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Atlas of
Abdominal Wall
Reconstruction
Second Edition
Michael J. Rosen, MD, FACS

Professor of Surgery
Lerner College of Medicine;
Director, Cleveland Clinic Comprehensive Hernia Center
Cleveland Clinic Foundation
Cleveland Ohio
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
ATLAS OF ABDOMINAL WALL RECONSTRUCTION, SECOND EDITION ISBN: 978-0-323-37459-0

Copyright © 2017 by Elsevier, Inc. All rights reserved.
Jeffrey Janis retains copyright for the original figures in Chapter 11.
No part of this publication may be reproduced or transmitted in any form or by any means, electronic or me-
chanical, including photocopying, recording, or any information storage and retrieval system, without permis-
sion in writing from the publisher. Details on how to seek permission, further information about the Publisher’s
permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the
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This book and the individual contributions contained in it are protected under copyright by the Publisher (other
than as may be noted herein).
Notices
Knowledge and best practice in this field are constantly changing. As new research and experience broaden
our understanding, changes in research methods, professional practices, or medical treatment may become
necessary.
Practitioners and researchers must always rely on their own experience and knowledge in evaluating and
using any information, methods, compounds, or experiments described herein. In using such information or
methods they should be mindful of their own safety and the safety of others, including parties for whom they
have a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to check the most
current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be
administered, to verify the recommended dose or formula, the method and duration of administration, and
contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of
their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient,
and to take all appropriate safety precautions.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume
any liability for any injury and/or damage to persons or property as a matter of products liability, negligence
or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the
material herein.
Previous edition copyrighted 2011.
International Standard Book Number: 978-0-323-37459-0
Content Strategist: Michael Houston

Content Development Specialist: Ann Ruzycka Anderson
Publishing Services Manager: Catherine Jackson
Senior Project Manager: Rachel E. McMullen
Design Direction: Ryan Cook
Printed in China
Last digit is the print number: 9 8 7 6 5 4 3 2 1

I would like to dedicate this atlas to all of my patients.
It is through their surgical treatment that we constantly improve and find the
best surgical approaches for their disorders.
Contributors
Conrad Ballecer, MD, FACS Jorge Daes, MD, FACS
Co-director of the Center for Minimally Invasive and Director
Robotic Surgery Minimally Invasive Surgery
Peoria, Arizona Clinica Bautista
Barranquilla, Atlantico, Columbia
Laurel J. Blair, MD
Minimally Invasive Surgery Fellow George DeNoto III, MD, FACS
Department of Gastrointestinal and Minimally Chief, Division of General Surgery
Invasive Surgery St. Francis Hospital
Carolinas Medical Center Roslyn, New York;
Charlotte, North Carolina Clinical Associate Professor of Surgery
Hofstra Northwell School of Medicine
Alfredo M. Carbonell II, DO Hempstead, New York
Chief, Division of Minimal Access & Bariatric Surgery
Department of Surgery Gregory A. Dumanian, MD
Greenville Health System; Stuteville Professor of Surgery
Associate Professor of Surgery Division of Plastic Surgery
University of South Carolina School of Medicine— Northwestern Feinberg School of Medicine
Greenville Chicago, Illinois
Greenville, South Carolina
Karen Kim Evans, MD
Harvey Chim, MD Associate Professor of Plastic Surgery
Assistant Professor Center for Wound Healing
Surgery/ Plastic Surgery Georgetown University Medical Center
University of Miami Miller School of Medicine Washington, D.C.
Miami, Florida
Brian Gastman, MD
William S. Cobb IV, MD Associate Professor/Staff
Associate Professor of Clinical Surgery, University of Department of Plastic Surgery
South Carolina—Greenville Cleveland Clinic
Vice Chair of Clinical Affairs Cleveland, Ohio
Co-Director, Hernia Center
Department of Surgery A. Daniel Guerron, MD
Greenville Health System General Surgery Resident
Greenville, South Carolina Digestive Disease Institute/General Surgery
Cleveland Clinic
Michelle Coriddi, MD Cleveland, Ohio
Resident
Department of Plastic Surgery Raffi Gurunluoglu, MD, PhD, FACS
Ohio State University Professor of Surgery
Columbus, Ohio Cleveland Clinic Lerner College of Medicine
Case Western Reserve University
Cory N. Criss, MD Department of Plastic and Reconstructive Surgery
Resident, Department of Surgery Cleveland Clinic
University Hospitals Case Medical Center Cleveland, Ohio
Cleveland, Ohio
v
vi Contributors
William W. Hope, MD Melissa Phillips LaPinska, MD, FACS

Assistant Professor Assistant Professor
Department of Surgery Department of Surgery
New Hanover Regional Medical Center University of Tennessee Health Science Center
University of North Carolina, Chapel Hill Knoxville, Tennessee
Wilmington, North Carolina
Samir Mardini, MD
Ron Israeli, MD, FACS Professor and Program Director
Clinical Assistant Professor of Surgery Division of Plastic Surgery
Division of Plastic Surgery Department of Surgery
Hofstra Northwell School of Medicine Mayo Clinic
Hempstead, New York Rochester, Minnesota
Jeffrey E. Janis, MD, FACS Jay Mittal, MD

Professor of Plastic Surgery Chief Resident
Neurosurgery, Neurology, and Surgery; Department of Surgery
Executive Vice Chairman Cleveland Clinic Foundation
Department of Plastic Surgery; Cleveland, Ohio
Chief of Plastic Surgery
University Hospitals Matthew L. Moorman, MD, FACS
Ohio State University Director, Division of Acute Care Surgery
Wexner Medical Center General Surgery
Columbus, Ohio Cleveland Clinic;
Assistant Professor of Surgery
Donald H. Jenkins, MD Case Western Reserve University, Cleveland Clinic
Consultant; Lerner College of Medicine
Associate Professor of Surgery; Cleveland, Ohio
College of Medicine Medical Director
Division of Trauma, Critical Care and General Surgery Maurice Y. Nahabedian, MD, FACS
Trauma Center Mayo Clinic Professor
Rochester, Minnesota Department of Plastic Surgery
Georgetown University
Kent W. Kercher, MD, FACS Washington, D.C.;
Professor Associate Professor
Division of Gastrointestinal and Minimally Invasive Department of Plastic Surgery
Surgery Johns Hopkins University
Department of Surgery Baltimore, Maryland
Carolinas Medical Center
Charlotte, North Carolina Sean B. Orenstein, MD
Assistant Professor
David M. Krpata, MD Department of Surgery
Fellow Oregon Health & Science University
General Surgery Portland, Oregon
Cleveland Clinic
Cleveland, Ohio Cemile Nurdan Ozturk, MD
Assistant Professor
Gregory A. Lamaris, MD, PhD Department of Head, Neck and Plastic Surgery
Plastic Surgery Fellow Roswell Park Cancer Institute
Department of Plastic and Reconstructive Surgery Buffalo, New York
The Cleveland Clinic Foundation
Cleveland, Ohio
Contributors vii
Eduardo Parra-Davila, MD, FACS, FASCRS Carley E. Schroering

Director of Minimally Invasive and Colorectal Surgery Medical Student
Director of Hernia and Abdominal Wall University of Kentucky
Reconstruction Lexington, Kentucky
Celebration Health Florida Hospital
Celebration, Florida Nathaniel F. Stoikes, MD, FACS
Assistant Professor of Surgery
Eric M. Pauli, MD University of Tennessee Health Science Center
Assistant Professor of Surgery Memphis, Tennessee
Director of Endoscopic Surgery
Department of General Surgery Jeffrey Ustin, MD, MS, FACS
Penn State Milton S. Hershey Medical Center Acute Care Surgeon
Hershey, Pennsylvania General Surgery
Cleveland Clinic
Clayton C. Petro, MD Cleveland, Ohio
General Surgery Resident
University Hospitals Case Medical Center Guy R. Voeller, MD, FACS
Cleveland, Ohio Professor of Surgery
University of Tennessee Health Science Center
Ajita S. Prabhu, MD Memphis, Tennessee
Assistant Professor
Department of Surgery David L. Webb, MD, FACS
University Hospitals Case Medical Center Assistant Professor
Cleveland, Ohio Department of Surgery
University of Tennessee Health Science Center
Michael J. Rosen, MD, FACS Memphis, Tennessee
Professor of Surgery
Lerner College of Medicine; Joshua S. Winder, MD
Director, Cleveland Clinic Comprehensive Hernia Research Fellow
Center Department of General Surgery
Cleveland Clinic Foundation Penn State Milton S. Hershey Medical Center
Cleveland Ohio Hershey, Pennsylvania
Steven Rosenblatt, MD, FACS Benjamin Zendejas-Mummert, MD

Staff Surgeon Resident in Surgery
General Surgery Mayo Clinic
Cleveland Clinic Rochester, Minnesota
Cleveland, Ohio
Martin D. Zielinski, MD, FACS
J. Scott Roth, MD, FACS Associate Professor
Professor of Surgery and Chief, Gastrointestinal Department of Surgery
Surgery Mayo Clinic
Department of Surgery Rochester, Minnesota
University of Kentucky
Lexington, Kentucky
Christopher J. Salgado, MD
Professor
Division of Plastic Surgery
Department of Surgery
University of Miami
Miami, Florida
Preface
The field of abdominal wall reconstruction and hernia repair has seen an explosion of innova-
tive approaches, reconstructive options, and multi-disciplinary collaboration in the past decade.
Since our first edition of this atlas, the reconstructive surgeon can now push the boundaries of
hernia surgery utilizing the robot, laparoscope, or open techniques that are all designed to mini-
mize wound and mesh complications and maximize patient outcomes. With growing interest in
the complexities of many of the patients that present with hernias, a renewed interest in preop-
erative optimization has emerged. In this atlas, we have summarized some of the key steps that
every reconstructive surgeon can adhere to in order to adequately prepare a patient to undergo
complex abdominal wall reconstruction and expect the best possible results. This edition will
also highlight some of the rare types of hernias that can challenge even the most experienced
reconstructive surgeon including perineal defects, major soft tissue loss, loss of domain, and
hernias after TRAM procedures. Significant effort has been made to help the reader understand
the intricate anatomy of the abdominal wall in order to make each of these advanced recon-
structive procedures reproducible in their own hands. I am also excited to provide the reader
with a detailed description of approaches and the rationale for each technique for some of the
more routine types of hernia procedures including inguinal hernias, umbilical hernias, and
repair of rectus diastasis. Our field is seeing a rapid growth of robotic ventral hernia repairs as
well. This atlas will provide the surgeon with a detailed description of how to introduce the
robotic platform into their practice and perform minimally invasive complex abdominal wall
reconstructions.
Today it is clear that the reconstructive surgeon must individualize their approach to abdomi-
nal wall reconstruction, and likely no single technique or prosthetic will accomplish the goals for
all repairs. As this field has continued to expand, it now represents a collaborative effort amongst
general surgeons, plastic surgeons, trauma surgeons, and herniologists. This atlas represents the
compilation of these efforts and like reconstructive surgery would not be possible without each of
their respective contributions. Each of these procedures has been described in detail with particu-
lar attention to avoiding common surgical pitfalls and strategies to deal with technical challenges
once they are encountered. In addition, each chapter is accompanied by a representative video of
the reconstructive approach to guide the surgeon in the technical nuances of the procedure. In this
textbook, the robotic, laparoscopic, open, and hybrid approaches are described. While there are
often many ways to repair an abdominal wall defect, this atlas describes a multitude of safe and
effective strategies to deal with these challenging problems across the entire spectrum of ventral
hernia repair as described by experts in the field. I believe that the second edition of this atlas will
provide the practicing surgeon with a useful guide to optimize outcomes for their patients.
ix
CHAPTER
1
Abdominal Wall Anatomy
and Vascular Supply
Harvey Chim, MD, Karen Kim Evans, MD, Christopher J. Salgado, MD, and
Samir Mardini, MD
1. Clinical Anatomy
1. Overview
s The anterior abdominal wall (Figs. 1.1–1.3) is a hexagonal area defined superiorly by the
costal margin and xiphoid process; laterally by the midaxillary line; and inferiorly by the
symphysis pubis, pubic tubercle, inguinal ligament, anterior superior iliac spine (ASIS),
and iliac crest.
s Layers of the anterior abdominal wall include skin, subcutaneous tissue, superficial fascia,
deep fascia, muscle, extraperitoneal fascia, and peritoneum.
2. Superficial Fascial Layers (see Figs. 1.1 and 1.2)
s The superficial fascia of the abdominal wall consists of a single layer above the umbilicus,
comprising the fused Camper and Scarpa fasciae.
s Below the umbilicus, the superficial fascia consists of a fatty outer layer (Camper fascia)
and a membranous inner layer (Scarpa fascia).
s Camper fascia is continuous inferiorly with the superficial thigh fascia and extends inferi-
orly to the scrotum in males and labia majora in females.
s Scarpa fascia fuses inferiorly with the fascia lata of the thigh and continues posteriorly to
the perineum, where it is called Colles fascia.
2
Chapter 1 • Abdominal Wall Anatomy and Vascular Supply 3
Xiphoid process Pectoralis major

muscle
Serratus anterior
muscles
Costal margin 5
6 Rectus
Parietal abdominis
peritoneum 7 muscles
Extraperitoneal
8 Linea alba
(subserosa) fascia
9
Transversalis fascia Linea semilunaris
Transversus 10
abdominis muscle Tendinous inscriptions
Posterior rectus sheath Midaxillary line
(above arcuate line)
• Transversalis fascia External oblique
• Internal oblique fascia muscle and
aponeurosis
Internal oblique muscle
External oblique muscle Iliac crest
Anterior rectus sheath Anterior superior iliac

(above arcuate line) spine (ASIS)
• Internal oblique fascia
• External oblique fascia Umbilicus
Superficial fascia Arcuate line
• Camper fascia
• Scarpa fascia Inguinal ligament
Fascia lata Pyramidalis muscle
Superficial epigastric and Pubic tubercle
circumflex iliac arteries
Intercrural fibers Symphysis pubis
Femoral vessels
Fig. 1.1
Pectoralis major
muscle
External oblique
muscle
Serratus anterior
muscles
5
Xiphoid process
Midaxillary line 6
7 Costal margin
8 Linea alba
9 Rectus abdominis
Latissimus dorsi muscle muscles
10
11 Umbilicus
12
Tendinous inscriptions
Iliac crest
Linea semilunaris
Arcuate line
Pubic tubercle
Anterior superior iliac

spine (ASIS)
Inguinal ligament
External oblique aponeurosis
Fig. 1.2
4 Section I • Anatomy
Pearls and Pitfalls
s Scarpa fascia is usually a visible and durable structure and is closed separately during vari-
ous surgeries on the abdominal wall to achieve an optimal scar result.
3. Deep Fascial Layers (see Figs. 1.1 and 1.2)
s The rectus sheath is found in the midline.

s Laterally, layers of the abdominal wall deep to superficial fascia include external oblique,
internal oblique, transversus abdominis, and parietal peritoneum.
s The arcuate line (see Fig. 1.3) is located midway between the umbilicus and symphysis
pubis and is a transition point where the posterior rectus sheath transitions from being the
fusion of part of internal oblique fascia and transversalis fascia superiorly to only transver-
salis fascia inferiorly.
s Above the arcuate line, the anterior rectus sheath consists of external oblique fascia and
part of internal oblique fascia. The posterior rectus sheath consists of internal oblique fas-
cia and transversalis fascia. The anterior and posterior layers of the rectus fascia invest the
rectus abdominis muscles.
s Below the arcuate line, the external oblique and internal oblique fasciae merge to form
the anterior rectus sheath. The posterior rectus sheath consists of transversus abdominis
fascia, making this only a thin layer with minimal strength.
Xiphoid Linea alba Linea alba

Costal margin
process (midline) (midline)
Variations of anterior
and posterior
rectus sheath at
different levels
(right side)
Level
EO RA above
costal
margin
Right
Costal cartilage
rectus
5, 6, 7
muscle Superior epigastric
vessels
External
oblique
muscle
Level
EO RA above
arcuate
IO
line
Arcuate TA
line TF
Lateral and medial branch of
(behind type ll deep epigastric vessels
rectus (DIEA and DIEV)
muscle)
EO Level
RA below
IO arcuate
TA line
RA = Rectus abdominis TF
EO = External oblique Inferior epigastric
EO Level
IO = Internal oblique vessels above
IO
TA = Transversus abdominis TA pubic
TF symphysis
TF = Transversalis fascia Pyramidalis
muscle
Pubic RA
symphysis
Common branching patterns:

- Type l DIEA continues as a single vessel (29%).
- Type ll DIEA divides into two vessels (57%).
- Type lll DIEA is a trifurcation (14%).
Fig. 1.3
s The linea alba results from fusion of the anterior and posterior rectus sheaths and lies in
the midline, extending cranially from the xiphoid process to the pubic symphysis caudally.
Fig. 1.4 shows the anterior wall fascia after dissection of the abdominal wall skin and sub-
cutaneous tissue, demonstrating the linea alba and linea semilunaris.
Pearls and Pitfalls
s Incision, release, and dissection of the anterior external oblique fascia can be done for re-
pair of ventral hernias; this is called the components separation technique (Fig. 1.5). The
incision in the external oblique fascia is made 1–2 cm lateral to the linea semilunaris, and
the fascia is released to attain primary closure. Incisions also can be made in the posterior
rectus sheath to gain additional length.
4. Abdominal Wall Musculature (see Figs. 1.1–1.3)
s The paired rectus abdominis muscles are the principal flexors of the anterior abdominal
wall. They function to stabilize the pelvis while walking. They also protect the abdominal
organs and help in forced expiration.
s The rectus abdominis muscles originate from the pubic symphysis and pubic crest and in-
sert on the anterior surfaces of the fifth, sixth, and seventh costal cartilages and the xiphoid
processes. Laterally, the rectus sheath merges with the aponeurosis of the external oblique
muscles to form the linea semilunaris (see Fig. 1.4).
s Three to four tendinous inscriptions, which are adherent to the anterior rectus sheath,
interrupt the rectus abdominis along its length (Fig. 1.6).
s The external oblique muscle is the most superficial and thickest of the three lateral abdom-
inal wall muscles. It originates from the lower eight ribs and courses in an inferomedial
direction. Inferiorly, it folds back on itself and forms the inguinal ligament, which extends
between the ASIS and pubic tubercle. It is attached medially to the pubic crest.
s The internal oblique muscle is deep to the external oblique muscle, and its aponeurosis
splits medially above the arcuate line to form part of the anterior rectus sheath and part of
the posterior rectus sheath. Below the arcuate line, the inferior oblique aponeurosis does
not split and fuses with the external oblique fascia to form the anterior rectus sheath. The
internal oblique muscle runs in a superomedial direction, perpendicular to the external
oblique muscle. It originates from the thoracolumbar fascia, anterior two-thirds of the iliac
crest, and lateral half of the inguinal ligament. It inserts on the inferior and posterior bor-
ders of the 10th through 12th ribs superiorly. Inferiorly, the internal oblique inserts on the
pectineal line with fibers from the transversus abdominis, forming the conjoint tendon,
which inserts on the pubic crest.
s The transversus abdominis muscle is the deepest of the three lateral abdominal wall mus-
cles and courses in a horizontal direction. It originates from the anterior three-fourths
of the iliac crest; lateral third of the inguinal ligament; and inner surface of the lower six
costal cartilages, interdigitating with fibers of the diaphragm. The muscle ends medially in
a broad flat aponeurosis, merging above the arcuate line with the posterior lamella of the
internal oblique aponeurosis and the linea alba. Below the arcuate line, it inserts into the
pubic crest and pectineal line, forming the conjoint tendon with the internal oblique.
External
oblique fascia
release
Linea
semilunaris
Linea alba
Fig. 1.4 Fig. 1.5
Tendinous
inscriptions
Fig. 1.6
s
The pyramidalis is a small triangular muscle found anterior to the inferior aspect of the
rectus abdominis; it is absent in about 20% of the population. It originates from the body
of the pubis and inserts into the linea alba inferior to the umbilicus.
s
The semilunar lines are formed by fusion of the external oblique, internal oblique, and
transversus abdominis aponeuroses at the lateral border of the rectus abdominis.
Pearls and Pitfalls
s Of all the muscles in the abdominal wall, the rectus abdominis muscle is the most versatile
and useful for flap procedures. The rectus muscle can be harvested as a free flap for mi-
crosurgical transfer of tissue to various defects. It also can be harvested as a pedicled flap,
based on the superior or inferior epigastric arteries, and rotated to fill groin, chest wall,
vaginal, and perianal wounds and mastectomy defects.
s Functional loss results if the rectus abdominis muscle is harvested. Using isometric dyna-
mometry, studies have shown that there is at least a 20% functional loss in trunk flexion.
Bilateral harvest of the rectus abdominis muscles can be debilitating for patients who are
very active because there is a 40% functional loss in trunk flexion, which may infringe on
activities of daily living.
5. Neurovascular Supply of the Abdominal Wall
s
The blood supply of the abdominal wall can be divided into three zones (Huger, 1979).
s Zone I comprises the upper and midcentral abdominal walls and is supplied by the verti-
cally oriented deep superior (Fig. 1.7A) and deep inferior epigastric arteries (Fig. 1.7B).
s Zone II comprises the lower abdominal wall and is supplied by the epigastric arcade, su-
perficial inferior epigastric, superficial external pudendal, and superficial circumflex iliac
arteries. Perforators from the deep circumflex iliac arteries also supply a region of skin
posterior and cephalad to the ASIS along the axis of the iliac crest.
Left subclavian artery
Internal thoracic
(mammary) artery
6 Musculophrenic artery
Deep superior
epigastric artery
Diaphragm
Zone I
Posterior rectus sheath
Choke vessels
Zone lll Zone lll
Transversus abdominis
Umbilicus
Arcuate line
Zone ll Inguinal ligament
Deep inferior
epigastric artery
External iliac artery
Femoral artery
Fig. 1.7
Zone I
Zone lll Zone lll
Perforators from deep

circumflex iliac artery
Zone ll
Superficial circumflex
iliac artery
Superficial inferior
epigastric artery
Femoral artery
and vein
Superficial external
B pudendal artery
Fig. 1.7—cont’d
s ZoneIII comprises the lateral abdominal wall (flank region) and is supplied by the mus-
culophrenic, lower intercostals (Fig. 1.8A), and lumbar arteries (Fig. 1.8B).
Vascular Supply
s
Knowledge of these zones of blood supply to the anterior abdominal wall is important
when planning incisions for surgical procedures. A previous subcostal incision can com-
promise the circulation to Huger’s zone III of the abdominal wall. In transverse rectus ab-
dominis myocutaneous flap harvest, the presence of a subcostal scar was found to increase
donor site complications, with a significantly higher incidence of abdominal wall skin
necrosis (25%) compared with patients without abdominal wall scars (5%).
s The superior epigastric artery (SEA) and deep inferior epigastric artery (DIEA) lie on the
posterior aspect of the rectus abdominis muscles and supply the muscle and overlying
skin and subcutaneous tissue through musculocutaneous perforators (Fig. 1.9).
s A study by Saber et al. (2004) provided guidelines for location of the epigastric vessels
based on computed tomography scan data in 100 patients. At the xiphoid process, the
SEA was 4.41 ± 0.13 cm from the midline on the right and 4.53 ± 0.14 cm from the mid-
line on the left. Midway between the xiphoid and umbilicus, the SEA was 5.50 ± 0.16
cm from the midline on the right and 5.36 ± 0.16 cm from the midline on the left. At the
umbilicus, the epigastric vessels were 5.88 ± 0.14 cm from the midline on the right and
5.55 ± 0.13 from the midline on the left. Midway between the umbilicus and symphysis
pubis, the inferior epigastric artery was 5.32 ± 0.12 cm from the midline on the right and
5.25 ± 0.11 cm from the midline on the left. At the symphysis pubis, the inferior epigas-
tric artery was 7.47 ± 0.10 cm from the midline on the right and 7.49 ± 0.09 cm from the
midline on the left.
s The DIEA is dominant in the vascular supply of the abdominal muscles compared with the
SEA. The two arborizing vascular systems converge within the rectus abdominis muscle at
a point between the xiphoid process and umbilicus. In a study by Taylor (2003), the mean
diameter of the DIEA at its point of origin was 3.4 mm compared with 1.6 mm for the SEA,
perhaps explaining the dominant arterial supply of the DIEA.
Left subclavian artery
Internal thoracic
(mammary) artery
8 Diaphragm
9
Musculophrenic artery
Lower intercostal
Zone I and lumbar
Zone lll arteries
External oblique muscle (removed)
Internal oblique muscle (removed)
muscle
Zone ll
Ascending branch of
deep circumflex
iliac artery
Inguinal ligament

A
Musculocutaneous perforators
Lateral division Deep inferior
rows epigastric artery
Femoral artery Medial division Superficial circumflex
rows iliac artery
Superficial inferior
Inguinal ligament epigastric artery
Subdermal plexus
Camper fascia
ASIS Deep
circumflex
Scarpa iliac artery
fascia
Rectus
Deep abdominis
fascia muscles
Deep inferior epigastric arteries

External oblique muscle
Internal oblique muscle
B muscle
Fig. 1.8
Deep inferior
epigastric artery
and vein
Fig. 1.9
s Magnetic resonance angiography of the abdominal wall shows the converging systems of
the SEA and DIEA in the abdominal wall giving off perforators to the skin (Fig. 1.10).
s The DIEA arises from the medial aspect of the external iliac artery opposite the origin of
the deep circumflex iliac artery, approximately 1 cm above the inguinal ligament. It passes
superomedially behind the transversalis fascia and toward the lateral border of the rectus
abdominis muscle. It then enters the rectus sheath, passing anterior to the arcuate line,
midway between pubis and umbilicus.
s The SEA originates at the bifurcation of the internal mammary artery into the muscu-
lophrenic artery and deep SEA, around the region of the sixth costal cartilage. It subse-
quently passes inferolaterally and pierces the posterior rectus sheath to lie on the posterior
surface of the abdominal muscle. It then gives off two or more branches before anastomos-
ing with the branches of the DIEA.
s The SEA, when described, refers in general to the deep SEA. A superficial SEA has been
noted in anatomic studies, but it is not clinically significant.
s The musculophrenic artery passes inferolaterally behind the seventh, eighth, and ninth
costal cartilages and provides large branches to the intercostal spaces, which become con-
tinuous with the posterior intercostal vessels. Together with the lumbar arteries, it supplies
the lateral part of the abdominal wall. The musculophrenic artery provides an alternative
vascular supply for a pedicled transverse rectus abdominis myocutaneous flap when the
proximal portion of the internal mammary artery has been divided or is obstructed.
s Three patterns of blood supply of the rectus abdominis muscle were described by Taylor
(2003), based on divisions of the DIEA at the level of the arcuate line. In type 1 (29%),
there was a single intramuscular artery. In type 2 (57%), the DIEA divided at the arcuate
line into two major intramuscular vessels. In type 3 (14%), the DIEA divided into three
branches at the arcuate line.
s Musculocutaneous perforators arise from the DIEA and lie in a medial and lateral subdivi-
sion in the form of longitudinal rows of perforators parallel to the sagittal plane.
s Medial row perforators in general tend to have a vascular territory that is larger and crosses
the midline, well perfusing Hartrampf zones I and II.
s Lateral row perforators tend to have a zone of perfusion that is localized to a hemiabdo-
men and may be used preferentially when a smaller flap is required.
s Chowdhry et al. (2010) reported that the DIEA encountered the lateral border of the rec-
tus abdominis at a mean distance of 10.45 ± 1.58 cm from the umbilicus, with the first
perforator traversing the rectus abdominis muscle approximately 7.4 ± 1.64 cm from the
umbilicus.
s Veins draining the anterior abdominal wall (Fig. 1.11) run as venae comitantes, accom-
panying the perforators and subsequently main arteries of the DIEA and SEA. These ulti-
mately drain into the azygos system and external iliac veins.
s The superficial inferior epigastric artery (SIEA) arises from the external iliac artery or su-
perficial circumflex iliac artery and, together with the superficial inferior epigastric vein
(SIEV), lies in the plane between the Camper and Scarpa fasciae, lateral to the rectus ab-
dominis muscles. The SIEA and SIEV provide an accessory blood supply to the anterior
abdominal wall, which may be used in the harvesting of flaps.
s The SIEA was reported to have a mean diameter of 0.6 mm, with a diameter greater than
1.5 mm only in 24% of patients. Location of the SIEA is highly variable, with a mean posi-
tion 2 cm lateral to the linea semilunaris (range, 0–8 cm).
s The location of the SIEV is highly variable compared with the SIEA, with the distance be-
tween the SIEA and SIEV ranging from 0.3 to 8.5 cm. In contrast to the veins accompany-
ing the other arteries supplying the anterior abdominal wall, the SIEV often runs a distance
away from its corresponding artery, the SIEA.
s The lower intercostals and lumbar arteries supplying the abdominal wall lie in the plane
between the internal oblique and transversalis muscles.
Fig. 1.10
Left subclavian vein
Internal thoracic
(mammary) artery
6
Musculophrenic vein
7
Superior epigastric veins
8 Thoracoepigastric vein
9 Overlying semilunaris
Lower intercostal
veins
Transversus abdominis muscle
Lumbar veins
External oblique muscle (removed)
Internal oblique muscle (removed)
Deep circumflex
iliac vein tributaries
Scarpa’s fascia
Camper’s fascia
Thoracoepigastric vein
Inferior epigastric veins
Inguinal ligament
Superficial circumflex veins

Superficial epigastric veins
External iliac vein
Femoral vein
Fig. 1.11
Nerve Supply (Fig. 1.12)
s
Sensory innervation of the abdominal wall is derived from the anterior branches of the
intercostals and subcostal nerves, from T7 to L1. These nerves run together with the in-
tercostal and lumbar arteries in the plane between the internal oblique and transversalis
muscles. Fig. 1.13 shows the motor nerves to the rectus abdominis muscle. The internal
oblique muscle has been divided, showing the nerve deep to the internal oblique muscle
and superficial to the transversus abdominis muscle.
s T7 through T9 supply the skin superior to the umbilicus.
s T10 supplies the skin around the umbilicus.
s T11 through L1 supply the skin inferior to the umbilicus.
s Lateral cutaneous branches of the intercostal nerves supply the lateral areas of the
abdominal wall.
s Motor innervation is supplied by the 7th through 12th intercostal nerves, iliohypogastric
nerves, and ilioinguinal nerves.
s The rectus abdominis muscle is innervated segmentally by ventral rami of the lower six
intercostal nerves.
s The external oblique is innervated by the lower six thoracic and upper two lumbar anterior
rami.
s The internal oblique is innervated by the lower thoracic intercostal nerves (T6 through
T12) and the iliohypogastric and ilioinguinal nerves.
s The transversus abdominis muscle is innervated by the lower intercostal nerves (T7
through T12) and the iliohypogastric and ilioinguinal nerves.
Pearls and Pitfalls
s Knowledge of the anatomy and course of abdominal wall nerves is important. Painful neu-
romas of the ilioinguinal and iliohypogastric nerves have been well documented following
anterior abdominal wall incisions for herniorrhaphy, iliac bone crest harvest, laparoscopic
port placement, and appendectomy. Surrounding scar tissue usually entraps the nerve
leading to the development of a neuroma, which causes severe pain, point tenderness, and
pain radiating to the groin. Surgery involving neuroma resection and scar division usually
treats the pain.
2. Abdominal Wall Physiology
1. Function in Respiration
s
The abdominal wall plays an accessory role to the intercostal muscles, thorax, and dia-
phragm in respiration.
s The diaphragm maintains a constant positive pressure differential between the abdomen
and thorax, increasing the volume of the thorax in inspiration and decreasing the volume
of the thorax in expiration.
s The abdominal wall primarily functions in expiration, whereas the transversus abdominis
and external and internal obliques increase intra-abdominal pressure to meet increased
Ventral rami of intercostal

nerves T2–11
T2
T3
T2
T3
T4 T4
T5 T5
T6
T6
T7
T7
T8 Posterior layer of
Lateral cutaneous T8
T8 rectus sheath
branches of intercostal T9
T9
nerves T2–11 T10 Transversus abdominis
T9 T10 muscle
T11 T11 Internal oblique muscle
Lateral cutaneous T10
branch of subcostal T12
T12 External oblique muscle
nerve T12
T11 Anterior branch of subcostal
Lateral cutaneous
branch of iliohypogastric nerves T12
nerve L1 T12
Iliohypogastric nerve L1
Lateral femoral Ilioinguinal nerve L1
cutaneous nerve
Overlying semilunaris
Ventral rami of subcostal
nerve T12
Fig. 1.12
Fig. 1.13
demands of breathing during exercise. This increase in intra-abdominal pressure is trans-

mitted through the diaphragm to the thorax and forces air from the lungs.
s In the absence of exertion or exercise, expiration is largely passive and relies on relaxation
of the intercostal muscles and diaphragm.
s In inspiration, the abdominal wall provides anterior support for the abdominal cavity, al-
lowing for generation of a pressure differential between the abdomen and thorax through
the diaphragm.
s The large mass of the intra-abdominal contents hydraulically transmits a negative pressure
to the thorax at steady state, through gravity, when a person is upright. When a person is
supine, this effect is diminished, resulting in a decrease of functional respiratory capacity
of the lungs by approximately 15%–20% of vital capacity.
2. Muscle Function
s The musculature of the anterior abdominal wall works in a synkinetic fashion to protect
intra-abdominal contents and increase abdominal pressure where required.
s An increase in intra-abdominal pressure facilitates expiration, micturition, defecation, and
parturition.
s The rectus abdominis muscle tenses the abdominal wall and flexes the vertebral column.
s The diaphragm interdigitates with the abdominal wall.
s The diaphragm, iliopsoas, and quadratus lumborum muscle form a kinetic chain that inte-
grates upper and lower body activity, allowing coordinated movement and weight shifts.
s Together with this kinetic chain, the rectus abdominis muscle stabilizes the pelvis during
walking, running, and jumping.
s Many studies have been performed to evaluate function of the abdominal wall after bilat-
eral transverse rectus abdominis myocutaneous flaps for breast reconstruction. Although
results are highly variable, it is generally agreed that loss of both rectus muscles results in
some back pain and decreased flexor strength of the anterior abdominal wall.
3. Abdominal Wall Disruption Relevant to Anatomy
1. Rectus Diastasis
s Diastasis of the rectus abdominis muscles is defined as separation of the paired recti at the
midline (Fig. 1.14).
s Rectus diastasis occurs physiologically in newborns and pregnant women.
s The inter-recti distance (IRD) has been reported to be up to 58 mm in the prenatal period,
with a continuing increase in IRD up to four times in the postpartum period.
s Severe cases in adults, typically in postpartum women, can be treated by plication of the
rectus abdominis muscles.
s Another reported association with diastasis recti is abdominal aortic aneurysm, particu-
larly in men.
s HIV-associated lipodystrophy has been reported to be associated with diastasis recti.
s A rare congenital cause is Beckwith-Wiedemann syndrome.
s Rectus diastasis is more pronounced with increased intra-abdominal pressure (Fig. 1.15);
although not visible at rest (Fig. 1.15A), it is seen with a sit-up (Fig. 1.15B).
Linea alba
(torn)
IRD
Normal rectus abdominis muscles

Rectus diastasis
(rectus abdominis
A B muscles separated)
Fig. 1.14
A B
Fig. 1.15
2. Ventral Hernia
s
Ventral hernia typically develops as an incisional hernia following a midline laparotomy
through the linea alba; it is due to incomplete healing that results in a fascial defect.
s Greater than 10% of patients undergoing abdominal surgical procedures develop inci-
sional hernias (>150,000 incisional hernias per year).
s Risk factors for developing an incisional hernia are obesity, smoking, aneurysmal disease,
malnourishment, steroid dependency, renal disease, and malignancy.
s Patients present with a mass protruding through the fascia defect and causing localized
protuberance of the anterior abdominal wall (Figs. 1.16 and 1.17).
s Possible complications include incarceration and strangulation.
s Repair can be achieved with laparoscopic or open ventral hernia repairs with or without
mesh or components separation techniques.
s Optimization of nutrition is essential for wound healing after reconstructive surgery in
the anterior abdominal wall. During closure, it is important to ensure proper alignment
of layers of the abdominal wall and tension-free closure. Meticulous surgical technique
and avoidance of smoking in patients before and after surgery minimize the incidence of
abdominal wall complications.
3. Physiology of Ventral Hernia Formation
s
Most incisional hernias resulting from disruption of laparotomy wounds begin forming
within 30 days after surgery.
s In mechanical failure of the midline laparotomy wound, fibrosis, myopathic disuse atro-
phy, and change in muscle fiber type occur in abdominal wall musculature.
s Abnormal load signaling, together with the abovementioned pathologic changes, results in
reduced abdominal wall compliance.
s Animal studies confirm lateral abdominal wall shortening and atrophy of internal oblique
muscles, leading to decreased extensibility and increased stiffness of the abdominal wall.
This results in persistent mechanical disruption of the hernia at a lower force compared
with nonherniated abdominal walls.
s Biologic changes resulting from mechanical failure of the abdominal wall include decreased
fibroblast contraction, decreased extracellular matrix formation, and collagen deposition.
s An incisional hernia is a chronic wound with abnormal tissue repair pathways and is prone
to fail in the presence of a lower mechanical disruptive force compared with a normal
physiologic abdominal wall.
Fascial defect
Incisional ventral hernia
Fig. 1.16
Fig. 1.17
4. Congenital Abnormalities
s
Defects in abdominal wall closure during embryogenesis include omphalocele and
gastroschisis.
s Omphalocele is the protrusion of abdominal wall contents from a midline defect in the
abdominal wall at the base of the umbilicus. The herniated contents are covered by a very
thin membrane of tissue and can become dry and necrotic after birth. In infants with
omphalocele, the incidence of other congenital anomalies, such as bowel atresia, chromo-
somal abnormalities, and cardiac and renal anomalies, is very high (up to 70%).
s Gastroschisis is the protrusion of abdominal wall contents through a defect in the abdomi-
nal wall that is not midline, usually to the right of the umbilicus. No membrane covers the
abdominal wall contents, and the bowel is usually very edematous and inflamed. There are
no associated congenital anomalies in these infants.
Selected References
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reconstruction, Ann Plast Surg 63:222–230, 2009.
Blanchard PD: Diastasis recti abdominis in HIV-infected men with lipodystrophy, HIV Med 6:54–56, 2005.
Boyd JB, Taylor GI, Corlett R: The vascular territories of the superior epigastric and the deep inferior epigastric systems, Plast Reconstr Surg
73:1–16, 1984.
Chowdhry S, Hazani R, Collis P, Wilhelmi BJ: Anatomical landmarks for safe elevation of the deep inferior epigastric perforator flap: a
cadaveric study, Eplasty 10, 2010. e41.
DuBay DA, Choi W, Urbanchek MG, et al.: Incisional herniation induces decreased abdominal wall compliance via oblique muscle atrophy
and fibrosis, Ann Surg 245:140–146, 2007.
Ducic I, Moxley M, Al-Attar A: Algorithm for treatment of postoperative incisional groin pain after cesarean delivery or hysterectomy,
Obstet Gynecol 108:27–31, 2006.
El-Mrakby HH, Milner RH: The vascular anatomy of the lower anterior abdominal wall: a microdissection study on the deep inferior
epigastric vessels and the perforator branches, Plast Reconstr Surg 109:539–543, 2002.
Franz MG: The biology of hernia formation, Surg Clin North Am 88:1–15, 2008.
Hartrampf CR, Scheflan M, Black PW: Breast reconstruction with a transverse abdominal island flap, Plast Reconstr Surg 69:216–225,
1982.
Hsia M, Jones S: Natural resolution of rectus abdominis diastasis. Two single case studies, Aust J Physiother 46:301–307, 2000.
Huger Jr WE: The anatomic rationale for abdominal lipectomy, Am Surg 45:612–617, 1979.
Losken A, Carlson GW, Jones GE, Culbertson JH, Schoemann M, Bostwick 3rd J: Importance of right subcostal incisions in patients
undergoing TRAM flap breast reconstruction, Ann Plast Surg 49:115–119, 2002.
Moesbergen T, Law A, Roake J, Lewis DR: Diastasis recti and abdominal aortic aneurysm, Vascular 17:325–329, 2009.
Moon HK, Taylor GI: The vascular anatomy of rectus abdominis musculocutaneous flaps based on the deep superior epigastric system,
Plast Reconstr Surg 82:815–832, 1988.
Ramirez OM, Ruas E, Dellon AL: “Components separation” method for closure of abdominal-wall defects: an anatomic and clinical study,
Plast Reconstr Surg 86:519–526, 1990.
Rozen WM, Chubb D, Grinsell D, Ashton MW: The variability of the superficial inferior epigastric artery (SIEA) and its angiosome: a
clinical anatomical study, Microsurgery 30:386–391, 2010.
Saber AA, Meslemani AM, Davis R, Pimental R: Safety zones for anterior abdominal wall entry during laparoscopy: a CT scan mapping of
epigastric vessels, Ann Surg 239:182–185, 2004.
Schneid H, Vazquez MP, Vacher C, Gormelen M, Cabrol S, Le Bouc Y: The Beckwith-Wiedemann syndrome phenotype and the risk of
cancer, Med Pediatr Oncol 28:411–415, 1997.
Taylor GI: The angiosomes of the body and their supply to perforator flaps, Clin Plast Surg 30:331–342, 2003.
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 125:772–782, 2010.
CHAPTER
2
Laparoscopic Repair of
Ventral Hernias: Standard
Sean B. Orenstein, MD, and William S. Cobb IV, MD
1. Introduction and Clinical Anatomy
s
Compared with traditional open ventral hernia repair, minimally invasive approaches
offer several advantages, including reduced wound and mesh infections, quicker return
of bowel function, and reduced length of hospitalization as well as improved cosmesis.
However, not everyone is a candidate for laparoscopic repair. Size and complexity of de-
fects, history of infection, prior hernia repairs or abdominal surgeries, body habitus, and
comorbidities all are factors that should be weighed to determine if laparoscopic repair is
appropriate.
s Laparoscopic repair of ventral hernias borrows much from the open techniques espoused
by Rives and Stoppa. It maintains the tenets of large mesh overlap with transabdomi-
nal fixation of the prosthetic. In a standard laparoscopic ventral herniorrhaphy, the mesh
prosthetic is placed intra-abdominally in an underlay position. Because the mesh lies jux-
taposed to the underlying viscera, a tissue-separating mesh is required to reduce visceral
adhesions to the mesh.
s Traditionally, the hernia defect is bridged with mesh; however, some surgeons advocate
closing the defect with transabdominal sutures. Potential benefits of defect closure include
reduced seromas and mesh exposure in the event of superficial infection as a result of
dead space obliteration above the mesh. Additionally, the law of LaPlace dictates that there
will be increased tension on the bridged portion of mesh from a hernia repair without de-
fect closure. This increased tension may ultimately lead to mesh “eventration,” or bulging
of the mesh within the hernia sac. Based on Pascal’s principle, closing the defect would
equalize pressure across the mesh. Another theoretical benefit of defect closure is akin to
open repairs with reapproximation of the midline, restoring a more native and functional
abdominal wall with medialization of the rectus muscles. The biggest drawbacks of defect
closure are additional operative time spent closing the defect and increased postoperative
pain from additional transfascial sutures.
s The amount of mesh overlap required for a durable ventral hernia repair is unknown. Based
on Pascal’s principle, the intra-abdominal pressure is evenly distributed over a large surface
area of mesh. The initial experience with laparoscopic ventral herniorrhaphy reported a
3-cm overlap of mesh, but the current recommendation is at least a 4- to 5-cm margin. The
amount of overlap depends on the diameter of the largest hernia defect and the thickness
of the patient’s abdominal wall. One large defect warrants at least 5 cm, whereas numerous
small defects (“Swiss cheese” defects) may require only 4 cm of additional mesh. If hernia
defect closure is chosen at the time of repair, a generous overlap of at least 5 cm is still recom-
mended; therefore a minimum of 10- to 12-cm-wide mesh should be used.
22
Chapter 2 • Laparoscopic Repair of Ventral Hernias: Standard 23
s In a laparoscopic ventral hernia repair, the mesh is placed in an insufflated abdominal cav-
ity. Ideally there is a slight degree of tension on the mesh at the completion of the repair.
The mesh does not lie flush against the underside of the abdominal wall. Rather it transects
the abdominal space, so that when the abdominal cavity is desufflated, the mesh will not
occupy the hernia sac (Fig. 2.1).
2. Preoperative Considerations
s When considering candidates for a laparoscopic ventral hernia repair, certain patient char-
acteristics must be considered. Contraindications include the following:
• Inability to tolerate general anesthesia
• Hypercoagulability
• Active infection
• Loss of domain
• Poor skin quality overlying hernia (ulceration, skin graft)
• Patient expectations (scar revision or panniculectomy desired)
s Surgeon skill, particularly in the area of adhesiolysis, needs to be factored in when choosing
a laparoscopic ventral hernia repair. Factors that portend a more difficult case requiring
experience with the technique include the following:
• Multiple previous laparotomies
• Previous intra-abdominal mesh
• History of peritonitis
• Atypical location of hernia (suprapubic, subxiphoid, flank)
Mesh sutures placed and tied

to anterior abdominal wall
Previous
incision
and ventral
hernia
Tacks
Insufflated
abdominal
cavity
4- to 5-cm
mesh
overlap
Mesh pulled taut while transecting abdominal wall
Fig. 2.1
24 Section II • Laparoscopic Repairs
s The preoperative consultation is critical in a patient undergoing laparoscopic ventral her-

niorrhaphy. Although a minimally invasive approach, laparoscopic ventral hernia repair
can result in significant postoperative pain and is not much different from an open repair
in terms of postoperative discomfort. The real benefit of the laparoscopic approach is the
well-documented reduction in wound- and mesh-related infectious complications. The
likelihood of postoperative seroma formation should be discussed. The need for conver-
sion to an open repair and the possibility of an enterotomy should be considered as well.
The anticipated options if an enterotomy occurs should be explained to the patient, in-
cluding delayed repair of the hernia defect until the abdomen is free from contamination.
s Because ventral hernias can usually be identified on physical examination, no further
work-up generally is required. However, computed tomography (CT) of the abdominal
wall can be helpful in a patient who is morbidly obese, has a recurrent hernia (particularly
with intra-abdominal mesh), demonstrates a defect in proximity to a bony structure
(ie, suprapubic, subxiphoid, flank defects), or has concern for loss of domain.
s Patients with previous failed attempts at repair can be difficult to treat. The reasons for
recurrence are usually unknown, but efforts should be made not to repeat errors of the
past. All operative reports that pertain to prior hernia repairs should be obtained to deter-
mine the mesh or meshes used and planes disrupted by prior repairs. Before approaching
a recurrent defect, the surgeon should feel extremely confident with adhesiolysis and have
a low threshold to convert to an open procedure. Patients who have had previous mesh
infections that required removal of the prosthesis pose an extremely difficult challenge and
should be considered for open repair.
s The preoperative orders consist of antibiotic and deep venous thrombosis prophylaxis. A
first-generation cephalosporin is typically given, and the dosage is adjusted for morbidly
obese patients. Because patients with ventral hernia are frequently obese, will be less mo-
bile postoperatively, and will experience increased intra-abdominal pressure from pneu-
moperitoneum, sequential compression devices and subcutaneous heparin are employed
preoperatively.
3. Operative Steps (Video 2.1)
1. Patient Positioning
s For most patients with defects in the midline, supine positioning with both arms tucked
is optimal, as this allows superior access for trocar placement and instrumentation. The
pressure points at the elbow and wrist should be padded (Fig. 2.2). For larger patients,
arm sleds may be required. In patients with defects off the midline or lumbar defects, a
bump may be placed under the hip on the side of the hernia, or a true lateral position may
be necessary with the aid of a beanbag.
s A Foley catheter is placed for bladder decompression; a three-way Foley catheter may be
used to insufflate the bladder for identification in the repair of suprapubic defects. Gastric
decompression is usually reserved for patients requiring a difficult orotracheal intubation
and may be achieved with orogastric tube decompression.
s The patient should be prepared and draped widely to allow lateral trocar placement. An
iodine-impregnated adhesive drape is applied to the patient’s skin after preparation and
draping to protect the biomaterial from the patient’s skin flora.
Fig. 2.2
2. Abdominal Access
s Abdominal entry can be the most difficult step in a patient who has undergone multiple
abdominal operations. Selecting the location for entry can be challenging because many
of these patients have had numerous abdominal incisions. The upper quadrant at the tip
of the 11th rib is generally a safe place to gain access even in such cases. The side of entry
should avoid previous incisions. For example, in a patient with an open cholecystectomy
incision, the left upper quadrant should be chosen. Because of the wide availability of
high-definition 5-mm laparoscopes and instruments, most of the trocars can be 5 mm in
size; however, at least one 12- to 15-mm trocar is necessary for mesh placement.
s Several safe methods for initial access have been described. A cutdown technique works
very well. Through a small incision in the upper quadrant, each layer of the abdominal
wall is divided down to the peritoneum. The peritoneum can be sharply entered with a
scalpel or bluntly penetrated with the finger to gain safe access to the abdominal cavity. An
optical trocar can also be used safely in the upper quadrant just below the rib line. Some
surgeons prefer the Veress needle. The best technique is the one with which the surgeon is
most comfortable and familiar.
s Once initial entry into the abdominal cavity is achieved, at least one and preferably two
additional trocars are placed laterally on the side of entry. Typically, one trocar can be
placed inferiorly, taking care not to be too close to the iliac crest, and an additional one can
be inserted between these two trocars. Two trocars are commonly placed on the opposite
side to provide additional viewing perspective for adhesiolysis, to aid in retraction, and
for contralateral tacking of the mesh (Fig. 2.3); however, new articulating and angulating
tacking devices may obviate the need for contralateral trocar placement.
3. Adhesiolysis
s The Achilles’ heel of the laparoscopic ventral hernia repair is the lysis of adhesions. This
step can be the most time-consuming and usually determines the length and complexity
of the case.
s A 30-degree laparoscope is mandatory to adequately visualize the anterior abdominal wall.
A 5-mm laparoscope provides more flexibility in moving the camera; however, if the visual
clarity is poor, a 10-mm laparoscope should be used.
s Energy sources should be avoided during adhesiolysis. Ultrasonic energy sources or bipo-
lar coagulating shears should not be used. Thermal injuries seal at the time of dissection
and may not be apparent for 3–5 days postoperatively. Sharp, cold, endoscopic scissor
dissection should dominate the dissection. Blunt bowel graspers are crucial to aid in re-
traction of the viscera and can be used to provide gentle blunt dissection as well. Typically,
during lysis of adhesions, the outer rind of adhesions may be sharply cut, giving way to a
“cotton candy” appearance to the loose areolar tissue that comprises most of the adhesions
(Fig. 2.4). Blunt dissection with gentle, short sweeps is very effective in this situation.
s External pressure applied on the abdominal wall by the assistant aids adhesiolysis. This
move can be critical in a morbidly obese patient or in a situation in which adhesions are
up within the hernia sac. By bringing the dissection into the abdomen with pressure, visu-
alization of the proper tissue planes is made possible.
Tip of 11th rib
10/12 mm
5 mm
5 mm
5 mm
(optional) 5 mm
ASIS
LOCATION OF TROCARS
Fig. 2.3
SHARP ADHESIOLYSIS
Fig. 2.4
s Previous intra-abdominal mesh can pose a hazard to performing adhesiolysis. If the previ-
ous mesh contains a polypropylene or polyester component that becomes directly exposed
to the bowel, a clear plane of dissection is typically absent. Attempts to mobilize the bowel
off the adherent mesh will result in an enterotomy. In this situation, the mesh should be
cut down off of the abdominal wall, leaving a swatch of prosthetic attached to the bowel
(Fig. 2.5). Any concern for bowel injury should mandate conversion to an open proce-
dure. Some cases of intense adhesion formation to the prosthetic may require a bowel
resection.
s Bleeding during adhesiolysis can be very problematic. Slight oozing that typically occurs
should be largely ignored. It rarely continues, and chasing it, especially with cautery, may
lead to a bowel injury. If the area of oozing can be isolated from viscera, judicious mo-
nopolar cautery may be used. An oozing area of adipose tissue can be lifted away from
underlying bowel and cauterized. Laparoscopic clip appliers can be extremely helpful in
controlling bleeding in areas adjacent to bowel or where the location of bowel is unknown.
Laparoscopic pre-tied suture loops, taking care not to secure around a loop of bowel, assist
with bleeding sections of omentum or mesenteric fat.
s Clearing the abdominal wall of all adhesions for the entire extent of the prior surgical inci-
sion is imperative. “Swiss cheese” defects not apparent preoperatively may become evident
at this time. Extra time in this step is worthwhile to avoid the “early recurrence”—actually
a defect missed at the initial repair.
s For defects above the umbilicus, the falciform ligament has to be taken down close to the
abdominal wall to allow for flush placement of mesh against the abdominal wall. This
move is best performed with electrocautery attached to the endoshears. The falciform liga-
ment is divided just below its insertion to the underside of the abdominal wall fascia and
taken up superiorly at least 5 cm above the defect to allow sufficient mesh overlap.
4. Sizing the Hernia Defect
s Measuring the defect is a critical step in the procedure. Many times, particularly following
a lengthy adhesiolysis, this step may not be given much attention. A durable repair relies
on adequate mesh overlap with proper placement, both of which are a direct result of ac-
curately measuring the defect.
s The edges of the hernia defect are best delineated with the aid of 3.5-inch, 20-gauge spinal
needles placed at each edge of the defect. The needle is inserted into the abdominal wall at
a 90-degree angle to the floor so that it can emerge at the defect edge within the abdomen.
A metric ruler should be used to measure the vertical and horizontal dimensions of the
defect between the needles. For multiple defects, the needles are placed to encompass all
fascial defects, measuring them as one large defect.
s Three techniques have been described for measuring the defect: (1) externally with abdo-
men insufflated, (2) externally with abdomen desufflated, and (3) internally with abdo-
men insufflated. Because the mesh is being placed intracorporeally, it makes sense to make
all measurements internally. The external measuring techniques overestimate the defect,
which is more pronounced in larger defects and obese patients with thick anterior ab-
dominal walls.
s The defect should be measured internally under pneumoperitoneum. A plastic metric
ruler is cut in half lengthwise and introduced via a 5-mm trocar. Two Maryland graspers
manipulate the ruler and measure the defect between the spinal needles in the abdomen
(Fig. 2.6). If the defect is longer than the ruler, another spinal needle can be inserted
along the axis of the defect within the length of the ruler. The sum of the two is the true
measurement.
Leaving swatches of
prosthetic on bowel
CUTTING DOWN PREVIOUS MESH

Fig. 2.5
Fig. 2.6
5. Hernia Defect Closure
s
As previously discussed, defect closure is an adjunct to traditional laparoscopic ventral
hernia repair. Although benefits of defect closure have been demonstrated in several case
series and routine closure by surgeons has increased, no randomized trials demonstrating
its use exist at the present time. Because of extra tension placed on the wound, permanent
monofilament sutures are used throughout the closure. Because multiple transfascial pass-
es are typically needed, a sharp suture passer is required, preferably disposable to ensure
a fresh sharp tip.
s To start defect closure, an external vertical line is drawn on the skin through the central
portion of the defect. Using spinal needles, the superior and inferior edges are identified
and marked. Sites for figure-of-eight sutures are marked approximately every 3 cm on the
vertical line. No. 1 polypropylene (Prolene) sutures are prepared by cutting the needle off,
placing a hemostat on one end to prevent pull-through, and grasping the other end with
the suture passer.
s Starting at one end, a stab incision is made with a No. 11 blade. Under direct visualiza-
tion, using the suture passer, the first No. 1 Prolene suture is passed through the stab
incision centrally and then advanced through one fascial edge approximately 1 cm from
the edge (Fig. 2.7A). A Maryland dissector is used to grasp the suture from the suture
passer. Using the same stab incision, the empty suture passer is advanced through the
contralateral fascial edge, the suture is grasped, and the suture passer is withdrawn ex-
ternally leaving the suture within the suture passer so that it is ready for the next pass
(Fig. 2.7B). Using the same stab incision, the suture passer with suture is advanced into
the ipsilateral fascial edge, advancing approximately 1 cm along the midline. After passing
the suture to the Maryland dissector, the suture passer is replaced in the contralateral fas-
cia to grasp the suture and withdraw it externally. Both ends of the suture are grasped with
the preplaced hemostat, completing placement of one figure-of-eight suture. All sutures
are placed before closure.
s A dditional figure-of-eight sutures are placed along the length of the premarked line
approximately every 3 cm in an identical manner, taking care to avoid locking subse-
quent sutures on previously placed figure-of-eight sutures. Gentle outward traction
of previously placed sutures may help by reducing excess suture within the hernia
cavity.
s After placement of all figure-of-eight sutures and ensuring adequate patient paralysis,
the sutures are tied down. Knots should be tied down sequentially from the ends,
proceeding toward the center to reduce wound tension (Fig. 2.7C). Reducing the
pneumoperitoneum to low levels (3–5 mm Hg) with direct visualization aids in defect
#1 Prolene suture passed through

central stab incision
Advancement through fascial edge
Maryland dissector
Suture grasper
Center line
of defect
Figure-of-eight sites
for suture placement
3 cm
A
Fig. 2.7
Second pass complete, advancing 1 cm along each fascial edge

of hernia and then back out same stab incision and placed in hemostat
First pass complete,

suture passer ready for
second pass back through
same stab incision
B
Fig. 2.7—cont’d
Knots below
Scarpa’s fascia
Knots tied down sequentially

1 from the ends,
reducing wound tension.
2
Placement of all
figure-of-eight sutures
C
Fig. 2.7—cont’d
closure. The surgeon must ensure no omentum or visceral structure becomes en-
trapped within the closure; pulling up and maintaining tension on the sutures exter-
nally during desufflation helps reduce entrapment. Placing a hemostat into the small
skin incision and lifting it allows the knot to fall below Scarpa fascia and not dimple
the skin (Fig. 2.8).
s Because defect closure creates tension on the newly reapproximated fascia, some of that
tension needs to be offloaded to the mesh. After mesh placement (see next section), addi-
tional buttressing sutures are placed alongside the defect closure. Using permanent mono-
filament sutures (No. 1 Prolene), full-thickness transabdominal (including mesh) simple
U-stitches are placed every 4–5 cm bilaterally, approximately 1–2 cm lateral to the midline
(see Fig. 2.7D).
s Other techniques for defect closure include intracorporeal suturing using a laparoscopic
suture-assist device, use of a running stitch with barbed suture, and robotic techniques.
The use of robotic-assisted laparoscopy may be beneficial, as it allows precise intracorpo-
real defect closure as well as the potential for preperitoneal mesh placement, isolating the
mesh from direct contact with the abdominal cavity; however, this is beyond the scope of
this chapter.
6. Mesh Introduction, Orientation, and Mesh-Positioning Devices
s Not all hernia defects are perfectly circular, and they are not all located exactly in the mid-
line of the abdomen. To ensure that the mesh will be centered reliably over the defect every
time, it is necessary to draw a grid of the x- and y-axes of the hernia defect on the external
abdominal wall (Fig. 2.9).
Full thickness (including mesh),

trans-abdominal simple U-stitches
Buttressing sutures aid

D in offloading tension to mesh
Fig. 2.7—cont’d
Place hemostat into small incision and lift

to release Scarpa’s fascia which allows knot
to go underneath
Skin dimple
after tying down
Scarpa’s fascia
Mesh
Fig. 2.8
Fig. 2.9
s With a ruler outside the abdomen, the distance halfway between the most superior and
most inferior spinal needles is measured. This determines the x-axis, the horizontal mid-
point of the hernia. Half the horizontal distance between the lateralmost spinal needles
marks the y-axis, or the vertical midpoint. Both axes are drawn on the skin with a per-
manent marker to grid the abdomen and mark the center of the hernia defect. Once the
mesh is brought into the abdomen, any attempt to retrieve one of the vertical or lateral
cardinal sutures should be made along the corresponding x- or y-axis line to align the
mesh over the defect and ensure the most accurate placement to achieve desired overlap
(Fig. 2.10).
s The type of mesh chosen for repair should have a favorable adhesion profile. Various ab-
sorbable barriers that coat polypropylene or polyester mesh have been shown to provide
reduction in adhesions. Expanded polytetrafluoroethylene (ePTFE) has a permanent an-
tiadhesion side. The infection profile of the biomaterial also should be considered; ePTFE
and polyester are less likely to resist infection.
s Classically, the mesh is marked, and sutures are placed in the mesh before introduction
into the abdomen. For preplaced sutures, the sheet is folded in half vertically and horizon-
tally. The midpoint of each mesh edge is marked. The cardinal sutures are placed at the
four midpoints, taking a 1-cm bite in from the edge. Permanent sutures should be used to
provide ongoing transfascial fixation. Polytetrafluoroethylene suture works well because
it has less memory and recoil; however, Prolene sutures also work well. The tails of the
cardinal sutures are tucked in, and the mesh is rolled from both ends toward the middle
like a scroll along the horizontal axis. After a brief soak in saline, meshes with temporary
antiadhesion barriers should be rolled with the barrier on the inside of the roll to prevent
it from scraping off during passage through the trocar.
s Once rolled, the mesh can be compressed and twisted to expunge air. The rolled mesh
may be passed directly through a 12- or 15-mm trocar (Fig. 2.11). Ideally this larger tro-
car would be inserted in an area eventually covered by mesh. However, it should not be
passed through the hernia defect itself, as this would allow a large superficial wound to be
in close contact with the mesh. A laparoscopic suture passer can be used to close the tro-
car defect with an absorbable monofilament suture after removal of this temporary trocar
and before mesh fixation. Very large pieces of mesh can be dragged into the abdomen by
passing an empty heavy grasper across the abdomen through a 5-mm trocar and out the
contralateral side trocar. The cap of the trocar is removed, and the mesh is pulled into the
abdominal cavity (Fig. 2.12). Every effort should be made to introduce the mesh through
the trocar. This maneuver avoids contact with the patient’s skin.
Fig. 2.10
MESH ROLLED AROUND GRASPER AND

PASSED THROUGH 10+ MM TROCAR
Fig. 2.11
LARGE MESH PULLED THROUGH

FROM CONTRALATERAL SIDE GRASPER
Fig. 2.12
s The mesh is unfurled inside the abdominal cavity. A grasper holds one end of the rolled
mesh while the Maryland grasper uncoils the mesh (Fig. 2.13). It is important to maintain
the proper orientation of the mesh, ensuring proper x- and y-axes as well as the antiadhe-
sion surface toward the viscera. It may be helpful with larger pieces to mark a line across
the horizontal axis of the mesh before insertion to ensure that the line runs from side to
side.
s Alternatively, mesh manufacturers have developed laparoscopic mesh-positioning devices
that may obviate the need for such precise external measurements as well as eliminate
the need to preplace sutures. However, it is still important to determine the center of the
defect and to gain an accurate internal measurement of the defect to implant an appropri-
ately sized mesh. Such devices are introduced within the abdomen and stabilize the mesh
against the anterior abdominal wall with balloons or semirigid frames, or both, and then
are removed after mesh fixation.
7. Securing the Mesh
s The steps for securing the mesh are different depending on whether or not a mesh-posi-
tioning device is used. Classically, if a mesh-positioning device is not used, after unrolling
the mesh, the cardinal suture is retrieved at the vertical site where there is the least amount
of adjustment first. For example, if the defect is in the lower abdomen, the inferior suture
should be placed initially to avoid having to move its location caudally toward the bladder
when stretching the mesh. Likewise, if the defect approximates the xiphoid, the superior
suture is placed first. The edge of the defect at the site of cardinal suture placement is
marked with the spinal needle. An additional spinal needle is “walked out” the axis line for
a distance of 5 cm to ensure overlap (Fig. 2.14). This measured spot is injected with local
anesthesia, and a stab incision is made through which the suture passer is introduced. The
suture passer retrieves each tail of the initial cardinal suture through the same small inci-
sion but at a different angle to achieve a separate fascial bite. Both suture tails are tagged
but are left untied.
Fig. 2.13
OVERLAP MEASUREMENT
FOR FIRST CARDINAL
SUTURE PLACEMENT
4 cm
Order of primary
suture placement 1
(1-4)
2 4
Abdominal grid for

mesh orientation 3
Mesh
outline
Fig. 2.14
Another random document with
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other hand, though they may show a degenerate condition of the
ovigerous appendages (Fig. 72, D), never develop a single positively
male characteristic. On dissecting crabs of these various categories it
is found that the generative organs are in varying conditions of
degeneration and disintegration.
The most remarkable fact in this history is the subsequent
behaviour of males which have assumed perfect female external
characters, if the Sacculina drops off and the crabs recover from the
disease. It is found that under these circumstances these males may
regenerate from the remains of their gonads a perfect hermaphrodite
gland, capable of producing mature ova and spermatozoa. The
females appear quite incapable, on the other hand, of producing the
male primary elements of sex on recovery, any more than they can
produce the secondary. Exactly analogous facts have been observed
in the case of the hermit-crabs parasitised by Peltogaster, but here
the affected males produce small ova in their testes before the
parasite is got rid of. Here, too, the females seem incapable of
assuming male characters under the influence of the parasite.
To summarise shortly the conclusions to be deduced from these
facts—certain animals react to the presence of parasites by altering
their sexual condition. This alteration consists in the female sex in an
arrest of reproductive activity, in the male sex in the arrest of
reproductive activity coupled with the assumption of all the external
characters proper to the female. But in these males it is not merely
the external characters that have been altered; their capacity for
subsequently developing hermaphrodite glands shows that their
whole organisation has been converted towards the female state.
That this alteration consists in a reorganisation of the metabolic
activities of the body is clearly suggested, and in the succeeding
paragraph we furnish some further evidence in support of this view.
Fig. 73.—Inachus mauritanicus, × 1. A, Low male; B, middle
male; C, high male; the great chela of the right side is the only
appendage represented.
Partial and Temporary Hermaphroditism. High and Low Dimorphism.
The reproductive phases of animals are frequently rhythmic,

periods of growth alternating with periods of reproduction. This is
well exemplified in the case of the ordinary males of Inachus
mauritanicus, of some other Oxyrhynchous crabs, and of the
Crayfish Cambarus.[77] During the breeding season the males of I.
mauritanicus fall into three chief categories: Small males with
swollen chelae (Fig. 73, A), middle-sized males with flattened chelae
(B), and large males with enormously swollen chelae (C). On
dissecting specimens of the first and third categories it is found that
the testes occupy a large part of the thoracic cavity and are full of
spermatozoa, while in the middle-sized males with female-like chelae
the testes appear shrivelled and contain few spermatozoa. These
non-breeding crabs are, in fact, undergoing a period of active growth
and sexual suppression before attaining the final state of
development exhibited by the large breeding males. This
phenomenon is obviously parallel to the “high and low
dimorphism”[78] so common in Lamellicorn beetles, where the males
of many species are divided into two chief categories, viz. “low
males” of small size in which the secondary sexual characters are
poorly developed, and “high males” of large size in which these
characters are proportionately much more highly developed than in
the low males. The only difference between the two cases is that
whereas in the beetles growth ceases on the attainment of maturity
in the low degree, in the Crustacea the low male passes through a
period of growth and sexual suppression to reach the high degree of
development.
The condition of the middle-sized males may be looked upon as
one of partial hermaphroditism, indications of the female state being
found in the flattened chelae and in the reduced state of the testes.
This interpretation is greatly strengthened by the state of affairs
observed in the life-history of the male Sand-hoppers, Amphipods of
the genus Orchestia.[79] In the young males of several species of this
genus, at the time of year when they are not actively breeding, small
ova are developed in the upper part of the testes of more than half of
the male individuals, these ova being broken down and reabsorbed
as the breeding season reaches its height. Nor is this phenomenon
confined to this genus; in the males of a number of widely different
Crustacea these small ova are found in the testes at certain periods of
the life-history (e.g. Astacus[80]), when the animal is not breeding.
The foregoing facts indicate unmistakably that the males of a
number of Crustacea under certain metabolic conditions, i.e. when a
stage of active growth as opposed to a stage of reproductive activity is
initiated, alter their sexual constitution in such a way that the latent
female characteristics are developed, and the organism appears as a
partial hermaphrodite. In the preceding paragraph we saw that the
males of a number of animals, especially Crustacea, react to the
metabolic disturbance set up by the presence of a parasite in exactly
the same way, i.e. by developing into partial or total hermaphrodites.
From these two converging bodies of facts we may conclude, firstly,
that sex and metabolism are two closely connected phenomena; and,
secondly, that the male sex is especially liable to assume
hermaphrodite characters whenever its metabolic requirements are
conservative, assimilatory, or in a preponderating degree anabolic, as
when a phase of active growth is initiated, or the drain on the system,
due to the presence of a parasite, is to be made good.
Normal Hermaphroditism in Cirripedia and Isopoda Epicarida.
The above-mentioned groups contain the only normally

hermaphrodite Crustacea, and since they are in most respects highly
specialised, we may be certain that they have been secondarily
derived from dioecious ancestors. They both lead a sessile or
parasitic life, and it is noteworthy that this habit is often associated
with hermaphroditism, e.g. in Tunicates. A sessile or parasitic mode
of life is one in which the metabolic functions are vegetative and
assimilatory rather than actively kinetic or metabolic. It is in this
state that we have seen the males of a number of Crustacea taking on
a temporary or partial hermaphroditism. We may, therefore, inquire,
whether in these cases of normal hermaphroditism there is any
evidence to show that here too the hermaphroditism has been
acquired by the male sex as a response to the change in the metabolic
conditions. In the parasitic Isopoda Epicarida (see pp. 129–136) the
hermaphroditism is of a very simple kind; all the individuals are at
first males, whose function it is to fix on and fertilise the adult
parasites. These subsequently develop into females which are in their
turn cross-fertilised by the young larvae derived from a previous
generation. All the individuals being alike, it seems probable that
they have been derived from one sex, and the general nature of
hermaphroditism deduced above may lead us to suppose that that
sex was originally male, the female having been suppressed. In
certain Cirripedia, e.g. most species of Scalpellum, there exist,
besides the hermaphrodite individuals, complemental males, so that
here a superficial conclusion might be drawn that the
hermaphrodites represent the female sex. But if we can suggest that
the complemental males are in reality similar in derivation to the
hermaphrodite individuals, we shall be in a position to claim that the
hermaphrodite Cirripedes are similar to the Isopoda Epicarida, and
have probably also been derived from the male sex. There is decided
evidence pointing to this conclusion. In the first place, the
complemental males of at least one species of Scalpellum, S. peronii,
do show an incipient hermaphroditism[81] in the presence of small
ova in their generative glands, which, however, never come to
maturity.
The condition of the degenerate males in the Rhizocephala may
also be interpreted in the same manner. These never pass beyond the
Cypris stage of development, in which they resemble in detail the
Cypris larvae of the ordinary hermaphrodite individuals, and they
are quite useless in the propagation of their species.
It is more reasonable to suppose that these Cypris larvae, which fix
on the mantle-openings of adult parasites, are in reality identical
with the ordinary Cypris which infest crabs and develop into the
hermaphrodites, than that they represent a whole male sex doomed
beforehand to uselessness and degeneration. If we suppose that the
Cirripedes have passed through a state of protandric
hermaphroditism similar to that of the Isopoda Epicarida, it is plain
that all the larvae must have originally possessed the instinct of first
fixing on the adult parasites, and we may suppose that this instinct
has been retained in the Rhizocephala, but is now only actually
fulfilled by a certain proportion of the larvae, which, under existing
circumstances, are useless and fail to develop further; while the rest
of the larvae, not finding an adult parasite to fix upon, go straight on
to infect their hosts and develop into the adult hermaphrodites.
The same explanation would apply to the complemental males in
Scalpellum, etc., these individuals being also potential
hermaphrodites, which are arrested in development, though not so
completely as in the Rhizocephala, owing to the position they have
taken up.
This theory throws light on another dark feature of Cirripede life-
history, namely, the gregarious instinct. The associations of
Cirripedes are not formed by a number of Cypris larvae fixing
together on the same spot, but rather by the Cypris larvae seeking
out adolescent individuals of their own species and fixing on or near
them. Now, if we suppose that the Cirripedes have passed through a
condition of protandric hermaphroditism similar to that of the
Isopoda Epicarida, it is clear that a slight modification of the sexual
instinct of the larvae would lead to the gregarious habit, while its
retention in some individuals in its original form accounts for their
finding their way to the mantles of adult individuals and developing
into the so-called complemental males.
Certain Cirripedes, viz. certain species of Scalpellum and Ibla and
all the Acrothoracica, are dioecious. It is impossible to decide at
present whether these species retain the primitive dioecious
condition of the ancestral Cirripedes, or whether they too have been
derived from an hermaphrodite state, but in the present state of
knowledge they hardly affect the validity of the theory that has been
proposed to account for the nature of the complemental males and
the hermaphrodite individuals.
Order IV. Ostracoda.
The Ostracoda are small Crustacea, the body consisting of very few
—about eight—segments, and being completely enclosed in a
carapace, which has the form of a bivalve shell. Development is
direct, without a Nauplius stage.
The Ostracoda[82] are marine and fresh-water animals that can be
divided into several families, differing slightly in habits and in
structures correlated with those habits.
The Cypridae and
Cytheridae include all the fresh-
water and a vast majority of
marine genera, adapted for a
sluggish life among water-plants,
though some can swim with
considerable activity. The
common Cypris and Candona of
our ponds and streams are
familiar instances. The Fig. 74.—Candona reptans. A, Natural
movements of these animals are size; B, X 15. a, 1st antennae; b, 2nd
effected by means of the two pairs antennae; c, walking legs. (After Baird.)
of uniramous pediform antennae
which move together and in a vertical straight line. In the Cypridae
(Fig. 74) there are, besides the mandibles, two pairs of maxillae, a
pair of walking legs, and, lastly, a pair of appendages, which are
doubled up into the carapace, and are used for cleaning purposes. In
the marine Cytheridae there is only one maxilla, the last three
appendages being pediform and used in walking. The telson in the
Cytheridae is rudimentary, but is well developed in the Cypridae. The
heart is altogether absent.
In many of the fresh-water forms, e.g. common species of
Candona and Cypris, males are never found, and parthenogenetic
reproduction by the females appears to proceed uninterruptedly.
Weismann[83] kept females of Cypris reptans breeding
parthenogenetically for eight years. He also remarks on the fact that
these, and indeed all parthenogenetic female Ostracoda, retain the
receptaculum seminis, used normally for storing the spermatozoa
derived from the male, unimpaired.
Some of the Cytheridae occur in deep water. Thus Cythere dictyon
was frequently taken by the Challenger in depths of over 1000
fathoms, but the majority prefer shallow water.
Fig. 75.—Asterope oblonga, ♀ , removed from its carapace, × 25.

A, Alimentary canal; A1, A2, 1st and 2nd antennae; E, eye; G, gills;
G.O, generative opening; H, heart; M, mandible; T, 6th
appendage; T′, last appendage (cleaning foot). (After Claus.)
The Halocypridae and Cypridinidae comprise marine genera

of a pelagic habit. The first antennae are chiefly sensory, but the
second antennae are biramous, and they do not merely move up and
down, as in the preceding families, but sideways like oars, the valves
of the shells being excavated to admit of free movements. There are
two pairs of maxillae; the succeeding limbs differ in the two families.
In the Cypridinidae, e.g. Asterope (Fig. 75), the first leg (T) is
lamelliform and is used as an accessory maxilla, while the second leg
(T’) is turned upwards into the shell as a cleaning organ. In the
Halocypridae the first leg is pediform, and differs in the two sexes,
while the second leg is rudimentary and points backwards. In
Asterope peculiar branchial organs (G) are present on the back. Both
families possess a heart; the Halocypridae are blind, while the
Cypridinidae possess eyes.
The Polycopidae and Cytherellidae are curious marine families
of a pelagic habit, with biramous second antennae well adapted for
swimming, and very broad. The first maxilla in the Polycopidae is
also employed in swimming, while the second is modified into a
branchial organ; the maxillae of the Cytherellidae are more normal
in structure, but both carry branchial lamellae. The posterior limbs
are altogether absent in Polycopidae, and in the Cytherellidae are
only represented by the copulatory organs of the male.
CHAPTER V
CRUSTACEA (CONTINUED):
MALACOSTRACA: LEPTOSTRACA—
PHYLLOCARIDA: EUMALACOSTRACA:
SYNCARIDA—ANASPIDACEA: PERACARIDA
—MYSIDACEA—CUMACEA—ISOPODA—
AMPHIPODA: HOPLOCARIDA—
STOMATOPODA
SUB-CLASS II.—MALACOSTRACA.
The Malacostraca are generally large Crustacea, and they are

characterised by the presence of a definite and constant number of
segments composing the body. In addition to the paired eyes we can
distinguish two pairs of antennae, a mandibular segment, and two
maxillary segments composing the head region proper; there then
follow eight thoracic segments, the limbs belonging to the anterior
thoracic segments being often turned forwards towards the mouth,
and modified in structure to act as maxillipedes, while at any rate the
last four are used in locomotion and are termed “pereiopods.”[84] The
abdomen is composed of six segments, which typically carry as many
pairs of biramous “pleopods,” and the body terminates in a telson.
Not counting the paired eyes or the telson, there are present nineteen
segments. The excretory organs in the adult open at the bases of the
second antennae, and are known as “green glands,” but in the larva
maxillary glands may be present homologous to those which persist
in the adult Entomostraca. This is the typical arrangement, but
sometimes the maxillary glands persist in adult Malacostraca, e.g.
Nebalia, Anaspides, and some Isopods.
The hepato-pancreatic diverticula are directed posteriorly, and not
anteriorly as in most Entomostraca, and the stomach is often
furnished with chitinous teeth and ridges forming an elaborate
gastric mill, especially in the larger Decapods.
SERIES 1. LEPTOSTRACA.
Division. Phyllocarida.
The small shrimp-like Crustacean Nebalia, which is found

burrowing in the superficial layers of sand in the littoral and
sometimes the deeper regions of most seas, has been regarded, ever
since its anatomy was made out by Claus,[85] as a connecting link
between Entomostraca and Malacostraca, and has been placed in a
separate group Leptostraca.
The segmentation of the body is Malacostracan, save that two
extra segments are present in the abdomen, and the paired
compound eyes are borne upon stalks. The eight thoracic limbs are
all very similar; they are built on the typical biramous plan, and each
carries a bract; they have been compared, owing to their flattened,
expanded shape, to the foliaceous limbs of the Phyllopods. The
abdominal appendages are also biramous. The heart is greatly
elongated, stretching through thorax and abdomen; there are present
both the antennary excretory glands characteristic of adult
Malacostraca and the maxillary glands characteristic of adult
Entomostraca, and both the posterior and anterior livers
characteristic of the two Orders respectively are present. This
combination of characters justifies the belief that Nebalia represents
a primitive form, standing to some extent in an intermediate position
between Entomostraca and Malacostraca, but it may be doubted if
the special relationship to the Phyllopoda, claimed on the strength of
the foliaceous appearance of the thoracic limbs, can be legitimately
pressed.
Nebalia shows the clearest signs of relationship to the other
primitive Malacostraca, and especially to the Mysidae, which it
resembles not only in general form and in the essentially biramous
character of its appendages, but also in many embryological points
and in the similarity in development of the brood-pouch.[86]
A large number of very ancient palaeozoic fossils are known which
are placed provisionally with Nebalia in the Division Phyllocarida,
and some of these are no doubt closely related to the existing isolated
genus. Hymenocaris from the Cambrian.
Fig. 76.—Nebalia geoffroyi, ♀ , × 20.
A.1, A.2, 1st and 2nd antennae; Ab.1,
Ab.6, 1st and 6th abdominal
appendages; A.G. antennary gland; C,
half of caudal fork; E, eye; G, ventral
ganglionic chain; H, heart; I, intestine;
L, upper liver-diverticulum; M,
adductor muscle of halves of carapace;
MX, palp of 1st maxilla; O, ovary; R,
rostrum. (After Claus.)
SERIES 2. EUMALACOSTRACA.
Before entering on a description of the members of this Series it is
necessary to introduce and justify a new scheme of classification
which has been proposed by Dr. W. T. Calman. This scheme
necessitates the abandonment of the old Order Schizopoda, and also
ignores the distinction which used to be considered fundamental
between the sessile-eyed Crustacea (Edriophthalmata) and the stalk-
eyed forms (Podophthalmata).
The old group of Schizopoda, to which Nebalia and the isolated
form Anaspides, to be considered later, are undoubtedly related,
represent very clearly the stem-forms from which the various
branches of the Malacostracan stock diverge. No doubt they are
themselves specialised in many directions, since they are a dominant
group in present day seas, but their organisation is fundamentally of
a primitive type. We see this especially in the comparative absence of
fusion or reduction of the segments of the body externally and of the
nervous system internally, and in the simple undifferentiated
character of the trunk-limbs, all of which conform to the primitive
biramous type. The most anterior thoracic limbs of the Schizopods
are of particular interest. In the higher Malacostraca three of these
limbs are usually turned forwards towards the mouth to act as
maxillipedes, and the most anterior of all, the first maxillipede, is
apt, especially in the Decapoda, to take on a flattened foliaceous form
owing to the expansion of the basal segments to act as gnathobases
(see Fig. 1, A, p. 10). Now this appendage in the Schizopods preserves
its typical biramous character, and resembles the succeeding thoracic
limbs, but in many of the species the basal joints show a tendency to
be produced into biting blades (Fig. 1, E, p. 10), thus indicating the
first step in the evolution of the foliaceous first maxillipede of the
Decapoda. The primitive character of the Schizopods is also
indicated by the fact that most of the Decapoda with uniramous
limbs on the five hinder thoracic segments pass through what is
known as the “Mysis stage” in development, when these limbs are
biramous, the exopodites being subsequently lost in most cases.
The “Schizopoda” include a very large number of pelagic Crustacea
of moderate size, which superficially appear to resemble one another
very closely. The slender, elongated body, the presence of biramous
limbs on all the thoracic and abdominal segments, and the
possession of a single row of gills at the bases of the thoracic limbs,
are, generally speaking, typical of the families Mysidae,
Lophogastridae, Eucopiidae, and Euphausiidae, which go to make up
the old Order Schizopoda.
It has, however, been pointed out first by Boas,[87] and
subsequently by Hansen and Calman,[88] that the Euphausiidae are in
many respects distinct from the other three families, and agree with
the Decapoda, while the Eucopiidae, Lophogastridae, and Mysidae
agree with the Cumacea, Isopoda, and Amphipoda.
It has, therefore, been suggested by these authors that the
classification of the Malacostraca should be revised, and Calman (loc.
cit.) has brought forward the following scheme:—
The division Peracarida, including the Eucopiidae,
Lophogastridae, and Mysidae (= Mysidacea), the Cumacea, Isopoda,
and Amphipoda, is characterised by the fact that when a carapace is
present it leaves at least four of the thoracic segments free and
uncoalesced: by the presence of a brood-pouch formed from the
oostegites on the thoracic limbs of the female: by the elongated
heart: by the few and simple hepatic caeca: by the filiform
spermatozoa: and by the direct method of development without a
complicated larval metamorphosis. The biting face of the mandible
has a movable joint, the “lacinia mobilis.”[89]
The division Eucarida, on the other hand, including the
Euphausiidae and the Decapoda, shows the converse of these
characters. The carapace coalesces with all the thoracic segments,
there is never a brood-pouch formed from oostegites, the hepatic
caeca are much ramified, the heart is short, the spermatozoa are
spherical with radiating pseudopodia, the development is indirect
with a complicated metamorphosis, and the mandible is without a
lacinia mobilis.
Corresponding divisions are made by Calman to receive the other
Malacostraca, namely, the Phyllocarida for Nebalia, the Syncarida
for Anaspides, and the Hoplocarida for the Stomatopoda or
Squillidae.
The important array of characters which separates the
Euphausiidae from the other Schizopods and unites them with the
Decapoda can no longer be neglected, and the consideration of
Anaspides and its allies will further emphasise the extreme difficulty
of retaining the Schizopoda as a natural group. In the sequel
Calman’s proposed scheme will be adopted.
DIVISION 1. SYNCARIDA.
There is no carapace, and all the eight thoracic segments may be

free and distinct. Eyes may be pedunculate or sessile. The mandible
is without a lacinia mobilis. There is no brood-pouch, the eggs being
deposited and hidden after fertilisation. The spermatozoa are
filiform, the hepatic caeca very numerous, and the heart tubular and
elongated, with ostia only in one place in the anterior thoracic
region. The auditory organ is at the base of the first antennae.
Order. Anaspidacea.
Fam. 1. Anaspididae.—The mountain-shrimp of Tasmania,

Anaspides tasmaniae, was first described by Thomson[90] in 1893
from specimens taken in a little pool near the summit of Mount
Wellington; it was redescribed by Calman,[91] who drew attention to
its remarkable resemblance to certain Carboniferous fossils of
Europe and N. America (Gampsonyx, Palaeocaris, etc.).
The creature appears to be confined to the deep pools of the rivers
and tarns on the mountains of the southern and western portions of
Tasmania.[92] The waters in which it occurs are always cold and
absolutely clear, and there is no record of its living at altitudes much
below 2000 feet, while it frequently occurs at 4000 feet. The body
may attain upwards of two inches in length; it is deeply pigmented
with black chromatophores, and it is held perfectly horizontal
without any flexure. The animal rarely swims unless disturbed,
usually walking about on stones and water-plants at the bottom of
deep pools. In walking the endopodites of the thoracic limbs are
chiefly instrumental, but they are assisted by the exopodites of the
abdominal limbs.
When frightened the shrimp can dart rapidly forwards or sideways
by the strokes of its powerful tail-fan, but it never jumps backwards
as do the other Malacostraca. It appears to browse upon the algal
slime covering the rocks and on the submerged liver-worts and
mosses, but it does not refuse animal food, even feeding on the dead
bodies of members of its own species. The thoracic limbs, which are
all biramous except the last pair, carry a double series of remarkable
plate-like gills on their coxopodites. The slender and setose
exopodites of the thoracic limbs are respiratory in function, being
kept in continual motion even when the animal is at rest, and serving
to keep up a current of fresh water round the gills.
Anaspides shows a remarkable combination of structural
characters, some of which are peculiar, while others are possessed in
common with the Peracarida or Eucarida. The chief peculiar
characters are the entire absence of a carapace, and the freedom of
the eight thoracic segments, with eight free thoracic ganglia in the
nerve-cord; the peculiar double series of plate-like gills; the structure
of the alimentary canal; and the fact that the eggs, instead of being
carried in a brood-pouch, or affixed to the abdominal limbs, are
deposited under stones and among water-plants.[93]
Fig. 77.—Anaspides tasmaniae in natural position for walking, ×
1. The last two pereiopods point backwards and are overlapped by
the first two pleopods.
The Peracaridan features, uniting it especially with the Mysidacea,

are the structure of the elongated heart, the filiform spermatozoa,
and the fact that no complicated metamorphosis is passed through,
the young hatching out in a condition similar to, though possibly not
identical with, the adult form.
The Eucaridan, especially Decapodan, features are the presence of
an auditory sac on the basal joint of the antennules, and the
modification of the endopodites of the first two abdominal
appendages in the male to form a copulatory organ.
A type of a new genus of this family was found by me in the littoral
zone of the Great Lake of Tasmania at an elevation of 3700 feet, and
named Paranaspides lacustris.
This little shrimp (Fig. 78), which does not appear to grow to more
than an inch in length, is totally different in appearance from
Anaspides, being pale green and transparent, with a very marked
dorsal hump as in Mysis, to which it bears a very striking superficial
resemblance. It leads a more active swimming life than Anaspides,
and with this habit is correlated the flexure of the body and the
greater size of the tail-fan and the scale of the second antenna. The
mandible is peculiar in being furnished with a four-jointed biramous
palp, while that of Anaspides is three-jointed and uniramous, and
the first thoracic appendage is provided with a setose biting lobe on
the antepenultimate joint, thus more resembling a maxillipede. In
other respects it agrees essentially in structure with Anaspides.
Fig. 78.—Paranaspides lacustris, × 4. a1, a2, First and second

antennae; Ab.1, first abdominal segment; ep, epipodites or gills on
the thoracic legs; md, mandible; Pl.1, first pleopod; T, telson;
Th.8, eighth free thoracic segment; U, uropod, or sixth pleopod.
Fam. 2. Koonungidae.—The sole representative of this family,

Koonunga cursor, has been recently described by Mr. O. A. Sayce,[94]
of Melbourne University, from a small stream some miles to the west
of Melbourne. Although plainly belonging to the Anaspidacea, this
interesting little animal, which only measures a few millimetres in
length, and follows a similar habit to Anaspides, running about with
its body unflexed, differs from all the other members of the Division
in possessing sessile instead of stalked eyes, in the first thoracic
segment being fixed to the head, and in a number of minor
anatomical points.
It is impossible at present to assign the Carboniferous forms
(Gampsonyx, Palaeocaris, etc.) to their exact position in the
Division, but it seems that they agreed more closely with Anaspides
than with the other two genera. From the position in which the
fossils are preserved, it would appear that they followed a similar
walking habit to Anaspides, and that the body was unflexed.
DIVISION 2. PERACARIDA.
The carapace, when present, leaves at least four of the thoracic

somites distinct; the first thoracic segment is always fused with the
head. The eyes are pedunculate or sessile.
The mandible possesses a lacinia mobilis. A brood-pouch is
formed in the female from oostegites attached to the thoracic limbs.
The hepatic caeca are few and simple; the heart is elongated and
tubular; the spermatozoa are filiform, and development takes place
without a complicated metamorphosis.
Order I. Mysidacea.
The Mysidacea, although pelagic, are not very often met with in
the true plankton on the surface; they generally swim some way
below the surface, going down in many cases into the abysses. For
this reason they thrive excellently in aquaria, and the common Mysis
vulgaris is often present in such numbers in the tanks at the
Zoological station at Naples as to damage the other inmates by the
mere press of numbers. The Mysidacea, like the majority of the
Peracarida, undergo a direct development, and hatch out with the
structure of the adult fully formed.
Many of the Mysidacea bear auditory sacs upon the sixth pair of
pleopods, a characteristic not found in the Euphausiacea.
Fam. 1. Eucopiidae.—The curious form Eucopia australis (Fig.
79) described by Sars,[95] may be chosen as an example of the
Mysidacea.
The peculiarity of this form consists chiefly in the immense
elongation of the endopodites of the fifth, sixth, and seventh thoracic
appendages. Characteristic of the Mysidacea is the freedom of the
hinder thoracic segments from fusion with the carapace, otherwise
this animal is seen closely to resemble the Euphausia figured (Fig.
102). Eucopia australis, like so many of the Mysidacea, is a deep-sea
animal, being brought up with the dredge from over 1000 fathoms; it
is very widely distributed over the Atlantic Ocean.
Fig. 79.—Eucopia australis, young female, × 3. A, 1st antenna;

Ab.1, 1st abdominal segment; Ab.6, 6th abdominal appendage; E,
eye; T, telson; Th, 5th thoracic appendage. (After Sars.)
Fam. 2. Lophogastridae.—The members of this family

(Lophogaster, Gnathophausia) agree with the Eucopiidae in the
possession of branched gills on some of the thoracic limbs, in the
absence of auditory sacs on the sixth pair of pleopods, in the
presence of normally developed pleopods in both the male and
female, and in the brood-lamellae being developed on all seven of the
thoracic limbs. The endopodites of the posterior thoracic limbs are,
however, of a normal size.
Fam. 3. Mysidae.—These differ from both the foregoing families
in the absence of gills, in the presence of an auditory sac on the sixth
pleopods, in the reduction of the other pleopods in the female, and in
the brood-lamellae being developed only on the more posterior pairs
of thoracic limbs. A number of closely related genera compose this
family, of which Mysis,
Boreomysis, and Siriella may be
mentioned. Mysis oculata, var.
relicta, is a fresh-water form from
the lakes of northern and central
Europe.

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Atlas of Abdominal Wall

Reconstruction - eBook PDF

Michael J. Rosen, MD, FACS

ATLAS OF ABDOMINAL WALL RECONSTRUCTION, SECOND EDITION ISBN: 978-0-323-37459-0

Previous edition copyrighted 2011.

International Standard Book Number: 978-0-323-37459-0

Content Strategist: Michael Houston

Last digit is the print number: 9 8 7 6 5 4 3 2 1

William W. Hope, MD Melissa Phillips LaPinska, MD, FACS

Jeffrey E. Janis, MD, FACS Jay Mittal, MD

Eduardo Parra-Davila, MD, FACS, FASCRS Carley E. Schroering

Steven Rosenblatt, MD, FACS Benjamin Zendejas-Mummert, MD

2. Superficial Fascial Layers (see Figs. 1.1 and 1.2)

Xiphoid process Pectoralis major

Anterior rectus sheath Anterior superior iliac

Anterior superior iliac

Pearls and Pitfalls

3. Deep Fascial Layers (see Figs. 1.1 and 1.2)

s The rectus sheath is found in the midline.

Xiphoid Linea alba Linea alba

Common branching patterns:

Pearls and Pitfalls

4. Abdominal Wall Musculature (see Figs. 1.1–1.3)

Fig. 1.4 Fig. 1.5

Pearls and Pitfalls

5. Neurovascular Supply of the Abdominal Wall

Left subclavian artery

External iliac artery

Zone lll Zone lll

Perforators from deep

Left subclavian artery

External iliac artery

Deep inferior epigastric arteries

Left subclavian vein

Superficial circumflex veins

Nerve Supply (Fig. 1.12)

Pearls and Pitfalls

2. Abdominal Wall Physiology

Ventral rami of intercostal

demands of breathing during exercise. This increase in intra-abdominal pressure is trans-

3. Abdominal Wall Disruption Relevant to Anatomy

Normal rectus abdominis muscles

3. Physiology of Ventral Hernia Formation

Incisional ventral hernia

1. Introduction and Clinical Anatomy

Mesh sutures placed and tied

s The preoperative consultation is critical in a patient undergoing laparoscopic ventral her-

3. Operative Steps (Video 2.1)

Tip of 11th rib

4. Sizing the Hernia Defect

CUTTING DOWN PREVIOUS MESH

5. Hernia Defect Closure

#1 Prolene suture passed through

Advancement through fascial edge

Second pass complete, advancing 1 cm along each fascial edge

First pass complete,

Knots tied down sequentially

6. Mesh Introduction, Orientation, and Mesh-Positioning Devices

Full thickness (including mesh),

Buttressing sutures aid

Place hemostat into small incision and lift

MESH ROLLED AROUND GRASPER AND

LARGE MESH PULLED THROUGH

ATLAS OF ABDOMINAL WALL RECONSTRUCTION, SECOND EDITION ISBN: 978-0-323-37459-0

s The rectus sheath is found in the midline.

s The preoperative consultation is critical in a patient undergoing laparoscopic ventral her-