 868–869
marking for, 869–870, 870f
operative technique, 870–871
patient selection, 868–869
postoperative considerations, 871
tissue availability, 870f
acellular dermal matrix in, 573–581
aesthetic considerations, 726–729
insetting, 726–728
shaping, 726–729
augmented patients, 676–678
autogenous
in thin patients, 873–878
with TRAM, 762–769
autologous-based
delayed versus immediate, 725–750
hernias after, 844
operative technique, 725–750
outcomes, 725–750
preoperative planning, 725
benefits of, 188, 638
bilateral, operative technique, 686
breast augmentation after
subfascial, 993–994
breast lift, contralateral breast, 350
breast reduction, contralateral breast, 350
complications, 613–619
contraindications, 450
delayed, 690–691
flaps in, 731
history of, 522
immediate versus, 522–524
indications, 522–527
LDMF and, 690–691
operative risk and, 608
direct-to-implant (DTI), 530, 639
operative risk and, 608
donor-site tissue, 869
effect of smoking, 1180–1181
evolution of, 472–473
expansion phase of, 553
failure of
case study, 741f
implant exposure and, 614–615
in irradiated breasts, 669–670
pathways to, 615f
fat transfer, 350
form-stable implant-based
decision making, 473–474
high-BMI patients
failure rates, 1187
history of, 349–350, 472, 530, 1225
“hot porridge” option, 821
hybrid reconstruction, 484–487, 485f–486f
immediate
flaps in, 731
LDMF and, 691–694, 701f
operative risk and, 608
immediate versus delayed
post-mastectomy radiation therapy and, 861
radiation and, 858–863
immediate versus staged
outcomes, 890
implant-based, 631f
after unilateral mastectomy, 638–646
augmented patients and, 675–682
case studies, 453f–455f
chemotherapy and, 645
contraindications, 639
drains, 644–645
failed, 779f
history, 449, 627, 647
implant salvage, 798f
indications, 638–639
intraoperative care, 452
operative, 880–881
operative technique, 450–452
outcomes, 456f
postoperative care, 452, 644–645
postoperative images, 454f
preoperative marking, 455f
preoperative planning, 639–641
prepectoral, 450
prepectoral versus subpectoral, 449–456
radiation therapy and, 645, 652f
shared decision making, 302–303
symmetry and, 631f
timing of procedures, 627–629
incisions, 640–641
indications, 450, 780
intraoperative care, 787
latissimus dorsi musculocutaneous flap, 683–705
mastectomy specimen
BMI and, 731f
dimensions of, 731f
guide for, 731f
one stage, 632–633
operative technique, 641–644
outcomes, 1225
partial flaps, 325f
patient reported outcomes
scale for assessment of, 647–648
patient satisfaction and, 211, 647
patient selection for, 780
PMRT and
clinical complications associated with, 859
postmastectomy, 168, 647
radiation therapy and, 859–864
post-mastectomy radiation therapy
timing of, 859
postoperative care, 787
preoperative oncoplastic
postoperative nipple malposition and, 654f
preoperative planning, 450, 532–533
prepectoral, 445, 483f
ADM and, 575, 575f
conversion
operative technique, 622–623
outcomes, 642f
trends in, 649
prosthetic, 530
rippling and wrinkling, 578
subcutaneous, 443
submuscular, 443–444
quality of life and, 302
recurrence after, 188
recurrence-free survival rates, 189f
revision, 696–698
ADM and, 578–579, 579f
decision-making algorithm, 736f
informed consent and, 1237
prepectoral conversion, 621–622
secondary, 398–404, 632–633, 731–735
capsule management, 633
case studies, 401–403
change of plane in, 633
complication rates, 403–404
contraindications, 398
fat injections, 632
history, 398
implant changes, 632–633
indications, 398
operative technique, 399–400
outcomes, 403–404
preoperative planning, 398–399
shared decision making and, 209
single stage, 639
skin excision patterns, 640–641
staged, 640
subpectoral
case studies, 461f–463f
complications, 464
contraindications, 458
history, 457
implant placement, 449
indications, 457–458
one-stage, 457–465
operative technique, 459–460
outcomes, 464
postoperative care, 460
preoperative planning, 458
revision rates, 464
symmetry procedures
pitfalls in, 349–357
unilateral implants, 627–636
techniques
shared decision making in, 302–304
templating in, 747f
timing of, 640
operative risk and, 608
tissue expanders and, 524f
two-stage, 632, 639
contralatreral augmentation and, 476f
implant exchange, 644
radiation delivery in, 708
type of
operative risk and, 608
Breast reconstructive surgery
decision-making in, 473
delayed
patient positioning, 772
dual plane, 533–535
immediate
patient positioning, 772
subpectoral, 533
two-stage
contraindications, 530–532
history, 530
immediate, 530–539
indications, 530
operative technique, 533–538
postoperative care, 535–537
second stage, 537–538
Breast reduction surgery
breast-conserving surgery and, 337
complications
asymmetry, 385–386
bottoming out, 385
hematomas, 384, 385f
infections, 385
puckers, 385
seromas, 384–385
underresection, 385
wound healing problems, 385
complications of
displaced NAC, 405–414
cosmetic
nipple malposition after, 650
displaced NAC, 405–414
fat removal, 883
indications, 389
intraoperative care
bandaging, 380–382
drains, 380
outcomes, 382f
taping, 380–382
liposuction, 883
male, 426t
liposuction, 418–422
liposuction versus excision, 416–440
massive weight loss
mastopexy and, 358–366
NAC malposition in, 412f
NAC placement in, 406
case studies, 411f–413f
outcomes, 414
postoperative care, 410
oncoplastic operative techniques, 376–380
complications, 383–386
dermis closure, 376–379
infiltration, 376
liposuction, 379–380
pedicle creation, 376
pedicle insetting, 376
pillar closure, 376
positioning, 376
recovery, 382
risks, 382–383
skin closure, 380
preoperative consultation, 372f
rereduction, 390f
principles of, 392f
risks
breastfeeding, 383
scarring, 382–383
sensation, 383
superomedial pedicle vertical
benefits of, 367–369
superomedial vertical
outcomes, 386f–389f
symmetry procedures, 633
Breast reduction/mastopexy
leval II oncoplastic surgery and, 80
operative technique, 351–352
Breast revision surgery
patient expectations
management of, 1130
postoperative care, 1130
secondary
contraindications, 1125
history of, 1123
indications, 1123–1125
intraoperative care, 1125–1130
operative technique, 1125–1127
patient assessment, 1123–1125
preoperative planning, 1125
Breast surgeons, social media for, 1241–1246
Breast surgery
aesthetic
polyurethane implants in, 1039
early mobilization after, 721
evolution of, 443–448
bioengineered concept of, 444–448
impact of smoking on, 1178–1181
informed consent for, 1233–1240
medicolegal considerations, 1239–1240
oncoplastic
decision making in, 299–307
operative risk factors, 607
pain and, 712
perioperative principles of, 1263–1270
previous
necrosis risk and, 606–607
regional pain control in, 718–720
risk factors
patient expectations, 1226–1227
Breast tissue
coverage classification for, 475f
reconstruction choices and, 476f
dense, 35
density of, 1055
effects of radiation on, 665
fascial system, 995–996
forces exerted on
weight and, 1026
glandular, 371
levels of, 1058f
morphovolumentric characteristics
reconstruction choices and, 476f
standard examination of, 1158–1159
stress-strain curves, 1027f
viscoelastic responses, 1027–1028
volume of
breast deformities, 944
Breast tissue coverage classification (BTCC), 506–507, 506t
measures in, 474
Breast-conserving surgery (BCS)
eligability for, 106
history of, 337–348
neoadjuvant therapy and, 111–112
oncologic safety of, 186
oncoplastic techniques for, 337
radiotherapy after, 91
Breastfeeding, 6
breast cancer risk and, 35, 41
breast reduction surgery and, 383
involutional hypomastia and, 921
ptosis after, 1069f
BREAST-Q questionnaire, 212, 357, 665
analysis for patient satisfaction, 570
BR-postoperative module, 357
Expectations module, 1226
patient-reported outcomes, 647–648
use of, 725
BRIP1 gene
breast cancer risk and, 10
cancer risk and, 46t
British Medical Devices Agency, 926
Brownian motion, biofilm adhesion and, 1212
Bupivacaine (Exparel)
liposomal, 1266
nerve block using, 719
BW distance. See Base width (BW) distance

C
CAF (cyclophosphamide, adriamycin, 5-FU) therapy, 111
Calcifications. See also Microcalcifications
benign, 20
sclerosing adenosis and, 193
dystrophic, 20
mammographic images of, 138
on mammography, 178–179
mammography of
behind LWBI, 1036f
scar tissue, 136f
warranting biopsy, 896
Calcium as secondary messenger, 6
Calcium-rich diets, breast cancer risk and, 6
CALLER Toolbox, 79
Cancer. See also Breast cancer; Specific cancers
models of
limitations, 888
recurrence rates
augmented breasts, 143t, 144f
screening for, 961
Cancer Intervention and Surveillance Modeling Network (CISNET)
models, 18
Cancer stem cells, removal of, 107
Cannulas
barbed, 910f
fat harvest, 904
in grafting mode, 912f
liposuction, 904
in motion
for fat grafting, 912f
selection of
for fat injection, 900–901
Capecitabine, NAT and, 121
Capillary ingrowth, 893
Capillary leak, radiation therapy and, 665
Caprini Risk Assessment Model, 717
Capsular activity, degree of, 1008
Capsular contracture (CC), 957f
acellular dermal matrix and, 575–576
ADM use and, 1118
after implants, 136
after LDMF surgery, 702
bacterial contamination and, 1204–1206
Baker grades of, 1205t, 1214
BIA-ALCL and, 1193
bilateral, 1147f
biofilms and, 1213–1214
history of, 1212
causes of, 1117–1118
correction of, 1145, 1147f, 1148f
definition of, 565
dermal substitute use after, 565
discussion of, informed consent and, 1236
etiology of, 1145, 1204–1206
example of, 1213f
factors contributing to, 938
biofilms, 996
inflammation, 996
skin contamination, 996
formation of, 1208t
grade 3, 1043f
grade 4, 1041f, 1042f
implant malpositions and, 1085, 1110–1115
implant rupture and, 1248
implant-related, 1039
infectious etiology for, 938
latissimus flap reconstruction and, 88
management of, 1085
mastopexy-augmentation and, 1083
minimization of, 1208t
patient education about, 956
periprosthetic
after augmentation mammaplasty, 938–939
circumferential linear fibrosis and, 930–931
porcine model of, 1205
postmastectomy radiation therapy and, 666, 708
prevention of, 565
aseptic maneuvers in, 996–997
experimental methods for, 1208–1209
proactive approach to, 1204–1211
radiation and, 672f
rates of, 472, 565, 1083
reconstructive surgery, 548f
reduced, factors associated with, 965t
revision procedures, 569–572
revisional surgery and, 1128–1129
risk of, 443
Capsular contractures
gel bleed and, 1204
Capsule dissection
examination of, 1114f
neopectoral technique, 1111–1112, 1113f
sutures, 1114f
Capsulectomy
ADM following, 577f
in BIA-ALCL, 1196–1198, 1199f
capsule recurrence and, 1128–1129
complete or partial, 676–677
for contractures
history of, 1204
en bloc, 1117–1118, 1119f
indications for
infections, 938
preoperative marking, 704f
Capsulorrhaphy, pocket modified by, 1144–1145
Capsulotomy, 632, 672f
Carbohydrate loading, preoperative, 717
Carbon monoxide, 1178
binding affinity of, 1265
Carboplatin
DNA damage and, 50
neoadjuvant chemotherapy and, 119
Carotinoids, breast cancer risk and, 6
Castile soap, 1215
Cauterization
Colorado tip in, 1021
monopolar, 753–754
monopolar cautery, 753–754
CC. See Capsular contracture (CC)
CCH. See Columnar cell hyperplasia (CCH)
CD30 immunohistochemistry
BIA-ALCL diagnosis and, 1194, 1195, 1195f
lymphoma staging, 1198f
CDH1 genes
breast cancer risk and, 19–20, 45t
breast cancer screening guidelines, 47t, 51
CEE. See Conjugated equine estrogen (CEE)
Cefamezin, 583
Cefazolin, 938, 996
Celecoxib, pain management using, 1266
Cell block cytology, 1194
Cell death, radiation and, 665
Cephalic vein transposition, 782
Cephalosporines
biofilm prophylaxis and, 1214–1215
postoperative, 467–468
Checkpoint serine-threonine kinase 2 (CHEK2) gene. See CHEK 2 gene
CHEK 2 gene
breast cancer risk and, 10, 19–20, 177
breast cancer screening guidelines, 47t, 51
cancer risk and, 46, 46t
Chemotherapy. See also Adjuvant chemotherapy; Specific regimes
adjuvant RT and
clinical trials, 157
anthracycline-based
for BIA-ALCL, 1198–1199
delayed
breast reconstruction and, 302
neoadjuvant
nipple-sparing mastectomy and, 217
side effects related to, 124–125
Chest
circumference of, 1016
width of
transgender patients, 1168
Chest feminization
in gender dysphoria, 1167
outcomes, 1170
Chest masculinization
case studies, 1163f–1164f
circumareolar technique, 1160
contraindications, 1159
focused assessments, 1158–1159
general considerations, 1157–1158
generic risks of, 1164–1165
history of, 1157
indications, 1159
intraoperative care, 1160, 1160f
outcomes, 1165
postoperative care, 1162–1164
preoperative evaluations, 1157–1158, 1158–1159
for transmasculine individuals, 1157–1166
Chest wall
deformities of
shaped implants in, 1009–1010
evaluation of, 1055–1056
fibrosis of, RT and, 859
irradiation of, 863
muscle contouring of, 1157
muscles
indications for resection, 106
tissue coverage using, 443
Childbirth, ptosis after, 1067f
Chlorhexidine
antisepsis and, 1207
prep skin preparation, 717
Chlorhexidine gluconate (CHG), 845
“Choice talk,” 299–300
CHOP regimen for BIA-ALCL, 1198–1199
Chronic pain. See also Pain management
breast surgery and, 712
inflammatory, 712
CINPT. See Closed incision negative pressure therapy (CINPT)
Circulating tumor cells (CTCs), 118
Circumareolar incisions, 73, 74f
Circumareolar mastopexy pattern, 1058–1059, 1061f
markings, 1065f
operative technique, 1062–1065, 1065f
Circumferential linear fibrosis, 930–931
Circum-mammary ligament, 996, 996f
Cisplatin, DNA damage and, 50
Classification of Postreconstruction Breast Defects checklist, 735, 736t
Classmates.com, 1241
Claus model, breast cancer risk, 42t, 43
Clavipectoral fascia incision, 243
Clodronate, adjuvant therapy and, 129
Clonidine, 37, 1266
Closed incision negative pressure therapy (CINPT), 567, 569
CMF therapy in breast cancer, 122
Coatings, implant, 1214
Cobbs v. Grant, 950
COC. See Combined oral contraception (COC)
Cold therapy, pain management using, 1266
Coleman cannulas, 900–901
Collaborative Group on Hormonal Factors in Breast Cancer, 9
Collagen
deposition of, 665
disrupted architecture of, 1206
radiation therapy and, 665
synthesis of, 1264
wound healing and, 1264
College of American Pathologists (CAP), 24
Columnar cell hyperplasia (CCH), 194
Combined oral contraception (COC), 9
Communication. See also Informed consent
breast and plastic surgeons, 218
informed consent and, 962, 1233–1240
language and, 951
physician-patient relationships and, 951–952
augmentation mastopexy and, 1052–1054
“teach back” techniques, 951
of test results, 1239
Complete decongestive therapy, 274–279, 274f
arm sections for, 277f
compression bandages, 277f
Complications. See also Specific conditions
discussion of, 1235
informed consent and, 1235
patient dissatisfaction and, 1228
patient risk factors for, 604–607
Compression dressings, postoperative, 1078
Compression mammography, 141f
Compression therapy
bandaging and, 277, 279, 281, 285
for lymphedema, 285
postsurgical lymphedema, 277, 280f
Computed tomography
BIA-ALCL and, 1193
perforators identified by, 771
Computerized tomographic angiography (CTA)
preoperative, 836
Concentric skin-reduction techniques, 435t
Congenital breast deformities
augmentation in patient with, 943–949
anatomic basis of deformities, 943–944
history, 943
core volume fat transplantation for, 1133f
Congenital hypoplastic breasts, 908
Congestive heart failure, chemotherapy-related, 125
Conjugated equine estrogen (CEE)
breast cancer risk and, 9
Connective tissue disease, BCT contraindication in, 57
Consent forms, language of, 951
Contractures. See also Capsular contracture (CC)
radiation-related, 146, 146f
Contralateral matching procedures, 758
Contralateral prophylactic mastectomy (CPM)
breast cancer risk and, 356–357
IBTR and, 89
outcomes, 355–356
patient satisfaction and, 211
reconstructive procedures after, 349
symmetry and, 349
Convection, biofilm adhesion and, 1212
Conventional fractionation (CF), 96–97
Cooper ligaments, 171, 506, 996f, 1057f
Cord cell tumors, ovarian, 45–46
Core body strength in high-BMI patients, 514
Core Clinical Studies, implant manufacturer, 1144–1154
Core needle biopsies
in augmented patients, 138
breast cancer diagnosis and, 105
inflammatory breast cancer, 110–111
Core technique, 550f
Core volume augmentation, fat for, 1134f–1136f
Corneal opacities, tamoxifen and, 127
Corpus mammae, anatomy of, 996f
Costochondral junction excision, 782f
Cotinine tests
blood, 1182
saliva, 1182
urine, 1182
“Cover-Roll” tape, 552
Cowden syndrome
breast cancer screening guidelines, 47t
cancer risk and, 45
PTEN gene and, 35
screening in, 51
syndromes related to, 45
Cox-1 inhibitors, 1266
C-peptide levels, breast cancer risk and, 8
CPM. See Contralateral prophylactic mastectomy (CPM)
Crescent lift mastopexy, 1061–1062, 1065f
Crescent lift mastopexy pattern, 1057–1058
Crescent mastopexy, 74–75, 74f
for nipple malposition, 658, 658f
Cryoablation
breast cancer studies, 66–67, 66t
limitations of, 68
Crystalloids, euvolemia management and, 754
Cultural barriers, patient education and, 956
Cushing disease, impacts on tissue, 391f
Cyberbullying, 952
Cyclooxygenase-2 inhibitors, 720
Cyclophosphamide. See also CHOP regimen
amenorrhea related to, 124
CAF therapy and
outcomes, 111
myelodysplastic syndrome and, 124
Cyclophosphamide, methotrexate, and 5-fluorouracil (CMF). See CMF
therapy
Cystic breast masses, 192–193
Cytokines
expression after radiation therapy, 859
inflammation and, 1264
Cytotoxic therapy, administration of, 119

D
Dairy foods, breast cancer risk and, 6
DBR. See Delayed breast reconstruction (DBR)
DCIS. See Ductal carcinoma in situ (DCIS)
Deaver retractors, 549, 553, 977, 987f, 988
DeBakey forceps, 934
Decision making
aids to, 211
flap selection, 756
gynaecomastia, 416
informed consent and, 950–952
partial breast reconstruction, 324f
paternalistic style of, 1227
patient choice and, 208–214
patient decision aids and, 951
patient satisfaction and, 208–214, 211
pre-breast augmentation, 1000
preference-sensitive, 952
shared
patient choice and satisfaction, 208–214
“Decision talk,” 300
Decongestive lymphatic therapy (DLT), 292
Decongestive therapy, 274–279, 285
Deep inferior epigastric artery perforator (DIEAP) flap
breast reconstruction
outcomes, 759f
LAP flaps as alternative to, 812–814
in reconstructed breast, 850, 853f, 854f, 855f, 856f
Deep inferior epigastric perforator (DIEP) flap, 714
abdominal wall morbidity and, 782
advantages of, 762
algorithm for insert of, 725
autologous, case study, 748f
bilateral, case studies, 737f–740f
breast reconstruction using, 881f
complications, 869
contraindications, 868–869
delayed reconstruction case study, 742f, 746f
dissection of, 784f
donor sites, 844–847
failed, 838f–839f, 841f
hernia rates after, 844
in high BMI patients, 1186
history of, 762, 843
immediate reconstruction
case study, 748f
fat grafting after, 749f
indications, 868–869
in irradiated patients, 669
near-equivalent backups for, 755
nerve coaptation and, 832f
neurotization of
case study, 788f, 789f
outcomes of, 833–834
sensory, 778–792
techniques for, 832–833
operative technique, 780–787
patient satisfaction with, 526
patient selection, 868–869
PMRT timing and reconstruction using
patient satisfaction and, 860
popularity of, 843
preoperative planning, 780–787, 781f
prior to revision surgery, 745f
salvage use of, 669, 670, 671f
with sensory neurotization, 778–792
sensory return of, 834
shaping of, 726
vessel anastomosis, 832f
Deep inferior epigastric vessel anastomoses, 785f
Deep thoracic fascia release, 687f
Deep vein thrombosis (DVT)
in high-BMI patients, 1188
preoperative evaluation, 717
prevention of, 816
prophylaxis, 717, 1188
risk of, 394, 717, 876
tamoxifen and, 36, 127
Delayed breast reconstruction (DBR), 690–691. See also Delayed
expander/implant-based breast reconstruction
autologous
immediate versus delayed, 861
indications, 525
bilateral mastectomy and, 851f
complication rates, 523
deep inferior epigastric perforator flaps
case study, 742f, 746f
fat grafting in, 731
flaps in, 731
history of, 522
immediate versus, 522–524, 858–863
implant-based
bilateral, 527f
indications for, 525
implant-based versus autologous, 524–525
indications, 522–527
LDMF and, 690–691
modified radical mastectomy after, 1187f
operative risk and, 608
patient positioning, 772
psychosocial well-being and, 861
radiation and, 858–863
Delayed expander/implant-based breast reconstruction
case studies, 554f–558f
contraindications, 546–547
history of, 540
implant selection, 553
indications, 540–546
marking for, 542f, 545f, 546f, 554f–558f
operative technique
core technique, 550f
delayed expander insertion, 549–553
implant placement, 553–559
outcomes, 543f, 544f
preoperative planning, 547–549
surgical risks of, 559–562
timing of, 540–546
Delayed wound healing, prophylactic antibiotics and, 1215
Delayed-immediate breast reconstruction
postmastectomy radiation therapy and, 670, 861–864
patient selection for, 862
schema for, 862f
tissue expanders in, 525–528
two-staged, 863
outcomes, 864f
Dental prophylaxis, 1238
Dermabond, 1106
Dermahooks, 754
Dermal flaps, creation of, 514f
Dermal matrices, 349, 565–566. See also Acellular dermal matrix (ADM)
Dermal substitutes
anatomic landmark reinforcement and, 565–566
implant pocket definition and, 565
prepectoral reconstruction and, 564–565
prepectoral reconstruction without, 566–572
purpose of, 564–572
Dermatitis
radiation therapy and, 859
Dermoglandular flap
inferior, 1081
raising of, 1078
superior, 426
Dermoglandular wedge excisions, 396
Desquamation
moist, 859
prevention of, 163
treatment breaks and, 163
NAC, 155, 155f
radiation-induced, 163, 670
Dexmedetomidine (Precedex), 1266
Diabetes
complications related to, 72, 639
contraindications related to, 150, 510, 511t, 516, 812
delayed chemotherapy and, 302
flap necrosis and, 613, 847
glycemic management, 1265
high-BMI patients and, 516
macrovascular disease and, 1265
NAC malposition and, 651
nipple-sparing mastectomy and
NAC malposition in, 651
presurgical assessments, 398
uncontrolled, 450, 625, 763, 780
vascular disease and, 1265
Diarrhea, chemotherapy-related, 124–125
DIEP flap. See Deep inferior epigastric perforator (DIEP) flap
Diet
bleeding and, 1236
breast cancer risk and, 40–41
cancer risk and, 6, 40–41
ERAS protocol and, 780
fibrocystic disease and, 790–791
gynaecomastia management and, 417
postoperative, 234, 488, 720, 756
pseudogynaecomastia management and, 417
weight loss and, 358
Diethylstilbestrol (DES), breast cancer risk and, 4–6, 32t
Diffuse large cell B-cell lymphomas, 1190
Digital mammography
augmented breasts and, 141
saline implants on, 142f
Dimpling, assessment of, 105
Dingman-Agris dissectors, 983, 986, 988, 989
Direct-to-implant (DTI) reconstruction, 490f, 639
acellular dermal matrices and, 473
ADM-assisted, 582–583
indications for, 583
preoperative considerations, 583
nipple areolar complex, 504
operative techniques
dual plane, 494
prepectoral plane, 494
reduction for NAC perfusion delay, 494–495
reduction pattern, 494
outcomes, 508f
postmastectomy radiation therapy and, 667
prepectoral
complication rates, 570–572
outcomes, 570–572
two-stage, 571
without dermal substitutes, 566–572
prepectoral reconstruction, 458, 459
shared decision making and, 302–303
single-stage
implant radiation and, 709
tissue expander radiation and, 709
in small breasts, 478–480
subpectoral breast augmentation and, 463f
surgical techniques, 493t
Dissatisfaction, risk factors for, 1228t
DNA microarrays, 26, 26f
Docetaxel, 50, 119–121, 249
Docetaxel/cyclophosphamide (TC). See TC therapy
Docetaxel/doxorubicin/cyclophosphamide (TAC), 119
Documentation
breast measurements, 1055f, 1103
of informed consent, 1238
of patient education, 960–961
Stowers doctrine, 1238–1239
Dog-ear deformities, 359, 367, 382, 385, 776
Donor sites
anesthesia, 904
body mass index in
thin patients, 873
bulging
abdominal fascia, 779
closure
umbilicoplasty, 786
closure of, 773
complications at, 776, 843–849
DIEP flaps, 844–847
dressings, 1140
fat grafting, 904, 945
free TRAM flaps, 1181
hemiabdominal flaps, 728f
irregularities, 1142
latissimus dorsi flaps, 335f
lumbar artery perforator flap, 814f
marking
autologous fat transfer (AFT), 913–916
fat grafting, 913–916
morbidity at, 779, 1187
necrosis at, 1187
seromas, 336, 702, 1142
surgical site occurrences, 844–847
tissue for breast reconstruction, 869
transverse upper gracilis flaps, 804f
vascularized, 284–291
lymph nodes, 284–291
VLNT, 286f, 287–288
Donut mastopexy
algorithm, 79t
technique, 72, 75–76, 76f
Doppler imaging
perforator identification, 794
postoperative monitoring, 836
Dorsal intercostal artery perforator (CICAP) flap, 326
Double-bubble deformity, 1007, 1009f
correction of, 1111
lawsuits and, 1237
tuberous breast correction and, 1176
Doxorubicin. See also CHOP regimen
congestive heart failure related to, 125
Doxorubicin/cyclophosphamide. See AC regimens
Drains
abdominal, 846
antibiotic protocol, 1269
breast reduction surgery, 380
closed suction, 1208
insertion of, 1114f
management of, 1269
seroma prevention, 845, 846
Draping, antisepsis and, 1207
Dressings
adhesive tape in, 1162
antibiotic-impregnated, 977
biofilm prophylaxis and, 1214
changes of
stress of, 1227
drain site, 1267
fat donor sites, 1140
incisional negative-pressure
in high BMI patients, 1187
negative pressure, 845
occlusive, 1267
postoperative, 997–998
VAC, 847–848
DTI reconstruction. See Direct-to-implant (DTI) reconstruction
Dual Gel Implants, 474
Dual plane technique, 533–535
Ductal carcinoma in situ (DCIS), 200
breast hyperplasia and, 192–203
chemoresistance in, 80
description of, 198
incidence of, 198
invasive breast carcinoma and, 57, 93
lumpectomy in, 57
male breast cancer, 179–180
mammographic imaging of, 198–199
management of, 186–187
margins, 186–187
nipple-sparing mastectomy and, 220, 221f, 222, 222f
pathologic classification of, 199
posttreatment surveillance of, 200
presentation of, 198
radiation therapy in, 93
recurrence risk for, 186
risk factors for, 198
risk of recurrence, 185–186
sentinel node biopsy in, 238
survival rates, 19
treatment of, 199
radiation therapy in, 200
surgical, 199–200
systemic treatment, 200
Ductal hyperplasia
atypical, 21t, 31, 194
cancer risk and, 8
characteristics of, 193
histology of, 193f, 195f
Dufourmentel-Mouly procedure, 429–430
E
Eclampsia, breast cancer risk and, 5
Edema. See also Lymphedema
breast, 96, 183
breast cancer and, 110, 216
chronic, 912
compression therapy and, 280, 282
flap, 499
macular, 127
postoperative, 20, 294, 690
radiation therapy and, 325, 665, 709
reduction of, 847, 905, 1093, 1266–1267
stromal, 355
Education levels, decision making and, 299
Efficiency
concepts for, 751
definition of, 751
Egypt, breast cancer mortality rates and, 3
Ehlers-Danlos syndrome, 1102
Elastin, wound healing and, 1264
Electrocautery
in augmentation mastopexy, 934
blunt-tipped, 138
breast augmentation surgery, 977f
breast implants and, 138
breast parenchyma, 977f
hemostasis maintained by, 934, 980
lighted, 977
operative risks of, 608
seroma formation and, 846
subdermal plexus thrombosis and, 467
Electromagnetic radiation, biofilm prophylaxis and, 1215
Electronic cigarettes (e-cigs), 604–605
Electrostatic interactions, biofilm adhesion and, 1212
Elliptical excision techniques, 429–430, 433f, 434f
Embryo cryopreservation, 124
Emory Breast Retractor sheath, 983
Endocrine therapy, 64–69. See also Adjuvant endocrine therapy
Endometrial cancer, tamoxifen and, 127
EndoMT, acellular dermal matrices and, 667
EndoPredict
description of, 29
in early-stage breast cancer, 117t
Endoscopes
bowel screening by, 51
electrocautery with, 996
Laser-assisted lipolysis, 417t
liposuction assisted by, 420, 422, 436t
transaxillary approach and, 982–991, 984f
use of, 996
visualization using, 934, 977, 978f, 987f, 991f
Endothelial growth factor (EGF) expression, 285, 859, 888
Enhanced Recovery After Surgery (ERAS) protocol, 780
breast, 713–714
components of, 714–717
historical perspective, 713
length of stay and, 714
preadmission interventions, 714–717
protocols, 716f
recommendations, 715t–716t
intraoperative interventions, 717
perioperative multimodal pain, 717–718
preoperative fasting, 717
preoperative holding interventions, 717
surgical efficiency and, 752
Enoxaparin
bowel prep using, 232
VTE prophylaxis, 1266
EPCAM gene, cancer risk and, 46t
Epidermal growth factor (EGF), 6
Epidermal growth factor receptor inhibitor. See Lapatinib
Epidermolysis, smoking and, 1181
Epidural anesthesia, 1266
Epinephrine, 1266
bupivacaine with, 1266
fat donor sites, 904
lidocaine and, 170, 376, 396, 549, 904, 1085
local anesthetics with, 782, 852, 966, 966t, 977, 1004
Marcaine with, 1105
operative conditions and, 172
vasoconstriction by, 608, 855
Epineural repair, 833f
Epithelialization, radiation therapy and, 859
ERAS. See Enhanced Recovery After Surgery (ERAS) protocol
Erosions, assessment of, 105
Erysipelas, frequency of, 284
Erythema, inflammatory breast cancer and, 109
Escherichia coli, capsular contractures and, 1204
Esmarch bandages, 294
Estrogen receptors (ERs). See also Hormone receptor expression
inflammatory breast cancer and, 109
RMRT outcomes in, 159
tumors positive for, 159
Estrogens
adipose-induced, 7
interactions with SERMs, 37
maternal, 5
synthesis of, 896
therapy using, 1167
transfeminine mammogenesis and, 1167
Ethical concerns, social media and, 1244–1245
Ethics, patient autonomy and, 952
Euvolemia, maintenance of, 754
EVE. See External vacuum expansion (EVE)
Events, social media and, 1244
Everolimus, use in early breast cancer, 128
Evidence-based guidelines, patient education and, 952
Excisions
open
complications of, 430–435
limitations of, 430–435
periareolar, 423–426
techniques, 423–426
Weber open excision, 424f–425f
Exemestane
breast cancer risk reduction and, 36
in ER positive tumors, 121
Exercise, postoperative, 1023
Expanded polyvinylalcohol formaldehyde (Ivalon sponge), 921
Expander/implant reconstruction
selection of, 597–598
Expanders
deflated, 594f
delayed-immediate insertion, 558
fill, 552
full-delayed
insertion of, 545
immediate
failed, 561f
Exparel®, 533, 535
Extensive metabolizers (EMs), 713
External beam radiation
trials of, 99–100
External oblique muscles
fascia covering, 995
External vacuum expansion (EVE)
AFT and
angiogenesis and, 911–912
graft delivery, 911–912
operative technique, 909–912
postgraft care, 912
site preparation, 911
autologous fat grafting and, 908
autologous fat transfer and
generic risks of, 916
preoperative education, 909f
preparation protocol, 908
Extracellular matrix
biofilms and, 1212
composition of, 1212
wound healing and, 1264

F
Facebook, targeted advertising on, 1241–1242
Factor V Leiden mutation, 1266
thrombosis and, 837–838, 837–839
Factor VIII elevation, thrombosis and, 839
Family histories
BRCA1/2 carriers, 49
breast cancer risk and, 9, 31, 40, 41
chest wall masculinization and, 1158
discussion of
informed consent and, 1235
risk reduction mastectomy and, 37t
Fascial system
breast, 995–996
deep, 996
superficial
anatomy of, 996f
Fast Track Surgery. See Enhanced recovery after surgery (ERAS) protocol
Fat
centrifugation of, 900
donor sites, 904
G forces on, 900
harvest techniques, 904
preparation for injection, 900
processing of, 904–905
reinjection of, 900
vascular insufficiency, 605
Fat grafting, 727f. See also Autologous fat grafting (AFG)
access options, 900–901
adjunct, implants and, 901–902
ancillary procedures, 914
augmentation mastopexy, 1066–1067
autologous, volume issues, 881–882, 881f
autologous fat breast reconstruction and, 903–907
bolus injections of
failure of, 909–910
breast cancer detection and, 887–888
breast cancer recurrence and, 888–891, 901
case-controlled studies, 889–890, 889t
observational studies of, 888–889
breast cancer risk and, 887–892
breast imaging and, 896
breast reconstruction using, 649
buildup of patient prior to, 732f, 733f
case studies, 894f–895f
categories of, 1132–1133
controversies, 896–897
for core volume, 1132, 1132f
core volume augmentation
outcomes, 1134f–1136f
outcomes with fat only, 1132
in delayed reconstruction, 731
delivery of, 911–912
donor site dressing, 1140
donor site irregularities, 1142
donor site marking, 913–916
donor sites, 945
fat placement, 1139
fat preparation, 900
fat reinjection, 900
fat retention and, 896–897
free
blood supply to, 909
graft survival, 1142
graft volumes, 897
grafting techniques, 914
harvest techniques, 899–900
harvesting, 852–853, 911f
harvesting seeds for, 910–911
history of, 1132–1133
in implant-based breast reconstruction, 899
irradiated skin flaps after, 528f
“mountains of sand” analogy, 1132, 1133f
oncologic safety, 896
partial mastectomy defects, 893–898
history of, 893
indications, 893
radiation change and, 893–895
patient safety and, 901
percentage survival, 913f
placement of, 894
postgraft care, 912
preoperative marking for, 703f
primary augmentation and, 997
principles of delivery, 910f
in radiated breast, 852
radiation therapy and, 894f
recipient site marking, 914
secondary breast augmentation and, 1126
serial, 837
simultaneous implant exchange with (SIEF), 1132
third space, 1133
tissue coverage and, 1127
for upper pole hollowness, 735f
Fat Grafting Task Force (FDA), 894
Fat grafts, free
blood supply to, 909
Fat harvesting, seeds, 910–911
Fat injections
breast reconstruction, 634
contralateral breast
symmetry procedures, 634
prepectoral implants and, 631f
subpectoral implants and, 631f
Fat necrosis
breast, 197
causes of, 910
EVE and AFT risks, 916
flap harvest sites, 776
PMRT and, 524
Fat tissue, coverage thickness, 504–505, 506t
Fat to implant ratios, 1138–1139, 1138f
outcomes and, 1141f
Fat transfer
bed preparation, 945
breast reconstruction and, 350
contralateral mastopexy, 355f
implant revision, 355f
radiated breast, 355f
reverse abdominoplasty and, 915–916
techniques, 905
Fat transplantation, focused, 1132
Fatigue
chemotherapy-related, 124–125
radiation therapy and, 163, 859
Feminizing augmentation, 207
in transgender patients, 1167
Femoral nerve, medial sensory branch of, 834
Fertility preservation
LHRH analogs and, 124
shared decision making in, 208
Fibrin sealants, 846
Fibroadenoma
description of, 195
histology of, 195f
juvenile, 195
presentation of, 195
recommendations, 197t
Fibroadipose tissue, hypertrophied, 293
Fibroblasts
acellular dermal matrices and, 667
collagen synthesis and, 1264
impact of radiation on, 576, 859
inflammation and, 1264
ingrowth of, 576
Fibrocystic changes, 192, 192f
Fibrofatty accumulation, lymphedema and, 229
Fibromatosis, breast, 197
Fibrosis
capsular contractures and, 666
chest wall, 859
inflammation and, 1205
postmastectomy radiation therapy and, 669f
radiation therapy and, 163, 606, 665, 837, 859, 893
Fibrous pseudobursa, 845
Financial concerns
discussion of, 1236
informed consent and, 1236
shared decision making and, 209
Fine-needle aspiration (FNA)
BIA-ALCL diagnosis, 1198f
biopsies, 1198f
cystic breast masses, 192–193
inflammatory breast cancer diagnosis by, 110
Fisher, Bernard, 260
Fisher Grading System, 1158, 1158t
grade 2, 1159f
grade 3, 1159f
grade I, 1158f
transmales, 1163f–1164f
Fisher hypothesis, 237
Flap necrosis. See also Necrosis
BMI and, 605–606
DIEP flaps, 869
donor site morbidity and, 1187
full thickiness, 611
implant exposure and, 613
LDMF reconstructive surgery, 698
mastectomy-related
rates of, 604
partial thickness, 611
pedicled vs. free flaps, 762
periareolar incisions and, 218
rates of, 762
Flaps. See also Specific flaps
abdominal
aesthetic concerns, 867–868
anastomosis, 755–756
autologous
neurotization of, 831–834
backups for, 755
compromised circulation, 835–836
donor site morbidity, 779, 1187
donor sites
surgical site occurrences, 844–847
elevation of, 753–754
evaluation of
surgical efficiency and, 752
excess skin and, 729, 729f
failed
preventative maneuvers, 836
prosthetic reconstruction, 837
secondary reconstruction, 837
innervated, 832
temperature perception, 832
insetting of, 726–728
local
for partial mastectomy, 324–336
microvascular reconstruction, 837–838
monitoring of, 836
neurotization, 778–792
nutrient vessels for, 337–338
perfusion of, 845
ICG assessment of, 499
intra-operative findings, 523
periareolar
delayed, 733f
positioning of, 753
preoperative imaging, 843, 844
preoperative marking of, 771
selection of, 756
shaping of, 726
immediate versus delayed reconstruction, 725–750
sizes of
BMI and, 345, 346f
planning for, 341
success rates, 835
tailor tacking, 513f
thickness of, 218, 553, 566
complication rates and, 604
operative risk and, 607
SSM and, 187–188
vascularity of, 511
complication rates and, 564
evaluation of, 641
width of
planning for, 341
Flat epithelial atypia, breast cancer risk and, 8, 8t, 194
FLOSEAL Hemostatic Matrix, 846
Fluid homeostasis, lymphatic system and, 284–285
Fluid retention, tamoxifen and, 127. See also Edema; Lymphedema
Fluorescence angiography. See also Indocyanine green (ICG)
intraoperative, 523f
after mastectomy, 523f
nipple areolar complex and, 153f
operative assessment using
predictive accuracy of, 609
skin flap viability, 608
Fluoroquinolones, biofilm prophylaxis and, 1215
5-fluorouracil (5-FU), CAF therapy and, 111
FNA. See Fine-needle aspiration (FNA)
Follow-up appointments, informed consent and, 1238
Food and Drug Administration (FDA)
classification of breast implants, 950
Fat Grafting Task Force, 894
Guidance Document, 1247
moratorium on silicone implants, 950, 956
screening for implant rupture, 1247
For marking
vertical mastopexy pattern, 1066f
Foreign bodies, implants as, 135–136
Formenti, Sylvia, 99
Free flaps
abdominal, 88
failed
after leech therapy, 835f
management of, 835–842
irradiated implants and, 670
smoking and, 1181
Free nipple grafts
mastectomy and, 429
NAC position and, 399
for nipple malposition, 659–660, 660f
nipple-sparing mastectomy, 217
Free tissue transfer, contraindications, 763, 780
Fulvestrant, function of, 180
Funnels
bacterial exposure reduced by, 980, 996–997, 1057, 1214
forces on implants and, 981
Keller type, 459, 569, 591
bacterial exposure reduced by, 1022
incision length and, 1020
“no touch” implant placement, 948, 971, 971f, 1140

G
Gabapentin
hot flashes minimized by, 37
pain management using, 1266
postoperative, 720
presurgical, 460, 717, 780, 1103
Gadolinium-based contrast media
side effects of, 47
Gail/BCRAT model
breast cancer risk, 31, 35–36, 42t, 43
GalaFLEX, 1118
ADM with, 1150
composition of, 1126
placement of, 1126
Galaform 3D
insertion of, 1098f
Galveston scale, 394
Garamycin, in triple-antibiotic solution, 583
GAS. See Gender-affirmation surgery (GAS)
Gastroepiploic flaps, 231, 233, 233f, 287–288
Gel bleed
capsular contractures and, 1204, 1207
diagnosis of, 1034
gel leaks versus, 939
inflammatory response to, 137
irritation caused by, 938
LBWIs and, 1034
reduction of, 923, 1037
Gelpi self-retaining instruments, 754
Gender, breast cancer risk and, 3–6
Gender diversity, definition of, 1167
Gender dysphoria
diagnosis of, 1167
ICD-10 classification of, 1157
incidence of, 1157
Gender identity, issues concerning, 1157
Gender nonbinary patients, health care needs of, 1157–1158
Gender-affirmation surgery (GAS), 204–207
case studies, 206
intraoperative care, 205
postoperative care, 205–206
Gene chips, 26f
Gene expression profiling
breast cancer subtypes, 116–117
breast tumors, 24, 27f
clinical applications of, 28
description of, 26
early-stage breast cancer, 117–118
multi-gene panels, 117t
Genetic counseling
breast cancer risk and, 32, 33t
guidelines for, 43
risk/benefits assessment
components of
Genetic Information Nondiscrimination Act of 2008, 43–44
Genetic testing
breast cancer risk and, 32, 33t
considerations, 43–44
family histories and, 44t
indications for, 44t
low-penetrance genes, 47
moderate-penetrance genes, 46, 46t
multigene panel, 44–45
Genetics
breast cancer risk and, 9
recurrence risk and, 183
Genomic cancer risk assessment, 43
Gentamicin in triple antibiotic solutions, 938, 996
GeoCities, 1241
Glandular hypomastia, 921, 928
Glandular necrosis
post oncoplastic surgery, 77
Glandular tissue, density of, 1056
Gluteal artery perforator (GAP) flap, 863. See also Inferior gluteal artery
perforator (IGAP) flap; Superior gluteal artery perforator (SGAP) flap
flap failure and, 835, 837
Gluteus maximus muscle
harvesting of, 770
Glycemic control, surgical risk reduction and, 1264. See also Diabetes
Godoy manual lymph drainage technique, 293
Goldilocks
mastectomy
patient counseling, 822
Goldilocks mastectomy, 821–830
after care, 826
bilateral, 825f
case study, 747f
flap insets, 826
follow-up, 826
history, 821
indications, 821–822, 827t
marking for, 823
mound with nipple excision, 825
operative technique, 823–829
deepithelialization timing, 823, 824f
flap creation, 824
marking, 823
outcomes, 825f
steps, 824f
patient selection, 822
perioperative considerations, 822–823
preoperative considerations, 822–823
preoperative evaluation, 822–823
preoperative planning, 822–823
with SWIM nipple preservation, 828f, 829f
outcomes, 828–829
Gonadotropin releasing hormone (GnRH)
treatment with, 1167
Google reviews, 1244
Goserelin
adjuvant therapy using, 128, 129
ovarian ablation with, 128
Gracilis muscle. See also Transverse upper gracilis (TUG) flap
central axis of, 802, 802f
exposure of, 796f
functional loss of, 809
harvesting of, 805
marking of, 794
orientation of, 803f
position of, 802f
vascular supply to, 874
Grafts, avascular, 915
Graft-to-recipient interfaces, optimization of, 910
Grant, Cobbs v., 950
Granulocyte growth factor (GGF), 123
Granulomatous mastitis
description of, 197–198
Gravity
force of, 1025–1026
negative effects of, 367
Greater saphenous vein, preservation of, 805
Groin flaps
harvesting of, 287
VLNT donor sites, 286–287, 286f
Grolleau classification, 944, 1172–1174
Growth factors, breast cancer risk and, 8–9. See also Specific growth factors
Guatemala, breast cancer mortality rates and, 3
Gynaecomastia
algorithm for surgery, 437f
benign, 178f
breast reduction surgery
liposuction versus excision, 416–440
classification of, 417f
description of, 178–179
elliptical excision techniques, 429–430, 433f, 434f
excision, 423–435
incisions, 423
open glandular, 423t
techniques, 423–430
idiopathic, 416
liposuction for
outcomes, 420–422
liposuction +open excision, 427f–428f
male breast cancer and, 177
male breast reduction
complications of, 435t
mastectomy
free nipple grafting and, 429
open excision
complications of, 430–435
limitations of, 430–435
postoperative care, 435–437
treatment, 417
treatment algorithms, 416
ultrasonic, 418–420
ultrasound-assisted, 418–420
unilateral, 416
VASER liposuction for, 420

H
Halstead, William, 167, 237
Halsted mastectomy, survival rates after, 54
Hamartomas, 197
Harmonic scalpels, operative risk and, 608
Hartrampf zones of perfusion, 762–763, 843, 1187
Headlights, 977
Head-of-bed elevation, postoperative, 871
Health care, waste in, 951
Health Grades, 1244
Health Insurance Portability and Accountability Act, 1243
Health outcomes, patient expectations and, 1226–1227
Heart disease, radiation therapy and, 859
Heavy metals
drinking water limits for, 1222t
silicone implants and, 1221t
Height, breast cancer risk and, 8–9
Hematomas
after breast augmentation, 936
after breast reduction, 384, 385f
breast augmentation outcomes, 1169–1170
coagulated, capsular contractures and, 1206
in DIEP flap patients, 845
flap recipient sites, 776
male breast reduction surgery and, 435
mastopexy-augmentation and, 1083
rates of, 1083
Hematoxylin and eosin (H&E) staining, 24
Hemiabdominal flaps within donor sites, 728f
Hemi-batwing resection incisions, 72, 75, 76f
Hemithorax, foreshortening of, 949
Hemostasis. See also Bleeding
Bovie electrocautery device and, 934
cautery and, 1021
confirmation of, 980
endoscopes and, 996
maintenance of, 934
pocket formation and, 1000
post-mastectomy, 641
wound healing and, 1263
Hepatic steatosis, tamoxifen and, 127
HER-2. See Human epidermal growth factor receptor 2 (HER-2) oncogene
Hereditary breast syndromes, management of, 50–51
“Hermunculus,” 831
Hernia rates after autologous breast reconstruction, 844
Heyer-Schulte implants, 922
Hibiclens shower, 938, 1103
HIFU. See High-intensity focused ultrasound (HIFU)
“High five” principles of implant selection, 1133, 1140
High Five System analysis, 967
High-intensity focused ultrasound (HIFU)
in breast cancer, 66t, 67–68
MRI guided, 67–68
ultrasound-guided, 67
High-resolution ultrasound (HRUS). See also Ultrasound
accuracy of
history of, 1248
increases in, 1248
advancements in, 1248
case studies, 1253, 1254f
cost of, 1248
popularity of, 961
sensitivity of, 1248
studies, 1249f
Hodgkin lymphoma
arterial stiffness in, 859
breast cancer risk and, 5
radiation therapy in, 859
Homunculus, 831
Honey, impact on biofilms, 1215
Hooke’s Law, 1026, 1027f
Hormone receptor expression. See also Estrogen receptors (ERs)
breast cancer diagnosis and, 105
breast cancer prognosis and, 15, 116
Hormone replacement therapy (HRT)
breast cancer risk and, 9
breast cancer risk reduction and, 48
NCCN recommendations, –35
Hormone therapy (HT)
chest wall masculinization and, 1157–1158
long-term risks of
transfemales and, 204–205
transfeminine mammogenesis and, 1167
transmasculine individuals, 1160
“Hot porridge” option, reconstruction surgery, 821
HT. See Hormone therapy (HT)
Human epidermal growth factor receptor 2 (HER-2) oncogene
breast cancer and, 26
breast cancer prognosis and, 15, 116
inflammatory breast cancer and, 109
survival data, 109
RMRT outcomes in, 159
targeted therapy, 125–126
tumors positive for, 159
Hydrodynamic interactions, biofilm adhesion and, 1212
Hydrogel
antibiotics in, 1215
implants filled with, 926
Hydrophobic interactions, biofilm adhesion and, 1212
Hypercoaguable states
contraindication in, 780
flap failure and, 837
thrombosis and, 837, 839
Hyperglycemia, wound healing and, 1265. See also Diabetes
Hyperhomocysteinemia, thrombosis and, 837, 839
Hyperpigmentation, radiation therapy and, 163, 590, 598, 859
Hyperplasias, atypical, 194
Hypertension, necrosis risk and, 606
Hypochlorus acid solution, pocket irrigation with, 1119
Hypofractionation (HF)
CF versus, 96–97
efficacy
outcomes, 96–97
Hypoplasia
implant placement in, 945–946
tuberous breast with, 1173
Hypothermia, intraoperative, 452, 715t, 717, 774, 901
Hypothyroidism, radiation therapy and, 859
Hypotrophic breasts, second degree, 1079f
Hypoxia
adipocytes and, 910
gene expression and, 671, 888
high-BMI patients and, 516
smoking and, 605
Hypoxia-inducible factor-1α, 888

I
IBC. See Inflammatory breast cancer (IBC)
IBRs. See In-breast recurrences (IBRs)
IBTR. See Ipsilateral breast tumor recurrence (IBTR)
Ibuprofen, postoperative, 720, 1103, 1162, 1166
ICAP flap, intercostal artery perforator (ICAP) flap
ICBN. See Intercostobranchial nerve (ICBN)
ICE method, IMF incision placement and, 1168
ICG. See Indocyanine green (ICG)
ICNs. See Intercostal nerves (ICNs)
IDC. See Invasive ductal carcinoma (IDC)
IDEAL. See Immediate-DElayed AutoLogous (IDEAL)
IGAP flap. See Inferior gluteal artery perforator (IGAP) flap
Iinseio taping
for lymphedema, 292
ILC. See Invasive lobular carcinoma (ILC)
Imaging, sensitivity trends, 472
IMAP flaps. See Internal mammary artery perforator (IMAP) flap
IMF. See Inframammary fold (IMF)
Immediate breast reconstruction (IBR)
complication rates, 523
delayed versus, 522–524
drawbacks of, 523
post-mastectomy radiation therapy and, 860–861
psychosocial well-being and, 861
risk factors, 523
Immediate versus delayed reconstructive surgery
post-mastectomy radiation therapy and, 861
Immediate-DElayed AutoLogous (IDEAL)
breast reconstruction protocol, 525–528
criteria, 128t, 303
Immune responses. See also Inflammation
breast implants and, 135–136
lymphatics and, 275–277
Immunohistochemistry (IHC), breast pathology, 24
Immunosuppression, tumor-related, 107
IMNs. See Internal mammary lymph nodes (IMNs)
Implant funnels. See also Funnels
benefits of, 996–997
Implant-based breast reconstruction (IBBR)
algorithm for, 475f
animation deformity
management of, 621–626
animation deformity in, 621–626
bilateral
delayed, 527f
indications for, 540
delayed
bilateral, 527f
indications, 525
fat grafting in, 899–902
history of, 899
outcomes, 902
history of, 540–563, 621
nipple-sparing mastectomy and, 488–496
operative techniques
dual plane, 494
prepectoral plane, 494
reduction for NAC perfusion delay, 494–495
reduction pattern, 494
post-mastectomy radiation therapy and, 859–864
previously radiated patients
case studies, 591, 592f–594f
generic risks of, 597
history of, 590
intraoperative care, 591
operative technique, 591
outcomes, 597–598
postoperative care, 591
role of, 590–599
ptotic patients, 488–496
radiation therapy and, 665–668, 706
contraindications, 707
outcomes, 708–709
reduction pattern incisions, 493f
smoking and, 1181
Implants. See also Breast implant-associated anaplastic large cell
lymphoma (BIA-ALCL); Gel bleed
acoustic impedance of, 1250
adjunct fat grafting, 901–902
alternative filling materials, 925–926
anatomical, 1015f (See also Implants, shaped)
indications for, 1009–1010
non-formstable, 1013, 1013f
textured, 1010f
availability of, 445f
bacterial contact with, reduction of, 1129t
Biocell textured surface
adhesive effect with, 931
creation of, 931
biofilms and, 1212–1217
breast cancer screening and, 961
breast implant-related illness, 1239
breast reconstruction surgery, 349–357
after unilateral mastectomy, 638–646
prepectoral versus subpectoral, 449–456
symmetry procedures, 627–636
cancer risk and, 135–136
characteristics of, 631
N-IMF and, 1127t
plane of, 631
types, 631
chronic antigenic stimulation by, 1191
circumferential linear fibrosis, 930–931
coatings of, biofilms and, 1214
complications related to
deformities, 1132–1133
content of, 1250
contracted radiated, salvage of, 665–674
core volume projection, 1132
coverage of, 564–565
deflation of, 939–940
deformities related to, 1132–1133
displacement of, 570–572, 578–579
double-lumen, HRUS image, 1260f
dual plane position, 676
as educational tools, 956
exchange of, 622
reoperation for, 709
excision of, 1196–1198
exposed, 613–619
case studies, 617f–619f
incidence of, 613–614
infections and, 613–614
management of, 615–616, 616f
risk factors for, 613–614
fat coverage needed for, 1139f
fat to implant ratios, 1138f
fat transfer and, risks of, 905–906
FDA classification of, 950
features to consider, 640t
feel of, 923
filling choices, 1008, 1169
footprint of, 1016
form-stable
breast reconstruction with, 472–489
history, 472
glandular cover for, 1007–1008
height of, 1007, 1007f, 1014–1015
herniation of, 136
high BMI reconstruction based on, 510–521
immediate mesh-assisted reconstructions
shared decision making and, 303
immobility, softness and, 931
impacts
disease prognosis and, 142–144
disease stage and, 142–144
improvements in, 649
indications for, 350
infections related to, 464
intact, imaging of, 1252f
irradiated, 665–668
irradiation of, 706–711
perspectives on, 706–711
reconstructive failure and, 708
in isolation
aesthetic outcomes, 1132
revision rates, 1132
Johnson & Johnson, 922
large, complications related to, 948
LDMF reconstruction and, 694f, 695f
limitations of, 953t
longevity of, 961
low-cohesive non-formstable, 1013f
lower pole, 1018f
LVC value, 1016
malposition of, 570–572, 578–579, 957f, 1118, 1142
case studies, 1115f–1116f
correction of, 1151f
history, 1110
management of, 1118
neopectoral technique for, 1110–1115
patient education about, 956
pocket overdissection and, 1144
submuscular positioning and, 1080
“worm’s eye view” assessment, 1056f
manufacturer-specific disease risks, 1191
mastectomy in patients with, 676
non-form stable, 1013f
no-touch technique, 938, 1120
observation angles, 1008–1009
patient education about, 953t
periprosthetic seromas, persistent, 936
placement of, 460f, 553–559, 621, 930f, 971
augmentation mastopexy and, 1057
contamination and, 1205
incision closure and, 971–972
Keller funnel in, 569, 971, 971t, 1020, 1022, 1140
mastectomy after, 676
“no-touch” method, 1140
prepectoral, 644f
submuscular, 643f
plane of, 632
pockets
oversized, 938
prophylactic antibiotics in, 938
subpectoral, 934–935
polyurethane
contraindications, 1040
history of, 1039
indications, 1039
operative technique, 1040–1050
preoperative planning, 1040
positioning of, 928–929
partial subpectoral, 929
subfascial, 929
subglandular, 928
subpectoral, 928–929
preclinical development of, 1028–1029
prepectoral
postmastectomy, 515f
site conversion, 1145
PUF-coated
concerns about, 931
popularity with surgeons, 931
radiopaque shadows from, 138
reconstruction using, 351
augmented patients and, 675–682
selection of, 853–854
removal of, 677f
rippling of, 570–572
management of, 1118
tuberous breast correction and, 1176
risk of bacterial contamination, 938
risks of, patient education about, 953t
round, shaped versus, 1006–1011
round gel, 354f
rupture of, 939–940
HRUS of, 1258f
MRI studies of, 939–940
screening for, 1247, 1247t
silent, 1247, 1248
saline-filled, 921–922
characteristics of, 640t
disadvantages of, 922
informed consent forms, 955t
placement of, 980f
selection of, 640
2Q Principle, 1013–1018
AK method, 1013–1018
case-by-case basis for, 1009
filling materials, 929
guide for, 479f–480f, 482f, 533f, 1013–1018, 1080, 1125–1126
implant sizes, 929–930
informed consent and, 956, 1236
patient education about, 954t
preoperative marking and, 1015f
shape and, 932–933
in subfascial augmentation, 997
surface textures, 930–932
surgical planning, 1056–1057
width limits, 931f
shape choices, 1169
selection of, 1077–1082
shaped (See also Implants, anatomical)
complications related to, 1011
history of, 1006
round versus, 1006–1011
shaped versus round, 1009
shared decision making, 302–303
shell types, imaging of, 1252–1253
silicone-filled
characteristics of, 640t
FDA moratorium on, 956
history of, 443, 1006
informed consent forms, 955t
patient labeling, 1247t
physician labeling, 1247t
placement of, 980–981
previous augmentation, 641f
selection of, 625
systemic disease and, 1218–1220
Siltex-textured surface, 931–932
size of
choice of, 1169
informed consent and, 1236–1237
patient education about, 953t
selection of, 953t, 1040
sizing tool for, 643f, 927
skin coverage, 1016
smooth
classifications, 1192t
description of, 1056
HRUS image, 1255f, 1257f
selection of, 1056
smooth round, BIA-ALCL risk and, 1006
stages of, 632
subglandular, 1207
disadvantages, 993
history of, 1117
mastectomy in patients with, 676
submuscular positioning, 1080–1082
subpectoral pocket changes, 1144–1145
support for, 1091f
surface technology, 1009
textured
Allergan withdrawal, 1024
anatomical, 1010f
BIA-ALCL and, 997
choices, 1169
classifications, 1192t
collagen deposition and, 1205–1206
contamination of, 1206
description of, 1056–1057
history of, 1006
HRUS image, 1254f, 1256f
informed consent and, 1239
microbiome studies of, 1191
outcomes, 1013f
selection of, 996, 1056
texturing techniques, 1205–1206
tissue coverage, 1016
tissue expanders versus
LDMF reconstruction and, 689–690, 692f, 693f
tissue ingrowth, 930, 932, 1040, 1057, 1267
two-stage reconstruction using, 530–539
volume of
operative risk and, 608
weight and, 1028
volumization by, 1083
washes, 1057
weight loss and, 958f
weight of, 1025–1038
volume and, 1028
width of, 1007, 1007f
analysis, 1015–1016
In situ ablation
breast cancer therapy, 65–68
outcomes, 65
patient selection for, 65–66
limitations of, 68–69
In vitro fertilization (IVF), BRCA mutations and, 49
Inamed. See Allergan implants
In-breast recurrences (IBRs)
DCIS and risk of, 186–187
mechanisms of, 183
In-breast tumor recurrences (IBTRs), 99
Incisions
areolar, 996–997
axillary, 996–997
basic techniques, 73
breast reconstruction surgery, 640–641
care of, 1174
circumareolar techniques, 73, 74f
closure of, 460f, 1162
complication rates and, 604
diagraming of, 1000
drawbacks to, 979f
informed consent and, 1236
inframammary, 73–74, 74f, 996–997, 1000, 1207
inframammary fold (IMF), 1126f
lateral, 491, 492f
length of, 1000
midlateral, 567f
NAC malposition and, 651
patterns of, 604
periareolar, 218
planning of, 504
reduction pattern, 492–493, 492f
S. epidermidis prophylaxis, 1214
selection of, 1236
size of, 979f
skin-reducing mastectomy
in large breasts, 680f
in ptotic breasts, 680f
soft tissue management and, 1266–1268
T, 380f
vertical, 491–492, 492f
Wise pattern, 368f
India, breast cancer survival and, 3
Indocyanine green (ICG)
description of, 608
flap perfusion assessed by, 499
half life of, 608
intraoperative, 218, 467, 523f
in lymphedema diagnosis, 230
preoperative planning, 232
reverse lymph node mapping using, 288–289, 289f
sentinel lymph node mapping with, 255, 257f
contraindications for, 256
indications for, 256
intraoperative care, 257
intraoperative technique, 256–257
postoperative care, 257
preoperative planning, 256
risks of, 257f
Indocyanine green (ICG) angiography, 783, 1187
flap perfusion testing, 172
intraoperative, 218, 467, 523f, 707
operative assessment using
predictive accuracy of, 608
skin flap viability, 608
tissue perfusion assessed by, 706
Infections
acellular dermal matrices and, 566–567
ADMs and rates of, 588
ALND complications, 245
biofilms and, 1213
breast reduction surgery, 385
capsular contractures and, 1205
capsulectomy indications, 938
discussion of, 1236
exposed implants and, 464, 613–614
implants and, 1214
informed consent and, 1236
pocket, 566–567
postoperative, 938
prophylactic antibiotics and, 1215
range of severity of, 938
rates of, 1083
reduction of, 1129t
reduction surgery complications, 385
S.epidermidis, postoperative, 938
SLNB complications, 245
subclinical, 1205, 1206
surgical site, 667, 717, 776, 845
Inferior cluneal nerves, 834
Inferior dermal mastectomy flap, de-epithelized, 152–153, 153f
Inferior gluteal artery perforator (IGAP) flap
history, 843
neurotization of, 834
in reconstructed breast, 850
shaping of, 726
Inferior pedicle, history of, 394
Inferior pole resection, NAC position and, 399
Infinity Irrigator Set, 784f
Inflammation. See also Immune responses
capsular contractures and, 996, 1205, 1214
cytokines and, 1264
fibroblasts and, 1264
fibrosis and, 1205
fibrotic response to, 1205
interleukin-8 (IL-8) and, 1205
irradiation and, 665
leukocytes and, 1264
lymphatic vessel injury and, 229
mesenchymal stem cells (MSCs) and, 1264
monocytes and, 1264
neutrophils and, 1264
perioperative, 1263
stem cell trafficking and, 1264
T-cell dysplasia and, 1191
white blood cells and, 1263–1264
wound healing and, 1263–1264
Inflammatory breast cancer (IBC)
adjuvant treatment of, 112
ALND in, 240
BCT contraindication in, 56
diagnosis, 109–111, 110
epidemiology, 109
imaging in, 110
incidence of, 109
medical photograph, 112f
neoadjuvant systemic treatment for, 111
skin changes and, 110f
SLNB in, 240
stage IV, outcomes, 112
surgical management of, 111–112
trimodal treatment for, 111
Inflammatory cascade, lymphatic vessel injury and, 229
Informed consent. See also Communication; Patient education
breast surgery, 1233–1240
components of learning, 1234–1235
decision making and, 950–952
description of, 1233
documentation of, 960–961, 1238
failed expectations and, 1234
forms for, 951
future care and, 1238
inclusions of, 1235–1237
lack of, 1227
lawsuits and, 1238–1239
learning styles and, 1234–1235
patient autonomy and, 952
patient education and, 950–952
patient understanding of, 951
responsibility for, 1234
second visit form, 955t
social media and, 1243
standards for, 1233–1234
traditional, 951
trust and, 950–951
Inframammary approach
augmentation mammaplasty, 1000–1005
operative technique, 1004–1005
incisions, location of, 1016f
Inframammary fold (IMF)
ACM suturing to, 536f
ADM and, 1145
asymmetry, 1003f–1004f
breast deformities, 944
capsule access from, 1111f
control of, 449
correction of, 855–856
flap raising, 537f
implant placement and, 971–972, 1007
incisions, 491f, 967, 967f
closure of, 971–972
ICE method for placement of, 1168
location of, 1126f
placement of, 1002, 1003f, 1168
landmarks, 458
malpositioned, 1095–1096
marking, 395, 395f, 970f
new, nipple and, 1016–1018
nipple and, 405
nipple transposition from, 406
obliteration of, 1157
persistent, implant size and, 948
position variability, 1052
positioning, 967–968, 967f
preoperative appearance, 1003f–1004f
preoperative assessment, 928, 928f
scar, 382–383
skin irritations along, 394
tissue thickness at, 993, 994f
tuberous breast deformity
release of, 944–945
surgical management of, 944–945
viability of, 1039
Inherited breast syndromes, psychosocial issues in, 51
Instagram, 1242
Instruments. See also Specific instruments
for microsurgical reconstruction, 753f
self-retaining, 753
setup, 753f
standardization of, 752
Insulin-like growth factor (IGF-1)
breast cancer risk and, 5, 7, 8–9
maternal, 5
upregulation of, 888
Intensive care units (ICUs), flap failures and, 836
Intercostal artery perforator (ICAP) flap
anatomy of, 326–327
lateral, 337
outcomes, 734f
vascular supply, 568f
Intercostal artery (IC) perforators, 324
Intercostal multiperforator flaps, 734f
Intercostal nerves (ICNs)
anatomy of, 781f
branches of, 783
flap innervation by, 832
nipple innervation by, 370–371
Intercostobranchial nerve (ICBN), 243
Interferon-1 (INF-1) expression, 859
Interferon-gamma expression, 671
Interleukin-1 (IL-1) expression, 859
Interleukin-8 (IL-8)
expression of, 859
inflammation and, 1205
Intermammary artery, pedicle supply by, 1093–1094
Intermammary distance (IMD), preoperative assessment, 928f
Intermittent pneumatic compression devices (PCDs)
for lymphedema, 282
prophylactic, 816
Internal mammary artery perforator (IMAP) flap, 854
Internal mammary fold, location of, 536f
Internal mammary lymph nodes (IMNs)
irradiation of, 706
radiation therapy and
controversy over, 161
treatment approaches, 162–163
Internal mammary (IM) vessels, 755–756
Internet, health-related information on, 952
Intimacy, breast sensation and, 831
Intracytoplasmic sperm injection (ICSI), 49
Intraductal papillomas
description of, 196
excision of, 196
histology of, 196f
Intra-operative fluorescence angiography
after mastectomy, 523f
Invasive breast cancers
BCT for, 92t
radiation therapy after, 92t
fibroadenomas and, 195
mastectomy versus BCT trials, 55t
risk of recurrence, 185–186
Invasive ductal carcinoma (IDC)
BCS for, 99–100
incidence of, 57
lumpectomy after, 82f
mammogram of, 178f
quadrantectomy, 84f
risk of recurrence in, 187
Invasive lobular carcinoma (ILC)
bilaral wire-localized lumpectomy, 83f
incidence of, 57
Inverted T scar mastopexy pattern, 1059, 1063f
marking, 1066f
operative technique
marking, 1066f
Involutional hypomastia, development of, 921
Ipsilateral breast tumor recurrence (IBTR)
diagnosis of, 87–88
follow up after, 89
prognosis following, 89
rates of, 87
treatment of, 88–89
axilla management, 88–89
ipsilateral mastectomy, 88
ipsilateral reconservation, 88
workup of, 87–88
Ipsilateral ribs, absences of, 949
Irrigation
antibiotics for, 569, 980
fluids, 1208
hypochlorus acid solution, 1119
of pockets, 533, 996, 1119
using Betadine, 459, 948, 971, 996
of wounds, 980
Ischemic complications, risk factors for, 473
Isometric resistance exercises for lymphedema, 279

J
Jejunal mesenteric lymph node flaps, 288
Johnson & Johnson implants, 922
Juvenile fibroadenoma, 195

K
Kehlet, Henrik, 713
Keller funnel, 459, 1020, 1022, 1140
implant insertion using, 569, 971, 971f
Keratinocytes
impact of radiation on, 859
wound healing and, 1264
Keratins, breast cancer expression of, 26
Ketorolac, postoperative, 718, 720, 1266
Keyhole mastopexy
skin envelopes and, 729
Ki-67, breast cancer and, 26
Ki-67 proliferative index, prognostic value of, 116
Kinesio taping
for lymphedema, 281, 282f
Kinesthetic learning, informed consent and, 1235
Klebsiella pneumoniae biofilms, 1213
Klinefelter syndrome
breast cancer and, 177
gynaecomastia and, 423
male breast cancer and, 180
Kocher clamps, 376, 422, 844
Korean Americans, breast cancer incidence, 4

L
Lactation, impacts of, 6
Lactational adenomas, description of, 195
Lalonde technique, 426t, 428–430, 430f–432f, 437, 437f
Lamellar release, 1153f
Laminar fat, anatomy of, 996f
Language, communication and, 951
LAP flap. See Lumbar artery perforator (LAP) flap
Lapatinib
description of, 126
HER-2-targeted therapy using, 119t
Laser ablation, breast cancer studies of, 66t
Laser thermotherapy in breast cancer, 68
Laser-assisted lipolysis (LAL), 418
in gynaecomastia, 420
Late Effects on Normal Tissue-Subjective, Objective, Management,
Analytic (LENT-SOMA) scale, 671
Lateral decubitus position, 815f
Lateral femoral cutaneous nerve, 834
Lateral intercostal artery perforator (LICAP) flap
breast reconstruction and, 311
deepithelialized, 826f
defect filled with, 339f, 340f
description of, 337
operative technique, 341–342
rotation of, 344f
turnover, 345f, 346f
perfusion by, 821
in reconstructed breast, 854
reconstructive plan, 328
selection of, 338, 340
sites for, 338f
turnover, 339f
Lateral pedicle, benefits of, 367
Lateral thigh flap, operative technique, 874
Lateral thoracic artery perrforator (LTAP) flap
defect filled with, 338, 340f
description of, 337
operative technique for, 341–342
radiotherapy and, 347f
turnover, 345f
selection of, 338
sites for, 338f
Lateral thoracic lymph node flap, VLNT donor site, 288
Latissimus dorsi (LD) flap, 352f–353f
in autologous reconstruction, 874
blood supply, 326
contraindications, 1186
donor site, 335f
in high BMI patients, morbidity rates, 1187
loss of function and, 337
morbidity in, 88
muscle-sparing, 333f, 843
noninnervated, 832
outcomes, 547f
reconstruction using, 837
fat grafting and, 905–906
salvage use of
in irradiated patients, 669
shaping of, 726
Latissimus dorsi muscle
autogenous reconstruction, 694–696, 696f
blood supply to, 683, 684f
related muscles, 684f
Latissimus dorsi musculocutaneous (LDMF) flap
anatomy of, 683–685
autogenous reconstruction using, 694, 696, 697f
bilateral, 703f–704f
breast reconstruction using, 683–705
complications, 698, 698f–704f, 702
history of, 683
indications for, 685
operative technique
flap harvest, 686, 687f, 696f
inset, 689f
postoperative recovery, 689
preoperative marking, 685, 686f, 691f, 692f, 695f, 697f, 699f, 703f
tissue expander versus implant, 689–690
reconstruction using, 683–705, 850
anatomy, 683–685
contralateral breast, 690
elevation of, 688f
history, 683
indications for, 685
inset, 689f
operative technique, 685–705
preoperative marking, 686f
tissue expander vs. implant, 689–690
volume-added, 695f
preoperative marking, 699f
revision reconstruction, 696–697
Latissimus dorsi musculocutaneous muscle
anatomy of, 683, 684f, 685
blood supply to, 684f
dissection of, 686–687, 687f
elevation of, 688f, 700f
LD flap. See Latissimus dorsi (LD) flap
LDMF FLAP. See Latissimus dorsi musculocutaneous (LDMF) flap
Leech therapy, failed flaps, 835f
Lejour vertical scar pattern, 428, 429f
LENT-SOMA (Late Effects on Normal Tissue-Subjective, Objective,
Management, Analytic) scale, 671
Leukocytes, inflammation and, 1264
Leukotriene antagonists
capsular contracture management and, 667
postoperative, 1208–1209
Leukotriene inhibitors, postoperative, 1208
Leukotriene receptor antagonists for capsular contractures, 938–939
Leuprolide, ovarian ablation with, 128
Levobupivacaine, nerve block using, 719
Leydig cells, testosterone production by, 180
LFS. See Li-Fraumeni syndrome (LFS)
Liability issues, reduction of, 1239
Liability policies, lawsuits and, 1238–1239
LICAP. See Lateral intercostal artery perforator (LICAP) flap
Lidocaine
epinephrine and, 170, 376, 396, 549, 1085
fat donor sites, 904
Life stages, brain plasticity and, 831
Lifestyle, breast cancer risk and, 40
Li-Fraumeni syndrome (LFS)
breast cancer screening guidelines, 47t
cancer risk and, 45
genetic counseling in, 44
Lighting, operating room, 977
Light-weight breast implant (LWBI)
B-Lite, 1028f
breast augmentation and, 1025–1038
clinical reports
case studies, 1031f–1034f
clinical survey reports, 1030
retrospective studies, 1030–1034
contraindications, 1029
indications, 1029
intraoperative care, 1029
operative techniques, 1029–1030
postoperative care, 1029
precautions, 1029
preclinical development, 1028–1029
preliminary benefits, 1034–1037
preoperative planning, 1029
Linear array transducers, 1251f
Lipoaspirate
composition of, 888
processing of, 904
sedimentation of, 910–911
spinning of, 904
washing of, 904
Lipofilling, 856
autologous flaps combined with, 882
outcomes, 894
postmastectomy, 901
salvage use of, 671
use of, 881
Lipografters, 911f
Lipomas, breast, 197
Lipomastia, 416
LipoMatrix Corporation, 926
Liponecrosis, 1177
Liposomal bupivacaine (Exparel), 1266
Liposomal infiltration protocol, 718t
Liposuction
augmentation mastopexy and, 1068
axillary, 1070f
benefits of, 418
breast reduction surgery, 418–422, 883
cannulas, 904
complications of, 420–422
contraindications, 295–296
conventional, 418
description of, 854–855
end-stage upper extremity lymphedema, 292–297
for gynaecomastia, 420–422
history of, 416, 418
incisions, 418
laser-assisted, 418
for lymphedema, 230–231
male, 418–422
NAC position and, 399
nonconventional, 418–420
open excision and, 427f–428f, 435–437, 436t
operative technique, 418–422
outcomes, 295, 295f, 390f, 1105f
postoperative care, 294–295, 435–437
power-assisted
conventional, 418
in lymphedema, 294, 294f
radiofrequency-assisted, 418
shape refined by, 379–380, 381f
surgical technique, 294
ultrasonic, 418–420
ultrasound-assisted, 418–420
VASER, 418
Liposuction mastopexy, 1102–1109
contraindications, 1102
general risks of, 1108
history of, 1102
indications, 1102
intraoperative care, 1106
operative technique, 1103–1106
anesthesia, 1105
marking, 1103f, 1104f
outcomes, 1103f, 1107f–1108f, 1108
postoperative care, 1106–1108
preoperative planning, 1102–1103
Lipotransfers, 484
Literacy barriers, patient education and, 956
LLLT (low-level laser therapy) for lymphedema, 281
Lobular carcinoma, 8
Lobular carcinoma in situ (LCIS)
CCH and, 194
description of, 198
histology of, 198f
incidence, 198
pleomorphic
description of, 198
recommendations, 197t
recommendations, 197t
Localizer of the BRCA2 gene. See PALB2 gene
“Lollipop scar” mastopexy, 1059
Long thoracic nerve, identification of, 243
Loperamide, 122
Low-level laser therapy (LLLT) for lymphedema, 281, 281f
Low-molecular-weight heparin (LWMH)
postoperative, 329
prophylactic, 816
VTE prophylaxis, 1266
Low-weight breast implants (LWBI)
gels on absorbent paper, 1035f
mammography of, 1035, 1036f
MRI and, 1035
oil release over time, 1035f
ultrasonography of, 1035, 1036f
LTAP flap. See Lateral thoracic artery perrforator (LTAP) flap
Lumbar arteries (LAs), anatomy of, 811f
Lumbar artery perforator (LAP) flap, 812
anatomy, 811–812
in autologous reconstruction, 875
breast reconstruction using, 811–820
case studies, 817f–818f
contraindications, 812, 817f
generic risks of, 819
history, 811
indications, 812
intraoperative care, 816
operative technique, 814–816
outcomes, 819
postoperative care, 816
preoperative planning, 812–814, 813f
donor sites, 814f
harvesting of, 815–816, 815f, 816f, 818f
indications, 812
operative technique, 875
Luminal A tumors
breast cancer and, 26
chemoresistance in, 80
gene expression profiling, 116–117
Luminal B tumors, breast cancer and, 26
Lumpectomy
adjuvant tamoxifen and RT, 93–95
ALND versus targeted RT, 263–265
APBI after, 98
in DCIS, 199
decision making process, 209
fat grafting after, 897
level II
candidates for, 80–81
local recurrence rates, 79
oncoplastic approach, 78–86
patient-reported outcomes, 79
safety issues, 79–80
mastectomy versus, 91–93
NAC malposition in, 651
nipple-sparing mastectomy and, 651
node-positive patients, 263–265
radiation after
recurrence rates, 57
trials of, 96
recurrences after, 93–95
reexcision +/- mammoplasty, 79
scars, 592
sites of, imaging, 20
total mastectomy versus, survival rates, 54
with/without radiotherapy for DCIS, 93t
Luteinizing hormone-releasing hormone (LHRH) agonists, 128
Luteinizing hormone-releasing hormone (LHRH) analogs, 124
LVB. See Lymphovenous bypass (LVB)
LVC values
definition of, 1016, 1017t
measurement of, 1018f
LVI (lymphovascular invasion), 15
LWBI. See Light-weight breast implant (LWBI)
LWMH. See Low-molecular-weight heparin (LWMH)
Lymph, flow of, 284–285
Lymph nodes. See also Axillary lymph node dissection (ALND); Axillary
sentinel lymph node biopsy; Sentinel lymph node biopsies (SLNB);
Vascularized lymph node transplants (VLNT)
assessment of, 105
axillary, on mammogram, 106f
breast cancer diagnosis and, 105
bulky, 106–107
clipping of, 251
excisional biopsy, 1197
internal mammary, 161, 162–163
internal mammary lymph nodes, 706
jejunal mesenteric, 288
lymphangiogenic growth factor secretion, 285
lymphedema management and, 229–236
mapping of, 255
PMRT indications and, 706
positive, 706
regional, 260–272
tattooing, 251
vascular endothelial growth factor C secretion, 285–286
vascularized donor sites, 284–291
vascularized transplant, 229–236
wire localization, 251
Lymphadenectomy, lymph stasis and, 229
Lymphadenopathy, BIA-ALCL and, 1193
Lymphangiogenesis, description of, 285
Lymphangiogenic growth factor, 285
Lymphangiography, ICG, 230f
Lymphangiomotoricity, 275
Lymphatic system
lymph vessels
ingrowth of, 231
transplantation for lymphedema, 292
lymphedema and, 284–285
reverse lymphatic mapping
node harvest and, 288–289, 289f
watersheds of, 276f
Lymphaticovenous-lymphatic bypass, 292
Lymphatic-venous shunt for lymphedema, 292
Lymphedema. See also Edema
after ALND, 244
after regional nodal radiation, 101
decongestive lymphatic therapy (DLT) for, 292
diagnosis of, 230
end-stage upper extremity
liposuction for, 292–297
fibroadipose tissue removal, 293
fibrosis and, 275
history of, 273, 292
incidence, 161
long-term, 275
lymphatic system and, 284–285
postsurgical
alternative therapies, 280–282
complete decongestive therapy, 274–279
compression therapy, 277, 280f
diagnosis of, 230
flexibility exercises, 278–279
history of, 229
incidence of, 273
intermittent pneumatic compression devices, 282
low-level laser therapy for, 281
management of, 229–236, 273–283
pathophysiology of, 229
phases of care for, 279–280, 279f
rehabilitation, 282
remedial exercises, 277–278, 278f
resistance exercises for, 279
risk reduction, 274t
self-care in, 275–277
stretching for, 278–279
taping for, 281–282
therapeutic exercises, 277
prediction of, 161
radiation therapy and, 163, 859
risk reduction education, 273–274
secondary, 284, 292
SLNB versus ALND, 250
staging of, 293t
surveillance for, 229
treatment of, 244, 285
Lymphomas
breast
incidence of, 1190
extranodal, 1190
staging, 1198f
Lymphoscintigraphy (LSG), preoperative, 232, 238–239, 293
Lymphovascular invasion (LVI), 15
Lymphovenous bypass (LVB)
axillary dissection and, 231f
distal, 231f
indications, 230–231

M
Macromastia, 501f
bilateral, 1047f
NAC malposition in, 411f, 413f
necrosis rates and, 606–607
nipple-sparing mastectomy, 217
obesity and, 1185
posture seen in, 394f
secondary, 398
Macronutrients, 1265
Macrophages, ADMs and, 667
Macrovascular disease, diabetes and, 1265
Macular edema, tamoxifen and, 127
Magnesium, wound healing and, 1265
Magnetic resonance angiography (MRA), preoperative, 232, 836
Magnetic resonance imaging (MRI)
augmented breasts and, 141–142
BCT patient selection and, 55
BIA-ALCL and, 1193
breast implant integrity evaluated using, 939–940
contraindications, 1247
cost of, 1247
DCIS on, 199
low-weight breast implants, 1035
newly diagnosed breast cancer and, 55
perforators identified by, 771
preoperative, 169f
screening for implant rupture, 1247
sensitivity of, 1247, 1248
specificity of, 1248
Male breast cancer
BRCA genes, 9–10
clinical presentation of, 177
history of treatment for, 177–182
incidence of, 4
medical oncology management, 180–181
pathology of, 179–180
presentation of, 178f
radiation oncology management of, 181
radiology of, 178–179
risk factors, 177
surgical management, 180
transfemales and, 204–205
Male breast reduction
complications of, 435t
decision algorith, 437t
history of, 416
indications, 416–417, 416t
liposuction vs. excision, 416–440, 436t
postoperative recovery, 436t
skin-reduction techniques, 426t
Male breasts, enlarged, 417f. See also Gynaecomastia
Malignancies, secondary
radiation therapy and, 859
Mallucci’s 45:55 ideal breast ratio, 1132
Malnutrition, wound healing and, 1265
Mammaplasty. See also Augmentation mammaplasty
augmentation
general considerations, 921–942
oncoplastic reduction
NSM and, 152
reduction
outcomes, 1268f
MammaPrint, 29
in early-stage breast cancer, 117t
predictive use of
adjuvant chemotherapy and, 123
Mammary cells, fat-induced proliferation and, 6
Mammary duct ectasia, 197
Mammary hypertrophy, 153f
preoperative view of, 395f, 397f
Mammatome excision, ultrasound-guided, 422
Mammography
of augmented breasts, 138, 140–141
compression issues in, 138
augmented patients
breast cancer in, 138f
before/after fat grafting, 896
breast cancer screening, 47, 47t, 55
DCIS on, 198–199
diagnostic use of
in inflammatory breast cancer, 110
digital, 504, 505f, 506f
augmented breasts and, 141
results of, 474
saline implants on, 142f
displacement and
augmented breast, 141f
false positive rates, 17
harm-benefit ratios, 17–18
impact on cancer mortality, 17, 18–19
of low-weight breast implants, 1035, 1036f
male, 49
post augmentation
impact of contractures on, 140, 140f
reduction, 887f
ruptured silicone implants on, 137f
screening, age and, 15–18
sensitivity in palpable cancers, 141t
silicone implants, 1036f
standard film, 504, 505f
transmasculine individuals, 1159–1160
Mammoplasty
oncoplastic reduction, 78–79
therapeutic
shared decision making, 301–302
uncertainty and, 301–302
MammoSite, 97–98
Manual lymphatic drainage (MLD)
for lymphedema, 274, 292, 293
technique, 275f
Marionette sutures, 533, 1119, 1120f
schematic, 1120f
Marketing
social media content, 1243–1244
specials, 1244
Marking
for abdominal-based breast reconstruction, 869–870, 870f
AFT donor sites, 913–916
AFT recipient sites, 914
for “Akademikliniken Method,” 1017t
for anatomical implants, 1015f
for augmentation mastopexy, 1059–1060, 1064f, 1066f, 1073, 1073f
universal markings, 1064f
for bilateral simple mastectomy, 695f
for breast augmentation, 1018–1020
preoperative, 965f
transaxillary approach, 982–983, 983f
of breast meridian, 373
of breast upper border, 373, 374f
circumareolar mastopexy pattern, 1065f
for delayed expander/implant-based breast reconstruction, 542f, 545f,
546f, 554f–558f
of fat grafting sites, 703f
of FAT recipient sites, 914
of flaps, 771
for Goldilocks mastectomy, 823
gracilis muscle, 794
for implant-based breast reconstruction, 455f
inframammary fold, 395, 395f, 970f
of inverted T scar pattern, 1066f
for latissimus dorsi musculocutaneous flap, 685, 686f, 691f, 692f, 695f,
697f, 699f, 703f
for liposuction mastopexy, 1103f, 1104f
of nipple position, 373, 1084
for nipple transfer procedure, 655
for nipple-areola reconstruction, 489f
for nipple-sparing mastectomy, 493, 500f
for partial mastectomy, 332f–333f
for pseudoptosis management, 1093f
for skin reduction, 513f
for skin removal, 1104f
for transverse upper gracilis flaps, 805f
“2Q principle,” 1019, 1019f
universal, 1059–1060, 1064f
using Sharpie pens, 549
vertical pattern, 1066f
for Wise pattern incisions, 310, 592f, 824f
for Wise-pattern mastectomy, 569f
Massive weight loss (MWL)
breast reduction
adequate breast volume, 359
contraindications, 359
excessive breast volume, 358–359
inadequate volume, 358
mastopexy and, 358–366
preoperative planning, 359
reconstruction after
case studies, 362f–365f
complications, 366
outcomes, 366
Mastectomy
5-year survival, 62
BCT versus
in invasive breast cancer, 55t
locoregional recurrences, 87
patient preferences, 55–56
bilateral
delayed reconstruction, 851f
immediate reconstruction after, 526f
bilateral versus unilateral
patient satisfaction in, 647–649
in breast implant patients, 675–676, 676f
breast reconstruction after, 522
conservative, 504
contractures after, 914
contralateral
algorithm for, 474–484, 474f
decision making issues, 208
IBTR and, 89
in DCIS, 200
decision making process, 209
dissection, 171f
early breast cancer and, 473
excess skin removal, 729f
flaps
breast anatomy and, 167–176
dissection, 167–170
necrosis, 613
perfusion of, 167
thickness of, 169–171
free nipple grafting and, 429
gender-affirming, 1157
goals of, 167
Goldilocks, 821–830
after care, 826
bilateral, 825f
case study, 747f
flap insets, 826
follow-up, 826
history, 821
indications, 821–822, 827t
marking for, 823
mound with nipple excision, 825
operative technique, 823–829
deepithelialization timing, 823, 824f
flap creation, 824
marking, 823
outcomes, 825f
steps, 824f
patient counseling, 822
patient selection, 822
perioperative considerations, 822–823
preoperative considerations, 822–823
preoperative evaluation, 822–823
preoperative planning, 822–823
with SWIM nipple preservation, 828f, 829f
outcomes, 828–829
Halsted style, 54
history of, 504
implants following, 590–591
contraindications, 590
indications, 590
preoperative planning, 590–591
incidence of, 522
indications for, 87
intra-operative fluorescence angiography after, 523f
ipsilateral breast, 88
lipofilling after, 901
male breast cancer, 181
masculinizing, 204
operative technique, 205–207
modern approaches, 564
modified radical
delayed reconstruction after, 1187f
history of, 150, 167
in inflammatory breast cancer, 111–112
postmastectomy RT and, 158
previous, 691f
trends toward, 91
nipple-sparing, 81
history of, 150
patient selection criteria, 150–156
node-positive patients
ALND versus targeted RT, 263–265
oncoplastic reduction and, 155f
partial
case studies, 311f–320f, 329f–335f
contraindications, 309, 325
fat grafting in, 893–898
indications for reconstruction, 309, 309t, 324–325
intraoperative care, 328
local flaps for, 324–336
operative techniques, 310–318, 310t, 327–329
outcomes, 321t
postoperative care, 329
preoperative planning, 309–310, 325–326
reconstruction of defects, 696, 696f
residual disease after, 111–112
surgical exposure, 328
surgical marking, 332f–333f
periareolar skin-sparing, 697f–698f
prophylactic
bilateral, 215
contralateral, 208
efficacy of, 48
high-risk patients, 204
immediate reconstruction after, 526f
risk reduction and, 638
shared decision making in, 208
quality of life and, 522
radiation therapy after, 157–166
breast reconstruction and, 760f
radical
BCT versus, 54
outcomes, 91–92
radical, BCT versus, 54
reconstruction after
fat transfer in, 350
resections for
informed consent, 301
shared decision making, 301
selection of, decision making, 507
site following excision, 542f
skin flaps, 452
irradiated after fat grafts, 528f
skin-reducing, 477f, 478f, 480, 635f, 642–643
skin-sparing, 150
specimens as guide, 593f, 731f
in stage IV breast cancer, survival data, 107
total versus lumpectomy
survival rates, 54
tumescent technique, operative risks and, 608
two-stage reconstruction, 624f
Wise-pattern, 535, 567–568
completion of, 569f–570f
markings, 569f
outcomes, 571f
without PMRT
recurrence rates, 161
survival rates, 161
Mastectomy, tumor location and
reconstruction issues, 676
Mastectomy, unilateral
implant based reconstruction surgery after, 638–646
Mastectomy flap necrosis (MFN)
methylene blue and, 608
postoperative management of, 609–611, 609f
nonoperative, 609–610
operative, 610–611
rates of, 604
Mastectomy flaps
factors in complications with, 489
Mastectomy pockets, oversized, 511, 511f
Mastectomy Reconstruction Outcomes Consortium (MROC) study, 670
Mastisol, postoperative, 1130
Mastitis, history of, 110
Mastopexy
ADM and, 577f
batwing, 526f
breast augmentation, 1072–1076
breast reduction surgery, 883
breast-conserving surgery and, 337
concentric pattern, 426
effect of smoking on, 1179–1180
fat transfer and
outcomes, 1135f
goals of, 1083
inverted T, 1080
keyhole
skin envelopes and, 729
liposuction, 1102–1109
massive weight loss and, 358–366
ovoid periareolar, 410f
periareolar, complications related to, 948
revision outcomes, 1095f
sailboat type, 1085
secondary, outcomes of, 1096f
smile type, 1085
Wise-pattern, skin envelopes and, 729
Mastopexy-augmentation. See also Augmentation mastopexy
complication rates, 1083
contraindications, 1083
effect of smoking on, 1179–1180
generic risks of, 1088
implant decisions, 1101
indications, 1083
operative technique, 1085–1086
case studies, 1086f–1088f
intraoperative care, 1086
postoperative care, 1086
outcomes, 1088–1089
patient selection for, 1090
pitfalls of
avoiding, 1083–1089
implant-related, 1084f
tissue-related, 1084f
preoperative planning, 1084f
recurrent ptosis following, 1090–1101, 1093–1094
two stage, reoperation rates, 1083
Matching procedures, breast symmetry and, 758–760
Matrix metalloproteinases (MMPs), after RT, 859
Maturation, wound healing and, 1263–1264
Maximal skin stretch, 1123
Mayo stand setup, 754t
MCFA (medial circumflex femoral artery perforator) flap, 875
MD-M (midline to meridian at IMF) measurement, 1103–1105
MD-N (midline to nipple) measurement, 1103–1105
MDS (myelodysplastic syndrome), 124
Mechanical injuries, cryoablation and, 66
Medial circumflex femoral artery perforator (MCFA) flap, 875
Medial intercostal artery perforator (MICAP) flap
defect filled with, 340f, 341f
description of, 337
sites for, 338f
Medial pectoral nerve dissection, 242–243
Medial pedicles
benefits of, 367
blood supply, 370f
design of, 375
Medical Device Amendments, FDC&A Act of 1938, 950
Medical histories
discussion of, 1235
informed consent and, 1235
patient decision making and, 300–301
Medical malpractice lawsuits, informed consent issues and, 1238–1239
Medical records, documentation in, 1238
Medicolegal considerations, 1239–1240. See also Informed consent;
Medical malpractice lawsuits
MEGADYNE Mega Soft cautery grounding pad, 754
Menarche, age at, 5, 41
Menopause
age of, 5
premature
chemotherapy-related, 124–125
Mentor Corporation
MemoryShape series, 932, 939
silicone implants, 527f, 924, 924t
Siltex implants
disease risk with, 1191
Style 1000 implants, 543f
Style 1600 implants, 544f, 548f
Style 2000 implants, 550f, 551f, 553, 554f–558f
Mesenchymal stem cells (MSCs), 1264
Meshed acellular dermal matrix, 582–589, 584f. See also Acellular dermal
matrix (ADM)
adjunct use of, 586
complications, 588
history of, 582–583
operative technique, 583–587
outcomes, 583f
tissue expanders with, 585f–587f
Meshes, bioresorbable, 1118, 1121, 1121f
Metaplastic carcinomas, prognosis in, 28, 116, 179
Metastatic disease
breast cancer
removal of primary tumor in, 108
tamoxifen-resistant, 127
treatment of, 49–50
non-breast sites for, 107
Methemoglobin, 1178
Methylene blue
biofilm detection and, 1215–1216, 1216f
operative risk and, 608
Mexico, breast cancer mortality rates and, 3
MFN. See Mastectomy flap necrosis (MFN)
MICAP flap. See Medial intercostal artery perforator (MICAP) flap
Microbial Surface Component Matrix Molecules, 1212
Microblogging, 1242
Microcalcifications, 20, 301, 321, 887, 897, 1035, 1036f. See also
Calcifications
in DCIS, 197–198, 200
ultrasound imaging, 142
Microdebrider excision, 423
Micromastia
bilateral, 1044f, 1045f
secondary health problems, 1027
Microneurorrhaphy, performance of, 785
Micronutrients, wound healing and, 1265
Micropapillary carcinomas, 116, 194, 199
Micropore paper tape, 3M, 380–382, 1022
Microscopes, operating, 756
Microsphere-enhanced silicone
displacement of, 1034–1035
samples of, 1035f
structure of, 1028–1029, 1028f
Microsurgical free tissue transfer, risks of, 776
Microvascular disease, diabetes and, 1265
Microvascular occlusion, smoking and, 1178
Microwave ablation
in breast cancer, 68
breast cancer studies of, 66t
Midline to meridian at IMF (MD-M) measurement, 1103–1105
Midline to nipple (MD-N) measurement, 1103–1105
MINDACT, description of, 29
Minimally invasive excisional techniques
for gynaecomastia
arthroscopic shavers, 422
endoscopic techniques, 422
microdebrider excision, 423
pull-through techniques, 422
VAB techniques, 422
MiraLAX 2, bowel prep using, 232
Misti Gold implant, 138, 926
MLD. See Manual lymphatic drainage (MLD)
MLH1 gene, cancer risk and, 46t
Mobilization, early, 721
Modified radical mastectomy (MSM)
delayed reconstruction after, 1187f
history of, 150, 167
in inflammatory breast cancer, 111–112
postmastectomy RT and, 158
previous, 691f
trends toward, 91
Moist desquamation, treatment breaks and, 163
Moldova, breast cancer mortality rates in, 3
Molecular diagnostics, 24
Molecular oncology, molecular diagnostics and, 24
Mometasone, preventive use of, 163
Mondor disease, 938
Monocryl sutures, 376, 380, 707
Monocytes, inflammation and, 1264
Monopolar cautery, 753–754
Monopolar diathermy, dissection using, 772
Montelukast (Singulair)
for capsular contractures, 464, 667, 939
Morphovolumetric characteristics
breast
reconstruction choices and, 474, 475f, 476f
Motiva Ergonomic devices
rupture rates, 1248
Motiva silicone implants, 924t
Movement, amplitude of
weight and, 1026–1027
MRI. See Magnetic resonance imaging (MRI)
MSH2 genes, cancer risk and, 46t
MS-TRAM flaps, bilateral free, 869
MTOR inhibitors, studies of, 128t
Mucositis, chemotherapy-related, 124–125
Multicatheter brachytherapy, APBI and, 97, 98f
Multifocal tumors, 80
Multigene assays, 185–186
Multiplex PCR, 25
Muscle relaxants, postoperative, 720
Muscle strength reduction, submuscular positioning and, 1080
Muscle “window-shading,” 1061
Muscle-sparing free-TRAM flap, 843
Muscle-sparing latissimus dorsi (MSLD) flap, 843
Musculocutaneous flaps, 813f
MWL. See Massive weight loss (MWL)
Myalgias, chemotherapy-related, 124–125
Myelodysplasia, chemotherapy-related, 124–125
Myelodysplastic syndrome (MDS), 124
Myelosuppression, chemotherapy-related, 124–125
Myodermal gluteus maximus flap, free, 770
Myofibroblasts
acellular dermal matrices and, 667
alpha-SMA+, 667
capsular contractures and, 1206
stimulation of, 938
N
NAC. See Neoadjuvant chemotherapy (NAC); Nipple areolar complex
(NAC)
Nanoparticles
metal, biofilms and, 1215
SPIO, 255
National Cancer Institute Breast Cancer Risk Assessment Tool (BCRAT),
31
National Comprehensive Cancer Network (NCCN)
on BCT, 54
breast cancer risk stratification, 31
consensus guidelines for BIA-ALCL diagnosis and management,
1191–1193, 1193f
guidelines, 28, 29
for cancer diagnosis, 110
posttreatment mammograms
timing of, 20–21
National Institute for Health and Care Excellence, 33t
National Surgical Quality Improvement Program (NSQIP), 835–836
Natrelle 410 (Allergan), capsular contracture data, 939
Natrelle Inspira implants, 526f
“Natural Y” polyurethane, 1205–1206
Nausea, tamoxifen and, 127
NBN gene
breast cancer screening guidelines, 47t, 51
cancer risk and, 46t
NCCN. See National Comprehensive Cancer Network (NCCN)
Near-infrared spectroscopy, 836
Necrosis. See also Flap necrosis
autologous reconstruction and, 172
bacterial growth and, 916
cell death and, 665
depth of, 604
management of, 604–612
nipple areolar complex, 605f
partial-thickness, 604
prevention of, 604–612
skin flaps
rates of, 651
smoking and, 1181
Needle biopsies, breast implants and, 137–138
Negative pressure therapy
benefits of, 1267, 1267f, 1268f
incisional
benefits of, 610
complication rates and, 610
cost benefits of, 610
outcomes, 1268f
Negative pressure wound therapy (NPWT), 847–848
Neoadjuvant chemotherapy (NAC)
ALND
indications for, 252
axillary recurrences after, 249
HER-2 targeted, 119–120, 119t
for inflammatory breast cancer, 111
locoregional recurrences after, 160–161
nipple-sparing mastectomy and, 217
nodal positivity rates after, 249, 249t
node positive patients
ALND after, 264–265
intraoperative technique, 266
postoperative care, 266–267
preoperative planning, 265–266
PMRT and, 160–161
SLNB after
feasibility of, 248
timing of, 248
surgery after, in node-positive patients, 264–265
in TNBC, 118–119
Neoadjuvant endocrine therapy (NET), 120–121
Neoadjuvant therapy, 115–134
in breast cancer, 118–121
locally advanced, 106
stage IV, 108
breast-conserving surgery and, 111–112
for inflammatory breast cancer, 111
Neoangiogenesis. See also Angiogenesis
fat grafting and, 910
process of, 910
Neopectoral pockets
closure of, 1115f
creation of, 1113
Neopectoral technique
capsule dissection, 1111–1112
preoperative planning for, 1111
Neosubpectoral pockets, 1118, 1118f
implant malposition and, 1126
Neovascularization. See also Angiogenesis; Neoangiogenesis
angiogenesis and, 1264
wound healing and, 1264
Neratinib
adjuvant treatment, 122
HER-2-targeted therapy using, 119t
Nerve blocks
brachial plexus, 718
imaging and, 1252
intercostal, 460, 549
paravertebral, 1266
pectoral, 718, 719–720, 780, 1266
regional, 569, 718, 1266
Nerve coaptation, 833, 833f
Nerve conduit tubes, composition of, 833
Nested PCR, 25
NET (neoadjuvant endocrine therapy), 120–121
Neural connector tubes, 786f
Neuromuscular blocks, 754
Neuropathic pain, breast surgery and, 712
Neurotization
autologous, 785f
outcomes, 833–834
techniques, 832–833
Neutrophils, inflammation and, 1264
NF1 gene
breast cancer risk and, 10
breast cancer screening guidelines, 47t
cancer risk and, 46t
Nicotine
cessation of, 1265
complication rates and, 604–605
surgery outcomes and, 1178
N-IMF measurement. See Nipple to inframammary fold (N-IMF)
measurement
Nipple
cancer involvement of, 216
innervation of, 370–371
ischemia of, 216–217
malposition
pedicled nipple transposition, 660–661
pocket revision for, 659, 659f
malposition following RT, 652f
malposition of
postoperative changes in, 651
surgical correction of, 657
surgical treatment for, 650–664
necrosis
after breast reduction, 383–384
breast reduction surgery and, 368
pedicle length and, 371
necrosis of
management of, 604–612
prevention of, 604–612
new inframammary fold and, 1016–1018
position marking, 1084
preoperative, 373
position of, 1129–1130
horizontal transfer of, 1014
inferior, 1129–1130
lateral, 1129–1130
medial, 1129–1130
postoperative, 1014
superior, 1129–1130
preoperative asymmetry of, 653
preservation with free graft, 826
preservation with local flap, 825–826
sensitivity of
postoperative, 936
viability of, 222
Nipple adenomas, 196–197
Nipple areola, size variability of, 1052
Nipple areolar complex (NAC)
anatomy of, 220–223, 393
blood supply of, 81, 85, 393, 393f, 650, 1093–1094, 1094f, 1127
circumareolar approach, 512
complications after nipple-sparing mastectomy, 650
deepithelialization of, 73
direct-to-implant reconstruction, 504
displaced, 405–410
case studies, 411f–413f
elevation of, 409, 1014
expansion of, 943
implants placement and, 1007, 1008
incisions, 73–74
ischemia, 413–414
after nipple-sparing mastectomy, 650
patient identification and, 504
localization of, 1162f
malposition of after nipple-sparing mastectomy, 650
management of central tumors, 85
mastectomy sparing, 479f, 481f
measures of, 725
necrosis of, 300, 413–414, 605f, 1165
BRAND4P procedure and, 466
methylene blue and, 608
operative technique and, 1088
patient identification and, 504
rates of, 604
pedicle of, 394
placement of, 406
symmetry, 1106f
position of, 393, 1060f, 1083
implant positioning and, 656
postoperative care, 410
postoperative complications, 77
preservation of, 187
quality of life and, 215
reciprocal rotation flaps in, 408f
reconstructed, tattooing of, 698f
recurrence at, NSM and, 188
removal of, 642, 686
repositioning of, 73, 394
contraindications for, 406–407
generic risks, 413–414
indications for, 406–407
intraoperative care, 407–410
outcomes, 414
preoperative planning, 407
in pseudoptosis, 1093–1094
techniques, 414t
shape of, transgender patients, 1169
superiorly displaced, 407–409
tethering of, 660, 660f
undermining of, 72–73, 72f
V-Y advancement flaps, 409, 409f
Nipple areolar reconstruction, 788f
Nipple asymmetry, preoperative
postoperative asymmetry and, 656
Nipple changes, assessment of, 105
Nipple grafting
double-incision free technique, 1160–1162, 1160f, 1161f
free, 1157, 1158f, 1160f, 1161f
Nipple shields, 966f
bacterial exposure reduced by, 996
Tegaderm, 997f
use of, 1057
Nipple to inframammary fold (N-IMF) measurement, 1103–1105, 1123f
measurement of, 1054, 1123f
preoperative assessment, 928f
Nipple to navel (N-N) measurement, 1103–1105
Nipple transfer procedure, marking for, 655
Nipple-areola reconstruction
outcomes, 759f
preoperative marking, 489f
procedure, 856
Nipple-areolar complex, removal of, 106
Nipple-sparing mastectomy (NSM), 81
aims of, 215
bilateral, 453f, 461f, 507f, 610f
bioengineered breast concept, 447f
breast conservation surgery and
approach algorithm, 498f
capsular contractures, 651
cases, 173f–174f, 789f
complication rates and, 604
contractures after, 651
NAC malposition in, 651
contraindications for, 150, 216, 487–490, 497
deepithelized inferior dermal mastectomy flap and, 152–153, 153f
definition of, 187
device-based reconstruction, 657f
flap quality, 217–218
flap thicknesses, 175f
gel implant and, 354f
generic risks, 174
history of, 150, 167, 215, 488, 497, 504, 564, 650–651
implants after, 350
in-breast recurrence risk and, 183
incisions, 151–152, 168–169, 490–493
locations of, 218–220
options for, 218f
indications for, 150, 216, 489, 497–498
intraoperative care, 171–172
local recurrence after, 175
marking for, 493
NAC malposition in, 651
NAC recurrence and, 188
nipple malposition after
contraindications for correction of, 657–658
correction of, 658–661, 658f
indications for correction of, 657
intraoperative prevention of, 653–657
outcomes, 661–662
patient selection for, 651–653
postoperative care after correction of, 661
rates of, 650
risk factors for, 651–653
risks of corrective surgery for, 663
surgical treatment for, 650–664
oncological safety of, 216, 662–663
oncoplastic reduction mammaplasty and, 152
oncoplastic surgery, 504–507
operative risk factors, 607
operative techniques, 151–153, 151f–153f, 170–171
outcomes, 153–156, 174–175, 219f–220f, 223f, 531f
patient satisfaction and, 211
patient selection criteria, 150–156, 504–509
post radiation therapy, 152f
postoperative care, 172–173
postoperative necrosis, 610f
postoperative photos, 152f
preoperative planning, 151, 153f
prepectoral reconstruction and, 707
ptotic patients, 488–496
radiation therapy and, 156, 216–217
reconstruction after, 155f, 349, 457, 650–651
reduction pattern incisions, 493, 493f
risk-reduction, 215
shared decision making and, 209
in situ SWIM technique, 825f
skin flap, case study, 742f
skin redundancy after, 552
surgical techniques, 221t, 222f, 493t
symmetry procedures, timing of, 627–629
team approach to, 215–225
technical aspects, 217–218, 217–223
technique, 647
therapeutic, 215–217
two-stage
candidate selection, 497–498
operative technique, 499, 500f–501f
outcomes, 502
postoperative care, 499–501
preoperative marking, 500f
preoperative planning for, 498
stage one, 499
stage two, 499
timing of stages, 502
two-staged, 497–503, 661f
Nipple-sparing reduction mastectomy (NSRM), 219–220
Nipple-sternum (NS) line, 1014, 1015f, 1019, 1020f
Nipple-to-anterior axillary fold distance, 654
Nipple-to-fold (N-IMF) distance, 967, 967f
Nipple-to-new IFM distance (N-NIMF), 1017f, 1018–1020
Nipple-to-nipple (N-N) distance, 1054
Niraparib for ovarian cancer, 50
Nitric oxide
expression after radiation therapy, 859
smoking and, 1178
Nitroglycerin ointment, 172, 610
N-N (nipple to navel) measurement, 1103–1105
Nodal disease
confirmation of, 251
residual
management of, 252
Nodularity, implant rupture and, 1248
Nonsteroidal anti-inflammatory drugs (NSAIDs). See also Specific drugs
pain management using, 1266
postoperative, 720
Norwegian Women and Cancer Study (NOWAC), 9
Notch-to-nipple measurements
breast asymmetry and, 937f
preoperative, 936f
supersternal, 935f
No-touch technique
acellular dermal matrix and, 583
implant placement and, 938, 980–981, 1120, 1140
Nottingham grading system, prognosis and, 116
NPWT (negative pressure wound therapy), 847–848
NSAPB P-1, breast cancer risk and, 7
NSM. See Nipple-sparing mastectomy (NSM)
NSQIP (National Surgical Quality Improvement Program), 835–836
NSRM (nipple-sparing reduction mastectomy), 219–220
Numeracy, patient, 960
Nutrition
breast cancer and, 6
breast cancer risk and, 7
postoperative, 720
surgical risk reduction and, 1264
Nylon Gillies-type sutures, 871
O
Obesity
breast cancer risk and, 7, 40
complication rates and, 604, 605–606
complications
necrosis and, 300–301
in TRAM flap reconstruction, 768
contraindications
to prosthetic breast reconstruction, 639
to TRAM flap reconstruction, 763
definition of, 1185
epidemiology of, 1185–1186
high BMI definitions and, 510
massive weight loss after, 358
nipple-sparing mastectomy and, 488–489
outcomes and, 516–520
surgical complications and, 639
Oil cysts, 1177
Olaparib for ovarian cancer, 50
Omega-3 fats, breast cancer risk and, 40–41
Omentum, exposure of, 233f
Oncologic parameters, 488
Oncoplastic approach
breast cancer
postoperative complications, 77
level 1, 70–77
level 1 versus level 2, 70
level 2, 70, 71f
option talk in, 301
team talk in, 301
three talks model and, 299–301
preliminary phase of, 300–301
Oncoplastic surgery
algorithm for options in, 79f
benefits of, 78–79
breast cancer
cancer resection, 73
defect closure, 73
incision location, 71–72
incision techniques, 73–76
patient selection, 70–71
procedures, 71–73
surgical planning, 71
undermining of skin, 72, 72f
undermining the nipple areolar complex, 72f
NSM and, 152
patient evaluation
history, 80
imaging, 80
physical examination, 80
reduction mammaplasty, 152
technique, 81, 85
timing of, 81
volume replacement approaches, 85
Oncotype DX
description of, 28
in early-stage breast cancer, 117t
predictive value of
adjuvant chemotherapy and, 123
Recurrence Scores, 49, 117, 185–186
133 LV expanders, 545f, 546f, 548f, 549, 550f, 552f, 554f–562f
Oocyte cryopreservation, 124
Oophorectomy
breast cancer regression and, 126
prophylactic, 37
risk reduction mastectomy and, 37t
Open biopsies in augmented patients, 138
Open glandular excision
indications, 423t
methods, 423t
Operating rooms
lighting of, 977
positioning in, 756
setup of, 752f
surgical efficiency and, 752f
Opioids
metabolism of, 713
pain management using, 1266
Oppenheimer effect, 135–136
“Option talk,” 300
Opus Curve implants (Sientra), 932
Oral contraception (OCP)
breast cancer risk and, 9, 41
breast cancer risk reduction and, 48
Oral mucositis, chemotherapy-related, 124–125
Osmotic injuries, cryoablation and, 66
Ovarian ablation
in early breast cancer, 128–129
methods of, 128–129
Ovarian cancer syndromes, psychosocial issues in, 51
Ovarian functional suppression, 128–129
Overall response rates (ORRs), 50

P
P53, breast cancer risk and, 177
Paclitaxel in inflammatory breast cancer, 111
Pain
discussion of, 1236
implant rupture and, 1248
informed consent and, 1236
Pain management
clinical, 713
environmental factors in, 712–713
intraoperative, 1263, 1266
liposomal infiltration protocol, 718t
numbing medications, 535–537
pectoral nerve blocks, 719–720
perioperative, 712–722, 1263
current understanding, 712–713
history of, 712
postoperative, 352
postoperative analgesia, 720
preoperative paravertebral blocks (PPVB), 719
regional anesthesia, 1266
trends in, 1266
PALB2 gene
breast cancer risk and, 10, 19–20, 177
breast cancer screening guidelines, 47t, 51
cancer risk and, 46, 46t
PAM50 (Prosigna)
description of, 29
recurrence scores, 186
PAP (perfunda artery perforator) flap, 843
Papillary lesions, 197t
Papillomas, breast cancer risk and, 8
Paravertebral blocks (PVBs), 1266
Parenchymal mobilization, 337
Parenchymal resection, 377f–378f
Parity
breast cancer risk and, 5, 41
impact of alcohol on, 7t
Paroxetine, hot flashes minimized by, 37
Patient autonomy
informed consent and, 950–951
self-determination and, 952
Patient choice, decision making and, 209
Patient consent, social media and, 1243
Patient decision aids (PDAs)
acceptance of, 951
certification of, 950
Patient decision checklists, 951
Patient dissatisfaction, risk factors for, 1228t
Patient education. See also Informed consent; Well-informed patients
3D simulations in, 957–959, 959f, 960f
before and after photos, 956
on breast augmentation, 950–964, 954–959
cultural barriers and, 956
decision-making and, 959
documentation of, 960–961
ERAS and, 714
implant-based reconstruction and, 638
information gaps and, 210
informed consent and, 950–952
initial consultations, 952–954, 953t
literacy barriers and, 956
misinformation available and, 952
numeracy and outcomes of, 960
patient expectations and, 961–962
patient satisfaction and, 212
preoperative, 952–953
shared decision making and, 209
social media and, 1227, 1243
staged patient learning and, 952–953
surgical efficiency and, 752
“teach back” techniques, 951
Patient educators
initial consultation forms, 953t
second consultation forms, 954t
Patient expectations
appearance in, 1226–1227
informed consent and, 1234
management of, 1130
preoperative evaluation and, 1052–1054
patient education and, 961–962
patient satisfaction and, 212
sizer systems and, 1011–1012
social media and, 1245
surgery risks and, 1226–1227
Patient immobilization devices, 95f
Patient loyalty, informed consent and, 1233–1234
Patient positioning, postoperative, 871
Patient preferences, breast width, 1016
Patient satisfaction
algorithm for reconstruction in, 680f
bilateral versus unilateral mastectomy, 647–649
breast reconstruction and, 647, 648–649
breast sensation and, 831–832
BREAST-Q analysis, 570
BREAST-Q survey, 725
clinical choices and, 648
cultural differences and, 212
with current breasts, 680f
data on, 648
dissatisfaction
apologies and, 1228
avoiding, 1225–1229
with cosmetic results, 1237
management of, 1225–1229
reasons for, 868
risk factors for, 1228t
listening skills and, 1228
male breast reduction surgery and, 435
patient education and, 955–956
PMRT and, 163
shared decision making and, 210–212, 299–307
visuals and, 955–956
Patient testimonials on social media, 1244
Patient values, decision making and, 304
Patient-controlled anesthesia (PCA), 1266
Patient-Reported Outcomes Measures (PROMs), 1225
PCA (patient-controlled anesthesia), 1266
PCDs. See Intermittent pneumatic compression devices (PCDs)
Peau d’orange
assessment of, 105
inflammatory breast cancer and, 109
Pectoral nerve, 243
Pectoral nerve blocks (PEBs), 718, 719–720, 719f, 780, 1266
Pectoralis major fascia, 978f
anatomy of, 995
incision under, 996
overrelease of, 1128
Pectoralis major flap, 880
Pectoralis major muscle
division of, 970f
identification of, 1112f
implant removal and, 677f
inferior attachment of, 443
lateral border of, 969f
origins, 1055
pocket beneath, 1118
radiated, 837
release of, 969f
shearing effect on skin flaps, 514
spacing of, 1055
subpectoral implant and, 515f
tissue release from, 1098f
Pectoralis minor muscle
division of, 243
protection of, 978
Pectoralis muscle, release of, 459f
Pectus excavatum, medial malposition and, 1055–1056
Pedicle
creation of, 377f
flaps, reconstruction of, 837
Pedicled nipple transposition, 660–661, 662f
Pembrolizumab, NACT plus, 119
Pentoxifylline (Trental), prophylactic use of, 668
Percutaneous aponeurectomy, 894
Perforasomes, 843
Perforator flaps. See also Anterior intercostal artery perforator (AICAP)
flap; Deep inferior epigastric artery perforator (DIEAP) flap; Deep inferior
epigastric perforator (DIEP) flap; Dorsal intercostal artery perforator
(CICAP) flap; Gluteal artery perforator (GAP) flap; Inferior gluteal artery
perforator (IGAP) flap; Intercostal artery perforator (ICAP) flap; Internal
mammary artery perforator (IMAP) flap; Lateral intercostal artery
perforator (LICAP) flap; Lumbar artery perforator (LAP) flap; Medial
circumflex femoral artery perforator (MCFA) flap; Medial intercostal artery
perforator (MICAP) flap; Perfundal artery perforator (PAP) flap; Superior
epigastric artery perforator (DEAP) flap; Superior gluteal artery perforator
(SGAP) flap; Thoracodorsal artery perforator (TDAP) flap; Transverse
profunda artery perforator (T-PAP) flap
anatomy of, 869
benefits of, 647
contraindications, 325f
harvest of, 337
history of, 324
local, 324
nutrient vessels for, 337–338
planning, 338–341
shaping of, 726
Perforators
location of, 330f, 334f, 338
mapping of, 771
sites for, 338f
Perfundal artery perforator (PAP) flap, 843
Periareolar concentric mastopexy, 426–428
Periareolar excision, 423–426
Periareolar flaps, delayed, 733f
Periareolar incisions
augmentation mammaplasty, 976–981
nipple-sparing mastectomy and
NAC malposition in, 651
placement of, 977f
techniques, 218
Periareolar mastopexy, complications related to, 948
Perioperative period
pain management, 1263
patient care during, 1263–1270
smoking during, 1182–1183
Peripheral nerves, ingrowth of, 832
Periprosthetic capsular contractures, 930–931. See also Capsular
contracture (CC)
Periprosthetic fluid
biopsies of, 1194, 1197
pathologic evaluation of, 1197
Periumbilical medial row perforator, 755
Persister cells, metabolism of, 1213
Personality traits, patient satisfaction and, 210
Pertuzumab, 111
HER-2-targeted therapy using, 119t
neoadjuvant therapy using, 120
trastuzumab and, 120, 126
Petit, Jean Louis, 237
Peutz-Jeghers syndrome
breast cancer screening guidelines, 47t, 51
description of, 45
Pexy reduction techniques, breast symmetrization and, 472
Phagocytosis, biofilm resistance to, 1213
Pharmacogenomics, 713
Phosphate and tensin homolog (PTEN) gene. See PTEN genes
Photographs
informed consent and, 1237–1238
outcomes, 1237–1238
Phyllodes tumors
description of, 195–196
histology of, 196f
incidence of, 195
recommendations, 197t
Physical activity, breast cancer risk and, 7–8, 35, 41
Physician-patient relationships. See also Informed consent; Patient
education; Well-informed patients
communication and, 951–952
informed consent and, 950–952
Physicians, self protection by, 1239
Physician/team communication, 210
Phytochemicals, breast cancer risk and, 6
Pilosebaceous glands, reduction of, 606
Pinch tests, upper pole, 1100f
Pitanguy maneuver, 1077–1078
Pitanguy point, 71, 71f
Plasmakinetic cautery, 846
Plastic surgeons
follow-up appointments, 1238
social media for, 1241–1246
Plastic surgery, ultrasound applications, 1253f
Platelet adhesion, smoking and, 1178
Platelet-derived growth factor (PDGF)-B, 667
PMRT. See Postmastectomy radiation therapy (PMRT)
PMS2 gene, cancer risk and, 46t
Pneumatic compression pumps (PCPs), 292
Pneumonitis after regional nodal radiation, 101
Pocket control, recurrent ptosis management and, 1097–1098
Pocket revision for nipple malposition, 659
Pocketplasty, use of, 567
Pockets
antimicrobial treatment of, 1204
assessment of, 1124
boundaries of, 1144–1145
characteristics of
dermal matrix use and, 567t
choice of, 1169
dissection for, 1000
infections
acellular dermal matrices and, 566–567
intraoperative preparation of, 863
irrigation of, 533, 996
with hypochlorus acid solution, 1119
triple antibiotic betadine solution, 1119
mastectomy, oversized, 511, 511f
neosubpectoral, 1118f
overdissection of, 1144–1145
reinforcement of, 1144–1145
revision of, 659, 659f
standard culture of, 1205
subfascial, 1100
submuscular, 1100
subpectoral, 1100f
creation of, 1119f
Poland syndrome
description of, 948–949, 948f
development of, 921
reconstructive surgery, 949
Poly ADP-ribose polymerase (PARP) inhibitors
DNA damage and, 50
neoadjuvant chemotherapy and, 119, 122
Poly-4-hydroxybutarate, 1126
Polydimethyl siloxane, silicone and, 922
Polydimethylsiloxane (PDMS; (CH3)2SiO), 1219f
Polygenic risk scores (PRS), cancer risk and, 47
Polymerase chain reactions (PCRs)
usefulness of, 24–25
variants of, 25, 25f
Polysaccharide gels, implants filled with, 926
Polytetrafluoroethylene (Teflon), breast augmentation with, 921
Polyurethane, breast augmentation wth, 921
Polyurethane foam
for breast reconstruction, 930
structure of, 925f
Polyurethane (PU) implants
in aesthetic breast surgery, 1039–1040
history of, 1039
indications, 1039–1040
outcomes, 1051
operative technique, 1040–1050
outcomes, 1041f–1050f, 1051
textured, 1205–1206
Polyvinylpyrrolidone (PVP) implants, 926
Popcorn capsulorrhaphy. See Thermal (popcorn) capsulorrhaphy technique
Positron emission tomography (PET)
BIA-ALCL and, 1193–1194
diagnostic use of
in inflammatory breast cancer, 110
Postanesthesia care units (PACUs), 787
Posterior medial thigh (PMT) flap, 875
Postmastectomy radiation therapy (PMRT), 157–166. See also Radiation
therapy (RT)
autologous tissue-based reconstructive surgery and, 860
breast reconstruction and
clinical complications associated with, 859
immediate versus delayed, 858–859
patient satisfaction and, 523–525
timing of, 859
capsular contracture and, 565, 666
clinical scenarios, 706
delayed-immediate breast reconstruction and, 670, 861–864
direct-to-implant (DTI) and, 667
exposed implants and, 614
fibrosis and, 669f
history of, 157, 665, 706
immediate breast reconstruction and, 860–861
implant positioning and, 777
implant-based reconstructive surgery and, 859–864
indications for, 627, 706–707
levels of, 707
locoregional recurrences, 158–160, 159t
need for, 640
negative effects of, 565
neoadjuvant chemotherapy and, 160–161
in node-negative populations, 160
original trials of, 157–160
preoperative planning and, 707
prosthetic reconstruction and, 639
radiation dosages, 161–163
radiation fractionation in, 161–163
radiation targets, 161–163
reconstructive failures and, 708, 861
regenerative tissue matrices and, 565
shared decision making and, 303
side effects of, 163–164
techniques, immobilization and, 162
timing of, 706
outcomes and, 708
reoperations and, 709
value of, 157
Postmenopausal women
NET in, 121
recurrence risk and, 183
Postneoadjuvant therapy, residual disease in, 121–122
Postoperative care
acellular dermal matrix and, 584–587
after augmentation mammaplasty, 935–936
after augmentation mastopexy, 1068–1070, 1078
after autologous breast reconstruction, 856, 875
after autologous fat grafting, 905
after BRAND4P procedure, 467–468, 468f–470f
after breast augmentation, 1022–1023, 1074–1076, 1140
exercise during healing, 1009–1010
transaxillary approach, 988, 988f
transgender patients, 1169
after breast conservation surgery, 311
symmetry procedures, 352
after breast reconstruction, 787
after breast reduction surgery, 410
after chest masculinization, 1162–1164
after gender-affirmation surgery, 205–206
after gynaecomastia surgery, 435–437
after ICG sentinel lymph node mapping, 257
after implant-based breast reconstruction, 452, 591, 644–645
after light-weight breast implant, 1029
after liposuction, 294–295, 435–437
after liposuction mastopexy, 1106–1108
after lumbar artery perforator flap, 816
after mastopexy-augmentation, 1086
after neoadjuvant chemotherapy, 266–267
after nipple areolar complex surgery, 410
after nipple-sparing mastectomy, 172–173, 661
after profunda artery perforator flap, 796
after SPIO sentinel lymph node mapping, 257–258
after subfascial augmentation mammaplasty, 997
after subfascial breast augmentation, 997–998
after subpectoral breast reconstruction, 460
after superior gluteal artery perforator (SGAP) flap, 774
after transverse upper gracilis flap, 806–809
after two-stage breast reconstructive surgery, 535–537
after two-stage nipple-sparing mastectomy, 499–501
breast mound, 452, 1140
breast revision surgery, 1130
exercise, 1023
patient education about, 954t
polyurethane implants and, 1040–1041
pseudogynaecomastia surgery, 435–437
standardization of, 756–757
support garments, 1013f
wound healing in, 1263–1264
Postoperative puckers, 375
Postoperative wound infections, 938
PPVB (preoperative paravertebral blocks), 718
Practice management, 1247–1262
Practice updates, social media, 1244
Prediction Analysis of Microarray (PAM-50), 117–118
Preeclampsia, breast cancer risk and, 5
Pregnancy
BCT contraindication in, 56
lactational adenomas in, 195
Preimplantation genetic diagnosis (PGD), 49
Premature menopause, chemotherapy-related, 124–125
Premenopausal women
NET in, 121
recurrence risk and, 183
Prenatal diagnoses (PND), BRCA mutations and, 49
Preoperative imaging, surgical efficiency and, 752
Preoperative paravertebral blocks (PPVB), 718, 719
Prepectoral approach
complication rates and, 564
two-stage reconstruction and, 535
Prepectoral conversion
contraindications, 625t
operative technique, 622–623
clinical experience, 622–623
complication rates, 622–623
implant exchange, 622
incision, 622
prepectoral plane change, 622
revision options, 623f
outcomes, 623–626
patient selection, 623–625
Prepectoral fascia
endoscopic view of, 987f
implant placement, 621
Prepectoral implant-based reconstruction (IBR)
one-stage, 466–471
BRAND4P procedure, 466–467
history of, 466
patient selection, 466
Prepectoral implants, history of, 1117
Prepectoral pockets
definition of, 565
development of, 551
vascular supply, 568f
Prepectoral reconstruction
acellular dermal matrix and, 668f
ADM-wrap-around technique, 584, 584f
approaches, 445
bioengineered breast concept and, 445–447
contraindications, 511t
oncologic, 511t
reconstructive, 511t
dermal matrices in, 565–566
direct-to-implant
dermal substitutes and, 564–565
history of, 564
modern methods, 564–565
in high BMI patients, 510–520
operative planning, 510–511
impact on fat grafting, 899
implants, outcomes, 668f
indications, 565–566
postmastectomy radiation therapy and, 709
radiation and, 666–667
revision procedures, 569–572
two-staged procedure, 511–512
without dermal substitutes, 566–572
PREPLANT technology, 1011, 1012f, 1013f
Pressure-Specified Sensory Device (PSSD), 832, 833–834
Prevena negative pressure dressings, 845
Process mapping
reliable backups and, 755
revaluation of, 757
surgical efficiency and, 751–757
Professionalism, social media and, 1243
PROFILE registry, 1191, 1195
Profunda artery perforator (PAP) flap
in autologous reconstruction, 875
case studies, 797f–799f
computed tomographic angiography of, 793f
contraindications, 794
history of, 793
indications, 793–794
neurotization of, 834
operative technique, 795–796
intraoperative care, 796
outcomes, 796
photographs, 795f–796f
postoperative care, 796
preoperative planning, 794
reconstruction using, 799f
Progesterone interactions with SERMs, 37
Progesterone receptors
inflammatory breast cancer and, 109
tumors positive for, 159
Progestin therapy, transfeminine mammogenesis and, 1167
Progestin-only contraception (POC), 9
Progression-free survival (PFS) rates, 50
Progressive tension sutures (PTS)
placement of, 846
seroma prevention, 845
Proliferation, wound healing and, 1263–1264
PROMs (Patient-Reported Outcomes Measures), 1225
Propionibacterium acnes, capsular contractures and, 1204
Prosigna/PAM-50 in early-stage breast cancer, 117t
Prostate gland biopsy, 49
Prostate-specific antigen (PSA), 49
Prostheses. See also Implants
breast examination and, 136
complications related to, 702
irradiated
complications associated with, 665–666
nonoperative adjunct treatments, 667–668
muscle coverage of, 444
Prosthetic reconstruction, fat grafting after, 897
Protein C deficiency, 837, 839
Protein depletion, wound healing and, 1265
Proteus and Proteus-like syndrome, 45
Prothrombin gene mutations, 839
Pseudoangiomatosus hyperplasia of the mammary stroma (PASH), 197
Pseudogynaecomastia, 416
male breast reduction
complications of, 435t
postoperative care, 435–437
treatment of, 417
Pseudoptosis
after breast reduction, 385
anterior view of, 1091f
etiology of, 1090–1091
implant malposition and, 1096f
management of
marking for, 1093f
relifting the breast, 1093–1097
mastopexy-augmentation technique, 1085, 1087f
presentation of, 1126–1127
shaped implants in, 1009–1010
volume displacement approaches, 81
Psychological consults, informed decision making and, 212
Psychosocial well-being
delayed breast reconstruction and, 861
immediate breast reconstruction and, 861
PTEN genes
breast cancer risk and, 10, 35, 45t, 177
cancers-related to, 10
mutations
risk reduction mastectomy and, 37t
screening in, 51
PTEN hamartoma tumor syndrome (PHTS), 45
Ptosis
after breastfeeding, 1069f
after childbirth, 1067f
bilateral, atrophy and, 1050f
breast deformities, 944
breast lift in, 350
breast reconstruction, 362f–365f
case studies, 362f–365f
classification of, 300
degree of, 1052, 1053f
preoperative planning and, 1103
glandular, 1059f, 1060f
grade 2, 1061f, 1062f
childbirth changes and, 1063f
grade 3
symmetry procedures in, 629f
implant-based reconstruction and, 567–569
necrosis rates and, 606
nipple-sparing mastectomy
implant-based reconstruction and, 488–496
outcomes, 219–220
nipple-sparing mastectomy and, 217
preoperative
nipple malposition after surgery, 653, 653f, 662
outcomes and, 662
rates of
mastopexy-augmentation and, 1083
recurrent, 1083
etiology of, 1090–1092, 1090t
management of, 1093–1101
mastopexy-augmentation and, 1090–1101
mastopexy-augmentation technique, 1085
pocket control in management of, 1097–1098
second degree, 1079f
skin-reducing mastectomy in, 680f
treatment of, 1090
Puckers, breast reduction surgery, 385
Puckett technique, modified, 945
Pulmonary emboli, tamoxifen and, 127

Q
Quadrantectomy, 84f, 334f
Quality improvement, Best Practice Standardization and, 751–757
Quality of life
breast conservation surgery and, 321
breast reconstruction and
self-esteem and, 522
breast reconstruction surgery and, 211
decision-making process and, 209
gender dysphoria and, 1157
lymphedema and, 273
mastectomies and, 301–302
PMRT and, 163
Quantitative PCR, 25

R
Race/ethnicity
breast cancer incidence and, 4f
breast cancer risk and, 3–6, 41
stage IV breast cancer and, 107
RAD51C gene
breast cancer risk and, 10
cancer risk and, 46t
RAD51D gene
breast cancer risk and, 10
cancer risk and, 46t
Radial scars
description of, 194–195, 195f
recommendations, 197t
Radiation dermatitis, 859
Radiation exposure
breast cancer risk and, 5, 31
Hodgkin lymphoma and, 5
Radiation pneumonitis, 859
Radiation therapy (RT). See also Postmastectomy radiation therapy
(PMRT)
acute toxicities, 859
adjuvant endocrine therapy versus, 94–95
after BCS
recurrence risk and, 189f
after BCT, 91–104, 92–93, 92t
after mastectomy, 157–166
APBI, 98f
arterial stiffness after, 859
autologous reconstruction and, 882
in BIA-ALCL, 1199
breast reconstruction after, 527f, 672
breast recurrence rates and, 189–190, 190f
chronic toxicities of, 859
complication rates and, 604
contractures related to, 146, 146f
in DCIS, 200
dosage in breast cancer, 95–100
epidermal changes and, 606
exposed implants after, 614
fat grafting and, 893
fibrosis after, 657–658
flap failure and, 835
fractionation in breast cancer, 95–100
guidelines
field design, 267f
node positive patients, 266–267
history of, 858–859
implant reconstruction after, 590–599
implant-based breast reconstruction and, 645, 665–668, 706
implant-based salvage and, 672
in inflammatory breast cancer, 112
microvasculature and, 670
neoadjuvant, skin necrosis and, 464
nipple malposition following, 652f
nipple-sparing mastectomy and, 156, 216–217, 651
node-positive patients
contraindications, 265
SLNB versus ALND, 262–263, 267f
omission in select populations, 93–95
patient satisfaction and, 211
post-breast-conservation surgery, 300–301
postmastectomy, 635
premastectomy, 216–217
prepectoral reconstruction and, 666–667
regional nodal, 100–102–11
secondary malignancies and, 859
sentinel node positive cancer, 263f
SGAP flap failure and, 840f
side effects of, 161
skin necrosis and, 606
subpectoral reconstruction and, 666
surgery versus, 260–272
symmetry procedures and, 635
timing of, 577
implant-based reconstruction and, 473
TRAM flap contraindications and, 763
volume in breast cancer, 95–100
whole breast, 97
Radiofrequency ablation (RFA), breast cancer studies, 66t, 67–68
Radiofrequency-assisted liposuction (RFAL), 418
Radiologic imaging of augmented breasts, 138–142
RAFT Suture, 915–916, 915f
Rake retractors, 977
Raloxifene
adverse reactions to, 36–37
breast cancer risk reduction and, 35–36
Ralstonia pickettii
Betadine use and, 996
BIA-ALCL and, 996
RealSelf, 1242
Real-time PCR, 25
Reasonable Patient Standard for informed consent, 1233
Reasonable Physician Standard for informed consent, 1233–1234
Reconstructive breast surgery. See also Breast reconstruction
autologous fat grafting with
tissue expansion, 908–917
bilateral, 776
breast symmetry after, 760–761
contraindications, 167
decision making, 507
dual plane technique, 444, 444f
failed, 443
PMRT and, 861
indications, 167
mastectomy and, 305
maximum reshape, 305
microsurgical tissue transfer, 790
minimal aggressiveness, 305
oncoplastic, 308
partial-muscle, 444
PMRT and, 163
selection of, 507
staged approach to, 163
timing of
matching procedures and, 758–760
PMRT and, 163–164
types of reconstruction, 758
Rectus abdominus muscle
fascia covering, 995
incision under, 996
Rectus muscle, infraumbilical segment of, 783
Redness, assessment of, 105
Reduction mammaplasty. See also Wise-pattern reduction mammaplasty
effect of smoking, 1180
in high BMI patients, 1186
history of, 393, 405–406
inverted-T incision, 393–398
history of, 394
indications, 394
inferior pedicle, 396–397
operative technique, 396–397
patient markings, 394–395, 395f
preoperative considerations, 394
nipple-sparing mastectomy, 217
oncoplastic, 152
outcomes, 1268f
patient selection, 1186
Wise-pattern, excessive breast volume and, 358–359
Reed-Sternberg-like cells, 1195
Reflection, ultrasound, 1250
Regional lymph nodal irradiation (RNI)
benefits of, 252–253
field of, 706
Regional lymph nodes, axillary surgery vs. RT, 260–272
Regional neural blocks, 718
Rehabilitation, breast surgery and, 1269
Renault breast ptosis classification, 300, 489t
Reproductive history, breast cancer risk and, 5
Research, social media and, 1243
Rete pegs, effacement of, 606
Retinal opacities, tamoxifen and, 127
Retractors, lighted, 977
Reverberation artifacts, ultrasound, 1252f
Reverse abdominoplasty and fat transfer (RAFT), 915–916, 915f, 916f
Reverse latissimus dorsi flaps. See Lumbar artery perforator (LAP) flap
Reverse lymphatic mapping, 288–289, 289f
Reverse transcriptase (RT-PCR), 25
Revision surgeries, informed consent and, 1237
Revolve system, 900
Rheumatoid arthritis, breast implant illness and, 1220
Rib fractures, radiation therapy and, 859
Right internal mammary artery, 781f
Right internal mammary vein, 781f
Rigotomy
description of, 914, 914f, 915f
procedures, 882
Rippling, saline implant, 1056
Risk reduction, perioperative, 1264
Risk-reducing mastectomy (RRM)
breast cancer risk and, 37
efficacy of, 48
in hereditary breast cancer, 50
Risk-reducing salpingo-oophorectomy (RRSO)
for breast/ovarian cancer risk, 37–38
efficacy of, 48
Ropivacaine, nerve block using, 719
Rotter nodes, removal of, 243
RT. See Radiation therapy (RT)
Ruben fat pad in autologous reconstruction, 875
Rucaparib for ovarian cancer, 50
Running barbed sutures, 1022

S
SAFE-Lipo, 1140
Sailboat mastopexy, 1085, 1087f
Saline-filled implants. See also Implants
construction of, 137
deflation of, 939
on digital mammography, 141, 142f
disadvantages of, 922
examples of, 922t
history of, 921–922
incisions, 985f
leaks, 939–940
mammographic shadows, 138
rippling of, 1056
subpectoral
outcomes, 935f
underfilling of, 922
valves, 137
Sarcoidosis, breast implant illness and, 1220
Scar tissue
breast parenchyma, 976
breast reduction surgery and, 382–383
calcification of, 136f
capsular contracture and, 1213–1214
discussion of, 1236
existing, 843–844
flap harvest sites, 776
“hockey stick,” 373
hypertrophy, 776
informed consent and, 1236
inverted T, 373
massage of, 1269
mastopexy-augmentation for, 1085–1086
minimization of, 1157
patient satisfaction and, 210
postsurgical care and, 1023f
preoperative planning and, 1103
rates of, 1083
reduction of, 367, 368
release of, 914, 914f
supraumbilical, 845
umbilical, 868
widening of, 1023f
“Scar wars” debate, 1081
Scarpa fascia closure, 972f
Sciatic nerve damage, 770
Scleroderma, breast implant illness and, 1220
Sclerosing adenosis, 193, 193f
Sclerosing lesions, complex, 194–195
Scrub nurses, 753, 754t, 756
Sebbin implant rupture rates, 1248
Segmentectomy, central, 106
Self-anchoring monofilament sutures, 847
Self-determination, patient autonomy and, 952
Self-esteem
breast surgery and, 1225–1226
mastectomy and, 850
Self-retaining instruments, 753
Semmes-Weinstein monofilaments, 832
Sensation
breast tissue and, 831
lack of, 832
outcomes and, 1227
recovery of, 383
testing of, 833–834
Sensory intercostal nerve allograft, 786f
Sensory neurotization, DIEP flap reconstruction and, 778–792
Sentinel lymph node biopsies (SLNB)
after neoadjuvant chemotherapy
feasibility of, 248, 250–252
optimization of, 250–252
timing of, 248
ALND and, 106
ALND versus, 262–263
alternative methods for, 255–259
axillary nodal recurrence and, 60
axillary staging and, 106
case selection for, 238
case studies, 267–268
complications of, 244–245
axillary web syndrome, 244–245
infection, 245
lymphedema, 244
sensory morbidity, 245
shoulder dysfunction, 245
failed, 240
history of, 157, 255
incisions for, 242f
indications for, 240t
invasive ductal carcinoma, 84f
isolated locoregional recurrence, 240
lymphedema after, 273
in node-positive breast cancer
trials of, 261t, 262, 269t–270t
pathology, 239
PMRT and, 160, 706
positive nodes, 160
prognostic value of, 106
regional nodal RT and, 100–102–11
surgery, 238–239
targeted radiation and, 262–263
technique for, 238–239
unavailability of, 240
Septocutaneous perforators, 813f
SERMs
estrogen interactions with, 37
progesterone interactions with, 37
Seromas
acellular dermal matrices and, 566–567
ADMs and risk of, 588
after breast reduction, 384–385
after breast surgery, 464
aspiration of, 936
BIA-ALCL and, 1193
delayed, 1193
in DIEP flap patients, 845
discussion of, 1236
donor site, 336, 702, 1142
drainage of, 936
formation of, 515f, 573
HRUS imaging, 1260f
infected, 845
informed consent, 1236
LDMF and, 702
periprosthetic, 936
persistent, 936
postoperative, 1164f
prevention of, 846–847
rates of, 1083
shaped implants and, 1011
Serratus anterior muscle
fascia covering, 995
incision under, 996
location of, 687
protection of, 978
“The $75,000 breast,” 1237–1238
informed consent and, 1237–1238
Severity of Postreconstruction Breast Defects checklist, 735, 736t
Sexual function, postmastectomy reconstruction and, 1228
Sexual well-being, breast reconstruction and, 302
SGAP flaps. See Superior gluteal artery perforator (SGAP) flap
Shared decision making (SDM)
cultural differences and, 212
decision aids and, 211
general concepts in, 299–301
history of, 208
messaging to patients, 304
oncologic, 304
reconstructive, 304
in oncoplastic breast surgery, 299–307
patient choice
fear of recurrence and, 208
time allotment in, 208
patient choice and satisfaction, 208–214
patient satisfaction and, 210–212
patient values and, 304
regret over time and, 211
Sharpie pens, marking using, 549
SIEF (simultaneous implant exchange with fat)
BRAVA pre-expansion, 1137f
core volume augmentation and, 1132
selection of, 1132–1133
Sientra cohesive implant rupture rates, 1248
Sientra silicone implants, 924t
capsular contracture data, 939
Silicon dioxide (silica, SiO2), 1218–1220
Silicone gel
chemistry of, 922–923
microsphere-enhanced, 1028f
samples of, 1035f
Silicone Gel-Filled Breast Implant Adjunct Clinical Study, 926t
Silicone-filled implants
bleed from, 923
evolution of, 923–924, 923t
examples of, 924t
exchange of
in pseudoptosis, 1098
FDA approval of, 924
FDA moratorium on, 950, 956
feel of, 923
fill selection, 1169
heavy metal concentrations, 1221t
herniated, 136, 136f
history of, 706, 921
incisions, 985f
insertion sleeve, 987f
leakage from, 137, 939–940
life span of, 1248
mammographic shadows, 138
moratorium on, 924
MRI of, false results with, 939
patient labeling, 1247t
physician labeling, 1247t
placement, preoperative photo, 989f, 990f
rupture of
rates of, 1248
screening for, 1247
ruptured, 137f
scar tissue calcification of, 136f
silicone chemistry, 922–923
Silicones
consumer products with, 926
elemental, 926
Siliconomas, 137, 137f
Silimed polyurethane implants, 1191
Siltex, structure of, 925f
Siltex-textured surfaces, 931–932
Simultaneous implant exchange with fat (SIEF)
BRAVA pre-expansion, 1137f
core volume augmentation and, 1132
selection of, 1132–1133
Simultaneous separation tumescence (SST), 1140
Single-isocenter photon technique, 162f
Sjögren syndrome, breast implant illness and, 1220
Skin
breast parenchyma and, 188f
changes to
assessment of, 105
inflammatory breast cancer and, 109, 110f
radiation therapy and, 163
closure of, 514f
complications, 385
contamination by, 996
elasticity of, 1000
assessment of, 1055
stretch marks and, 1123–1124
variability, 1052
excess, treatment of, 1127
excision patterns, 532f
fibrosis
irradiation and, 216–217
necrosis of
management of, 604–612
post RT, 464
prevention of, 604–612
puckers, 375, 385
quality of, 1123–1124
radiation therapy and, 606
rashes
BIA-ALCL and, 1193
over implants, 1041
reducing tension on, 1267
reduction of
extra-areolar scars and, 428–430
markings, 513f
redundancy, management of, 512
removal of
marking for, 1104f
stretch
deformity, 957f
maximal, 1123, 1124f
patient education about, 956
thickness variability, 1052
Skin envelopes
breast deformities, 944
deficit, 779f
delayed
categories of, 731
flap reconstruction, 729
inadequate, 1000
preservation of
history of, 604
tissue expanders and, 862–863
Skin excision patterns
breast reconstruction surgery, 640–641
staged/delayed, 426
Skin flaps
decreased compliance of, 566
immobilization of, 1267
irradiated
after fat grafts, 528f
necrosis
rates of, 651
smoking and, 1181
operative assessment of, 608–609
perfusion, 593f
viability of, 523
assessment of, 608–609
Skin glue, 1174
Skin hooks, placement of, 977
Skin ischemia and necrosis (SKIN) scores, 604, 605f
Skin pinch thickness, 1123, 1124f
Skin-reducing mastectomy (SRM)
incisions, 680f
in large breasts, 680f
in patients with previous augmentation, 679, 681
in ptotic breasts, 680f
reconstructive surgery after, 642–643
Skin-reduction techniques
open excision techniques and, 426–430
without extra-areolar scars, 426–428
Skin-sparing mastectomy (SSM)
contraindications, 216
delayed-immediate reconstruction and, 670
flap thickness, 187–188
history of, 150, 215
in-breast recurrence risk and, 183
incisions, 458
large breasts, 643f
nipple malposition after, 650
operative risk factors, 607
periareolar, 697f–698f
ptotic breasts, 643f
reconstruction, 349
residual disease after, 111–112
symmetry procedures, 627–629
timing of, 627–629
SLNB. See Sentinel lymph node biopsies (SLNB)
Small-duct papillomas, 193–194
Smile mastopexy, 1085
Smoking
breast cancer risk and, 7
complications related to
necrosis and, 300–301
rates of, 604–605
in TRAM flap reconstruction, 768
contraindications to flap reconstruction, 763
discussion of, 1235
electronic cigarettes (e-cigs), 604–605
flap failure and, 835
high-BMI patients and, 516
informed consent and, 1235
nipple-sparing mastectomy and, 489, 651
pathophysiology of, 1178
perioperative, 1181–1183
PMRT and, 163
resource utilization and, 1183
surgical outcomes and, 163, 909, 1178–1184
vascular supply and, 1178
Smoking cessation, 1159
monitoring compliance, 605f
surgical risk reduction and, 1264, 1265
wound healing and, 1182f
SnapChat, 1242
Snoopy deformity, 1152f. See also Waterfall deformity
Snoopy-nose deformities, 929
Social media
anonymity and, 1245
for breast surgeons, 1241–1246
ethical concerns, 1244–1245
events and, 1244
health-related information on, 952
history of, 1241
impact of, 1227
marketing content, 1243–1244
misinformation and, 1220
patient expectations and, 1245
patient testimonials on, 1244
personal postings on, 1244–1245
platforms, 1241–1243
practice updates, 1244
professional postings, 1245
reviews on, 1242
Society for Gynecologic Oncology, 33t
Society of Breast Imaging, 21t
Society of Surgical Oncology (SSO), 22t
Socioeconomic position (SEP), breast cancer risk and, 41
Soft tissue
coverage evaluation
pre-breast augmentation, 965
management of
incisions and, 1266–1268
support
sewing in, 1128
Soft tissue matrix, 494f
Solid tumor staging, 1196f
Sonication, maceration and, 1205
Sore throats, radiation therapy and, 859
Sound frequency in tissue, 1250
Specimen weight, necrosis rates and, 606
Specular reflection, 1250–1251
Spider silk proteins, 1208
SPIO. See Superparamagnetic iron oxide (SPIO)
Sponges, biofilm prophylaxis and, 1214
Sports bras, tight, 1011
SRM. See Skin-reducing mastectomy (SRM)
SSIs. See Surgical site infections (SSIs)
SSM. See Skin-sparing mastectomy (SSM)
SST (simultaneous separation tumescence), 1140
St. Gallen guidelines, 116
Standards of Care for the Health of Transsexual, Transgender, and Gender
Nonforming People (SOC), 1167
Staphylococcus epidermidis
capsular contractures and, 1204–1206, 1214
postoperative wound infections
management of, 938
prophylactic techniques, 1214
Staples, flap positioning and, 753
Stellate ganglion block, 292
Stem cell trafficking, inflammation and, 1264
Stem cells, loss of, 606
Stereotactic core needle biopsy, 199
Steric interactions, biofilm adhesion and, 1212
Steri-Strips, 1130, 1174
Sternal notch to nipple (SN) distance, 1123
cleavage and, 654
measurement of, 1054, 1103–1105
nipple-sparing mastectomy and, 651
nipple-to-anterior axillary fold distance and, 654
STK11 genes
breast cancer risk and, 19–20, 45t
cancers-associated with, 45
function of, 45
Stowers doctrine, 1238–1239
Strattice, 1128
Stress-strain curves, breast tissue, 1027f
Stretch marks, skin elasticity and, 1123
Stretching, breast, 1027f
Stromal vascular fraction (SVF) isolation, 888
Subcutaneous fat, tissue quality and, 676
Subcutaneous tissue
excess, 511f
lateral anterior, 512f
regeneration of, 893
repositioning of, 512f
thickness of, 1055
Subdermal plane, access to, 900–901
Subdermal plexus thrombosis, 467
Subfascial augmentation
implant selection, 997
outcomes, 1008f
round implants and, 1008f
Subfascial pockets, operative technique, 971
Subglandular implants
applications of, 1117–1118
history of, 1117
operative technique, 1119–1121
placement of, 1117, 1124
superior fullness and, 1117
tissue coverage, 1127
Subglandular pockets
creation of, 978–979, 978f
implant placement, 971
operative technique, 971
subpectoral pocket conversion to, 1110–1111
Submental flaps, VLNT donor site, 287
Subpectoral augmentation
pocket selection, 1169
technique, 978f
transgender patients, 1169
Subpectoral pockets
creation of, 1119f
neopectoral pocket conversion from, 1111
subglandular pocket conversion from, 1110–1111
tissue expander placement and, 534f
Subpectoral reconstruction, 533
radiation and, 666
Subpectoral space, 1119f
Suction-assisted lipectomy (SAL), 352, 418, 419f, 854–855
Superficial fascial system (SCARPA), 934
Superficial inferior epigastric artery (SIEA), 782
as backup for DIEP, 755
pedicle assessment, 755
in reconstructed breast, 850
Superficial inferior epigastric vein (SIEV)
dissection of, 845
preservation of, 836
Superior epigastric artery perforator (SEAP) flap, 311, 854
Superior gluteal artery, anatomy of, 771
Superior gluteal artery perforator (SGAP) flap, 770–777. See also Gluteal
artery perforator (GAP) flap
in autologous reconstruction, 874
contraindications, 771
failed, 837, 840f
harvest of, 774f
donor site closure, 773
donor site complications, 776
fat recruitment during, 772f
outcomes of, 773f, 775f, 776–777
patient positioning, 772
time involved in, 770
history of, 770, 843
indications for, 770–771
neurotization of, 834
operative technique, 772–774
intraoperative care, 774
learning curves, 776–777
postoperative care, 774
preoperative planning, 771, 771f
in reconstructed breast, 850, 852f
risks of tissue transfer, 776
selection of, 770
shaping of, 726
Superior inferior epigastric artery (SIEP) flap
in high BMI patients, 1186
shaping of, 726
Superomedial pedicle
blood supply, 370f
design of, 375
insetting of, 379f
nipple necrosis and, 384f
vascular supply, 368f
vertical breast reduction
benefits of, 367–369
contraindications, 371
indications, 371
postoperative puckers, 375
preoperative assessment, 371–373
preoperative planning, 373–375
projection, 375f
skin opening, 374–375
Superparamagnetic iron oxide (SPIO)
sentinel lymph node mapping with, 255
contraindications for, 255
indications for, 255
intraoperative care, 256–257
postoperative care, 257–258
preoperative planning, 255
risks of, 257–258
Support garments
IPOMIA bras, 1022–1023
postoperative care, 1013f
Supraclavicular flaps, 287
Suprascapular plane, dissection of, 1112f
Suprasternal notch to the nipple areolar complex (SSN-N) distance, 928
Surfactants
biofilm integrity and, 1215
biofilm resistance to, 1213
Surgeons
operative technique and, 754–755
practice variability, 752
roles of, 753–754
Surgery
changes caused by, 299
effects of smoking on, 1178–1184
efficient processes, 751–757
informed consent for, 1233–1240
outcomes, 1178–1184
perioperative management, 1263
risk reduction, 1264–1265
risks of
informed consent and, 1235
stress of, 1265
team role standardization, 752
wound healing and stress of, 1265
Surgical efficiency
concepts for, 751
process mapping and, 751–757
Surgical instruments. See Specific instruments
Surgical site infections (SSIs)
breast surgery, 717
in DIEP flap patients, 845
flap harvest sites, 776
irradiated tissue and, 667
Surgical site occurrences (SSOs), 844–847
Surgical sites, preparation of, 1207
Sutures
anchoring, 728–729, 728f
barbed, 847, 856, 1022
deep dermal relaxation, 1023f
flap positioning and, 753
marionette, 533, 1120, 1120f
Monocryl, 376, 380, 707
nylon Gillies-type, 871
pocket-defining, 565
progressive tension
placement of, 846
seroma prevention, 845
RAFT, 915–916, 915f
self-anchoring monofilament, 847
umbilicoplasty use of, 871
Vicryl, 584, 871
Vicryl 2-0, 459
wagon-wheel permanent, 1174
Symmastia
assessment of, 1124
breast augmentation outcomes, 1169–1170
mastopexy and, 1085
operative technique and, 1085
patient education about, 956
Symmetry
determination of, 630f
factors in, 629–630
procedures
case studies, 352f–355f
contralateral breast, 634–635
factures influencing, 629t
fat injections, 634
LDMF and, 690
mastoplexy, 635
reduction and augmentation, 634–635
timing of
postmastectomy RT, 635
size and shape, 635
Synthetic meshes, 649
Systemic sclerosis, 1220

T
T cell lymphomas. See also Breast implant-associated anaplastic large cell
lymphoma (BIA-ALCL)
T helper cells (Th1 cells), 1191
Tailor tacking, 513f
Tamoxifen
adjuvant therapy using, 112, 129
adverse reactions to, 36–37
breast cancer risk reduction and, 20, 35–36, 48
breast cancer trials of, 126–127
in elderly women, 93–95
function of, 126–127
in inflammatory breast cancer, 112
in lymph-node negative disease
PMRT and, 159–160
recurrence scores, 159–160
side effects of, 127
surgery versus, 64–65
Taping
bandaging and, 380, 382
breast reduction surgery, 380–382
for lymphedema, 281–282, 282f
Tattooing, 826
lymph nodes, 251
reconstructed NAC, 698f
Taxane-containing chemotherapy, 124t
Taxanes
administration of, 119
combination therapy using, 123
99mTc radiotracers, 255
TC therapy, administration of, 119
T-cell lymphoma
breast cancer and, 961
breast implants and, 1190
T-cells, lifespan of, 1191
TDAP flap. See Thoracodorsal artery perforator (TDAP) flap
T-DM1. See Ado-trastuzumab emtansine (T-DM1)
Team roles
confidence of, 755
morale and, 755
process evaluation and, 757
standardization of, 752
Tegaderm, 452, 997f, 1106, 1130
Telangiectasia, radiation therapy and, 163, 893
Telfa, 1106, 1130
Temperature discrimination, 832
Tensor fascia lata (TFL) flap, 874
TEPID assessment system, 927
TEs. See Tissue expanders (TEs)
Test results, communication of, 1239
Testosterone
Leydig cell production by, 180
transmasculine individuals, 1157–1158
Thermal (popcorn) capsulorrhaphy technique
malpositioned IMF and, 1095–1096, 1096f, 1097f
thermal damage and, 1126
Thermoablation, breast cancer therapy, 65–68
Thigh, profunda artery flap harvest, 794f
Thoracic hypoplasia, 921
Thoracoacromial vessels, 243
Thoracodorsal artery perforator (TDAP) flap, 311, 324
anatomy of, 325, 326f
description of, 337–338
history, 843
operative technique for, 342–345
muscle patch in, 343f
patient positioning, 342
in reconstructed breast, 850, 854, 854f
reconstructive plan, 325
Thoracodorsal nerve
identification of, 243
location of, 334f
preservation of function, 343f
3-D imaging, breast, 1011
3-D printing, scaffolds, 484, 487
Threshold phenomenon, bacterial load and, 1206
Thrombocytosis, thrombosis and, 839
Thromboembolism
microsurgical free tissue transfer, 776
Thyroid disorders, symptoms of, 1220
“Time gain compensation” (TGC), 1252
TISSEEL Fibrin Sealant, 846
Tissue augmentation, fundamental concepts of, 913
Tissue expanders (TEs), 692f
ADM and fit of, 582–583
advantages, 88
autologous fat grafting with
total breast reconstruction and, 908–917
breast reconstruction and, 457–458
case studies, 739f–740f
coverage of, 641
in delayed-immediate breast reconstruction, 525–528
evolution of, 538
exchange
reoperation for, 709
exposure, 619f
extrusion of tabs, 617f
history of, 530
implants versus
LDMF reconstruction and, 689–690, 692f, 693f
irradiation of, 863
perspectives on, 706–711
reconstructive failure and, 708
with meshed ADM, 585f–587f
operative risk and, 608
placement, 707
subpectoral pockets and, 534f
placement of, 641, 797f–798f
position of
PMRT and, 862–863
reconstruction based o, 172
replacement of
NAC malposition and, 651
saline-filled, 443
selection of, 532
staged reconstruction and, 640
subcutaneous
placement, 730f
in total breast reconstruction
operative technique, 909–912
in radiated breast, 525
two-stage reconstruction using, 530–539
Tissue oximetry, 172
Tissue perfusion devices, 511
TNBC. See Triple-negative breast cancer (TNBC)
Tobacco metabolites, 1178
Top of breast to nipple (TB-N) measurement, 1103–1105
Total body fat, breast cancer risk and, 7
Total breast reconstruction, AFT and TE, 909–912
Total volume (TV) measurement, 1103–1105
TP53 mutations
breast cancer risk and, 19–20, 45t
LFS and, 50
risk reduction mastectomy and, 37t
TP53 transcription factor, 45
Traction injuries, augmented patients, 936
TRAM flap. See Transverse rectus abdominis musculocutaneus (TRAM)
flap
Tranexamic acid, 569
Transaxillary breast augmentation, 982–992
Transfemales
case studies, 205–206
feminizing augmentation, 207
hormone therapy in, 204–205
indications for mastectomy in, 204–205
postoperative follow-up in, 205–206
Transfeminine mammogenesis, 1167
hormone treatments, 1167
Transforming growth factor (TGF), 859
Transforming growth factor-B1, 667
Transgender patients, 1168
aesthetic breast surgery in, 1167–1171
breast cancer management in, 204–207
breast cancer screening in, 204–207
chest feminization in
outcomes, 1170
chest width issues, 1168
health care needs of, 1157–1158
prevalence, 1167
“top surgery” in, 204
U.S. population of, 1157
vocabulary choices, 1168
Transma, 204
Transmales
chest wall masculinization, 1163f
indications for mastectomy in, 204
postoperative follow-up in, 206
preoperative planning, 205
Transmasculine individuals
cancer screening in, 1159–1160
chest masculinization for, 1157–1166
Transverse myocutaneous gracilis (TMG) flap
harvest, 803f
history, 801, 843
operative technique, 874
Transverse profunda artery perforator (T-PAP) flap, 794f
Transverse rectus abdominis musculocutaneus (TRAM) flap
bipedicled, 766, 767f
breast reconstruction using, 356
breast salvage and, 670
complications, 767–768
contraindications, 763–767, 868–869
flap shaping, 766–767
free
donor sites, 1181
history of, 762
impact of smoking on, 1181
free versus pedicled, 762–769
in high BMI patients, 1186
history of use in reconstruction, 683, 762–763
indications, 763–767, 868–869
muscle-sparing
case study, 743f, 749f–750f
hernia rates after, 844
necrosis, 685
noninnervated, 832
operative techniques, 765–768
patient selection, 868–869
pedicled
history of, 762
whole-muscle technique, 765f
radiation therapy and, 763
in reconstructed breast, 850
shaping of, 726
transverse orientation
history of, 762
vascularization of, 762
blood supply zones, 762–763
Transverse upper gracilis (TUG) flap, 801–810
breast reconstruction using
case studies, 807f–809f
outcomes, 809
case study, 744f–745f
contraindications, 802
design optimization, 806f
donor site, 804f
history, 801
indications, 801–802
intraoperative care, 806
modifications, 804t
neurotization of, 834
operative technique, 805–806
partial dissection of, 802f
postoperative care, 806–809
preoperative planning, 802–805
in reconstructed breast, 850
shaping, 805f
skin marking, 805f
skin paddle design, 806f
vascularity, 801f
Transversus abdominis plan block, 720
Trastuzumab
adjuvant use of, 125–126
chemotherapy containing, 125t
description of, 125
docetaxel with pertuzumag and
in inflammatory breast cancer, 111
HER-2-targeted therapy using, 119–120, 119t
in inflammatory breast cancer, 111
optimum duration of, 125–126
pertuzumab and, 120, 126
pertuzumag with
in inflammatory breast cancer, 111
subcutaneous formulation of
efficacy of, 126
Trauma, lymphedema and, 273
Trichilemmomas, Cowden syndrome and, 45
Triglyceride (soybean-derived) filled implants, 926
Trimodal therapy in inflammatory breast cancer, 111
Triple-negative breast cancer (TNBC)
BARD1 and risk of, 46
BRCA-related, 49
neoadjuvant chemotherapy in, 118–119
residual disease in, 121–122
Triptoreline, ovarian ablation with, 128
TRUE Texture, structure of, 925f
Trust, informed consent and, 950–951
Tuberous breast deformities, 943f, 1172f
anatomic basis of, 943–944
anatomical implants in, 1009f, 1010f
augmentation in patients with, 943–949
base, 944f
characteristics of, 1172
classification of, 1172
correction of, 1172–1177
contraindications, 1173
history of, 1172
indications, 1173
operative technique, 1173–1174
outcomes, 1176–1177
postoperative care, 1174
preoperative planning for, 1173
risks of, 1176
first description of, 1172
postoperative appearance, 1176f
preoperative appearance, 946f, 947f, 1175f
presentation of, 943
surgical outcomes, 946f, 947f
type 1, 944
Tubular adenomas, 195
TUG flap. See Transverse upper gracilis (TUG) flap
Tumeric, impact on biofilms, 1215
Tumescent technique
complication rates and, 604
mastectomy, operative risks and, 608
mastopexy-augmentation, 1085–1086
Tumor, Node, Metastasis (TNM) staging system, 115
Tumor ablation therapy, 64–69
Tumors
biology of, 183
microenvironments of, 888
recurrence risk and, 183
size of
augmented breasts, 143t
leval II oncoplastic surgery and, 80–81
patient outcomes and, 115
PMRT indications and, 706
ultrasound imaging of, 142
Twitter, 1242
“2Q principle,” 1013–1018, 1019, 1019f
Tylenol, postoperative, 720
Tyrer-Cruzick model of breast cancer risk, 42t, 43

U
Ultrarapid metabolizers (UM), 713
Ultrasonic liposuction (UAL), 418–420, 421f
Ultrasonography. See also High-resolution ultrasound (HRUS)
acoustic impedance, 1250
acoustic shadowing artifact, 1253f
basics of, 1249–1253
BIA-ALCL evaluation by, 1193
biofilm prophylaxis and, 1215
B-mode, 1250
breast, 168f
high-frequency devices
biofilm prophylaxis and, 1215
imaging controls, 1252
implant detection on, 142
implant leakage on, 142
linear array transducers, 1251f
of low-weight breast implants, 1035, 1036f
postmastectomy, 170f
reflection, 1250
reverberation artifacts, 1252f
specular reflection, 1250–1251
wave frequencies, 1250
Ultrasound systems
components of, 1249–1250, 1249f
displays, 1249
transducers, 1250, 1251, 1251f
Ultrasound transducers
electronic focusing, 1250, 1251, 1251f
Ultrasound-guided mammatome excision, 422
Umbilicoplasty
donor site closure, 786
horizontal, 871
Umbilicus
appearance of, 868
closure of, 871
Underresection after breast reduction, 385
Unfractionated heparin (UFH), 1266
United States
breast cancer incidence in, 3, 4f
breast cancer mortality rates in, 4f
breast cancer survival and, 3
United States Preventive Services Taskforce (USPSTF), 33t, 1168
cancer screening guidelines, 15, 16t
policy makers, 19
Upper pole pinch test, 1100f

V
VAC (vacuum-assisted wound closure), stress of, 1227
Vacuum-assisted biopsies in augmented patients, 138
Vacuum-assisted wound closure (VAC), stress of, 1227
Vaginal discharge, tamoxifen and, 127
Van der Waals forces, biofilm adhesion and, 1212
Van Nuys Prognostic Index, 94
Variants of unknown significance (VUS), 43
Vascular endothelial growth factor (VEGF), 888
Vascular endothelial growth factor C (VEGF-C) secretion, 285–286
Vascular injuries, cryoablation and, 66
Vascularity, acellular dermal matrices and, 667
Vascularized lymph node transplants (VLNT)
donor site options for, 286–288
harvest of, 232–233
for lymphedema, 229–236, 285, 292
donor sites, 231
operative technique, 232–234
preoperative planning, 232
mechanism of, 285–286
outcomes of, 235
recipient site options, 286f
risks of, 235
Vascularized omentum lymphatic transplant (VOLT)
anastomosis, 234f
harvest of, 232, 233f
postoperative results, 234f, 235f
Vasculitis, post skin-sparing mastectomy, 184f
VASER (vibration amplification of sound energy at resonance), 418
Vasoconstriction, smoking and, 1178
Vasodilation, wound healing and, 1263
Vasomotor instability, tamoxifen and, 127
Vasopressors, 754
Vectra 3D imaging, 1125
Vegetables, non-starchy, 6
Venlafaxine, hot flashes minimized by, 37
Venous thromboembolism (VTE)
compression devices and, 352
prophylaxis, 1265–1266
risk of, 352
surgical risk reduction and, 1264
Venous thrombosis, flap failure and, 836
Vertical breast reduction
history of, 367
principles of, 367–369
rereduction and, 367–392
superomedial pedicle
contraindications, 371
indications, 371
postoperative puckers, 375
preoperative assessment, 371–373
preoperative planning, 373–375
Vertical mastopexy pattern, 1059
marking for, 1066f
operative technique, 1065–1066
Vibration amplification of sound energy at resonance (VASER) liposuction,
418, 420
Vicini, Frank, 99
Vicryl deep fixating sutures, 660, 871
Vicryl Plus sutures, 584
Videos, social media and, 1241–1243
Videotaping, process efficiency and, 757
Viscoelastic responses, breast, 1027–1028
Visual acuity, tamoxifen and, 127
Visual aids, patient education and, 955–956
Vitamin A, wound healing and, 1265
Vitamin C, wound healing and, 1265
Vitamin D deficiency, symptoms of, 1220
Vitamin E, prophylactic use of, 668
VLNT. See Vascularized lymph node transplants (VLNT)
VOLT. See Vascularized omentum lymphatic transplant (VOLT)
Volume difference (VD) measurement, 1103–1105
Volume displacement techniques, 81, 85
Volume replacement approaches
breast-conserving surgery and, 337
oncoplastic surgery, 85
partial mastectomy and, 324
preoperative planning, 325–326
Vomiting, chemotherapy-related, 124–125
VTE. See Venous thromboembolism (VTE)
V-Y advancement flap, 409, 409f

W
Wagon-wheel permanent sutures, 1174
Waterfall deformity, 1066
anterior view of, 1092f
etiology of, 1090–1092, 1091t, 1099f
implant decisions, 1101
implant exchange, 1100f
lateral view of, 1092f
management of, 1098–1101
outcomes, 1099f
relifting breast, 1098–1099
Waterfall effect, submuscular positioning and, 1080
Weber open excision technique, 424f–425f
WebMD, 1244
Websites, health-related information on, 952
Weight, movement amplitude and, 1026–1027
Weight loss, involutional hypomastia and, 921
Weitlaner self-retaining instruments, 753
Well-informed patients. See also Patient education; Physician-patient
relationships
preferences of, 952
White blood cells, inflammation and, 1263–1264
Wire localization, lymph node, 251
Wire-localized lumpectomy, bilateral, 71, 83f
Wire-localized mastectomy, 314f
Wise keyhole patterns, customization of, 1077–1078
Wise pattern incisions, 169, 368f
complications of, 458
liposuction + open excision, 430f
marking, 310, 592f, 824f
nipple-sparing mastectomy, 217, 538f
operative risk factors, 607
in ptotic breasts, 428–429
skin envelopes and, 729
skin redundancy and, 552
technique, 395, 395f
Wise-pattern reduction mammaplasty
case studies, 362f–365f
excessive breast volume and, 358–359
intraoperative care, 359–362
markings, 359
technique, 359–362, 360f–362f
postoperative car, 362
Wise-pattern reduction/mastopexy, 81, 82f
Women’s Health initiative cohort, 7–8
World Professional Association for Transgender Health (WPATH),
1157–1158, 1167
Wound dehiscence
acellular dermal matrices and, 566–567
exposed implants and, 613
flap harvest sites, 776
incidence of
waistline incisions, 847
risk factors, 847
Wound healing
breakdown, 1180f
breast reduction surgery, 385
cytokines and, 859
delayed, 1180, 1215
high-BMI patients, 516
inflammatory phase of, 1178
postoperative, 1263–1264
prophylactic antibiotics and, 1215
radiation therapy and, 606, 859
recovery and, 1269
smoking and, 1178, 1179f
smoking cessation and, 1182–1183, 1182f
stabilization and, 1264
Wound infections. See Infections
Wound stabilization, wound healing and, 1264
Wounds, irrigation of, 980
WPATH (World Professional Association for Transgender Health),
1157–1158
Wrinkling
ADM and, 578
patient education about, 956

X
Xeroform gauze, 1174

Y
Yelp, 1244
YouTube, 1242–1243

Z
Zafirlukast (Accolate), 667, 939, 1128
Zinc, wound healing and, 1265
Zoledronic acid, 129

You might also like