Clinical Algorithms

in General Surgery
A Practical Guide
Salvatore Docimo Jr.
Eric M. Pauli
Editors

123
Clinical Algorithms in General Surgery
Salvatore Docimo Jr.  •  Eric M. Pauli
Editors

Clinical Algorithms
in General Surgery
A Practical Guide
Editors
Salvatore Docimo Jr. Eric M. Pauli
Department of Surgery Department of Surgery
Stony Brook Medicine Penn State Milton S. Hershey Medical
Stony Brook, NY Center
USA Hershey, PA
USA

ISBN 978-3-319-98496-4    ISBN 978-3-319-98497-1 (eBook)

https://doi.org/10.1007/978-3-319-98497-1

Library of Congress Control Number: 2019930648

© Springer Nature Switzerland AG 2019

This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or
part of the material is concerned, specifically the rights of translation, reprinting, reuse of
illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way,
and transmission or information storage and retrieval, electronic adaptation, computer software,
or by similar or dissimilar methodology now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this
publication does not imply, even in the absence of a specific statement, that such names are
exempt from the relevant protective laws and regulations and therefore free for general use.
The publisher, the authors, and the editors are safe to assume that the advice and information in
this book are believed to be true and accurate at the date of publication. Neither the publisher nor
the authors or the editors give a warranty, express or implied, with respect to the material
contained herein or for any errors or omissions that may have been made. The publisher remains
neutral with regard to jurisdictional claims in published maps and institutional affiliations.

This Springer imprint is published by the registered company Springer Nature Switzerland AG
The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
To my wife, Aisa, and our son, Massimo, thank you for the
unwavering support and patience. To my parents, I am forever
indebted to you. To my colleagues and friends throughout the
surgical world who contributed their expertise to these
algorithms, thanks. I will always be grateful to those who had a
part in my training and continue to offer their wisdom and
insight.
Salvatore Docimo, Jr., DO, MS

My surgical career has been the epitome of dumb luck. I have

had the good fortune to train under and with amazing
surgeons, I work with dynamic colleagues, and I get to train
eager students, residents, and fellows. I would like to thank all
those individuals who have contributed to my success,
especially those who were willing to share their expertise
through these algorithms. Thanks in particular to the three Jeffs
(you can rank yourselves in order), Yuri, Mike, Randy, Peter,
Ann, Evan, Abraham, Lou, and Chris.
Eric M. Pauli, MD
Preface

With the rapid expansion of surgical knowledge, it has never been more chal-
lenging to organize and articulate a simple and safe surgical plan. Traditional
textbooks, in an attempt to keep pace with the growth of surgical science,
have become encyclopedic reference books. Young surgeons, with a finite
amount of time to pore over such tomes and an increasing load of clinical
responsibilities, often search for educational materials that offer basic, safe
principles of general surgery. For the more seasoned surgeon, a brief review
of vital surgical topics does not require the comprehensive perspective offered
by traditional surgical textbooks.
We created this book of surgical algorithms in order to meet the needs of
both of these groups of surgeons. The goal of an algorithm is to create a set of
rules, permit data processing, and establish a solution in the most efficient
manner. An algorithmic approach to surgical scenarios allows for concise
organization of clinical information, application of basic and safe principles,
and, finally, formation of an unambiguous surgical solution. The algorithms
are also accompanied with a synopsis to provide a more comprehensive
review, if desired.
Students, residents, and surgeons will find the algorithms concise enough
to read to completion in moments of spare time. For the surgical trainee, they
should provide a foundation upon which future learning can be built. For the
more senior surgeon, they will provide an up-to-date overview of commonly
encountered topics from the “20,000 foot view.” For chief residents and
recent graduates, we hope this book enables crystallization of their knowl-
edge base as they prepare for the American Board of Surgery certifying
examination.

Stony Brook, NY, USA Salvatore Docimo Jr.

Hershey, PA, USA Eric M. Pauli

vii
Contents

Part I Skin and Soft Tissue

1 Management of Cutaneous Melanoma������������������������������������������   3

Julie A. DiSano and Colette R. Pameijer
2 Basal Cell Carcinoma����������������������������������������������������������������������   5
Julie A. DiSano and Colette R. Pameijer
3 Squamous Cell Carcinoma��������������������������������������������������������������   7
Julie A. DiSano and Colette R. Pameijer
4 Management of Soft Tissue Sarcoma ��������������������������������������������   9
Julie A. DiSano and Colette R. Pameijer
5 Necrotizing Soft Tissue Infection����������������������������������������������������  11
Julie A. DiSano and Colette R. Pameijer

Part II Head and Neck

6 Management of Squamous Cell Carcinoma

of the Oropharynx����������������������������������������������������������������������������  17
Laila Siddique, Tom Shokri, and Neerav Goyal
7 Evaluation of Neck Mass ����������������������������������������������������������������  21
Tom Shokri, Laila Siddique, and Neerav Goyal
8 Evaluation of an Enlarged Cervical Lymph Node������������������������  25
Laila Siddique, Tom Shokri, and Neerav Goyal
9 Salivary Gland Tumors��������������������������������������������������������������������  29
Tom Shokri, Laila Siddique, and Neerav Goyal

Part III Thoracic

10 Massive Hemoptysis������������������������������������������������������������������������  35

Henry Tannous, Joanna Chikwe, and Maroun B. Yammine
11 Mediastinal Masses��������������������������������������������������������������������������  39
Henry Tannous, Joanna Chikwe, and Maroun B. Yammine
12 Tracheal Stenosis������������������������������������������������������������������������������  43
Henry Tannous, Joanna Chikwe, and Maroun B. Yammine

ix
x Contents

13 Incidental Lung Nodule������������������������������������������������������������������  47

Henry Tannous, Joanna Chikwe, and Maroun B. Yammine
14 Management of Lung Cancer ��������������������������������������������������������  51
Scott C. Tiedebohl and Matthew D. Taylor
15 Management of Empyema��������������������������������������������������������������  55
Shannon R. Kotch and Matthew D. Taylor
16 Management of Spontaneous Pneumothorax��������������������������������  59
Shannon R. Kotch and Matthew D. Taylor
17 Thoracoabdominal Aortic Aneurysm��������������������������������������������  63
Albert G. Pavalonis and Anil Hingorani

Part IV Breast

18 Nipple Discharge������������������������������������������������������������������������������  69

Anjali R. Thawani and Lillian M. Erdahl
19 Breast Mass Evaluation ������������������������������������������������������������������  73
Anjali R. Thawani and Lillian M. Erdahl
20 Ductal Carcinoma In Situ���������������������������������������������������������������  77
Anjali R. Thawani and Lillian M. Erdahl
21 Lobular Carcinoma In Situ������������������������������������������������������������  81
Anjali R. Thawani and Lillian M. Erdahl
22 Enlarged Axillary Lymph Node������������������������������������������������������  85
Zeynep Bostanci and Laura Kruper
23 Metastatic Breast Cancer����������������������������������������������������������������  87
Zeynep Bostanci and Laura Kruper
24 Recurrent Breast Cancer����������������������������������������������������������������  91
Zeynep Bostanci and Laura Kruper
25 Paget’s Disease����������������������������������������������������������������������������������  95
Zeynep Bostanci and Laura Kruper
26 Locoregional Recurrence of Breast Cancer����������������������������������  97
Jessica C. Gooch and Freya Schnabel
27 Metastatic Breast Cancer���������������������������������������������������������������� 101
Jessica C. Gooch and Freya Schnabel
28 Inflammatory Breast Cancer���������������������������������������������������������� 105
Jessica C. Gooch and Freya Schnabel
29 Breast Reconstruction��������������������������������������������������������������������� 109
Jessica C. Gooch and Freya Schnabel
30 Management of Male Breast Cancer���������������������������������������������� 113
Jessica C. Gooch and Freya Schnabel
Contents xi

Part V Esophagus

31 Management of Esophageal Motility Disorders���������������������������� 119

Anthony R. Tascone and Caitlin A. Halbert
32 Management of Achalasia �������������������������������������������������������������� 123
Anthony R. Tascone and Caitlin A. Halbert
33 Barrett’s Esophagitis ���������������������������������������������������������������������� 127
Caitlin A. Halbert and Anthony R. Tascone
34 Gastroesophageal Reflux Disease �������������������������������������������������� 129
Caitlin A. Halbert and Anthony R. Tascone
35 Hiatal Hernia������������������������������������������������������������������������������������ 133
Wanda Lam, Ruel Neupane, and Jeffrey M. Marks
36 Esophageal Carcinoma�������������������������������������������������������������������� 135
Ruel Neupane, Wanda Lam, and Jeffrey M. Marks
37 Esophageal Perforation ������������������������������������������������������������������ 139
Ruel Neupane, Wanda Lam, and Jeffrey M. Marks
38 Acidic and Basic Injuries���������������������������������������������������������������� 143
Wanda Lam, Ruel Neupane, and Jeffrey M. Marks

Part VI Stomach and Duodenum

39 Gastric Ulcer Management ������������������������������������������������������������ 149

Maria S. Altieri and Konstantinos Spaniolas
40 Duodenal Ulcer Management �������������������������������������������������������� 153
Maria S. Altieri and Konstantinos Spaniolas
41 Complications of Peptic Ulcer Disease ������������������������������������������ 157
Carl J. Dickler and Konstantinos Spaniolas
42 Management of Recurrent Peptic Ulcer Disease�������������������������� 161
Carl J. Dickler and Konstantinos Spaniolas
43 Management of Gastric Cancer������������������������������������������������������ 165
Christina L. Wolchok and Georgios V. Georgakis
44 Management of Gastrointestinal Stromal Tumors����������������������� 169
Igor G. Elyash
45 Management of Upper Gastrointestinal Hemorrhage������������������ 171
Igor G. Elyash

Part VII Small Bowel

46 Small Bowel Obstruction���������������������������������������������������������������� 175

Ryan M. Juza and Vamsi V. Alli
47 Small Bowel Tumors������������������������������������������������������������������������ 181
Vamsi V. Alli and Ryan M. Juza
xii Contents

48 Management of Small Bowel Neuroendocrine Tumors���������������� 185

Michele A. Riordon and Calvin H. L. Law
49 Management of Enterocutaneous Fistulas������������������������������������ 191
Maria Michailidou
50 Management of Crohn’s Disease���������������������������������������������������� 195
Igor G. Elyash
51 Management of Postoperative Ileus ���������������������������������������������� 197
Igor G. Elyash
52 Management of Gallstone Ileus������������������������������������������������������ 199
Igor G. Elyash
53 Management of Short Bowel Syndrome���������������������������������������� 201
Igor G. Elyash

Part VIII Large Bowel

54 Management of Lower Gastrointestinal Bleeding������������������������ 205

Audrey S. Kulaylat and David B. Stewart Jr.
55 Management of Diverticulitis���������������������������������������������������������� 209
Audrey S. Kulaylat and David B. Stewart Jr.
56 Management of Large Bowel Obstruction������������������������������������ 213
Audrey S. Kulaylat and David B. Stewart Jr.
57 Management of Colonic Pseudo-­Obstruction ������������������������������ 217
Audrey S. Kulaylat and David B. Stewart Jr.
58 Management of Colonic Volvulus �������������������������������������������������� 221
Audrey S. Kulaylat and David B. Stewart Jr.
59 Appendicitis�������������������������������������������������������������������������������������� 225
Kristen T. Crowell and Evangelos Messaris
60 Ulcerative Colitis������������������������������������������������������������������������������ 229
Kristen T. Crowell and Evangelos Messaris
61 Crohn’s Colitis���������������������������������������������������������������������������������� 233
Maria Michailidou and Evangelos Messaris
62 Ischemic Colitis�������������������������������������������������������������������������������� 237
William Sangster and Evangelos Messaris
63 Clostridium difficile Colitis�������������������������������������������������������������� 241
Kristen T. Crowell and Evangelos Messaris
64 Hereditary Colorectal Cancer Syndromes������������������������������������ 243
Emily Huang and Michael F. McGee
65 Colorectal Polyps������������������������������������������������������������������������������ 251
Emily Huang and Michael F. McGee
66 Colon Cancer������������������������������������������������������������������������������������ 255
Emily Huang and Michael F. McGee
Contents xiii

Part IX Rectum and Anus

67 Rectal Prolapse�������������������������������������������������������������������������������� 263

Quinton Morrow Hatch and Eric K. Johnson
68 Solitary Rectal Ulcer Syndrome ���������������������������������������������������� 269
John Kuckelman and Eric K. Johnson
69 Rectal Cancer ���������������������������������������������������������������������������������� 275
Quinton Morrow Hatch and Eric K. Johnson
70 Rectovaginal Fistula������������������������������������������������������������������������ 283
John Kuckelman and Eric K. Johnson
71 Management of Hemorrhoids�������������������������������������������������������� 289
Matthew Z. Wilson and Joseph R. Notaro
72 Management of Anal Fissure���������������������������������������������������������� 293
Matthew Z. Wilson and Kirsten Bass Wilkins
73 Management of Perianal Abscess and Fistula-in-Ano������������������ 297
Matthew Z. Wilson and Bertram T. Chinn
74 Management of Anal Cancer���������������������������������������������������������� 301
Matthew Z. Wilson and Kirsten Bass Wilkins
75 Management of Fecal Incontinence������������������������������������������������ 303
Matthew Z. Wilson and Suraj Alva

Part X Liver

76 Evaluation of Liver Nodule ������������������������������������������������������������ 307

Katelin A. Mirkin and Niraj J. Gusani
77 Cystic Diseases of the Liver������������������������������������������������������������ 313
Laura M. Enomoto and Niraj J. Gusani
78 Management of Benign Liver Masses�������������������������������������������� 319
Katelin A. Mirkin and Niraj J. Gusani
79 Hepatic Abscess�������������������������������������������������������������������������������� 323
Jasvinder Singh and Niraj J. Gusani
80 Malignant Liver Tumors (Metastatic Liver Disease)�������������������� 327
Neal M. Mineyev, Karla M. Chaffee, and Joyce Wong
81 Diagnosis and Management of Hepatocellular Carcinoma��������� 331
Neal M. Mineyev, Karla M. Chaffee, and Joyce Wong
82 Diagnosis and Management of Primary Sclerosing Cholangitis 335
Neal M. Mineyev, Karla M. Chaffee, and Joyce Wong
83 Portal Hypertension and Shunting������������������������������������������������ 339
Neal M. Mineyev, Karla M. Chaffee, and Joyce Wong
xiv Contents

Part XI Biliary

84 Acute Cholecystitis and Biliary Colic�������������������������������������������� 345

Chanak J. Chantachote and Samer Sbayi
85 Acalculous Cholecystitis������������������������������������������������������������������ 349
Chanak J. Chantachote and Samer Sbayi
86 Postcholecystectomy������������������������������������������������������������������������ 351
Chanak J. Chantachote and Samer Sbayi
87 Management of Postcholecystectomy Cholangitis������������������������ 355
Joel VanderVelde and Ross F. Goldberg
88 Management of Choledocholithiasis���������������������������������������������� 357
Joel VanderVelde and Ross F. Goldberg
89 Acute Cholangitis ���������������������������������������������������������������������������� 359
Joel Vandervelde and Ross F. Goldberg
90 Cholangiocarcinoma������������������������������������������������������������������������ 361
Zachary J. Senders, John B. Ammori, and Jeffrey M. Hardacre
91 Diagnosis and Management of Gallbladder Cancer�������������������� 365
Joshua L. Lyons, John B. Ammori, and Jeffrey M. Hardacre
92 Choledochal Cysts���������������������������������������������������������������������������� 369
Shreya Gupta, Jeffrey M. Hardacre, and John B. Ammori
93 Cholecystectomy of the Pregnant Patient�������������������������������������� 373
Avi Hameroff and Jaimey M. Pauli

Part XII Pancreas

94 Acute Pancreatitis���������������������������������������������������������������������������� 379

Kayla M. Hartz and Jennifer Maranki
95 Chronic Pancreatitis������������������������������������������������������������������������ 383
Kayla M. Hartz and Jennifer Maranki
96 Pancreas Divisum���������������������������������������������������������������������������� 387
Kayla M. Hartz and Jennifer Maranki
97 Walled-Off Pancreatic Fluid Collections �������������������������������������� 391
Kayla M. Hartz and Jennifer Maranki
98 Periampullary Carcinoma�������������������������������������������������������������� 395
Heidi N. Overton and Matthew J. Weiss
99 Management of Intraductal Papillary Mucinous Neoplasms������ 399
Jonathan G. Sham and Matthew J. Weiss
100 Pancreatic Necrosis�������������������������������������������������������������������������� 403
Ammar Asrar Javed and Matthew J. Weiss
Contents xv

Part XIII Spleen

101 Management of Splenic Abscess ���������������������������������������������������� 409

Andrew T. Bates and Michael G. Svestka
102 Atraumatic Indications for Splenectomy�������������������������������������� 413
Maria S. Altieri and Andrew T. Bates

Part XIV Thyroid/Parathyroid

103 Hypothyroidism�������������������������������������������������������������������������������� 419

Lukasz Czerwonka
104 Hyperthyroidism������������������������������������������������������������������������������ 423
Ewen Chao and Lukasz Czerwonka
105 Thyroiditis���������������������������������������������������������������������������������������� 427
Lukasz Czerwonka
106 Goiter������������������������������������������������������������������������������������������������ 431
Lukasz Czerwonka
107 Thyroid Nodule�������������������������������������������������������������������������������� 435
Melissa Boltz
108 Thyroid Cancer�������������������������������������������������������������������������������� 439
Melissa Boltz
109 Hyperparathyroidism���������������������������������������������������������������������� 443
Melissa Boltz

Part XV Endocrine

110 Cushing’s Syndrome and Disease �������������������������������������������������� 449

Edwina Moore and Vikram D. Krishnamurthy
111 Primary Hyperaldosteronism (Conn’s Syndrome) ���������������������� 453
Iuliana Bobanga, Cassandre Bénay, and Vikram D.
Krishnamurthy
112 Glucagonoma������������������������������������������������������������������������������������ 457
Talia Burneikis and Vikram D. Krishnamurthy
113 Management of Pheochromocytoma���������������������������������������������� 461
Hadley E. Ritter and Benjamin C. James
114 Management of Aldosteronoma������������������������������������������������������ 465
Hadley E. Ritter and Benjamin C. James
115 Management of Gastrinoma ���������������������������������������������������������� 469
Rachel E. Simpson and Benjamin C. James
116 Management of Insulinoma������������������������������������������������������������ 473
Rachel E. Simpson and Benjamin C. James
xvi Contents

117 Management of Somatostatinoma�������������������������������������������������� 477

Rachel E. Simpson and Benjamin C. James
118 Management of VIPoma������������������������������������������������������������������ 481
Rachel E. Simpson and Benjamin C. James

Part XVI Pediatric

119 Congenital Diaphragmatic Hernia ������������������������������������������������ 487

Christopher J. McLaughlin, Rachel E. Hanke,
and Robert E. Cilley
120 Tracheoesophageal Fistula�������������������������������������������������������������� 491
Rachel E. Hanke, Morgan K. Moroi, and Robert E. Cilley
121 Other Diaphragmatic Hernias: Late-Presenting
Bochdalek Hernia, Morgagni Hernia, and Giant
Hiatal Hernia of Infancy ���������������������������������������������������������������� 495
Morgan K. Moroi, Christopher J. McLaughlin,
and Robert E. Cilley
122 Duodenal Obstruction in Newborns���������������������������������������������� 499
Abdulraouf Y. Lamoshi, Sophia Abdulhai,
and Todd A. Ponsky
123 Small Intestinal Atresia ������������������������������������������������������������������ 501
Abdulraouf Y. Lamoshi, Sophia Abdulhai,
and Todd A. Ponsky
124 Management of Malrotation ���������������������������������������������������������� 505
Sophia Abdulhai, Abdulraouf Y. Lamoshi,
and Todd A. Ponsky
125 Management of Imperforate Anus ������������������������������������������������ 509
Sophia Abdulhai and Aaron Garrison
126 Hirschsprung Disease���������������������������������������������������������������������� 513
Rachel E. Hanke, Morgan K. Moroi, and Kathryn Lynn
Martin
127 Pediatric Inguinal Hernia���������������������������������������������������������������� 517
Afif N. Kulaylat and Kathryn Lynn Martin
128 Meconium Ileus�������������������������������������������������������������������������������� 521
Kathryn Lynn Martin and Afif N. Kulaylat
129 Pediatric Intussusception���������������������������������������������������������������� 525
Afif N. Kulaylat and Kathryn Lynn Martin
130 Pyloric Stenosis�������������������������������������������������������������������������������� 529
Dan W. Parrish, Jonathan H. DeAntonio,
and David A. Lanning
131 Necrotizing Enterocolitis ���������������������������������������������������������������� 533
Jonathan H. DeAntonio, Dan W. Parrish,
and David A. Lanning
Contents xvii

132 Omphalocele and Gastroschisis������������������������������������������������������ 537

Jonathan H. DeAntonio, Dan W. Parrish,
and David A. Lanning
133 Biliary Atresia���������������������������������������������������������������������������������� 541
Dan W. Parrish, Jonathan H. DeAntonio,
and David A. Lanning

Part XVII Vascular

134 Carotid Artery Stenosis ������������������������������������������������������������������ 547

Ian Bailey and Faisal Aziz
135 Abdominal Aortic Aneurysm���������������������������������������������������������� 551
Erin K. Greenleaf and Faisal Aziz
136 Ruptured Abdominal Aortic Aneurysm���������������������������������������� 555
Faisal Aziz
137 Aortic Dissection������������������������������������������������������������������������������ 559
Katelynn Ferranti and Faisal Aziz
138 Acute Lower Extremity Ischemia�������������������������������������������������� 565
Afsha Aurshina and Anil Hingorani
139 Chronic Lower Extremity Ischemia ���������������������������������������������� 569
Afsha Aurshina and Anil Hingorani
140 Intermittent Claudication �������������������������������������������������������������� 573
Afsha Aurshina and Anil Hingorani
141 Acute Deep Venous Thrombosis����������������������������������������������������� 577
Afsha Aurshina and Anil Hingorani
142 Management of Acute Mesenteric Ischemia���������������������������������� 581
Josh Radtka
143 Management of Chronic Mesenteric Ischemia������������������������������ 585
Josh Radtka
144 Thoracic Outlet Syndrome�������������������������������������������������������������� 589
Tarik Z. Ali and Josh Radtka
145 AV Shunt Complications ���������������������������������������������������������������� 593
Josh Radtka

Part XVIII Genitourinary

146 Management of the Renal Mass������������������������������������������������������ 597

J. Chris Riney, Neil J. Kocher, and Matthew Kaag
147 Prostate Cancer�������������������������������������������������������������������������������� 601
Rosa Park and Matthew Kaag
148 Management of Scrotal/Testicular Mass���������������������������������������� 605
Brian M. Blair and Matthew Kaag
xviii Contents

149 Diagnosis and Management of Fournier’s Gangrene ������������������ 609

Augustyna Gogoj and Matthew Kaag

Part XIX Trauma

150 Hypotension and Blunt Abdominal Trauma �������������������������������� 615

Cheyenne C. Sonntag and Steven R. Allen
151 Traumatic Brain Injury������������������������������������������������������������������ 619
Shannon R. Kotch and Steven R. Allen
152 Penetrating Neck Trauma �������������������������������������������������������������� 623
Alexis Lauria and Steven R. Allen
153 Penetrating Chest Trauma�������������������������������������������������������������� 627
Melissa Linskey and Steven R. Allen
154 ED Thoracotomy������������������������������������������������������������������������������ 631
Nathan R. Manley and George O. Maish III
155 Blunt Chest Wall Trauma���������������������������������������������������������������� 633
Nathan R. Manley and George O. Maish III
156 Blunt Cardiac Injury ���������������������������������������������������������������������� 637
Nathan R. Manley and George O. Maish III
157 Deceleration Injury: Blunt Aortic Injury�������������������������������������� 641
Nathan R. Manley and George O. Maish III
158 Penetrating Abdominal Trauma ���������������������������������������������������� 645
Michael Smith and Fausto Vinces
159 Blunt Abdominal Trauma��������������������������������������������������������������� 649
Michael Smith and Fausto Vinces
160 Management Algorithm for Acute and Chronic
Diaphragmatic Injuries ������������������������������������������������������������������ 653
Elif Onursal and Fausto Vinces
161 Management of Traumatic Liver Injuries ������������������������������������ 657
Melissa Amberger and Fausto Vinces
162 Management of Pancreatic Trauma ���������������������������������������������� 661
Shreya Jammula and Eric H. Bradburn
163 Management of Traumatic Splenic Injuries���������������������������������� 665
Eric H. Bradburn, Kameron Durante, and Shreya Jammula
164 Management of Kidney and Ureter Injuries �������������������������������� 669
Eric H. Bradburn, Madison Morgan, and Danielle Von Nieda
165 Urethral Trauma������������������������������������������������������������������������������ 675
Cheyenne C. Sonntag and Susan MacDonald
166 Pelvic Fractures�������������������������������������������������������������������������������� 679
Ryan M. Staszak and Lacee Jay Laufenberg
Contents xix

167 Bladder Injuries ������������������������������������������������������������������������������ 683

Ryan M. Staszak and Lacee Jay Laufenberg
168 Rectal Injuries���������������������������������������������������������������������������������� 687
Amanda E. Lee, Karima Fitzgerald, and Lacee Jay Laufenberg
169 Extremity Compartment Syndrome���������������������������������������������� 693
Karima Fitzgerald, Amanda E. Lee, and Lacee Jay Laufenberg

Part XX Critical Care

170 Management of Intracranial Hemorrhage������������������������������������ 701

Ariel P. Santos
171 Airway Management ���������������������������������������������������������������������� 707
Robert S. Schoaps and Sprague W. Hazard III
172 Intubation and Extubation�������������������������������������������������������������� 711
Ariel P. Santos
173 Acute Respiratory Distress Syndrome (ARDS)���������������������������� 719
Dan A. Galvan
174 Management of Sepsis �������������������������������������������������������������������� 723
Jacklyn Engelbart and Luis J. Garcia
175 Management of Shock �������������������������������������������������������������������� 727
Jacklyn Engelbart and Luis J. Garcia
176 Blood Transfusion Indications�������������������������������������������������������� 731
Jacklyn Engelbart and Luis J. Garcia
177 Abdominal Compartment Syndrome�������������������������������������������� 735
Jacklyn Engelbart and Luis J. Garcia
178 Acute Renal Failure ������������������������������������������������������������������������ 739
Kathleen A. Iles and Richard J. King
179 Postoperative Pulmonary Emboli�������������������������������������������������� 743
Kathleen A. Iles and Richard J. King
180 Burns Management�������������������������������������������������������������������������� 747
Kathleen A. Iles and Richard J. King
181 Acid-Base Disorders������������������������������������������������������������������������ 751
Kathleen A. Iles and Richard J. King

Part XXI Electrolytes

182 Hyponatremia���������������������������������������������������������������������������������� 757

Kathryn W. Shaw and Andre A. S. Dick
183 Hypernatremia �������������������������������������������������������������������������������� 761
Kathryn W. Shaw and Andre A. S. Dick
xx Contents

184 Hypokalemia������������������������������������������������������������������������������������ 765

Kathryn W. Shaw and Andre A. S. Dick
185 Hyperkalemia ���������������������������������������������������������������������������������� 767
Kathryn W. Shaw and Andre A. S. Dick
186 Management of Hypocalcemia�������������������������������������������������������� 771
Robert S. Schoaps and Sprague W. Hazard III
187 Management of Hypercalcemia������������������������������������������������������ 775
Robert S. Schoaps and Sprague W. Hazard III
188 Paradoxical Aciduria ���������������������������������������������������������������������� 779
Robert S. Schoaps and Sprague W. Hazard III

Part XXII Hernia

189 Inguinal Hernia�������������������������������������������������������������������������������� 783

Q. Lina Hu and David C. Chen
190 Recurrent Inguinal Hernia�������������������������������������������������������������� 789
Q. Lina Hu and David C. Chen
191 Femoral Hernia�������������������������������������������������������������������������������� 793
Q. Lina Hu and David C. Chen
192 Obturator Hernia���������������������������������������������������������������������������� 797
Q. Lina Hu and David C. Chen
193 Ventral Hernia Repair �������������������������������������������������������������������� 801
Justin A. Doble and Eric M. Pauli
194 Incarcerated and Strangulated Hernia������������������������������������������ 805
Justin A. Doble and Eric M. Pauli
195 Management of Open Abdomen ���������������������������������������������������� 809
Justin A. Doble and Eric M. Pauli
196 Abdominal Wall Reconstruction���������������������������������������������������� 813
Justin A. Doble and Eric M. Pauli

Part XXIII Bariatric Surgery

197 Indications for Bariatric Surgery �������������������������������������������������� 819

Jin Sun Kim and Ann M. Rogers
198 Work-Up of Abdominal Pain in the Bariatric Patient������������������ 821
Sarayna S. McGuire and Ann M. Rogers
199 Internal Hernia: Diagnosis and Treatment������������������������������������ 825
Brandon LaBarge and Ann M. Rogers
200 Marginal Ulcer: Diagnosis and Treatment������������������������������������ 827
Ye Tian and Ann M. Rogers
201 Ventral Hernia Repair in Bariatric Patients �������������������������������� 831
Anish Shah and Salvatore Docimo Jr.
Contents xxi

202 Acute Leak Following Bariatric Surgery: Endoscopic Stent

Management ������������������������������������������������������������������������������������ 835
Salvatore Docimo Jr.
203 Vitamin and Micronutrient Deficiencies After
Bariatric Surgery ���������������������������������������������������������������������������� 839
Salvatore Docimo Jr.

Part XXIV Pregnancy and General Surgery

204 Pregnancy and Cholelithiasis���������������������������������������������������������� 845

Jaimey M. Pauli
205 Pregnancy and Appendicitis������������������������������������������������������������ 849
Emily Smith and Jaimey M. Pauli
206 Pregnancy and Breast Cancer�������������������������������������������������������� 853
James M. O’Brien and Jaimey M. Pauli
207 Pregnancy and Hernia �������������������������������������������������������������������� 857
Jaimey M. Pauli

Index���������������������������������������������������������������������������������������������������������� 861
Contributors

Sophia  Abdulhai, MD Division of Pediatric Surgery, Akron Children’s

Hospital, Akron, OH, USA
Tarik Z. Ali, MD  Division of Vascular Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Steven  R.  Allen, MD Department of Surgery, Penn State Health Milton
S. Hershey Medical Center, Hershey, PA, USA
Vamsi V. Alli, MD  Department of Surgery, Division of Minimally Invasive
and Bariatric Surgery, Penn State Milton S. Hershey Medical Center, Hershey,
PA, USA
Maria  S. Altieri, MD, MS  Department of General Surgery, Stony Brook
University Hospital, Stony Brook, NY, USA
Suraj Alva, MD, FACD, FASCRS  Department of Surgery, Rutgers Robert
Wood Johnson Medical School, Edison, NJ, USA
Melissa  Amberger, DO Department of Surgery, St. Barnabas Health
System, Bronx, NY, USA
John  B.  Ammori, MD Department of Surgery, University Hospitals
Cleveland Medical Center, Cleveland, OH, USA
Afsha Aurshina, MBBS  Department of Vascular Surgery, Vascular Institute
of New York, Brooklyn, NY, USA
Faisal Aziz, MD, FACS  Division of Vascular Surgery, Penn State Heart and
Vascular Institute, Pennsylvania State University College of Medicine,
Hershey, PA, USA
Department of Surgery, Penn State Milton S.  Hershey Medical Center,
Hershey, PA, USA
Ian Bailey, MD  Division of Vascular Surgery, Penn State Heart and Vascular
Institute, Pennsylvania State University College of Medicine, Hershey, PA,
USA
Penn State Health Milton S. Hershey Medical Center, Hershey, PA, USA
Andrew  T.  Bates, MD Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA

xxiii
xxiv Contributors

Cassandre  Bénay, MD, MSc Department of Endocrine Surgery, The

Cleveland Clinic, Cleveland, OH, USA
Brian  M.  Blair, MD  Division of Urology, Penn State Milton S.  Hershey
Medical Center, Hershey, PA, USA
Iuliana  Bobanga, MD Department of Endocrine Surgery, The Cleveland
Clinic, Cleveland, OH, USA
Melissa  Boltz, DO, MBA Department of Surgery, Penn State Hershey
Medical Center, Hershey, PA, USA
Zeynep  Bostanci, MD Breast Surgical Oncology, Ironwood Cancer and
Research Centers, Avondale, AZ, USA
Eric H. Bradburn, DO, MS, FACS  Department of Trauma and Acute Care
Surgery, Penn Medicine Lancaster General Health, Lancaster, PA, USA
Talia  Burneikis, MD Department of Endocrine Surgery, The Cleveland
Clinic, Cleveland, OH, USA
Karla  M.  Chaffee, MD Department of General Surgery, Lenox Hill
Hospital, New York, NY, USA
Chanak  J.  Chantachote, MD Department of Surgery, Stony Brook
University Hospital, Stony Brook, NY, USA
Ewen  Chao, MD Department of Surgery, Division of Otolaryngology  –
Head and Neck Surgery, Stony Brook University Hospital, Stony Brook, NY,
USA
David  C.  Chen, MD Department of Surgery, Lichtenstein Amid Hernia
Clinic at University of California at Los Angeles, Los Angeles, CA, USA
Joanna  Chikwe, MD Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA
Department of Cardiovascular Surgery, Icahn School of Medicine at Mount
Sinai, New York, NY, USA
Bertram T. Chinn, MD  Department of Colon and Rectal Surgery, Rutgers
Robert Wood Johnson Medical School, Edison, NJ, USA
Robert E. Cilley, MD  Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Kristen  T.  Crowell, MD Department of Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
Lukasz  Czerwonka, MD  Department of Surgery, Division of
Otolaryngology – Head and Neck Surgery, Stony Brook University Hospital,
Stony Brook, NY, USA
Jonathan H. DeAntonio, MD  Division of Pediatric Surgery, Department of
General Surgery, Virginia Commonwealth University Health, Richmond, VA,
USA
Contributors xxv

Department of Surgery, Virginia Commonwealth University School of

Medicine, Richmond, VA, USA
Andre A. S. Dick, MD, MPH  Department of Surgery, Section of Pediatric
Transplantation, Seattle Children’s Hospital and University of Washington,
Seattle, WA, USA
Carl J. Dickler, MD  Department of General Surgery, SUNY Stony Brook
University Hospital, Health Sciences Center T19-030, Stony Brook, NY,
USA
Julie  A.  DiSano, MD  Department of General Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
Justin A. Doble, MD  Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Salvatore Docimo Jr., DO, MS  Division of Bariatric, Foregut, and Advanced
Gastrointestinal Surgery, Stony Brook Medicine, Stony Brook, NY, USA
Kameron  Durante  Department of Trauma and Acute Care Surgery, Penn
Medicine Lancaster General Health, Lancaster, PA, USA
Igor G. Elyash, DO  Morristown Surgical Associates, Morristown Medical
Center, Morristown, NJ, USA
Jacklyn  Engelbart, BSE Department of Surgery, University of Iowa
Hospitals and Clinics, Iowa City, IA, USA
Laura  M.  Enomoto, MD Department of Surgery, Program for Liver,
Pancreas, and Foregut Tumors, Penn State College of Medicine, Penn State
Cancer Institute, Hershey, PA, USA
Lillian M. Erdahl, MD, FACS  Department of Surgery, University of Iowa,
Iowa City, IA, USA
Katelynn Ferranti, MD  Division of Vascular Surgery, Penn State Heart and
Vascular Institute, Pennsylvania State University College of Medicine,
Hershey, PA, USA
Department of Vascular Surgery, Penn State Health, Milton S.  Hershey
Medical Center, Hershey, PA, USA
Karima Fitzgerald, MD  Division of Trauma, Acute Care, and Critical Care
Surgery, Penn State Milton S. Hershey Medical Center, Hershey, PA, USA
Dan A. Galvan, MD  Geisinger Holy Spirit Hospital, Harrisburg, PA, USA
Luis  J.  Garcia, MD, FACS Department of Surgery, University of Iowa
Hospitals and Clinics, Iowa City, IA, USA
Aaron  Garrison, MD Division of Pediatric Surgery, Akron Children’s
Hospital, Akron, OH, USA
Georgios  V.  Georgakis, MD, PhD Department of Surgery, Division of
Surgical Oncology, Stony Brook University Hospital, Stony Brook, NY, USA
xxvi Contributors

Augustyna Gogoj, BS  Division of Urology, Penn State Milton S. Hershey

Medical Center, Hershey, PA, USA
Ross F. Goldberg, MD  Creighton University School of Medicine, Phoenix,
AZ, USA
University of Arizona College of Medicine – Phoenix, Phoenix, AZ, USA
Jessica C. Gooch, MD  Department of Surgery, NYU Langone Health, NYU
Perlmutter Cancer Center, New York, NY, USA
Neerav  Goyal, MD, MPH Division of Otolaryngology-Head and Neck
Surgery, Department of Surgery, Penn State Milton S. Hershey Medical
Center, Hershey, PA, USA
Penn State Cancer Institute, Penn State Milton S. Hershey Medical Center,
Hershey, PA, USA
Erin K. Greenleaf, MD, MS  Division of Vascular Surgery, Penn State Heart
and Vascular Institute, Pennsylvania State University College of Medicine,
Hershey, PA, USA
Penn State Milton S. Hershey Medical Center, Hershey, PA, USA
Shreya Gupta, MD  Department of Surgery, University Hospitals Cleveland
Medical Center, Cleveland, OH, USA
Niraj  J.  Gusani, MD, MS, FACS Department of Surgery, Program for
Liver, Pancreas, and Foregut Tumors, Penn State College of Medicine, Penn
State Cancer Institute, Hershey, PA, USA
Caitlin A. Halbert, DO  Advanced GI and Bariatric Surgery, Department of
General Surgery, Christiana Care Health System, Newark, DE, USA
Avi Hameroff, MD  Maternal Fetal Medicine, Department of Obstetrics and
Gynecology, Penn State Health Milton S. Hershey Medical Center, Hershey,
PA, USA
Rachel E. Hanke, MD  Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Jeffrey  M.  Hardacre, MD Department of Surgery, University Hospitals
Cleveland Medical Center, Cleveland, OH, USA
Kayla  M.  Hartz, BA Edward Via College of Osteopathic Medicine,
Blacksburg, PA, USA
Quinton  Morrow  Hatch, MD Department of Surgery, Madigan Army
Medical Center, Tacoma, WA, USA
Sprague  W.  Hazard III, MD Department of Anesthesiology and
Perioperative Medicine, Penn State Hershey Medical Center, Hershey, PA,
USA
Anil Hingorani, MD, FACS  Division of Vascular Services, NYU Langone
Hospital-Brooklyn, Brooklyn, NY, USA
Contributors xxvii

Q. Lina Hu, MD  Department of Surgery, David Geffen School of Medicine

at University of California, Los Angeles, Los Angeles, CA, USA
Emily Huang, MD, MA Ed  Department of Surgery, University of Chicago,
Chicago, IL, USA
Kathleen  A.  Iles, MD SUNY Upstate Medical University College of
Medicine, Syracuse, NY, USA
Department of Surgery, University of North Carolina Hospitals, Chapel Hill,
NC, USA
Benjamin  C.  James, MD, MS Department of Surgery, Harvard Medical
School, Boston, MA, USA
Department of Surgery, Beth Israel Deaconess Medical Center, Boston, MA,
USA
Shreya Jammula, BS  Department of Trauma and Acute Care Surgery, Penn
Medicine Lancaster General Health, Lancaster, PA, USA
Ammar Asrar Javed, MD  Department of Surgery, Johns Hopkins Hospital,
Baltimore, MD, USA
Eric K. Johnson, MD  Cleveland Clinic Foundation, Cleveland, OH, USA
Department of Surgery, Division of Colorectal Surgery, Hillcrest Hospital,
Mayfield Heights, OH, USA
Ryan M. Juza, MD  Department of Surgery, Division of Minimally Invasive
and Bariatric Surgery, Penn State Milton S. Hershey Medical Center, Hershey,
PA, USA
Matthew  Kaag, MD  Division of Urology, Penn State Milton S.  Hershey
Medical Center, Hershey, PA, USA
Jin Sun Kim, BS, BA  Pennsylvania State University College of Medicine,
Hershey, PA, USA
Richard  J.  King, MD, FACS Department of Surgery, SUNY Upstate
Medical University, Syracuse, NY, USA
Neil  J.  Kocher, MD Division of Urology, Penn State Milton S.  Hershey
Medical Center, Hershey, PA, USA
Shannon R. Kotch, MD  Department of General Surgery, Penn State Health
Milton S. Hershey Medical Center, Hershey, PA, USA
Vikram  D.  Krishnamurthy, MD  Department of Endocrine Surgery, The
Cleveland Clinic, Cleveland, OH, USA
Laura  Kruper, MD, MSCE Breast Surgical Oncology, Department of
Surgery, City of Hope Hospital, Duarte, CA, USA
John  Kuckelman, DO Department of General Surgery, Madigan Army
Medical Center, Tacoma, WA, USA
Uniformed Services University of the Health Sciences, Bethesda, MD, USA
xxviii Contributors

Afif N. Kulaylat, MD, MSc  Department of Surgery, Division of Pediatric

Surgery, Penn State Milton S. Hershey Medical Center, Hershey, PA, USA
Audrey  S.  Kulaylat, MD Department of Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
Brandon  LaBarge, BA Department of Surgery, Penn State College of
Medicine, Penn State Milton S. Hershey Medical Center, Hershey, PA, USA
Wanda Lam, MD  Department of Surgery, University Hospitals Cleveland
Medical Center, Cleveland, OH, USA
Abdulraouf Y. Lamoshi, MD, MPH, CTS, ABPS, MS  Division of Pediatric
Surgery, Akron Children’s Hospital, Akron, OH, USA
David A. Lanning, MD, PhD  Division of Pediatric Surgery, Department of
General Surgery, Virginia Commonwealth University Health, Richmond, VA,
USA
Department of Surgery and Pediatrics, Children’s Hospital of Richmond,
Richmond, VA, USA
Department of Surgery, Virginia Commonwealth University School of
Medicine, Richmond, VA, USA
Alexis Lauria, MD  Department of Surgery, Walter Reed National Military
Medical Center, Bethesda, MD, USA
Lacee Jay Laufenberg, MD  Department of Surgery, Division of Trauma,
Acute Care, and Critical Care Surgery, Penn State Milton S. Hershey Medical
Center, Hershey, PA, USA
Calvin H. L. Law, MD, MPH, FRCSC  Department of Surgical Oncology,
Sunnybrook Health Sciences Centre, Toronto, ON, Canada
Amanda E. Lee, MD  Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Melissa  Linskey, MD Department of Surgery, Penn State Health Milton
S. Hershey Medical Center, Hershey, PA, USA
Joshua  L.  Lyons, MD Department of Surgery, University Hospitals
Cleveland Medical Center, Cleveland, OH, USA
George O. Maish III, MD  Department of Surgery, University of Tennessee
Health Science Center, Memphis, TN, USA
Nathan  R.  Manley, MD, MPH Department of Surgery, University of
Tennessee Health Science Center, Memphis, TN, USA
Jennifer  Maranki, MD, MSc Department of Gastroenterology and
Hepatology, Penn State Milton S.  Hershey Medical Center, Hershey, PA,
USA
Contributors xxix

Jeffrey M. Marks, MD, FACS, FASGE  Department of Surgery, University

Hospitals Cleveland Medical Center, Cleveland, OH, USA
Kathryn Lynn Martin, MD, FRCSC  Department of Surgery, Division of
Pediatric Surgery, Penn State Milton S.  Hershey Medical Center, Hershey,
PA, USA
Michael  F.  McGee, MD, FACS, FASCRS Department of Surgery,
Northwestern Memorial Hospital, Chicago, IL, USA
Sarayna  S.  McGuire, BS Department of Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
Susan MacDonald, MD  Division of Urology, Department of Surgery, Penn
State Milton S. Hershey Medical Center, Hershey, PA, USA
Christopher  J.  McLaughlin, MD Department of Surgery, Penn State
Milton S. Hershey Medical Center, Hershey, PA, USA
Evangelos Messaris, MD, PhD, FACS, FASCRS  Department of Surgery,
Penn State Milton S. Hershey Medical Center, Hershey, PA, USA
Division of Colon and Rectal Surgery, Beth Israel Medical Center, Harvard
Medical Center, Boston, MA, USA
Maria Michailidou  Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Neal M. Mineyev, MD  Department of General Surgery, Lenox Hill Hospital,
New York, NY, USA
Katelin  A.  Mirkin, MD Department of Surgery, Program for Liver,
Pancreas, and Foregut Tumors, Penn State College of Medicine, Penn State
Cancer Institute, Hershey, PA, USA
Edwina  Moore, MD Department of Endocrine Surgery, The Cleveland
Clinic, Cleveland, OH, USA
Madison  Morgan Department of Trauma and Acute Care Surgery, Penn
Medicine Lancaster General Health, Lancaster, PA, USA
Morgan K. Moroi, BS  Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Ruel Neupane, MD  Department of Surgery, University Hospitals Cleveland
Medical Center, Cleveland, OH, USA
Joseph R. Notaro, MD, FACS, FASCRS  Department of Surgery, Rutgers
Robert Wood Johnson Medical School, New Brunswick, NJ, USA
James M. O’Brien, MD  Maternal Fetal Medicine, Department of Obstetrics
and Gynecology, Penn State Health, Milton S.  Hershey Medical Center,
Hershey, PA, USA
xxx Contributors

Elif  Onursal, DO, MS Department of General Surgery, St. Barnabas

Hospital Health System, Bronx, NY, USA
Heidi  N.  Overton, MD  Department of Surgery, Johns Hopkins Hospital,
Baltimore, MD, USA
Colette  R.  Pameijer, MD Department of General Surgery, Penn State
Milton S. Hershey Medical Center, Hershey, PA, USA
Rosa Park, MD  Division of Urology, Penn State Milton S. Hershey Medical
Center, Hershey, PA, USA
Dan W. Parrish, MD  Department of Pediatric Surgery, Batson Children’s
Hospital, University of Mississippi Medical Center, Jackson, MS, USA
Albert G. Pavalonis, DO  Department of Vascular Surgery, NYU Langone
Hospital-Brooklyn, Brooklyn, NY, USA
Eric  M.  Pauli, MD, FACS, FASGE Department of Surgery, Penn State
Milton S. Hershey Medical Center, Hershey, PA, USA
Jaimey M. Pauli, MD  Maternal-Fetal Medicine, Department of Obstetrics
and Gynecology, Penn State Health Milton S. Hershey Medical Center,
Hershey, PA, USA
Todd A. Ponsky, MD, FACS  Division of Pediatric Surgery, Akron Children’s
Hospital, Akron, OH, USA
Josh  Radtka, MD Division of Vascular Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
J.  Chris  Riney, MD Division of Urology, Penn State Milton S.  Hershey
Medical Center, Hershey, PA, USA
Michele A. Riordon, MD, FRCSC  Department of Surgery, Royal Victoria
Regional Health Centre, Barrie, ON, Canada
Hadley  E.  Ritter, MD Department of Surgery, Indiana University,
Indianapolis, IN, USA
Ann M. Rogers, MD  Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
William Sangster, MD  Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Ariel P. Santos, MD, MPH, FRCSC, FACS  Department of Surgery, Texas
Tech University Health Sciences Center, Lubbock, TX, USA
Samer  Sbayi, MD, MBA, FACS Department of General Surgery, Stony
Brook University Hospital, Stony Brook, NY, USA
Freya Schnabel, MD  Department of Surgery, NYU Langone Health, NYU
Perlmutter Cancer Center, New York, NY, USA
Robert S. Schoaps, MD  Department of Anesthesiology and Perioperative
Medicine, Penn State Hershey Medical Center, Hershey, PA, USA
Contributors xxxi

Zachary  J.  Senders, MD Department of Surgery, University Hospitals

Cleveland Medical Center, Cleveland, OH, USA
Anish Shah, MD  Department of Surgery, Stony Brook University Hospital,
Stony Brook, NY, USA
Jonathan G. Sham, MD  Department of Surgery, Johns Hopkins Hospital,
Baltimore, MD, USA
Kathryn  W.  Shaw, MD Department of Surgery, Division of Transplant
Surgery, University of Washington Medical Center, Seattle, WA, USA
Tom  Shokri, MD Division of Otolaryngology-Head and Neck Surgery,
Department of Surgery, Penn State Milton S.  Hershey Medical Center,
Hershey, PA, USA
Laila  Siddique, BA  Division of Otolaryngology-Head and Neck Surgery,
Department of Surgery, Penn State Milton S. Hershey Medical Center,
Hershey, PA, USA
Department of Otolaryngology-Head and Neck Surgery, University of Miami
Miller School of Medicine, Miami, FL, USA
Rachel  E.  Simpson, MD Department of Surgery, Indiana University,
Indianapolis, IN, USA
Jasvinder Singh, MD  Department of Surgery, Program for Liver, Pancreas,
and Foregut Tumors, Penn State College of Medicine, Penn State Cancer
Institute, Hershey, PA, USA
Emily Smith, MD  Maternal-Fetal Medicine, Department of Obstetrics and
Gynecology, Medical College of Wisconsin, Milwaukee, WI, USA
Michael  Smith, DO  Department of Surgery, Westchester Medical Center,
Valhalla, NY, USA
Cheyenne C. Sonntag, MD, MS  Department of Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
Konstantinos  Spaniolas, MD Department of Surgery, Stony Brook
University Hospital, Stony Brook, NY, USA
Ryan M. Staszak, MD  Department of Surgery, Division of Trauma, Acute
Care, and Critical Care Surgery, Penn State Milton S.  Hershey Medical
Center, Hershey, PA, USA
David B. Stewart Jr., MD, FACS, FASCRS  Department of Surgery, Banner
University Medical Center – Tucson, Tucson, AZ, USA
Michael G. Svestka, MD  Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA
Henry  Tannous, MD Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA
Department of Cardiovascular Surgery, Icahn School of Medicine at Mount
Sinai, New York, NY, USA
xxxii Contributors

Anthony  R.  Tascone, MD Department of General Surgery, Saint Luke’s

Health System, Kansas City, MO, USA
Matthew D. Taylor, MD  Department of Surgery, Penn State Health Milton
S. Hershey Medical Center, Hershey, PA, USA
Division of Thoracic Surgery, Penn State Health Milton S. Hershey Medical
Center, Hershey, PA, USA
Ye Tian, BA  Penn State Health Milton S. Hershey Medical Center, Hershey,
PA, USA
Anjali  R.  Thawani, MD Division of Surgical Oncology, AMITA Health
System, Elk Grove Village, IL, USA
Scott C. Tiedebohl, MD  Department of Surgery, Penn State Health Milton
S. Hershey Medical Center, Hershey, PA, USA
Division of Thoracic Surgery, Penn State Health Milton S. Hershey Medical
Center, Hershey, PA, USA
Joel VanderVelde, MD  Department of Surgery, Maricopa Integrated Health
System, Phoenix, AZ, USA
Fausto Vinces, DO, FACS, FICS  Department of Surgery, Vassar Brothers
Medical Center, Poughkeepsie, NY, USA
Danielle Von Nieda  Department of Trauma and Acute Care Surgery, Penn
Medicine Lancaster General Health, Lancaster, PA, USA
Matthew  J.  Weiss, MD  Department of Surgery, Johns Hopkins Hospital,
Baltimore, MD, USA
Kirsten  Bass  Wilkins, MD, FACS, FASCRS Department of Surgery,
Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ, USA
Matthew  Z.  Wilson, MD, MSc Department of Surgery, Dartmouth
Hitchcock Medical Center, One Medical Center Drive, Lebanon, NH, USA
Christina  L.  Wolchok, DO Graduate Medical Education, Department of
General Surgery, Stony Brook University Hospital, Stony Brook, NY, USA
Joyce  Wong, MD Department of General Surgery, Lenox Hill Hospital,
New York, NY, USA
Maroun  B.  Yammine, MD  Department of Cardiovascular Surgery, Icahn
School of Medicine at Mount Sinai, New York, NY, USA
 Part I
Skin and Soft Tissue
 Management of Cutaneous
Melanoma
Julie A. DiSano and Colette R. Pameijer
Algorithmic Approach
A. The history and physical examination should
include risk factors for melanoma and family
history. The lesion should be evaluated by the
ABCDE criteria: A, asymmetry; B, borders;
C, color; D, diameter; E, evolution. If the
lesion meets any one of these criteria, it
should be biopsied.
B. Key pathologic criteria that impact stage and
treatment include depth, ulceration, mitotic rate,
and satellitosis. Lesions ≤ 0.8 mm deep without
ulceration or mitoses are considered low-risk
lesions. These patients should undergo wide
local excision (WLE) with a 1 cm margin. There
is no consensus regarding high-risk features in a
thin melanoma.*
C. High-risk lesions should undergo WLE with a
1–2 cm margin and sentinel lymph node biopsy.
Sentinel lymph node biopsy should consist of
preoperative lymphoscintigraphy and intraop-
erative use of gamma probe with or without
vital blue dye injection, followed by meticu-
lous pathologic exam of sentinel lymph node.
D. If the sentinel node is positive for malignancy,
the patient should undergo staging workup,
including either a CT of the chest, abdomen,
J. A. DiSano · C. R. Pameijer (*)
Department of General Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: cpameijer@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_1
1
and pelvis with IV contrast or full body PET/
CT, and consider brain MRI.  If there is evi-
dence of metastasis, the patient should consider
systemic therapy or a clinical trial. If there is no
evidence of metastasis, the patient should be
offered a completion lymphadenectomy and
consider systemic therapy or a clinical trial.
E. If at the time of diagnosis there is suspicion for
metastatic disease or palpable lymph nodes on
exam, the patient should undergo staging
imaging including either a CT chest, abdomen,
pelvis with IV contrast or a full body PET/CT
as well as fine needle aspiration or core biopsy
of suspicious nodes. If the disease is contained
in the nodes, the patient should undergo wide
local excision with lymph node dissection and
be considered for systemic therapy or a clinical
trial postoperatively. If the disease is meta-
static at the time of diagnosis, the patient
should receive systemic therapy or enroll in a
clinical trial. Limited metastatic disease may
be resected in carefully selected patients.
F. Follow-up care: Patient should have a com-
plete skin exam every 3–12  months for the
first 5  years and at least annually for life.
Imaging should be performed for signs or
symptoms of metastasis in any patient and
considered every 3–12 months for 3 years for
stage IIB-IV. Patient should be educated about
sun protection and self-examination.
*NCCN should be visited regularly for updated
guidelines.
3
4 J. A. DiSano and C. R. Pameijer

• History and Physical Exam: pigmented cutaneous lesion

A • Complete skin exam and nodal exam
• Biopsy

Primary Melanoma with

melanoma suspicion of mets,
palpable LN E

B
• Staging imaging
Low High or • FNA/core biopsy of suspicious
WLE with low nodes or metastatic lesions
1 cm margin risk?

C High Metastatic Regional

disease disease

WLE with 1-2 cm margin and

sentinel lymph node biopsy Systemic chemotherapy WLE and
or clinical trial lymph node dissection

Consider systemic
Sentinel node Sentinel node chemotherapy or
negative for positive for
malignancy malignancy
D clinical trial

Staging imaging

Regional Metastatic
disease disease

Completion Consider systemic chemotherapy

lymphadenectomy or clinical trial

Follow-up care: Regular complete skin exam and sun protection education F

Algorithm 1.1

Suggested Reading
National Comprehensive Cancer Network. NCCN clinical
practice guidelines in oncology: melanoma (version
1.2017). https://www.nccn.org/professionals/physi-
cian_gls/pdf/melanoma.pdf. Accessed 17 July 2017.
 Basal Cell Carcinoma
Julie A. DiSano and Colette R. Pameijer
Algorithmic Approach
A. The first step in the evaluation of a patient
with a suspicious skin lesion is the history
and physical examination. The typical appear-
ance of basal cell carcinoma is a pearly, flesh-­
colored bump on sun-exposed skin. A
complete skin exam should be performed as
well as a nodal exam. The lesion should be
biopsied; lymph nodes should only be biop-
sied if palpable on exam.
B. Once diagnosis of basal cell carcinoma is
established, surgical excision is the treatment E. Patients with high-risk lesions should be con-
of choice. The choice of Mohs micrographic
surgery or surgical excision is based on size,
location, cosmesis, and patient comorbidities.
Excision should achieve at least a 4  mm
margin.
C. If the lesion is not able to be excised, the
patient should undergo radiation therapy.
Treatment with a hedgehog pathway inhibitor
(vismodegib or sonidegib) can be considered.
J. A. DiSano · C. R. Pameijer (*)
Department of General Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: cpameijer@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_2
2
D. The lesion should be risk stratified to deter-
mine if there is a high risk or low risk for recur-
rence. High-risk lesions have any of the
following features: Location on mask areas of
the face, genitalia, hands, or feet; lesion greater
than 20 mm on the trunk or extremities; lesion
greater than 10 mm on the cheeks, forehead,
scalp, neck, and feet; poorly defined borders;
recurrent disease; patient on immunosuppres-
sion; lesion at the site of prior radiation ther-
apy; perineural involvement; and pathology
showing aggressive growth pattern.
sidered for further treatment with radiation
therapy. Addition of a hedgehog pathway
inhibitor (vismodegib or sonidegib) should
also be considered.
F. Follow-up care: Patient should have a com-
plete skin exam every 6–12  months for the
first 5  years and at least annually for life.
Patient should be educated about sun protec-
tion and self-examination.
5
6 J. A. DiSano and C. R. Pameijer

History and Physical Exam:

Suspicious skin lesion

A
• Complete skin exam and nodal exam
• Biopsy

Basal Cell
Carcinoma

Candidate No Consider radiation therapy or

B for surgical hedgehog pathway inhibitor
excision?

Yes

Surgical excision
+/- Mohs

High or
D low High risk
risk?

Low risk Consider radiation therapy or

hedgehog pathway inhibitor

Follow-up care: Regular complete skin exam

F and sun protection education

Algorithm 2.1

Suggested Reading
National Comprehensive Cancer Network. NCCN clinical
practice guidelines in oncology: basal cell skin cancer
(version 1.2017). https://www.nccn.org/professionals/
physician_gls/pdf/nmsc.pdf. Accessed 17 July 2017.
 Squamous Cell Carcinoma
Julie A. DiSano and Colette R. Pameijer
Algorithmic Approach
A. The typical appearance of squamous cell car-
cinoma is an ulcerated cutaneous lesion. A
complete skin exam should be performed as
well as a nodal exam. The lesion should be
biopsied.
B. Any palpable lymph nodes should be further
evaluated with fine needle aspiration or core
needle biopsy. If the nodes are positive for
malignancy, a staging CT of the chest, abdo-
men, and pelvis should be done. If disease is
limited to the regional lymph nodes, the
patient should have wide excision of the pri-
mary site and lymphadenectomy.
C. If there are no palpable nodes or the node
biopsy shows no evidence of malignancy, sur-
gical excision should be performed. If the
lesion is amenable to excision (based on size,
location, patient comorbidities, cosmesis, and
need for reconstruction), it should be excised
with 4–6  mm margins. If margins are posi-
tive, patient should undergo Mohs micro-
graphic surgery to achieve negative margins.
J. A. DiSano · C. R. Pameijer (*)
Department of General Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: cpameijer@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_3
3
If excision is not possible, the patient should
undergo radiation therapy with or without
systemic chemotherapy.
D. The lesion should be risk stratified to deter-
mine risk of recurrence. High-risk lesions
have any of the following features: Location
on mask areas of the face, genitalia, hands, or
feet; lesion greater than 20  mm on trunk or
extremities; lesion greater than 10 mm on the
cheeks, forehead, scalp, neck, and feet; poorly
defined borders; recurrent disease; patient is
immunosuppressed; lesion at site of prior
radiation therapy or chronic inflammation;
perineural or lymphovascular involvement;
and lesion with greater than 2 mm depth.
E. Patients with high-risk lesions should be con-
sidered for further treatment with radiation
therapy.
F. Follow-up care: Patients should have a com-
plete skin exam every 3–12  months for the
first 2  years, then every 6–12  months for
3 years, and at least annually for life. Patient
should be educated about sun protection and
self-examination.
7
8 J. A. DiSano and C. R. Pameijer

History and Physical Exam:

Skin lesion that is ulcerated.

A
· Complete skin exam and nodal exam
· Biopsy

Squamous cell
carcinoma

Palpable Yes FNA or core needle

nodes? biopsy of node

No

Benign Malignant
C

No Candidate
Consider radiation Staging CT
for surgical
therapy Excision of primary and
excision?
lymph node dissection if
limited to regional disease.

Yes

High or
D low High risk
risk?
E

Consider radiation therapy

Low risk

Follow-up care: Regular complete skin exam

F and sun protection education

Algorithm 3.1

Suggested Reading
National Comprehensive Cancer Network. NCCN clinical
practice guidelines in oncology: squamous cell skin
cancer (version 1.2017). https://www.nccn.org/pro-
fessionals/physician_gls/pdf/squamous.pdf. Accessed
17 July 2017.
 Management of Soft Tissue
Sarcoma
Julie A. DiSano and Colette R. Pameijer
Algorithmic Approach
A. Patients with sarcoma typically present with a
painless mass that is increasing in size. The
history obtained from the patient should
include duration of mass, changes over time,
symptoms related to the mass, and any his-
tory of radiation to the area. Patients often
report a history of trauma, which is not caus-
ative but likely draws attention to the area.
B. Imaging of the lesion should be obtained with
either MRI or CT scan. Biopsy should be
obtained to establish histologic subtype and
grade. Percutaneous biopsy is acceptable.
Patients should undergo chest imaging for
staging with either chest X-ray or CT.
C. Once the diagnosis of sarcoma is estab-
lished, it should be determined if the lesion
is low or high grade and if it is resectable.
Patients with rhabdomyosarcoma should be
referred to a specialty center for further
management. Patients with unresectable
tumors, desmoid tumors, or Ewing’s sar-
coma should be referred for chemotherapy
and/or radiation. Following treatment, they
J. A. DiSano · C. R. Pameijer (*)
Department of General Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: cpameijer@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_4
4
should be reassessed for possible resection
based on their response to treatment.
D. Patients with low-grade or resectable tumors
should undergo margin-negative resection.
The biopsy site should be resected en bloc with
the surgical specimen. Postoperative radiation
therapy should be considered based on the
tumor grade, size, and margin status. Positive
margins should be re-excised if possible.
E. Patients with high-grade or borderline resectable
tumors should undergo neoadjuvant therapy
prior to resection; this can consist of radiation,
chemotherapy, or both. Following treatment,
they should be reassessed with imaging, and a
margin-negative resection should be performed
if possible. Attempts should be made to spare
limb function if possible. After resection, con-
sider further therapy with radiation or chemo-
therapy, depending on preoperative treatment.
F. Follow-up care: Patients should be followed
with complete history and physical every
3–6  months for 3–5  years. They should
undergo surveillance with local imaging of
the primary site as well as chest imaging for
evidence of metastasis.
9
10 J. A. DiSano and C. R. Pameijer

History and Physical Exam:

A Painless mass, increasing in size.

B · Imaging with MRI or CT

· Image guided biopsy

C Refer to
Sarcoma Rhabdomyosarcoma
specialty center

D E

· Low grade · High grade · Unresectable

· Resectable · Borderline resectable · Desmoid
· Ewings

Margin negative Neoadjuvant

Systemic chemotherapy
resection therapy
and radiation

Consider radiation Reassess with Consider resection based

therapy imaging (MRI/CT) on response to treatment

Margin negative
resection

Follow-up Care:
F Local imaging of primary site
and chest imaging

Algorithm 4.1

Suggested Reading
National Comprehensive Cancer Network. NCCN clini-
cal practice guidelines in oncology: sarcoma (version
1.2017). https://www.nccn.org/professionals/physi-
cian_gls/pdf/sarcoma.pdf. Accessed 17 July 2017.
 Necrotizing Soft Tissue Infection
Julie A. DiSano and Colette R. Pameijer
Algorithmic Approach
A. Patients with necrotizing soft tissue infec-
tions (NSTI) will often have a history of
obesity, diabetes, immunosuppression, or
recent surgery or trauma. A hallmark is
pain out of proportion to the physical exam
findings. They may have fever, tense edema,
bullae, ecchymosis or necrosis of the skin,
cutaneous anesthesia, and evidence of sys-
temic toxicity. NSTIs most commonly
involve the extremities, perineum, and gen-
italia [1, 2].
B. Laboratory analysis should include a CBC,
complete metabolic panel, and CRP.  The
LRINEC (laboratory risk indicatory for nec-
rotizing fasciitis) can aid in decision-making.
This score includes WBC (1 point for WBC
15–25, 2 points for WBC >25), hemoglobin
(1 point for Hgb 11–13.5, 2 points for Hgb
<11), CRP (4 points for CRP ≥150), sodium
(2 points for Na <135), glucose (1 point for
glucose >180), and creatinine (2 points for
Cre >1.6). If the LRINEC score is ≥6, there is
a high likelihood of NSTI [3].
C. The patient should be appropriately resusci-
tated. NSTIs are often polymicrobial, and the
J. A. DiSano · C. R. Pameijer (*)
Department of General Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: cpameijer@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_5
5
patient should be started on broad-spectrum
antibiotics, including coverage for gram-­
positive cocci, gram-negative rods, and anaer-
obes, including clostridial species (penicillin
G, vancomycin, gentamicin, clindamycin).
NSTI is a surgical emergency, and nonopera-
tive management is associated with almost
100% mortality [4]. Excision should extend
to healthy, bleeding tissue at all margins and
tissue should be sent for culture.
D. Patients typically require ongoing critical
care support after surgery, including resusci-
tation, broad-spectrum antibiotics, and man-
agement of comorbidities. They should return
to the operating room within 24 h for further
evaluation, and debridement if necessary.
Patients with necrotizing soft tissue infec-
tions will likely require serial debridement
with most patients requiring 3–4 operative
debridements.
E. Patients with lower index of suspicion can be
evaluated by bedside debridement. If the sur-
geon is easily able to slide a finger along the
fascial plane and finds evidence of necrotic
tissue or “dish water fluid” on bedside I&D,
the patient should be taken to the OR for sur-
gical debridement.
F. Follow-up care: Patients will require a multi-
disciplinary team to aid in recovery. They will
require rehabilitation, wound management,
and possible flap coverage.
11
12 J. A. DiSano and C. R. Pameijer

History:
A Pain, cellulitis, history of obesity, diabetes, or
immunosuppression.

Obtain vital signs, blood work, and perform physical exam

Calculate LRINEC score

B

Yes
OR for debridement
C
High
suspicion
for NSTI?
D
Yes

No

Broad, spectrum antibiotics,

resuscitation, serial
debridement
E Bedside I&D
reveals
NSTI?

No

Broad, spectrum antibiotics,

IVF resuscitation, close
observation

Follow-up Care: Wound management, flap coverage,

F and rehabilitation

Algorithm 5.1
5  Necrotizing Soft Tissue Infection 13

References PubMed PMID: 25069713; PubMed Central PMCID:

PMCPMC4199388.
3. Wong CH, Khin LW, Heng KS, Tan KC, Low
1. Bonne SL, Kadri SS. Evaluation and management of
CO.  The LRINEC (laboratory risk indicator for
necrotizing soft tissue infections. Infect Dis Clin N
necrotizing fasciitis) score: a tool for distinguishing
Am. 2017;31(3):497–511. https://doi.org/10.1016/j.
necrotizing ­fasciitis from other soft tissue infections.
idc.2017.05.011.
Crit Care Med. 2004;32(7):1535–41. PubMed PMID:
2. Hakkarainen TW, Kopari NM, Pham TN, Evans
15241098.
HL.  Necrotizing soft tissue infections: review and
4. Anaya DA, Dellinger EP.  Necrotizing soft-tissue
current concepts in treatment, systems of care, and
infection:diagnosis and management. Clin Infect Dis.
outcomes. Curr Probl Surg. 2014;51(8):344–62.
2007;44(5):705. Pubmed PMID: 17278065.
https://doi.org/10.1067/j.cpsurg.2014.06.001.
 Part II
Head and Neck
 Management of Squamous Cell
Carcinoma of the Oropharynx
Laila Siddique, Tom Shokri, and Neerav Goyal
Algorithmic Approach
A. The first step in the evaluation of a patient with
suspected oropharyngeal squamous cell carci-
noma (OPSCC) is the history and physical
examination. Questions regarding the presence
of dysphagia, odynophagia, oral bleeding,
otalgia, change in speech, airway compromise,
B symptoms, and use of tobacco or alcohol
raise clinical suspicion for malignancy. A sex-
ual history should be obtained to assess the
likelihood of HPV-associated OPSCC [1].
B. A thorough physical exam involves inspection
and palpation of the soft palate, tonsils, base of
L. Siddique
Division of Otolaryngology-Head and Neck Surgery,
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Department of Otolaryngology-Head and Neck
D. Definitive diagnosis requires histopathologi-
Surgery, University of Miami Miller School of
Medicine, Miami, FL, USA
e-mail: laila.siddique@jhsmiami.org
T. Shokri
Division of Otolaryngology-Head and Neck Surgery,
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
N. Goyal (*)
Division of Otolaryngology-Head and Neck Surgery,
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Penn State Cancer Institute, Penn State Milton
S. Hershey Medical Center​, Hershey, PA, USA
e-mail: ngoyal1@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_6
6
tongue, and posterior oropharyngeal wall.
Lesions may appear exophytic, flat, ulcerated,
verrucoid, or papillary. Fiberoptic endoscopy
should be performed in the office to visualize
the extent of the lesion or to search for syn-
chronous lesions. Cranial nerve IX-XII func-
tion should be assessed for possible neurotropic
involvement and palpation of the neck should
be performed for irregular lymph nodes [1].
C. Patients with clinical findings suspicious for
OPSCC should undergo a contrast-
enhanced CT or MRI of the head and neck
for precise evaluation, staging, and treat-
ment planning [2]. Patients with lymph
node irregularities and an unknown primary
lesion should first undergo an ultrasound-
guided fine needle aspiration of the node,
followed by imaging if the results are posi-
tive for malignancy [3].
cal evaluation of a tissue sample. Biopsies of
the tonsil and soft palate can be performed in
the office, whereas difficult to reach regions
may require rigid endoscopy under general
anesthesia for biopsy [1, 4].
E. Once the diagnosis of OPSCC is confirmed and
staged, PET/CT or chest CT should be per-
formed to evaluate for metastatic disease [5]
and stage-dependent treatment discussed with
a head and neck surgeon, including s­urgical
resection with possible reconstruction, radio-
therapy, and/or chemotherapy [1, 6].
17
18 L. Siddique et al.

F. Postoperative maintenance of the three major initiated. A temporary tracheotomy may

functions of the oropharynx (swallowing,
speech, and airway) is vital. Nasogastric
tubes can be used for feeding in smaller
defects (with an expected temporary need),
gastrostomy tube feeding with larger defects,
and those requiring adjuvant radiotherapy.
Swallow and speech rehabilitation should be
rarely be required to maintain a patent air-
way. All patients should maintain adequate
oral hygiene with regular suctioning and use
of antiseptic mouthwashes. Patients should
regularly be monitored for detection of pos-
sible recurrence and subsequent early inter-
vention [1].

A History and Physical Exam:

Dysphagia, odynophagia, bleeding, otalgia, and change in speech
Social Hx: alcohol, tobacco, sexual history

Inspection and palpation of soft palate, tonsils, base of tongue, posterior oropharyngeal wall,
+/- Flexible fiberoptic endoscopy, cranial nerve exam IX-XII, bimanual palpation of neck for lymphadenopathy

Suspicious lesion Irregular lymph node with

+/- lymphadenopathy unknown primary

Ultrasound-guided FNA:
Suspicious for malignancy

C CT/MRI of the head and neck for evaluation, staging, and treatment planning

Does tumor
invade local
structures?
Do neck lymph
nodes enhance?

D Biopsy primary lesion in the office or with rigid endoscopy under anesthesia

Diagnosis of Oropharyngeal
SCC E

T1-T2 (cancer </= 4 cm) T3-T4a ( >4 cm-local invasion) Unresectable (T4b +)
or or or

1º resection, Radiotherapy 1º resection,

Chemoradiation Chemoradiation Palliation
selective ND +/- chemo bilateral ND

RT +/- chemo Salvage surgery RT +/- chemo

if high risk if high risk

Follow-up: Oral hygiene, NG /G-tube, speech rehab, +/-tracheostomy, and regular follow-up F

Algorithm 6.1
6  Management of Squamous Cell Carcinoma of the Oropharynx 19

References 4. Lewis JS, Thorstad WL, Chernock RD, et  al. p16
positive oropharyngeal squamous cell carcinoma:
an entity with a favorable prognosis regard-
1. Flint PW, Cummings WC.  Malignant neoplasms of
less of tumor HPV status. Am J Surg Pathol.
the oropharynx. In: Cummings otolaryngology: head
2010;34(8):1088–96.
and neck surgery. Philadelphia: Elsevier, Saunders;
5. Quon A, Fischbein NJ, McDougall IR, et al. Clinical
2015.
role of F-FDG PET/CT in the management of squa-
2. Wippold FJ. Head and neck imaging: the role of CT
mous cell carcinoma of the head and neck and thyroid
and MRI. J Magn Reson Imaging. 2007;25:453.
carcinoma. J Nucl Med. 2007;48(Suppl 1):58S–67S.
3. Righi PD, Kopecky KK, Caldemeyer KS, et  al.
6. Yousem DM, Gad K, Tufano RP. Resectability
Comparison of the ultrasound- fine needle aspiration
issues with head and neck cancer. Am J Neuroradiol.
and computed tomography in patients undergoing elec-
2006;27(10):2024–36.
tive neck dissection. Head Neck. 1997;19(7):604–10.
 Evaluation of Neck Mass
Tom Shokri, Laila Siddique, and Neerav Goyal
Algorithmic Approach
A. A thorough history and physical exam remain
the mainstay of initial evaluation of a neck
mass. Key red flag symptoms to delineate
include rapid growth, dysphagia, weight loss,
otalgia, aural fullness, hearing loss, hemopty-
sis, epistaxis, paresthesia, and dyspnea [1, 2].
Ninety percent of pediatric neck masses are
benign lesions, related to an inflammatory
response or congenital anomaly. With the
exclusion of thyroid masses, 80% of adult
neck masses are malignant [3]. Signs and
T. Shokri
Division of Otolaryngology-Head and Neck Surgery,
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
L. Siddique
Division of Otolaryngology-Head and Neck Surgery,
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Department of Otolaryngology-Head and Neck
Surgery, University of Miami Miller School of
Medicine, Miami, FL, USA
e-mail: laila.siddique@jhsmiami.org
N. Goyal (*)
Division of Otolaryngology-Head and Neck Surgery,
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Penn State Cancer Institute, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: ngoyal1@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_7
7
symptoms of infection including symptoms
of fever, chills, fluctuance, erythema, tender-
ness, or warmth should prompt treatment
with antibiotics and re-evaluation.
B. A detailed head and neck examination is criti-
cal. Mobility, tenderness, location within the
neck, firmness, fluctuance, erythema, and
palpable bruits are some of the features that
should be initially noted. The aerodigestive
tract must be evaluated through palpation and
visualization of the floor of mouth, oral
tongue, palate, tonsils, base of tongue, buccal
mucosa, nasopharynx, oropharynx, larynx,
and nasal cavity [4].
C. Computed tomography (CT) is the most com-
monly utilized imaging modality. To avoid
ionizing radiation, ultrasonography may be
initially useful in the pediatric population as
they have a higher likelihood of an inflamma-
tory, infectious, or congenital process [5].
Ultrasonography should also be considered
for thyroid masses, as use of CT with iodine
contrast can delay potential radioiodine treat-
ment. MRI is useful in delineating soft tissue
anatomy, particularly if perineural disease is
suspected. CTA or MRA can be considered if
there is suspicion for a vascular lesion.
D. Fine needle aspiration (FNA) or core needle
biopsy may be performed. If this does not
yield a diagnosis, an excisional biopsy may
be performed. However, the surgeon must be
cognizant of the risk of tumor seeding.
21
22 T. Shokri et al.

E. If the lesion is found to be infectious, conser- head and neck oncologic surgeon for further
vative therapy with antibiotic treatment and workup for staging and appropriate
possible steroids may be administered while management.
congenital lesions should undergo observa-
tion with reassessment for surgical excision.
Neoplastic lesions should be referred to a

A-B History and physical

Signs of Yes
Antibiotics with re-
infection evaluation

No

Diagnostic Imaging
CT: Standard
C CTA/MRA: Vascular lesion
MRI: Soft tissue concern
Ultrasound: Pediatric/thyroid

E
D No
Concern for
malignancy? Congenital or inflammatory

Yes
Trial of antibiotics ± steroids.
Biopsy and referral to head Refer to otolaryngologist.
and neck oncologic surgeon

Algorithm 7.1
7  Evaluation of Neck Mass 23

References Cummings otolaryngology: head and neck surgery.

5th ed. Philadelphia: Elsevier; 2010.
4. Kadom N, Lee EY.  Neck masses in children: cur-
1. Goff CJ, Allred C, Glade RS.  Current management
rent imaging guidelines and imaging findings. Semin
of congenital branchial cleft cysts, sinuses and fis-
Roentgenol. 2012;47:7–20.
tulae. Curr Opin Otolaryngol Head Neck Surg.
5. Layfield L.  Fine-needle aspiration in the diagnosis
2012;20:533–9.
of head and neck lesions: a review and discussion of
2. Tracy TF, Muratore CS. Management of common head
problems in differential diagnosis. Diagn Cytopathol.
and neck masses. Semin Pediatr Surg. 2007;16:3–13.
2007;35:798–805.
3. Chen AY, Otto KJ.  Differential diagnosis of neck
masses. In: Flint PW, Haughey BH, Lund VJ, editors.
 Evaluation of an Enlarged Cervical
Lymph Node
Laila Siddique, Tom Shokri, and Neerav Goyal
Algorithmic Approach
A. The differential diagnosis of a neck mass
includes congenital anomalies, inflammatory/
infectious lymphadenopathy, and malig-
nancy. Neck masses in children are more
commonly congenital or associated with
inflammatory lymph nodes, whereas neck
masses in adults raise a higher concern for
malignancy [1]. A thorough history and phys-
ical exam are first required in evaluation.
Questions regarding the onset of the neck
L. Siddique
Division of Otolaryngology-Head and Neck Surgery,
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Department of Otolaryngology-Head and Neck
Surgery, University of Miami Miller School of
Medicine, Miami, FL, USA
e-mail: laila.siddique@jhsmiami.org
T. Shokri
Division of Otolaryngology-Head and Neck Surgery,
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
N. Goyal (*)
Division of Otolaryngology-Head and Neck Surgery,
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Penn State Cancer Institute, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: ngoyal1@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_8
8
mass as well as its rate of growth are impor-
tant, as well as the presence of symptoms of
infection and B symptoms. Information about
travel and contact with sick individuals or
animals should be obtained [2].
B. On physical examination, inspection and
bimanual palpation of the neck should be
carefully performed to assess for location,
size, tenderness, and symmetry [3]. Hard and
tender lymph nodes are associated with infec-
tions; hard nodes fixed to the skin or deeper
structures can suggest malignancy; and fluc-
tuant masses can be seen with an abscess or
cyst [4]. A comprehensive physical exam
should also be performed to assess for other
signs of infection, peripheral lymphadenopa-
thy, or systemic inflammatory processes.
C. If the history and physical exam suggest an
infectious etiology, consider initiating a trial
of oral antibiotics. If symptoms do not begin
to improve within 2–3 days, obtain (1) a neck
ultrasound to rule out a neck abscess or an
infected congenital cyst [5]; (2) CBC, CRP,
LDH, and chest radiograph for systemic
inflammatory processes; (3) PPD to rule out
tuberculosis lymphadenitis; (4) serology for
HIV, EBV, CMV, and toxoplasmosis; and (5)
referral to a head and neck surgeon or infec-
tious disease physician as appropriate.
D. If the history and physical exam are suggestive
of a malignant process, or if infectious and
inflammatory etiologies have been ruled out, a
25
26 L. Siddique et al.

CBC, blood smear, and fine needle aspiration
should be performed to assess for malignancy
and atypical mycobacterial infection, followed
by referral to a head and neck surgeon, oncolo-
gist, or infectious disease internist [6].
E. If a total diagnostic workup is negative and
the patient is otherwise asymptomatic, the
etiology may be cervical lymphadenopathy
secondary to drug reactions, a developmental
mass such as a thyroglossal duct cyst or der-
moid cyst, vascular malformation, or benign
processes. In this situation, it is appropriate to
observe and follow-up with the patient in
4–6  weeks [5], with referral to a head and
neck surgeon if the mass enlarges during this
time or remains larger than 2 cm [7].

A History and Physical Exam: Rate of growth? Other infectious symptoms?

B symptoms? Social Hx: sick contacts, travel?

Inspection and bimanual palpation of neck: location, size, tenderness, hardness, fixation, cystic?
B Comprehensive physical exam with HEENT, cardiovascular, pulmonary, abdominal evaluation.

Signs of infection:
C YES
tenderness and
NO
erythema of node, D
chills, fatigue?

Trial of oral antibiotics Developmental mass

suspected?
E
NO
YES

CBC, blood smear, FNA/

Improvement in 2-3 days? excisional biopsy Developmental
Referral to ENT mass suspected?

YES NO

YES
• Ultrasound with reflex CT for
NO
abscess vs. cyst
Complete 10 • CBC, CRP, LDH, CXR for
daycourse inflammatory process Consider LAD
• HIV, EBV, CMV, toxo serology secondary to drug
Referral to ENT
reaction or benign
etiology

Positive results?
YES NO Observe for 4-6
weeks

Treat and follow up Evaluate for possible

with ENT and/or malignancy (see D) Refer to ENT if
infectious disease as node increases in
appropriate size or remains
>2 cm

Algorithm 8.1
8  Evaluation of an Enlarged Cervical Lymph Node 27

References 4. Acierno SP, Waldhausen JH.  Congenital cervical

cysts, sinuses and fistulae. Otolaryngol Clin N Am.
2007;40(1):161–76. vii–viii.
1. Connolly AA, MacKenzie K.  Paediatric neck
5. Leung AK, Robson WL.  Childhood cervical lymph-
masses—a diagnostic dilemma. J Laryngol Otol.
adenopathy. J Pediatr Health Care. 2004;18(1):3–7.
1997;111(6):541–5.
6. Anne S, Teot LA, Mandell DL.  Fine needle aspi-
2. Bauer PW, Lusk RP.  Neck masses. In: Bluestone CD,
ration biopsy: role in diagnosis of pediatric head
Stool SE, Alper CM, et al., editors. Pediatric otolaryngol-
and neck masses. Int J Pediatr Otorhinolaryngol.
ogy. 4th ed. Philadelphia: Saunders; 2003. p. 1629–47.
2008;72(10):1547–53.
3. Torsiglieri AJ Jr, Tom LW, Ross AJ III, Wetmore RF,
7. Dickson PV, Davidoff AM.  Malignant neo-
Handler SD, Potsic WP. Pediatric neck masses: guide-
plasms of the head and neck. Semin Pediatr Surg.
lines for evaluation. Int J Pediatr Otorhinolaryngol.
2006;15(2):92–8.
1988;16(3):199–210.
 Salivary Gland Tumors
Tom Shokri, Laila Siddique, and Neerav Goyal
Algorithmic Approach
A. The initial step in evaluation is a detailed history
and physical. The most common presenting
symptom of a major salivary gland neoplasm is
asymptomatic swelling. Pain is more com-
monly reported in malignant lesions and may
suggest perineural invasion (PNI) [1].
B. Physical findings that increase the index of
suspicion for malignancy include facial pare-
sis, cervical lymphadenopathy, and fixation
of mass to overlying skin or deep structures
[2]. Lymphadenopathy is seen on presenta-
tion in 10–30% of cases.
T. Shokri
Division of Otolaryngology-Head and Neck Surgery,
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
L. Siddique
Division of Otolaryngology-Head and Neck Surgery,
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Department of Otolaryngology-Head and Neck Surgery,
University of Miami Miller School of Medicine,
Miami, FL, USA
e-mail: laila.siddique@jhsmiami.org
N. Goyal (*)
Division of Otolaryngology-Head and Neck Surgery,
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Penn State Cancer Institute, Penn State Milton
S. Hershey Medical Center​, Hershey, PA, USA
e-mail: ngoyal1@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_9
9
C. Diagnostic imaging is warranted if there is a
concern for extragrandular extension.
Ultrasonography is an appropriate initial step
in evaluation. Computed Tomography (CT)
and Magnetic Resonance Imaging (MRI) are
useful for further delineating anatomy [3].
D. Fine needle aspiration cytology (FNAC) is rec-
ommended for major salivary gland lesions,
allowing for tissue diagnosis. Core needle biopsy
(CNB) yields greater diagnostic accuracy.
However, CNB is more painful and for parotid
masses risks injury to the facial nerve [4, 5].
E. Standard of care for benign lesions continues
to be removal, particularly if causing symp-
toms or growing in size. However, a subset of
patients may choose watchful waiting.
F. If positive for malignancy, staging, according
to AJCC guidelines [6], should be performed
for both prognostic measures and to guide
management strategy.
G. Surgery remains the gold standard for primary
and regionally metastatic cancer of the salivary
glands. Patients with clinically positive nodal
disease, T3/T4 staging, or high-grade histol-
ogy should undergo neck dissection (ND).
H. Adjuvant radiotherapy should be considered
in cases of high grade, T3/T4, close (<2 mm)/
positive margins, PNI, recurrent disease, or
positive cervical lymph nodes following neck
dissection. Chemotherapy may be considered
as palliative treatment in unresectable or dis-
tantly metastatic disease.
29
30 T. Shokri et al.

History and Physical Exam:

A Vague asymptomatic swelling of the neck, pain, gland obstruction/sialadenitis
Palpable Mass

Assess for facial paresis, cervical lymphadenopathy, and fixation of

B mass to overlying skin or deep structures

Findings
concerning for
malignancy?

C Diagnostic Imaging: Ultrasonography, CT, or MRI

D Obtain Tissue Sample: FNAC or CNB

E/F Benign lesion Malignant lesion

· Surgical excision
G/H · Observant management
· Surgical excision · ND and adjuvant radiation if nodal
disease, T3/T4, high grade, and + margin

Algorithm 9.1
9  Salivary Gland Tumors 31

References a systematic review. J Oral Maxillofac Surg.

2010;68:2146–53.
5. Schmidt RL, Hall BJ, Wilson AR, et al. A system-
1. Spiro RH, Hajdu SI, Strong EW. Tumors of the sub-
atic review and meta-analysis of the diagnostic
maxillary gland. Am J Surg. 1976;132:463–8.
accuracy of ultrasoundguided core needle biopsy
2. Terhaard C, Lubsen H, Tan B, et al. Facial nerve func-
for salivary gland lesions. Am J Clin Pathol. 2011;
tion in carcinoma of the parotid gland. Eur J Cancer.
136:516–26.
2006;42:2744–50.
6. Edge SB, Byrd DR, Compton CC, Fritz AG, Greene
3. Lee YY, Wong KT, King AD, Ahuja AT. Imaging of
FL, Trotti A, editors. AJCC cancer staging manual.
salivary gland tumors. Eur J Radiol. 2008;66:300–4.
7th ed. New York: Springer; 2010.
4. Colella G, Cannavale R, Flamminio F, et  al. Fine-­
needle aspiration cytology of salivary gland lesions:
 Part III
Thoracic
 Massive Hemoptysis
Henry Tannous, Joanna Chikwe,
and Maroun B. Yammine
Algorithmic Approach
A. Other sources of bleeding like nasopharyngeal
and upper GI bleeding can present as hemop-
tysis and have to be ruled out. A true massive
hemoptysis will be defined in this chapter as
life-threatening blood loss from the airways
causing respiratory distress or hemodynamic
instability. Usually the rate of blood loss would
exceed 100 cc/h or 500 cc/24 h [1, 2].
B. The priority is to secure the airway to main-
tain gas exchange and support the hemody-
namics as needed. If a specific side is
suspected to be the source of bleeding, then
the patient should be positioned in lateral
decubitus with the suspected bleeding side
down to prevent drowning of the unaffected
side. A more detailed history and physical
exam should be taken and blood samples
sent to rule out anemia, thrombocytopenia,
and coagulopathy [3].
H. Tannous (*) ∙ J. Chikwe
Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA
Department of Cardiovascular Surgery, Icahn School
of Medicine at Mount Sinai, New York, NY, USA
e-mail: Henry.Tannous@stonybrookmedicine.edu
M. B. Yammine
Department of Cardiovascular Surgery, Icahn School
of Medicine at Mount Sinai, New York, NY, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_10
10
C. After the initial stabilization, a bronchos-
copy is warranted. The patient should be
intubated with a large ET tube (size [>8])
to allow for an interventional bronchos-
copy. Flexible bronchoscopy is key to
evacuate clots, identify the source, and
control the bleeding. Cold saline, epineph-
rine wash, and direct pressure (with the
scope or balloon) are commonly used
effective modalities. Other possible modal-
ities include cryoablation, laser therapy,
and procoagulants application. [Rigid
bronchoscopy can also be used; it provides
better suction but is reserved for proximal
airway bleeding [4, 5]].
D1. If the bronchoscopy was successful, further
workup and treatment would be directed
based on the underlying etiology. Possible
etiologies of massive hemoptysis include
pulmonary infections (fungal, TB, etc.),
vasculitis, AVMs, bronchiectasis, tumors,
airway inflammation or ecchymosis, iatro-
genic injuries, and fistulae.
D2. If bronchoscopy was unsuccessful, further
actions should be taken to protect and venti-
late the unaffected lung, pending definite
treatment. This can be achieved by placing
an endobronchial blocker on the affected
side, switching the ET tube to a double
lumen tube, or advancing the ET tube into
the unaffected side. The latter option is con-
35
36 H. Tannous et al.

sidered as a last resort since it does not help
tamponade the bleed [3].
E. Subsequently, the definitive treatment of air-
way (tracheal or bronchial) bleed includes
angiography with ­embolization. However, a
parenchymal bleed is better treated with
lung resection [6–8].
Tracheo-innominate fistula is a potential cause
of massive hemoptysis in intubated patients or
patients with a tracheostomy. It requires
immediate intervention with cuff overinfla-
tion, digital compression of the artery against
the sternum, and transfer to the operating room
for sternotomy and fistulae repair [9].

A
Massive Hemoptysis: Life-threatening blood loss from airways causing respiratory
distress or hemodynamic instability, >100cc/hr or >500cc/24hrs

Simultaneously
B
- Support hemodynamics
Secure the airway to maintain gas exchange
- Correct coagulopathy
- Position patient in lateral decubitus
(bleeding side down) - Transfuse as needed
- Intubate with large ET tube - Complete Hx and physical exam
(while bronchoscopy is being set up)

C
BRONCHOSCOPY
- Cold saline and epinephrine wash
- Direct pressure
- Cryotherapy/procoagulant application

Is the
bleeding
controlled?
D Yes No

Protect and ventilate unaffected lung

Address underlying etiology
- Endobronchial blocker in bleeding side
- Switch to a double lumen ET tube
- Advance ET tube to unaffected side

E What is the
source of
bleeding?
Airways Parenchyma Tracheoesophageal

Angiography with embolization Lung resection TE fistulae repair

Algorithm 10.1
10  Massive Hemoptysis 37

References choscopy before bronchial artery embolization

for massive hemoptysis. AJR Am J Roentgenol.
2001;177(4):861–7.
1. Ibrahim WH.  Massive haemoptysis: the defini-
6. Shigemura N, Wan IY, Yu SC, Wong RH, Hsin MK,
tion should be revised. Eur Respir J. 2008;32.
Thung HK, et  al. Multidisciplinary management of
England:1131–2.
life-threatening massive hemoptysis: a 10-year expe-
2. Fartoukh M, Khoshnood B, Parrot A, Khalil A,
rience. Ann Thorac Surg. 2009;87(3):849–53.
Carette MF, Stoclin A, et  al. Early prediction of in-­
7. Chun JY, Morgan R, Belli AM. Radiological manage-
hospital mortality of patients with hemoptysis: an
ment of hemoptysis: a comprehensive review of diag-
approach to defining severe hemoptysis. Respiration.
nostic imaging and bronchial arterial embolization.
2012;83(2):106–14.
Cardiovasc Intervent Radiol. 2010;33(2):240–50.
3. Jean-Baptiste E.  Clinical assessment and man-
8. Andrejak C, Parrot A, Bazelly B, Ancel PY, Djibre
agement of massive hemoptysis. Crit Care Med.
M, Khalil A, et al. Surgical lung resection for severe
2000;28(5):1642–7.
hemoptysis. Ann Thorac Surg. 2009;88(5):1556–65.
4. Sakr L, Dutau H. Massive hemoptysis: an update on
9. Scalise P, Prunk SR, Healy D, Votto J. The incidence of
the role of bronchoscopy in diagnosis and manage-
tracheoarterial fistula in patients with chronic trache-
ment. Respiration. 2010;80(1):38–58.
ostomy tubes: a retrospective study of 544 patients in
5. Hsiao EI, Kirsch CM, Kagawa FT, Wehner JH,
a long-term care facility. Chest. 2005;128(6):3906–9.
Jensen WA, Baxter RB.  Utility of fiberoptic bron-
 Mediastinal Masses
Henry Tannous, Joanna Chikwe,
and Maroun B. Yammine
Algorithmic Approach
Mediastinal Mass
The mediastinum is defined as the area between the
thoracic inlet, the diaphragm, and the pleural cavi-
ties laterally. A mediastinal mass is classified
according to its location [1, 2]. An anterior mass is
located between the sternum and the pericardium.
The differential diagnosis includes thymomas, tera-
tomas [and other germ cell tumors], thyroid tumors,
and lymphomas [3]. A mass in the middle mediasti-
nal compartment, which houses the visceral organ
and structures, is usually a cyst [cardiac, broncho-
genic, esophageal]. A posterior mediastinal mass is
located around the spine and paraspinal structures
and is usually a neurogenic tumor.
A. A mediastinal mass can have local or systemic
symptoms or be completely asymptomatic. An
extensive H&P should screen for previous Hx
of cancer, superior vena cava syndrome, myas-
H. Tannous (*) ∙ J. Chikwe
Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA
Department of Cardiovascular Surgery, Icahn School
of Medicine at Mount Sinai, New York, NY, USA
e-mail: Henry.Tannous@stonybrookmedicine.edu
M. B. Yammine
Department of Cardiovascular Surgery, Icahn School
of Medicine at Mount Sinai, New York, NY, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_11
11
thenia gravis, Horner syndrome, paraneoplas-
tic syndromes, lymphadenopathy, neural
deficit, stridor, dysphagia, or hoarseness [2].
B. A CT with IV contrast will narrow down the
differential based on the location of the mass
and evaluate the mass density, size, and inva-
sion of surrounding structures.
C. For posterior mediastinal tumors, an MRI may
be needed to fully assess the neurologic tumor.
A tissue biopsy may be possible to rule other
etiologies. Neurogenic masses warrant resec-
tion in conjunction with neurosurgery [4–6].
D. Middle mediastinal tumors are usually cystic
in nature and warrant resection if they are
symptomatic. Bronchoscopic and esophageal
cysts might need endoscopic studies as part
of their evaluation [7, 8].
E. Anterior mediastinal masses require more
extensive workup:
(a) PET/CT to diagnose regional and sys-
temic disease [9].
(b) Technetium scan to locate ectopic thy-
roid tissue.
(c) Scrotal ultrasound for germ cell/gonadal
primary tumors.
(d) Tumor markers: AFP and B-HCG for
germ cell tumors [10, 11].
(e) Serum anti-acetylcholine receptor
antibodies.
(f) Tissue sampling if lymphoma is sus-
pected [percutaneous vs. endobronchial
vs. surgical].
39
40 H. Tannous et al.

Germ cell tumors are treated by chemother- Thymomas: Most common neoplasm of the ante-
apy, lymphomas with ChemoRad, and thyroid rior mediastinum [12, 13]. The decision to oper-
and thymic tumors with resection. ate should take into consideration the presence of
myasthenia gravis [2].

A
Complete H&P should screen for previous Hx of cancer, superior
vena cava syndrome, myasthenia gravis, Horner syndrome, signs
of tamponade, B symptoms, paraneoplastic syndromes, stridor,
dysphagia, and hoarseness

CT scan:
Assesses location of mass and
invasion of surrounding structures

E Anterior Middle Posterior

D C

Yes AFP/B- Surgical resection Tissue Bx may be helpful

Treatment of germ cell HCG recommended if
tumors [chemotherapy] +ve? symptomatic

No
Surgical resection
recommended in
conjunction with
Needle Bx followed by Yes Lymphoma neurosurgery
ChemoRad if confirmed suspected?

No

Vital organs invaded

Tissue biopsy needed prior Yes
(arch vessel, SVC,
to definitive ChemoRad pulmonary hilum)

No

Tumor resection with curative intent for thymic

tumor [thoracoscopic vs. median sternotomy]

Algorithm 11.1
11  Mediastinal Masses 41

References 7. Takeda S, Miyoshi S, Minami M, Ohta M, Masaoka

A, Matsuda H. Clinical spectrum of mediastinal cysts.
Chest. 2003;124(1):125–32.
1. Carter BW, Tomiyama N, Bhora FY, Rosado de
8. Esme H, Eren S, Sezer M, Solak O. Primary mediasti-
Christenson ML, Nakajima J, Boiselle PM, et  al. A
nal cysts: clinical evaluation and surgical results of 32
modern definition of mediastinal compartments. J
cases. Tex Heart Inst J. 2011;38(4):371–4.
Thorac Oncol. 2014;9(9 Suppl 2):S97–101.
9. Schiepers C, Filmont JE, Czernin J.  PET for stag-
2. Duwe BV, Sterman DH, Musani AI.  Tumors of the
ing of Hodgkin’s disease and non-Hodgkin’s lym-
mediastinum. Chest. 2005;128(4):2893–909.
phoma. Eur J Nucl Med Mol Imaging. 2003;30(Suppl
3. Carter BW, Marom EM, Detterbeck FC. Approaching
1):S82–8.
the patient with an anterior mediastinal mass: a
10.
Javadpour N.  Significance of elevated serum
guide for clinicians. J Thorac Oncol. 2014;9(9 Suppl
alphafetoprotein (AFP) in seminoma. Cancer.
2):S102–9.
1980;45(8):2166–8.
4. Reeder LB.  Neurogenic tumors of the mediastinum.
11. Hori K, Uematsu K, Yasoshima H, Yamada A,

Semin Thorac Cardiovasc Surg. 2000;12(4):261–7.
Sakurai K, Ohya M.  Testicular seminoma with
5. Mazel C, Grunenwald D, Laudrin P, Marmorat
human chorionic gonadotropin production. Pathol Int.
JL.  Radical excision in the management of thoracic
1997;47(9):592–9.
and cervicothoracic tumors involving the spine:
12. Mullen B, Richardson JD. Primary anterior mediasti-
results in a series of 36 cases. Spine (Phila Pa 1976).
nal tumors in children and adults. Ann Thorac Surg.
2003;28(8):782–92. discussion 92.
1986;42(3):338–45.
6. Forsythe A, Volpe J, Muller R. Posterior mediastinal
13. Gerein AN, Srivastava SP, Burgess J. Thymoma: a ten
ganglioneuroma. Radiographics. 2004;24(2):594–7.
year review. Am J Surg. 1978;136(1):49–53.
 Tracheal Stenosis
Henry Tannous, Joanna Chikwe,
and Maroun B. Yammine
Algorithmic Approach
A. Tracheal stenosis develops in patients with
prolonged intubation due to scarring around
the ET tube or tracheostomy. It could also
be due to a tumor, injury, chest radiation,
autoimmune disorder, or infection [1–3].
B. Initial evaluation should assess for respira-
tory distress and include a complete history
and physical exam. Suspicious symptoms
include SOB nonresponsive to bronchodila-
tors and adult new-onset stridor. Other
symptoms may include cough, dyspnea,
hemoptysis, and wheezing [4–6].
C1. For life-threatening stenosis, oxygen therapy
and airway management are paramount.
Bronchoscopy-­ guided intubation or emer-
gent tracheostomy/cricothyroidotomy might
be needed. Rigid bronchoscopy intubation is
reserved for extreme cases. It allows
H. Tannous (*) ∙ J. Chikwe
Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA
Department of Cardiovascular Surgery, Icahn School
of Medicine at Mount Sinai, New York, NY, USA
e-mail: Henry.Tannous@stonybrookmedicine.edu
M. B. Yammine
Department of Cardiovascular Surgery, Icahn School
of Medicine at Mount Sinai, New York, NY, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_12
12
v­entilation and therapeutic coring or dila-
tion. Once the airway is secured, the severity,
extent, and location of the stenosis should be
fully assessed bronchoscopically [7].
C2. Subsequent workup includes a CXR and CT
scan of the chest, which may show tracheal
deviation, foreign body, or mediastinal shift.
While CXR has low sensitivity and specific-
ity, a CT is more useful in diagnosing and
assessing severity [3].
D. Following airway establishment and for
non-­life-­threatening stenosis, further man-
agement should take into consideration the
following factors: Etiology of the lesion,
prognosis, life expectancy, and ability to tol-
erate planned procedures.
E1. For extrinsic compression of the trachea or
systemic diseases causing stenosis, a
disease-­ specific plan should be imple-
mented. For example, ChemoRad for lym-
phoma, vascular intervention for aneurysms
and rings, and resection for substernal thy-
roid tumors and thymomas [3].
E2. For intrinsic pathologies, the following
treatment options are available [7–9]:
(a) Tracheal resection of the affected seg-
mented and end-to-end reconstruction
provides excellent long-term relief [10].
(b) Tracheal stenting provides short- or
long-­
term relief and is done with a
metal or silicone stent [11].
43
44 H. Tannous et al.

(c) Tracheal dilation provides temporary

(d) Tracheal laser ablation and brachyther-
relief and is achieved with dilators or apy are used to excise scar tissue and
balloons [9]. provide temporary relief [6, 12].

A
History and Physical exam:
Adult with a history of recent hospitalization and prolonged intubation presenting
with new-onset stridor and SOB non responsive to bronchodilators

Is the
patient in
respiratory
distress?

Yes No
C

- O2 therapy Once stable - CXR: r/o foreign body and tracheal

- Bronchoscopy-guided intubation or
deviation and mediastinal shift
surgical airway
- CT Chest: Superior in diagnosis and
- Bronchoscopic assessment of
assessing severity, extent, and
severity, extent, and location of
location of stenosis
stenosis

D
- Etiology
- Prognosis/life expectancy
- Ability to tolerate therapeutic
intervention

Intrinsic compression:
Extrinsic compression:
Implement a disease-specific plan, for - Tracheal resection
example, ChemoRad for lymphoma - Tracheal stenting/dilation
- Tracheal laser ablation

Algorithm 12.1
12  Tracheal Stenosis 45

References 7. Li WT, Xiao YB, Liu GN, Huang SM, Ling Y,

Zhang JQ, et  al. Management of benign tracheal
stenosis by intubation dilatation under flexible
1. Zias N, Chroneou A, Tabba MK, Gonzalez AV, Gray
bronchoscopic guidance. Zhonghua Yi Xue Za Zhi.
AW, Lamb CR, et al. Post tracheostomy and post intu-
2011;91(42):2995–8.
bation tracheal stenosis: report of 31 cases and review
8. Ciccone AM, De Giacomo T, Venuta F, Ibrahim M,
of the literature. BMC Pulm Med. 2008;8:18.
Diso D, Coloni GF, et al. Operative and non-operative
2. Koshkareva Y, Gaughan JP, Soliman AM. Risk factors
treatment of benign subglottic laryngotracheal steno-
for adult laryngotracheal stenosis: a review of 74 cases.
sis. Eur J Cardiothorac Surg. 2004;26(4):818–22.
Ann Otol Rhinol Laryngol. 2007;116(3):206–10.
9. Dalar L, Karasulu L, Abul Y, Ozdemir C, Sokucu SN,
3. Bacon JL, Patterson CM, Madden BP. Indications and
Tarhan M, et al. Bronchoscopic treatment in the man-
interventional options for non-resectable tracheal ste-
agement of benign tracheal stenosis: choices for sim-
nosis. J Thorac Dis. 2014;6:258–70.
ple and complex tracheal stenosis. Ann Thorac Surg.
4. Majid A, Guerrero J, Gangadharan S, Feller-Kopman
2016;101(4):1310–7.
D, Boiselle P, DeCamp M, et al. Tracheobronchoplasty
10. Yamamoto K, Kojima F, Tomiyama K, Nakamura T,
for severe tracheobronchomalacia: a prospective out-
Hayashino Y. Meta-analysis of therapeutic procedures
come analysis. Chest. 2008;134(4):801–7.
for acquired subglottic stenosis in adults. Ann Thorac
5. Papla B, Dyduch G, Frasik W, Olechnowicz H. Post-­
Surg. 2011;91(6):1747–53.
intubation tracheal stenosis  – morphological-clinical
11. Chin CS, Litle V, Yun J, Weiser T, Swanson SJ. Airway
investigations. Pol J Pathol. 2003;54(4):261–6.
stents. Ann Thorac Surg. 2008;85(2):S792–6.
6. Allen AM, Abdelrahman N, Silvern D, Fenig E,
12. Leventhal DD, Krebs E, Rosen MR.  Flexible

Fruchter O, Kramer MR.  Endobronchial brachy-
laser bronchoscopy for subglottic stenosis in the
therapy provides excellent long-term control of
awake patient. Arch Otolaryngol Head Neck Surg.
recurrent granulation tissue after tracheal stenosis.
2009;135(5):467–71.
Brachytherapy. 2012;11(4):322–6.
 Incidental Lung Nodule
Henry Tannous, Joanna Chikwe,
and Maroun B. Yammine
Algorithmic Approach
Incidental lung nodule is a solid parenchymal lung
lesion picked up incidentally by CXR, CT scan, or
MRI done during a screening or workup for other
pathologies. When larger than 3 cm, the nodule is
considered a “mass.” For the purpose of this discus-
sion, all solid or part-solid parenchymal lesions less
than 3 cm will be referred to as lung nodules [1, 2].
A. History and physical exam are key: Smoking
history, exposure to carcinogens (asbestos or
silica, etc.), recent travel history, previous
cancer history, or a family history of malig-
nancy. The differential diagnosis includes
infectious and inflammatory processes as
well as benign and malignant tumors [3].
B. For patients with no previous history of can-
cer and no prior imaging for comparison, a
nodule ≤8  mm can be followed up in
6 months with a CT scan [4, 5].
H. Tannous (*) ∙ J. Chikwe
Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA
Department of Cardiovascular Surgery, Icahn School
of Medicine at Mount Sinai, New York, NY, USA
e-mail: Henry.Tannous@stonybrookmedicine.edu
M. B. Yammine
Department of Cardiovascular Surgery, Icahn School
of Medicine at Mount Sinai, New York, NY, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_13
13
C. If the nodule is >8 mm, a PET/CT is indi-
cated to help categorize it. A hypometa-
bolic nodule can undergo a repeat CT
scan at 6  months, whereas a hypermeta-
bolic one should undergo tissue biopsy
(CT guided, endobronchial, or excisional)
[4, 6, 7].
D1. If primary lung cancer is confirmed, stag-
ing workup and preoperative evaluation
are initiated. For stage 1 or 2 lung cancer,
surgery is the mainstay of treatment with
lobectomy being the gold standard of ther-
apy. For stage 3 or 4, chemoradiation is the
most common treatment. For patients who
are poor candidates for surgery, alternative
local therapies include cryoablation, ste-
reotactic radiation, and radiofrequency
ablation [8].
D2. For a metastatic lung nodule, a complete
metastatectomy is reserved for controlled
primary malignancies with favorable prog-
nosis and no other metastatic sites.
E. If the mass is not cancerous, treatment
should target the underlying pathology:
Fungal infection, TB, and vasculitis [1].
NB: Ground glass opacifications should
be followed up through regular serial imag-
ing unless they develop an enlarging solid
component, become >2.5 cm, or increase in
size by 25%. In this case, it would require a
tissue biopsy.
47
48 H. Tannous et al.

History and Physical exam:

Smoking history, exposure to carcinogens (asbestos, silica, etc.), recent travel,
A previous malignancy, or family Hx of malignancy

Follow up CT in 6 months only if there

No is low index of suspicion:
Is the
B - No previous Hx of cancer
nodule
- Prior imaging comparison
> 8 mm?

Yes

PET/CT

No
Active imaging surveillance
Is the lesion (documenting interval growth
hypermetabolic? warrants repeat PET/CT)

Yes

Tissue biopsy (CT guided, endobronchial, 1- Primary lung CA: Staging

or excisional) workup, preoperative
evaluation, definitive resection
2- Metastatic nodule: Consider
metastasectomy
Yes
D
Is the lesion
malignant?

No Address underlying etiology

E (autoimmune, infectious, etc.)

Algorithm 13.1
13  Incidental Lung Nodule 49

References images: from the Fleischner Society 2017. Radiology.

2017;284(1):228–43.
6. Jaklitsch MT, Jacobson FL, Austin JH, Field JK, Jett
1. Ost D, Fein AM, Feinsilver SH.  Clinical practice.
JR, Keshavjee S, et al. The American Association for
The solitary pulmonary nodule. N Engl J Med.
Thoracic Surgery guidelines for lung cancer screening
2003;348(25):2535–42.
using low-dose computed tomography scans for lung
2. Gould MK, Donington J, Lynch WR, Mazzone PJ,
cancer survivors and other high-risk groups. J Thorac
Midthun DE, Naidich DP, et  al. Evaluation of indi-
Cardiovasc Surg. 2012;144(1):33–8.
viduals with pulmonary nodules: when is it lung can-
7. Berghmans T, Dusart M, Paesmans M, Hossein-­
cer? Diagnosis and management of lung cancer, 3rd
Foucher C, Buvat I, Castaigne C, et al. Primary tumor
ed: American College of Chest Physicians evidence-­
standardized uptake value (SUVmax) measured on
based clinical practice guidelines. Chest. 2013;143(5
fluorodeoxyglucose positron emission tomography
Suppl):e93S–e120S.
(FDG-PET) is of prognostic value for survival in non-­
3. McWilliams A, Tammemagi MC, Mayo JR, Roberts
small cell lung cancer (NSCLC): a systematic review
H, Liu G, Soghrati K, et al. Probability of cancer in
and meta-analysis (MA) by the European Lung
pulmonary nodules detected on first screening CT. N
Cancer Working Party for the IASLC Lung Cancer
Engl J Med. 2013;369(10):910–9.
Staging Project. J Thorac Oncol. 2008;3(1):6–12.
4. Wood DE. National Comprehensive Cancer Network
8. Rivera MP, Mehta AC, Wahidi MM. Establishing the
(NCCN) clinical practice guidelines for lung cancer
diagnosis of lung cancer: diagnosis and management
screening. Thorac Surg Clin. 2015;25(2):185–97.
of lung cancer, 3rd ed: American College of Chest
5. MacMahon H, Naidich DP, Goo JM, Lee KS, Leung
Physicians evidence-based clinical practice guide-
ANC, Mayo JR, et  al. Guidelines for management
lines. Chest. 2013;143(5 Suppl):e142S–e65S.
of incidental pulmonary nodules detected on CT
 Management of Lung Cancer
Scott C. Tiedebohl and Matthew D. Taylor
Algorithmic Approach
A. Lung cancer should be included in the differ-
ential diagnosis of any pulmonary nodule dis-
covered on imaging. A complete history and
physical exam should be completed, noting
the patient’s prior exposures to smoking and
other environmental risk factors along with
pulmonary symptoms [1].
B. A CT scan should then be obtained to better
characterize the lesion. A lesion that is spicu-
lated and not calcified is concerning for
malignancy. It is important to compare new
studies to all previous studies to see if the
lesion has grown or changed in character [2].
C. If after reviewing a patient’s history, physical
examination, and CT findings the suspicion
for a malignancy remains low, no further
workup is necessary, and the nodule can be
observed with repeat imaging based on the
Fleischner society guidelines.
S. C. Tiedebohl ∙ M. D. Taylor (*)
Department of Surgery, Penn State Health Milton
S. Hershey Medical Center, Hershey, PA, USA
Division of Thoracic Surgery, Penn State Health
Milton S. Hershey Medical Center,
Hershey, PA, USA
e-mail: mtaylor6@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_14
14
D. If the nodule is suspicious for malignancy, a
PET/CT is used to evaluate for nodal involve-
ment and metastatic disease [2].
E. If there is no evidence of lymph node involve-
ment or metastatic disease, the determination
of the patient’s ability to tolerate surgery
must be made. Patients should have a recent
EKG and pulmonary function tests.
Postoperative predictive values of FEV1 and
DLCO of >60% indicate that the patient should
be able to tolerate a major lung resection.
Values between 30% and 60% require cardio-
pulmonary exercise testing. If the values are
<30%, then the patient is high risk, and
VO2max should be obtained. If this is less than
10  mL/kg/min, the patient is not a surgical
candidate [3].
F. For those patients who are not surgical candi-
dates, definitive chemoradiation or SBRT
should be offered [1].
G. If the patient is an operative candidate based
on preoperative assessment and the lesion is
deemed resectable, the patient can proceed to
surgery. Ideally, patients should undergo
lobectomy or pneumonectomy with additional
mediastinal lymph node assessment. If a
patient cannot tolerate these lobectomy, then a
more limited resection should be performed.
Regardless of the resection, it should be per-
formed minimally invasively, if possible [1].
H. If there are suspicious lymph nodes on PET
imaging, biopsy of the suspicious nodes
51
52 S. C. Tiedebohl and M. D. Taylor

should be undertaken via endobronchial
ultrasound (EBUS) or mediastinoscopy in
order to appropriately stage the patient and
direct further management [1].
I. If after biopsy, there is no evidence of lymph
node disease or only N1 disease, then the
patient can undergo preoperative evaluation
and proceed to surgery [1].
J. If there is evidence of N2 disease on biopsy,
then the patient’s case should be discussed
in a multidisciplinary conference which
should include the surgical team, medical
oncology, and radiation oncology. The
patient can then proceed directly to surgery
after preoperative evaluation and receive
induction chemotherapy, or definitive che-
motherapy or SBRT [1].
K. If there is evidence of unresectable disease
or metastatic disease, the patient is not a
surgical candidate, and referral to medical
and radiation oncology should be under-
taken [1].

History:
Elderly male, current smoker
Pulmonary nodule found on
CXR for cough

A
Full history/physical exam

B CT

C Low suspicion of malignancy High suspicion of malignancy

D
Surveillance PET/CT

Suspicious
K
lymph nodes
E No evidence of lymph node Unresectable disease or obvious
involvement or metastatic disease metastatic disease
EBUS or
H mediastinoscopy
Operative Definitive
candidate? chemoradiation
J or SBRT

No Yes
Negative or locally +Mediastinal lymph nodes
positive lymph nodes (N1) (N2)
Definitive
radiation or
I
SBRT
Single-level N2
disease Multilevel N2
F disease
Surgery

G Multidisciplinary
evaluation

Algorithm 14.1
14  Management of Lung Cancer 53

References Johns Hopkins textbook of cardiothoracic surgery.

2nd ed. New York: McGraw Hill Publishing; 2014.
3. Arndt A. Pulmonary physiology and pulmonary func-
1. University of Texas. MD Anderson Cancer Center.
tion tests. In: DM LP, Mery CM, Turek JW, editors.
Thoracic Center Faculty. Non-small cell lung cancer. MD
TSRA review of cardiothoracic surgery. 2nd ed.
Anderson: Department of Clinical Effectiveness; 2017.
Chicago: Thoracic Surgery Residents Association;
2. Kim MP, Vaporciyan AA.  Primary lung cancer. In:
2015.
Yuh DD, Yang SC, Vricella LA, Doty JR, editors.
 Management of Empyema
Shannon R. Kotch and Matthew D. Taylor
Algorithmic Approach
A. In a patient with a history of current or recent
pneumonia with ongoing symptoms, parapneu-
monic effusion should be suspected. Pneumonia
can be associated with pleural effusions around
60% of the time; however, less than 5% typi-
cally progress to empyema. Causes of empy-
ema other than infection include trauma and
iatrogenic instrumentation [1, 2].
B. Vital signs consistent with infection (i.e.,
tachycardia, fever), leukocytosis, and physi-
cal exam findings consistent with a pulmo-
nary process should lead the clinician to
suspect a parapneumonic effusion [1].
C. Physical exam findings and a history sugges-
tive of a parapneumonic effusion warrant imag-
ing. This usually begins with a chest radiograph,
which often demonstrates findings of a pleural
effusion. CT scan is the gold standard for imag-
ing a pleural abnormality as it can differentiate
pleural fluid from a parenchymal abnormality.
CT can also demonstrate loculations within a
S. R. Kotch
Department of General Surgery, Penn State Health
Milton S. Hershey Medical Center, Hershey, PA, USA
M. D. Taylor (*)
Department of Surgery, Penn State Health Milton
S. Hershey Medical Center, Hershey, PA, USA
Division of Thoracic Surgery, Penn State Health
Milton S. Hershey Medical Center,
Hershey, PA, USA
e-mail: mtaylor6@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_15
15
collection or a dense fibrous peel, important for
planning the appropriate treatment [1].
D. After demonstration of a fluid collection on
imaging, thoracentesis with pleural fluid anal-
ysis is the next step in management. This can
be done with image-guided technique, either
ultrasonographically or by CT guidance. Fluid
can then be analyzed by Light’s criteria. A pH
less than 7.2 or glucose less than 60 is diagnos-
tic of infection. Pleural fluid can be cultured;
however, sensitivity has been reported to be
between 40% and 60% [1, 2].
E. After identification of an infected pleural col-
lection (empyema), tube thoracostomy should
then be performed. Fluid should be sent for
gram stain and culture. Empiric antibiotics
should be started after fluid has been sent [1, 2].
F. If, after adequate drainage for 24 h, there is
evidence of a persistent fluid collection, CT
should be repeated.
G. Fibrinolytics, consisting of tPA and DNase,
can be instilled into the collection if it is a
simple collection and is still in the early
phase, typically less than 3 days. Fibrinolytics
have been shown to decrease the need for sur-
gical intervention. This benefit is seen when
the two agents are used together; when used
alone, they are ineffective [3].
H. If there is evidence of pleural thickening, the col-
lection is multiloculated, or the collection is sim-
ple, but has been present for more than 3 days,
then the patient should undergo video-­assisted
thoracoscopic surgery (VATS) with decortica-
55
56 S. R. Kotch and M. D. Taylor

tion. If VATS is felt to be unsafe due to the poten- I. If a simple collection fails fibrinolytic ther-
tial for parenchymal injury due to a dense fibrous apy, surgical treatment is indicated by VATS
peel, open thoracotomy is indicated [2]. or thoracotomy [2].

History:
Productive cough, fever, dyspnea, pleuritic chest pain
A
Current or recent history of pneumonia

Obtain vital signs and blood work, and perform physical exam

38.6, BP 115/70, HR 90, RR 20, WBC 20,000

B Diminished breath sounds, dullness to percussion, fremitus, and egophony

Obtain chest radiograph or CT scan

Chest radiograph shows unilateral pleural effusion

C CT scan shows pleural fluid collection consistent with parapneumonic effusion

Sample pleural fluid (thoracentesis) with pleural

D fluid analysis

pH <7.2 or glucose <60

Tube thoracostomy with Gram

E
stain and fluid cultures. Begin
antibiotics

F Obtain CT if collection persists >24 hr

Simple collection, early (<3 days) Multiloculated, pleural thickening

Simple collection, late (>3 days)
G
H
Fibrinolytics
VATS/thoracotomy

Failure to improve at 24 hr
I

Algorithm 15.1
15  Management of Empyema 57

References 3. Rahman NM, Maskell NA, West A, Teoh R, Arnold A,

Mackinlay C, Peckham D, Davies CW, Ali N, Kinnear
W, Bentley A, Kahan BC, Wrightson JM, Davies HE,
1. Raymond D. Surgical intervention for thoracic infec-
Hooper CE, Lee YC, Hedley EL, Crosthwaite N, Choo L,
tions. Surg Clin North Am. 2014;94(6):1283–303.
Helm EJ, Gleeson FV, Nunn AJ, Davies RJ. Intrapleural
https://doi.org/10.1016/j.suc.2014.08.004.
use of tissue plasminogen activator and DNase in
2. Bhatnagar R, Maskell NA. Treatment of complicated pleu-
pleural infection. N Engl J Med. 2011;365(6):518–26.
ral effusions in 2013. Clin Chest Med. 2013;34(1):47–62.
https://doi.org/10.1056/NEJMoa1012740.
https://doi.org/10.1016/j.ccm.2012.11.004.
 Management of Spontaneous
Pneumothorax 16
Shannon R. Kotch and Matthew D. Taylor

Algorithmic Approach C. Imaging consists of a simple upright chest

radiograph. CT may also be obtained to
A. In a patient who presents with a chief com- assess for underlying lung disease; however,
plaint of sudden-onset dyspnea and pleuritic-­ in the acute setting, it is not necessary [1].
type chest pain, pneumothorax must be D. Determining the patient’s stability is key to
included in the differential diagnosis. providing the best treatment [1].
Pneumothorax may be asymptomatic in 10% E. In patients who are hemodynamically stable and
of patients. Primary spontaneous pneumotho- have a small pneumothorax, typically less than
rax is typically seen in young male smokers 2 cm, observation is appropriate. Intervention is
who are otherwise healthy and tend to be tall not necessary unless the pneumothorax enlarges
and thin. These patients have apical subpleu- or the patient’s condition declines [1, 2].
ral blebs which rupture. Secondary spontane- F. Patients who are hemodynamically unstable
ous pneumothorax occurs in patients with at presentation or who have a large pneumo-
known lung disease including COPD, infec- thorax on chest radiography should undergo
tion, cystic fibrosis, and catamenial [1]. tube thoracostomy. This can be accomplished
B. The physical exam findings are many and vary by means of a small-bore catheter (14F or
between stable and unstable patients. In patients less) or a 16F to 22F chest tube [2].
experiencing significant respiratory distress, G. Once there is radiographic resolution of the
are tachypniec, have distended neck veins and pneumothorax, the clinician should consider
tracheal deviation, or are otherwise hemody- removal of the chest tube. If there is no air leak
namically unstable, the clinician should be con- after suction has been discontinued, a second
cerned about a tension pneumothorax [1]. chest radiograph may be obtained to confirm
that there has not been recurrence of the pneu-
S. R. Kotch mothorax. The timing of the radiograph varies
Department of General Surgery, Penn State Health with most (67%) of clinicians waiting 5–12 h
Milton S. Hershey Medical Center, Hershey, PA, USA
after the last documented air leak [2].
M. D. Taylor (*) H. However, in patients with radiographic reso-
Department of Surgery, Penn State Health Milton
lution of the pneumothorax, but who have a
S. Hershey Medical Center, Hershey, PA, USA
persistent air leak after 4–5 days, evaluation
Division of Thoracic Surgery, Penn State Health
for surgical management is indicated.
Milton S. Hershey Medical Center,
Hershey, PA, USA ­Thoracoscopy with bullectomy and mechani-
e-mail: mtaylor6@pennstatehealth.psu.edu cal pleurodesis can be performed in these

© Springer Nature Switzerland AG 2019 59

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_16
60 S. R. Kotch and M. D. Taylor

patients. In patients who are poor surgical
candidates or those who decline surgery,
chemical pleurodesis with talc or doxycy-
cline can be instilled via the chest tube to
achieve pleural symphysis [2].
I. Thoracoscopy with pleurodesis is also per-
formed to prevent recurrence. For those
patients with primary pneumothorax, this
does not typically occur until after the sec-
ond recurrence unless the patient is involved
in high-risk activities such as flying or
scuba diving. Patients with secondary
pneumothoraces typically undergo inter-
vention after the first occurrence due to the
potential morbidity and mortality of a
recurrence [2].

History:
A Sudden onset of dyspnea, and chest pain

Obtain vital signs, and perform physical exam

• 37.6, BP 110/65, HR 95, RR 25

• Unilateral decreased breath sounds, hyper resonance, decreased chest excursion, and
B subcutaneous emphysema
• Significant respiratory distress, tachypnea, pulsus paradoxus, distended neck veins, and
tracheal deviation

C Obtain chest radiograph confirming pneumothorax

D Hemodynamically stable Hemodynamically unstable

F
Tube thoracostomy
Small pneumothorax Large pneumothorax

E
Observation Radiographic resolution of Radiographic resolution of
pneumothorax, no air leak pneumothorax, air leak present

H
G Pull chest tube Thoracoscopy or
chemical pleurodesis

Prevention of recurrence
I

Algorithm 16.1
16  Management of Spontaneous Pneumothorax 61

References 2. Baumann MH, Strange C, Heffner JE, Light R, Kirby

TJ, Klein J, Luketich JD, Panacek EA, Sahn SA, AACP
Pneumothorax Consensus Group. Management of
1. van Berkel V, Kuo E, Meyers BF.  Pneumothorax,
spontaneous pneumothorax: an American College of
bullous disease, and emphysema. Surg Clin North
Chest Physicians Delphi consensus statement. Chest.
Am. 2010;90(5):935–53. https://doi.org/10.1016/j.
2001;119(2):590–602.
suc.2010.06.008.
 Thoracoabdominal Aortic
Aneurysm
Albert G. Pavalonis and Anil Hingorani
Algorithmic Approach
A. The diagnostic imaging for a patient with a
thoracoabdominal aneurysm is usually done
by the time he/she is seen by the surgeon. In a
majority of cases, a TAAA is found inciden-
tally on imaging done for other reasons. The
two preferred imaging modalities for TAAA
are CT angiography and MR angiography (if
contrast allergy or significant concern for
renal failure). High-quality imaging of the
thoracoabdominal aorta is essential for accu-
rate classification of the aneurysm because
this determines treatment options [1].
B. Once high-quality imaging is available, the
next step is classifying the specific TAAA
subtype. The Crawford classification is the
standardized identification system. This sys-
tem is based on anatomic location of the
aneurysm and not size [2]. The Crawford
classification is:
A. G. Pavalonis
Department of Vascular Surgery, NYU Langone
Hospital-Brooklyn, Brooklyn, NY, USA
A. Hingorani (*)
Division of Vascular Services, NYU Langone
Hospital-Brooklyn, Brooklyn, NY, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_17
17
Type I: distal to left subclavian and proximal
to the renal arteries.
Type II: distal to left subclavian and inferior
to the renal arteries.
Type III: 6th intercostal space and inferior to
the renal arteries.
Type IV: inferior to the diaphragm extending
to the aortic bifurcation.
Type V: 6th intercostal space and proximal to
the renal arteries.
C. After the aneurysm has been anatomically
delineated based on the Crawford classifica-
tion, then the next important thing is the risk
of rupture. A TAAA with a size greater than
6 cm carries a yearly risk of rupture of 14.1%
[4]. Aneurysm growth of more than 2 mm per
year also carries an increased risk of rupture.
Patients with the following characteristics
exhibit higher propensity for rupture: Female,
COPD, and uncontrolled hypertension (espe-
cially diastolic >100 mmHg) [6].
63
64
D. The perioperative management/workup of
TAAA patients is important for optimal out-
come. Ideally, management and extended
workup should occur at a center that special-
izes in the treatment of TAAA (high-volume
center). It is important to consider the follow-
ing management [3, 6]:
1. Cardiac risk assessment
2. Strict control of hypertension
3. Initiation of statin therapy (found to
decrease risk of rupture)
4. Pulmonary assessment (FEV1  >  1.4
required for single lung ventilation during
open repair)
E. All repair options carry considerable risk for
complications. The most significant compli-
cations are the following: Paralysis, renal
failure, visceral ischemia, and myocardial
infarction [3]. Given the high risk of opera-
tion, the repair of a TAAA should only be
A. G. Pavalonis and A. Hingorani
considered when the risk of rupture overshad-
ows potential complications.
F. Repair options involve open repair, endovascular
repair, and hybrid repair. Open repair is the origi-
nal modality of TAAA repair and is still a viable
option in the setting of anatomy that may not be
adequate for endovascular repair. Endovascular
repair involves intraluminal insertion of a cus-
tom-made stent graft; however, this is not always
an option in cases of rupture as it requires
4–6  weeks to manufacture a patient-specific
stent graft [7]. That being said, endovascular
repair has been successfully performed in cases
of rupture with the utilization of chimney grafts
in conjunction with off-the-shelf stent grafts [1].
Finally, a hybrid repair could be considered. This
involves open debranching of visceral and aortic
arch vessels to maintain perfusion with subse-
quent placement of a stent graft to exclude the
aneurysmal aortic segment [5].
17  Thoracoabdominal Aortic Aneurysm 65

History and Physical Exam:

Thoracoabdominal aortic aneurysms usually found incidentally during the evaluation
and work up of other medical conditions
A

Obtain high-quality imaging (CT angiography or MR angiography)

Classification of TAAA based on the Crawford system

B
Type I: Distal to left subclavian and proximal to the renal arteries
Type II: Distal to left subclavian and inferior to the renal arteries
Type III: Sixth intercostal space and inferior to the renal arteries
Type IV: Inferior to the diaphragm extending to the aortic bifurcation
Type V: Sixth intercostal space and proximal to the renal arteries

Identify risk of rupture

C
> 6 cm carries a yearly risk of rupture of 14.1%.

Aneurysm growth of more than 2 mm

Patients with the following characteristics exhibit higher

propensity for rupture: female, COPD, uncontrolled hypertension
(especially diastolic >100 mmHg).

Peri operative Management

D 1. Cardiac risk sssessment

2. Strict control of hypertension
3. Initiation of statin therapy
4. Pulmonary assessment

E
Discussion of Risks and Complications Related to Therapeutic Intervention

F Referral to High-Volume Center for Repair

Algorithm 17.1
66 A. G. Pavalonis and A. Hingorani

Suggested Reading Fredric JR, Woo YJ. Thoracoabdominal aortic aneurysm.

Ann Cardiovasc Surg. 2012;1(3):227–85.
Kabbani LS, Criado E, Upchurch GR Jr, et  al. Hybrid
Black SA, Wolfe JH, Clark M, et  al. Complex thora-
repair of aortic aneurysms involving the visceral and
coabdominal aortic aneurysms: endovascular exclu-
renal vessels. Ann Vasc Surg. 2010;24:219–24.
sion with visceral revascularization. J Vasc Surg.
Stein LH, Berger J, Tranquilli M, et  al. Effect of statin
2006;43:1081–9.
drugs in thoracic aortic aneurysms. Am J Cardiol.
Davies RR, Goldstein LJ, Coady MA, et  al. Yearly rup-
2010;55:841–57.
ture or dissection rates for thoracic aortic aneurysms:
Zinganshin BA, Elefteriades JA.  Surgical manage-
simple prediction based on size. Ann Thorac Surg.
ment of thoracoabdominal aneurysms. Heart.
2006;81:169–77.
2014;100:1577–82.
Escobar GA, Upchurch GR Jr. Management of thora-
coabdominal aortic aneurysms. Curr Probl Surg.
2011;48:70–133.
Part IV
Breast
 Nipple Discharge
Anjali R. Thawani and Lillian M. Erdahl
Algorithmic Approach
A. The first step in the evaluation of a patient
with nipple discharge is a history to differenti-
ate pathologic from physiologic discharge.
Questions regarding the timing (spontaneous
vs. expressed), side, color/character, single vs.
multiple ducts, history of pregnancy and nurs-
ing, nipple trauma, smoking, signs of mastitis,
prior history of nipple discharge, as well as
breast cancer risk assessment will help to
determine the type of discharge present [1].
B. Physiologic nipple discharge is generally
bilateral, involves multiple ducts, and is often
nonspontaneous. The consistency of physio-
logic discharge may be serous, milky (galac-
torrhea), green, or brown [1, 2].
C. Pathologic nipple discharge is generally uni-
lateral, spontaneous, and serous or bloody, but
can also be brown. It is often from a single
duct but can involve multiple ducts [2, 3]. It is
more often associated with carcinoma, espe-
cially when serous or bloody [4]. Cytology of
nipple aspirate has a very low sensitivity for
A. R. Thawani
Division of Surgical Oncology, AMITA Health
System, Elk Grove Village, IL, USA
L. M. Erdahl (*)
Department of Surgery, University of Iowa,
Iowa City, IA, USA
e-mail: Lillian-erdahl@uiowa.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_18
18
cancer, and therefore generally is not helpful
in diagnosing malignancy [5].
D. Physical exam should focus on any skin or
nipple changes, nipple retraction, masses, or
nodules. An attempt at expressing the dis-
charge should be made, within reason.
Regional lymphadenopathy should also be
assessed [1, 2].
E. In the case of physiologic discharge, appropri-
ate work-up may include mammogram, ultra-
sound, and hormone levels to include prolactin
and TSH. Galactorrhea can be caused by ele-
vated prolactin levels, which in turn can be
caused by many medications which increase
prolactin levels, including psychotropics, anti-
hypertensives, gastrointestinal drugs, anesthet-
ics, amphetamines, marijuana, and estrogens [1,
2]. If prolactin levels are elevated in the absence
of drugs/medications, an MRI of the brain may
be required to r/o prolactinoma. It is important
to note that lactation can last up to 2 years after
pregnancy and occasionally longer.
F. Green or brown discharge is typically associ-
ated with periductal mastitis and generally
resolves on its own, as long as no active infec-
tion is present [2].
G. In the case of pathologic nipple discharge,
diagnostic mammogram and subareolar ultra-
sound are the imaging modalities of choice.
Although historically the sensitivity and
specificity of mammogram and US was
­considered low for diagnosis of malignancy
69
70
[3, 5], newer data suggests otherwise [6, 7]. If
no abnormalities (defined as a mass, indeter-
minate/suspicious calcifications, or architec-
tural distortion) are seen on mammogram and
subareolar US every 6 months for 2 years or
until the discharge is resolved, the upstage
risk to carcinoma is <3%. Surgical therapy to
excise the duct is typically unnecessary. In
the presence of an imaging abnormality,
biopsy is recommended to evaluate the cause.
Most often, surgery is also indicated to
remove the affected duct and underlying
lesion in order to rule out an associated carci-
noma [6, 7].
. Some institutions also utilize ductography for
H women of child-bearing age that surgery may
imaging of the affected duct. The perfor-
A. R. Thawani and L. M. Erdahl
mance of ductography is dependent on a phy-
sician who is experienced with this technique,
but is often poorly correlated with the surgi-
cal diagnosis [2, 8]. In some cases, MRI may
be considered for suspicious bloody dis-
charge with no imaging abnormality seen on
mammogram and ultrasound, especially in
those women at high risk for breast cancer
based on family history, age, or both.
I. Surgical options include ductoscopy, image/
discharge-guided single duct excision, and
major subareolar duct excision (the last of
these is defined as excision of all the central
nipple ducts) [9]. It is important to counsel
affect future lactation.
18  Nipple Discharge 71

A Nipple discharge
History and physical

Spontaneous Spontaneous
B/C Non Spontaneous
Unilateral Bilateral
Milky/white
D Green/gray/tan
Bloody Copious
Straw colored Milky

Mammogram and
Observe Endocrine work up
subareolar
E/F Routine screening including TSH and
ultrasound
and exams prolactin

G Abnormal
Negative
mammogram
mammogram
and/or
/US
subareolar US

Image guide
Counsel low
percutaneous biopsy
risk of
and/or subareolar duct
carcinoma
excision
(<3%)

Major or localized Q6-month follow-up

*Subareolar ducts can be
imaging and exams
I subareolar duct
until resolved or for
localized using a lacrimal
excision * probe, methylene blue dye,
1–2 years
ductography, or ductoscopy.

Algorithm 18.1
72 A. R. Thawani and L. M. Erdahl

References 5. Simmons R, Adamovich T, Brennan M, et  al.

Nonsurgical evaluation of pathologic nipple dis-
charge. Ann Surg Oncol. 2003;10(2):113–6.
1. Laronga C, Tollin S, Turanga K.  History, physi-
6. Gray RJ, Pockaj BA, Karstaedt PJ. Navigating murky
cal examination, and staging. In: Keurer H, editor.
waters: a modern treatment algorithm for nipple
Keurer’s breast surgical oncology. New York: The
discharge. Am J Surg. 2007;194:850–4; discussion,
Mc-Graw Hill Companies; 2010. p. 126–8.
854–5.
2. Kato M, Simmons R. The evaluation and treatment of
7. Ashfaq A, Senior D, Pockaj B, et al. Validation of a
nipple discharge. In: Scott-Conner C, Dirbas F, edi-
modern treatment algorithm for nipple discharge. Am
tors. Breast surgical techniques and interdisciplinary
J Surg. 2014;208:222–7.
management. New York: Springer; 2011. p. 179–86.
8. Cabioglu N, Hunt K, Singletary SE, et  al. Surgical
3. Adepoju LJ, Chun J, El-Tamer M, et al. The value of
decision making and factors determining a diagnosis
clinical characteristics and breast imaging studies in
of breast carcinoma in women presenting with nipple
predicting a histopathologic diagnosis of cancer or
discharge. J Am Coll Surg. 2003;196(3):354–64.
high-risk lesion in patients with spontaneous nipple
9. Sharma R, Dietz J, Wirght H, et al. Comparative anal-
discharge. Am J Surg. 2005;190:644–6.
ysis of minimally invasive microductectomy versus
4. Neslon RS, Hoehn JL. Twenty year outcome follow-
major duct excision in patients with pathologic nip-
ing central duct resection for bloody nipple discharge.
ple discharge. Surgery. 2005;138:591–6; discussion,
Ann Surg. 2006;243:522–4.
596–7.
 Breast Mass Evaluation
Anjali R. Thawani and Lillian M. Erdahl
Algorithmic Approach
A. Workup of any breast mass starts with taking
a focused history and performing a physical
exam. Key components of the history include
onset, duration, size, change in size, associ-
ated pain, cyclical changes, nipple discharge,
and personal history of breast disease. In
addition, the history should include a gyneco-
logic and personal family history of cancer
including but not limited to breast cancer. The
physical exam should include examination of
the regional lymph nodes in the neck, chest,
and axilla. Breast exam components include
inspection, palpation seated and supine, and
examination for nipple discharge. There are
limited data regarding the most effective
technique for breast exam. Based on research
using sensor-based breast models, it appears
the rubbing movement is the most effective
technique for detecting masses [1].
B. Once the history and exam are complete, the
practitioner can determine the best type of
imaging for further evaluation. Correlation
A. R. Thawani
Division of Surgical Oncology, AMITA Health
System, Elk Grove Village, IL, USA
L. M. Erdahl (*)
Department of Surgery, University of Iowa,
Iowa City, IA, USA
e-mail: Lillian-erdahl@uiowa.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_19
19
between clinical and radiographic findings
should always be evaluated.
C. Mammography is typically the preferred
imaging modality for palpable breast lesions.
For young women and women with dense
breast tissue, mammogram may miss lesions.
If a woman is under 40, we recommend first
discussing the optimal imaging with the radi-
ologist performing the study. Ultrasound is
the study of choice in the evaluation of a pal-
pable breast mass in women under the age of
30 or who are lactating or pregnant. Women
aged 30–39 may benefit from starting with
ultrasound according to the American College
of Radiology Appropriateness Criteria© [2].
D. After mammogram, ultrasound of a palpable
mass is usually recommended to provide fur-
ther detail on the characteristics of the mass.
Diagnostic ultrasound can also be used to
determine the best method of biopsy if a
biopsy is recommended [2].
E. It is rarely necessary to perform MRI for
diagnostic evaluation of a palpable mass.
However, it may be indicated for further eval-
uation after initial imaging and biopsy [2].
F. Suspicious masses on imaging, BIRADS cat-
egory 4 or 5 should be biopsied with core
biopsy and placement of a radiologic marker
for future identification. Medical or surgical
treatment will then be based on both patho-
logic findings and radiologic-pathologic
concordance. Discordant biopsy results
­
73
74
should be reviewed with the performing radi-
ologist and pathologist to determine next
steps and surgical excisional biopsy should
be considered [2].
G. Solid masses interpreted as probably benign
on imaging, BIRADS 3, should be reviewed
and core biopsy considered if they are new in
a patient with prior imaging within the past
year. Lesions that are not biopsied should be
followed with short interval exam and imag-
ing [2]. Perform repeat history and physical
exam in 3  months to evaluate for change in
the mass that might require additional evalua-
tion. Continue to follow every 6 months until
the lesion is stable for 2 years. These lesions
A. R. Thawani and L. M. Erdahl
have a 2.6–6.9% rate of progressing to appear
more suspicious and require biopsy [3, 4].
The majority of lesions that progress will do
so in the first 6 months [3].
H. Benign or negative imaging findings of
BIRADS 2 and 1, respectively, should be
reviewed. If physical exam is concerning, dis-
cuss with a radiologist possible additional
imaging to evaluate the finding. If no addi-
tional imaging will be beneficial, consider
fine needle aspiration of palpable mass. Treat
the patient based on pathology results [2].
I. Cysts presenting as palpable masses should
not be routinely aspirated. Aspiration of a
painful cyst may be considered [2].
19  Breast Mass Evaluation 75

A B Breast mass
History and physical

Age <30
Pregnant Age 30–39 Age ≥ 40
Lactating

Diagnostic
Diagnostic targeted Diagnostic
mammogram or
ultrasound mammogram
targeted ultrasound

Review imaging findings, if BIRADS 0-incomplete

Order additional testing to complete

BIRADS 1 : Negative BIRADS 4 : Suspicious

BIRADS 3 : Probably Benign
BIRADS 2 : Benign BIRADS 5 : Highly Suspicious

G New on imaging

Further workup only on Follow-up in 3 months Image-guided percutaneous

H suspicious masses Monitor on physical exam core needle biopsy with F
Consider FNA in select cases Repeat imaging 3-6 months radiologic clip placement

Are radiology and

Follow solid lesions 3-6 pathology concordant?
months until stable 2 years

NO
YES
Consider excisional
Treat tissue diagnosis
biopsy

Algorithm 19.1
76 A. R. Thawani and L. M. Erdahl

References 3. Buch K, Qureshi M, Bloch B, et  al. Surveillance of

probably benign (BI- RADS 3) lesions in mammog-
raphy: what is the right follow-up protocol? Breast J.
1. Laufer S, D’Angelo AD, Kwan C, Ray RD, Yudkowsky
2015;21(2):168–74.
R, Boulet JR, McGaghie WC, Pugh CM. Rescuing the
4. Harvey JA, Nicholson BT, Lorusso AP, Cohen MA,
clinical breast examination: advances in classifying
Bovbjerg VE. Shortterm follow-up of palpable breast
technique and assessing physician competency. Ann
lesions with benign imaging features: evaluation of
Surg. 2017;266(6):1069–74.
375 lesions in 320 women. AJR Am J Roentgenol.
2. Harvey JA, et al. ACR appropriateness criteria palpable
2009;193:1723–30.
breast masses. J Am Coll Radiol. 2016;13(11):e31–42.
 Ductal Carcinoma In Situ
Anjali R. Thawani and Lillian M. Erdahl
Algorithmic Approach
A. Ductal carcinoma in situ (DCIS) of the breast
is a heterogenous group of lesions with
diverse malignant potential and several treat-
ment options. It is generally considered a
“preinvasive” lesion, meaning that it has not
crossed the basement membrane of the cell
into adjacent tissue. It is a nonobligate pre-
cursor to invasive cancer. Overall, if left
alone, 25–40% of patients will develop an
invasive cancer, which constitutes the ratio-
nale for treatment. When appropriately
treated, the mortality from DCIS remains
low, at 0.5–1.0% [1–4].
B. Most DCIS is found on mammography.
Eighty percent are associated with calcifica-
tions seen on mammogram. These calcifica-
tions are generally a good guide, but do not
always predict the extent of DCIS. The final
pathology may be larger, smaller, or the same
as the mammographic imaging [1, 5].
C. The first step in the evaluation of the patient
with biopsy-proven DCIS is a complete his-
A. R. Thawani
Division of Surgical Oncology, AMITA Health
System, Elk Grove Village, IL, USA
L. M. Erdahl (*)
Department of Surgery, University of Iowa,
Iowa City, IA, USA
e-mail: Lillian-erdahl@uiowa.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_20
20
tory and physical exam. Key aspects of the
history include family history of breast can-
cer, time of unopposed estrogen (i.e., early
menarche, late parity, late menopause), pres-
ence of a mass, nipple discharge or retraction,
history of hormone replacement therapy, his-
tory of previous chest or neck radiation ther-
apy, BMI, and presence of previous breast
biopsies [6]. A strong family history should
warrant a consultation with a genetic counsel-
lor for genetic testing. * Refer to NCCN
guidelines on hereditary testing [7]. Physical
exam should include a detailed breast exam,
expression of nipple discharge if present,
breast size, and the presence of lymphade-
nopathy [2].
D. DCIS is classified based on nuclear grade and
the presence of necrosis in many systems.
This classification allows for prediction of
local recurrence risk when combined with
tumor size, age, and margin status. The high-
est local recurrence risk is for high-grade
lesions. Non-high-grade lesions with necrosis
recur more often than those without necrosis
[2, 8, 9].
E. Treatment for DCIS includes excision alone,
excision and radiation therapy (RT) +/− hor-
mone therapy (HT), and mastectomy. Choice
of operation does not alter overall survival,
although local recurrence is higher after
breast-conserving surgery. The addition of RT
will generally decrease the local recurrence
77
78
risk by 50%. The addition of HT will also
reduce the local recurrence risk by at least
30% [10–16].
F. The choice of treatment is based upon the
extent of disease, patient preference, and esti-
mation of local recurrence. The van Nuys pre-
diction Index incorporates size, age, margin
status, and pathology and is a useful tool to esti-
mate local recurrence and to determine future
therapy. Genomic testing (currently Oncotype
DCIS) can be performed on the lumpectomy
specimens to better quantify recurrence risk
and need for adjuvant therapies [9, 17, 18].
G. Sentinel lymph node biopsy is not indicated
for pure DCIS on core biopsy, unless the
patient has to undergo mastectomy.
A. R. Thawani and L. M. Erdahl
Microinvasion is defined as the extension of
cancer beyond the basement membrane into
adjacent tissues with no focus greater than
1 mm in dimension. In general, the incidence
of occult invasion is less than 10%. A delayed
sentinel lymph node biopsy when invasion is
found at final pathology is safe, accurate, and
prevents unnecessary axillary surgery, since
the majority of patients will not have invasive
cancer on final excision [1, 2].
H. The most recent consensus statement on mar-
gins recommends a 2 mm margin for DCIS,
which has been thought to decrease the local
recurrence risk while minimizing unneces-
sary surgery in the form of re-excisions or
mastectomy [19, 20].
20  Ductal Carcinoma In Situ 79

DCIS diagnosed on
A percutaneous core biopsy

Review imaging and obtain

B/C additional imaging if needed
to confirm extent of disease

Favorable breast size to tumor

size ratio or
E favorable for oncoplastic
Multicentric disease
Diffuse, malignant, calcifications
technique
Early to mid-pregnancy
History of previous breast radiation
*History of scleroderma, active lupus
*Unfavorable tumor to breast size ratio
Lumpectomy
Image localization with marker

F
Invasion present Mastectomy
with sentinel lymph node biopsy
No invasion present

Invasive cancer algorithm G

Margins < Margins > or
H 2 mm = 2 mm

Mastectomy Re-excision

*Denotes relative contraindication

**Radiation therapy
**May be avoided in select patients

**Hormonal therapy
in ER + PR + patients

Algorithm 20.1
80 A. R. Thawani and L. M. Erdahl

References New Zealand: randomized controlled trial. Lancet.

2003;362:95–102.
12. Viani GA, Stefano EJ, Alfonso SL, et  al. Breast-

1. Silverstein M, Lagios M. Ductal carcinoma in situ. In:
conserving surgery with or without radiotherapy in
Keurer H, editor. Keurer’s breast surgical ­oncology.
women with ductal carcinoma in situ: a metaanalysis
New York: The McGraw Hill Companies; 2010.
of randomized trials. Radiat Oncol. 2007;2:28–39.
p. 189–207.
13.
Fisher B, Constantino J, Redmond C, et  al.
2. Lagios M.  Duct carcinoma in situ: a Gordian knot
Lumpectomy compared with lumpectomy and radia-
untied. In: Scott-Conner C, Dirbas F, editors. Breast
tion therapy for the treatment of intraductal breast
surgical techniques and interdisciplinary manage-
cancer. N Engl J Med. 1993;328:1581–6.
ment. New York: Springer; 2011. p. 623–31.
14. Fisher B, Dignam J, Wolmark N, et al. Lumpectomy
3. Sanders M, Schuyler P, Dupont W, Page D. The natu-
and radiation therapy for the treatment of intraductal
ral history of low grade ductal carcinoma in suit of the
breast cancer: findings from the National Surgical
breast in women treated by biopsy only revealed over 30
Adjuvant Breast and Bowel Project B-17. J Clin
years of long term follow-up. Cancer. 2005;103:2481–4.
Oncol. 1998;16:441–52.
4. Rosen P, Senie R, Schottenfeld D, Ashikari
15. Julien J, Bijker N, Fentiman I, et al. Radiotherapy in
R. Noninvasive breast carcinoma: frequency of unsus-
breast conserving treatment for ducal carcinoma in
pected invasion and implications for treatment. Ann
situ: first results of EORTC randomized phase III trial
Surg. 1979;1989:377–82.
10853. Lancet. 2000;355:528–33.
5. Holland R, Hendriks J, Verbeek A, et  al. Extend,
16. Fisher B, Dignam J, Wolmark N, et  al. Tamoxifen
distribution, and mammographic/histological cor-
in treatment of intraductal breast cancer: National
reclations of breast ductal carcinoma in situ. Lancet.
Surgical Adjuvant Breast and Bowel Project B-24 ran-
1990;335:519–22.
domised controlled trial. Lancet. 1999;353:1993–2000.
6. Eva SS. Rating the risk factors for breast cancer. Ann
17. Solin LJ, Gray R, Bahner FL, et  al. A multigene
Surg. 2003;237(4):474–82.
expression assay to predict local recurrence risk for
7. National Comprehensive Cancer Network. Breast
ductal carcinoma in situ of the breast. J Natl Cancer
cancer. Genetic/familial high-risk assessment: breast
Inst. 2013;105(10):701–10.
and ovarian. Version 3.2017. https://www.nccn.org/
18. Rackovich E, Nofech-Mozes S, Henna W, et  al. A
professionals/physician_gls/pdf/genetics_screening.
population-based validation study of the DCIS score
pdf. Accessed 2/2018.
predicting recurrence risk in individuals treated by
8. Holland R, Peterse J, Millis R, et al. Ductal carcinoma
breast-conserving surgery alone. Breast Cancer Res
in situ: a proposal for a new classification. Semin
Treat. 2015;152(2):389–98.
Diagn Pathol. 1994;11:167–80.
19. Moran MS, Schnitt SJ, Giuliano AE, et al. Society of
9. Silverstein MJ, Poller D, Waisman J, et al. Prognostic
Surgical Oncology-American Society for Radiation
classification of breast ductal carcinoma-in-situ.
Oncology consensus guideline on margins for breast-
Lancet. 1995;345:1154–7.
conserving surgery with whole-breast irradiation in
10. Fisher B, Land S, Mamounas E, et  al. Prevention
stages I and II invasive breast cancer. Ann Surg Oncol.
of invasive breast cancer in women with ductal car-
2014;21(3):704–16.
cinoma in situ: an update of the National Surgical
20. Rosenberger LH, Mamtani A, Fuzesi S, et  al. Early
Adjuvant Breast and Bowel Project experience.
adoption of the SSO-ASTRO consensus guide-
Semin Oncol. 2001;28:400–18.
lines on margins for breast-conserving surgery with
11. UK Coordinating Committee on Cancer Research
whole-breast irradiation in stage I and II invasive
(UKCCR), Ductal Carcinoma in Situ (DCIS)
breast cancer: initial experience from Memorial
Working Party. Radiotherapy and tamoxifen in
Sloan Kettering Cancer Center. Ann Surg Oncol.
women with completely excised ductal carcinoma
2016;23(10):3239–46.
in situe of the breast in the UK, Australia, and
 Lobular Carcinoma In Situ
Anjali R. Thawani and Lillian M. Erdahl
Algorithmic Approach
A. LCIS is a high-risk atypical breast lesion.
Women diagnosed with classic type LCIS
have a 20–25% 10-year risk of developing
invasive breast cancer [1]. Studies show that
this risk exists for both breasts. Historically, it
had been shown that the risk of developing
invasive cancer was equal in the ipsilateral
and contralateral breasts [1]. More recent
studies suggest that the risk is somewhat
higher in the ipsilateral breast although both
breasts are still at risk.
B. The first step in evaluation of a patient with
LCIS is to determine how and why the biopsy
was performed and whether other disease was
associated with the LCIS. Most often, LCIS is
thought of as an incidental finding on biopsy
of an imaging abnormality such as mass, cal-
cifications, or MRI enhancement [2].
C. Excisional biopsy should be performed if a
mass was present or there is another finding,
such as radial scar, for which excision is rec-
ommended. Excisional biopsy should also be
A. R. Thawani
Division of Surgical Oncology, AMITA Health
System, Elk Grove Village, IL, USA
L. M. Erdahl (*)
Department of Surgery, University of Iowa,
Iowa City, IA, USA
e-mail: Lillian-erdahl@uiowa.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_21
21
performed if radiologic and pathologic find-
ings are discordant, as this carries a risk of
upgrade to cancer at excisional biopsy as high
as 38% in modern series [2, 3]. Excisional
biopsy is performed with localization of the
biopsy site and any residual imaging findings.
It is not necessary to achieve a negative mar-
gin for classic LCIS if specimen radiograph
and pathology confirm removal of the suspi-
cious area without additional findings. If can-
cer is found, margins should be assessed
following the margin guidelines outlined in
the corresponding chapters.
D. While some studies suggest classic LCIS
diagnosed on core biopsy in normal risk
patients diagnosed on screening mammogra-
phy with confirmed radiology-pathology con-
cordance can be monitored on imaging and
do not require excisional biopsy, this has not
been widely adopted as practice. The most
recent NCCN guidelines for breast cancer
recommend not excising LCIS with concor-
dance (biopsy otherwise benign) [4].
Confirming concordance is the responsibility
of the surgeon and requires discussion with
the radiologist and the pathologist to ensure
agreement [5]. Pursuing this option requires
monitoring the biopsied area with imaging
[5]. Evidence demonstrating a higher upstage
rate at excisional biopsy in women who had
LCIS found on high-risk screening protocol
had the following: imaging for a clinically
81
82
palpable mass, >4 foci of atypia at biopsy,
LCIS with associated atypical ductal hyper-
plasia, or LCIS found with a history of partial
mastectomy for breast cancer [3].
E. The risk of upstage to cancer in a woman
undergoing surgical excision of LCIS is 3%
overall with higher risk if excision is per-
formed for high-risk features listed in point D
up to 38% [3, 6]. Women should be counseled
prior to excision that additional therapy may
be recommended depending on the final
excision.
F. Women with a personal history of LCIS are at
increased risk of developing cancer of
approximately 1–2% per year [1, 7]. Due to
the increased risk, high-risk screening should
be recommended. Screening should include
clinical breast exam every 6  months and
yearly mammogram with consideration of
yearly MRI [5, 8].
G. After excision or biopsy of classic LCIS,
women should be offered risk-reducing
­hormonal therapy which has been shown to
A. R. Thawani and L. M. Erdahl
reduce the risk of breast cancer by more than
50% [9, 10]. Modifiable risk factors for breast
cancer should also be discussed including
obesity, sedentary lifestyle, and alcohol
intake. Another strategy that is sometimes
considered for risk reduction is bilateral pro-
phylactic mastectomies. Comorbidities that
impact risk and alternatives of high-risk
screening, hormonal therapy, and lifestyle
modification should be discussed with a
woman considering prophylactic mastecto-
mies for LCIS.
H. Pleomorphic LCIS is a special type of LCIS
and there is little research with long-term
follow-up looking at the outcomes of PLCIS
[11]. Excision to negative margins may
require mastectomy and the impact of clear
margins on long-term outcome is not clear
[11, 12]. Multidisciplinary discussion of
cases can aid in developing a treatment plan
as the role of radiation therapy is unclear.
Hormonal therapy should be offered as in
all LCIS.
21  Lobular Carcinoma In Situ 83

B LCIS diagnosed on core biopsy

Pleiomorphic LCIS Classic LCIS

Radiologic-pathologic
Review pathology, discuss Discordant or
high risk
concordance no D
excision to negative other lesion
margins

C
High risk screening F
Consider radiation Excisional biopsy with and
Consider hormonal therapy marker localization* discuss risk
reduction G

DCIS or invasive
cancer Classic LCIS

Use algorithms for

High risk screening F
and
DCIS or invasive
discuss risk
cancer
reduction
G

Algorithm 21.1

5. Landercasper J, Linebarger JH. Contemporary breast

References
1. Haagensen CD, Lane N, Lattes R, et al. Lobular neo-
plasia (so-called lobular carcinoma in situ) of the
breast. Cancer. 1978;42(2):737–69.
2. Degnim AC, King TA.  Surgical management of
high-risk breast lesions. Surg Clin North Am.
2013;93(2):329–40.
3. Rendi MH, Dintzis SM, Lehman CD, et  al. Lobular
in-situ neoplasia on breast core needle biopsy: imag-
ing indication and pathologic extent can identify
which patients require excisional biopsy. Ann Surg
Oncol. 2012;19(3):914–21.
4. National Comprehensive Cancer Network. Clinical
practice guidelines in oncology. Breast cancer.
Version 4.2017. https://www.nccn.org/professionals/
physician_gls/pdf/breast.pdf. Accessed 2/2018.
imaging and concordance assessment: a surgical per-
spective. Surg Clin North Am. 2011;91(1):33–58.
6. Murray MP, Luedtke C, Liberman L, et al. Classic
lobular carcinoma in situ and atypical lobular
hyperplasia at percutaneous breast core biopsy:
outcomes of prospective excision. Cancer.
2012;119(5):1073–9.
7. King TA, Pilewskie M, Muhsen S, et  al. Lobular
carcinoma in situ: a 29-year longitudinal experience
evaluating clinicopathologic features and breast can-
cer risk. J Clin Oncol. 2015;33(33):3945–52.
8. National Comprehensive Cancer Network. Clinical
practice guidelines in oncology. Breast cancer.
Genetic/familial high-risk assessment: breast and
ovarian. Version 3.2017. https://www.nccn.org/pro-
fessionals/physician_gls/pdf/genetics_screening.pdf.
Accessed 2/2018.
84
9. Fisher B, Costantino JP, Wickerham DL, et  al.
Tamoxifen for prevention of breast cancer: report of the
National Surgical Adjuvant Breast and Bowel Project
P-1 Study. J Natl Cancer Inst. 1998;90(18):1371–88.
10. Vogel VG, Costantino JP, Wickerham DL, et al. Effects
of tamoxifen vs raloxifene on the risk of developing
invasive breast cancer and other disease outcomes: the
NSABP study of tamoxifen and raloxifene (STAR)
P-2 trial. JAMA. 2006;295(23):2727–41.
A. R. Thawani and L. M. Erdahl
11. De Brot M, Mautner SK, Muhsen S, et al. Pleomorphic
lobular carcinoma in situ of the breast: a single insti-
tution experience with clinical follow-up and cen-
tralized pathology review. Breast Cancer Res Treat.
2017;165:411–20.
12. Flanagan MR, Rendi MH, Calhoun KE, Anderson
BO, Javid SH. Pleomorphic lobular carcinoma in situ:
radiologic-pathologic features and clinical manage-
ment. Ann Surg Oncol. 2015;22(13):4263–9.
 Enlarged Axillary Lymph Node
Zeynep Bostanci and Laura Kruper
Algorithmic Approach
A. The differential diagnosis of an enlarged axil-
lary lymph node includes reactive lymphade-
nopathy, lymphoma, and metastatic
carcinoma. When a patient presents with an
enlarged axillary node, a detailed history and
physical are essential, focusing on details
such as tobacco use, recent travel, recent ill-
ness, history of prior cancers (particularly
breast cancer), and symptoms such as cough,
night sweats, or weight loss. A thorough
breast examination should be performed, and
imaging including mammography and ultra-
sound should be ordered.
B. One of the first steps in a patient presenting
with new onset axillary adenopathy is a biopsy
of the lymph node; core needle is preferred
over FNA.  Once a malignancy is identified,
tumor markers are evaluated to identify the
primary site of disease and to guide manage-
ment. Neoplasms presenting with axillary
nodal involvement include lymphomas, breast
Z. Bostanci (*)
Breast Surgical Oncology, Ironwood Cancer and
Research Centers, Avondale, AZ, USA
L. Kruper
Breast Surgical Oncology, Department of Surgery,
City of Hope Hospital, Duarte, CA, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_22
22
cancers, melanomas, thyroid cancers, skin
cancers, sarcomas, lung cancers, and gastric
cancers [1]. Tumor markers can help narrow
the diagnosis and include carcinoembryonic
antigen (CEA), estrogen receptor (ER) and
progesterone receptor (PR), mammaglobin,
cytokeratins 7 and 20, CA 125, and thyroid
transcription factor (TTF-1). If the biopsy
demonstrates metastatic breast cancer and
mammography and ultrasound is unable to
demonstrate a primary breast lesion, MRI is
recommended as it can detect 50% of occult
breast cancers [2]. In addition, staging should
be completed with CT chest, abdomen, pelvis,
and bone scan, or PET CT if indicated. If a
primary lesion is identified on MRI, it should
be biopsied under MRI guidance. The patient
should then be managed depending on the
clinical stage and receptors.
C. If the biopsy is consistent with a breast pri-
mary and no primary lesion is identified, this
is referred to as “occult breast cancer,” repre-
senting 0.1–0.8% of all newly diagnosed
breast cancers [3, 4]. In this patient popula-
tion, in addition to systemic therapy, the
options include mastectomy with axillary dis-
section or, alternatively, axillary node dissec-
tion and radiation to the breast with equivalent
survival outcomes [5]. Adjuvant systemic
therapies are given, depending on the tumor
markers (ER, PR, Her2neu). Neoadjuvant
chemotherapy may be considered.
85
86 Z. Bostanci and L. Kruper

A 55-year-old woman palpated an axillary mass. She has no other complaints. On physical
A eamination she has a mobile, solitary lymph node at the right axilla. Examination of
bilateral breasts is within normal limits. She has no supraclavicular or cervical adenopathy

Obtain bilateral mammogram and ultrasound and right axillary ultrasound with biopsy of the
lymph node, if suspicious appearing on ultrasound

B Bilateral mammogram shows scattered fibroglandular breasts.

No suspicious lesions on mammography or ultrasound.
Axillary ultrasound shows a solitary, enlarged lymph node
with cortical thickening and loss of fatty hilum which was
biopsied. Biopsy shows adenocarcinoma consistent with
breast primary

Obtain bilateral breast MRI with contrast (also obtain CT chest

abdomen, pelvis, and bone scan to rule out metastatic disease)

Primary lesion
identified on
MRI?

C Yes D No

MRI-guided biopsy and Discussion with the patient about right

management directed by mastectomy and axillary node dissection vs
biopsy results axillary node dissection and radiation

Algorithm 22.1

4. Walker GV, Smith GL, Perkins GH, Oh JL, Woodward

References
1. NCCN clinical practice guidelines in oncology occult
primary version 2.2017 [Internet]. 2016 [cited 2017
Sep 4.]. Available from: https://www.nccn.org/profes-
sionals/physician_gls/pdf/occult.pdf.
2. Buchanan CL, Morris EA, Dorn PL, Borgen PI, Van
Zee KJ.  Utility of breast magnetic resonance imag-
ing in patients with occult primary breast cancer. Ann
Surg Oncol. 2005;12(12):1045–53.
3. Foroudi F, Tiver KW.  Occult breast carcinoma pre-
senting as axillary metastases. Int J Radiat Oncol Biol
Phys. 2000;47(1):143–7.
W, Yu T-K, et al. Population-based analysis of occult
primary breast cancer with axillary lymph node
metastasis. Cancer. 2010;116(17):4000–6.
5. He M, Tang L-C, Yu K-D, Cao A-Y, Shen Z-Z, Shao
Z-M, et al. Treatment outcomes and unfavorable prog-
nostic factors in patients with occult breast cancer.
Eur J Surg Oncol J Eur Soc Surg Oncol Br Assoc Surg
Oncol. 2012;38(11):1022–8.
 Metastatic Breast Cancer
Zeynep Bostanci and Laura Kruper
Algorithmic Approach
A. When a patient presents with history and
physical examination findings concerning
metastatic breast cancer, initial workup
should include breast imaging and tissue
biopsy. This should include bilateral diagnos-
tic mammography, ultrasound(s), and biop-
sies of any breast masses and suspicious
lymph nodes for characterization of the tumor
and confirming metastatic disease in the
axilla, infraclavicular, or supraclavicular
areas.
B. Metastatic breast cancer at the time of initial
diagnosis (de novo stage IV breast cancer)
compromises 5–6% of women with newly
diagnosed breast cancer [1]. According to
NCCN guidelines, patients who present with
clinical stage IIIA disease or higher or lower
stage with symptoms concerning metastatic
disease will need systemic staging with CT
chest, abdomen, and pelvis and bone scan.
Z. Bostanci (*)
Breast Surgical Oncology, Ironwood Cancer and
Research Centers, Avondale, AZ, USA
L. Kruper
Breast Surgical Oncology, Department of Surgery,
City of Hope Hospital, Duarte, CA, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_23
23
PET CT may be used if the CT scan or bone
scan is equivocal or suspicious. PET CT is not
indicated for early stage breast cancer or oper-
able stage III disease [2]. In addition to the
staging work up, any patient (<60 years old)
diagnosed with triple negative breast cancer
should be referred for genetic testing [3].
C. Depending on the practice setting, patient
should be referred to medical oncology once
there is a suspicion for metastatic disease. If
staging scans are concerning for metastatic
disease, biopsy should be performed to con-
firm the diagnosis. The tumor markers ER,
PR, and Her2neu should be tested from the
metastatic focus as these will guide treat-
ment. It is important to involve medical
oncologists early as systemic therapy should
be started urgently after diagnosis.
D. The role of surgery is limited in metastatic
breast cancer. When there is an excellent
response to systemic therapy, resection of the
metastatic focus (lung, liver) may be consid-
ered if there is no prohibitive risk to surgery
[4, 5]. Surgery on the primary breast tumor is
controversial. Surgery should not be recom-
mended if the distant disease is progressing;
however, breast surgery may be considered in
selected patients with well-controlled oligo-
metastatic distant disease with multidisci-
plinary input [6]. Ultimately, some patients
might require a palliative mastectomy to con-
trol infection, bleeding, or pain.
87
88 Z. Bostanci and L. Kruper

A
A 55-year-old woman felt a mass in her right breast a couple months ago. She never had screening
mammography. Recently, she noticed that the mass was getting larger and she also felt a lump at
her armpit. She has no other complaints. On physical examination, she has a 6 cm mass taking up
most of the right breast with nipple retraction. She also has bulky lymphadenopathy at right axilla

Obtain bilateral mammogram and right breast and axillary ultrasound with biopsy
of the mass and lymph nodes

Mammogram shows a 6 cm spiculated mass at the central right

breast. Ultrasound shows a 5.8 cm hypodense mass with irregular
borders and posterior shadowing at retroareolar position. There are
several suspicious lymph nodes with cortical thickening and loss of
fatty hilum. Biopsy of the mass shows invasive ductal carcinoma,
grade 3, triple negative. Biopsy of a representative lymph node
confirms metastatic adenocarcinoma consistent with breast primary

B Obtain CBC, CMP, CT chest, abdomen, pelvis, bone scan or PET CT, and genetic testing

C CT scan shows a solitary liver mass; biopsy was performed and

shows metastatic triple negative breast cancer. Patient referred to
medical oncology

Chemotherapy

Response?
Stable or regression Worsening disease

E Consider metastetectomy
Management per medical
oncology (change chemotherapy
and reassess)

Algorithm 23.1
23  Metastatic Breast Cancer 89

References 3]. Available from: https://www.nccn.org/profession-

als/physician_gls/pdf/genetics_screening.pdf.
4. Sadot E, Lee SY, Sofocleous CT, Solomon SB, Gönen
1. Breast cancer facts & figures. American Cancer
M, Kingham TP, et al. Hepatic resection or ablation
Society [Internet]. [cited 2017 Sept 3]. Available
for isolated breast cancer liver metastasis: a case-
from: https://www.cancer.org/research/cancer-facts-
control study with comparison to medically treated
statistics/breast-cancer-facts-figures.html.
patients. Ann Surg. 2016;264(1):147–54.
2. NCCN clinical practice guidelines in oncology breast
5. Macherey S, Mallmann P, Malter W, Doerr F,
cancer, version 2.2017 [Internet]. 2017 [cited 2017
Heldwein M, Wahlers T, et  al. Lung metastasec-
Sept 3]. Available from: https://www.nccn.org/profes-
tomy for pulmonary metastatic breast carcinoma.
sionals/physician_gls/pdf/breast.pdf.
Geburtshilfe Frauenheilkd. 2017;77(6):645–50.
3. NCCN clinical practice guidelines in oncology
6. Khan SA. Surgical management of de novo stage IV
genetic/familial high risk assessment: breast and ovar-
breast cancer. Semin Radiat Oncol. 2016;26(1):79–86.
ian version 2.2017 [Internet]. 2016 [cited 2017 Sept
 Recurrent Breast Cancer
Zeynep Bostanci and Laura Kruper
Algorithmic Approach
A. Patients with history of breast cancer are rou-
tinely followed to monitor for recurrence.
Most breast cancer recurrences occur within
the first 5 years of diagnosis [1]. For this rea-
son, National Comprehensive Cancer
Network Guidelines recommend that patients
treated for breast cancer undergo a history
and physical examination 1–4 times per year
(as clinically indicated) for 5 years and then
annually thereafter [2]. For patients who have
undergone breast conserving therapy (BCT),
mammography is performed every 12 months.
Ultrasound can be utilized to complement
mammography when specified. In following
the patient with prior breast cancer, it is
important to note the details of treatment
including surgery, adjuvant therapies, and, if
a component of prior therapy, response to
neoadjuvant chemotherapy and type of radia-
tion. Whether the patient had a lumpectomy
or mastectomy, sentinel lymph node biopsy
or axillary node dissection, whole breast radi-
ation (WBI) or accelerated partial breast irra-
Z. Bostanci (*)
Breast Surgical Oncology, Ironwood Cancer and
Research Centers, Avondale, AZ, USA
L. Kruper
Breast Surgical Oncology, Department of Surgery,
City of Hope Hospital, Duarte, CA, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_24
24
diation (APBI), and the presence of a genetic
mutation, all factors into how the patient
should be followed and what findings raise
clinical suspicion. Other important details
include initial stage of disease, response to
neoadjuvant chemotherapy, and tumor type
(i.e., hormone receptor positive, Her2neu
positive, triple negative) since the risk of
recurrence is dependent on such factors. A
careful review of systems should be per-
formed at each visit, assessing symptoms
such as abdominal pain, chest pain, cough,
bone pain, weakness, recent weight loss, per-
sistent headache, and blurred vision.
B. Once a breast cancer recurrence is suspected,
whether by examination or imaging, a tissue
diagnosis is needed. It is important to know
the status of estrogen, progesterone, and
Her2neu receptors as these will guide sys-
temic therapies.
C. After confirming breast cancer recurrence,
metastatic disease should be ruled out with
staging scans and labs (CBC and CMP). A
CT scan of the chest, abdomen, and pelvis
along with a bone scan are indicated. PET/CT
is most helpful in situations where standard
imaging studies are equivocal [2]. Brain MRI
is indicated if central nervous system symp-
toms present.
D. If there is no evidence of distant metastasis on
imaging, the case should be discussed in a
multidisciplinary fashion including surgery,
91
92 Z. Bostanci and L. Kruper

medical oncology, and radiation oncology Table 24.1  Management of local recurrence
with plastic surgery and genetics as indicated. Primary breast cancer Recurrent breast cancer
Systemic therapy is indicated for patients treatment treatment
with recurrent disease. If the recurrence is Lumpectomy + WBI Mastectomy
Lumpectomy + Mastectomy or lumpectomy +
unresectable upon presentation, systemic
APBI WBI
therapy should be the first step of treatment. Mastectomy without Excision of chest wall
Otherwise, there is no consensus on whether reconstruction mass + radiation
systemic therapies should be given before or Mastectomy + Excision of chest wall mass
after surgery. In cases where the recurrence implant-based with possible removal of the
reconstruction implant + radiation
has a more aggressive phenotype such as tri-
Mastectomy + Excision of chest wall
ple negative or Her2neu positive, chemother- tissue-based mass + radiation
apy may be recommended prior to surgery. If reconstruction
metastatic disease is identified, patient should
be referred to medical oncology and radiation
oncology. (Please see metastatic breast can- If patient had sentinel node biopsy at the time
cer topic.) of lumpectomy, repeat sentinel node biopsy at the
E. The patient’s previous treatment history is time of surgery may be performed.
taken into account when deciding surgical Regional recurrence is treated with surgery and
management. Table  24.1 shows the most radiation (axillary recurrence) or radiation alone
common treatment option in each circum- (supraclavicular or internal mammary nodes) in
stance, and alterations to these may be neces- addition to systemic therapy. There are multiple
sary depending on patient preferences and layers of complexity with each patient, and multi-
input from medical oncology, radiation disciplinary decision-making is fundamental when
oncology, and plastic surgery. treating a patient with recurrent breast cancer.
24  Recurrent Breast Cancer 93

A 55-year-old woman with a history of Stage I left breast cancer treated with breast
A conservation therapy (lumpectomy and radiation) presents with a new density
adjacent to the surgical bed on surveillance mammography

Perform physical examination, left breast ultrasound, ultrasound guided vs.

stereotactic biopsy of the area of concern

B
No distinct mass palpated at the area of concern. No palpable axillary lymphadenopathy.
1.1 × 1.2 × 1.5 cm mass was seen on ultrasound and biopsied which shows invasive
ductal carcinoma

C Obtain CBC, CMP, CT chest, abdomen, pelvis and bone scan or PET CT

Evidence of
distant
metastasis?

CT scan shows bone lesions at L2,

No evidence of distant metastasis on imaging
L3, L4, and femur

Multidisciplinary Refer the patient to medical oncology and

discussion for upfront radiation oncology
surgery or surgery
following chemotherapy

Systemic therapies are recommended

Surgery and systemic depending on receptor status. Radiation
therapies depending on therapy can be offered to treat bone pain
E receptor status

Algorithm 24.1
94 Z. Bostanci and L. Kruper

References tomy, and total mastectomy followed by irradiation. N

Engl J Med. 2002;347(8):567–75.
2. NCCN clinical practice guidelines in oncology breast
1. Fisher B, Jeong J-H, Anderson S, Bryant J, Fisher ER, cancer, version 2.2017 [Internet]. 2017 [cited 2017
Wolmark N. Twenty-five-year follow-up of a random- Sept 3]. Available from: https://www.nccn.org/profes-
ized trial comparing radical mastectomy, total mastec- sionals/physician_gls/pdf/breast.pdf.
 Paget’s Disease
Zeynep Bostanci and Laura Kruper
Algorithmic Approach
A. A concern for Paget’s disease is raised in any
patient presenting with eczema of the nipple
or areola, bleeding, yellowish exudate, and
itching or ulceration of the nipple. Paget’s
disease of the breast is rare, accounting for
1–3% of newly diagnosed breast cancers.
With Paget’s, greater than 90% are associated
with intraductal or invasive breast cancer [1].
The presentation may be confused by derma-
tologic conditions which may delay the
diagnosis.
B. When Paget’s disease is suspected, a thor-
ough physical examination of the breast
should be performed. If there is an underlying
cancer in the breast, the cancer may be remote
from the nipple-areolar complex (NAC). A
punch biopsy of the affected nipple skin
should be obtained for diagnosis.
C. Initial evaluation includes mammography
and ultrasound. If the nipple biopsy demon-
strates Paget’s and initial imaging fails to
detect a cancer within the breast, breast MRI
Z. Bostanci (*)
Breast Surgical Oncology, Ironwood Cancer and
Research Centers, Avondale, AZ, USA
L. Kruper
Breast Surgical Oncology, Department of Surgery,
City of Hope Hospital, Duarte, CA, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_25
25
should be obtained [2]. Of note, even when a
mass is identified with mammography or
ultrasound and diagnosis confirmed with
biopsy, MRI may still be useful in evaluating
the extent of disease (i.e., continuity between
the mass and NAC) which can aid in surgical
planning (central lumpectomy vs.
mastectomy).
D. If MRI demonstrates a mass not visualized on
mammography or ultrasound, an MRI-guided
biopsy should be performed. Depending on
the size of the mass and the relationship
between the mass and NAC, mastectomy
with sentinel lymph node biopsy (SLNB) or
lumpectomy including NAC (central lumpec-
tomy)  ±  SLNB may be considered and dis-
cussed with the patient [3]. Patients treated
with breast conservation will need radiation
therapy.
E. If no underlying cancer is identified within
the breast and the patient has isolated Paget’s
disease of the nipple, options include central
lumpectomy ± SLNB and radiation or mas-
tectomy with SLNB [3].
95
96 Z. Bostanci and L. Kruper

A 55-year-old woman is complaining of itching and burning sensation of the right nipple. She
A also noticed that it is red and scaly. She does not have nipple discharge. On examination,
right nipple has eczematous changes. There are no distinct masses or skin changes at the rest
of the breast, no lymphadenopathy. Her last mammogram was a year ago and normal.

Obtain bilateral mammogram and right breast

B
ultrasound, punch biopsy of the nipple

Bilateral mammogram shows heterogeneously dense breasts.

No suspicious lesions on mammography or ultrasound. Punch
abiopsy shows tumor cells in the epidermis consistent with
Paget’s disease

Obtain breast MRI with contrast

Concomitant
malignancy
identified on MRI?

D Yes E No

MRI-guided biopsy Discuss with the patient about right

mastectomy and sentinel node biopsy or right
breast central lumpectomy + radiation

Depending on the biopsy results and the

relationship between the mass and the
nipple-areolar complex (NAC),
mastectomy with SLNB, excision of NAC
and lumpectomy, ± SLNB, or central
lumpectomy including the mass and nipple
± SLNB may be considered

Algorithm 25.1

disease in select patients with Paget disease of the

References nipple. J Am Coll Surg. 2008;206(2):316–21.
3. NCCN clinical practice guidelines in oncology breast
1. Yim JH, Wick MR, Philpott GW, Norton JA, Doherty cancer, version 2.2017 [Internet]. 2017 [cited 2017
GM. Underlying pathology in mammary Paget’s dis- Sept 3]. Available from: https://www.nccn.org/profes-
ease. Ann Surg Oncol. 1997;4(4):287–92. sionals/physician_gls/pdf/breast.pdf.
2. Morrogh M, Morris EA, Liberman L, Van Zee K,
Cody HS, King TA. MRI identifies otherwise occult
 Locoregional Recurrence of Breast
Cancer
Jessica C. Gooch and Freya Schnabel
Algorithmic Approach
A. Patients who have had breast cancer should
undergo close follow-up after management of
their primary disease. A patient with a per-
sonal history of breast cancer is at risk for the
development of recurrence in the ipsilateral
breast after breast-conserving surgery (BCT)
and for the development of a contralateral
second primary [1, 2]. The most significant
risk factor for in-breast recurrence after BCT
is a positive lumpectomy margin [2]. Other
risk factors for in-breast recurrence include
young age, larger tumor size, lymphovascular
invasion, multifocal disease, high nuclear
grade, lymph node positivity, LCIS, triple
negative or HER-2/neu positive disease, and
the lack of radiation therapy to the breast after
a lumpectomy [2, 3]. Isolated regional lymph
node recurrences are uncommon, with vari-
ous studies citing rates of 0.2–1.6% in clini-
cally node-negative patients who undergo
sentinel node biopsy [4–6]. In-breast recur-
rence after BCT has recently been shown to
be 2% at 5 years and 5% at 10 years in a large
cohort from the Netherlands [7]. After mas-
tectomy surgery, patients may develop recur-
J. C. Gooch · F. Schnabel (*)
Department of Surgery, NYU Langone Health, NYU
Perlmutter Cancer Center, New York, NY, USA
e-mail: Freya.Schnabel@nyumc.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_26
26
rent disease on the chest wall or reconstructed
breast. Chest wall recurrence after mastec-
tomy is associated with the development of
metastatic disease. Most LRR occurs within a
median of 4 years of the original cancer diag-
nosis [2]. Triple negative and HER-2/neu-­
positive tumors are more likely to develop
LRR than tumors that are hormone receptor
positive [8–10].
B. Surveillance recommendations include peri-
odic history and physical examination by the
surgeon every 3–6 months for the first 3 years,
every 6–12 months for the next 2 years, and
annually after 5  years of follow-up is com-
pleted [11]. Patients who have undergone
BCT are at risk for ipsilateral breast tumor
recurrence, along with the development of a
contralateral second primary breast cancer.
Mammography of the affected breast every
6 months for the first 2 years after treatment is
recommended, followed by annual exams.
Other imaging may also be incorporated as
indicated, based on breast density and other
factors. After mastectomy, LRR may present
as a palpable superficial mass on the chest
wall (or reconstructed breast) or in the axilla.
Most patients will also be followed by their
medical oncologists, who may recommend
blood work and other imaging as per proto-
col. The workup for a suspected locoregional
recurrence starts with a full history and physi-
cal exam. The history should include the
97
98
r­elevant details of the patient’s previous
breast cancer, including the clinicopathologic
features of the tumor, the hormone, and
HER-2/neu status as well as the type of breast
and axillary surgery, radiation treatment (RT),
and systemic therapy.
C. The patient should undergo a thorough workup
to evaluate the extent of the recurrent disease.
When LRR is suspected after breast-­
conserving surgery, patients should undergo
diagnostic mammography with ultrasound
and/or MRI as clinically indicated. Tissue
sampling of all suspect areas is required to
confirm diagnosis and establish the biomarker
profile. Extensive or high-risk local disease
may also necessitate imaging to rule out dis-
tant metastases. Chest wall recurrences after E. After local management is complete, the
mastectomy are associated with the develop-
ment of distant metastases, and these patients
should be evaluated to rule out distant disease.
PET/CT or CT of the chest, abdomen, and pel-
vis and bone scan are useful in this regard [3].
D. Local recurrences may be categorized as
either an in-breast recurrence after breast
conservation, axillary recurrence, or a chest
wall recurrence after mastectomy. In patients
who had previous lumpectomy without radia- F. The patient with LRR will require careful
tion, it may be possible to perform a second
breast-conserving surgery with the addition
of post-lumpectomy radiation. In the case of
the patient who has had prior lumpectomy
with radiation treatment, a completion total
mastectomy is the standard approach [3]. If
the patient had a prior sentinel node biopsy
and is clinically node negative, it is appropri-
ate to attempt to map the axilla and perform a
second sentinel node biopsy. In patients who
have had previous mastectomy, a chest wall
J. C. Gooch and F. Schnabel
recurrence should be widely excised, remap-
ping sentinel nodes should be done if possi-
ble, and the patient referred for radiation
treatment (RT) as well as systemic therapy
[3]. Patients with isolated axillary recurrence
after sentinel node biopsy should undergo a
completion axillary dissection followed by
radiation treatment and systemic therapy as
appropriate. In cases of axillary recurrence
after prior axillary dissection, surgical resec-
tion should be performed for local control of
disease and followed by radiation treatment
and systemic therapy as appropriate.
Recurrences involving the internal mammary
or supraclavicular nodes should be referred
for radiation and systemic treatment [3].
patient should be referred to a medical oncol-
ogist for a discussion of their systemic treat-
ment options. The purpose of systemic therapy
is to reduce the risk for the development of
metastatic disease. Recommendations for sys-
temic treatment will be based on the patient’s
prior disease and treatment along with the
details of the recurrence, including the histo-
pathologic factors and biomarker profile [12].
follow-up. Regular breast imaging is impor-
tant to monitor any remaining breast tissue.
Annual mammography and physical exam
every 6–12 months with the surgeon is war-
ranted. Blood work and other imaging may be
directed by the medical oncologist, with the
focus on potential sites of disease. Any new
symptoms should have further evaluation.
The following algorithm for management of
locoregional recurrence is adapted from the
NCCN guidelines [11].
26  Locoregional Recurrence of Breast Cancer 99

Patient presents with palpable mass

A or
a new lesion is seen on routine
imaging/surveillance

B History and Physical Exam

-Previous cancer treatment: lumpectomy vs. mastectomy?
-Previous radiation and what dose
-Previous chemotherapy
-Previous endocrine therapy
-Palpable mass vs. imaging finding?

-Perform full physical exam, including bilateral breasts and lymph node basins

Imaging and Labs

C -Diagnostic mammogram if previous BCT and/or intact contralateral breast
-Full staging workup–consider US/CT/MRI for extent of breast/chest wall involvement
-Consider CT chest/abdomen/pelvis, PET/CT, bone scan, and CT/MRI of the brain to
evaluate for distant disease
-Biopsy of disease sites and evaluation of receptor status
-Check labs: CBC, CMP, LFTs, serum tumor markers

D In-breast recurrence Chest wall recurrence Nodal recurrence

-If previous BCT -If skin/chest wall -If axillary, resect if

with RT, perform recurrence, resect if possibleand refer for
mastectomy possible and radiation
consider radiation -If supraclavicular or
treatment internal mammary,
refer for radiation
treatment

E Referral to medical oncology for systemic chemotherapy and endocrine therapy

if hormone receptor positive
-Anti-Her2 therapy for Her2 positive disease

F
Follow-up

Algorithm 26.1
100 J. C. Gooch and F. Schnabel

References B-32 randomised phase 3 trial. Lancet Oncol.

2010;11(10):927–33.
7. Bosma SC, et al. Very low local recurrence rates after
1. Lin NU, et  al. International guidelines for manage-
breast-conserving therapy: analysis of 8485 patients
ment of metastatic breast cancer (MBC) from the
treated over a 28-year period. Breast Cancer Res
European School of Oncology (ESO)-MBC Task
Treat. 2016;156(2):391–400.
Force: surveillance, staging, and evaluation of patients
8. Lowery AJ, et al. Locoregional recurrence after breast
with early-stage and metastatic breast cancer. Breast.
cancer surger: a systematic review by receptor pheno-
2013;22(3):203–10.
type. Breast Cancer Res Treat. 2012;133:831–41.
2. Grotz TE, Boughey JC. Recurrent breast cancer. In: Wilke
9. Hattangadi-Gluth JA, et  al. Basal subtype of inva-
LG, Chagpar AB, editors. American Society of Breast
sive breast cancer is associated with a higher
Surgeons breast surgery manual: American Society of
risk of true recurrence after conventional breast-­
Breast Surgeons; 2012. www.breastsurgeons.org.
conserving therapy. Int J Radiat Oncol Biol Phys.
3. Shikama N, Sekiguchi K, Nakamura N. Management
2012;82(3):1185–91.
of locoregional recurrence of breast cancer. Breast
10. Gillon P, et  al. Factors predictive of locoregional

Cancer. 2011;18(4):252–8.
recurrence following neoadjuvant chemotherapy in
4. Navarro-Rodriguez E, et  al. Factors associated with
patients with large operable or locally advanced breast
disease recurrence in breast cancer patients with nega-
cancer: an analysis of the EORTC 10994/BIG 1-00
tive sentinel lymph node biopsy. Clin Breast Cancer.
study. Eur J Cancer. 2017;79:226–34.
2016;16(6):e181–6.
11.
Network, N.C.C.  NCCN-evidence blocks–recur-
5. de Boniface J, et al. Ten-year report on axillary recur-
rent or stage IV disease. In: NCCN guidelines ver-
rence after negative sentinel node biopsy for breast
sion 2.2016–invasive breast cancer. Fort Washington.
cancer from the Swedish Multicentre Cohort Study.
www.nccn.org: National Comprehensive Cancer
Br J Surg. 2017;104(3):238–47.
Network; 2016. p. 17–23.
6. Krag DN, et al. Sentinel-lymph-node resection com-
12. Aebi S, et al. Chemotherapy for isolated locoregional
pared with conventional axillary-lymph-node dissec-
recurrence of breast cancer (CALOR): a randomised
tion in clinically node-negative patients with breast
trial. Lancet Oncol. 2014;15(2):156–63.
cancer: overall survival findings from the NSABP
 Metastatic Breast Cancer
27
Jessica C. Gooch and Freya Schnabel

Algorithmic Approach nodes) should be evaluated with PET/CT (or

A. Metastatic breast cancer accounts for about
6% of all newly diagnosed breast cancers, an
incidence which has not changed despite
improvements in prognosis in recent years [1,
2]. Once breast cancer is metastatic, it is no
longer considered curable; however, a variety
of treatment options to extend survival and
palliate symptoms are available. Five-year sur-
vival in stage IV disease is approximately 26%
although recent studies suggest this may be C. Systemic therapy is the initial treatment for
increasing to as much as 36% [2–4]. The algo-
rithm is adapted from the NCCN guidelines
for management of recurrent and metastatic
disease. This is a highly complex topic, the full therapeutic options. If the disease is ER/PR
scope of which is beyond this brief review [5].
B. Patients presenting with a new breast cancer
diagnosis should undergo a full history, phys-
ical exam, and complete breast imaging.
Biopsy of the primary site should be done to
confirm the tumor histology and for bio-
marker analysis. Most commonly, this is done
via percutaneous or image-guided core nee-
dle biopsy. Patients presenting with locally
advanced breast cancer or those with high-­
risk disease (large primaries, positive axillary have suggested a benefit of surgical excision
J. C. Gooch · F. Schnabel (*)
Department of Surgery, NYU Langone Health, NYU
Perlmutter Cancer Center, New York, NY, USA
e-mail: Freya.Schnabel@nyumc.org
CT chest, abdomen, and pelvis and bone
scan) to rule out metastatic disease. The most
common first site of metastasis in breast can-
cer is bone, with ribs and spine frequently
involved. Other common sites for breast can-
cer metastasis include the liver and lungs.
Biopsy of a suspected metastatic site is often
required to confirm the diagnosis and provide
information on the biomarker profile which
may be different from the primary.
patients with metastatic disease at the time of
presentation. The biomarker profile of the
tumor will dictate some of the appropriate
positive, hormonal therapy (tamoxifen in pre-
menopausal patients, tamoxifen or aromatase
inhibitors in postmenopausal patients) is the
recommended first treatment. If the disease is
not hormone sensitive, chemotherapy is gen-
erally given. Anti-HER-2/neu therapy is rec-
ommended for patients with HER-2/
neu-positive disease. These patients should
be monitored closely to assess for response of
the primary tumor. Although some studies
of the primary tumor, the mainstay of treat-
ment for metastatic disease is systemic
­therapy, with surgery or radiation treatment
for local control and palliation of symptoms
[6–9]. A multidisciplinary approach is key.

© Springer Nature Switzerland AG 2019 101

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_27
102
D. Patients may present with metastatic disease at
some time after their initial breast cancer treat-
ment. Important factors to ascertain at the time
of diagnosis of metastatic disease include
patient performance status, menopausal status,
current symptoms, and history of prior treat-
ments. The physical exam should include exam-
ination of the breasts and axillary, supraclavicular treatment, studies have shown that the addi-
and cervical lymph node basins, auscultation of
the chest, and palpation of the abdomen, at a
minimum. Diagnostic breast imaging should be
performed to rule out a new primary breast can-
cer. A full set of labs including CBC, CMP, F. Patients may progress through several lines of
LFTs, and serum tumor markers should also be
ordered. The full staging workup includes imag-
ing of the chest, abdomen, pelvis, skeletal sys-
tem, and brain using CT, MRI, PET/CT, or bone
scan. Any sites suspicious for metastatic disease
should be biopsied to confirm the diagnosis and
to evaluate the biomarker profile of the tumor,
which may differ from that of the original pri-
mary tumor [10, 11].
E. For patients with hormone-receptor-positive
metastatic breast cancer, endocrine therapy is
appropriate as a first step. Targeted anti-­
HER-­2/neu therapy may be used for patients
whose tumors overexpress HER-2/neu. For
hormone-receptor-negative patients, the
mainstay of treatment is chemotherapy.
While multidrug regimens have been demon-
strated to provide a survival benefit when
given as adjuvant therapy for local disease,
the role of these regimens in metastatic dis-
ease is still open to discussion [12]. However,
some studies have advocated polychemo-
therapy for metastatic disease [13], citing
longer survival and better overall quality of
life. For premenopausal patients, tamoxifen
is the mainstay of hormonal treatment, with G. Palliative care referrals for assistance with
the option of ovarian suppression and an aro-
matase inhibitor in selected cases. In post-
menopausal patients, an aromatase inhibitor
is the most common first-line hormonal ther-
apy. Patients with metastatic ER/PR positive
breast cancer are treated with a hormonal
agent until the time of progression of dis-
ease, at which time the treatment is changed
J. C. Gooch and F. Schnabel
to other endocrine options. In this manner,
patients may cycle through tamoxifen and all
three aromatase inhibitors. Other endocrine
treatments may include fulvestrant, which is
approved for treatment of metastatic breast
cancer in postmenopausal women [3]. In the
case of disease that is resistant to endocrine
tion of mTOR or CDK inhibitors such as
everolimus or palbociclib in combination
with endocrine treatment may improve pro-
gression-free survival [3].
therapy during the course of their disease. All
recurrent or metastatic patients should be
offered the option of enrollment in clinical
trials. Patients may benefit from surgical
resection or radiation therapy for symptom-
atic control of selected lesions [6–9].
Radiation to bony metastasis may improve
pain control and reduce risk of pathologic
fractures, while surgery and radiation in con-
junction with systemic therapy has been
shown to increase median survival in some
studies of patients with brain metastasis [9].
The initial follow-up for patients with meta-
static disease will occur primarily in the med-
ical oncologist’s office. Labs should be
repeated as needed while actively on systemic
treatment. Bone density testing should be
ordered every 2 years while on an aromatase
inhibitor and echocardiogram every 3 months
while on Herceptin. Imaging and follow-up
with the surgeon should be considered on an
as-­needed basis. Any new symptoms should
prompt a return to the physician’s office for
an exam and imaging to rule out progression
of disease.
symptoms such as pain or nausea may be
appropriate. Hospice referral is appropriate
when patients have progression of disease
despite multiple lines of therapy and are
approaching the end of life. Maintenance of
qualify of life and attention to the patient’s
goals of care is key throughout the manage-
ment of metastatic breast cancer.
27  Metastatic Breast Cancer 103

A Patient presents for evaluation of

breast cancer

New breast cancer diagnosis; Previous breast cancer diagnosis;

concern for advanced disease concern for recurrence or metastasis

B D

History and Physical Exam History and Physical Exam

-Perform full physical exam, including bilateral -Evaluate performance status, menopausal status,
breasts and lymph node basins current symptoms and previous treatment regimens

-Diagnostic mammogram and ultrasound
-Full staging workup–consider US/CT/MRI for extent
of breast/chest wall involvement
-Consider CT chest/abdomen/pelvis, PET/CT, bone
scan, and CT/MRI of the brain to evaluate for distant
disease
-Biopsy of disease sites and evaluation of receptor
status
-Check labs: CBC, CMP, LFTs,
and serum tumor markers
-Perform full physical exam including bilateral breasts
and lymph node basins, auscultation of chest and
examination of abdomen
-Diagnostic mammogram if previous BCT and/or intact
contralateral breast
-Full staging workup – consider US/CT/MRI for extent
of breast/chest wall involvement
-Consider CT Chest/Abdomen/Pelvis, PET/CT, bone
scan and CT/MRI of the brain to evaluate for distant
disease

-Biopsy of disease sites and evaluation of receptor

For ER/PR-positive disease:
C -Tamoxifen (premenopausal) or aromatase inhibitor
status
(postmenopausal) -Check labs: CBC, CMP, LFTs, serum tumor markers
-Evaluation for systemic chemotherapy
E
For Her-2/neu-positive disease:
Add Trastuzumab/Pertuzumab
For ER/PR-positive disease:
-Tamoxifen (premenopausal) or aromatase inhibitor
For hormone-receptor-negative disease: (postmenopausal)
-Systemic chemotherapy -Consider ovarian ablation/suppression
-Evaluation for systemic chemotherapy
Local treatments:
-RT or surgery for symptom control as needed
For Her-2/neu-positive disease:
Stable disease Disease progression Add Trastuzumab/Pertuzumab

For hormone-receptor-negative disease:

F Follow-up -Chemotherapy -Systemic chemotherapy
-Consider second-
or third-line endocrine
Local treatments;
regimens
-RT or surgery for symptom control as needed

Stable
G Consider second- disease
or third-line
Disease Stable
chemotherapy
progression disease
Hospice/palliative regimens and/or
Follow-up
care referral clinical trial
enrollment

Algorithm 27.1
104 J. C. Gooch and F. Schnabel

References 7. Ruiterkamp J, et  al. Surgical resection of the pri-

mary tumour is associated with improved survival in
patients with distant metastatic breast cancer at diag-
1. Barinoff J, et  al. Primary metastatic breast cancer
nosis. Eur J Surg Oncol. 2009;35(11):1146–51.
in the era of targeted therapy  – prognostic impact
8. Ruiterkamp J, Ernst MF. The role of surgery in meta-
and the role of breast tumour surgery. Eur J Cancer.
static breast cancer. Eur J Cancer. 2011;47:S6–S22.
2017;83:116–24.
9. Budach W.  Radiotherapy in patients with metastatic
2. Surveillance, E.a.E.R.P.  Cancer stat facts: female
breast cancer. Eur J Cancer. 2011;47:S23–7.
breast cancer. In: Cancer stat facts. National Cancer
10. Van Poznak C, et  al. Use of biomarkers to guide
Institute Surveillance, Epidemiology and End Results
decisions on systemic therapy for women with meta-
Program (SEER). seer.cancer.gov. 1975–2014.
static breast cancer: American Society of Clinical
3. Kaklamani V, Gradishar WJ.  Endocrine therapy in
Oncology clinical practice guideline. J Clin Oncol.
the current management of postmenopausal estrogen
2015;33(24):2695–704.
receptor positive metastatic breast cancer. Oncologist.
11. Lin NU, et  al. International guidelines for manage-
2017;22:507–17.
ment of metastatic breast cancer (MBC) from the
4. Mariotto AB, et  al. Estimation of the number of
European School of Oncology (ESO)-MBC Task
women living with metastatic breast cancer in the
Force: surveillance, staging, and evaluation of patients
United States. Cancer Epidemiol Biomarkers Prev.
with early-stage and metastatic breast cancer. Breast.
2017;26(6):809–15.
2013;22(3):203–10.
5. Network, N.C.C.  NCCN- evidence blocks  – recur-
12. Cardoso F, et  al. International guidelines for man-
rent or stage IV disease. In: NCCN guidelines ver-
agement of metastatic breast cancer: combination vs
sion 2.2016 – invasive breast cancer. Fort Washington.
sequential single-agent chemotherapy. J Natl Cancer
www.nccn.org: National Comprehensive Cancer
Inst. 2009;101(17):1174–81.
Network; 2016. p. 17–23.
13. Stockler M, et al. Systematic reviews of chemother-
6. Leung AM, et al. Effects of surgical excision on sur-
apy and endocrine therapy in metastatic breast cancer.
vival of patients with stage IV breast cancer. J Surg
Cancer Treat Rev. 2000;26(3):151–68.
Res. 2010;161(1):83–8.
 Inflammatory Breast Cancer
Jessica C. Gooch and Freya Schnabel
Algorithmic Approach
A. Inflammatory breast cancer is a rare presenta-
tion of invasive breast cancer that is associ-
ated with a poor prognosis. Between 1% and
5% of all newly diagnosed breast cancers in
the United States each year present in this
manner [1–3]. The diagnosis is suggested by
the clinical features at presentation and con-
firmed on tissue sampling. According to the
most recent AJCC staging criteria, inflamma-
tory cancer is by definition a T4d lesion. As a
result, these patients are at a minimum stage
IIIB at diagnosis [4, 5].
B. The first step in management is a full and
thorough history and physical exam. The
diagnosis of inflammatory breast cancer
relies on several clinical criteria [1]. These
include the rapid onset of breast erythema,
edema, and/or peau d’orange, with or without
the presence of an underlying mass. The ery-
thema should occupy at least 1/3 of the breast.
There may be nipple involvement such as
flattening, crusting, or retraction. The symp-
toms should have been present for no longer
than 6  months. Involved lymph nodes are
J. C. Gooch · F. Schnabel (*)
Department of Surgery, NYU Langone Health, NYU
Perlmutter Cancer Center, New York, NY, USA
e-mail: Freya.Schnabel@nyumc.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_28
28
common, presenting in nearly 80% of
patients, according to one study [6]. The dif-
ferential diagnosis at presentation may
include mastitis, and an initial course of anti-
biotics may be a reasonable strategy.
However, failure to respond promptly to
treatment should be the cause for concern and
should trigger additional investigation with-
out delay [1–3].
C. Patients with suspected inflammatory breast
cancer should undergo diagnostic breast
imaging, including bilateral mammography
and additional imaging as appropriate.
Imaging should include an evaluation of the
axillary nodes. MRI may also be helpful and
will demonstrate over 90% of cancers as well
as skin thickening and enhancement [1, 3].
Core biopsies of any suspicious breast masses
should be done to confirm the diagnosis and
for biomarker analysis. In addition, a punch
biopsy of involved skin should be done, as the
histologic hallmark of inflammatory breast
cancer is tumor involvement of the dermal
lymphatics, which produces the characteristic
presentation.
D. Once there is tissue confirmation of the dis-
ease, the patient should proceed expeditiously
to a workup to exclude metastatic disease,
including labs, bone scan, chest X-ray, CT, or
PET/CT. Regional nodal disease is common
in inflammatory cancer, and 30% of patients
are found to have metastatic disease at
105
106
­diagnosis [1, 3]. Suspicious axillary nodes
should be biopsied to confirm the extent of
disease. The treatment of patients with meta-
static breast cancer is discussed elsewhere in
this text.
E. The contemporary approach to treatment for
patients with inflammatory breast cancer
includes neoadjuvant chemotherapy, fol-
lowed by surgery and other treatment modali-
ties (including radiation treatment and
endocrine therapy) as appropriate. The typi-
cal chemotherapy regimens include anthracy-
clines and taxanes [2–4]. Those patients
whose tumors overexpress HER-2/neu should
also receive trastuzumab, and dual blockade
with pertuzumab is also approved for neoad-
juvant treatment of HER-2/neu-positive
patients [3, 4]. Patients should be followed
clinically during neoadjuvant treatment, with
repeat MRI at the completion of therapy to
evaluate for objective response.
F. Patients who respond to chemotherapy and
have resectable disease are candidates for sur-
gical resection. The most common procedure
is a total mastectomy with evaluation of the
axillary nodes as appropriate. However, a
patient with excellent response to neoadjuvant
treatment may be a candidate for less exten-
sive procedures [2]. Axillary nodal involve-
ment is noted in up to 85% of patients, making
those patients ineligible for sentinel node
­procedures [3]. Following surgery, most
patients are candidates for post-mastectomy
J. C. Gooch and F. Schnabel
radiation. Comprehensive nodal irradiation
(including the ipsilateral axilla, infraclavicu-
lar and supraclavicular nodes) is recom-
mended for patients with extensive nodal
disease [2, 4]. Breast reconstruction may be
offered to patients with good response to neo-
adjuvant treatment; however, the impact of
post-mastectomy radiation should be taken
into consideration (see Chap. 29, Breast
Reconstruction).
G. After surgery, patients with HER-2/neu-­
positive disease will continue anti-HER-2
treatment for 1  year. As noted above, post-­
mastectomy radiation is commonly recom-
mended for patients with inflammatory breast
cancer. Although up to 83% of inflammatory
breast cancers lack hormone receptor expres-
sion, endocrine therapy is appropriate for
patients with ER/PR-positive disease [2].
Following treatment, the patient should con-
tinue close clinical follow-up including phys-
ical examination every 3–6  months and
regular imaging of the contralateral breast.
These patients should also be monitored for
the possibility of chest wall recurrence. As
these patients are at increased risk for the
development of metastatic disease, additional
follow-­up with lab work and body imaging is
appropriate and may be directed by the
patient’s medical oncologist. Any new symp-
tom referable to the common sites for metas-
tasis from breast cancer (bone, lung, liver)
should be evaluated promptly.
28  Inflammatory Breast Cancer 107

History and physical exam

A Patient presents with painful erythematous
breast with rapid onset and progression of
symptoms

B Assess for presence of diagnostic criteria

–Rapid onset of breast erythema, edema, peau d’orange, with or without an underlying mass
–Flattening, crusting or retraction of the nipple may be present
–Duration of no more than 6 months
–History of mastitis not responding to antibiotics
–Examination reveals erythema occupying at least 1/3 of the breast and may reveal an underlying
mass or palpable lymph nodes

Imaging: Diagnostic mammography and ultrasound; consider MRI

–Evaluate axilla
C

–Biopsy of mass
–Skin punch biopsy

D Metastatic Workup
–Labs
–Bone Scan
–CT Yes Biopsy No
Course of
–PET/CT consistent with
antibiotics
E –biopsy of suspicious carcinoma
nodes

Metastatic disease absent Metastatic disease present

Close follow
–Definitive systemic chemotherapy up for
–Primary systemic chemotherapy improvement;
–Endocrine therapy for HR+ Insufficient –Endocrine therapy for HR+ tumors
–Trastuzumab/Pertuzumab for continue
tumors response workup
–Trastuzumab/Pertuzumab for HER2+ tumors
HER2+ tumors

Response to treatment
F Monitor for response to
therapy
–Modified Radical Mastectomy
–Axillary Lymph Node Dissection

G
Postmastectomy radiation
therapy –Continue systemic therapy Follow up: physical exam q3–6mo
–Consider delayed –imaging for contralateral breast
reconstruction –symptom directed workup for
suspicion of recurrence

Algorithm 28.1
108 J. C. Gooch and F. Schnabel

References 3. Yamauchi H, et al. Inflammatory breast cancer: what

we know and what we need to learn. Oncologist.
2012;17(7):891–9.
1. Dawood S, et  al. International expert panel on
4. Network NCC.  NCCN  – evidence blocks  – inflam-
inflammatory breast cancer: consensus statement for
matory breast cancer, in NCCN guidelines version
standardized diagnosis and treatment. Ann Oncol.
2.2016 – Invasive breast cancer. 2016. p. 1–2.
2011;22(3):515–23.
5. Cancer AJCO. Breast cancer staging. 8th ed: Chicago,
2. van Uden DJ, et al. Inflammatory breast cancer: an over-
Illinois: A. C. Society; 2017.
view. Crit Rev Oncol Hematol. 2015;93(2):116–26.
6. Wecsler JS, et  al. Lymph node status in inflam-
matory breast cancer. Breast Cancer Res Treat.
2015;151(1):113–20.
 Breast Reconstruction
Jessica C. Gooch and Freya Schnabel
Algorithmic Approach
A. The initial stage in planning for breast recon-
struction is evaluation by the surgeon who will
perform the oncologic operation. The initial
evaluation focuses on the disease being treated
and the appropriate options for the surgical
phase of treatment. Referral to a plastic surgeon
for discussion of applicable reconstructive
options may follow. Women should be edu-
cated about the option for breast reconstruction
as it has significant benefits for quality of life
and emotional outcomes for the patient [1–3].
By federal law (Women’s Health and Cancer
Rights Act), the cost of breast reconstruction
after mastectomy is covered by medical insur-
ance, and in New York State, a discussion of all
of the various breast reconstruction options,
including contralateral symmetry procedures,
is also mandated by state law.
B. Plastic surgery consultation should include a
full history and physical exam, including a
focus on the cancer treatment plan, the patient’s
desires and concerns as related to breast sur-
gery, the body habitus, smoking history, and
general medical condition and comorbidities.
Smoking and significant medical comorbidi-
J. C. Gooch · F. Schnabel (*)
Department of Surgery, NYU Langone Health, NYU
Perlmutter Cancer Center, New York, NY, USA
e-mail: Freya.Schnabel@nyumc.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_29
29
ties as well as obesity are risk factors that may
increase the likelihood of postoperative
wound-healing complications, and these
should be identified in the preoperative evalua-
tion [1, 4]. Inflammatory breast cancer may be
a relative contraindication to immediate breast
reconstruction due to the need to resect
involved skin, the risk of recurrence, and the
need to move directly to postoperative radio-
therapy as soon as possible [1]. However, in
current practice, the majority of these patients
undergo neoadjuvant chemotherapy, and the
response to treatment may have an effect on
the posttreatment surgical options.
C. The role of breast reconstruction varies with
the type of oncologic surgery planned for
treatment of the patient’s cancer. Patients
undergoing breast-conserving therapy should
be evaluated for the likely magnitude of cos-
metic defect after lumpectomy and the poten-
tial benefit of oncoplastic techniques as part
of the procedure. Oncoplastic surgery aims to
improve the cosmetic results of breast cancer
surgery by mitigating the effects of resection
of a volume of breast tissue and reducing the
deformities that may result. These techniques
make use of advancement flaps of glandular
tissue and skin to fill the lumpectomy cavity
and may allow patients with unfavorable fea-
tures to undergo a breast-conserving approach
with an acceptable cosmetic outcome [5].
These patients often require a contralateral
reduction and/or mastopexy for symmetry.
109
110
D. As part of the preoperative evaluation, it is
important to determine whether or not the
patient is likely to require post-mastectomy
radiation therapy (PMRT) as this impacts on
the reconstructive decision-making. PMRT is
felt to adversely affect autologous tissue
reconstruction and increases the rate of cap-
sular contracture of implant reconstructions
[6]. Patients who are likely to undergo PMRT
may be best served by placement of a tissue
expander and expansion prior to beginning
radiation treatments. This preserves the skin
envelope and allows for the options of either
continued implant-based reconstruction or
conversion to autologous tissue reconstruc-
tion after the completion of radiation treat-
ment [1]. PMRT increases the risk of capsular
contracture, poor cosmetic outcome, poor
wound healing, and implant loss compared to
the non-radiated scenario.
E. Most patients undergoing mastectomy proce-
dures are able to undergo immediate recon-
struction. In patients undergoing mastectomy
procedures, the two reconstructive options
are implant-based reconstruction and recon-
struction using autologous tissue. Implant-­
based reconstruction is the most widely
performed procedure in the United States for
post-mastectomy reconstruction. Most often,
a tissue expander is placed at the time of the
mastectomy. The expander is filled over the
course of several months after the patient has
healed from the initial operation. The
expander is exchanged for a permanent
implant at a follow-up procedure. Some
patients may be able to undergo one-step
implant-based reconstruction, with a perma-
nent implant placed at the time of mastec-
tomy. Typically, this approach requires them
to accept a smaller implant than the size of
their breast before surgery. Currently, most
patients will opt to have silicone implants
placed [2]. Implant-based reconstruction has F. All patients may find that their reconstruc-
the advantage of being relatively simple and
straightforward with fewer surgical morbidi-
ties than autologous reconstruction. Implant-­
based reconstruction does not involve the
added morbidity of the donor site required in
autologous tissue reconstructions. However,
J. C. Gooch and F. Schnabel
this approach does require multiple outpa-
tient visits for expansion, and requires a sec-
ond surgical procedure. In addition, a breast
implant for reconstruction may not provide
an acceptable match for a contralateral native
breast, especially in women with large and
pendulous breasts [2–4].
Autologous reconstruction may be per-
formed via any number of different flaps,
including the TRAM, DIEP, SIEA, and GAP
flaps [7], depending on patient body habitus
and availability of sufficient tissue. These
flaps may be transferred on a vascular pedicle
or may utilize free tissue transfer techniques
with microvascular anastomoses to place the
flap into position. Autologous reconstruction
with free flaps and microsurgical anastomosis
requires significantly more technical exper-
tise than implant-based reconstruction, and
the procedures are time and resource inten-
sive. However, the patient has the benefit of
the natural feel of their own tissues and fre-
quently a better match of the native contralat-
eral breast. Autologous reconstruction has the
added advantage that the reconstructed breast
will change with changes in the patient’s
body habitus over time. The additional donor
site morbidity and significantly higher num-
bers of overall postoperative complications
including DVT/PE, blood transfusion require-
ments and surgical site infections when com-
pared to implant-based reconstruction are
drawbacks to this procedure [4]. Most studies
cite an overall complication rate for free tis-
sue transfer techniques in the range of
23–30% [4]. In addition, a small percentage
of patients, ranging from 1% to 5% will expe-
rience complete flap loss, depending on the
type of flap and whether it relies on a pedicle
or a microvascular anastomosis [4]. However,
patient satisfaction with autologous recon-
struction is quite high over time [1–4].
tion requires revision after the initial
operation(s) are completed. Scar revision,
fat grafting, and, in the case of implant
reconstruction, capsulotomy or capsulec-
tomy may all be required at some point.
Patients who have had total mastectomies
29  Breast Reconstruction 111

may also choose to undergo nipple recon-
struction with any one of a variety of local
flap techniques to recreate a nipple-areola
complex. The flap can subsequently be tat-
tooed to simulate the natural pigmentation
of the nipple and areola. Patients may also
choose to have contralateral mastopexy or
other surgery for symmetry [2].
G. Following the conclusion of reconstruction,
patients should continue screening with their
breast surgeon or oncologist. MRI may be
useful in evaluating implant integrity.

Initial Evaluation by Breast/General Surgeon

A and Referral to Plastic Surgeon

History and Physical Exam Considerations

B Focus:Cancer treatment plan, body habitus, smoking Significant comorbidities
history, medical comorbidities, patient desires/concerns -Body Habitus
-Active smoking

Contraindications
-Inflammatory Cancer
C Mastectomy -Patient does not desire

Breast Conserving
Therapy

Post-Mastectomy
D Radiation Therapy
planned? Oncoplastic
reconstruction if
appropriate with
Yes No consideration for
contralateral symmetry
procedures if necessary
E “Delayed” vs.
Immediate Immediate
Reconstruction Reconstruction

Tissue Expander
during Radiation Autologous Implant
Therapy Reconstruction Reconstruction

Expander exchange for

Implant after
Radiation Therapy

F
-Revision as needed
-Contralateral symmetry procedures
-Nipple Reconstruction

G Follow up

Algorithm 29.1
112 J. C. Gooch and F. Schnabel

References 4. Gart MS, et  al. Autologous options for postmastec-

tomy breast reconstruction: a comparison of outcomes
based on the American College of Surgeons National
1. Network NCC NCCN – Evidence blocks – Principles
Surgical Quality Improvement Program. J Am Coll
of breast reconstruction following surgery, in NCCN
Surg. 2013;216(2):229–38.
guidelines version 2.2016  – Invasive Breast Cancer.
5. Savalia NB, Silverstein MJ. Oncoplastic breast recon-
2016. p. 1–2.
struction: patient selection and surgical techniques. J
2. Djohan R, Gage E, Bernard S. Breast reconstruction
Surg Oncol. 2016;113(8):875–82.
options following mastectomy. Cleve Clin J Med.
6. Clemens MW, Kronowitz SJ. Current perspectives on
2008;75(Supplement 1):S17–23.
radiation therapy in autologous and prosthetic breast
3. Alderman AK, et  al. Does patient satisfaction with
reconstruction. Gland Surg. 2015;4(3):222–31.
breast reconstruction change over time? Two-year
7. Reconstruction options: a comparison chart. 2013,
results of the Michigan Breast Reconstruction
BreastCancer.org: www.breastcancer.org.
Outcomes Study. J Am Coll Surg. 2007;204(1):7–12.
 Management of Male Breast
Cancer
Jessica C. Gooch and Freya Schnabel
Algorithmic Approach
A. Male breast cancer accounts for only 1% of
all breast cancers and less than 1% of all
malignancies in men [1, 2]. In 2017, it is
estimated that there will be 2470 new cases
of breast cancer in men compared to 252,710
new cases in women, with a projected 460
deaths [3]. The mean age at diagnosis is typ-
ically quoted as 60–65 years [4, 5]. As male
breast cancer is a relatively rare clinical
entity, there are no established screening
protocols. As a result, male breast cancers
tend to present with painless palpable
masses rather than radiographic findings.
Some studies suggest a delay between onset
of symptoms and a final diagnosis of breast
cancer in males of over 10 months [5]. While
stage-for-stage they have similar outcomes
to female breast cancers, male patients tend
to present at a more advanced stage at diag-
nosis [1, 4, 5].
B. The workup of a male with a breast mass
begins with a full history and physical exam.
In a male patient, breast cancer risk factors
are predominantly related to family history of
J. C. Gooch · F. Schnabel (*)
Department of Surgery, NYU Langone Health, NYU
Perlmutter Cancer Center, New York, NY, USA
e-mail: Freya.Schnabel@nyumc.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_30
30
breast and other related cancers. Male
BRCA2 mutation carriers are known to be at
increased risk to develop breast cancer [2].
All men affected with breast cancer should
undergo genetic counselling and be recom-
mended for genetic testing [6]. Past medical
history and medication history are important
as increased exposure to estrogens is a risk
factor for breast cancer development.
Klinefelter syndrome, cryptorchidism, gyne-
comastia, liver disease, and prostate cancer
treated with hormonal therapy have been
associated with an increased risk for male
breast cancer, although some studies dispute
this fact [5, 7]. The patient should be ques-
tioned as to the location of the mass and
length of time it has been present, as well as
any other associated symptoms. As in
females, physical exam of the male patient
should focus on identification of any palpable
mass and whether it is fixed or involving the
skin. In males, due to the general paucity of
breast tissue, most breast cancers are located
in the subareolar aspect of the breast, where
the majority of the ductal tissue is present [5].
The contralateral breast should also be exam-
ined. The regional lymph nodes (including
axillary, cervical, and supraclavicular nodes)
should be evaluated for the presence of any
clinically positive nodes.
113
114
C. A male patient with a palpable breast mass
should be referred for diagnostic breast
­imaging. Mammography is generally feasi-
ble, particularly in the presence of gyneco-
mastia. Ultrasound may be useful for the
evaluation of any clinically suspicious axil-
lary nodes and may also guide the perfor-
mance of a biopsy. Biopsy samples should be
sent for histologic diagnosis and biomarker
analysis. The majority of male breast cancers
are hormone receptor positive (over 90%) and
mostly HER-2/neu negative, corresponding
to a Luminal A or Luminal B phenotype [5].
Preoperative assessment of the axilla should
follow the protocols for female patients
addressed elsewhere in the text.
D. The general approach to a male breast cancer
patient is similar to that of an affected female.
Patients who present with locally advanced
disease should be offered neoadjuvant che-
motherapy prior to surgery. The most com-
mon surgical procedure for male breast
cancer is a total mastectomy with evaluation
of the axillary nodes. The axilla should be
evaluated with sentinel node biopsy and com-
pletion axillary dissection as appropriate [2,
5]. Male breast cancer patients are more
likely to have axillary nodal involvement than
their female counterparts [5]. Breast recon-
struction is not often performed after male
breast cancer treatment. There is little experi-
ence with breast-conserving surgery in males,
and the typical subareolar primary location
decreases the cosmetic value of that approach.
J. C. Gooch and F. Schnabel
E. Adjuvant therapy after surgery for male breast
cancer should be recommended based on clini-
copathologic characteristics, following similar
protocol as for female breast cancer. Biomarker
analysis of the tumor (ER/PR, HER-2/neu sta-
tus, and Ki-67) is standard, and genomic
assays may also be employed to determine the
patient’s risk for recurrence and shed light on
the potential benefit for cytotoxic chemother-
apy. As in females, anthracyclines and taxanes
form the basis for most standard chemothera-
peutic regimens. Patients with hormone recep-
tor (ER/PR)-positive tumors should receive
hormonal therapy with tamoxifen or aroma-
tase inhibitors. There is discussion in the litera-
ture about the combination of an aromatase
inhibitor and an androgen suppressor for hor-
monal treatment of breast cancer, but this is not
the standard of care [1, 2]. Post-lumpectomy
radiation should be delivered to patients under-
going breast conservation surgery. The guide-
lines for post-­mastectomy radiation in males
follow those for females, with radiation rec-
ommended after mastectomy in cases of pri-
mary tumors greater than 5 cm in size and/or
lymph node involvement.
F. After treatment is completed, patients should
continue close clinical follow-up with their
healthcare team. Annual imaging of the contra-
lateral breast is appropriate as well. As noted
above, male breast cancer is associated with
BRCA2 mutations. If a man tests positive for a
mutation, close relatives should consider genetic
counselling and testing to clarify their status.
30  Management of Male Breast Cancer 115

History and physical exam

A
Patient presents with palpable breast mass

B
History
Mass: onset, location, symptoms
Past medical history/medications
Family history: breast or ovarian cancer in female relatives? Known genetic mutations?
Risks: Klinefelter syndrome, gynecomastia, BRCA 2, liver disease, DM, prostate cancer,
exogenous estrogen, and androgens

Physical exam
Mass: mobile vs. fixed location?
Axilla: palpable nodes, fixed/matted nodes?

C Imaging: mammography and ultrasound

Core biopsy – assess receptor status

D Workup demonstrates malignancy

Clinical T1, N0 Clinical T2 or above

E Clinical N1 or above

-Breast surgery – mastectomy vs. lumpectomy

-Consider neoadjuvant chemotherapy
-Axillary surgery – sentinel node biopsy, possible
-Axillary US and FNA
axillary dissection

-Consider chemotherapy
-Consider tamoxifen for ER+ tumors
-Consider PMRT

F Follow up

Algorithm 30.1
116 J. C. Gooch and F. Schnabel

References to race: a SEER population-based study. Oncotarget.

2017:1–11.
5. Javidiparsijani S, Rosen L, Gattuso P. Male breast car-
1. Kiluk JV, et  al. Male breast cancer: manage-
cinoma: a clinical and pathological review. Int J Surg
ment and follow-up recommendations. Breast J.
Pathol. 2017;25(3):200–5.
2011;17(5):503–9.
6. Network NCC. Breast and/or ovarian cancer genetic
2. Losurdo A, et al. Controversies in clinicopathological
assessment, in NCCN guidelines Version 2. 2017.
characteristics and treatment strategies of male breast
7. Hagberg KW, et al. Impact of 5-alpha reductase inhib-
cancer: a review of the literature. Crit Rev Oncol
itors for treatment of benign prostatic hyperplasia on
Hematol. 2017;113:283–91.
erectile dysfunction, treated depression, gynecomas-
3. Society AC.  Cancer facts and figures 2017. Cancer.
tia and breast cancer: a real world 20 year observa-
2017:1–74.
tional study. Clin Epidemiol. 2017;9:83–91.
4. Sun H, et  al. Clinicopathological characteristics and
survival outcomes of male breast cancer according
 Part V
Esophagus
 Management of Esophageal
Motility Disorders
Anthony R. Tascone and Caitlin A. Halbert
Algorithmic Approach
A. The first step in the evaluation of a patient
with a suspected esophageal motility disorder
is the history and physical examination.
Patients classically present with dysphagia
and chest pain. It is also important to inquire
about reflux symptoms, as gastroesophageal
reflux disease is the cause of most esophageal
motility disorders [1].
B. The next step in the workup of esophageal
motility disorders is to rule out mechanical
obstruction and esophageal cancer with esoph-
agogastroduodenoscopy (EGD) [2]. Barium
esophagram is an additional imaging modality,
which can help to rule out mechanical obstruc-
tion and give additional information about
esophageal and gastric anatomy. pH monitor-
ing may also be done to rule out reflux in
patients without classic symptoms [3].
C. After mechanical obstruction has been ruled
out, proceed with high-resolution manome-
try. The most recent version of the Chicago
Classification, released in May 2014, divides
A. R. Tascone
Department of General Surgery, Saint Luke’s Health
System, Kansas City, MO, USA
C. A. Halbert (*)
Advanced GI and Bariatric Surgery, Department
of General Surgery, Christiana Care Health System,
Newark, DE, USA
e-mail: Caitlin.a.halbert@christianacare.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_31
31
the “major disorders of peristalsis” into three
categories: distal esophageal spasm; hyper-
contractile, or jackhammer, esophagus; and
absent contractility. Distal esophageal spasm
is defined by premature contractions in at
least 20% of swallows with normal lower
esophageal sphincter (LES) relaxation.
Jackhammer esophagus is characterized by
hypercontractile peristalsis in at least 20% of
swallows. Absent contractility is character-
ized by aperistalsis in the setting of normal
LES relaxation [4].
D. It is important to note that there is a paucity of
data on treatment and outcomes for some of
the newly defined major disorders of peristal-
sis as described by the Chicago Classification
[4]. Treatment for each of the disorders begins
with avoiding trigger factors that cause symp-
toms, eating soft foods and chewing thor-
oughly, and reducing reflux with a proton
pump inhibitor (PPI) [2]. Distal esophageal
spasm is one of the new terms, and data is
scarce on the best treatment options.
Botulinum injections have shown promise in
reducing dysphagia symptoms in some small
studies [5]. Based on results from patients
with diffuse esophageal spasm, surgical myot-
omy with an extended myotomy showed good
results and can be used to treat patients who
fail botulinum injection therapy [6]. There is
also minimal data supporting the  best treat-
ment of jackhammer esophagus. A trial of cal-
119
120 A. R. Tascone and C. A. Halbert

cium channel blockers, nitrates, sildenafil, and
pain modulators (trazodone) may help with
pain [2]. Limited research suggests that botu-
linum injections and surgical myotomy may
be of some benefit in patients with continued
symptoms after pharmacologic treatment [2,
3]. Treatment of absent esophageal contractil-
ity entails dietary and lifestyle modifications,
as there is no specific treatment to restore or
improve peristalsis. Patients should be advised
to favor liquid and semisolid nutrition over
solids, consume meals in the upright position,
chew thoroughly, and drink during meals to
facilitate esophageal clearance. Reduction of
reflux symptoms with a PPI is also a target of
therapy [2].

A History and Physical:

Chest pain, dysphagia, reflux

B Esophagogastroduodenoscopy (EGD)
+/- Barium esophagram
+/- pH monitoring

No mechanical
obstruction?

Obtain high-resolution manometry

C

Findings consistent Absent Findings consistent

with distal esophageal with jackhammer
esophageal spasm contractility esophagus

Treatment: Treatment: Treatment:

1. Avoid trigger factors
and reduce reflux
2. Botulinum injections
3. Extended myotomy
Dietary and lifestyle
modifications, reflux
treatment
1. Avoid trigger factors
and reduce reflux
2. Pharmacologic
smooth muscle
relaxants
3. Botulinum injections
or surgical myotomy

Algorithm 31.1
31  Management of Esophageal Motility Disorders 121

References 4. Kahrilas PJ, Bredenoord AJ, Fox M, Gyawali

CP, Roman S, Smout AJPM, et  al. The Chicago
­classification of esophageal motility disorders, v3.0.
1. Diener U, Patti MG, Molena D, Fisichella PM, Way
Neurogastroenterol Motil. 2015;27(2):160–74.
LW.  Esophageal dysmotility and gastroesophageal
5. Bashashati M, Andrews C, Ghosh S, Storr
reflux disease. J Gastrointest Surg. 2001;5(3):260–5.
M.  Botulinum toxin in the treatment of diffuse
2. Zerbib F, Roman S.  Current therapeutic options for
esophageal spasm. Dis Esophagus [Internet].
esophageal motor disorders as defined by the Chicago
2010;23(7):554–60. Available from: http://www.ncbi.
classification. J Clin Gastroenterol. 2015;49(6):1–10.
nlm.nih.gov/pubmed/20459446.
3. Schlottmann F, Patti M. Primary esophageal motility
6. Leconte M, Douard R, Gaudric M, Dumontier I,
disorders: beyond achalasia. Int J Mol Sci [Internet].
Chaussade S, Dousset B.  Functional results after
2017;18(7):1399. Available from: http://www.mdpi.
extended myotomy for diffuse oesophageal spasm. Br
com/1422-0067/18/7/1399.
J Surg. 2007;94(9):1113–8.
 Management of Achalasia
Anthony R. Tascone and Caitlin A. Halbert
Algorithmic Approach
A. The first step in the evaluation of a patient
with achalasia is the history and physical
examination. Patients classically present with
dysphagia to solids and liquids associated
with regurgitation of undigested food or
saliva. Other common symptoms include
heartburn, noncardiac chest pain, epigastric
pain, cough or asthma, chronic aspiration,
and hoarseness [1]. An important part of the
examination of patients with potential achala-
sia is to rule out oropharyngeal dysphagia,
which can be done by watching the patient
drink water.
B. The next step in the workup of achalasia is to
rule out mechanical obstruction and esopha-
geal cancer, or pseudoachalasia, with esopha-
gogastroduodenoscopy (EGD). Findings
suggestive of achalasia on EGD include a
dilated or tortuous esophagus, food impac-
tions, fluid pooling in the esophagus, resis-
tance to intubation of the gastroesophageal
A. R. Tascone
Department of General Surgery, Saint Luke’s Health
System, Kansas City, MO, USA
C. A. Halbert (*)
Advanced GI and Bariatric Surgery, Department of
General Surgery, Christiana Care Health System,
Newark, DE, USA
e-mail: Caitlin.a.halbert@christianacare.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_32
32
junction, and candidiasis. Barium esopha-
gram is an additional imaging modality,
which can help to rule out mechanical
obstruction and, additionally, aid in diagnosis
of achalasia. It classically shows a dilated
esophagus with a narrow gastroesophageal
junction, otherwise known as a “bird’s beak”
appearance. Other suggestive features include
contrast filling the esophagus with poor emp-
tying, a “corkscrew appearance,” and aperi-
stalsis [2].
C. If there is no mechanical obstruction or other
cause for the patient’s symptoms found on
EGD or barium esophagram, proceed with
high-resolution manometry to secure the
diagnosis. Manometric findings of aperistal-
sis and incomplete lower esophageal sphinc-
ter relaxation diagnose achalasia. The most
recent version of the Chicago Classification
of esophageal motility disorders divides
achalasia into three distinct phenotypes,
which have prognostic and potential thera-
peutic implications [3, 4]. Type I achalasia
has the above findings with a normal esopha-
geal pressure. Type II achalasia is character-
ized by increased pan-esophageal pressure,
and Type III achalasia shows distal esopha-
geal spastic contractions [3].
D. The recommended first-line treatment of
achalasia depends on the specific phenotype.
Type I and Type II achalasia are treated with
either graded pneumatic dilation or laparo-
123
124 A. R. Tascone and C. A. Halbert

scopic surgical myotomy with partial or unwilling to undergo definitive therapy as

fundoplication, ideally performed at high-
­ described above, botulinum toxin therapy is
volume centers of excellence. First-line treat-
ment of Type III achalasia is laparoscopic
myotomy with partial fundoplication [5].
Peroral endoscopic myotomy (POEM) has
also emerged as a safe and reliable treatment
option when performed in expert centers but
carries a high prevalence of GERD due to the
fact that no antireflux procedure is performed
[6]. If the patient is a poor surgical candidate
recommended. Pharmacologic therapy with
calcium channel blockers, long-acting
nitrates, or the phosphodiesterase-5 inhibitor,
sildenafil, is reserved for patients who have
failed botulinum toxin therapy. Laparoscopic
surgical myotomy can be used for pneumatic
dilation failures and vice versa. Patients with
refractory achalasia can be offered repeat
myotomy or in rare cases esophagectomy [7].

A History and Exam:

Common symptoms: Progressive dysphagia, heartburn, regurgitation or vomiting,
noncardiac chest pain, epigastric pain, cough or asthma, chronic aspiration,
hoarseness
Rule out oropharyngeal dysphagia

B
Obtain imaging studies to rule out mechanical obstruction:
Esophagogastroduodenoscopy (EGD)
Barium esophagram

Obtain high-resolution manometry

C

Findings Pursue other

consistent with diagnosis
Achalasia?

High surgical risk

D Low surgical risk

Botulinum toxin
therapy
Type I-II Type III

Nitrates
Pneumatic Calcium channel blockers
Myotomy Sildenafil
dilation

Repeat myotomy or
dilation Esophagectomy

Algorithm 32.1
32  Management of Achalasia 125

References evant classification by high-resolution manometry.

Gastroenterology. 2008;135(5):1526–33.
5. Zerbib F, Roman S.  Current therapeutic options for
1. Tsuboi K, Hoshino M, Srinivasan A, Yano F,
esophageal motor disorders as defined by the Chicago
Hinder RA, Demeester TR, et  al. Insights gained
classification. J Clin Gastroenterol. 2015;49(6):1–10.
from symptom evaluation of esophageal motil-
6. Talukdar R, Inoue H, Reddy DN.  Efficacy of
ity disorders: a review of 4,215 patients. Digestion.
peroral endoscopic myotomy (POEM) in the
2012;85(3):236–42.
treatment of achalasia: a systematic review and meta-­
2. Pandolfino JE, Gawron AJ.  Achalasia. JAMA
analysis. Surg Endosc Other Interv Tech [Internet]
[Internet]. 2015;313(18):1841. Available from: http://
2015;29(11):3030–46. Available from: https://doi.
jama.jamanetwork.com/article.aspx?doi=10.1001/
org/10.1007/s00464-014-4040-6.
jama.2015.2996.
7. Vaezi MF, Pandolfino JE, Vela MF.  ACG clinical
3. Kahrilas PJ, Bredenoord AJ, Fox M, Gyawali CP,
guideline: diagnosis and management of achalasia.
Roman S, Smout AJPM, et  al. The Chicago clas-
Am J Gastroenterol [Internet] 2013;108(8):1238–
sification of esophageal motility disorders, v3.0.
49. Available from: http://www.nature.com/
Neurogastroenterol Motil. 2015;27(2):160–74.
doifinder/10.1038/ajg.2013.196.
4. Pandolfino JE, Kwiatek MA, Nealis T, Bulsiewicz W,
Post J, Kahrilas PJ.  Achalasia: a new clinically rel-
 Barrett’s Esophagitis
Caitlin A. Halbert and Anthony R. Tascone
Algorithmic Approach
A. Patients with multiple risk factors for Barrett’s
esophagitis should undergo screening endos-
copy. Risk factors include age greater than 50,
presence of symptoms for greater than 5 years,
presence of a hiatal hernia, obesity, white race,
and male sex. Screening for low-risk patients
with GERD is not routinely recommended [1].
B. Barrett’s esophagitis is a condition defined by
metaplasia of the distal esophageal mucosa.
On endoscopic biopsy, it consists of meta-
plastic columnar epithelium extending above
the gastroesophageal junction into the tubular
esophagus. White light endoscopy is recom-
mended with 4-quadrant mucosal biopsies of
the Barrett’s epithelium every 2  cm. The
interval is shortened to 1 cm for patients with
a history of dysplasia [1].
C. Treatment of patients with Barrett’s esophagus,
with or without GERD symptoms, consists of
long-term therapy with proton pump inhibitors
(PPI) [2]. Greater than standard dosing of PPI
C. A. Halbert (*)
Advanced GI and Bariatric Surgery, Department of
General Surgery, Christiana Care Health System,
Newark, DE, USA
e-mail: Caitlin.a.halbert@christianacare.org
A. R. Tascone
Department of General Surgery, Saint Luke’s Health
System, Kansas City, MO, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_33
33
therapy is not indicated for patients with
Barrett’s esophagitis. Endoscopic eradications
in the form of radiofrequency ablation (RFA),
photodynamic therapy (PDT), or endoscopic
mucosal resection (EMR) are recommended
for patients with high-grade dysplasia [1].
Eradication therapy should also be considered
in patients with low-grade dysplasia, especially
if persistent pathology is seen on repeat biopsy
[3]. EMR is preferred in patients with irregu-
larities of the mucosa on endoscopic visualiza-
tion. While endoscopic eradication therapy for
high-­grade dysplasia is successful for 70–80%
of patients, esophagectomy is an alternative
form of therapy. Esophagectomy should be
considered in patients with high-grade long-
segment or multifocal disease [1].
D. There are several indications for surgical
consultation for patients with Barrett’s
esophagus and GERD. Patients who are par-
tial responders to PPI, have severe regurgita-
tion, or cannot tolerate therapy with PPI. The
latter includes patients who elect surgical
intervention over lifelong need for medical
therapy [4]. While some experts recommend
antireflux surgery in any patient with
Barrett’s esophagus, there is no evidence to
prove that it is superior to medical manage-
ment [1, 5].
E. Surveillance endoscopy timing is dependent
on pathologic findings if no eradication ther-
apy has been performed [1].
127
128 C. A. Halbert and A. R. Tascone

Risk factors for Barrett’s esophagitis:

A Age greater than 50, presence of symptoms for greater than 5 years,
presence of a hiatal hernia, obesity, white race and male sex

Upper endoscopy

B Non-dysplastic Low-grade dysplasia High-grade dysplasia

Medical therapy for Medical therapy

Endoscopic eradication
C treatment of GERD Versus
therapy
symptoms and reflux Endoscopic eradication
esophagitis therapy

Consideration for Consideration for

D antireflux surgery antireflux surgery
Consideration for
antireflux surgery

Surveillance endoscopy: Surveillance endoscopy: Surveillance endoscopy:

E every 3-5 years every 6-12 months every 3 months

Algorithm 33.1

3. Kestens C, Offerhaus GJA, van Baal JWPM, Siersema

References
1. Spechler SJ, Sharma P, Souza RF, Inadomi JM,
Shaheen NJ.  American Gastroenterological
Association medical position statement on the man-
agement of Barrett’s esophagus. Gastroenterology.
2011;140(3):1084–91.
2. Freedberg DE, Kim LS, Yang Y-X.  The risks and
benefits of long-term use of proton pump inhibi-
tors: expert review and best practice advice from
the American Gastroenterological Association.
Gastroenterology [Internet]. 2017;152(4):706–15.
Available from: http://linkinghub.elsevier.com/
retrieve/pii/S0016508517300914.
PD.  Patients with Barrett’s esophagus and persis-
tent low-grade dysplasia have an increased risk for
high-grade dysplasia and cancer. Clin Gastroenterol
Hepatol. 2016;14(7):956–62.
4. Stefanidis D, Hope WW, Kohn GP, Reardon PR,
Richardson WS, Fanelli RD.  Guidelines for surgi-
cal treatment of gastroesophageal reflux disease.
Surg Endosc [Internet]. 2010;24(11):2647–69.
Available from: http://www.ncbi.nlm.nih.gov/
pubmed/20725747.
5. Wassenaar E, Oelschlager B.  Effect of medical and
surgical treatment of Barrett’s metaplasia. World J
Gastroenterol. 2010;16(30):3773–9.
 Gastroesophageal Reflux Disease
34
Caitlin A. Halbert and Anthony R. Tascone

Algorithmic Approach nal GERD.  Avoidance of tobacco, alcohol,

A. Gastroesophageal reflux disease can present
with a varying display of symptoms. They are
categorized into esophageal and extra-­
esophageal symptoms, according to the
Montreal Classification [1]. Important ques- C. Patients presenting with chest pain must have
tions for patients include but are not limited
to timing, duration, and association of reflux
symptoms, sleeping habits, frequency of
upper respiratory infections, and over-the-
counter medication use.
B. Patients presenting with classic symptoms
of heartburn and/or regurgitation may
achieve relief with lifestyle modifications.
Weight loss is strongly recommended for
patients with a BMI greater than 25.
Elevating the head of the bed can improve
symptoms, particularly for patients with D. Medical management includes proton pump
nocturnal GERD. Avoidance of meals, espe-
cially those with high-fat content, within
2–3 h of reclining can also improve noctur-
C. A. Halbert (*)
Advanced GI and Bariatric Surgery, Department of
General Surgery, Christiana Care Health System,
Newark, DE, USA
e-mail: Caitlin.a.halbert@christianacare.org
A. R. Tascone
Department of General Surgery, Saint Luke’s Health
System, Kansas City, MO, USA
chocolate, caffeine, spicy foods, citrus, and
carbonated beverages have limited effects in
GERD symptoms except in the case where
patient intake correlates with exacerbation
of clinical symptoms [2].
a cardiac etiology ruled out before consider-
ing GERD. Dysphagia is not classically asso-
ciated with GERD and can be an alarming
symptom representing something more
severe. Early workup is imperative and should
include upper endoscopy and barium radio-
graphs to rule out intraluminal pathology and
mechanical obstruction. If the diagnosis is
unclear, pH manometry may be necessary.
Patients with refractory GERD also require
further workup as described above [3].
inhibitors (PPIs), histamine-receptor (H2)
antagonists, and antacids. PPIs are the most
powerful and commonly prescribed acid sup-
pression medication. Patients should be
started on once-daily PPI therapy for an ini-
tial course of 8  weeks. If patients are only
partially responsive at this dosing, the PPI
therapy can be titrated to twice daily. H2
antagonists can be prescribed for symptom
relief in patients without erosive esophagitis,
especially for use with nocturnal GERD [3].
Patients in whom PPI therapy has success-
fully treated their symptoms should be trialed

© Springer Nature Switzerland AG 2019 129

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_34
130
off of PPIs. The exception would be patients
with known Barrett’s esophagus and severe
esophagitis. If patients are unable to tolerate a
trial off PPI therapy, further workup is indi-
cated [3].
E. There are several indications for surgical con-
sultation for patients suffering from GERD:
1. Failure of medical management: Patients
who are partial responders to PPI, have
severe regurgitation, or cannot tolerate
therapy with PPI.
2. Patients who elect surgical intervention
over lifelong need for medical therapy.
3. Severe, complicated GERD: Patients with
Barrett’s esophagus or peptic strictures.
4. Patients with extra-esophageal symp-
toms [4].
F. Many patients will already have some testing
completed by the time they are referred for
surgical consideration. If not already com-
pleted, they will need upper endoscopy.
Barium swallow is a consideration preoper-
atively to further delineate anatomy.
Esophageal manometry is important to rule
out achalasia or esophageal dysmotility.
This study can also help to tailor surgery
according to the functionality of the esopha-
gus [4]. Impedance-­pH ambulatory reflux
monitoring provides evidence of the pres-
C. A. Halbert and A. R. Tascone
ence of abnormal esophageal acid exposure
and symptom correlation, if not diagnosed
on previous testing. Telemetry capsule pH
and catheter-based pH monitoring are avail-
able, with the latter providing additional
information on weakly acidic or nonacid
reflux [3].
G. Traditionally, the Nissen fundoplication has
been the gold standard for the surgical treat-
ment of GERD.  There is evidence demon-
strating that the Toupet fundoplication has
equivalent heartburn control with a lower
dysphagia rate. Some experts advocate for
Toupet fundoplication over Nissen fundopli-
cation, thereby also rendering the manome-
try unnecessary in the preoperative workup
[4]. This remains a debated topic. The mag-
netic sphincter augmentation device was
approved by the US Food and Drug
Administration in 2012. Clinical trials in the
USA have shown significant reflux control
and minimal side effects at 5  years from
implantation [5]. In patients meeting indica-
tions for bariatric surgery, the roux-en-Y
gastric bypass should be considered. It has
been shown to have significant improvement
in typical and atypical GERD symptoms, as
well as additional obesity-­related comorbid-
ities [6].
34  Gastroesophageal Reflux Disease 131

A History and Physical Exam:

Esophageal and Extraesophageal Symptoms

Classic symptoms: Atypical symptoms:

Regurgitation, Chest pain, dysphagia,
heartburn weight loss

B Lifestyle Modification Upper endoscopy,

C Barium esophagram

Findings
Symptom
c/w GERD
relief?

D No
Medical
Management

Meets
indications
for surgical
referral?
E

Upper endoscopy,
Barium esophagram,
Esophageal manometry,
F Impedance pH

Normal Esophageal motility Impaired Esophageal motility

G BMI >35

Magnetic
Nissen/Toupet Roux-en-Y Toupet
Sphincter
Fundoplication Gastric Bypass Fundoplication
Augmentation

Algorithm 34.1
132 C. A. Halbert and A. R. Tascone

References 4. Stefanidis D, Hope WW, Kohn GP, Reardon PR,

Richardson WS, Fanelli RD.  Guidelines for surgi-
cal treatment of gastroesophageal reflux disease.
1. Vakil N, Van Zanten SV, Kahrilas P, Dent J, Jones R,
Surg Endosc [Internet]. 2010;24(11):2647–69.
Bianchi LK, et al. The Montreal definition and clas-
Available from: http://www.ncbi.nlm.nih.gov/
sification of gastroesophageal reflux disease: a global
pubmed/20725747.
evidence-based consensus. Am J Gastroenterol.
5. Ganz RA, Edmundowicz SA, Taiganides PA, Lipham
2006;101:1900–20.
JC, Smith CD, DeVault KR, et  al. Long-term out-
2. Kahrilas PJ, Shaheen NJ, Vaezi MF, Hiltz SW, Black
comes of patients receiving a magnetic sphincter aug-
E, Modlin IM, et  al. American Gastroenterological
mentation device for gastroesophageal reflux. Clin
Association medical position statement on the
Gastroenterol Hepatol. 2016;14(5):671–7.
management of gastroesophageal reflux disease.
6. Frezza EE, Ikramuddin S, Gourash W, Rakitt T,
Gastroenterology [Internet]. 2008;135(4):1383–91,
Kingston A, Luketich J, et al. Symptomatic improve-
1391-e5. Available from: http://www.ncbi.nlm.nih.
ment in gastroesophageal reflux disease (GERD) fol-
gov/pubmed/18789939.
lowing laparoscopic Roux-en-Y gastric bypass. Surg
3. Katz PO, Gerson LB, Vela MF.  Guidelines for the
Endosc. 2002;16(7):1027–31.
diagnosis and management of gastroesophageal reflux
disease. Am J Gastroenterol. 2013;108(10):1672.
 Hiatal Hernia
Wanda Lam, Ruel Neupane, and Jeffrey M. Marks
Algorithmic Approach
A. Patients with hiatal hernia can be asymptom-
atic or present to outpatient clinic with reflux
symptomatic, such as heartburn, abdominal
pain, anemia, and regurgitation, as well as
respiratory symptoms, such as dyspnea, chest
pain, or cough. There is a 1% risk per year for
these patients to develop acute complications
(hemorrhage, incarceration, gastric volvulus,
obstruction, and strangulation) that require
urgent surgical intervention [1]. Physical
exam findings in hiatal hernia lack specific-
ity; further imaging is warranted in the diag-
nosis of hiatal hernia.
B. There are four types of hiatal hernias [2]:
(a) Type 1: sliding hernia, where the GE
junction moves above the diaphragm
together with some or the entire stomach,
associated with esophageal shortening.
(b) Type 2: rolling or paraesophageal hernia,
where the gastric fundus herniates into
the mediastinum alongside the esopha-
gus, with the gastroesophageal junction
remaining in an intra-abdominal posi-
tion. Since the gastroesophageal sphinc-
teric mechanism functions normally in
W. Lam · R. Neupane · J. M. Marks (*)
Department of Surgery, University Hospitals
Cleveland Medical Center, Cleveland, OH, USA
e-mail: Jeffrey.Marks@UHhospitals.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_35
35
most of these cases, reflux of gastric con-
tents is uncommon.
(c) Type 3: mixed hernias involve herniation
of the stomach with the gastroesophageal
junction into the mediastinum.
(d) Type 4: giant paraesophageal hernia
characterized by intrathoracic stomach
along with associated viscera such as the
spleen, colon, small bowel, or pancreas.
C. Barium swallow and upper endoscopy are
useful in the diagnosis of hiatal hernia. In the
setting of acute symptoms, CT might be con-
sidered, while EGD provides a therapeutic
means to decompress and reduce the volvu-
lized stomach and to assess the viability of
the stomach [3]. In planning for elective
repair of hiatal hernia, additional pH, manom-
etry study, and gastric emptying studies can
be helpful in determining the surgical repair
of choice and if there is concomitant
achalasia.
D. Urgent intervention is indicated in the setting
of acute hemorrhage, incarceration, gastric
volvulus, obstruction, and strangulation.
Hiatal hernia reduction and gastropexy may
be warranted in certain emergent situations.
Elective repair is offered to patients with
symptomatic hiatal hernias refractory on
medical therapy (PPI or H2 blocker) who are
suitable surgical candidates [3].
E. In an elective repair of hiatal hernia, laparo-
scopic approach has become the standard of
133
134 W. Lam et al.

care. Transthoracic approach can be consid-
ered if esophageal lengthening is required.
The use of mesh has not been shown to
improve or worsen long-term outcome. While
a fundoplication is recommended as a step in
repairing a sliding or paraesophageal hernia
repair, there is no existing guideline on tailor-
ing the degree of fundoplication, which
include Nissen, a 360 degree wrapping of the
anterior and posterior walls of the stomach
around the esophagus, or partial anterior or
posterior wrapping [4, 5].

Presentation with dysphagia, heart burn, regurgitation.

A B Atypical symptoms can include dyspnea, chest or abdominal pain.

Barium swallow
C Endoscopy can be diagnostic and therapeutic
Consider pH and manometry studies if differential
diagnosis remains broad

Elective surgical intervention Unstable, requiring urgent

• Medical treatment failure,intolerance or non- intervention
compliance • Hemorrhage
D E • Prospect of lifelong medical therapy • Incarceration
• Severe esophagitis, Barrett’s • Volvulus
• Benign stricture • Obstruction
• Quality of life improvement • Strangulation

Surgical repair
Transabdominal
• Laparoscopic –standard of care, vs open
Transthoracic-failed/not candidate for transabdominal
approach

Fundoplication
• Nissen–complete
• Partial –anterior or
posterior

Algorithm 35.1

management of hiatal hernia. Surg Endosc [Internet].

References
1. Stylopoulos N, Gazelle GS, Rattner DW. Paraesophageal
hernias: operation or observation? Ann Surg [Internet].
2002;236(4).:492–500-­1. Available from: http://www.
ncbi.nlm.nih.gov/pubmed/12368678.
2. Townsend C, Bouchamp DB, Evers MB, Mattox
K. Sabiston textbook of surgery: the biological basis
of modern surgical practice. 20th ed. Philadelphia:
Elsevier; 2016.
3. Kohn GP, Price RR, DeMeester SR, Zehetner J,
Muensterer OJ, Awad Z, et  al. Guidelines for the
2013;27(12):4409–28. Available from: http://www.
ncbi.nlm.nih.gov/pubmed/24018762.
4. Peters JH.  SAGES guidelines for the manage-
ment of hiatal hernia. Surg Endosc [Internet].
2013;27(12):4407–8. Available from: http://www.
ncbi.nlm.nih.gov/pubmed/24196541.
5. Stylopoulos N, Rattner DW.  The history of hiatal
hernia surgery: from Bowditch to laparoscopy. Ann
Surg [Internet]. 2005;241(1):185–93. Available from:
http://www.ncbi.nlm.nih.gov/pubmed/15622007.
 Esophageal Carcinoma
Ruel Neupane, Wanda Lam, and Jeffrey M. Marks
Algorithmic Approach
A. Esophageal cancer is the sixth leading cause of
cancer death in the world and carries a 5-year
survival rate of only 15–25%. In the USA and
other developed countries, such as Western
Europe and Australia, esophageal adenocarci-
noma is the most common histological type,
whereas in the developing world, squamous cell
carcinoma is the predominate type. Esophageal
adenocarcinoma is associated with long-stand-
ing reflux disease, obesity, and Barrett’s esopha-
gus, whereas squamous cell carcinoma is
associated with smoking and alcohol use [1, 2].
B. Unintentional weight loss and dysphagia
likely represent late symptoms of esophageal
cancer since the esophagus can accommodate
distention that slowly progresses over a
period of time, evident by the fact that 50% of
patients have unresectable or metastatic dis-
ease at the time of diagnosis. Nodal spread is
also rapid, with 14–21% present in T1 lesions
(submucosa) and 38–60% in T2 lesions (mus-
cularis propria) [2].
C. Endoscopy is the gold standard for diagnos-
ing esophageal cancer with tissue biopsy, as
well as characterizing the size and location of
R. Neupane · W. Lam · J. M. Marks (*)
Department of Surgery, University Hospitals
Cleveland Medical Center, Cleveland, OH, USA
e-mail: Jeffrey.Marks@UHhospitals.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_36
36
the lesion. A barium swallow is a functional
study that provides the characteristic finding
of apple core lesion that is seen in esophageal
cancer. A chest and abdomen CT is recom-
mended in detecting metastatic lesions to the
liver and lungs for locally advanced disease.
PET/CT/MRI is also employed to improve
the accuracy in staging. Endoscopic ultra-
sound is essential in the staging of resectable
esophageal cancer by providing information
on depth of invasion, as well as lymph node
involvement. Data on the use of staging tho-
racoscopy or laparoscopy is lacking [3, 4].
D. In the TNM staging for esophageal cancer
(Table 36.1), T0 represents no evidence of dis-
ease; Tis high-grade dysplasia, defined as
malignant cells confined by the basement
membrane; T1 submucosa; T2 muscularis pro-
pria; T3 adventitia; and T4 adjacent structures.
N0 represents no regional lymph node involve-
ment; N1 up to 3 regional nodes; N2 up to 6
nodes, and N3 7 or more nodes [5]. For patients
with Barrett’s esophagus with high-grade dys-
plasia, endoscopic intervention is recom-
mended [6]. In patients with T1–T3 lesions,
esophagectomy is offered to patients who are
good surgical candidates. This is followed by
adjuvant therapy for advanced disease to
improve survival [2]. A Cochrane review of 13
studies has suggested survival benefits of neo-
adjuvant chemotherapy for resectable thoracic
esophageal cancer [7]. The type of surgical
135
136 R. Neupane et al.

Table 36.1 American Joint Committee on Cancer approach, namely the transhiatal, Ivor-Lewis,
(AJCC) tumor/node/metastasis (TNM) classification
or three-field, has not been shown to differ in
T – Primary tumor survival benefits or operative mortality, though
T0 No evidence of primary tumor the transhiatal approach is associated with a
Tis High grade dysplasia
lower postoperative morbidity [2]. Preoperative
T1 Lamina propria, muscularis mucosa, or
submucosa esophageal stenting is sometimes used for
T2 Muscularis propria patients with dysphagia as a bridge to surgery
T3 Adventitia while undergoing neoadjuvant therapy [8].
T4 Adjacent structures Some surgeons opt to establish enteral access
N – Regional lymph node for patients with significant weight loss by
N0 No lymph node involvement either gastrostomy or jejunostomy prior to sur-
N1 Metastasis in 1–2 regional lymph nodes gical resection for nutrition optimization.
N2 Metastasis in 3–6 regional lymph nodes
E. For unresectable lesions, palliative options
N3 Metastasis in 7+ regional lymph nodes
are offered, including chemoradiation, esoph-
M – Distant metastasis
M0 No distant metastasis
ageal stenting, feeding gastrostomy or jeju-
M1 Distant metastasis nostomy, and esophagectomy [3].

Presentation of GERD, dysphagia or asymptomatic/constitutional symptoms

Anatomic symptoms
A B • Fistula to airway,
• recurrent laryngeal nerve involvement - hoarseness
• metastases to liver bone and lung

Work up with barium swallow and endoscopy

C D Staging with CT, PET, MRI, EUS
Additional staging with bronchoscopy, mediastinocopy, thoracoscopy, laparoscopy

Chemoradiation
• Lymph node involvement
E • T3 and greater disease
• Significant co-morbidities or distant organ metastases
• Squamous cell carcinoma may respond completely
Surgery
• En bloc resection with T1-T2 disease
• After neoadjuvant chemoradiation for
lymph node involvement or T3 disease
• Palliation

Palliation Options
• Surgery
• Chemoradiation
• Stenting
• Lasar ablation
• Feeding gastrostomy, jejunostomy

Algorithm 36.1
36  Esophageal Carcinoma 137

References 5. Rice TW, Patil DT, Blackstone EH. 8th edition AJCC/
UICC staging of cancers of the esophagus and esoph-
agogastric junction: application to clinical practice.
1. José M, Arnal D, Arenas ÁF, Arbeloa ÁL. Esophageal
Ann Cardiothorac Surg. 2017;6(2):119–30.
cancer: risk factors, screening and endoscopic treat-
6. Spechler SJ.  Barrett esophagus and risk of esopha-
ment in Western and Eastern countries. World J
geal cancer: a clinical review. JAMA [Internet].
Gastroenterol. 2015;21(26):7933–43.
2013;310(6):627–36. Available from: http://www.
2. Enzinger PC, Mayer RJ. Esophageal cancer. N Engl
ncbi.nlm.nih.gov/pubmed/23942681.
J Med [Internet]. 2003;349(23):2241–52. Available
7. Kidane B, Coughlin S, Vogt K, Malthaner
from: https://doi.org/10.1056/NEJMra035010.
R.  Preoperative chemotherapy for resectable tho-
3. Townsend C, Bouchamp DB, Evers MB, Mattox
racic esophageal cancer. Cochrane Database Syst
K. Sabiston textbook of surgery: the biological basis
Rev [Internet]. 2015;(5):CD001556. Available from:
of modern surgical practice. 20th ed. Philadelphia:
http://www.ncbi.nlm.nih.gov/pubmed/25988291.
Elsevier; 2016.
8. Martin RCG, Cannon RM, Brown RE, Ellis SF,
4. Varghese TK, Hofstetter WL, Rizk NP, Low DE,
Williams S, Scoggins CR, et al. Evaluation of quality
Darling GE, Watson TJ, et al. The society of thoracic
of life following placement of self-expanding plastic
surgeons guidelines on the diagnosis and staging of
stents as a bridge to surgery in patients receiving neo-
patients with esophageal cancer. Ann Thorac Surg
adjuvant therapy for esophageal cancer. Oncologist
[Internet]. 2013;96(1):346–56. Available from: http://
[Internet]. 2014;19(3):259–65. Available from: http://
www.ncbi.nlm.nih.gov/pubmed/23752201.
www.ncbi.nlm.nih.gov/pmc/articles/PMC3958458/.
 Esophageal Perforation
Ruel Neupane, Wanda Lam, and Jeffrey M. Marks
Algorithmic Approach
A. Esophageal perforation is a medical and surgi-
cal emergency. One meta-analysis of 75 stud-
ies reported a pooled mortality of 11.9% [1]; a
12-year national study from England reported
a 30-day mortality of 30% among 2564
patients [2]. Mortality rate is doubled if the
diagnosis is delayed for more than 24  h [3].
The etiologies of esophageal perforation
include iatrogenic instrumentation, foreign
body ingestion, trauma, malignancy, or force-
ful emesis, also known as Boerhaave’s
Syndrome, when a transmural esophageal tear
occurs after retching. This is different from
Mallory-Weiss tear, which is a mucosal tear
that does not result in esophageal perforation.
B. Due to its high mortality, esophageal perfora-
tion must be considered in patients presenting
with neck, substernal, or epigastric pain, with a
history of instrumentation, trauma, foreign
body ingestion, malignancy, or vomiting. Fever,
tachycardia, tachypnea, subcutaneous emphy-
sema, diminished breath sounds, and abdominal
R. Neupane · W. Lam · J. M. Marks (*)
Department of Surgery, University Hospitals
Cleveland Medical Center, Cleveland, OH, USA
e-mail: Jeffrey.Marks@UHhospitals.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_37
37
tenderness might be present on physical exam.
Hemodynamic instability occurs as a result of
mediastinitis or pleuritis [4].
C. Once suspected, workup for esophageal per-
foration should be promptly undertaken.
Leukocytosis and elevated amylase level is
consistent with esophageal perforation.
Electrolytes, coagulation panel, and type and
screen should be obtained in anticipation of
need for surgical or endoscopic intervention.
Extravasation of contrast in an esophagram is
diagnostic; the contrast of choice depends on
location of suspected perforation to minimize
inflammatory response from contrast extrava-
sation. Gastrografin swallow evaluation
should be utilized first as the most useful ini-
tial test, as it will not cause mediastinitis,
unlike barium [5]. Mediastinal air and/or
fluid on CT scan helps localize the site of per-
foration [4].
D. Supportive measures, namely, fluid resuscita-
tion, broad-spectrum antimicrobials, NPO
status, close hemodynamic monitoring, and
support in an ICU setting, are critical in the
initial management of esophageal perfora-
tion. A 12-year retrospective study in England
advocated for centralization of care at high-
volume centers where multidisciplinary
approach led to improved outcomes [2]. In a
hemodynamically stable patient with
­contained perforation, conservative manage-
ment is acceptable. Esophageal stenting with
139
140 R. Neupane et al.

mediastinal and pleural drainage is a treat-
ment option for stable patients with limited
mediastinal or pleural contamination, though
its efficacy has not been compared with surgi-
cal intervention [6].
E. Surgical intervention is indicated for patients
who are hemodynamically unstable or show
no improvement on nonoperative manage-
ment. The operative approach is guided by
the location of perforation, whether it is con-
tained or not, and underlying pathology. A
cervical incision is made for a high esopha-
geal perforation: a right thoracotomy for the
upper 2/3 and a left thoracotomy for the lower
2/3 perforation. The possibility of primary
repair is dictated by the degree of tissue
inflammatory which often depends on timing
from onset of symptoms. Muscle flap has
been established as a safe approach for intra-
thoracic or cervical esophageal perforation
when primary repair is impossible or risky
[7]. In the face of severe inflammation, devi-
talized tissue should be debrided and esopha-
geal diversion should be considered if primary
repair is deemed high risk for anastomotic
leak. Temporary feeding access, such as gas-
trostomy or jejunostomy, and wide drainage
should be established.

Presentation with forceful emesis, foreign body ingestion, or trauma

A B Vitals, blood work, and physical exam

C D Resuscitation, foley, NG, NPO, antibiotics, +/– ICU

Discern cervical vs thoracic versus

abdominal symptoms? Confirm
with imaging or endoscopy

E Hemodynamically stable Hemodynamically unstable

Contained perforation–continue Uncontained Non/pre-perforation –

conservative therapy. Consider
stenting if limited mediastinal,
pleural contamination
Uncontained perforation
perforation – debridement, diversion,
– emergent surgical
operating room for drainage, gastrostomy/
exploration
exploration jejunostomy

Operative intervention
• Cervical approach – amenable to drainage and primary repair =/– muscle flap
• Thoracic and abdominal perforation – possible primary repair, muscle flap, and drainage. Jejunostomy
• Distal obstruction – resection, reconstruction, drainage, jejunostomy
• Possible esophagectomy and exclusion

Algorithm 37.1
37  Esophageal Perforation 141

References center 10-year experience. World J Gastroenterol.

2014;20(30):10613–9.
4. Townsend C, Bouchamp DB, Evers MB, Mattox
1. Biancari F, D’Andrea V, Paone R, Di Marco C, Savino
K. Sabiston textbook of surgery: the biological basis
G, Koivukangas V, et  al. Current treatment and out-
of modern surgical practice. 20th ed. Philadelphia:
come of esophageal perforations in adults: systematic
Elsevier; 2016.
review and meta-analysis of 75 studies. World J Surg.
5. Michel L, Grillo HC, Malt RA. Esophageal perfora-
2013;37(5):1051–9.
tion. Ann Thorac Surg. 1982;33(2):203–10.
2. Markar SR, Mackenzie H, Wiggins T, Askari A,
6. Dasari BVM, Neely D, Kennedy A, Spence G, Rice
Faiz O, Zaninotto G, et  al. Management and out-
P, Mackle E, et  al. The role of esophageal stents in
comes of esophageal perforation: a national study
the management of esophageal anastomotic leaks
of 2,564 patients in England. Am J Gastroenterol.
and benign esophageal perforations. Ann Surg.
2015;110(11):1559–66.
2014;259(5):852–60.
3. Persson S, Elbe P, Rouvelas I, Lindblad M, Kumagai
7. Richardson JD, Tobin GR.  Closure of esopha-
K, Lundell L, et al. Predictors for failure of stent treat-
geal defects with muscle flaps. Arch Surg.
ment for benign esophageal perforations  – a single
1994;129(5):541–7. discussion 547–8.
 Acidic and Basic Injuries
Wanda Lam, Ruel Neupane, and Jeffrey M. Marks
Algorithmic Approach
A. Caustic injuries are uncommon in the United
States with 5000 cases reported every year,
most of which occur in the pediatric popula-
C. Clinical and radiographic examination of
tion. Household disinfectants such as bleach
are common offending agents. Whereas acids
results in coagulation necrosis and eschar for-
mation that limits depth of penetration and
injury, alkalis leads to liquefactive necrosis
and saponification that promotes deeper tis-
sue penetration [1, 2].
B. In the initial evaluation of a patient with caus-
tic injuries, the management of airway,
breathing, and circulation is crucial. For
patients with rapidly progressing upper air-
way edema, stridors, emesis, respiratory dis-
tress, endotracheal intubation should be
considered; anesthesia and otolaryngology
teams should be involved early if there is con-
cern for difficult airway [3]. Intravenous
access should be established and hemody-
namic stability monitored closely. A thorough
history should be taken to determine the form
D. Patients with grades 1–2a injuries can be
W. Lam · R. Neupane · J. M. Marks (*)
Department of Surgery, University Hospitals
Cleveland Medical Center, Cleveland, OH, USA
e-mail: Jeffrey.Marks@UHhospitals.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_38
38
of ingested substance, timing of ingestion,
and duration of tissue contact. History taking
can be challenging in this patient population,
commonly of pediatrics and mental illnesses.
caustic injury alone is inadequate. Early inter-
vention with flexible fiber-optic endoscopy up
to 36 h was shown to be safe and accurate in
characterizing the location, extent, and sever-
ity of injury [4]. Zargar et  al. developed a
grading system to classify the caustic injuries
and predict prognosis: grade 0, normal exam;
grade 1, edema and mucosal hyperemia; grade
2a, superficial and noncircumferential ulcer-
ation; grade 2b, deep and circumferential
ulceration; grade 3a scatter necrosis; and
grade 3b, extensive necrosis with high risk of
stricture formation [4]. There is evidence to
support the safety in completely evaluating
the esophagus and stomach for additional
lesions beyond circumferential burns [5]. A
nasogastric tube should be placed under direct
visualization at this time for grade 2b and 3
injuries without significant gastric involve-
ment [6]. Emesis should be minimized and
neutralization is contraindicated due to the
risk of thermal injury.
safely managed on the regular nursing floor
and discharged home within 1–2  days with
good oral intake and antacids therapy. Patients
with grades 2b–3 injuries should be admitted
143
144 W. Lam et al.

to an intensive care unit with nutritional sup-
port and monitored for perforation for up to
1–2 weeks. The use of corticosteroids is con-
troversial and has not been shown to reduce
the formation of strictures in grade 3 patients.
Antibiotics should be used if there is evidence
of perforation with peritonitis or mediastini-
tis, but has not been shown to reduce the for-
mation of strictures [7].
E. Surgical intervention is indicated in the acute
setting of peritonitis and perforation, as well
as long-term stricture formation that is not
amenable to endoscopic dilation or stenting.
In a hemodynamically stable patient, laparo-
scopic exploration can be considered as ini-
tial operative approach [1]. Refer to
“Esophageal Perforation” chapter for details
of surgical management.
F. Serial endoscopy is performed to monitor
progression of injuries, iatrogenic perfora-
tion, as well as long-term stricture develop-
ment, which can take place 3 weeks to 1 year
after the initial exposure [2]. Barium esopha-
gram is an alternative diagnostic modality to
evaluate for strictures [5]. Local injection and
topical application of mitomycin C to esoph-
ageal mucosa has been described with good
outcome in preventing structure formation in
high-grade injuries, though further prospec-
tive studies are required to validate its effi-
cacy [8]. Serial dilation is commonly
performed every 1–3 weeks for strictures [2].
Nutrition should be optimized to support
healing, which might require establishing
enteral access with either gastrostomy or jeju-
nostomy early in the management plan.

History and physical: vitals, substance, duration

A B C Labs, CXR, AXR, or CT
Endoscopy

NPO, IVF, +/– ICU monitoring

D Antibiotics E

1st-degree burn 2nd-degree burn 3rd-degree burn

48 h ICU, monitor for sepsis

observation. PO ICU, IV antibiotics Airway involvement –
challenge. Repeat Swallow evaluation at 24 h Consider fiber-optic
endoscopy and Possible second look if intubation
esophagram with concernfor perforation/ Diagnostic laparoscopy if
follow-up necrosis question of perforation
Exploratory laparotomy in
unstable patient, full
thickness involvement

Surgical options include

debridement of devitalized
Stricture formation
tissue
and treatment • +/– esophagectomy
F options include • +/– gastric resection
serial dilation, stent, • cervical
and jejunostomy esophagostomy
feeding gastrostomy
or jejunostomy

Algorithm 38.1
38  Acidic and Basic Injuries 145

References of burns. Gastrointest Endosc [Internet]. 37(2):165–

9. Available from: http://www.ncbi.nlm.nih.gov/
pubmed/2032601.
1. Kluger Y, Ishay O Ben, Sartelli M, Katz A, Ansaloni
5. Temiz A, Oguzkurt P, Ezer SS, Ince E, Hicsonmez
L, Gomez CA, et al. Caustic ingestion management:
A.  Predictability of outcome of caustic ingestion by
world society of emergency surgery preliminary sur-
esophagogastroduodenoscopy in children. World
vey of expert opinion. World J Emerg Surg [Internet].
J Gastroenterol [Internet]. 2012;18(10):1098–103.
2015;10:48. Available from: http://www.ncbi.nlm.
Available from: http://www.ncbi.nlm.nih.gov/pmc/
nih.gov/pmc/articles/PMC4609064/.
articles/PMC3296984/.
2. Contini S, Scarpignato C.  Caustic injury of the upper
6. Shub MD.  Therapy of caustic ingestion: new treat-
gastrointestinal tract: a comprehensive review. World J
ment considerations. Curr Opin Pediatr [Internet].
Gastroenterol [Internet]. 2013;19(25):3918–30. Available
2015;27(5):609–13. Available from: http://www.ncbi.
from: http://www.ncbi.nlm.nih.gov/pubmed/23840136.
nlm.nih.gov/pubmed/26196260.
3. Struck MF, Beilicke A, Hoffmeister A, Gockel I,
7. Park KS. Evaluation and management of caustic inju-
Gries A, Wrigge H, et al. Acute emergency care and
ries from ingestion of Acid or alkaline substances. Clin
airway management of caustic ingestion in adults:
Endosc [Internet]. 2014;47(4):301–7. Available from:
single center observational study. Scand J Trauma
http://www.ncbi.nlm.nih.gov/pubmed/25133115.
Resusc Emerg Med [Internet]. 2016;24:45. Available
8. Berger M, Ure B, Lacher M.  Mitomycin C in the
from: http://www.ncbi.nlm.nih.gov/pmc/articles/
therapy of recurrent esophageal strictures: hype or
PMC4827211/.
hope? Eur J Pediatr Surg [Internet]. 2012;22(2):109–
4. Zargar SA, Kochhar R, Mehta S, Mehta SK. The role
16. Available from: http://www.ncbi.nlm.nih.gov/
of fiberoptic endoscopy in the management of corro-
pubmed/22517516.
sive ingestion and modified endoscopic classification
 Part VI
Stomach and Duodenum
 Gastric Ulcer Management
39
Maria S. Altieri and Konstantinos Spaniolas

Algorithmic Approach: Introduction lesser curvature of the stomach high along

­cardia; and type V, an ulcer due to NSAID use.
Gastric ulcer is one of the most common gastro-
intestinal diagnoses in the USA with a preva-
lence of 2%. Gastric ulcers are divided into five
types depending on the location and based on
the Modified Johnson classification: type I,
located on the lower lesser curvature of the
stomach; type II, two ulcers – one on the lower
curvature and the other a duodenal ulcer; type
III, a prepyloric ulcer; type IV, located on the
Types II and III are due to high acid secretion,
which is an important consideration in terms of
surgical management. Gastric ulcer manage-
ment primarily depends on the acute or chronic
presentation.
Common acute presentations of gastric ulcer
complications that may require surgical inter-
vention include bleeding, perforation, and
obstruction.

M. S. Altieri
Department of General Surgery, Stony Brook
University Hospital, Stony Brook, NY, USA
K. Spaniolas (*)
Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA
e-mail: Konstantinos.Spaniolas@
stonybrookmedicine.edu

© Springer Nature Switzerland AG 2019 149

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_39
150 M. S. Altieri and K. Spaniolas

Bleeding

Bleeding

Resuscitate
A Stable?
No IV fluids
PPI drip
Transfuse

Yes

Endoscopic
B assessment and
control

Yes No Yes
Successful? Stable? Angioembolization Successful?

No Yes No

Wedge resection Wedge resection

Monitor Monitor
or (include TV +
Serial H/H Serial H/H
Primary control via Pyloroplasty for
PPIs PPIs
gastrotomy II/III)

Algorithm 39.1

A. Initial treatment in the case of bleeding from a
gastric ulcer is based on resuscitation by
obtaining intravenous access, fluid resuscita-
tion, and placement of a nasogastric tube.
Nasogastric aspiration of blood is suggestive
of an upper GI bleed. any coagulopathy should
be corrected and transfusion should be initi-
C. Surgery depends on the stability of the
ated in case of instability or in case of signifi-
cant blood loss. Proton pump inhibitor (PPI)
therapy is particularly important, and should
be initiated early, while awaiting esophago-
gastroduodenoscopy (EGD), which, besides
establishing the diagnosis, is often the defini-
tive treatment for most ulcers either through
cautery, clipping, or epinephrine injection.
B. If endoscopic control fails, angioemboliza-
tion can be attempted. endoscopic marking of
the ulcer with a clip can facilitate endovascu-
lar control, if such expertise and institutional
experience is available. In the case of massive
hemorrhage with failed endoscopic control,
transfusion requirement of more than four
units of blood, recurrent hemorrhage after
one or more EGD attempts, repeated hospi-
talization for bleeding ulcer, and concurrent
indications for surgery such as perforation or
obstruction, surgical intervention is
indicated.
patient. If unstable, gastric ulcer can be
oversewn for bleeding control. in a stable
patient, resection of the gastric ulcer is the
preferred approach. For types I, IV, and V,
wedge resection alone is adequate (provided
that closure will not cause obstruction at the
GE junction or the pylorus). For types II and
III in a stable patient, the optimal surgical
options are pyloroplasty with oversewning
the ulcer or antrectomy; both options should
include a vagotomy, especially in patients
with history of chronic PPI use. If a formal
resection is not performed, a biopsy is
required as gastric ulcers are associated with
risk of malignancy.
39  Gastric Ulcer Management 151

Perforation

Perforation

Resuscitate
No IV fluids
A Stable?
PPI
Antibiotics

Yes

Primary closure
B Minimal No and/or Omental
contamination? Patch
H pylori treatment

Yes

Wedge resection
C (add TV +
Pyloroplasty for
II/III)

Algorithm 39.2

A. In case of an obstruction or perforation, initial
management should include ensuring ade-
quate intravenous access and fluid resuscita-
tion, PPI therapy, and antibiotics (in case of
perforation). For perforated gastric ulcers in
an unstable patient, the ulcer should be biop-
sied and a simple primary or omental patch
closure can be performed. if the location and
extent of the perforation is such that primary
closure would lead to an obstruction (overall
not common, but can be seen with type II or
III ulcers), inclusion of the perforation within
a pyloroplasty field may be advantageous.
B. If tissue quality will not allow for primary
closure, formal resection and reconstruction
(simple wedge resection for types I, IV, and
V; antrectomy with reconstruction  – See
above) may be performed if the patient is
stable.
C. For patients with extensive tissue damage and
large perforations in type II and III ulcers,
with instability or severe duodenal scarring,
wide drainage including a duodenostomy
tube or pyloric exclusion with gastrojejunos-
tomy should be considered.
152
Obstruction
Obstruction
Resuscitate
No IV fluids
A Stable? NGT
PPI
Yes
EGD with bx
B UGI after 1 week
Persistent Obstruction
Antrectomy
or
C Gastrojejunostomy
(consider addition
of TV)
Algorithm 39.3
A. This is almost an exclusive complication of
type II and III ulcers. Patients who present
with an acute obstruction may benefit from a
course of nasogastric decompression and PPI
therapy, as a mode to rehabilitate the gastric
body for longer term functional recovery, and
to improve quality of gastric tissues in antici-
pation of resection.
B. In patients with obstruction, endoscopic dila-
tion can relieve the symptoms. Biopsy is par-
amount to assess for underlying malignancy.
The addition of PPI therapy, eradication of
Helicobacter pylori, nutritional support, and
smoking cessation will decrease the chance
of obstruction recurrence following endo-
scopic or surgical therapy.
C. Surgical treatment is indicated if endoscopic
dilation fails or is not feasible, despite medi-
cal optimization. In this case, surgical
approach will depend on the quality of the
duodenum. Patients with marked duodenal
scarring should undergo biopsy of the ulcer
to rule out malignancy, and if negative, pro-
ceed with gastrojejunostomy (loop or Roux-
en-Y) to avoid the risk of the “difficult”
M. S. Altieri and K. Spaniolas
duodenal stump. When duodenal scarring is
minimal (commonly the case for gastric
ulcers), definitive treatment should consist of
antrectomy. Vagotomy should be considered
for all patients, especially if they have a his-
tory of chronic PPI use (PPI therapy failure).
Reconstruction can consist of Bilroth I,
Bilroth II, or Roux-en-Y gastrojejunostomy,
depending on tissue mobility and surgeon
experience.
Intractable Ulcer
The initial management for intractable chronic
ulcers includes EGD with biopsy to rule out malig-
nancy, in addition to removing any risk factors,
including smoking cessation, NSAID use, and
assuring compliance with PPIs. For patients with
family history or multiple ulcers in different loca-
tions, Zollinger Ellison syndrome should be ruled
out. Surgical treatment should be considered for
patients who have had multiple recurrences or
failed two trials of PPI therapy of 12 weeks each.
It is paramount to perform biopsies with each
EGD.  Surgery approach in this case depends on
the tissue quality of the duodenum. If the duode-
num demonstrates minimal scarring, antrectomy
and reconstruction (Bilroth I if there is enough
mobility; Bilroth II or Roux-­en-­Y gastrojejunos-
tomy if there is not enough mobility for gastroduo-
denostomy) are the treatments of choice. If the
duodenal tissues are profoundly scarred, and there
is a major concern for duodenal stump leak, repeat
biopsies and diversion with gastrojejunostomy
without resection remain as options. If resection is
unavoidable, the “difficult duodenum” can be
managed with Nissen stump closure (using the
pancreatic capsule) or with primary closure and
lateral duodenostomy tube drainage. Truncal
vagotomy may be added for type II and III ulcers.
Suggested Reading
Cameron JL, Cameron AM. Stomach. In: Current surgical
therapy. 11th ed. Philadelphia, PA: Saunders; 2014.
p. 69–107.
Kitagawa Y, Dempsey DT. Stomach. In: Schwartz’s prin-
ciples of surgery. New York City, NY: McGraw-Hill
Education\Medical; 2015. p. 1035–95.
 Duodenal Ulcer Management
Maria S. Altieri and Konstantinos Spaniolas
Algorithmic Approach
Duodenal ulcers are more common compared
to gastric ulcers. These ulcers tend to be asso-
ciated with Helicobacter pylori infection and
are most commonly found in the first portion of
the duodenum. Management of duodenal ulcer
begins with the assessment of hemodynamic
instability (see Chap. 39, Gastric Ulcer
Management).
A. Resuscitating the patient should be the initial
goal. Surgery, although at this time it is rarely
indicated, is needed in case of perforation,
protracted bleeding despite endoscopic ther-
apy, obstruction, intractability despite medi-
cal treatment, or inability to rule out cancer.
M. S. Altieri
Department of General Surgery, Stony Brook
University Hospital, Stony Brook, NY, USA
K. Spaniolas (*)
Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA
e-mail: Konstantinos.Spaniolas@
stonybrookmedicine.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_40
40
B. Bleeding is the most common complication
of duodenal ulcer. EGD is the best test for
both diagnosis and treatment. Biopsies can be
performed to test for H. pylori and anti-H.
pylori therapy initiated. Similar to bleeding
gastric ulcers, endoscopic approach can be
highly successful in bleeding control (see
Bleeding Gastric Ulcer section).
C. Surgical intervention is suggested for failure
of or inability to provide endoscopic therapy.
This involves anterior duodenotomy with
ligation of the gastroduodenal artery and
oversewing of the ulcer. For stable patients,
especially with a history of chronic PPI use
(failure of PPI therapy), vagotomy and pylo-
roplasty should be considered in this setting.
153
154 M. S. Altieri and K. Spaniolas

Bleeding

Resuscitate
No IV fluids
Stable? PPI drip
A
Transfuse

Yes

Endoscopic
assessment and
B control

No Duodenotomy and
Successful? suture ligation
C or pyloroplasty+TV

Yes

Monitor
Serial H/H
PPIs
H. pylori treatment

Algorithm 40.1
40  Duodenal Ulcer Management 155

A. Resuscitating the patient should be the initial
goal.
B. In case of obstruction, initial treatment should
concentrate on a trial of gastric decompression,
PPI therapy, and endoscopic assessment for pos-
sible dilation (as well as biopsy for H. pylori).
C. If endoscopic therapy is unsuccessful or not
indicated (see above—gastric ulcer obstruc-
tion) or if obstruction recurs, surgical therapy
is indicated (same as obstruction due to gas-
tric ulcer).

Obstruction

No Resuscitate
Stable? IV fluids
A
NGT
PPI

Yes

EGD with bx
B UGI after 1 week

Persistent obstruction

Antrectomy
or
C Gastrojejunostomy
(consider addition
of TV)

Algorithm 40.2
156 M. S. Altieri and K. Spaniolas

A. Contained perforation in a stable patient can
be treated conservatively. The diagnosis of a
contained perforation is established on a
patient with minimal or improving pain and
hemodynamic stability and illustrated on con-
trast imaging. This commonly occurs in cases
where the ulcer is in the retroperitoneal loca-
tion (segment III or IV of the duodenum).
B. In case of free perforation, peritonitis, or
instability, surgery is required. Placement of
omental patch (Graham patch) is the most
commonly performed surgery. The addition
of vagotomy should be considered for patients
on chronic PPI use (failure of PPI therapy).
For patients with extensive tissue damage and
large perforations, with instability or severe
duodenal scarring, wide drainage including a
duodenostomy tube or pyloric exclusion with
gastrojejunostomy should be considered
along with distal feeding jejunostomy.

Perforation

A No Resuscitate
Stable? Antibiotics
PPI

Yes

Antibiotics
PPI
H.Pylori Yes Contained on
treatment imaging?
Close monitor

No B

Primary closure
and/or Omental
Patch
(Antrectomy+TV
if PPI failure)
(Lateral
duodenostomy or
pyloric exclusion
for severe tissue
damage)

Algorithm 40.3

Suggested Reading
Gilliam AD, Speake WJ, Lobo DN, et  al. Current prac-
tice of emergency vagotomy and Helicobacter pylori
eradication for complicated peptic ulcer in the United
Kingdom. Br J Surg. 2003;90:88–90.
 Complications of Peptic Ulcer
Disease
Carl J. Dickler and Konstantinos Spaniolas
Algorithmic Approach
Surgical treatment of peptic ulcer disease (PUD)
traditionally involved one of the three operations:
highly selective vagotomy (HSV), vagotomy and
drainage (V + D), or vagotomy and antrectomy
(V + A). The choice of which procedure to per-
form depended on the patient’s condition and sur-
geon’s preference/experience. All are considered
acceptable treatments for PUD.  Currently, with
the use of proton pump inhibitors, surgery for
PUD is uncommon. However, occasionally the
practicing surgeon will encounter patients with
intractable disease or emergent manifestations of
PUD, requiring surgical intervention. The afore-
mentioned operations are not without complica-
tions and risks. Complications related to the
procedures are commonly the consequence of
different alterations they incur on the gastrointes-
tinal tract. These include dumping syndrome,
C. J. Dickler
Department of General Surgery, SUNY Stony Brook
University Hospital, Health Sciences Center T19-030,
Stony Brook, NY, USA
K. Spaniolas (*)
Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA
e-mail: Konstantinos.Spaniolas@
stonybrookmedicine.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_41
41
diarrhea, gastric stasis, bile reflux, and Roux syn-
drome (Algorithm 41.1).
Dumping syndrome is more common after
pyloroplasty or distal gastrectomy, affecting
5–10% of patients, but can occur after vagotomy
without an emptying procedure as well. Dumping
syndrome is further characterized into early or
late. Early dumping results in diaphoresis, weak-
ness, tachycardia, and lightheadedness that
develop 15–30 min postprandially. Late dumping
results in reactive hypoglycemia and hyperinsu-
linemia that occur 2–3  h after a meal. These
symptoms are thought to be related to the rapid
influx of hyperosmolar contents into the small
bowel due to lack of pylorus or pyloric function.
A. The primary treatments are dietary modifica-
tions and avoiding fluids during meals and
adding fibers.
B. Acarbose can be an effective medication for
late dumping syndrome.
C. Octreotide is the first line medication, which
can be started at 100 ug BID and up-titrated
to 500 ug TID.
D. If medical treatment fails, then the last resort
is surgical revision. Options include reversed/
antiperistaltic intestinal interpositions (which
have risks of obstruction) or conversion to
Roux-En-Y gastrojejunostomy with or with-
out a vagotomy (goals should be to minimize
size of gastric remnant to lower risks of stasis
and ulcers).
157
158 C. J. Dickler and K. Spaniolas

Prior surgery for peptic

ulcer disease

Dumping
Roux Syndrome Diarrhea
Syndrome

A
Positive
Early Late
Hydrogen
Antibiotics breath
UGI or gastric test
emptying scan
Dietary Modifications A
A Negative

Positive
Acarbose B B
Promotility agents,
anti-emetics, low Acid Fecal
Octreotide dose opioids suppression fat test

C B Negative

Surgical
D Medical management:
revision
Revise gastric cholestyramine
C octreotide
remnant or
subtotal/total codeine/loperamide
gastrectomy
Fails

C
Jejunal
D interposition or
anti-peristaltic
limb

Algorithm 41.1

A portion of patients (25–30%) who have had
Roux-En-Y reconstruction will experience Roux
or Afferent Limb Syndrome. It is more predomi-
nant with longer Roux limbs (>40 cm). Patients
can experience vomiting, epigastric pain, early
satiety, and weight loss. There can be dilation of
the Roux limb, gastric pouch, or distal efferent
limb on imaging.
A. UGI or gastric emptying scans will show
delayed gastric emptying. The syndrome is
thought to be due to disordered motility in the
limb as the reconstruction displaces the jeju-
num away from pacemaker cells in the duo-
denum. This leads to ectopic pacemaker
activity in the Roux limb that results in food
peristalsis going toward the gastric remnant
instead of away from it.
41  Complications of Peptic Ulcer Disease
B. Medical management starts with promotility
agents, antiemetics, and low-dose opioids.
C. Persistent symptoms can require surgical
revision with either partial resection of the
gastric remnant or subtotal or total
gastrectomy.
Diarrhea is a common symptom after PUD
surgery. Symptoms usually develop early postop-
eratively. It is thought to be caused by dysmotil-
ity or accelerated transit through the GI tract, or
related to bile acid malabsorption or bacterial
overgrowth.
A. The first step involves ruling out bacterial
overgrowth (hydrogen breath test, or trial of
empiric antibiotic therapy, when testing is not
available).
B. The next step is to rule out fat malabsorption
(fecal fat testing) which can be treated with
acid suppression.
C. If these tests are negative, the next medical
treatment is with cholestyramine, octreotide,
or antisecretory/antimotility agents (loper-
amide, opioids, etc.).
If medical treatment fails, the surgical treat-
ment involves revision with a possible jejunal
interposition segment vs. antiperistaltic intestinal
limb (distal ileal graft). Both surgeries have risks
of obstruction or bacterial overgrowth.
Gastric stasis and biliary reflux can also
develop after these surgeries with similar symp-
toms of nausea/vomiting, epigastric pain, bloat-
ing, and/or weight loss. They can both result
from disordered motility of the remaining stom-
ach, and gastric stasis can also result from
mechanical (anastomotic stricture) or functional
(retrograde peristalsis) obstruction. Gastric stasis
is usually suggested by emesis of undigested
food, while biliary reflux has biliary emesis
(Algorithm 41.2).
159
Gastric Stasis
A. The initial evaluation of gastric stasis is with
endoscopy to rule out anastomotic strictures.
Patients with gastric stasis resulting from
obstruction maybe relieved with endoscopic
dilation as a first step. If recurrence of PUD
coexists with anastomotic stricture and gas-
tric stasis, aggressive management of the
PUD (maximal PPI therapy, smoking cessa-
tion, and eradication of Helicobacter pylori),
concurrently with serial dilations, is of para-
mount importance.
B. If there is no evidence of stricture, the next diag-
nostic test would be a gastric emptying studies
or upper GI series to check for any delay.
C. Gastric stasis that results from motility issues
can usually be treated medically (diet modifi-
cations and promotility agents).
D. If treatment is refractory, then surgery (subto-
tal gastrectomy) is an option as a last resort.
Biliary Reflux
A. The initial evaluation is with endoscopy,
which can show bile during upper
endoscopy.
B. If there is no bile seen on upper endoscopy, the
diagnosis can be confirmed with a HIDA scan
which will show prolonged imaging (tracer
appears to pool into the residual stomach).
C. Patients with biliary reflux can be managed
first with cholestyramine and sucralfate.
Efferent loop obstruction may also cause bili-
ary reflux and can often be diagnosed, and
even managed, endoscopically.
D. Patients with biliary reflux and failure of
medical therapy are best managed with con-
version to Roux-en-Y gastrojejunostomy,
with or without subtotal gastrectomy. If bili-
ary reflux occurs in patients with Roux-en-Y
configuration, elongation of the Roux limb
will often alleviate the pathology.
160 C. J. Dickler and K. Spaniolas

Prior surgery for peptic

ulcer disease

Gastric stasis Biliary reflux Roux Syndrome

A A EGD Roux Syndrome

EGD

No

B HIDA Bile UGI or Gastric

Anastomotic Emptying Scan
stricture Dilate
Yes
C
Reflux Cholestyramine Promotility
Persists + Sucralfate Agents
No Yes

Persists
Revise Revise Gastric
B anastomosis Subtotal
Remnant or
D Subtotal/Total
gastrectomy Gastrectomy
Nuclear gastric Normal
emptying variant
study

Delayed No delay

Promotility C
agents

Persists

Subtotal D
gastrectomy

Algorithm 41.2

Kitagawa Y, Dempsey DT. Stomach. In: Schwartz’s prin-

Suggested Reading
Bolton JS, Charles Conway W.  Postgastrectomy syn-
dromes. Surg Clin N Am. 2011;91(5):1105–22.
https://doi.org/10.1016/j.suc.2011.07.001.
Cameron JL, Cameron AM. Stomach. In: Current surgical
therapy. 11th ed. Philadelphia, PA: Saunders; 2014.
p. 69–107.
ciples of surgery. New York City, NY: McGraw-Hill
Education\Medical; 2015. p. 1035–95.
Savas JF, Miller TA.  Postgastrectomy syndromes.
In: Shackelford’s surgery of the alimentary tract.
Philadelphia, PA: Elsevier/Saunders; 2013. p. 757–66.
Teitelbaum, Ezra N, et al. Stomach. In: Sabiston textbook
of surgery: the biological basis of modern surgical
practice. 12th ed. Philadephia, PA: Elsevier; 2017.
p. 1188–236.
 Management of Recurrent Peptic
Ulcer Disease
Carl J. Dickler and Konstantinos Spaniolas
Algorithmic Approach
Peptic ulcer disease (PUD) is a common cause of
epigastric pain and gastrointestinal symptoms
throughout the world. The most common causes
of PUD are Helicobacter pylori infection and the
use of nonsteroidal anti-inflammatory drugs
(NSAIDs). Treatment of the disease has advanced
significantly with the advent of proton pump
inhibitors (PPIs) and histamine-2 (H2) blockers.
They have shifted the disease from being man-
aged surgically to medically in most cases.
However, a small subset (5–10%) of patients will
be refractory to standard treatment with PPIs.
When presented with such a patient, one must
thoroughly investigate the possible causes of
recurrent or inadequately treated disease.
A. The most common causes of recurrent PUD
are medication noncompliance, smoking, H.
pylori infection, and NSAID use. Ensuring
patient medication compliance and counsel-
ing patients to adhere to lifestyle modifica-
C. J. Dickler
Department of General Surgery, SUNY Stony Brook
University Hospital, Health Sciences Center T19-030,
Stony Brook, NY, USA
K. Spaniolas (*)
Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA
e-mail: Konstantinos.Spaniolas@
stonybrookmedicine.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_42
42
tions (NSAIDs and smoking) can help patients
manage their disease. Clinicians must also be
vigilant to other possible causes. All patients
with recurrent disease should undergo esoph-
agogastroduodenoscopy (EGD) with biopsies
of any ulcers to rule out cancer and biopsy for
recurrent H. pylori infections.
B. Clinicians should have a high index of suspi-
cion for cancer if symptoms worsen despite
initial treatments. Patients with prior cancer
resections can have cancer manifest as new
ulcer at or near the anastomosis, which can be
ruled out with biopsy during esophagogastro-
duodenoscopy (EGD).
C. Having a thorough knowledge of a patient’s
prior surgical procedures can help rule out post-
surgical causes of recurrent disease. In the liter-
ature, this is most commonly the result of
retained antrum from an incomplete antrectomy
(proximal margins should be at the incisura of
the lesser curvature and the third branch of the
right gastroepiploic artery along the greater cur-
vature). This can be confirmed by performing a
sodium pertechnetate Tc 99 m scan.
D. If the prior history is not enlightening, basic
laboratory testing can help point one in the
right direction. Preliminary studies should
include evaluation for H. pylori and checking
of gastrin levels, with a plan to follow up with
a secretin test if the results are equivocal.
These will help rule out a gastrinoma
(Zollinger–Ellison syndrome, ZES).
161
162 C. J. Dickler and K. Spaniolas

E. If elevated gastrin levels are seen, but there is
a poor response to a secretion test (less than
200  pg/ml in gastrin levels), then pseudo-
Zollinger–Ellison syndrome or antral G-cell
hyperplasia must be suspected. This can be
distinguished from ZES by using a standard
meal test, which will show a 3× fold increase
in gastrin levels in pZES, but only about 40%
in ZES.
F. Ulcers that do not respond to maximal medical
therapy will require surgical revision with par-
tial gastrectomy with or without vagotomy.

Recurrent peptic ulcer

disease

Endoscopy with biopsy (Cancer vs. H. pylori A

Medical Management (PPI BID, Smoking cessation, Treat H. pylori

Rule out cancer Re-evaluation

(Repeat endoscopy with Biopsy of symptoms
or screen with CT Scan)

Equivalent

Negative
C

Prior surgical Tc-99 scan

history? (Retained antrum)
Yes
Surgical Positive
resection No

D
Completion antrectomy
Octreotide Zollinger–Ellis Gastrin levels with redo anastomosis or
scan Syndrome (Secretin test) conversion to Roux En Y
Elevated
Normal

E
Pseudo-Zollinger– Standard meal
Ellison Syndrome test
Elevated
Normal

Nonhypergastrinemia related ulcer

Revision gastrectomy
Medical management
+/- vagotomy
Fails

Algorithm 42.1
42  Management of Recurrent Peptic Ulcer Disease 163

Suggested Reading Keuppens F, et  al. Antral gastrin cell hyperplasia in

patients with peptic ulcer. Ann Surg. U.S.  National
Library of Medicine, 1980. www.ncbi.nlm.nih.gov/
Cameron JL, Cameron AM. Stomach. In: Current surgical
pubmed/7362294.
therapy. 11th ed. Philadelphia, PA: Saunders; 2014.
Kitagawa Y, Dempsey DT. Stomach. In: Schwartz’s prin-
p. 69–107.
ciples of surgery. New York City, NY: McGraw-Hill
Dacha S, et  al. Hypergastrinemia. Gastroenterol Rep.
Education\Medical; 2015. p. 1035–95.
2015;3(3):201–8. https://doi.org/10.1093/gastro/
Teitelbaum EN, et  al. Stomach. In: Sabiston textbook
gov004.
of surgery: the biological basis of modern surgical
Fisher WE, et  al. Pancreas. In: Schwartz’s principles of
practice. 12th ed. Philadephia, PA: Elsevier; 2017.
surgery. New York City, NY: McGraw-Hill Education\
p. 1188–236.
Medical; 2015. p. 1392–3.
Vakil N. Approach to refractory or recurrent peptic ulcer
Gray GR, et al. Extragastric gastrinoma or G-cell hyper-
disease. Approach to refractory or recurrent peptic
plasia of the antrum? The preoperative diagnosis in a
ulcer disease. UpToDate5, 5 July 2017, www.upto-
case of hypergastrinaemia. Br J Surg. 1976;63(8):596–
date.com/contents/approach-to-refractory-or-recur-
8. https://doi.org/10.1002/bjs.1800630809.
rent-peptic-ulcer-disease.
 Management of Gastric Cancer
Christina L. Wolchok and Georgios V. Georgakis
Algorithmic Approach
A. Patients with gastric cancer present most
commonly with nonspecific abdominal pain.
It is important to identify the presenting
symptom or sign (heart burn, dysphagia, nau-
sea, pain, obstruction, GI bleed, weight loss,
and anemia) as the presence of such symp-
toms signifies cancer at later stages. Signs
that are associated with advanced disease
include a palpable abdominal mass, Virchow’s
node (left supraclavicular), Sister Mary
Joseph’s node (umbilical), Irish node (left
axillary), Krukenberg’s tumor (adnexa/
ovary), Blumer’s shelf (pelvic cul-de-sac
mass), ascites, and jaundice.
B. Some patients present in extremis as a result
of dehydration from gastric outlet obstruc-
tion, malnutrition and weight loss from dys-
phagia, and/or severe anemia from
malabsorption. In these cases, restoring the
patient’s homeostasis precedes any workup.
C. L. Wolchok
Graduate Medical Education, Department of General
Surgery, Stony Brook University Hospital,
Stony Brook, NY, USA
G. V. Georgakis (*)
Department of Surgery, Division of Surgical
Oncology, Stony Brook University Hospital,
Stony Brook, NY, USA
e-mail: georgios.georgakis@stonybrookmedicine.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_43
43
C. Upper gastrointestinal endoscopy and biopsy
is important for confirmation of the diagno-
sis. Endoscopic ultrasound can give addi-
tional information about the T stage, the
presence of regional lymphadenopathy,
which permits nodal biopsy via fine needle
aspiration. An imaging study like CT scan of
the chest, abdomen and pelvis or a PET/CT
evaluation (skull base to mid-thigh) is also
used for staging [1].
D. Clinical staging is done by reviewing all the
clinical data (endoscopy, EUS, CT, or PET
CT) according to the AJCC guidelines, con-
sidering the tumor depth of invasion (T), the
presence or absence of regional lymph nodes
(N), and the presence or absence of distant
metastases (M). A multidisciplinary approach
should be taken at all disease stages [2].
E. Gastric cancer is deemed unresectable if there
suspicious or biopsy proven positive lymph
nodes at the root of the mesentery or para-aortic
nodes, distant metastases, or peritoneal seeding
(including positive peritoneal cytology).
F. In the case of unresectable disease, or in the
event the patient is unfit for surgery, chemo-
therapy, chemoradiation, and/or palliative pro-
cedures (stenting, resection for obstruction or
uncontrollable bleeding, and gastrostomy tube
placement for decompression) are the pre-
ferred modes of treatment. Once the treatment
is concluded, restaging may be ­performed to
re-evaluate the mass for possible resection.
165
166 C. L. Wolchok and G. V. Georgakis

G. When resectable, an initial diagnostic lapa-
roscopy with washings and cytology is
strongly recommended [3, 4].
H. If cytology is positive, then the patient should
receive chemotherapy according to the multi-
disciplinary approach. Once the treatment is
concluded, restaging may be performed to re-
evaluate the mass for resection [4].
I. If cytology is negative, surgery with periop-
erative chemotherapy or chemoradiation is
warranted [5, 6].

Vague abdominal pain or more specific symptoms

A Sings of obstruction, GI bleed, weight loss, anemia

In the event of a patient presenting in extremis (obstruction, dehydration,

B severe malnutrition), immediate measures to restore homeostasis (e.g., NG
decompression, IV hydration, and TPN initiation) are warranted.

· Esophagogastroduodenoscopy
· Endoscopic Ultrasound
C · CT Chest/abdomen/pelvis with IV contrast
· PET-CT for intestinal type and nonmucinous tumors
· CBC and comprehensive chemistry

D
Staging

Absence of metastatic disease Presence of metastatic disease

E Surgically resectable Surgically unresectable
Surgical candidate Nonsurgical candidate

Chemotherapy or Chemoradiation
Consider diagnostic laparoscopy
G with cytology
Palliative procedures for obstruction, F
uncontrollable bleeding, etc.

I Cytology negative Cytology positive H

Surgery
Perioperative chemotherapy Chemotherapy
Perioperative chemoradiation

Algorithm 43.1  Treatment algorithm for gastric cancer

43  Management of Gastric Cancer 167

References carcinoma for laparoscopic staging. Am J Surg.

2006;191(1):134–8.
4. Mezhir JJ, Shah MA, Jacks LM, Brennan MF, Coit DG,
1. Park SR, Lee JS, Kim CG, Kim HK, Kook MC,
Strong VE.  Positive peritoneal cytology in patients
Kim YW, et  al. Endoscopic ultrasound and com-
with gastric cancer: natural history and outcome of
puted tomography in restaging and predicting prog-
291 patients. Ann Surg Oncol. 2010;17(12):3173–80.
nosis after neoadjuvant chemotherapy in patients
5. Cunningham D, Allum WH, Stenning SP, Thompson
with locally advanced gastric cancer. Cancer.
JN, Van de Velde CJ, Nicolson M, et al. Perioperative
2008;112(11):2368–76.
chemotherapy versus surgery alone for resect-
2. Amin MB, Edge S, Greene F, Byrd DR, Brookland
able gastroesophageal cancer. N Engl J Med.
RK, Washington MK, Gershenwald JE, Compton
2006;355(1):11–20.
CC, Hess KR, Sullivan DC, Jessup JM, Brierley JD,
6. Smalley SR, Benedetti JK, Haller DG, Hundahl
Gaspar LE, Schilsky RL, Balch CM, Winchester DP,
SA, Estes NC, Ajani JA, et  al. Updated analysis of
Asare EA, Madera M, Gress DM, Meyer LR, edi-
SWOG-directed intergroup study 0116: a phase III
tors. AJCC Cancer staging manual. 8th ed. Chicago:
trial of adjuvant radiochemotherapy versus obser-
Springer; 2017. p. 1032.
vation after curative gastric cancer resection. J Clin
3. Sarela AI, Lefkowitz R, Brennan MF, Karpeh
Oncol. 2012;30(19):2327–33.
MS.  Selection of patients with gastric adeno-
 Management of Gastrointestinal
Stromal Tumors
Igor G. Elyash
Algorithmic Approach
A. Gastrointestinal stromal tumors (GISTs) are
the most common nonepithelial tumors of the
GI tract. They are characterized by genes
encoding receptor protein tyrosine kinases,
such as KIT and platelet-derived growth fac-
tor receptor alpha (PDGFRA). They can be
seen in any part of the gastrointestinal tract
but are usually found in the stomach. GISTs
typically present in middle age, and only a
small percentage of them present in a famil-
ial/genetic pattern; most are sporadic. They
are found in the wall of the gastrointestinal
tract and can have various types of presenta-
tion. Symptomatology includes early satiety,
abdominal discomfort, and bleeding. Other
times, they are asymptomatic and are inci-
dentally found on imaging and endoscopy.
B. Initial examination of patients begins with a
history and physical characterizing symp-
toms and their natural course. Basic blood
work can be ordered as part of the workup.
The diagnosis is often made by CT of the
abdomen with contrast. GISTs are often
smooth in appearance and enhance with con-
trast. CT scans can also identify any potential
sites of metastasis (majority of metastasis
I. G. Elyash (*)
Morristown Surgical Associates, Morristown Medical
Center, Morristown, NJ, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_44
44
tends to occur in the intraperitoneal cavity).
An esophagogastroduodenoscopy (EGD) is
also helpful in characterizing the mass and
often shows a smooth mass covered by nor-
mal mucosa. If there are any diagnostic dis-
crepancies, magnetic resonance imaging
(MRI) can also be completed as part of the
workup.
C. Once a radiologic or clinical diagnosis of a
GIST has been made, further management is
dependent on resectability and tumor spread.
If the primary tumor demonstrates no signs of
metastasis and is highly suspicious of a GIST
on imaging and endoscopy, there is no need for
a preoperative biopsy. Endoscopic ultrasound-
guided biopsy may assist in establishing a
diagnosis in metastatic disease or if any clini-
cal ambiguity exists. Resectable primary
tumors are managed with surgical resection
with negative margins. If tumors have a high
risk of recurrence (high mitotic rate, increased
size), they are postoperatively treated with the
tyrosine kinase inhibitor, imatinib. Large/unre-
sectable tumors are treated with neoadjuvant
imatinib and then surgery if downsized.
D. Resected tumors are followed with exams
and CT scans every 3 to 6  months for 3 to
5 years and then on a yearly basis.
169
170 I. G. Elyash

A
History: Patient presenting with early satiety, vague
abdominal discomfort, GI bleed. Can be
asymptomatic with incidental finding.

B History and Physical exam: Symptoms and their natural

course.

Basic blood work and then evaluate symptoms with CT

abdomen/ EGD. MRI if any diagnostic discrepancies.

C
Resectable lesion?

Yes No

Surgical resection with EUS guided biopsy for

negative margins. confirmation.

Imatinib treatment
High risk of Yes
reoccurrence?

No
Surgical resection if
D resectable tumor
Surveillance

Algorithm 44.1

Suggested Reading
Brunicardi FC. Schwartz’s principles of surgery. 10th ed.
New York: McGraw Hill; 2015.
Cameron JL, Cameron AM. Current surgical therapy. 11th
ed. Philadelphia: Elsevier; 2014.
Keung EZ, Raut CP. Management of gastrointestinal stro-
mal tumors. Surg Clin North Am. 2017;97(2):437–52.
 Management of Upper
Gastrointestinal Hemorrhage
Igor G. Elyash
Algorithmic Approach
A. Upper gastrointestinal hemorrhage can present
as hematemesis, melena, and also hematoche-
zia in the setting of significant hemorrhage.
The initial approach with all patients starts
with ensuring the maintenance/support of the
airway and proper resuscitation with intrave-
nous (IV) fluids and blood products as needed.
Patients should be in a monitored setting with
strict monitoring of outputs and hemodynam-
ics. The source of bleeding is further investi-
gated with a thorough history and physical
examination. History should focus on previous
episodes of bleeding, comorbidities, current
medications, previous surgical history, as well
as other symptoms. History of abdominal pain,
dysphagia, retching, and jaundice/ascites can
shed light on the cause of bleeding. Nasogastric
tube (NGT) and lavage are occasionally used if
source of bleeding is in question.
I. G. Elyash (*)
Morristown Surgical Associates, Morristown Medical
Center, Morristown, NJ, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_45
45
B. Baseline hemoglobin levels, coagulation pro-
files, basic chemistries, and liver functions
are helpful with management. After the
patient is resuscitated and hemodynamically
stable, the initial diagnostic study is an upper
endoscopy. Upper endoscopy allows for
localization of the source of bleeding and
intervention at the same time.
C. If the source is identified (i.e., peptic ulcers,
varicosities, Mallory-Weiss tears), the goal is
to control bleeding during endoscopy and
treat it accordingly. If no source is identified,
the next step is to proceed with either a tagged
red blood cell (RBC) scan for slow bleeding
or angiography for significant bleeding.
D. If unstable bleeding cannot be controlled with
endoscopy/angiography, the next step is sur-
gical intervention. Bleeding may be con-
trolled with oversewing and may occasionally
require resection. Recurrent bleeding often
requires surgical intervention as well.
171
172 I. G. Elyash

A History: Hematemesis, melena, hematochezia

Resuscitation with IVF and blood products if needed,

strict hemodynamic monitoring. History and physical:
Previous episodes of bleeding, comorbidities,
medications, other symptoms.

B
Order blood work (CBC, chemistries, LFTs, coagulation
profile). After proper resuscitation and suspicion of
upper GI bleed, endoscopy is the first test of choice.

Source of
bleeding is
identified?

Yes No

Slow Bleeding
Endoscopic control of or Massive
bleeding followed by
observation
Slow Massive

Consider RBC scan. If Angiography/surgical

D intervention
negative, observe or
If re-bleed, repeat
consider other source.
endoscopy. Additional
bleeding requires surgery.

Algorithm 45.1

Suggested Reading
Barkun AN, et  al. International Consensus recommen-
dations on the management of patients with nonvari-
ceal upper gastrointestinal bleeding. Ann Intern Med.
2010;152(2):101–13.
Brunicardi FC. Schwartz’s principles of surgery. 10th ed.
New York: McGraw Hill; 2015.
Cameron JL, Cameron AM. Current surgical therapy. 11th
ed. Philadelphia: Elsevier; 2014.
 Part VII
Small Bowel
 Small Bowel Obstruction
Ryan M. Juza and Vamsi V. Alli
Algorithmic Approach
A. Symptoms: Symptoms of small bowel
obstruction include progressive abdominal
pain and distention with accompanying nau-
sea and vomiting. Symptom development,
however, can be variable depending on the
degree of obstruction. Partial bowel obstruc-
tion results in delayed intestinal transit from
incomplete blockage of the bowel. Symptoms
may develop gradually over several days, and
patients can continue to pass flatus or bowel
movements despite the obstruction. Complete
or high-grade bowel obstructions develop
more rapidly as a result of complete intestinal
blockage. Patients decompress proximally
through emesis, and bowel function is absent.
Closed-loop obstructions present rapidly
without distention but with significant
abdominal pain and nausea. They result in an
isolated segment of bowel with both inflow
and outflow obstructions as a result of adhe-
sive disease, volvulus, or internal hernias,
R. M. Juza (*) ∙ V. V. Alli
Department of Surgery, Division of Minimally
Invasive and Bariatric Surgery, Penn State Milton S.
Hershey Medical Center, Hershey, PA, USA
e-mail: Ryan.Juza@UHhospitals.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_46
46
which can rapidly become ischemic. A high
level of suspicion is necessary to accurately
diagnose and appropriately treat a small
bowel obstruction.
B. Workup: The first step in evaluating a patient
with small bowel obstruction includes
obtaining a thorough history and physical
examination. Pertinent history includes
past surgeries and endoscopies, previous
episodes, bowel habits, and symptom pro-
gression. Physical exam should evaluate for
signs of dehydration, evidence of hernias,
presence and character of bowel sounds,
and signs of peritonitis. Digital rectal exam
is necessary to rule out an obstructing rec-
tal mass. The first diagnostic test typically
obtained is a plain abdominal X-ray, fol-
lowed shortly after with a computed tomog-
raphy (CT) of the abdomen, preferably with
oral contrast. Typical findings include con-
tinuously dilated loops of proximal small
bowel with air-fluid levels, with distal
decompression after a so-called transition
point. A fluid-filled stomach on imaging is
common but may be absent in the setting of
recent emesis. In addition to history, physi-
cal exam, and imaging, laboratory studies
are critical to the clinical care of the patient
and will help determine whether a patient
requires an operation. A complete blood
count, lactic acid, electrolyte and basic
metabolic panel, and international normal-
175
176
ized ratio are required. Depending on the
duration and severity of symptoms, signifi-
cant electrolyte a­bnormalities and acute
kidney injury are possible and require
aggressive fluid resuscitation with intrave-
nous crystalloid solution and electrolyte
replacement. In a patient without preexist-
ing kidney disease, endpoints of resuscita-
tion include achieving adequate urine
output [1].
(a) Concerning findings: Abdominal com-
plaints should be limited to mild general-
ized abdominal distention and discomfort.
Evidence of fevers, chills, or peritoneal
signs requires operative intervention.
Small bowel obstruction secondary to
adhesive disease should not typically
cause significant hemodynamic, hemato-
logic, or electrolyte abnormalities. The
presence of these findings should prompt
closer evaluation. Depending on the
duration of symptoms, patients may dem-
onstrate tachycardia associated with
hypovolemia, which should respond to
intravenous fluid resuscitation.
Additionally, hypotension that is unre-
sponsive to a weight-based fluid bolus is
abnormal and should prompt further
workup.
(b) Imaging: Findings on imaging include:
(i) Isolated segments of dilated bowel.
(ii) Nonphysiologic free fluid (i.e.,
male/amenorrheic females).
(iii) Dilation greater than 3  cm in
diameter.
(iv) Pneumotosis intestinalis.
(v) Free abdominal air.
(vi) Mesenteric edema.
(c) Laboratory: Significant leukocytosis is
suggestive of compromised bowel and
should lower the threshold for operative
intervention. A mild leukocytosis can be
seen with obstructive symptoms due to
bowel edema and hypovolemic state.
This should begin to normalize with
appropriate nasogastric decompression
and resuscitation. Likewise, lactic acido-
sis should prompt earlier surgical inter-
R. M. Juza and V. V. Alli
vention. It should, however, be regarded
carefully as a normal lactic acid level
does not rule out intestinal ischemia in
the setting of venous outflow
obstruction.
C. Special groups: Certain patient subgroups
require special attention.
(a) Virgin abdomen: Patients who present
with obstructive symptoms without prior
abdominal surgery warrant close surgical
scrutiny. Previous dogma stated that all
patients with a “virgin” abdomen and
obstruction warrant operative exploration
because of the risk of malignant obstruc-
tion [2]. Recent studies, however, suggest
that adhesive disease is still the most
likely culprit in patients without prior
surgical history [3]. Regardless, patients
who present with obstructive symptoms
without prior abdominal surgery com-
mand a lower threshold for operation.
(b) Altered gastrointestinal (GI) tract anat-
omy, such as roux-en-Y gastric bypass:
Patients with prior gastric bypass surgery
are at risk of internal hernia formation, in
addition to adhesive small bowel disease
as the source of bowel obstruction. Internal
hernias form through the mesenteric
defects created when performing a roux-
en-Y reconstruction. Bowel herniated
through these defects is at a high risk of
incarceration and strangulation. Any
patient with prior gastric bypass warrants
additional workup, including an upper
gastrointestinal (UGI) or CT scan with
oral and intravenous contrast to evaluate
for internal hernia. Typical radiographic
findings include swirling in the mesentery
and loops of dilated bowel with interven-
ing segments of decompressed bowel.
Some surgeons advocate diagnostic lapa-
roscopy in all gastric bypass patients who
present with obstructive symptoms
because of the risk of strangulated internal
hernia. The risk of internal hernia is not
unique to roux-en-Y reconstructions but
can occur anywhere a bowel resection and
anastomosis create a mesenteric defect.
46  Small Bowel Obstruction
(c) Hernia: Abdominal wall hernias are a
common cause of mechanical small
bowel obstruction. Herniated bowel is at
risk of incarceration and strangulation.
CT evidence of a hernia with a narrow
neck is more concerning for strangula-
tion than a hernia with a wide neck where
the bowel can easily self-reduce.
Attempts to manually reduce the hernia
can be performed and, if successful, often
D
alleviates the obstruction. If the patient
has exam findings suggestive of strangu-
lation, attempts to manually reduce the
hernia should be avoided, and the patient
should be taken to the operating room for
exploration as this is a sign of an underly-
ing ischemic bowel.
(d) Impaired patient: Nonoperative manage-
ment of patients with small bowel obstruc-
tion is contingent on the ability to serially
examine the patient for changes in clinical
177
exam. Patients who are elderly, obtunded,
or cognitively impaired may not have a
reliable abdominal examination.
Additionally, patients who are on steroids
or are immune suppressed may not mani-
fest the typical signs and symptoms of
bowel ischemia. A surgeon should have a
lower threshold for operative exploration
in this patient population.
. Treatment: Initial management with nasogas-
tric decompression, fluid resuscitation, and
close monitoring is indicated. Patients who
do not have signs of peritonitis or concerning
lab and imaging findings can be managed
with electrolyte replacement and often with a
provocative upper GI series utilizing hyperos-
motic water-soluble contrast dye, which may
decrease the time to return of bowel function
[4]. Patients who fail to resolve their symp-
toms after a 24–48-h trial of nonoperative
management require surgical exploration.
178 R. M. Juza and V. V. Alli

Patient with obstructive symptoms

A

Nasogastric tube
decompression, IV fluid
resuscitation

Thorough and focused history and physical

examination

Plan films – supine/upright Abdominal X-ray

CT abdomen/pelvis with oral and intravenous contrast
Laboratory studies

Workup consistent with small bowel obstruction

Yes
High-risk group OR

C
No

Yes
High-risk OR
features

No

24–48 hour trial nonoperative

management

Algorithm 46.1
46  Small Bowel Obstruction 179

Return of
bowel function

Partial

Consider small
bowel follow-
though study

Yes No

Contrast
reaches colon

No
Yes

Remove NG and OR
slow diet
advancement

Algorithm 46.1 (continued)

tion in the virgin abdomen: the need for a mandatory

References
1. Maung AA, Johnson DC, Piper GL, Barbosa RR,
Rowell SE, Bokhari F, Collins JN, Gordon JR, Ra JH,
Kerwin AJ, Eastern Association for the Surgery of
Trauma. Evaluation and management of small-bowel
obstruction: an Eastern Association for the Surgery
of Trauma practice management guideline. J Trauma
Acute Care Surg. 2012;73(5 Suppl 4):S362–9.
2. Beardsley C, Furtado R, Mosse C, Gananadha S,
Fergusson J, Jeans P, Beenen E. Small bowel obstruc-
laparotomy explored. Am J Surg. 2014;208(2):243–8.
3. Tavangari FR, Batech M, Collins JC, Tejirian T. Small
bowel obstructions in a virgin abdomen: is an opera-
tion mandatory? Am Surg. 2016;82(10):1038–42.
4. Di Saverio S, Catena F, Ansaloni L, Gavioli M,
Valentino M, Pinna AD.  Water-soluble contrast
medium (gastrografin) value in adhesive small
intestine obstruction (ASIO): a prospective, ran-
domized, controlled, clinical trial. World J Surg.
2008;32(10):2293–304.
 Small Bowel Tumors
Vamsi V. Alli and Ryan M. Juza
Algorithmic Approach
Small bowel tumors are a rare clinical entity but
one that the general surgeon should be prepared
to address. They comprise 3–5% of all GI tumors
and 0.5% of cancer in the United States [1].
Symptoms are often vague and nonspecific, with
frequent delays in diagnosis, reportedly up to
3  years for benign tumors and 18  months for
malignant tumors [2]. As a result, small bowel
tumors may be encountered as either an inciden-
tal finding or as an unexpected source of nonspe-
cific abdominal pain, weight loss, or anemia. In
the case of carcinoid tumors, diagnosis is made
following manifestation of systemic effects of
metastatic disease, i.e., carcinoid syndrome.
Types of Small Bowel Tumors
Primary: adenocarcinoma, neuroendocrine
tumors (including carcinoid), sarcoma
(including gastrointestinal stromal tumors
(GIST)), metastatic [3]
V. V. Alli (*) ∙ R. M. Juza
Department of Surgery, Division of Minimally
Invasive and Bariatric Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: valli@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_47
47
A. Clinical suspicion for small bowel mass.
The most common presentation of small
bowel tumors is abdominal pain, which occurs
in 44–90% of patients, followed by weight
loss in 24–44% and bleeding in 23–41% of
cases. Some patients remain asymptomatic
until tumors reach a critical mass, resulting in
obstruction from obliteration of the lumen or
intussusception. Obstructive symptoms such
as nausea and vomiting occur in 17–64% of
patients with small bowel tumors, while
22–26% of tumors present with bowel
obstruction and 6–9% with perforation and
jaundice in 6% of patients [4].
B. For patients with suspected gastrointestinal
malignancy, a thorough history should be
obtained, specifically inquiring regarding
abdominal pain, weight loss, fatigue, nausea,
vomiting, anorexia, early satiety, abdominal
distension, change in bowel habits, melena.
Past medical history should inquire about
prior oncologic history, specifically lung,
breast, cervical, colon cancers, as well as
melanoma and sarcomas, all of which may
metastasize to the bowel.
Personal and family history of conditions
predisposing to small bowel malignancy
should be elicited, including Peutz–Jeghers,
hereditary nonpolyposis colorectal cancer,
familial adenomatous polyposis syndrome,
Crohn’s d­isease, neurofibromatosis type 1,
and celiac disease [5].
181
182
Review of symptoms relevant to meta-
static disease should cover chest pain, short-
ness of breath, cough, wheezing, hemoptysis,
jaundice, acholic stool, neurologic symp-
toms, dermatitis, diarrhea, and mental status
changes.
A focused abdominal exam should evalu-
ate for distension, masses, organomegaly,
tenderness, and shifting dullness. Additional
attention should be paid to digital rectal
exam and fecal occult blood testing.
Examination of lymphatic basins may reveal
evidence of metastasis from visceral sources,
particularly the eponymous Sister Mary
Joseph node (umbilical) and Virchow’s node
(supraclavicular).
Laboratory examinations lack specificity.
However, complete blood count (CBC) with
differential basic metabolic panel (BMP),
liver function tests (LFTs), and coagulation
profile should be obtained to screen for ane-
mia and abnormal differential (may indicate
lymphoma) and assess nutrition and gross
abnormalities in liver function or electrolytes
prior to potential procedures.
Tumor specific markers  – Chromogranin
A in neuroendocrine tumors and 5-hydroxy-
indoleacetic acid (5-HIAA) in carcinoid
syndrome.
C. Testing
Initial options for radiographic imaging
include small bowel follow-through (50–60%
sensitivity) or axial imaging in the form of
computed tomography (CT) or magnetic res-
onance imaging (MRI) (both have >80%
sensitivity).
Endoscopic evaluation: Upper/lower
endoscopy for direct endoscopic identifica-
tion and potential biopsy. Twenty-five percent
of small bowel masses occur in the
duodenum.
. Additional Diagnostic Modalities
D are treated with a Whipple procedure.
Additional contrast-enhanced imaging of
the small bowel may be required if initial stud-
ies fail to localize the tumor. These options
include CT enterography (85% sensitivity) and
MR enterography (91–97% sensitivity).
V. V. Alli and R. M. Juza
Additional endoscopic evaluation may
identify the tumor. This includes capsule
endoscopy (passive study with purely diagnos-
tic capability, sensitivity of 1.5–9%) [2] and
either push (valuable until proximal jejunum)
or double-balloon enteroscopy which allow
biopsy and potentially endoscopic resection.
Once the mass is identified, metastatic
workup should be conducted as indicated.
. Treatment Based on Size, Location, and Tumor
E
Type
If size is <2  cm, assessment using endo-
scopic ultrasound (EUS) may reveal high-risk
characteristics. If no high-risk features are
noted, asymptomatic lesions found incidentally
may be surveilled, though there is a chance of
missed diagnosis of malignancy. *Lesions
<1 cm in size found to be carcinoid tumors may
be amenable to endoscopic resection alone.
If size is >2 cm, assess location and suitabil-
ity for resection. If the lesion is unresectable,
locally advanced, or workup reveals metastatic
disease, systemic chemotherapy (biopsy-
guided therapy) is indicated. Treatment of met-
astatic disease is largely palliative.
Surgery
When oncologically indicated and anatomically
feasible, surgical resection with primary anas-
tomosis is preferred. Segmental resections
may be performed, with adjacent lymphade-
nectomy. Care should be taken to assess the
remainder of the GI tract, particularly in the
case of carcinoid (~30% are multiple) or meta-
static lesions, where multiple sites of disease
are possible [3].
• Endoscopic resection: Biopsy-proven benign
lesions may be resected endoscopically.
• Difficult location: Tumors involving the
first and second portion of the duodenum
Distal ileal tumors require ileocolectomy.
• Metastatic disease may require palliative
resections for bleeding, or bypass for
malignant obstructions, and chemotherapy
for lymphoma.
47  Small Bowel Tumors 183

Concern for small bowelmalignancy A

Thorough and appropriate history & physical,

laboratory workup,evaluationfor signs of metastatic B
disease
Symptoms; Existing imaging
without any
imaging

C CT or MRI
Symptoms of
metastatic
disease
Endoscopic evaluation with EGD &/orcolonoscopy

Tumor
identified
D Yes

Metastatic
No Yes workup

Small bowel contrast studies (UGI, CTE, or MRE),

capsule studyor enteroscopy to identify small
bowel mass
No Metastatic disease
Positive for
Metastatic disease

E No Resectable
disease

Consider palliative
resection, bypass,
Yes
chemotherapyin cases of
lymphoma or carcinoid

Resection

Adjuvant
chemotherapy

Followup: Surveillence
& labs

Algorithm 47.1
184 V. V. Alli and R. M. Juza

References 4. Talamonti MS, Goetz LH, Rao S, Joehl RJ. Primary

cancers of the small bowel: analysis of prognostic fac-
tors and results of surgical management. Arch Surg.
1. Siegel RL, Miller KD, Jemal A.  Cancer statistics,
2002;137(5):564–70.
2018. CA Cancer J Clin. 2018;68:7.
5. Kim JS, Park SH, Hansel S, Fletcher JG. Imaging and
2. Emanuele R, Anastasios K, Diana Y, Reddy SN, Julius
screening of cancer of the small bowel. Radiol Clin
G, Marco P. Neoplastic diseases of the small bowel.
North Am. 2017;55(6):1273–91.
Gastrointest Endosc Clin N Am. 2017;27:93–112.
3. Ashley SW, editor. Scientific American surgery.
Hamilton/Ontario/Philadelphia: Decker Intellectual
Properties; 2018. ISSN 1547-1616.
 Management of Small Bowel
Neuroendocrine Tumors
Michele A. Riordon and Calvin H. L. Law
Algorithmic Approach
A. Small bowel neuroendocrine tumors (NETs)
include both foregut (duodenal) and midgut
(jejunal and ileal) types. Most foregut NETs
do not produce a biologically active hormone
and are often classified as nonfunctioning.
Functioning NETs are usually from the midgut
and typically produce and secret serotonin,
tachykinin, and prostaglandins. Both groups of
NETs most often present with nonspecific
symptoms, which often leads to delayed diag-
nosis. A careful history and physical exam can
help provide clues that will determine the next
steps in the investigation and which patients
are at risk of having functional tumors and
metastatic disease. Carcinoid syndrome, clas-
sically characterized by flushing, diarrhea, and
valvular heart disease, occurs most often in
metastatic NETs of the small bowel, but the
overall incidence is less than 13%. Biological
behavior and response to therapy are linked to
differentiation and the grade of tumor as mea-
M. A. Riordon
Department of Surgery, Royal Victoria Regional
Health Centre, Barrie, ON, Canada
C. H. L. Law (*)
Department of Surgical Oncology, Sunnybrook
Health Sciences Centre, Toronto, ON, Canada
e-mail: calvin.law@sunnybrook.ca
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_48
48
sured by Ki-67. Most recent classification by
Ki-67 includes G1 (<3%), G2 (3–20%), and
G3 (>20%) [1–5].
B. A multislice, triple phase computed tomogra-
phy (CT) of the chest, abdomen, and pelvis
(including an enterogram protocol) is the first
choice of imaging for both the detection and
staging of small bowel neuroendocrine
tumors. Magnetic resonance imaging (MRI)
can be used if there is diagnostic uncertainty
after CT, there is a contraindication to the con-
trast medium, or to further characterize liver
involvement. Functional imaging such as
111
In-pentetreotide (OctreoScan) or positron
emission tomography (PET)/CT imaging with
68Ga-labeled somatostatin analog are useful
in the localization of well-­differentiated small
bowel NETs, whereas a flurodeoxyglucose
(18FDG) PET/CT is more useful for poorly
differentiated tumor localization [5–7].
C. Biochemical workup with a serum chromo-
granin a (CgA) level and a 24-h
5-­hydroxyindole acetic acid (5-HIAA) urine
collection are not considered first-line diag-
nostic tests. The sensitivity of serum CgA is
in the range of 67–93%, but the specificity is
less than 50% [8, 9]. A 24-h urine 5-HIAA
level has a sensitivity that approaches 100%
but a specificity of only 35%, and it is falsely
elevated by serotonin-rich foods [9, 10].
However, carcinoid syndrome is a result of
metastases outside the portal circulation and
185
186
thus elevates serum serotonin by avoiding
first-pass effect. In this situation, 24-h urine
5-HIAA may confirm elevated serotonin and
identify this population of patients at risk of
carcinoid crisis.
D. Carcinoid crisis is associated with a rapid
release of hormones from metastatic tumor
deposits that can result in sudden fluctuations in
blood pressure (most commonly hypotension),
tachycardia, bronchospasm, and hyperthermia.
If a patient has features of carcinoid syndrome,
periprocedural prophylaxis with octreotide is
used in attempts to prevent a carcinoid crisis,
but recent data suggest that prophylactic octreo-
tide may not be beneficial. Shortening the dura-
tion of hemodynamic instability with prompt
usage of vasopressors does seem to decrease
complications from the crisis [11, 12].
E. Localized treatment: Curative intent surgery
includes exam for synchronous, multifocal
lesions and regional lymphadenectomy.
Avoidance of short-gut syndrome is an impor-
tant consideration.
M. A. Riordon and C. H. L. Law
Metastatic treatment: Tissue diagnosis for
differentiation and Ki-67 index are key to
choosing the optimal treatment. Options
include observation; somatostatin analogs;
palliative surgery to prevent symptoms (small
bowel resection to prevent obstruction and
cholecystectomy to decrease somatostatin
side effects); surgical cytoreduction (particu-
larly for functional tumors); liver-directed
therapy, including embolization options; and
chemotherapy for high Ki-67 or poorly dif-
ferentiated tumors.
F. Disease progression:
–– G1 and G2 (Ki-67  <  20%)  – Targeted
molecular therapy: Tyrosine kinase inhibi-
tors (i.E., everolimus), peptide receptor
radionuclide therapy (177-lutetium).
–– G3 and/or poorly differentiated (Ki-­
67 > 20%): Platinum-based chemotherapy.
–– For all tumors  – Additional symptom
control may also be achieved with telo-
tristat in patients with functional midgut
tumors.
48  Management of Small Bowel Neuroendocrine Tumors 187

History
-Local symptoms: abdominalpain, mass, obstructive symptoms, bloating,
gastrointestinal bleeding
-Systemic symptoms: weight loss,
-Functional neuroendocrine symptoms from small bowel tumors
-Carcinoid syndrome: flushing, diarrhea, valvular heart disease
-Bronchospasm: (wheezing, chestpain, cough)
A

Physical exam
Cardiac: elevated JVP, cardiomegaly, murmurs, edema
Respiratory: wheezing
Abdominal: mass, signs of bowel obstruction, hepatomegaly, stigmata
of liver disease
General: evidence of flushing, signs of weight loss

CT scan (enterogram protocol)

showing small bowel primary,
mesenteric mass or clinical features
suggestive of a small bowel neuro
endocine tumor?
B

Workup

1. Multiphase CT abdomen and pelvis for primary tumor evaluation and to rule out
metastatic liver disease
2. MRI if CT nondiagnostic or further liver evaluation required
3. Octreotide scan – (111-In-labelled pentetreotide) for primary tumor evaluation
and metastatic disease (or preferably 68GA scan if available)
4. PET/CTscan – especially if there is negative octreotide/68GA scan
5. Cardiac consult and ECHO if abnormal cardiac exam

Algorithm 48.1
188
Evidence of carcinoid syndrome
metastatic disease on imaging?
E, F
Localized and resectable disease
1. Inspect for synchronous lesions
2. En-bloc margin-negative resection
3. Adequate lymphadenectomy
Algorithm 48.1 (continued)
on history, exam or
Yes
No
Localized, advanced,
or metastatic disease?
Locally advanced disease
1. Resection of primary and
metastatic disease with
curative intent
2. Avoid short guy syndrome
M. A. Riordon and C. H. L. Law
1. Chromogran in A level
2. 24-hour urine 5-HIAA
Elevat
Yes
No
Perioperative
octreotide
prophylaxis prior to
any biopsy or surgery
Metastatic disease
1. Obtain tissue for diagnosis and
differentiation with Ki-67 index
2. Observation
3. Somatostatin analogues
4. Surgical cytoreduction
5. Palliative surgery for symptoms
6. Liver directed therapy
7. Chemotherapy for high Ki-
67/poorly differentiated tumors
48  Management of Small Bowel Neuroendocrine Tumors 189

Disease progression
G (consider re-biopsy to
ensure no change in Ki-67)

G1, G2 (KI-67<20%) G3 (KI-67>20%)

Targeted molecular therapy

1. Tyrosine kinase inhibitors (i.e.,
everolimus) Platinum-based chemotherapy
2. Peptide receptor radionuclide therapy
(i.e.,177-Lutetium)

Functional Functional
tumor? tumor?

Consider telotristat for

additional symptom control

Algorithm 48.1 (continued)

metastatic presentation, and outcomes. Cancer.

References
1. Strosberg JR, Weber JM, Feldman M, et al. Prognostic
validity of the American Joint Committee on can-
cer staging classification for midgut neuroendocrine
tumors. J Clin Oncol. 2013;31:420–5.
2. Modlin IM, Oberg K, Chung DC, et  al.
Gastroenteropancreatic neuroendocrine tumors.
Lancet Oncol. 2008;9:61–72.
3. Hallet J, Law CHL, Cukier M, et  al. Exploring
the risking incidence of neuroendocrine tumors:
a population-­ based analysis of epidemiology,
2015;121:589–97.
4. Pape UF, Berndt U, Muller-Nordhorn J.  Prognostic
factors of long-term outcome in gastroenteropancre-
atic neuroendocrine tumors. Endocr Relat Cancer.
2008;15:183–97.
5. Raphael MJ, Chan DL, Law C, et  al. Principles of
diagnosis and management of neuroendocrine tumors.
CMAJ. 2017;189:E398–404.
6. Onaitis MW, Kirshbom PM, Hayward TZ, et  al.
Gastrointestinal carcinoids: characteristics by
site of origin and hormone production. Ann Surg.
2000;232:549–56.
190
7. Grimaldi F, Fazio N, Attanasio R, et  al. Italian
Association of Clinical endocrinologists (AME)
position statement: a stepwise clinical approach
to the diagnosis of gastroenteropancreatic neu-
roendocrine neoplasms. J Endocrinol Investig.
2014;37:875–909.
8. Stridsberg M, Eriksson B, Oberg K, et al. A compari-
son between three commercial kits for chromogranin
a measurements. J Endocinol. 2003;177:337–41.
9. Singh S, Law C.  Chromogranin a: a sensitive bio-
marker for the detection and post-treatment monitor-
ing of gastroenteropancreatic neuroendocrine tumors.
Expert Rev Gastroenterol Hepatol. 2012;6:313–34.
M. A. Riordon and C. H. L. Law
10. Bajetta E, Ferrari L, Martinetti A, et al. Chromogranin
A, neuron specific enolase, carinoembryonic anti-
gen, and hydroxyindole acetic acid evaluation
in patients with neuroendocrine tumors. Cancer.
1999;86:858–65.
11. Woltering EA, Wright AE, Stevens MA, et  al.
Development of effective prophylaxis against
intraoperative carcinoid crisis. J Clin Anesth.
2016;32:189–93.
12. Condron ME, Pommier SJ, Pommier RF. Continuous
infusion of octreotide combined with perioperative
octreotide bolus does not prevent intraoperative car-
cinoid crisis. Surgery. 2016;159:358–65.
 Management of Enterocutaneous
Fistulas
Maria Michailidou
Algorithmic Approach
A. Patients with EC fistulas typically present
with drainage of enteric contents through the
abdominal wall or with occult findings of
abdominal pain, ileus, fevers, malaise, and a
CT consistent with an intraabdominal
abscess. Past medical and surgical history
should be obtained, including any history of
abdominal operations, trauma, malignancy,
radiation, or inflammatory bowel disease. EC
fistulas are categorized based on etiology (iat-
rogenic, mesh related, because of inflamma-
tory bowel disease, diverticulitis, radiation
effects, trauma, neoplastic process), location
(proximal or distal small bowel), and daily
output (low < 200 ml/day, intermediate 200–
500 ml/day, high > 500 ml).
B. EC fistulas carry high morbidity and mortal-
ity and therefore require a multidisciplinary
approach. Principal management involves
fluid resuscitation with electrolyte correction
and replacement of fluid losses, characteriza-
tion and control of sepsis, nutritional support,
and local wound care [1]. Patients should be
M. Michailidou (*)
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_49
49
initially made nil per os (NPO), undergo fluid
resuscitation, and have any electrolyte
derangements intravenously corrected. Sepsis
accounts for the majority of morbidity related
to EC fistulas, and therefore any sign of sep-
sis should mandate early administration of
broad spectrum antibiotics. In addition, cross-
sectional imaging with CT of the abdomen
and pelvis may identify any intraabdominal
fluid collections that require image-guided
drainage, as well as sites of distal obstruction.
Patients with peritonitis or persistent septic
shock should be taken to the operating room
for wide drainage and enteric diversion.
Many patients are nutritionally depleted upon
presentation and suffer from severe protein
losses from the EC fistula and therefore
require supplemental nutrition, mainly in the
form of total parenteral nutrition (TPN).
Nutritional goals should include an average
caloric and protein intake of 30  kcal/kg/day
and 1.5–2.5  g/kg/day, respectively. High-­
output fistulas may be controlled with TPN,
proton pump inhibitors (PPI), antidiarrheals,
and octreotide injections [2]. The goal of
enteric output should be <1.5  L/day. In
patients with no evidence of ileus or no
increase in the daily fistula output after intro-
duction of oral intake, enteral feeds are pre-
ferred over TPN or should be used
supplementarily to TPN.  Local wound care
should involve a wound care specialist and/or
191
192
enterostomal therapist and aim at controlling
the effluent and protect the adjacent skin site,
with either local wound barriers or negative
pressure vacuum dressings [3]. Special situa-
tions include patients with spontaneous fistu-
las secondary to inflammatory bowel disease
(IBD). Percutaneous drainage, along with the
use of a biologic agent, can aid in the sponta-
neous closure of the fistula [4].
C. About one third of fistulas will spontaneously
close by 4–6 weeks. Fistulas that remain open
after 12  weeks will require surgical manage-
ment. Factors associated with failure of sponta-
neous closure include retained foreign body
(most commonly permanent suture or mesh),
high-output (often proximal) fistulas such as
jejunal or ileal fistulas, presence of distal obstruc-
tion, spontaneous fistulas secondary to radiation,
IBD or malignancy, as well as short (<2 cm) fis-
tulas and those with epithelialized tracts.
M. Michailidou
D. Surgical management should be offered no
sooner than 12  weeks (ideally 6 months)
from the onset of the EC fistula in patients
whose nutrition has been optimized, sepsis
has resolved, and comorbidities managed
[5, 6]. Preoperatively, cross-sectional imag-
ing should be obtained to rule out occult
fluid collections, as well as a fistulogram to
rule out distal obstruction. Surgical princi-
ples include safe entry to the abdomen away
from the EC fistula, lysis of adhesions,
inspection of potential distal obstruction,
avoidance of enterotomies, removal of
retained foreign body, and takedown of EC
fistula with resection of involved segment(s)
and primary anastomosis. Often, full thick-
ness resection of the EC fistula and the
abdominal wall is required, which may
necessitate complex abdominal wall recon-
struction [7].
49  Management of Enterocutaneous Fistulas 193

Drainage of enteric contents through surgical site /abdominal wall

Ileus, abdominal pain, fevers, leukocytosis s/p abdominal operation

A Obtain past medical and surgical history

- Prior abdominal operations
- Radiation
- Malignancy
- Inflammatory bowel disease

Yes Operative
Early (<7 days) exploration,
postoperative, bowel
sepsis or resection,
peritonitis washout,
ostomy

No

B 1. NPO, IV fluid resuscitation, Electrolyte repletion

2. Sepsis Control / Define fistula
CT Abdomen/Pelvis to rule out abscess, distal
obstruction
Broad Spectrum Antibiotics
CT guided drainage of intra-abdominal abscess
3. Nutritional support with TPN
4. Local wound care
5. IBD related –CT Enterography/Biologic therapy

Yes No
Oral nutritional Proton Pump Inhibitors
Output <1.5 Octreotide
supplementation L/day?
Wean TPN if tolerated Loperamide

Yes

C Fistula Expectant Observation

Resolves?

No
Repeat CT Abdomen/Pelvis and Fistulogram
D Optimize nutrition
OR in 6 months for LOA, ECF takedown with bowel
resection, abdominal wall reconstruction

Algorithm 49.1
194 M. Michailidou

References neous fistula in patients with Crohn’s disease treated

with anti-TNF therapy: a cohort study from the
GETAID. Am J Gastroenterol. 2014;109(9):1443–9.
1. Gribovskaja-Rupp I, Melton GB.  Enterocutaneous
5. Brenner M, Clayton JL, Tillou A, Hiatt JR, Cryer
fistula: proven strategies and updates. Clin Colon
HG. Risk factors for recurrence after repair of entero-
Rectal Surg. 2016;29(2):130–7.
cutaneous fistula. Arch Surg (Chicago, Ill: 1960).
2. Rahbour G, Siddiqui MR, Ullah MR, Gabe SM,
2009;144(6):500–5.
Warusavitarne J, Vaizey CJ.  A meta-analysis of
6. Visschers RG, van Gemert WG, Winkens B, Soeters
­outcomes following use of somatostatin and its ana-
PB, Olde Damink SW.  Guided treatment improves
logues for the management of enterocutaneous fistu-
outcome of patients with enterocutaneous fistulas.
las. Ann Surg. 2012;256(6):946–54.
World J Surg. 2012;36(10):2341–8.
3. Misky A, Hotouras A, Ribas Y, Ramar S, Bhan C. A
7. Krpata DM, Stein SL, Eston M, Ermlich B, Blatnik
systematic literature review on the use of vacuum
JA, Novitsky YW, et  al. Outcomes of simultane-
assisted closure for enterocutaneous fistula. Color
ous large complex abdominal wall reconstruction
Dis. 2016;18(9):846–51.
and enterocutaneous fistula takedown. Am J Surg.
4. Amiot A, Setakhr V, Seksik P, Allez M, Treton X,
2013;205(3):354–8; discussion 8–9.
De Vos M, et  al. Long-term outcome of enterocuta-
 Management of Crohn’s Disease
Igor G. Elyash
Algorithmic Approach
A. Crohn’s disease usually presents in the third
and sixth decades of life as a focal inflamma-
tion that can occur at any location along the
GI tract from the mouth to anus, usually spar-
ing the rectum. Symptoms include intermit-
tent abdominal pain, diarrhea, and weight
loss. Patients can also present with extraintes-
tinal manifestations such as ocular disease,
skin lesions, and joint disease. Initial evalua-
tion includes a history and physical examina-
tion and should assess for previous episodes,
family history of inflammatory bowel dis-
ease, and any prior treatments.
B. A thorough workup of Crohn’s disease should
include blood work and endoscopic evalua-
tion to assess the level of inflammation and
also to rule out possible malignancy. A com-
puted tomography (CT) scan can be helpful
to rule out specific abdominal pathology and
may identify fistulas and abscess formation.
Testing for perinuclear antineutrophil cyto-
plasmic antibody (p-ANCA) may be consid-
ered when the diagnosis is unclear.
I. G. Elyash (*)
Morristown Surgical Associates, Morristown Medical
Center, Morristown, NJ, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_50
50
C. If the patient is having active disease, medical
therapy is initiated. Treatment consists of ste-
roids and biologic medications. If medical
therapy is successful, the patient is followed
closely and considered for remission therapy.
If medical therapy fails in treating active
inflammation and/or the patient’s symptoms
worsen due to medical treatment (i.e., ste-
roids), surgical intervention should be consid-
ered. Patients should also be considered for
surgery if they demonstrate signs of peritoni-
tis, bowel obstruction, signs of perforation,
toxic megacolon, concern for malignancy,
and/or fistulas.
D. In the operating room, the goal is disease
resection with gross margins. Patients with
Crohn’s disease will oftentimes require mul-
tiple surgeries in their lifetime. It is impor-
tant to be mindful of short-gut syndrome,
which can be a devastating complication of
multiple bowel resections. If large segments
of bowel are involved or a patient has mul-
tiple previous bowel resections, stricturo-
plasty should be considered over segmental
resection.
195
196 I. G. Elyash

A History: Diffuse abdominal pain, diarrhea,

weight loss with intermittent symptoms.

Perform a history and physical exam. Ask about

previous episodes, family history of inflammatory
bowel disease, previous skin or ophthalmic issues.

B Order blood work (CBC, chemistries, LFTs),

Endoscopy, CT scan with contrast. May consider
antibody testing.

C If signs of active inflammatory disease confirmed by

studies, start Medical Therapy (5-ASA, Steroids,
biologic medications)

Response to medical Poor response to Peritoneal signs, bowel

Therapy medication or complications obstruction, signs of perforation,
due to medications toxic megacolon, signs of mass,
fistulas.

D Close follow up-

consider
medication for Operative Intervention
remission

Resection of gross
disease only
Yes Risk of short
Consider Stricturoplasty gut syndrome? No

Algorithm 50.1

Suggested Reading
Brunicardi FC. Schwartz’s principles of surgery. 10th ed.
New York: McGraw Hill; 2015.
Cameron JL, Cameron AM. Current surgical therapy. 11th
ed. Philadelphia: Elsevier; 2014.
 Management of Postoperative
Ileus
Igor G. Elyash
Algorithmic Approach
A. Postoperative ileus typically presents with
symptoms of nausea, vomiting, abdominal
pain, and abdominal distention postopera-
tively. Evaluation begins with a comprehen-
sive history and physical examination. History
should include assessment of a patient’s past
medical history, events during the surgery, and
current medications.
B. After performing a history and physical
exam, blood work should be obtained to look
for elevations in white blood cells and
changes in electrolytes. An abdominal X-ray
with supine and upright images should be
ordered to look for signs of bowel distention.
This will confirm the diagnosis. If a patient
develops fevers, tachycardia, peritoneal signs,
and/or clinically deteriorates, this is an indi-
cation for operative exploration.
I. G. Elyash ()
Morristown Surgical Associates,
Morristown Medical Center, Morristown, NJ, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_51
51
C. Initial treatment for postoperative ileus is
supportive. Treat any infectious process with
appropriate antibiotics if needed. Provide
proper fluid and electrolyte replacement.
Medications that slow gastrointestinal (GI)
motility, such as opiates, should be limited.
Consider nasogastric tube (NGT) placement
and supplemental nutrition. Patients should
also be on bowel rest and have serial abdomi-
nal examinations.
D. If disease is prolonged without any clinical
improvement, a computed tomography (CT)
scan may be required to look for certain treat-
able causes such as fluid collections or
abscess formation. Specific disease processes
should be treated accordingly. If there is no
resolution of symptoms, surgical exploration
may be necessary.
197
198 I. G. Elyash

A History: Distended abdomen with diffuse tenderness,

nausea/vomiting a few days after abdominal surgery

Perform a history and physical exam. Review medical

history, medications patient is taking and operative events.

B Order blood work and supine/upright plain abdominal film.

Signs of fever,
X-ray shows dilated bowel tachycardia, generalized
loops in continuous pattern peritonitis.

C Supportive care: Treat infections, Operative Intervention

fluid/electrolyte replacement, limit
opiates, bowel rest, serial abdominal
exams. Consider NGT, may need
supplemental nutrition

D
Prolonged disease despite
conservative care

Order CT abdomen Treat specific findings. May

with contrast need surgical intervention.

Algorithm 51.1

Suggested Reading
Brunicardi FC. Schwartz’s principles of surgery. 10th ed.
New York: McGraw Hill; 2015.
Cameron JL, Cameron AM. Current surgical therapy. 11th
ed. Philadelphia: Elsevier; 2014.
 Management of Gallstone Ileus
Igor G. Elyash
Algorithmic Approach
A. Gallstone ileus classically presents with
symptoms of episodic bowel obstruction.
Usually, this involves nausea, vomiting, dif-
fuse abdominal pain, and constipation.
Patients are often female and are elderly. A
detailed history and physical examination
should be taken, with a focus on any history of
biliary disease and prior episodes of small
bowel obstruction. Following a history and
physical exam, supportive care such as intra-
venous (IV) hydration and nasogastric inser-
tion should be started. Any diffuse peritoneal
signs should prompt emergency surgical
exploration. Blood work should look for
changes in white blood cell count and any
electrolyte abnormalities. Liver function tests
will usually be nonspecific. If patient is hemo-
dynamically stable, proceed with a computed
tomography (CT) of the abdomen and pelvis.
B. CT scan is the test of choice for gallstone
ileus. It will show signs that are suspicious
for the diagnosis such as bowel obstruction or
gallbladder thickening. The most characteris-
tic and pathognomonic finding is Rigler’s
triad. It is characterized by pneumobilia,
I. G. Elyash (*)
Morristown Surgical Associates, Morristown Medical
Center, Morristown, NJ, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_52
52
signs of small bowel obstruction, and pres-
ence of a radiolucent gallstone. If no signs of
gallstone ileus are present, appropriate care is
continued.
C. When signs of gallstone ileus are seen on CT
or if patient is having diffuse peritoneal signs,
surgical exploration after resuscitation is nec-
essary. During laparotomy, the entire bowel
should be inspected as multiple stones in vari-
ous locations are possible. Once the area of
obstruction is localized, a longitudinal enter-
otomy should be made proximal to the area of
obstruction and the stone removed. Any
necrotic bowel should be resected if necessary.
If bowel is viable, the enterotomy should be
closed in two layers in a transverse fashion.
D. Once enterolithotomy is performed, a deci-
sion should be made regarding a cholecystec-
tomy and fistula take down. Patients that have
minimal comorbidities, are hemodynamically
stable, and with limited inflammatory changes
can undergo cholecystectomy and bilioen-
teric fistula closure at the time of initial oper-
ation. All other patients (hemodynamically
unstable, severe comorbidities) should
undergo a cholecystectomy and fistula take-
down electively once medically optimized.
199
200 I. G. Elyash

A
History: Episodes of nausea/vomiting with diffuse
abdominal pain and constipation that are
intermittent in nature.

B
Perform a physical exam. Start IVF and consider NGT
placement. Order labs and CT scan with contrast.

Any signs of
Rigler’s triad on
CT?

Yes No
Appropriate
C Resuscitation followed by laparotomy: Inspect care
entire bowel, identify site of obstruction and
perform longitudinal enterolithotomy to
obstruction. Resect necrotic bowel

D
Is the patient
high risk?

No
Yes

Can perform cholecystectomy and fistula take

Finish operation. Patient can have an elective
down at same time as laparotomy
cholecystectomy if recurrent symptoms and if
medically optimized.

Algorithm 52.1

Suggested Reading
Nuno-Guzman CM, et  al. Gallstone ileus, clinical pre-
sentation, diagnostic and treatment approach. World J
Gastrointest Surg. 2016;8(1):65–76.
Ravikumar R, Williams JG.  The operative manage-
ment of gallstone ileus. Ann R Coll Surg Engl.
2010;92:279–81.
 Management of Short Bowel
Syndrome
Igor G. Elyash
Algorithmic Approach
A. Short bowel syndrome is characterized by
compromised intestinal absorption leading to
symptoms of malabsorption. These include
diarrhea, dehydration, electrolyte abnormali-
ties, and/or malnutrition. Evaluation begins
with a thorough history and physical exami-
nation. History should include prior medical
history with a focus on symptoms of Crohn’s
disease and any prior bowel surgery. Increased
risk of short bowel syndrome occurs with a
shortened small bowel length, previous
colonic surgery, and absence of a functional
ileocecal valve.
B. After a thorough history and physical exam,
the next step in evaluation is to obtain blood
work. Electrolyte abnormalities will need to
be corrected, as with any vitamin deficien-
cies. An albumin level can be helpful in
assessing overall nutrition status. It is also
important to rule out other potential causes of
malabsorption and malnutrition such as pan-
creatitis, celiac disease, and infectious causes.
Stool studies may be helpful. Endoscopy can
be considered to assess the quality of bowel
as well.
I. G. Elyash (*)
Morristown Surgical Associates,
Morristown Medical Center, Morristown, NJ, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_53
53
C. The first step in the management of short
bowel syndrome is supportive. Treat any
underlying disorders, replete fluids and elec-
trolytes, consider antimotility agents, and
provide parenteral nutrition as needed. In
many cases, intestines will undergo adapta-
tion, and bowel absorption will be restored.
When medical therapy fails or patients
develop complications related to total paren-
teral nutrition (TPN) or chronic malabsorp-
tion, surgical options are considered.
D. If medical therapy fails and the patient has
not developed complications, such as sepsis,
organ failure from TPN or malabsorption,
certain surgical options are available. If the
patient has an ostomy, attempts should be
made to restore bowel continuity. Patients can
also undergo surgery to slow bowel transit
such as segmental reversal of small bowel or
interpositioning of colon between small
bowel. If bowels are dilated, patients can
undergo the longitudinal intestinal lengthen-
ing and tailoring (LILT) or serial transverse
enteroplasty procedure (STEP) to increase
intestinal length. Intestinal transplantation
should be considered if a patient develops
severe or life-threatening complications.
201
202 I. G. Elyash

A
History: Symptoms of diarrhea, steatorrhea,
dehydration, malnutrition.

Perform a history and physical: History should look for

previous bowel surgery, surgery for malignancy, history
of Crohn’s, pediatric intestinal disorders.

B
Order Lab work. May consider endoscopy and
additional studies as needed.

C Treat primary condition, fluid/electrolyte

replacement/parenteral nutrition, anti-motility
agents.

Symptoms not improving despite medical

treatment

Major Complications related to intestinal

failure/Long term artificial nutrition?
No Yes

Consider
Consider surgical option such as
Intestinal
LILT, STEP.
Transplantation.

Algorithm 53.1

Suggested Reading
Brunicardi FC. Schwartz’s principles of surgery. 10th ed.
New York: McGraw Hill; 2015.
Cameron JL, Cameron AM. Current surgical therapy. 11th
ed. Philadelphia: Elsevier; 2014.
Iyer KR. Surgical management of short bowel syndrome.
J Parenter Enter Nutr. 2014;38:53–9.
 Part VIII
Large Bowel
 Management of Lower
Gastrointestinal Bleeding 54
Audrey S. Kulaylat and David B. Stewart Jr.

Algorithmic Approach source masquerading as an LGIB (10–15% of

cases) [1]. If either of these is positive, appro-
A. Lower gastrointestinal bleeding (LGIB) can priate interventions to address the source
range from low-volume bleeding episodes of should be pursued.
no hemodynamic consequence to life-­ D. For patients with a self-limited bleeding epi-
threatening hemorrhage. A thorough history sode who respond to resuscitative efforts, an
eliciting the onset, frequency, duration, and early colonoscopy may be performed after
character (hematochezia vs. melena) of bleed- mechanical bowel preparation [3]. In this
ing is important, as is identifying associated instance, colonoscopy can be diagnostic (in
symptoms that help indicate the underlying over 75% of cases), as well as therapeutic [4].
pathology (e.g., weight loss and cancer) [1]. Endoscopic clipping, epinephrine injection,
B. For patients with massive LGIB, early resus- electrocautery, or a combination thereof can
citation with isotonic crystalloid and, if nec- be employed to address the source of bleed-
essary, blood products is critical prior to ing [3].
further diagnostic efforts. Repeat exams E. For patients who are hemodynamically stable
monitoring for the development or recurrence but who have ongoing bleeding, attempts at
of hypovolemic shock are necessary. localization should be made prior to further
Laboratory studies, including serial complete intervention. Depending upon the patient’s
blood counts and coagulation panels, can comorbidities (such as renal failure) and
help guide resuscitative efforts [2]. institutional availability, either CT angiogra-
C. A focused examination should be performed phy (CTA) or nuclear scintigraphy with
to rule out two common causes of GI bleed- 99m
Tc-labeled RBCs can be used. CTA
ing: anoscopy/proctoscopy to evaluate for requires higher rates of bleeding (>0.3  mL/
anorectal causes (5–20% of cases) and naso- min) to localize a source, but this study is able
gastric lavage to evaluate for an upper GI to localize the site of bleeding more effec-
tively than nuclear medicine studies, while
A. S. Kulaylat scintigraphy is able to detect lower rates of
Department of Surgery, Penn State Milton S. Hershey bleeding (>0.05  mL/min), and repeat scans
Medical Center, Hershey, PA, USA can be performed for up to 24 h if initial scans
D. B. Stewart Jr. (*) are negative. Scintigraphy is not precise
Department of Surgery, Banner University Medical enough to allow planning for a segmental
Center – Tucson, Tucson, AZ, USA ­colectomy [1].
e-mail: dbstewart@surgery.arizona.edu

© Springer Nature Switzerland AG 2019 205

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_54
206 A. S. Kulaylat and D. B. Stewart Jr.

F. For patients with negative CTA or repeatedly
negative scintigraphy, supportive care should
be continued while continually reassessing
the patient for signs of rebleeding. For
patients with a positive CTA or scintigraphy,
super selective embolization with mesenteric
angiography may successfully address the
bleed, particularly for patients with an active
“blush” on scintigraphy or a short time inter-
val between scintigraphy/CTA and mesen-
teric angiography, which predicts the success
of this intervention [5, 6].
G. For patients who initially present with hemo-
dynamic instability that is refractory to resus-
citative efforts, and for whom other sources
(upper GI and anorectal) have been ruled out,
emergent exploratory laparotomy should be
performed [1]. In the absence of an obvious
small bowel source during exploration, such
as a Meckel’s diverticulum, a total abdominal
colectomy with end ileostomy is the proce-
dure of choice, as this surgery has the lowest
incidence of postoperative bleeding. For
patients who rebleed after multiple therapeu-
tic attempts but who on the basis of angiogra-
phy have had the source of their bleeding
successfully localized, a segmental colec-
tomy can be performed.

History and Physical Examination:

A Elicit onset, duration, frequency, and character of bleeding
Assess for signs of hemodynamic instability
Symptoms for 36 hours

B Resuscitation with IV fluids +/– blood products, obtain laboratory parameters

C Rule out upper GI source (nasogastric lavage) or anorectal source (anoscopy/proctoscopy)

Response to
resuscitation?

Not responding to
Self-limited bleeding, resuscitation,
hemodynamically stable: G
D Mechanical bowel prep
hemodynamically
Ongoing bleeding, unstable: exploratory
followed by colonoscopy laparotomy
hemodynamically stable:
CTA or nuclear
scintigraphy

Positive
scan?

Negative: Continued Positive: Consider

supportive care, F intervention with
assess for rebleeding mesenteric angiography

Algorithm 54.1
54  Management of Lower Gastrointestinal Bleeding 207

References acute lower intestinal bleeding. Clin Gastroenterol

Hepatol Off Clin Pract J Am Gastroenterol Assoc.
2010;8(4):333–43; quiz e344.
1. Steele SR, Hull T, Read TE, Saclarides TJ, Senagore
5. Koh FH, Soong J, Lieske B, Cheong WK, Tan
AJ, Whitelow CB, editors. The ASCRS textbook of
KK.  Does the timing of an invasive mesenteric
colon and rectal surgery. 3rd ed. Arlington Heights:
angiography following a positive CT mesenteric
Springer; 2016.
angiography make a difference? Int J Color Dis.
2. Strate LL, Gralnek IM.  Management of patients
2015;30(1):57–61.
with acute lower gastrointestinal bleeding. Am J
6. Ng DA, Opelka FG, Beck DE, et al. Predictive value
Gastroenterol. 2016;111(4):459–74.
of technetium Tc 99m-labeled red blood cell scin-
3. Pasha SF, Shergill A, Acosta RD, et  al. The role of
tigraphy for positive angiogram in massive lower
endoscopy in the patient with lower GI bleeding.
gastrointestinal hemorrhage. Dis Colon Rectum.
Gastrointest Endosc. 2014;79(6):875–85.
1997;40(4):471–7.
4. Strate LL, Naumann CR.  The role of colonoscopy
and radiological procedures in the management of
 Management of Diverticulitis
Audrey S. Kulaylat and David B. Stewart Jr.
Algorithmic Approach
A. Abdominal pain, usually centered in the
D.
lower abdomen, is a frequent symptom.
Pneumaturia, fecaluria, or the passage of fla-
tus or stool per vagina in patients who have
undergone a hysterectomy is indicative of
colovesical and colovaginal fistulas, respec-
tively [1]. On physical examination, patients
should be evaluated for lower abdominal ten-
derness and, in the acute setting, for signs of
peritonitis.
B. Especially for acute diverticulitis, laboratory
evaluation should include a CBC, and CT
scanning is recommended to evaluate for
pericolic fat stranding, abscess formation,
and pneumoperitoneum [2].
C. Uncomplicated disease represents the most
common manifestation of diverticulitis and
can typically be managed with antibiotics
with Gram-negative and anaerobic coverage.
In hemodynamically stable, immunocompe-
tent and socially reliable patients who can
tolerate a diet, outpatient treatment with oral
antibiotics can be pursued; for others, admis-
A. S. Kulaylat
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
D. B. Stewart Jr. (*)
Department of Surgery, Banner University Medical
Center – Tucson, Tucson, AZ, USA
e-mail: dbstewart@surgery.arizona.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_55
55
sion for intravenous antibiotics and bowel
rest is indicated [2].
Uncomplicated disease is recurrent in
13–47% of patients [3]. In general, recurrent
episodes of disease tend to be of similar
severity to prior episodes. Therefore, the
decision to offer surgery to these patients
should be tailored to a patient’s number of
episodes, their history of dietary modification
to prevent recurrent disease, and their opera-
tive risk. Prior to elective resection, evalua-
tion of the large intestine with colonoscopy is
advised no sooner than 6 weeks following an
acute episode, if no recent evaluation has
been performed, in order to ensure the
absence of alternative diagnoses such as can-
cer or Crohn’s disease [1].
E. Complicated disease, including the formation
of an abscess (10–25%), a fistula (2%, most
commonly colovesicular), or a free perfora-
tion resulting in diffuse peritonitis (1%),
occurs in a minority of patients (~1%) but is
associated with a high incidence of morbidity
and even mortality [1]. For disease compli-
cated by an abscess 3 cm or larger, percutane-
ous drainage with antibiotic therapy is
recommended [2].
F. While prior recommendations to provide an
elective resection after the first episode of
complicated disease have been questioned,
certain disease-related complications such as
fistulas and strictures should prompt surgical
209
210
intervention. Elective resection should
include removing the entire sigmoid and rec-
tosigmoid colon, creating a true colorectal
anastomosis as opposed to a colocolostomy.
Failure to remove the rectosigmoid colon is
associated with a higher incidence of anasto-
motic leaks and recurrent diverticulitis. If the
surgeon is well versed in advanced laparo-
scopic techniques, then a minimally invasive
approach is preferable [4].
G. For patients with peritonitis due to free perfo-
ration, urgent sigmoid colectomy is recom-
mended. In many respects, a Hartmann’s
procedure (sigmoidectomy with the construc-
A. S. Kulaylat and D. B. Stewart Jr.
tion of a stapled rectosigmoid stump and an
end descending colostomy) is the safest sur-
gical option in the short term due to the
absence of an anastomosis. However, consid-
ering the historically high complication rates
associated with a subsequent colostomy clo-
sure, the option of an on-table colonic lavage
with the construction of a colorectal anasto-
mosis, with a possible diverting loop ileos-
tomy, can be considered based on the patient’s
physiologic status as well as the degree of
contamination [5]. Construction of an anasto-
mosis is generally contraindicated in the set-
ting of widespread feculent contamination.
55  Management of Diverticulitis 211

History and physical examination:

LLQ pain, fevers, altered bowel habits, abdominal distension
A LLQ tenderness +/- peritoneal signs
Symptoms for 36 hours

Obtain laboratory studies and CT scan

B

Generalized
peritonitis on exam
or free
perforation on CT?

No Yes: Urgent
surgical G
intervention

Complicated
disease?

Yes: Initial
No: Medical medical
C E
management management

Colonoscopy in 6-8 weeks Colonoscopy in six to eight weeks (if

(if no recent endoscopic exam), and no recent endoscopic exam), and F
D
then consider dietary modification then definitive surgical resection
versus elective resection

Algorithm 55.1
212 A. S. Kulaylat and D. B. Stewart Jr.

References 3. Buchs NC, Mortensen NJ, Ris F, Morel P, Gervaz

P. Natural history of uncomplicated sigmoid divertic-
ulitis. World J Gastrointest Surg. 2015;7(11):313–8.
1. Steele SR, Hull T, Read TE, Saclarides TJ, Senagore
4. Bachmann K, Krause G, Rawnaq T, et  al. Impact of
AJ, Whitelow CB, editors. The ASCRS textbook of
early or delayed elective resection in complicated diver-
colon and rectal surgery. 3rd ed. Arlington Heights:
ticulitis. World J Gastroenterol. 2011;17(48):5274–9.
Springer; 2016.
5. Salem L, Flum DR.  Primary anastomosis or
2. Feingold D, Steele SR, Lee S, et al. Practice param-
Hartmann's procedure for patients with diverticular
eters for the treatment of sigmoid diverticulitis. Dis
peritonitis? A systematic review. Dis Colon Rectum.
Colon Rectum. 2014;57(3):284–94.
2004;47(11):1953–64.
 Management of Large Bowel
Obstruction
Audrey S. Kulaylat and David B. Stewart Jr.
Algorithmic Approach
A. Since large bowel obstructions (LBO) can
result from a variety of both benign (e.g.,
diverticular disease, ischemic colitis) and
malignant (e.g., colorectal cancer, extrinsic
compression from ovarian cancer) diseases, a
detailed history is essential for determining
the diagnosis. Important factors to consider
include the onset and duration of obstructive
symptoms, as well as any associated symp-
toms. Patients will report complaints of
abdominal pain and distention, as well as pro-
gressively worsening obstipation.
Competency of the ileocecal valve can impact
patient presentation: patients with competent
valves are at risk for a closed-loop obstruc-
tion and are less likely to have nausea/vomit-
ing, which is commonly seen in large bowel
obstructions [1].
B. A thorough physical exam evaluating for
signs of peritonitis and systemic toxicity
should be performed, in additional to obtain-
ing laboratory studies to assess for electrolyte
derangements or signs of bowel ischemia.
A. S. Kulaylat
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
D. B. Stewart Jr. (*)
Department of Surgery, Banner University Medical
Center – Tucson, Tucson, AZ, USA
e-mail: dbstewart@surgery.arizona.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_56
56
Initial radiographic evaluation with an acute
abdominal series can be obtained, in order to
(1) evaluate for signs of perforation, (2)
assess the degree of colonic distention, and
(3) potentially identify an etiology, such as a
volvulus [1].
C. In patients with systemic toxicity or signs of
free perforation, intravenous broad-spectrum
antibiotics and emergent exploratory laparot-
omy are indicated. If unresectable disease
(e.g., carcinomatosis) or disease that requires
initial medical treatment (e.g., neoadjuvant
therapy for obstructing rectal cancer) is
encountered, then proximal diversion is an
appropriate procedure. If resectable disease is
found, resection of the diseased intestine is
indicated, along with careful inspection of the
remaining large intestine for either ischemia
or synchronous lesions.
D. In hemodynamically stable patients with a
clear diagnosis, such as colonic volvulus (10–
15% of LBO), acute colonic pseudoobstruc-
tion, or foreign body impaction, further
management should proceed according to the
underlying etiology of bowel obstruction
[1–3].
E. In hemodynamically stable patients without
signs of perforation, but for whom the diag-
nosis remains unclear, further imaging should
be obtained. Either contrast enema (particu-
larly for left-sided lesions) or CT scans can
be helpful in determining the etiology of the
213
214 A. S. Kulaylat and D. B. Stewart Jr.

obstruction. Colonoscopy, preferably with s­urgical resection, with the possibility of

CO2 insufflation, can also be used to obtain a
tissue diagnosis in patients with suspected
intraluminal disease, such as colorectal can-
cer (~50% of LBO) [1].
F. Further management of LBO in the none-
mergent setting is dependent upon etiology.
In general, the two main options are surgical
(either resection or diversion) or endoscopic
stenting, the latter of which can be used as a
bridge to surgery or as definitive palliation.
Stents offer lower initial morbidity than
converting a more urgent surgery to an elec-
tive procedure with a lower likelihood of
requiring a stoma [4]. However, stents are
often less effective at relieving the initial
obstruction (53% vs. 99%) and have high
rates of reobstruction [5]. Since stents are
safest when used as a bridge to elective sur-
gery within several weeks, careful consider-
ation of the goals of care is necessary in
choosing how to relieve the patient’s
­obstructive symptoms.

Detailed History:
A Abdominal pain and distention, obstipation, +/–nausea/vomiting

Thorough physical examination

B Obtain laboratory studies and abdominal plain films

Peritonitis?
Clear
diagnosis?

Hemodynamically
Hemodynamically
unstable or signs of
stable, no clear E
C Hemodynamically diagnosis
free perforation:
stable, clear
Exploratory surgery D diagnosis (e.g.
colonic volvulus,
foreign body, etc) Abdominal/pelvis CT
or contrast enema

Resectable
Definitive
disease?
management Consider definitive
depending upon
surgical resection or F
etiology
stenting, depending
upon etiology

Yes: Resect
with proximal No: Proximal
diversion diversion

Algorithm 56.1
56  Management of Large Bowel Obstruction 215

References 3. Chudzinski AP, Thompson EV, Ayscue JM.  Acute

colonic pseudoobstruction. Clin Colon Rectal Surg.
2015;28(2):112–7.
1. Steele SR, Hull T, Read TE, Saclarides TJ, Senagore
4. van Hooft JE, van Halsema EE, Vanbiervliet G,
AJ, Whitelow CB, editors. The ASCRS textbook of
et  al. Self-expandable metal stents for obstructing
colon and rectal surgery. 3rd ed. Arlington Heights:
colonic and extracolonic cancer: European Society of
Springer; 2016.
Gastrointestinal Endoscopy (ESGE) clinical guide-
2. Vogel JD, Feingold DL, Stewart DB, et  al. Clinical
line. Endoscopy. 2014;46(11):990–1053.
practice guidelines for colon volvulus and acute
5. Sagar J.  Colorectal stents for the management of
colonic pseudo-obstruction. Dis Colon Rectum.
malignant colonic obstructions. Cochrane Database
2016;59(7):589–600.
Syst Rev. 2011(11):CD007378.
 Management of Colonic Pseudo-­
Obstruction 57
Audrey S. Kulaylat and David B. Stewart Jr.

Algorithmic Approach dilatation of the cecum (>12 cm), endoscopic

A. The primary goals in the evaluation of
patients with suspected colonic pseudo-­ D. For patients without the above indications,
obstruction (CPO) are (1) to exclude other
etiologies of obstruction, particularly
mechanical etiologies, and (2) to determine if
signs of perforation or ischemia are present.
Patients will report absent or decreased bowel
function, with increasing abdominal disten-
tion and discomfort [1]. Depending on the
competency of the ileocecal valve, nausea
and vomiting may not be present in the acute
setting. Physical examination should include
a digital anorectal examination to ensure the
absence of an obstructing anorectal mass.
B. Laboratory studies are essential to identify
contributory electrolyte abnormalities.
Although colonic dilation can be seen on E. For patients who do not respond to these con-
plain films, either CT or contrast enemas
should be used to rule out a mechanical
obstruction in these patients [2].
C. If a patient presents with or develops signs of • Prior to administration, patients should be
perforation or ischemia, surgical intervention
is mandated [3]. In the scenario of significant
A. S. Kulaylat
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
D. B. Stewart Jr. (*)
Department of Surgery, Banner University Medical
Center – Tucson, Tucson, AZ, USA
e-mail: dbstewart@surgery.arizona.edu
decompression or surgical intervention is
required.
conservative interventions for 48–72 h are the
recommended first treatment and result in
resolution in 70–90% of cases [3, 4].
• Bowel rest, IV fluid resuscitation, electro-
lyte correction, and discontinuation of
instigating agents (e.g., opioids) are main-
stays of treatment.
• Serial abdominal exams and plain films to
assess for worsening colonic dilation and/
or signs of perforation are indicated.
• Nasogastric and/or rectal tube decompres-
sion can be considered depending on the
patient’s symptoms and radiographic
findings.
servative measures, intravenous neostigmine
is the next therapeutic option for patients
without contraindications to its use [5].
in a monitored setting with reversal agents
(atropine and glycopyrrolate) available in
case hypotension or bradycardia resulting
in hemodynamic instability, or severe
abdominal cramps, develops.
• A dose of 2–2.5 mg IV administered over
2–5 min is effective in ~90% of cases [1].
• If ineffective or bowel dilation recurs (17–
38% of cases) [6], a provider may ­administer

© Springer Nature Switzerland AG 2019 217

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_57
218 A. S. Kulaylat and D. B. Stewart Jr.

repeat doses after waiting for at least 80 min
for some of the drugs to be eliminated.
F. Endoscopic decompression can be performed
in patients for whom the above measures are
ineffective and results in sustained resolution
in 70–90% of cases [3].
• No bowel preps or laxatives should be given
prior to endoscopy, and sedation with ben-
zodiazepines (not opioids) is preferred [6].
• CO2 insufflation should be used when
available, given its faster resorption.
• Decompression to the hepatic flexure with
the placement of a colonic tube is the goal
of the intervention, which can be repeated
multiple times if dilation recurs.
G. In cases that are refractory to the above
measures, surgical intervention may be
required, which can range from an ileoco-
lectomy to a subtotal colectomy, depending
on the distribution of nonviable colon. In
this setting, an ileostomy should be
constructed.

History and Physical Examination (Including a Digital Anorectal Exam):

A Increasing abdominal distention and pain, with absence of bowel movements
Distended abdomen +/– peritonitis

Obtain laboratory studies and plain films, +/– CT scan or

B contrast enema: rule out mechanical obstruction

Signs of
ischemia or perforation?

Yes: Surgical
No: Bowel rest, IVF, electrolyte correction, C
D discontinue narcotics, +/– NG or rectal tube intervention

E Trial of neostigmine

F Trial of endoscopic decompression

G Surgical intervention

Algorithm 57.1
57  Management of Colonic Pseudo-Obstruction 219

References colonic pseudo-obstruction. Dis Colon Rectum.

2016;59(7):589–600.
4. Trevisani GT, Hyman NH, Church JM. Neostigmine:
1. Chudzinski AP, Thompson EV, Ayscue JM.  Acute
safe and effective treatment for acute colonic pseudo-­
colonic pseudoobstruction. Clin Colon Rectal Surg.
obstruction. Dis Colon Rectum. 2000;43(5):599–603.
2015;28(2):112–7.
5. Steele SR, Hull T, Read TE, Saclarides TJ, Senagore
2. Harrison ME, Anderson MA, Appalaneni V, et al. The
AJ, Whitelow CB, editors. The ASCRS textbook of
role of endoscopy in the management of patients with
colon and rectal surgery. 3rd ed. Arlington Heights:
known and suspected colonic obstruction and pseudo-­
Springer; 2016.
obstruction. Gastrointest Endosc. 2010;71(4):669–79.
6. Jain A, Vargas HD. Advances and challenges in the man-
3. Vogel JD, Feingold DL, Stewart DB, et  al. Clinical
agement of acute colonic pseudo-­obstruction (ogilvie
practice guidelines for colon volvulus and acute
syndrome). Clin Colon Rectal Surg. 2012;25(1):37–45.
 Management of Colonic Volvulus
Audrey S. Kulaylat and David B. Stewart Jr.
Algorithmic Approach
A. In suspected colonic volvulus, a full history
and physical exam should be expeditiously
performed. Unlike malignant obstruction,
symptoms from a volvulus evolve more
acutely. Patients may report abdominal pain,
increasing abdominal distention, and a lack
of bowel function; in the case of sigmoid vol-
vulus, a history of being institutionalized,
either due to mental health issues or due to
senescence, is a frequent historical element.
While chronic constipation is a common fea-
ture of sigmoid volvulus, cecal volvulus can
be associated with prior surgeries which
mobilized the cecum resulting in a pathologic
degree of mobility as a risk factor for volvu-
lus. On physical examination, a distended and
tympanitic abdomen will be encountered,
with or without tenderness to palpation [1].
B. Laboratory studies, including a CBC, electro-
lytes, and a renal function panel, should be
obtained.
C. If plain films are obtained, they may be diag-
nostic for a sigmoid volvulus (50–70% of
A. S. Kulaylat
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
D. B. Stewart Jr. (*)
Department of Surgery, Banner University Medical
Center – Tucson, Tucson, AZ, USA
e-mail: dbstewart@surgery.arizona.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_58
58
cases) by revealing a “bent inner tube” or
“omega loop” pointing toward the right
upper quadrant. In the case of a cecal vol-
vulus, a “coffee bean” pointing toward the
left upper quadrant is sometimes evident
(20%) [2].
D. CT scans provide more details, and in most
cases of volvulus they demonstrate a mesen-
teric swirl, as well as distinguish the laterality
of the volvulus and assess for intestinal perfo-
ration. Water-soluble contrast enemas may
also be used to establish the diagnosis of a
volvulus and to distinguish between sigmoid
and cecal volvuluses, though this study is
often difficult to obtain during off-hours, and
it can delay intervention [2].
E. For sigmoid volvulus, if peritonitis or perfo-
ration is present, an emergent exploratory
laparotomy with resection should be per-
formed. Depending upon patient status and
degree of peritoneal contamination, a
Hartmann’s procedure (sigmoidectomy with
the construction of an end descending colos-
tomy and a stapled rectosigmoid stump) may
be indicated rather than a sigmoidectomy
with the construction of a colorectal anasto-
mosis [3].
F. For sigmoid volvulus (50–75% of cases), in
the absence of peritonitis or radiographic evi-
dence of perforation, detorsion with flexible
endoscopy is the first-line treatment for sig-
moid volvulus, and this intervention is
221
222
s­ uccessful in 60–95% of cases. If nonviable
colon is encountered during this procedure,
then immediate surgical resection is indi-
cated, usually in the form of a Hartmann’s
procedure [4].
G. In the setting of successful endoscopic
decompression of a volvulus, elective sig-
moid resection prior to discharge is recom-
mended, given high recurrence rates
(20–90%) and the significant incidence of
complications associated with recurrent epi-
sodes. A full evaluation of the colon with
colonoscopy should be performed prior to
resection. Unless contraindicated by the
patient’s overall status, primary anastomosis
should be attempted. Resection of all redun-
A. S. Kulaylat and D. B. Stewart Jr.
dant colon should be performed to reduce the
risk of recurrence [1].
H. Because of low success rates, attempts at
endoscopic decompression should be avoided
in the setting of cecal volvulus, and instead
immediate surgical resection should be per-
formed. If no significant contamination or
gangrene is present, and if the patient is sta-
ble, primary anastomosis can be performed.
Otherwise, resection with ileostomy and
mucus fistula, or the construction of an anas-
tomosis with a diverting loop ileostomy,
should be considered. Detorsion alone, ceco-
pexy or cecostomy tube insertion should not
be performed due to high recurrence and
mortality rates [5].
58  Management of Colonic Volvulus 223

History and physical examination:

A Abdominal pain, increasing distention, lack of bowel movement
Distended, tympanitic abdomen +/– peritonitis
Symptoms for 36 hours

B Obtain vital signs, laboratory studies, and plain films

Does plain film

C distinguish sigmoid from cecal
volvulus?

D No: obtain CT
SIGMOID or contrast CECAL
enema

Peritoneal Emergent right

H colectomy
signs?
F
No: endoscopic
intervention

Yes: immediate
E surgical Elective resection
intervention G prior to discharge

Algorithm 58.1

3. Akcan A, Akyildiz H, Artis T, Yilmaz N, Sozuer

References
1. Vogel JD, Feingold DL, Stewart DB, et al. Clinical practice
guidelines for colon volvulus and acute colonic pseudo-
obstruction. Dis Colon Rectum. 2016;59(7):589–600.
2. Steele SR, Hull T, Read TE, Saclarides TJ, Senagore
AJ, Whitelow CB, editors. The ASCRS textbook of
Colon and Rectal surgery. 3rd ed. Arlington Heights:
Springer; 2016.
E.  Feasibility of single-stage resection and primary
anastomosis in patients with acute noncomplicated
sigmoid volvulus. Am J Surg. 2007;193(4):421–6.
4. Atamanalp SS.  Treatment of sigmoid volvulus: a
single-­center experience of 952 patients over 46.5
years. Tech Coloproctol. 2013;17(5):561–9.
5. Kapadia MR. Volvulus of the small bowel and Colon.
Clin Colon Rectal Surg. 2017;30(1):40–5.
 Appendicitis
Kristen T. Crowell and Evangelos Messaris
Algorithmic Approach
A. Acute appendicitis is suspected in patients
with acute abdominal pain that begins at the
umbilicus and is associated with anorexia,
nausea, or vomiting. The pain migrates to the
right lower quadrant (RLQ) as the inflamma-
tory process progresses to involve the overly-
ing peritoneum. Duration of pain in acute
uncomplicated appendicitis is less than 48 h,
whereas there is increased risk of perforated
or complicated appendicitis when pain is
present for >48–72 h [1]. Physical exam is a
reliable indicator of appendicitis when there
is rebound tenderness in the RLQ; other exam
signs include Rovsing sign and RLQ pain
when the LLQ is palpated. Diffuse peritonitis
should be evaluated for perforated appendici-
tis or other causes of an acute abdomen.
B. In addition to the exam, laboratories should
be obtained focusing on the white blood cell
K. T. Crowell
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
E. Messaris (*)
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Division of Colon and Rectal Surgery, Beth Israel
Medical Center, Harvard Medical Center,
Boston, MA, USA
e-mail: emessaris@pennstatehealth.psu.edu,
emessari@bidmc.harvard.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_59
59
count (WBC). An elevated WBC >10 sup-
ports acute appendicitis; however, when it is
very high (>15), this suggests complicated,
perforated, or gangrenous appendicitis. Vital
signs should be obtained, and tachycardia
could represent dehydration that would
require rehydration in the ED.
C. Patients with a history consistent with the
above, a mild elevation of the WBC, fever,
and rebound tenderness in the RLQ, are
highly suspicious for acute uncomplicated
appendicitis. Male patients do not require any
imaging, and a laparoscopic appendectomy
should be performed [2]. Imaging, CT scan,
or ultrasound should be considered in female
patients to rule out other sources of RLQ or
pelvic pain, including pelvic inflammatory
disease, tuboovarian abscess, ovarian cyst or
torsion, or other gynecologic causes.
D. In patients with a suspicious history, but the
signs are not as clear, such as the WBC is less
than 15, they do not have fever, and the exam
is only mildly concerning for rebound in the
RLQ, imaging should be performed to delin-
eate the diagnosis [2]. A CT scan should be
obtained on adults as it can be cost saving
compared to ultrasound, but ultrasound or
MRI should be obtained in the pediatric
population.
E. Imaging that shows an inflamed appendix
(>10 mm), wall thickening, and periappendi-
ceal fluid with no sign of perforation or
225
226
g­angrene is suggestive of acute uncompli-
cated appendicitis [3]. If imaging suggests
acute appendicitis, then the patient should
undergo laparoscopic appendectomy as lapa-
roscopy decreases length of stay and postop-
erative pain. Complications of appendectomy
are surgical site infection, small bowel
obstruction, and abscess [4].
F. If the imaging shows a normal appendix or
the appendix is not visualized, then the patient
can either be discharged to home or observed
based upon the clinical suspicion [2].
G. Imaging demonstrating a contained fluid col-
lection indicating an abscess raises suspicion
for perforation. A contained perforation with
an abscess may be treated with a nonopera-
tive modality. Intravenous antibiotics, bowel
rest, and CT-guided percutaneous drainage
are the hallmarks of nonoperative treatment.
K. T. Crowell and E. Messaris
Nonoperative treatment is associated with a
lower morbidity profile than immediate
appendectomy. An interval appendectomy
6–8 weeks later should be considered for pre-
vention of recurrence (risk >10%) and identi-
fication of cancer especially in adults or
Crohn’s disease. Patients over the age of 40
should undergo a screening colonoscopy
prior to an interval appendectomy [5].
H. Immediate surgery for complicated appendi-
citis is indicated when free perforation is
found on imaging, surgical exploration is
warranted, and the use of laparoscopy is
appropriate depending on the comfort of the
surgeon. Complicated appendicitis carries the
same postoperative morbidity, although with
increased risk of wound infection, 20%, and
potential for ileocecal resection or right hemi-
colectomy [6].
59 Appendicitis 227

History and Physical

A Acute onset, Migratory abdominal pain: periumbilical to RLQ,
Anorexia, Fever, Tenderness in RLQ

B Obtain vital signs, laboratory studies

High suspicion Lowersuspicion

C WBC > 15, Temp > 38.5°C, WBC < 14.9, afebrile, light
Rebound/Guarding in RLQ tenderness in RLQ

Laparoscopic Imaging:
appendectomy Ultrasound vs CT scan

Does imaging
Laparoscopic Yes suggest acute No Discharge vs.
E F
appendectomy uncomplicated observe
appendicitis?

CT Scan: Fluid collection in RLQ signifying a contained abscess

Start antibiotics, NPO, IVF, CT-guided drainage

Fever, tenderness, leukocytosis Sepsis, persistent fever, increasing

improve leukocytosis

Immediate H
G • Discharge home on antibiotics. Appendectomy
• Interval appendectomy is
recommended, preceded by
colonoscopy if >50

Algorithm 59.1
228 K. T. Crowell and E. Messaris

References appendix on treatment of patients and use of hospital

resources. N Engl J Med. 1998;338(3):141–6.
4. Long KH, Bannon MP, Zietlow SP, Helgeson ER,
1. Atema JJ, van Rossem CC, Leeuwenburgh MM,
Harmsen WS, Smith CD, et al. A prospective random-
Stoker J, Boermeester MA. Scoring system to distin-
ized comparison of laparoscopic appendectomy with
guish uncomplicated from complicated acute appen-
open appendectomy: clinical and economic analyses.
dicitis. Br J Surg. 2015;102(8):979–90.
Surgery. 2001;129(4):390–400.
2. Scott AJ, Mason SE, Arunakirinathan M, Reissis
5. Andersson RE, Petzold MG. Nonsurgical treatment of
Y, Kinross JM, Smith JJ.  Risk stratification by the
appendiceal abscess or phlegmon: a systematic review
appendicitis inflammatory response score to guide
and meta-analysis. Ann Surg. 2007;246(5):741–8.
decision-making in patients with suspected appendi-
6. Mentula P, Sammalkorpi H, Leppaniemi
citis. Br J Surg. 2015;102(5):563–72.
A.  Laparoscopic surgery or conservative treatment
3. Rao PM, Rhea JT, Novelline RA, Mostafavi AA,
for appendiceal abscess in adults? A randomized con-
McCabe CJ.  Effect of computed tomography of the
trolled trial. Ann Surg. 2015;262(2):237–42.
 Ulcerative Colitis
Kristen T. Crowell and Evangelos Messaris
Algorithmic Approach
A. Patients with suspected ulcerative colitis
(UC) have a history of abdominal pain and
bloody diarrhea, rectal urgency, or tenesmus.
There is a bimodal presentation in adolescent
and middle-age men and women, more com-
monly in white and black individuals [1].
B. In the evaluation of the patient with UC, mul-
tiple serum markers should be obtained,
including CBC, electrolytes, renal function,
albumin, ESR/CRP, and LFTs to evaluate leu-
kocytosis, anemia, electrolyte abnormality
related to diarrhea, nutritional status, and
inflammatory markers. Stool cultures are
obtained to evaluate for secondary infection,
especially cytomegalovirus (CMV) and
Clostridium difficile [2].
C. Based upon exam, vitals, and labs, patients
should be categorized according to signs of
systemic toxicity. Toxicity signs include
K. T. Crowell
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
E. Messaris (*)
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Division of Colon and Rectal Surgery, Beth Israel
Medical Center, Harvard Medical Center,
Boston, MA, USA
e-mail: emessaris@pennstatehealth.psu.edu,
emessari@bidmc.harvard.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_60
60
fever, tachycardia, hypotension, abdominal
tenderness, or end organ failure and should
warrant an inpatient admission with support-
ive care and a CT scan to evaluate the degree
of colonic inflammation and colonic dilata-
tion and the presence of perforation.
D. If CT scan shows colonic inflammation cor-
relating with UC with no additional compli-
cations, a flexible sigmoidoscopy can be
performed to establish the diagnosis.
Flexible sigmoidoscopy is safe in acute
colonic inflammation, and biopsies help
determine the extent of inflammation and
the presence of CMV infection. IV steroids
are started immediately, and if there is no
improvement in 3  days, then IV cyclospo-
rine or infliximab should be initiated [2].
E. Patients who do not improve in 3–5  days
after rescue therapy or worsen clinically
(fever, leukocytosis, megacolon >6  cm)
likely will not respond to medical therapy,
and total abdominal colectomy with end ile-
ostomy is indicated. Ileal pouch-anal anasto-
mosis (IPAA) is the recommended operation
for UC patients, either in a one-, two-, or
three-stage procedure depending on the
severity of ­illness [3].
F. Patients who improve with IV steroids and
cyclosporine or infliximab can be fed orally,
can be transitioned to PO medications, and
should continue on maintenance cyclosporine
or infliximab. Of the patients with acute
229
230
severe UC, around 86% do not require sur-
gery for UC in the following 1 year after dis-
charge [4].
G. Patients with acute severe colitis with signs of
fulminant colitis including perforation or
colonic ischemia should undergo emergent
colectomy. Unstable patients should undergo
subtotal colectomy with ileostomy, and after
the patient is stable plans to undergo IPAA
should be made [3].
H. Stable patients should undergo elective
colonoscopy with biopsy, as it is the diag-
nostic study of choice. Endoscopic features
include vascular congestion, loss of vascu-
lar pattern, erythema, mucosal friability,
and ulceration which occur in a continuous
manner from the rectum proximally in the
colon. The terminal ileum is only involved
in backwash ileitis. “Skip” lesions are only
K. T. Crowell and E. Messaris
seen in Crohn’s disease (CD), and if found
then UC should be ruled out. Biopsies are
obtained to verify histology, e.g., crypt dis-
tortion, decreased crypt density, and trans-
mucosal inflammation. In patients with
severe colitis, flexible sigmoidoscopy is
safer and preferred over colonoscopy [5].
Medical management depends on the sever-
ity of illness. 5-ASA or mesalamine for
mild disease, induction therapy can include
steroids and/or thiopurines. For more
severe diseases, biologic therapy is indi-
cated including anti-TNF agents or vedoli-
zumab. Patients should be monitored for
response to medical therapy and indica-
tions for colectomy: medically refractory
disease, concern for carcinoma, perfora-
tion, toxic megacolon, and uncontrolled
colonic hemorrhage [2].
60  Ulcerative Colitis 231

History and Physical Exam:

A
Chronic abdominal pain, bloody diarrhea, tenesmus

Vitals
B CBC, CMP, stool cultures, C diff assay

Systemic Yes
C CT scan of
toxicity? abdomen/pelvis

D G

No
Colitis, no perforation Perforation

H Colonoscopy with
biopsy
Flex sigmoidoscopy Emergent total
confirms UC abdominal
colectomy, end
Medical management: ileostomy
5-ASA/mesalamine
Steroids
IV steroids and rescue
Thiopurine
infliximab or CSA
Biologic therapy
F

Clinical Discharge home

Yes on steroids and
improvement
? continue TNF
antagonist tx

No

Emergent total
E
abdominal
colectomy, end
ileostomy

Algorithm 60.1
232 K. T. Crowell and E. Messaris

References proctocolectomy for ulcerative colitis: preoperative

status and long-term results. Inflamm Bowel Dis.
2007;13(10):1228–35.
1. Rao SS, Holdsworth CD, Read NW.  Symptoms and
4. Aratari A, Papi C, Clemente V, Moretti A, Luchetti
stool patterns in patients with ulcerative colitis. Gut.
R, Koch M, et  al. Colectomy rate in acute severe
1988;29(3):342–5.
ulcerative colitis in the infliximab era. Dig Liver Dis.
2. Kornbluth A, Sachar DB, Practice Parameters
2008;40(10):821–6.
Committee of the American College of Gastro­
5. Dignass A, Eliakim R, Magro F, Maaser C, Chowers
enterology. Ulcerative colitis practice guidelines
Y, Geboes K, et al. Second European evidence-based
in adults: American College of Gastroenterology,
consensus on the diagnosis and management of ulcer-
Practice Parameters Committee. Am J Gastroenterol.
ative colitis part 1: definitions and diagnosis. J Crohns
2010;105(3):501–23; quiz 524.
Colitis. 2012;6(10):965–90.
3. Tariverdian M, Leowardi C, Hinz U, Welsch T,
Schmidt J, Kienle P.  Quality of life after restorative
 Crohn’s Colitis
Maria Michailidou and Evangelos Messaris
Algorithmic Approach
A. Clinical manifestations vary based on the
behavior of the disease (nonstricturing and
nonpenetrating, stricturing or penetrating,
associated perianal disease) [1]. In general,
patients present with crampy abdominal pain,
bloody diarrhea, fevers, weight loss, or
obstructive symptoms. Extraintestinal mani-
festations include pyoderma gangrenosum,
erythema nodosum apththous stomatitis, pri-
mary sclerosing cholangitis, and peripheral
arthritis. Belonging to the Ashkenazi Jew
population, living in urban areas, and positive
family history of inflammatory bowel disease
(IBD) are all risk factors for developing the
disease. The current theory of pathogenesis
suggests that an environmental trigger in a
predisposed individual with an altered host
defense leads to mucosal inflammation and
the development of IBD.  Tobacco smoking
M. Michailidou
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
E. Messaris (*)
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Division of Colon and Rectal Surgery, Beth Israel
Medical Center, Harvard Medical Center,
Boston, MA, USA
e-mail: emessaris@pennstatehealth.psu.edu,
emessari@bidmc.harvard.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_61
61
has been associated with increased risk of
developing Crohn’s disease, as well as
increased severity, need for surgical interven-
tion, and recurrence of the disease after sur-
gery [2].
B. B. Diagnosis of Crohn’s colitis is based on a
combination of clinical, endoscopic, and
pathologic findings as well as laboratory
markers. Endoscopic features of Crohn’s
colitis include segmental inflammation with
skip lesions, apthoid ulcers, cobblestone
appearance of mucosa, and presence of fistu-
las or strictures. In about 50% of patients, the
rectum is spared. Microscopically they pres-
ent with focal transmural chronic inflamma-
tion, lymphoid aggregates, and granulomas.
Presence of anti-Saccharomyces cerevisiae
antibodies (ASCA), although not specific,
along with absence of perinuclear antineutro-
phil cytoplasmic antibodies (P-ANCA) is
highly suggestive of Crohn’s disease [3].
Nevertheless, 10–15% of patients are diag-
nosed with indeterminate colitis.
C. Small bowel follow through, computed tomog-
raphy (CT), and magnetic resonance imaging
(MRI) enterography are useful adjuncts that
should be used to assess the presence and
extent of associated small bowel disease.
D. Medical treatment remains the mainstay ther-
apy for Crohn’s colitis. High-dose systemic
steroids or budesonide, an enteric coated
oral steroid, is an effective medication for
233
234
induction of remission of disease. Azathioprine
and 6-mercaptopurine are immunomodulators
being used in moderate disease as monother-
apy or in conjunction with biologic agents to
achieve remission. Biologic agents, which
mainly act as monoclonal antibodies against
TNF-a, are highly effective in inducing and
maintaining remission in steroid-dependent,
steroid refractory, or fistulizing disease. Early
administration of biologic agents, often with
conjunction of immunomodulators, after
diagnosis of Crohn’s disease is linked with
better outcomes [4]. In addition, they are
being used as an effective medical prophy-
laxis after surgery.
E. Indications for surgery include failure of or
intolerance to medical therapy, chronic
obstruction, fistula formation, local perfora-
tion with abscess formation, toxic colitis, fail-
ure to thrive, and presence of dysplasia or
malignancy [5]. Patients with rectal involve-
ment benefit from total proctocolectomy with
end ileostomy. Patients with single segment
or multiple segment colonic disease and
spared rectum should undergo segmental col-
ectomy and total abdominal colectomy with
ileorectal anastomosis, respectively [6].
M. Michailidou and E. Messaris
Patients with medically refractory toxic coli-
tis should undergo total abdominal colectomy
with end ileostomy [7].
F. Patients with severe colitis typically present
with six or more bloody bowel movements
per day, plus one systemic sign of toxicity
that includes anemia (<10.5  g/dL), ESR
(>30 mm/h), fever (>37.5 °C), or tachycardia
(>90 beats per minute). Patients with total or
segmental dilation of the colon with associ-
ated systemic toxicity have toxic megacolon
[7]. Treatment involves intravenous hydra-
tion and antibiotics with high-dose systemic
corticosteroids. CMV and Clostridium diffi-
cile colitis need to be ruled out since they can
present parallel to severe colitis. Although
most data originate from fulminant ulcer-
ative colitis cases [8], patients who fail to
respond to systemic steroids within 2–3 days
of initiation should be offered either rescue
therapy with infliximab (5 mg/kg) or cyclo-
sporine (2–4  mg/kg) [9] or total abdominal
colectomy with end ileostomy. Patients who
fail medical management with rescue ther-
apy, typically within 5–7  days, should be
offered total abdominal colectomy with end
ileostomy.
61  Crohn’s Colitis 235

A Clinical presentation suspicious for inflammatory bowel disease

(abdominal pain, diarrhea, weight loss, obstructive symptoms)

B Rule out other causes of colitis (ischemic, infectious)

C. difficile toxin, CMV, stool cultures for ova and parasites
CBC, ESR, CRP, P-ANCA, ASCA, rule out concomitant celiac disease
CT A/P
Colonoscopy with biopsies and intubation of terminal ileum

Severe colitis (six or more bloody stools per day plus one sign of systemic
toxicity) which includes anemia (<10.5 g/dL), ESR (>30 mm/h), fever (>37.5°C),
and tachycardia (>90 beats per minute) +/-megacolon

Yes No

F NPO, IV fluids, IV antibiotics Colonoscopy with intubation of C

Rule out CMV/C.diff colitis terminal ileum
IV steroids +/-rescue anti-TNF-a CT or MRI enterography

Improvement Diagnosis consistent

No improvement
with Crohn’s Colitis

E Steroids D
Total abdominal colectomy
Immunomodulators
with end ileostomy
Biologic agents

• Failed medical management • Multiple areas of

• Failure to thrive low-grade dysplasia
• Stricture • High-grade dysplasia
• Perforation • Colon adenocarcinoma

E Total proctocolectomy with end

ileostomy

– Single segment colonic disease

Segmental colectomy
– Multiple segment colonic disease
with no rectal involvement
TAC with ileorectal anastomosis
– Colonic disease with rectal
involvement
Total proctocolectomy with end
ileostomy

Algorithm 61.1
236 M. Michailidou and E. Messaris

References (REACT): a cluster randomised controlled trial.

Lancet. 2015;386(10006):1825–34.
5. Toh JW, Stewart P, Rickard MJ, Leong R, Wang N,
1. Silverberg MS, Satsangi J, Ahmad T, Arnott ID,
Young CJ. Indications and surgical options for small
Bernstein CN, Brant SR, et al. Toward an integrated
bowel, large bowel and perianal Crohn’s disease.
clinical, molecular and serological classification of
World J Gastroenterol. 2016;22(40):8892–904.
inflammatory bowel disease: report of a Working
6. Strong S, Steele SR, Boutrous M, Bordineau L, Chun
Party of the 2005 Montreal World Congress of
J, Stewart DB, et al. Clinical practice guideline for the
Gastroenterology. Can J Gastroenterol = Journal cana-
surgical management of Crohn’s disease. Dis Colon
dien de gastroenterologie. 2005;19(Suppl A):5a–36a.
Rectum. 2015;58(11):1021–36.
2. Parkes GC, Whelan K, Lindsay JO.  Smoking in
7. Strong SA.  Management of acute colitis and
inflammatory bowel disease: impact on disease course
toxic megacolon. Clin Colon Rectal Surg.
and insights into the aetiology of its effect. J Crohns
2010;23(4):274–84.
Colitis. 2014;8(8):717–25.
8. Andrew RE, Messaris E.  Update on medical and
3. Smids C, Horjus Talabur Horje CS, Groenen MJM,
surgical options for patients with acute severe ulcer-
van Koolwijk EHM, Wahab PJ, van Lochem EG. The
ative colitis: what is new? World J Gastrointest Surg.
value of serum antibodies in differentiating inflam-
2016;8(9):598–605.
matory bowel disease, predicting disease activity and
9. Narula N, Marshall JK, Colombel JF, Leontiadis GI,
disease course in the newly diagnosed patient. Scand
Williams JG, Muqtadir Z, et  al. Systematic review
J Gastroenterol. 2017;52(10):1104–12.
and meta-analysis: infliximab or cyclosporine as
4. Khanna R, Bressler B, Levesque BG, Zou G, Stitt
rescue therapy in patients with severe ulcerative
LW, Greenberg GR, et  al. Early combined immuno-
colitis refractory to steroids. Am J Gastroenterol.
suppression for the management of Crohn’s disease
2016;111(4):477–91.
 Ischemic Colitis
William Sangster and Evangelos Messaris
Algorithmic Approach
A. Ischemic colitis can develop secondary to:
1. Acute arterial occlusion (embolic or
thrombotic)
2. Venous thrombosis
3. Hypoperfusion of the colonic vasculature
causing nonocclusive ischemia
B. Typically patients with ischemic colitis will
present with sudden, crampy abdominal pain
with an urgent desire to defecate and subse-
quent passage of bloody diarrhea within 24 h.
Abdominal tenderness is usually mild to
moderate with focal peritonitis which is
located in the distribution of the segment of
colon involved [1].
C. The differential diagnosis for ischemic colitis
includes:
1.
Infectious etiologies such as
Cytomegalovirus or Clostridium difficile
colitis, Shigella, or Salmonella
W. Sangster
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
E. Messaris (*)
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Division of Colon and Rectal Surgery, Beth Israel
Medical Center, Harvard Medical Center,
Boston, MA, USA
e-mail: emessaris@pennstatehealth.psu.edu,
emessari@bidmc.harvard.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_62
62
2. Inflammatory colitis such as Crohn’s dis-
ease or ulcerative colitis
3. Traumatic etiology other than ischemia
D. Laboratory assessment, though not diagnos-
tic, may aid in determining severity. Increased
white blood cell count, serum lactate, lactate
dehydrogenase (LDH), creatine phosphoki-
nase (CPK), or blood urea nitrogen (BUN)
may indicate advanced tissue damage [2].
Stool culture, ova and parasite testing, and
Clostridium difficile toxin assay should be
ordered to rule out infectious etiologies of
bloody diarrhea.
E. Computed tomography (CT) scan of the
abdomen with intravenous contrast is the
study of choice to initially diagnose ischemic
colitis. CT findings are nonspecific and in
early cases of ischemic colitis can be normal.
Typical findings of ischemic colitis include
abnormal wall enhancement, wall thickening,
and mesenteric fat stranding [3]. Pneumatosis
coli, gas in the mesenteric or portal veins, or
pneumoperitoneum is also not specific to
colonic ischemia but may be seen in more
advanced stages and indicate colonic necro-
sis/perforation [4].
F. If the patient is not improving or the diagno-
sis is in question, colonoscopy can be per-
formed as the diagnostic test of choice and
should be completed within 48 h of symptom
onset. Although nonspecific, features on
colonoscopy suggestive of ischemic colitis
237
238
include segmental erythema, edema, mucosal
friability, ulcerations, and blue-black nodules
with dark-dusky backgrounds suggestive of
gangrene [5].
G. Treatment of colonic ischemia depends upon
its etiology and severity. Supportive care with
bowel rest and observation is appropriate pro-
vided there is no evidence of colonic perfora-
tion, necrosis, or gangrene. Intravenous fluids
should be given to ensure adequate colonic
perfusion. Though there is no strong evidence
supporting the routine use of antibiotics for
the treatment of all patients with colonic isch-
emia, current guidelines suggest starting
empiric broad-spectrum antibiotics for most
patients with colonic ischemia, except those
with mild disease [6].
After instituting supportive care, most patients
with nonocclusive colonic ischemia will improve
within one or two days and have complete clini-
W. Sangster and E. Messaris
cal and radiologic resolution of symptoms within
1–2 weeks [7].
For embolic or thrombotic colonic ischemia,
anticoagulant therapy should be instituted. Unlike
in cases of mesenteric ischemia, embolectomy,
bypass graft, or endarterectomy is generally not
performed in cases of primary colonic ischemia.
If findings of severe colonic ischemia exist, such
as diffuse peritoneal signs on physical exami-
nation, pneumatosis or pneumoperitoneum
on radiographic examination, or gangrene on
colonoscopic examination, surgical explora-
tion is indicated. The specific operation depends
upon the location of the affected colon and may
require a segmental colectomy or total colec-
tomy. In cases where a segmental resection is
performed without the creation of a diverting
ostomy, a “second-look” operation within 12
to 24 h may be appropriate to assess the viabil-
ity of the remaining colon and integrity of any
anastomoses.
62  Ischemic Colitis 239

Clinical presentation concerning for ischemic colitis? (acute abdominal

pain with hematochezia)

Evidence of diffuse (nonfocal) peritonitis on physical examination?

No Yes

Perform laboratory assessment (white blood

cell count, lactate, LDH, CPK, BUN, stool
cultures)

Obtain CT scan with IV contrast (assess for

abnormal wall enhancement, wall thickening,
mesenteric fat stranding, pneumatosis coli,
mesenteric gas or pneumoperitoneum)

Evidence of severe colonic ischemia

or colonic perforation?
(WBC>15,000/mm3, BUN>20
mg/dL, LDH>350 units/L,
pneumatosis coli, pneumoperitoneum)

No Yes

1.Supportive care with Consider surgical exploration

IV fluids and IV
antibiotics and reassess
2. Consider
colonoscopic evaluation
within 48 hours if
symptoms persist to
confirm diagnosis
Stricture present

If patient develops chronic symptomatology,

obtain water-soluble enema study or
endoscopic evaluation to assess for stricture

No stricture present

Observe

Algorithm 62.1
240 W. Sangster and E. Messaris

References findings of pneumatosis and portomesenteric venous

gas in acute bowel ischemia. World J Gastroenterol.
2013;19(39):6579–84.
1. Feuerstadt P, Brandt LJ.  Colon ischemia: recent
5. Zou X, Cao J, Yao Y, Liu W, Chen L.  Endoscopic
insights and advances. Curr Gastroenterol Rep.
findings and clinicopathologic characteristics of
2010;12(5):383–90.
ischemic colitis: a report of 85 cases. Dig Dis Sci.
2. Mosele M, Cardin F, Inelmen EM, Coin A,
2009;54(9):2009–15.
Perissinotto E, Sergi G, et  al. Ischemic colitis in
6. Brandt LJ, Feuerstadt P, Longstreth GF, Boley
the elderly: predictors of the disease and prognostic
SJ.  ACG clinical guideline: epidemiology, risk fac-
factors to negative outcome. Scand J Gastroenterol.
tors, patterns of presentation, diagnosis, and manage-
2010;45(4):428–33.
ment of colon ischemia (CI). Am J Gastroenterol.
3. Cruz C, Abujudeh HH, Nazarian RM, Thrall JH. Ischemic
2015;110(1):18–44.
colitis: spectrum of CT findings, sites of involvement
7. O'Neill S, Yalamarthi S.  Systematic review of
and severity. Emerg Radiol. 2015;22(4):357–65.
the management of ischaemic colitis. Color Dis.
4. Milone M, Di Minno MN, Musella M, Maietta P,
2012;14(11):e751–63.
Iaccarino V, Barone G, et al. Computed tomography
 Clostridium difficile Colitis
Kristen T. Crowell and Evangelos Messaris
Algorithmic Approach
A. In the setting of new onset diarrhea, history
and physical examination are the first step
with specific inquiry about risk factors for C.
difficile colitis. Usually, the diarrhea is
watery. The strongest risk factor is recent
antibiotic use, and patients who are immuno-
suppressed or diagnosed with inflammatory
bowel disease are at higher risk [1]. Physical
examination should evaluate for abdominal
distention and peritoneal signs.
B. A diarrheal specimen should be evaluated for
C. difficile toxin [2].
C. With a positive assay, the severity of colitis is
determined next. Vital signs and laboratory
studies including complete blood count
(CBC), electrolytes, renal function, and albu-
min should be obtained.
D. Patients should be evaluated for fulminant C.
difficile colitis, which includes systemic tox-
K. T. Crowell
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
E. Messaris (*)
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
Division of Colon and Rectal Surgery, Beth Israel
Medical Center, Harvard Medical Center,
Boston, MA, USA
e-mail: emessaris@pennstatehealth.psu.edu,
emessari@bidmc.harvard.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_63
63
icity, hypotension, oliguria, tachycardia, or
perforation [3]. A plain abdominal X-ray may
be obtained to evaluate for toxic megacolon.
With a concerning physical exam, a CT scan
can assist in determining the extent of colonic
inflammation and can further characterize
signs of perforation or impending perforation
with pneumatosis.
E. If fulminant disease or perforation is identi-
fied, total abdominal colectomy with end ile-
ostomy and a stapled rectal stump is the safest
surgical option [4].
F. Without peritoneal signs or perforation, antibi-
otic therapy in addition to supportive care is
indicated. The antibiotic regimen chosen is
based upon disease severity as listed below [5]:
(a) Mild disease (WBC <15,000 and creatinine
(Cr) less than 1.5 times baseline) is treated
with oral or IV antibiotic therapy with met-
ronidazole 500 mg tid for 10–14 days.
(b) Severe disease (WBC  >15,000 and/or
Cr >1.5 times baseline Cr) is treated with
125 mg vancomycin PO qid for 10–14 days.
(c) Severe-complicated disease is character-
ized by additional complicating factors,
including ileus, shock requiring vaso-
pressors, and megacolon, or worsening
symptoms or lack of improvement after
5 days of antibiotic treatment. CT scans
of the abdomen/pelvis should be
obtained. Treatment: IV metronidazole
500 mg tid, PO vancomycin 125 mg qid,
241
242 K. T. Crowell and E. Messaris

and if ileus: add vancomycin enema
500 mg qid.
G. Continue to monitor patient for signs of C.
difficile colitis. Patients who clinically
worsen or do not respond to medical ther-
apy should be evaluated for surgical inter-
vention. Patients with refractory or recurrent
disease should be considered for fecal
microbiota transplant prior to surgical inter-
vention [6].

History:
A Duration of diarrhea, nausea, vomiting, abdominal pain
Recent antibiotic use, IBD, immunosuppression

Positive
B
Clostridium
difficile toxin
assay?

C Physical exam, vital signs, laboratories

Fulminant C.
D difficile colitis or
colonic G
perforation?
Continue
to
Yes No reassess

Initiate antibiotic
Immediate F
E therapy
surgical
intervention
Mild: Severe: Severe-
metronidazole vancomycin PO complicated:
PO vanco + IV
metro, ± vanco
enema
Algorithm 63.1

4. Kaiser AM, Hogen R, Bordeianou L, Alavi K, Wise

References
1. Ananthakrishnan AN.  Detecting and treating
Clostridium difficile infections in patients with
inflammatory bowel disease. Gastroenterol Clin N
Am. 2012;41(2):339–53.
2. Surawicz CM, Brandt LJ, Binion DG,
Ananthakrishnan AN, Curry SR, Gilligan PH, et  al.
Guidelines for diagnosis, treatment, and prevention of
Clostridium difficile infections. Am J Gastroenterol.
2013;108(4):478–98. quiz 99
3. Butala P, Divino CM.  Surgical aspects of ful-
minant Clostridium difficile colitis. Am J Surg.
2010;200(1):131–5.
PE, Sudan R, et  al. Clostridium difficile infection
from a surgical perspective. J Gastrointest Surg.
2015;19(7):1363–77.
5. Katzman M.  Antibiotic therapy for Clostridium
difficile infection. Semin Colon Rectal Surg.
2014;25(3):143–9.
6. Lee CH, Steiner T, Petrof EO, Smieja M, Roscoe
D, Nematallah A, et al. Frozen vs fresh fecal micro-
biota transplantation and clinical resolution of
diarrhea in patients with recurrent Clostridium dif-
ficile infection: a randomized clinical trial. JAMA.
2016;315(2):142–9.
 Hereditary Colorectal Cancer
Syndromes
Emily Huang and Michael F. McGee
Algorithmic Approach
Approximately 30% of colorectal cancer cases are
associated with a family history of colorectal pol-
yps or cancer, but only 3–5% of cases are associ-
ated with a specifically identifiable inheritable
colorectal cancer syndrome. The most commonly
identifiable cause of inheritable colorectal cancer is
Lynch syndrome, characterized by a specific muta-
tion in one of the DNA mismatch repair (MMR) or
EPCAM genes. Although the terms Lynch syn-
drome and hereditary nonpolyposis colorectal can-
cer (HNPCC) are often used interchangeably, the
term Lynch syndrome refers to patients with a spe-
cifically identifiable germline MMR defect,
whereas HNPCC refers to a patient or kindred who
meets the Amsterdam criteria (Table 64.1).
Hereditary polyposis syndromes are a group
of hereditary disorders characterized by a pleth-
ora of polyps throughout the gastrointestinal tract
that predispose the patient to cancer. It is impor-
tant to distinguish Lynch syndrome from polypo-
sis syndromes, as the former typically causes
isolated cancers with minimal adenomatous
polyp burden, rather than extensive polyposis.
E. Huang
Department of Surgery, University of Chicago,
Chicago, IL, USA
M. F. McGee (*)
Department of Surgery, Northwestern Memorial
Hospital, Chicago, IL, USA
e-mail: mmcgee1@nm.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_64
64
The surgeon typically encounters two clinical
situations which are outlined in this chapter’s
flow charts: [1] management of a patient or kin-
dred with recently diagnosed colorectal cancer
with suspicion of Lynch syndrome and [2] man-
agement of a patient with personal or family his-
tory of significant colonic polyposis.
A. A personal or family history of young (< age
50) colorectal, endometrial, or Lynch-­
associated cancers should trigger suspicion of
Lynch syndrome. A review of systems may
reveal symptoms such as gastritis or abnor-
mal vaginal bleeding that might provide clues
to concurrent malignancies in a patient who
presents with a known diagnosis of colon
cancer. Additionally, thorough personal and
family histories must be obtained evaluating
for colorectal cancers, polyps, and Lynch-­
associated cancers (endometrial, gastric,
ovarian, small bowel, and urinary tract can-
cers). The surgeon should be familiar with the
Amsterdam criteria to assess the suspected
kindred’s risk for hereditary nonpolyposis
colorectal cancer (Table 64.1).
B. Recent recommendations encourage routine
testing of all colorectal cancers for MMR
gene defects. Some institutions may limit
tumor MMR testing to patients using the
revised Bethesda criteria (see Table  64.2).
Most commonly, immunohistochemistry
(IHC) for the four most common defective
243
244 E. Huang and M. F. McGee

Table 64.1  Amsterdam II criteria for hereditary nonpolyposis colorectal cancer [1]
1 At least three family members affected, one of whom is a first-degree relative of the other two, with HNPCC-
related cancers (colorectal, endometrial, small bowel, ureter, renal pelvis)
2 Two successively related generations
3 At least one of the HNPCC-related cancers diagnosed before age 50
4 Familial adenomatous polyposis excluded

Table 64.2  Bethesda guidelines to guide tumor testing for MMR gene defects [2]
1 Colorectal cancer diagnosed in patient under 50 years of age
2 Synchronous or metachronous colorectal cancer or other HNPCC-associated tumors, regardless of age
3 Colorectal cancer with high levels of microsatellite instability (MSI-H) histology in a patient younger than
60 years old
4 Colorectal cancer in one or more first-degree relatives with an HNPCC-related tumor, with one of the cancers
diagnosed under 50 years of age
5 Colorectal cancer diagnosed in two or more first- or second-degree relatives with HNPCC-related tumors,
regardless of age

MMR genes (MLH1, MSH2, MSH6, PMS2)
is performed on tumor biopsies, although
some institutions additionally test for the
EPCAM gene as well. It should be noted that
nearly all testing can be done with endoscopic
biopsies alone.
C. Patients with abnormal tumor MLH1 testing
merit further tumor testing. The most com-
mon cause of abnormal MLH1 testing is
somatic promoter methylation caused by a
BRAF gene defect, a condition which is typi-
cally sporadic and not inheritable. Any patient
with a defective or missing MLH1 gene
should undergo reflexive BRAF gene testing
of the tumor biopsy. If a mutated BRAF gene
is found, the cancer is considered to be spo-
radic (not Lynch) and treated accordingly. If
BRAF testing is normal (i.e., wild type), then
the MLH1 defect is considered to arise from
Lynch or Lynch-like syndrome and should be
further evaluated with germline testing.
D. MLH1 and PMS2 are often coexpressed, so an
MLH1 defect may also cause a PMS2 defect.
A purely isolated PMS2 defect is likely to be
related to Lynch or Lynch-like syndrome.
E. Patients with other MMR defects not attrib-
uted to a BRAF mutation are likely to have
Lynch or Lynch-like syndrome and merit
confirmation through germline (blood) test-
ing with a genetic counselor. Patients with a
tumor MMR defect who fail to demonstrate a
germline genetic defect are considered to
have “Lynch-like syndrome” arising from a
somatic (i.e., not germline) defect of the
MMR genes. There is no consensus on man-
agement and surveillance of Lynch-like
patients; however, many advocate total colec-
tomy in lieu of segmental colectomy in
appropriate patients. For this reason, germ-
line testing typically should not delay surgi-
cal therapy for recently diagnosed Lynch-like
patients, since confirmation of a germline
MMR defect is more pertinent to the kindred
than to the patient in question. Patients who
screen positively for Amsterdam II criteria
and fail to possess a germline MMR defect
are considered to have familial colorectal
cancer type X, which is an entity distinct
from Lynch syndrome. There is no consensus
on management of colorectal cancer type X
patients; however, many advocate total colec-
tomy in appropriate patients and intensive
postoperative surveillance programs.
Polyposis disorders are characterized by a
known germline mutation, and new clinical data
on the genetics of polyposis syndromes continue
to arise with ongoing research. Whether establish-
ing a new diagnosis, performing surgery for cancer
or prophylaxis, or counseling members from a pol-
yposis kindred, the surgeon must be aware of pol-
yposis syndromes and their workup, diagnosis,
and treatments. Table 64.3 details the heritability
and characteristics of polyposis syndromes.
64  Hereditary Colorectal Cancer Syndromes
F. The most common presentations to the surgeon
in the context of hereditary polyposis syn-
dromes will be (1) the patient with a new colo-
noscopic finding of polyposis or diagnosis of
colorectal cancer who requires workup for a
hereditary syndrome and (2) the patient with a
known hereditary syndrome presenting for risk
reduction surgery or a new diagnosis of cancer.
G. The first encounter should begin with a detailed
and tailored history and physical exam. The
personal history focuses on (gastrointestinal)
GI symptoms and personal history of cancer.
The family history must be taken in an orga-
nized fashion and include any relatives (focus-
ing on first- or second-degree relatives) with
cancer, the type and location of the cancer
(colorectal vs. extraintestinal), and age at diag-
nosis. Using a pedigree to organize this infor-
mation can be helpful. Furthermore, because
phenotypes for the various polyposis and non-
polyposis syndromes can overlap, the clinician
should be alert and wary of any distinguishing
traits. The physical exam includes a complete
evaluation for surgical fitness and thorough
abdominal evaluation, as usual, but here we
point out a number of important and unusual
findings that are characteristic of polyposis
syndromes. A thorough clinical exam may
detect supernumerary teeth, epidermoid cysts,
thyroid nodules, and desmoid tumors, for
instance, which are characteristic of familial
adenomatous polyposis (FAP) [3].
H. Patients who present with a new finding of
polyposis on colonoscopy or who raise clini-
cal suspicion of a hereditary polyposis syn-
drome (e.g., the young patient with newly
diagnosed colon cancer with a duodenal ade-
noma) should be referred for genetic counsel-
ing and testing. Apart from determining the
risk for cancer for an individual patient,
genetic testing has significant implications
for the entire family and may inform subse-
quent decisions about surveillance or risk
reduction, as most of the hereditary polyposis
syndromes are autosomal dominant. Genetic
counseling guides patients through the often
complex decisions about treatment and pre-
vention that arise from a new genetic diagno-
sis and can adjust misperceptions [4].
245
I. Depending on the specific syndrome, surveil-
lance of the colon, the entire GI tract, or the GI
tract and other organs may be warranted.
Recommendations for modalities and inter-
vals are outlined in Table  64.3 by syndrome
[5–16]. For familial adenomatous polyposis
(FAP), recommendations are generally con-
current between the American College of
Gastroenterology (ACG), American Society
of Gastrointestinal Endoscopists (ASGE), and
various European guidelines [5–9]. Juvenile
polyposis syndrome is rare and thus without a
large burden of collective experience to guide
management [8]. In addition to the modalities
mentioned, capsule endoscopy, push enteros-
copy, and magnetic resonance imaging (MRI)
enterography are also used as screening
modalities for selected FAP patients at higher
risk of developing small bowel adenomas
(those with duodenal adenomas) and patients
with Peutz-Jeghers syndrome [17].
Recommendations for surveillance in Peutz-
Jeghers syndrome are taken from the work of
a Dutch multidisciplinary group and concur
closely with those from other European and
American societies.
J. Recommendations for segmental, total
abdominal colectomy, and proctocolectomy
vary depending on the specific polyposis syn-
drome. In classic FAP, where the colorectal
cancer risk reaches a lifetime risk of 100% by
around age 40, recommendations for procto-
colectomy are very strong, although proce-
dures can be staged to be tailored to patients’
individual needs, such as fecundity preserva-
tion or rectal polyp burden. In Peutz-Jeghers
syndrome, recommendations are targeted
toward symptomatic and nonmalignant com-
plications of the hamartomatous polyps,
including intussusception and bleeding. The
exact mechanism of carcinogenesis in Peutz-­
Jeghers syndrome is yet unknown, so surveil-
lance aims to detect malignancy early, with
polypectomy having the potential benefit of
removing premalignant lesions. Regardless
of treatment, the cycle of surveillance and
appropriate treatment continues throughout
the rest of life in these patients and begins
anew with subsequent generations.
Table 64.3  Hereditary polyposis syndromes, their characteristics, and recommended surveillance and treatment regimens [5–16]
246

Approximate
Polyp type Syndrome Genes Inheritance Clinical findings risk of CRC Recommended surveillance Treatment
Adenoma Familial APC Autosomal  Profuse: over 1000 polyps Classic: Annual flexible sigmoidoscopy starting from Total proctocolectomy
adenomatous dominant  Classic: hundreds of polyps 100% puberty, with colonoscopy if high risk/numerous by age 25 (usually late
polyposis  Attenuated: fewer than 100 Profuse: polyps found teens); eliminates
(FAP) polyps 100% Annual proctoscopy for patients with ileorectal cancer risk
Duodenal adenomas and Attenuated: anastomosis Total colectomy with
carcinomas, gastric fundic gland 70–80% Upper endoscopy every 3 years from age 30 ileorectal anastomosis
polyps; desmoid tumors, Screening can start slightly later/be spaced to every is an option for
epidermoid cysts, supernumerary 2 years for attenuated FAP individuals with few
teeth, osteomas polyps in the rectum
MUTYH- MYH Autosomal 0–1000 adenomas, CRC <50 years; 75% Colonoscopy beginning at age 25–30, and repeated Endoscopic
associated recessive gastric fundic gland polyps, every 3–5 years if no neoplasia found; repeated polypectomy where
polyposis duodenal adenomas, and every 1–2 years if polyps found, depending on possible. Surgery
(MAP) carcinomas histology indicated for
EGD to evaluate for duodenal adenomatous colorectal cancer,
neoplasia beginning at age 30, and repeated every high-grade dysplasia
3–5 years if exam is normal not amenable to
Annual thyroid ultrasound beginning at age 25–30 endoscopic
polypectomy, or high
polyp burden. Surgery
should be with total
colectomy (colon
cancer) and ileorectal
anastomosis, or total
proctocolectomy
(rectal cancer), as the
entire colon is at risk
E. Huang and M. F. McGee
Hamartoma Juvenile BMPR1A Autosomal Working definition by Jass et al. 40% EGD and colonoscopy, starting in the later teen No strong evidence
polyposis SMAD4, dominant [13]: years, every years regarding the role of
syndrome heterogeneous  At least 5 juvenile polyps preventative
 Juvenile polyps throughout GI proctocolectomy;
tract however, the decision
 Any number of juvenile polyp should be based on
with JPS family history number and size of
Typically, 50–200 polyps; 20–50% polyps
have JPS family history; presenting
by age 20 with rectal bleeding
Peutz-Jeghers STK11 Autosomal Orocutaneous pigmentation; 40% Annual physical exam, hemoglobin, starting at age Polypectomy for
syndrome dominant family history of PJP; cancer of 10 polyps over 1–1.5 cm
small bowel, colon, stomach, Video capsule endoscopy and/or MRI enterography both to prevent
pancreas, breast, ovary, testis every 2–3 years starting at age 10 nonmalignant
Upper endoscopy every 2–5 years starting at age 20 complications such as
Colonoscopy every 2–5 years starting at age 25–30 intussusception or
Annual breast exam and mammography/breast MRI, bleeding, and to
64  Hereditary Colorectal Cancer Syndromes

starting at age 25 (mammography at age 30) remove possible

Annual pelvic exam, Pap smear, transvaginal precursor to
ultrasonography, and CA-125, starting at age 25–30 malignancy
Treatment of
malignancy as
indicated
PTEN PTEN Autosomal Colorectal adenomas, lipomas, 10% As advocated by NCCN 2007 [14]: Colectomy or
hamartoma dominant fibromas, ganglioneuromas, (Cowden  Annual or biannual colonoscopy starting at age 35 proctocolectomy
tumor juvenile hamartomas; colorectal syndrome);  Breast self exam starting at age 18 based on polyp
syndrome cancer; macrocephaly, most  Annual clinical breast examinations starting at age burden, if endoscopic
trichilemmomas malignant 25 (or 5–10 years before earliest known breast management
potential is cancer in the family) inadequate. No good
extracolonic  Annual mammography and breast MRI starting at estimate of colorectal
age 35 (or 5–10 years before earliest known breast cancer risk given rarity
cancer in the family) of this syndrome
 Blind endometrial biopsy
 Annual physical exam with focus on breast and
thyroid starting at age 18 (or 5 years before
youngest age of cancer diagnosis in the family)
 Baseline thyroid ultrasound at age 18; consider
annual ultrasound depending on individual factors
(continued)
247
Table 64.3 (contiuned)
248

Approximate
Polyp type Syndrome Genes Inheritance Clinical findings risk of CRC Recommended surveillance Treatment
Serrated Serrated Unknown Unknown WHO criteria one of the following 25–40% Annual colonoscopy with removal of polyps larger Endoscopic
(hyperplastic) [16]: than 5 mm and biopsies of smaller clusters (likely polypectomy where
polyposis  At least 20 serrated polyps of hyperplastic); usually starting at age of diagnosis possible. Surgery
syndrome any size throughout the colon Colonoscopy interval can be lengthened in patients indicated for
 Any number of serrated polyps without polyps on subsequent colonoscopy colorectal cancer or
proximal to the sigmoid in an high polyp burden.
individual with family history of Surgery should be
SPS with total colectomy
 At least 5 serrated polyps and ileorectal
proximal to the sigmoid, 2 of anastomosis, with
which are over 1 cm diameter ongoing surveillance
of any remaining
sigmoid and/or rectum
E. Huang and M. F. McGee
64  Hereditary Colorectal Cancer Syndromes 249

Young patient diagnosed with colorectal,

A or HNPCC-related cancer; or strong
family history of HNPCC-related cancer

Tumor specimen microsatellite instability

B (MSI) determination and mismatch repair
protein (MMR) testing

MLH1defect or Yes
BRAF C
MLH1+PMS2
mutation?
defect?

No Yes No

Germline
PMS2 defect
D MMR
(isolated)?
Yes defect?

No
Yes No
Yes

MSH2 or
MSH6
defect?
Lynch syndrome: Strongly
Lynch-like syndrome: No
consider total colectomy
consensus on treatment,
No and TAH/BSO, family
consider total colectomy,
evaluation, surveillance
surveillance program
program

Amsterdam
criteria
positive? Yes

E
No

Familial colorectal cancer type X, no consensus

Traditional treatment and surveillance for
on treatment, consider total colectomy,
sporadic colorectal cancer
surveillance program

Patient with significant Patient with known family

polyposis on colonoscopy, no history of hereditary
F
known mutation polyposis syndrome

Thorough and appropriate personal history,

G family history, physical exam, endoscopic
staging

H Genetic counseling and testing; diagnosis

I Surveillance (See Table 64.1)

J
Treatment (See Table 64.1)

Algorithm 64.1  Management of Patients with Suspected Inheritable Colorectal Cancer Syndromes
250 E. Huang and M. F. McGee

References and Peutz-Jeghers syndrome. Gut. 2002;51(suppl

5):v21–7.
9. Mitchem JB, Hall JF.  Adenomatous Polyposis
1. Vasen HF, Watson P, Mecklin JP, Lynch HT.  New
Syndromes: Diagnosis and Management. Clin Colon
clinical criteria for hereditary nonpolyposis
Rectal Surg. 2016;29(04):321–9.
colorectal cancer (HNPCC, Lynch syndrome) pro-
10. Van Lier MG, Wagner A, Mathus-Vliegen EM,

posed by the International Collaborative group on
Kuipers EJ, Steyerberg EW, Van Leerdam ME. High
HNPCC. Gastroenterology. 1999;116(6):1453–6.
cancer risk in Peutz-Jeghers syndrome: a systematic
2. Umar A, Boland CR, Terdiman JP, Syngal S, Chapelle
review and surveillance recommendations. Am J
AD, Rüschoff J, Fishel R, Lindor NM, Burgart
Gastroenterol. 2010;105(6):1258.
LJ, Hamelin R, Hamilton SR.  Revised Bethesda
11. Steele SR, Hull TL, Read TE, Saclarides TJ, Senagore
Guidelines for hereditary nonpolyposis colorectal
AJ, Whitlow CB, editors. The ASCRS textbook of
cancer (Lynch syndrome) and microsatellite instabil-
colon and rectal surgery. Springer: New York; 2016.
ity. J Natl Cancer Inst. 2004;96(4):261–8.
12. Gordon PH, Nivatvongs S. Principles and practice of
3. Kalady MF, Heald B. Diagnostic approach to heredi-
surgery for the colon, rectum, and anus. CRC Press:
tary colorectal cancer syndromes. Clin Colon Rectal
New York; 2007.
Surg. 2015;28(04):205–14.
13.
Jass JR, Williams CB, Bussey HJ, Morson
4. Petersen GM, Boyd PA.  Gene tests and coun-
BC.  Juvenile polyposis–a precancerous condition.
seling for colorectal cancer risk: lessons from
Histopathology. 1988;13(6):619–30.
familial polyposis. J Natl Cancer Inst Monogr.
14. Blumenthal GM, Dennis PA. PTEN hamartoma tumor
1994;17:67–71.
syndromes. Eur J Hum Genet. 2008;16(11):1289.
5. Syngal S, Brand RE, Church JM, Giardiello FM,
15. Hazewinkel Y, Tytgat KM, Van Eeden S, Bastiaansen B,
Hampel HL, Burt RW.  ACG clinical guideline:
Tanis PJ, Boparai KS, Fockens P, Dekker E. Incidence
genetic testing and management of hereditary gas-
of colonic neoplasia in patients with serrated polypo-
trointestinal cancer syndromes. Am J Gastroenterol.
sis syndrome who undergo annual endoscopic surveil-
2015;110(2):223.
lance. Gastroenterology. 2014;147(1):88–95.
6. Davila RE, Rajan E, Baron TH.  ASGE guide-
16. Snover D, Ahnen D, Burt R, Odze RD. Serrated pol-
line: colorectal cancer screening and surveillance.
yps of the colon and rectum and serrated polyposis.
Gastrointest Endosc. 2006;63(4):546–57.
In: Bosman FT, Carneiro F, Hruban RH, editors.
7. Vasen HF, Moeslein G, Alonso A, Aretz S, Bernstein
WHO classification of tumours of the digestive sys-
I, Bertario L, Blanco I, Bülow S, Burn J, Capella
tem. 4th ed. Lyon: IARC; 2010.
G, Colas C.  Guidelines for the clinical manage-
17. Schulmann K, Hollerbach S, Kraus K, Willert J, Vogel
ment of familial adenomatous polyposis (FAP). Gut.
T, Möslein G, Pox C, Reiser M, Reinacher-Schick A,
2008;57(5):704–13.
Schmiegel W.  Feasibility and diagnostic utility of
8. Dunlop MG.  Guidance on gastrointestinal surveil-
video capsule endoscopy for the detection of small
lance for hereditary non-polyposis colorectal cancer,
bowel polyps in patients with hereditary polyposis
familial adenomatous polypolis, juvenile polyposis,
syndromes. Am J Gastroenterol. 2005;100(1):27.
 Colorectal Polyps
Emily Huang and Michael F. McGee
Algorithmic Approach
A. Adenomatous colon polyps are precursors to
colon cancer, and colonoscopic polypectomy
reduces both the incidence and mortality of
colorectal cancer [1]. Adequate bowel prepa-
ration, endoscopic irrigation, and meticulous
suctioning permit thorough and complete
mucosal evaluation to detect and treat all
colonic neoplasia.
B. Following polyp identification, thorough irri-
gation and suctioning are performed to ade-
quately assess polyp-specific features to
guide management and enable treatment.
Determination of polyp size, morphology,
and location is essential, and use of Paris
classification to characterize polyp morphol-
ogy is encouraged [2]. Malignant tumors are
differentiated from benign adenomas by size,
firmness, central depression, ulceration, and
fixation to the deeper bowel wall [3, 4].
Inability to expand peri-polyp submucosa
during saline lift (i.e., “non-lifting sign of
Uno”) is associated with invasive cancer or
scarring from prior polypectomy interven-
E. Huang
Department of Surgery, University of Chicago,
Chicago, IL, USA
M. F. McGee (*)
Department of Surgery, Northwestern Memorial
Hospital, Chicago, IL, USA
e-mail: mmcgee1@nm.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_65
65
tions. Narrow-band imaging, colonoscopic
microscopy, and chromoendoscopy may
yield additional information about the polyp
surface features. Nongranular surface fea-
tures and irregular nonstructured pits (Kudo
pit pattern type V) are both features that
should raise suspicion of submucosal inva-
sion and invasive adenocarcinoma [5].
C. Many suggest routinely tattooing all polyps
larger than 1–2  cm to facilitate endoscopic
surveillance or future surgical resection
should the lesion prove to be malignant.
D. Nearly all benign polyps are amenable to
endoscopic excision. Cold snare polypec-
tomy is the workhorse for most sessile polyps
smaller than 1 cm. Cold forceps can be used
to excise the smallest (1–2 mm) polyps; how-
ever, this technique is associated with high
rates of residual adenomatous tissue [6]. Hot
biopsy forceps polypectomy techniques have
fallen out of favor due to high rates of delayed
bleeding and perforation. Hot snare polypec-
tomy is typically used for pedunculated and
larger sessile (>1  cm) polyps. Saline-lift
endoscopic mucosal resection (EMR) is a
useful technique in which the submucosal
layer is first injected with saline to “lift” the
polyp, facilitating en bloc or piecemeal resec-
tion with a hot snare. EMR is helpful for large
polyps, those spanning many folds, and for
large right-sided polyps where the bowel wall
may be more susceptible to thermal injury.
251
252
Large postpolypectomy defects may benefit
from prophylactic clip closure to decrease the
risk of postpolypectomy hemorrhage.
E. Malignant appearing lesions should be biop-
sied and tattooed, and not removed, since
malignancy merits oncologic surgical resec-
tion. Indeterminately malignant lesions with
benign biopsy pathology may be referred to
expert endoscopists for consideration of
advanced polypectomy. The endoscopist
must be aware of his or her limitations prior
to attempting polypectomy because an
incomplete polypectomy may cause submu-
cosal scarring and prohibit later EMR
attempts by an expert. Special situations may
mandate surgical resection regardless of
polyp histology. For example, polyps grow-
ing into the appendiceal orifice or ileocecal
valve are frequently not amenable to endo-
scopic resection due to the difficulty of
obtaining a negative margin, as well as risk of
perforation or appendicitis. In these special
cases, patients should be referred for advanced
expert colonoscopic polypectomy or consid-
eration of surgical resection.
F. If polyp pathology demonstrates no evidence
of cancer, surveillance colonoscopy should
continue based on the number, size, histol-
ogy, completeness of polypectomy, bowel
preparation quality, and patient and family
history. Periodically updated guidelines dic-
tate the frequency of postpolypectomy sur-
veillance for commonly resected polyps in
average-risk individuals [7].
G. “Carcinoma in situ” or “intramucosal carci-
noma” are confusing terms that describe lack
E. Huang and M. F. McGee
of cancerous invasion of the muscularis
mucosa. These lesions are premalignant (i.e.,
Tis or T0), and colonoscopic resection alone
may be adequate. Histology, margins, and
depth of malignant invasion determine the
adequacy of colonoscopic polypectomy for
malignant pedunculated polyps. Haggitt’s
classification dictates that polypectomy alone
is sufficient for a favorable- histology tumor
confined to the polyp stalk with a 2 mm mar-
gin from the cut polyp edge [8]. The analo-
gous Kikuchi classification for sessile polyps
has shown polypectomy to be sufficient for
favorable-histology tumor penetration lim-
ited to the upper third (<1 mm) of submucosa
[9]. Sessile and pedunculated polyps with
deeper submucosal cancerous penetration
(>1 mm) should be considered for oncologic
surgical resection given the high frequency of
lymph node metastases. Regardless of polyp
morphology, high-risk pathologic features
such as poor differentiation, lymphovascular
invasion, and extensive budding increase the
risk of lymphatic metastasis and typically
mandate oncologic surgical resection [10].
H. Occasionally, polyp margins, histology, and
the endoscopist’s assessment of polypectomy
completeness may be unclear. In these situa-
tions, multidisciplinary review with the
endoscopist, surgeon, and pathologist can
guide decision-making. In this meeting, the
risks of local cancer recurrence and lymph
node metastasis should be balanced against
the risk of surgical resection, using the
patient’s wishes and operative risk to deter-
mine the course of subsequent care.
65  Colorectal Polyps 253

A Polyp identified

Evaluate polyp features: size, morphology,

firmness, villous pattern, ulceration,central
depression

Malignant Stop: Tattoo polyp site

features? and biopsy extensively
Yes

No

Consider tattooing all E

C polyps > 1–2 cm
D

Await pathology and

consider referral to
Any advanced endoscopist or
Sessile polyp
pedunculated oncologic surgical
Sessile polyp < >10 mm: hot Technically
polyp: hot snare, resection
10 mm: cold snare or EMR, infeasible
snare consider clipping consider clipping
base base Multi-disciplinary review:
consider oncologic
surgical resection, EMR,
endoscopic surveillance

Pathology: no
H
malignancy, OR Pathology:
no neoplasia malignancy
at margins G

Carcinoma in Pedunculated <1 mm Uncertain

situ, negative T1 cancer, margin, margins or
margins, no >2 mm margins, >1 mm SM uncertain
F high risk no high risk depth, high histologic
features features risk features features

Endoscopic surveillance Oncologic surgical resection

Algorithm 65.1
254 E. Huang and M. F. McGee

References Byth K.  Endoscopic mucosal resection outcomes

and prediction of submucosal cancer from advanced
colonic mucosal neoplasia. Gastroenterology.
1. Zauber AG, Winawer SJ, O'Brien MJ, Lansdorp-­
2011;140(7):1909–18.
Vogelaar I, van Ballegooijen M, Hankey BF, Shi
6. Efthymiou M, Taylor A, Desmond P, Allen B, Chen
W, Bond JH, Schapiro M, Panish JF, Stewart
R.  Biopsy forceps is inadequate for the resection of
ET.  Colonoscopic polypectomy and long-term pre-
diminutive polyps. Endoscopy. 2011;43(4):312–6.
vention of colorectal-cancer deaths. N Engl J Med.
7. Lieberman D, Rex D, Winawer S, Giardiello F, Johnson
2012;366(8):687–96.
D, Levin T. Guidelines for colonoscopy surveillance
2. Inoue H, Kashida H, Kudo S, Sasako M, Shimoda T,
after screening and polypectomy: a consensus update
Watanabe H, Yoshida S, Guelrud M, Lightdale CJ,
by the US Multi-Society Task Force on colorectal
Wang K, Riddell RH.  The Paris endoscopic classi-
cancer. Gastroenterology. 2012;143(3):844–57.
fication of superficial neoplastic lesions: esophagus,
8. Haggitt R, Glotzbach R, Soffer E, Wruble
stomach, and colon: November 30 to December 1,
L.  Prognostic factors in colorectal carcinomas aris-
2002. Gastrointest Endosc. 2003;58(6 Suppl):S3–43.
ing in adenomas: implications for lesions removed
3. Galandiuk S, Fazio VW, Jagelman DG, Lavery IC,
by endoscopic polypectomy. Gastroenterology.
Weakley FA, Petras RE, Badhwar K, McGonagle
1985;89:328–36.
B, Eastin K, Sutton T.  Villous and tubulovillous
9. Kikuchi R, Takano M, Takagi K, Fujimoto R, Nozaki
­adenomas of the colon and rectum: a retrospective
T, Fujiyoshi T, Uchida Y. Management of early inva-
review, 1964–1985. Am J Surg. 1987;153(1):41–7.
sive colorectal cancer. Risk of recurrence and clinical
4. Doniec JM, Löhnert MS, Schniewind B, Bokelmann
guidelines. Dis Colon Rectum. 1995;38(12):1286–95.
F, Kremer B, Grimm H.  Endoscopic removal
10. Resch A, Langner C.  Risk assessment in early

of large colorectal polyps. Dis Colon Rectum.
colorectal cancer: histological and molecular markers.
2003;46(3):340–8.
Dig Dis. 2015;33(1):77–85.
5. Moss A, Bourke MJ, Williams SJ, Hourigan LF,
Brown G, Tam W, Singh R, Zanati S, Chen RY,
 Colon Cancer
Emily Huang and Michael F. McGee
Algorithmic Approach
B. For patients with suspected colon cancer,
The surgeon may first encounter a patient at any
point along the timeline of the diagnosis, workup,
or treatment of colon adenocarcinoma. From an
emergent consultation for perforation to an elec-
tive clinic referral for newly diagnosed tumor to a
multidisciplinary tumor board evaluation for
complex multivisceral resection, surgeons must
be familiar with the clinical approach for many
scenarios [1].
A. Up to 30% of colorectal adenocarcinomas
may be asymptomatic at the time of diagno-
sis; however, the remainder of patients will
experience symptoms. The most common
symptoms of colon cancer are “alarm” symp-
toms such as changes in bowel habits or
bloody bowel movements. Abdominal pain,
which is infrequently associated with cancer,
is a worrisome sign associated with obstruc-
tion, local tumor ingrowth, or perforation and
merits expedited workup when cancer is
suspected.
E. Huang
Department of Surgery, University of Chicago,
Chicago, IL, USA
M. F. McGee (*)
Department of Surgery, Northwestern Memorial
Hospital, Chicago, IL, USA
e-mail: mmcgee1@nm.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_66
66
history-­taking should explore abdominal
symptoms (nausea, emesis, early satiety, pain,
changes in bowel habits, hematochezia) that
might suggest obstruction or help localize
pathology. Anorexia and weight loss should
be assessed. Extraabdominal symptoms such
as chest pain, cough, dyspnea, and jaun-
dice or anicteric stools may suggest pulmo-
nary or liver metastases. The patient’s fecal
continence status should be explored and
may occasionally impact surgical decision-­
making. As noted in the separate chapter on
hereditary colorectal cancer, a family history
of colon cancer or polyposis may prompt
referral for genetic counseling and testing
[2, 3]. Physical examination should focus on
the abdomen, noting any scars from previous
surgery that might affect operative planning,
areas of tenderness, or masses, as well as
hepatosplenomegaly or ascites. A thorough
lymph node exam may rarely discover meta-
static disease to the inguinal, supraclavicular,
or cervical lymph node chains. A digital rec-
tal exam may reveal a low-laying tumor and
allows qualitative assessment of sphincter
tone. Lower extremity edema may be seen
with hypoalbuminemia and may indicate a
malnourished state. The initial evaluation
should also assess baseline functional status,
frailty, and other comorbidities, which may
affect future surgical decision-making.
255
256
C. The first diagnostic procedure, if not already
performed, is colonoscopy with tumor local-
ization, diagnostic biopsy, and location tat-
tooing. As noted in the chapter on colon
polyps, endoscopic evaluation of the lesion is F. Stage IV colon cancer patients presenting
very important, as certain features are sug-
gestive of malignancy. Tattooing lesions is
essential and guides surgical resection,
whereas complete and thorough evaluation of
the remaining colon excludes synchronous
cancers or polyps and other conditions which
may impact surgical decision-making. Rarely,
occult adenocarcinoma may be discovered in
an initially benign-appearing adenomatous
polyp. Management of such malignant polyps
is discussed in the colon polyps section of
this text.
D. Following confirmation of colon cancer, stag-
ing computed tomography (CT) of the chest,
abdomen, and pelvis is performed.
Complementary ultrasound, magnetic reso-
nance imaging (MRI), or positron emission
tomography (PET) imaging and image-
guided biopsy may help characterize equivo-
cal findings found on initial staging studies. A
complete blood count (CBC), serum chemis-
try, liver function tests, and carcinoembry-
onic antigen (CEA) should be drawn at this
initial encounter. Unexplained anemia may
suggest a chronically bleeding lesion, abnor-
mal LFTs may raise suspicion for metastatic G. In the absence of metastatic disease, the sur-
disease and provide a nutritional evaluation,
and a baseline CEA level serves as a refer-
ence to guide postoperative survivorship [4].
E. Approximately one quarter of newly diag-
nosed colon cancer patients will present with
metastatic disease. Patients with metastatic
disease absent significant symptoms benefit
from multidisciplinary evaluation in conjunc-
tion with a medical oncologist. Curative-­
attempt multivisceral resection may confer
survival benefits in select situations with or
without neoadjuvant chemotherapy in
patients with isolated liver and/or lung metas-
tases [5, 6]. Patients with potentially resect-
able metastatic disease should be discussed
with a multidisciplinary team consisting of
surgeons (thoracic, hepatobiliary, and
E. Huang and M. F. McGee
colorectal), medical oncologists, patholo-
gists, radiologists, and radiation oncologists
and considered for neoadjuvant chemother-
apy versus primary surgery.
with significantly obstructing, bleeding, or
perforated tumors may be candidates for pal-
liative interventions in conjunction with input
from a multidisciplinary management team
and the patient. Obstructing lesions may be
evaluated for self-expanding metal stents,
proximal diverting loop stoma, or palliative
resection. Similarly, tumor-related hemor-
rhage may prompt palliative surgical resec-
tion or targeted palliative radiotherapy in
select patients. Perforated lesions should be
managed on clinical context and acuity, bal-
anced carefully on the desires of the patient,
surgical risks, and likelihood of meaningful
survival. Treatment of perforated cancers
ranges from nonoperative management with
antibiotics, bowel rest, and percutaneous
drain placement to emergent proximal divert-
ing stoma or colectomy. The surgeon must be
particularly conscientious when considering
palliative surgery and predicate all decision-­
making to be commensurate with patient’s
long-term wishes since comorbidities and
advanced disease may subject patients to
unacceptably high surgical risks.
geon should assess appropriateness of cura-
tive attempt surgery. Imaging typically guides
the surgeon to determine resectability of the
cancer while ensuring adequate margins and
lymphadenectomy without collateral damage
of adjacent structures. Moreover, the patient
should prove to be a good candidate for the
proposed intervention. Principles of onco-
logic colectomy include 5 cm margins proxi-
mally and distally along the colon wall,
grossly negative circumferential margins for
T4b cancers (where tumor directly invades
other structures), high ligation of the arterial
supply to the affected colon segment, and
complete en bloc lymphadenectomy to assure
a minimum of 12 lymph nodes for pathology
review. Patients with completely resected
66  Colon Cancer
tumors who are found to have nodal metasta-
ses (stage III) should be referred to a medical
oncologist for adjuvant chemotherapy. Stage
II (T3 or T4  N0) cancer patients should be
H. Occasionally, local resectability may be in
referred to a medical oncologist to discuss the
role of adjuvant chemotherapy; however, sur-
vival advantages conferred by adjuvant che-
motherapy for stage II colorectal cancers are
modest and merit balance of chemotherapy
risks and side effects with expected survival
benefits. Regardless of the prescribed adju-
vant treatments, all curative intent colectomy
patients follow surveillance protocols with
257
imaging, physical exams, CEA, and colonos-
copy determined by periodically updated
guidelines.
question, and multidisciplinary consultation
assists with treatment planning. Tumors found
to be invading or threatening surrounding
structures may require multivisceral resection
or neoadjuvant treatments aimed to enable
future resection with negative margins. The
National Comprehensive Cancer Network
(NCCN) guidelines lay out the recommended
treatment regimens for such situations.
258 E. Huang and M. F. McGee

Patient with “alarm” symptoms worrisome

A for colorectal cancer, or abnormal imaging

B Thorough and appropriate history and physical

Symptoms; no
colonoscopy yet

Colonoscopy already
Colonoscopy, completed (for symptoms
biopsy, tattoo or screening)
C

Endoscopic confirmation of adenocarcinoma

Metastatic workup: CT chest, abdomen, and

pelvis; CBC, chemistry, LFTs, CEA H
D

Multidisciplinary
discussion
Locally resectable
Special discussion of
Metastatic disease in
neoadjuvant
disease? medically
chemotherapy,
No operable patient? No
intraoperative
radiation therapy
Yes

Yes G

Significantly
Adjuvant
obstructing, Surgical chemotherapy,
bleeding, or resection surveillance
perforated tumor?

Yes

No

Multidisciplinary discussion Consider palliative

E Special cases: isolated liver and/or resection,
diversion, stenting,
F
lung metastases
or radiotherapy

Algorithm 66.1
66  Colon Cancer 259

References lines for hereditary nonpolyposis colorectal cancer

(Lynch syndrome) and microsatellite instability. J
Natl Cancer Inst. 2004;96(4):261–8.
1. National Comprehensive Cancer Network (NCCN).
4. Slentz K, Senagore A, Hibbert J, Mazier WP, Talbott
NCCN clinical practice guidelines in oncology: colon
TM.  Can preoperative and postoperative CEA pre-
cancer. Version 2.2017. Accessed at www.nccn.org/
dict survival after colon cancer resection? Am Surg.
professionals/physician_gls/PDF/colon.pdf on 7 Aug
1994;60(7):528–31.
2017.
5. Rosen SA, Buell JF, Yoshida A, Kazsuba S, Hurst R,
2. Vasen HF, Watson P, Mecklin JP, Lynch HT.  New
Michelassi F, Millis JM, Posner MC. Initial presenta-
clinical criteria for hereditary nonpolyposis
tion with stage IV colorectal cancer: how aggressive
colorectal cancer (HNPCC, Lynch syndrome) pro-
should we be? Arch Surg. 2000;135(5):530–4.
posed by the International Collaborative group on
6. Pfannschmidt J, Dienemann H, Hoffmann H. Surgical
HNPCC. Gastroenterology. 1999;116(6):1453–6.
resection of pulmonary metastases from colorectal
3. Umar A, Boland CR, Terdiman JP, Syngal S, Chapelle
cancer: a systematic review of published series. Ann
AD, Rüschoff J, Fishel R, Lindor NM, Burgart LJ,
Thorac Surg. 2007;84(1):324–38.
Hamelin R, Hamilton SR.  Revised Bethesda guide-
 Part IX
Rectum and Anus
 Rectal Prolapse
67
Quinton Morrow Hatch and Eric K. Johnson

Algorithmic Approach maximum conservative measures are undertaken.

Surgeons, therefore, are often called upon to take
Rectal prolapse (procidentia) is defined as full-­ care of these patients.
thickness intussusception of the rectum through Unfortunately, no consensus exists as to the
the anus [1]. It is a secondary disorder in adults, optimal management of rectal prolapse. This lack
generally arising from chronic pelvic dysfunction of unanimity has resulted in the development and
due to laxity in the muscles of the pelvic floor and adoption of a number of surgical endeavors, none
anal canal, an abnormally deep pouch of Douglas, of which has proven absolute superiority over the
and a lack of normal rectal fixation [2–7]. At others. This very fact has led to discordant prac-
times, these abnormalities are of congenital deri- tice patterns and some degree of confusion, par-
vation; however, in most cases, the weakened ticularly for providers who do not routinely see
pelvic floor is caused by old age, multiparity, these patients. This chapter will attempt to guide
large birth weight of vaginally delivered babies, the surgeon through the appropriate rectal pro-
prior pelvic surgery, increased body mass index, lapse workup and provide clarity in operative
chronic straining, chronic diarrhea, or chronic decision-making (Fig. 1).
constipation [2, 8–11]. Unfortunately, the pro-
lapse itself results in a self-perpetuating cycle of A. Patients with prolapse usually describe a rub-
worsening pelvic floor weakening as the chronic bery mass that protrudes from the anus. Some
stretch on the sphincters and nerves continuously have described it as feeling like a “hard-­boiled
exacerbates the problem [11]. As a result of this egg.” It is more pronounced with Valsalva and
vicious cycle, full-thickness rectal prolapse rarely in fact may spontaneously reduce between
resolves spontaneously, even in cases where bowel movements. Most patients will describe
some level of fecal soiling, bleeding, pelvic
discomfort, and altered bowel habits (consti-
Q. M. Hatch pation, diarrhea, incomplete evacuation) [11–
Department of Surgery, Madigan Army Medical
Center, Tacoma, WA, USA 15]. On physical exam, full-thickness rectal
prolapse must be differentiated from internal
E. K. Johnson (*)
Cleveland Clinic Foundation, Cleveland, hemorrhoids, which may also prolapse to an
OH, USA impressive degree. Prolapse will display either
Department of Surgery, Division of Colorectal concentric folds or will be completely smooth
Surgery, Hillcrest Hospital, Mayfield Heights, circumferentially. Hemorrhoids, in contrast,
OH, USA will always appear as radially oriented col-

© Springer Nature Switzerland AG 2019 263

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_67
264
umns. An additional point of differentiation is
that hemorrhoids rarely prolapse greater than
5 cm, whereas rectal prolapses routinely do so
[8]. While it is possible to have a patient dem-
onstrate rectal prolapse in the lateral decubitus
position, the most consistent way of evaluat-
ing the degree of rectal prolapse is to have
a patient sit on a toilet or squat over a towel
and then perform a Valsalva maneuver. A
digital rectal exam is important, as it will rule
out any masses that may be acting as a lead
point. It will also give a general sense as to the
function of the pelvic muscles of defecation
(sphincter, puborectalis). In-office testing of
the anal wink and/or bulbocavernosus reflex
is not required but can help the surgeon esti-
mate the likelihood of restoring continence
after surgical repair. Those with impaired
reflexes signifying nerve dysfunction may be
less likely to recover continence fully after
surgery. It is important to inspect the visible
rectal mucosa and establish whether or not the
rectum is reducible.
B. Tissue prolapsing through the anus is often
quite concerning to both patients and clini-
cians. In most cases, however, it is not an
acute matter, as the lax sphincter complex
and weak pelvic floor inherently provide
some degree of protection against acute incar-
ceration. Nevertheless, incarceration and
strangulation may occur, and delay in surgi-
cal intervention will result in grave conse-
quences for the patient [8].
If acutely incarcerated or strangulated rectum
is encountered, the appropriate surgical interven-
tion is a perineal proctectomy or Altemeier pro-
cedure. This procedure involves the full-thickness
excision of the rectum and, at times, a portion of
the sigmoid colon followed by a coloanal or low
colorectal anastomosis. In some cases of appar-
ent incarceration, application of sugar to the pro-
lapse may result in osmotic effect, reduction of
swelling, and the ability to reduce the prolapse—
Turning an acute scenario into an elective one.
C. While a large, strangulated rectal prolapse is
likely the most dramatic presentation, the
Q. M. Hatch and E. K. Johnson
majority of patients present with a chronic,
reducible, prolapse with healthy-appearing
mucosa. In such cases, sufficient time exists
for additional workup and patient counsel-
ing. Patients should be reassured that pro-
lapse is not dangerous, and people with
small, minimally symptomatic prolapse do
not require an operation.
Rectal prolapse may be thought of as a pelvic
hernia. As with hernias of the abdominal wall, the
natural tendency is to progress with time. Surgery
is therefore indicated (though not mandatory)
even in relatively mild cases. An assessment of
the patient’s overall health and ability to tolerate
an operation must be taken into account when
making a decision as to whether or not to offer
surgery. While there is nuance and subjective
interpretation involved in this assessment, it
stands to reason that patients with exceedingly
poor performance status who have mild proci-
dentia may not benefit from an operation of any
type. Such patients should be advised to optimize
their bowel habits with fiber and hydration.
Pelvic floor physical therapy and biofeedback
may treat the underlying etiology and in doing so
improve defecatory function [16–18].
D. Patients who are deemed operative candi-
dates should undergo further evaluation to
guide operative decision-making. The ratio-
nale behind this is that rectal prolapse is
rarely an isolated disorder but rather a mani-
festation of global pelvic floor herniation.
Cystoceles, enteroceles, rectoceles, sig-
moidoceles, or vaginal vault prolapses are
frequent cooccurrences and may necessitate
complex pelvic floor reconstruction in com-
bination with urogynecology. Dynamic pel-
vic floor imaging evaluates for such anatomic
abnormalities. Both cinedefecography and
dynamic pelvic magnetic resonance imaging
(MRI) are adequate radiographic studies.
The benefit of MRI is that it is noninvasive;
however, it does not allow the patient to
assume the normal sitting position (unless
the institution has a sitting MRI) that pro-
motes complete evacuation of stool. These
67  Rectal Prolapse
studies will affect the management strategy
in up to 40% of cases [19].
Prior to pursuing an operative procedure to
correct a prolapse in a patient with chronic con-
stipation, it is also important to rule out func-
tional obstruction as the underlying etiology. A
sitz marker study will assess the function of the
colon and rule out colonic inertia, while dynamic
pelvic floor imaging and anorectal manometry
will assess for obstructed defecation. A positive
finding on any of these studies will provide some
understanding of the ultimate causation of the
procidentia, but as already suggested, nonopera-
tive optimization of these abnormalities likely
will not correct the prolapse itself. In fact, the
prolapse will only serve to exacerbate the diffi-
culty with any of these processes and often must
be corrected prior to engaging in effective pelvic
floor physical therapy.
If desired, the anatomic construct and function
of the anal sphincter itself may be assessed with
anal ultrasound or electromyographic studies.
These tests are rarely utilized in practice, as clini-
cally relevant sphincter dysfunction is likely
exacerbated by the prolapse itself. The prolapse
must therefore be surgically corrected before the
true sphincter function may be accurately
assessed or effectively treated.
Complete prolapse is associated with a four-
fold increase in relative risk of colorectal malig-
nancy [20]. It is therefore wise practice to evaluate
for luminal lesions prior to planning any colorec-
tal operation in a patient who has not been recently
screened. It is unlikely that there is a causal rela-
tionship between the two disease processes
beyond the fact that they both occur in older
patients; however, the correlation highlights the
necessity of thorough and thoughtful evaluation.
E. As a general rule in treating difficult disor-
ders, the number of described treatments is
inversely proportional to the efficacy of any
one. This certainly holds true in cases of
procidentia, as multiple operations have
been described. In most cases, the proce-
dures rely on the fundamental principles of
prolapse repair, which are rectal fixation to
265
the sacrum and/or resection or plication of
redundant bowel [2, 5, 7, 11].
Two broad categories of approach and repair
exist: abdominal and perineal. Despite multiple
studies, including several randomized controlled
trials, no approach or procedure has shown supe-
riority, with recurrence rates ranging anywhere
from 0 to 50%, depending on the series [2, 11, 21,
22]. The recently published PROSPER trial,
which randomized patients to either suture recto-
pexy, resection rectopexy, Delorme, or Altemeier,
suggested a 10-year recurrence rate of approxi-
mately 40%, with no difference between proce-
dures [22].
F. Despite a lack of evidence, dogma holds that
perineal procedures have a higher recurrence
rate. The benefit, however, is that they spare
the patient an abdominal operation. Perineal
proctosigmoidectomy (Altemeier) has there-
fore become the procedure of choice for frail,
elderly patients suffering from rectal pro-
lapse. This procedure involves a circumferen-
tial, full-thickness incision just above the
dentate line, pulling through of redundant
rectum and sigmoid colon, resection of the
redundant segment, and a coloanal anastomo-
sis. Unfortunately, some of what is saved by
sparing abdominal surgery is lost in func-
tional morbidity, as proctectomy often results
in high rates of incontinence, soilage, and
urgency due to loss of the normal rectal resor-
vior [2, 11, 21, 23, 24]. Alternative perineal
options are the mucosal sleeve resection
(Delorme) and prosthetic anal encirclement
(Thiersch). These latter two procedures have
limited use in true full-thickness rectal pro-
lapse in the modern era.
G. Abdominal procedures are more often
selected in young, fit patients who are bet-
ter able to tolerate an abdominal operation.
While this approach has not produced a
definitive benefit in terms of recurrence or
functional outcomes in randomized con-
trolled trials, the prevailing sentiment is
that the abdominal approach is superior in
both regards.
266
Abdominal approaches to rectal prolapse
repair include suture rectopexy, resection recto-
pexy, posterior mesh rectopexy, and ventral mesh
rectopexy. There is considerable variation in the
technical aspects of each. Furthermore, any one
of them can be performed using laparoscopic or
robotic-assisted platforms. Suffice it to say that
the premise of each is to reduce the prolapse and
anchor it to the sacral promontory (except per-
haps in ventral mesh rectopexy, where the mech-
anism providing success is debated). In the case
of resection rectopexy, the fixation is combined
with resection of the sigmoid colon. A common
morbidity among these procedures is worsening
constipation [2, 11]. Advocates of resection rec-
topexy argue that constipation is reduced by
resecting the sigmoid colon. This assertion has
not consistently held true in the literature,
although most series do show some postoperative
improvement in constipation from baseline [2,
11]. There is an increasing trend toward ventral
mesh rectopexy, as a recent large series has
Q. M. Hatch and E. K. Johnson
shown significant improvement from baseline
constipation (48–16%) [25]. Whether or not this
holds true as our experience with ventral mesh
rectopexy increases is yet to be determined.
There does not appear to be a long-term differ-
ence in outcomes between minimally invasive
and open approaches, although avoidance of an
abdominal incision results in faster overall recov-
ery and earlier discharge [26].
H. There is no specific need for any follow-up
beyond routine postoperative care.
Nevertheless, it is critical to reemphasize the
importance of maintaining optimal bowel
habits. This includes a high-fiber diet (25–35
grams of soluble fiber a day) and 64  oz of
water a day. Fiber supplements such as psyl-
lium often help to achieve the goal of soft,
bulky stools that do not require straining.
Patients with obstructed defecation should be
referred for pelvic floor physical therapy and
biofeedback [16–18].
67  Rectal Prolapse 267

A History and Physical:

prolapsing tissue with
concentric folds on valsalva

Incarcerated
Reducible
or
strangulated

B C

Functional
evaluation:

Perineal Table –Defecography

–Consider Sitz
D
proctectomy sugar
(Altmeier) markers
–Consider
manometry
–Consider EMG

High-risk Low-risk
patient patient

F G

Observation Prosthetic Perineal Abdominal

with PRN anal prolapse prolapse repair:
manual encirclement repair:
reduction (Thiersch) –Suture
–Altemeier rectopexy
–Delorme –Resection
rectopexy
–Posterior mesh
rectopexy
–Ventral mesh
rectopexy

Algorithm 67.1
268 Q. M. Hatch and E. K. Johnson

References 15. Kim D, Tsang C, Wong W, et  al. Complete rectal

prolapse: evolution of management and results. Dis
Colon Rectum. 1999;42(4):460–6.
1. Jacobs L, Lin Y, Orkin B. The best operation for rectal
16. Ternent C, Bastawrous A, Morin N, et  al. Practice
prolapse. Surg Clin North Am. 1997;77:49–70.
parameters for the evaluation and management of
2. Madiba T, Baig M, Wexner S. Surgical management
constipation. Dis Colon Rectum. 2007;50:2013.
of rectal prolapse. Arch Surg. 2005;140:63–73.
17. Jorge J, Habr-Gama A, Wexner SD.  Biofeedback

3. Broden B, Snellman B.  Procidentia of the rectum
therapy in the colon and rectal practice. Appl
studied with cineradiography: a contribution to
Psychophysiol Biofeedback. 2003;28:47–61.
the discussion of causative mechanism. Dis Colon
18. Khaikin M, Wexner S.  Treatment strategies in

Rectum. 1968;11:330–47.
obstructed defecation and fecal incontinence. World
4. Roig J, Buch E, Alo´s R, et al. Anorectal function in
J Gastroenterol. 2006;12(20):3168–73.
patients with complete rectal prolapse: differences
19. Harvey C, Halligan S, Bartram C, et  al. Evacuation
between continent and incontinent individuals. Rev
proctography: a prospective study of diagnostic and
Esp Enferm Dig. 1998;90:794–805.
therapeutic effects. Radiology. 1999;211:223–37.
5. Kuijpers H. Treatment of complete rectal prolapse: to
20. Rashid Z, Basson M.  Association of rectal pro-

narrow, to wrap, to suspend, to fix, to encircle, to pli-
lapse with colorectal cancer surgery. Surgery.
cate or to resect? World J Surg. 1992;16:826–30.
1996;119:51–5.
6. Nicholls R. Rectal prolapse and the solitary ulcer syn-
21. Deen K, Grant E, Billingham C, et  al. Abdominal
drome. Ann Ital Chir. 1994;65:157–62.
resection rectopexy with pelvic floor repair ver-
7. Yakut M, Kaymakciioglu N, Simsek A, et al. Surgical
sus perineal rectosigmoidectomy and pelvic floor
treatment of rectal prolapse: a retrospective analysis
repair for full thickness rectal prolapse. Br J Surg.
of 94 cases. Int Surg. 1998;83:53–5.
1994;81(2):302–4.
8. Stein E, Stein DE.  Rectal procidentia: diagnosis
22. Senapati A, Gray RG, Middleton LJ, et al. PROSPER:
and management. Gastrointest Endosc Clin N Am.
a randomised comparison of surgical treatments for
2006;16:189–201.
rectal prolapse. Color Dis. 2013;15(7):858–68.
9. Marceau C, Parc Y, Debroux E, et al. Complete rectal
23. Johansen O, Wexner S, Daniel L, et al. Perineal rec-
prolapse in young patients: psychiatric disease a risk
tosigmoidectomy in the elderly. Dis Colon Rectum.
factor of poor outcome. Color Dis. 2005;7:360.
1993;36:767–72.
10. Mellgren A, Bremmer S, Johansson C, et  al.

24. Yoshioka K, Ogunbiyi O, Keighley M.  Pouch peri-
Defecography. Results of investigations in 2,816
neal rectosigmoidectomy gives better functional
patients. Dis Colon Rectum. 1994;37:1133.
results than conventional rectosigmoidectomy in
11. Hatch Q, Steele S.  Rectal prolapse and intussuscep-
elderly patients with rectal prolapse. Br J Surg.
tion. Gastroenterol Clin N Am. 2013;42:837–61.
1998;85:1525–6.
12. Hiltunen K, Matikainen M, Auvinen O, et al. Clinical
25. Consten EC, van Iersel JJ, Verheijen PM, et al. Long-­
and manometric evaluation of anal sphincter func-
term outcome after laparoscopic ventral mesh rec-
tion in patients with rectal prolapse. Am J Surg.
topexy: an observational study of 919 consecutive
1986;151:489.
patients. Ann Surg. 2015;262(5):742–7.
13.
Keighley M, Fielding J, Alexander-Williams
26. Kellokumpu I, Virozen J, Scheinin T.  Laparoscopic
J.  Results of Marlex mesh abdominal rectopexy for
repair of rectal prolapse: a prospective study evaluat-
rectal prolapse in 100 consecutive patients. Br J Surg.
ing surgical outcome and changes in symptoms and
1983;70:229.
bowel function. Surg Endosc. 2000;14:634–40.
14. Madoff R, Mellgren A.  One hundred years of rectal
prolapse surgery. Dis Colon Rectum. 1999;42:441.
 Solitary Rectal Ulcer Syndrome
John Kuckelman and Eric K. Johnson
Algorithmic Approach
Solitary rectal ulcer syndrome (SRUS) often
confused with colitis cystica profunda, rectal
neoplasia, or inflammatory bowel disease/procti-
tis is a rare benign disorder of defecation that can
cause significant distress for those affected.
There is a relative paucity of literature associated
with SRUS with the majority of the published
articles being limited to descriptive analysis and
case reports. Approximately 1  in 100,000 indi-
viduals per year will suffer from SRUS with
similar incidences in both female and male pop-
ulations with a slight dominance in women.
Diagnosis is usually in the third or fourth decade
of life although certain pediatric and geriatric
populations are also at higher risk [1]. The
pathophysiology of SRUS is poorly understood,
although there are several prevailing factors that
seem to be consistently associated. Most patients
display a dyssynergia between contraction of the
pelvic floor muscles and defecation causing high
J. Kuckelman
Department of General Surgery, Madigan Army
Medical Center, Tacoma, WA, USA
Uniformed Services University of the Health
Sciences, Bethesda, MD, USA
E. K. Johnson (*)
Cleveland Clinic Foundation, Cleveland, OH, USA
Department of Surgery, Division of Colorectal Surgery,
Hillcrest Hospital, Mayfield Heights, OH, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_68
68
rectal pressures resulting in a relative ischemia
of the mucosa while creating shearing of the rec-
tum against the pelvic floor muscles, namely the
puborectalis muscle. This phenomenon ulti-
mately results in repeated mucosal damage and
the formation of one or multiple (polypoid)
ulcers [2, 3].
In this chapter, we will present key findings
that will aid in correctly identifying SRUS and
provide a stepwise approach on how best to con-
servatively manage these patients. Unfortunately,
conservative management fails in approximately
one third of patients who require surgical inter-
vention for resolution. There are no official
guidelines regarding the surgical management of
these patients. As such, there have been many
surgical options developed overtime [4]. We
review the benefits and drawbacks to these vari-
ous approaches in hopes of providing a helpful
reference for surgeons who are called on to man-
age SRUS.
A. A complete history and physical exam in
the office is perhaps the single most impor-
tant step in determining if a patient has
SRUS.  Rectal ulcers can be due to vari-
ous etiologies (see B). The clinician should
attempt to elicit any and all underlying eti-
ologies at the initial patient encounter. The
focus of treatment should be on rectifying or
­optimizing the primary issue. Resolution of
the rectal ulcer will often follow.
269
270
The most common complaint is rectal bleed-
ing and/or a mucous discharge associated with a
feeling of incomplete evacuation. However, it is
important to realize that a quarter of patients will
present without any symptoms at all with rectal
ulcer being discovered on a screening exam or
colonoscopy or during the workup for rectal
bleeding or tenesmus [1, 4]. On physical exam,
the surgeon may see blood or mucous discharge
at the anus. Digital rectal exam may reveal muco-
sal disruption. Most SRUSs have been reported
to be found on the anterior wall at various lengths
from the anal margin up to 10 cm [5, 6]. A rectal
ulcer may also be directly visualized in the office
using anoscopy or proctosigmoidoscopy. If a rec-
tal ulcer is identified, it should be evaluated with
further studies to ensure a diagnosis of SRUS.
B. Patients with rectal ulcer should be screened
for history of inflammatory bowel disease—
Specifically ulcerative colitis and immuno-
suppressive disorders such as HIV/AIDS as
opportunistic viral infections may cause rec-
tal ulceration. These causes should be man-
aged with primary treatment being targeted at
the underlying cause [7]. The relationship of
rectal ulcer to rectal prolapse is a matter of
some debate as some view them as synony-
mous and related diagnoses, while others
view them as two separate entities.
Intussusception of the rectum may create an
ischemic environment that predisposes the
rectal mucosa to ulceration. In the presence of
prolapse, patients should be questioned about
or asked to demonstrate how they reduce their
prolapsed rectum as digital reduction may
cause ulceration through repeated trauma to
the area [8, 9]. Rectal prolapse identified in
the setting of SRUS should be repaired
(options discussed elsewhere). Circumstances
causing repeated trauma to the rectum (such
as anal-receptive intercourse) should be
avoided. Patients with history of vascular dis-
ease may be predisposed to ulceration at
Sudeck’s point, and treatment should be
aimed at optimizing blood flow to this area
[7]. Finally, all patients with a visualized rec-
tal ulcer should be questioned for any signs or
J. Kuckelman and E. K. Johnson
risk factors for rectal cancer. These examples
are independent ailments to SRUS and should
be managed separately from the algorithm
shown in Fig. 1. Several have devoted chap-
ters in this book.
C. The diagnosis of SRUS is often delayed due
to the large differential diagnosis for rectal
bleeding, as well as the need to rule out other
primary causes such as rectal cancer.
Performing a colonoscopy with biopsies of
normal and abnormal mucosa is crucial to
making the diagnosis of SRUS, as histologi-
cal analysis can confirm the diagnosis.
Solitary rectal ulcer syndrome may be dis-
covered to be a misleading name on endo-
scopic analysis, as there is a high variability
in the appearance of SRUS ranging from
simple mucosal erythema to a chronic-
appearing ulcer with nodular edges and a
white or sloughing base [1, 10]. Further, up
to one third of patients may have a polypoid
lesion with multiple ulcers present [1]. Once
biopsies are obtained, histological analysis
showing no evidence of malignancy with
obliterated lamina propria and hypertrophy
of the muscular layer with regenerative
changes of the crypts is diagnostic of SRUS
[1, 10, 11].
Dynamic imaging may play a vital role in
understanding the cause of SRUS, and it should
be performed prior to operative intervention to
help aid in preoperative planning. Defecography
either using fluoroscopy or magnetic resonance
imaging (MRI) may show a lack of coordination
between the involuntary pelvic floor muscles and
the external anal sphincter [12, 13]. Often, an
internal rectal intussusception will be seen with-
out evidence of full-thickness rectal prolapse.
These studies can aid both in supporting the diag-
nosis and in determining which intervention is
needed. Finally, endorectal ultrasound (ERUS)
has been shown to evaluate both ulcer depth and
the external and internal sphincter muscles. There
is some evidence that sphincter thickness on
ERUS correlates to internal rectal ­intussusception
leading to SRUS; and this information may guide
operative planning as well [14].
68  Solitary Rectal Ulcer Syndrome
D. Once benign SRUS has been confirmed, con-
servative management should be the first line
of treatment. On rare occasions, symptoms
may be so severe that early operative inter-
vention may be warranted; however, every
attempt at conservative management should
be made. The mainstay of conservative man-
agement includes patient education focusing
on behavioral modification. Patients should
understand the benefits of healthy stooling
habits including high-fiber diets, regular toi-
leting, and avoidance of straining. Bulking
agents and stool softeners may be added to
accomplish these goals. These modifications
are highly effective in asymptomatic or
mildly symptomatic patients.
Medical therapy can be used to aid in healing
and quell symptomatic patients. Topical agents
such as sucralfate or mesalamine may be adminis-
tered via enema and in some cases have been found
beneficial for acute management. Little evidence
exists to support long-term efficacy [1, 15, 16].
E. In patients who continue to experience symp-
toms without resolution of SRUS, the next
step should be biofeedback and pelvic floor
physical therapy. These methods target pelvic
floor behaviors to specifically reprogram
autonomic pathways associated with defeca-
tion. This effectively corrects dyssynergy and
prevents straining in the majority of patients.
Objective evidence suggests that biofeedback
therapy provides the best chance for patients
with SRUS with 50–75% of patients having
complete resolution of their ulcer and associ-
ated symptoms [3, 17, 18].
If conservative management fails, surgical
intervention remains an option. In fact, up to one
third of patients will require surgical interven-
tion. [1] There are multiple approaches that have
described that we will review. However, due to
the variability in  location, size, and potential
pathophysiology coupled with the relative rarity
of the disease, there is no one favored surgical
approach to SRUS, and each patient should be
treated based on findings discussed in A and C.
271
F. As this is a benign condition, the primary
goals of surgery are to manage the patient’s
symptoms while keeping the bowel in conti-
nuity. For patients without any evidence of
intussusception, a local repair should be
attempted. Depending on size and location of
the ulcer, transanal excision may be attempted
down to the muscular layer. Ulcers located
higher in the rectum may be amendable to
local excision using a transanal minimally
invasive approach (TAMIS) [19]. Other strat-
egies for local therapy have been described
using sclerotherapy. Direct therapies such as
serial application of argon beam coagulation
as well as fibrin glue have also been cited in
the literature [20]. Primary repair with suture
closure using healthy surrounding redundant
mucosa has been described, but these local
therapies usually provide short-term symp-
tomatic relief without significant long-term
benefits [4, 5]. These local therapies, although
described, typically have poor outcomes and
may even worsen the size and depth of the
ulcer; thus, they are generally not recom-
mended. If there is evidence of a hypertonic
or thickened sphincter muscle, injection of
botulinum toxin may relax the sphincter com-
plex and allow healing of the ulcer [21].
Although it has been described, division of
the puborectalis muscle is a particularly mor-
bid operation resulting in high rates of incon-
tinence and is not generally recommended
[22]. Overall, these surgical approaches may
provide some short-term relief, but they are
often not durable, and recurrence is common
[23, 24].
G. When there is either clinical or radiographic
evidence of full thickness or internal rectal
prolapse, then surgical repair of this disorder
should be considered first. Rectopexy with or
without the use of mesh using either an open
or laparoscopic abdominal approach is the
procedure of choice for these patients, as it
directly addresses the most likely attributed
pathophysiology. This approach will be effec-
tive and possible in either scenario and is sup-
ported by the largest amount of evidence,
with 55–83% of patients having symptomatic
272
improvement [22, 24, 25]. The decision to
perform a perineal proctectomy (Altemeier
procedure) will depend on the severity of the
prolapse (not applicable to internal intussus-
ception), the fitness of the patient for surgery,
as well as the depth of the ulcer. Ulcers
extending into muscular layers on ERUS
should be resected with proctectomy or trans-
anal excision if possible [26]. In some severe,
persistent, or recurrent cases, a low anterior
resection with coloanal anastomosis/recon-
struction can be effective. It should be noted
that this is a radical option associated with
significant morbidity and should be used only
as a last resort.
. In the case that all other treatments, conser-
H recurrence and frustration for both the
vative and surgical, have been exhausted,
J. Kuckelman and E. K. Johnson
fecal diversion should be discussed with the
patient. This may be done as a temporizing
measure or as a permanent solution in will-
ing patients. This is typically accomplished
with the formation of an end colostomy
which may only be required for a matter of
months. Endoscopic evidence of complete
healing should be obtained prior to consider-
ation of a restorative procedure. It is impor-
tant to consider the most likely etiology for
the disorder and to employ a strategy to cor-
rect it as a cornerstone in the patient’s treat-
ment plan. As mentioned earlier, any plan
that addresses the ulcer without attention to
the underlying cause will typically result in
patient and surgeon.
68  Solitary Rectal Ulcer Syndrome 273

History and Physical

Bleeding/Mucous
Discharge
Constipation
A Tenesmus/Straining
Digital rectal exam
Anoscopy
Proctosigmoidoscopy

-Colonoscopy with biopsies -

C Barium enema -Defecography
-
Manometry/Electromyograph
y -Rectal ultrasound

B -Cancer
-Prolapse -
Infectious -
Separate Algorithms Ulcerative colitis
-Ischemic colitis -
Retained foreign
body

Benign solitary
Conservative management
Rectal ulcer

D
-Patient education -
Behavior modification
Severe symptoms -High fiber, bulking -
Failure
Sulcralfate enema -
Topical steroids -
E Bio
Sulfasalazine

feedback

Failure

No
intussusception Intussusception

G
F
Surgical repair of
Local repair
prolapse

Failure

Sclerotherapy Botulinum toxin Local excision

Fecal diversion H
TAMIS Transanal

End colostomy

Algorithm 68.1
274 J. Kuckelman and E. K. Johnson

References 15. Zargar SA, Khuroo MS, Mahajan R.  Sucralfate

retention enemas in solitary rectal ulcer. Dis Colon
Rectum. 1991;34(6):455–7.
1. Zhu QC, et al. Solitary rectal ulcer syndrome: clinical
16. Aad G, et  al. Combined measurement of the Higgs
features, pathophysiology, diagnosis and treatment
boson mass in pp collisions at sqrt[s]=7 and 8 TeV
strategies. World J Gastroenterol. 2014;20(3):738–44.
with the ATLAS and CMS experiments. Phys Rev
2. Morio O, et al. Anorectal physiology in solitary ulcer
Lett. 2015;114(19):191803.
syndrome: a case-matched series. Dis Colon Rectum.
17. Rao SS, et  al. ANMS-ESNM position paper and

2005;48(10):1917–22.
consensus guidelines on biofeedback therapy for
3. Rao SS, et  al. Pathophysiology and role of biofeed-
anorectal disorders. Neurogastroenterol Motil.
back therapy in solitary rectal ulcer syndrome. Am J
2015;27(5):594–609.
Gastroenterol. 2006;101(3):613–8.
18. Vaizey CJ, Roy AJ, Kamm MA. Prospective evalua-
4. Bulut T, et  al. Solitary rectal ulcer syndrome:
tion of the treatment of solitary rectal ulcer syndrome
exploring possible management options. Int Surg.
with biofeedback. Gut. 1997;41(6):817–20.
2011;96(1):45–50.
19. Walega P, Kenig J, Richter P.  Transanal endoscopic
5. Niv Y, Bat L.  Solitary rectal ulcer syndrome--clin-
microsurgery combined with endoscopic posterior
ical, endoscopic, and histological spectrum. Am J
mesorectum resection in the treatment of patients with
Gastroenterol. 1986;81(6):486–91.
T1 rectal cancer - 3-year results. Wideochir Inne Tech
6. Vaizey CJ, et al. Solitary rectal ulcer syndrome. Br J
Maloinwazyjne. 2014;9(1):40–5.
Surg. 1998;85(12):1617–23.
20. Somani SK, et  al. Healing of a bleeding solitary

7. Tjandra JJ, et al. Clinical and pathologic factors asso-
rectal ulcer with multiple sessions of argon plasma.
ciated with delayed diagnosis in solitary rectal ulcer
Gastrointest Endosc. 2010;71(3):578–82.
syndrome. Dis Colon Rectum. 1993;36(2):146–53.
21. Keshtgar AS, et al. Botulinum toxin, a new treatment
8. Tjandra JJ, et al. Clinical conundrum of solitary rectal
modality for chronic idiopathic constipation in chil-
ulcer. Dis Colon Rectum. 1992;35(3):227–34.
dren: long-term follow-up of a double-blind random-
9. Mackle EJ, Parks TG.  The pathogenesis and patho-
ized trial. J Pediatr Surg. 2007;42(4):672–80.
physiology of rectal prolapse and solitary rectal ulcer
22. Sitzler PJ, et  al. Long-term clinical outcome of sur-
syndrome. Clin Gastroenterol. 1986;15(4):985–1002.
gery for solitary rectal ulcer syndrome. Br J Surg.
10. Chiang JM, Changchien CR, Chen JR.  Solitary rec-
1998;85(9):1246–50.
tal ulcer syndrome: an endoscopic and histological
23. Choi HJ, et al. Clinical presentation and surgical out-
presentation and literature review. Int J Color Dis.
come in patients with solitary rectal ulcer syndrome.
2006;21(4):348–56.
Surg Innov. 2005;12(4):307–13.
11. Madigan MR, Morson BC. Solitary ulcer of the rec-
24. Ihnat P, et  al. Novel combined approach in the

tum. Gut. 1969;10(11):871–81.
management of non-healing solitary rectal ulcer
12. Mahieu PH. Barium enema and defaecography in the
syndrome  - laparoscopic resection rectopexy and
diagnosis and evaluation of the solitary rectal ulcer
transanal endoscopic microsurgery. Wideochir Inne
syndrome. Int J Color Dis. 1986;1(2):85–90.
Tech Maloinwazyjne. 2015;10(2):295–8.
13. Goei R, Baeten C, Arends JW.  Solitary rectal ulcer
25. Tweedie DJ, Varma JS. Long-term outcome of lapa-
syndrome: findings at barium enema study and defe-
roscopic mesh rectopexy for solitary rectal ulcer syn-
cography. Radiology. 1988;168(2):303–6.
drome. Color Dis. 2005;7(2):151–5.
14. Marshall M, et  al. Predictive value of internal anal
26. Laubert T, et al. Obstructive defecation syndrome: 19
sphincter thickness for diagnosis of rectal intus-
years of experience with laparoscopic resection recto-
susception in patients with solitary rectal ulcer syn-
pexy. Tech Coloproctol. 2013;17(3):307–14.
drome. Br J Surg. 2002;89(10):1281–5.
 Rectal Cancer
Quinton Morrow Hatch and Eric K. Johnson
Algorithmic Approach
Rectal cancer has historically been associated
with substantial morbidity and mortality [1, 2].
This applies not only to the primary disease pro-
cess but to the treatment as well. An abdomino-
perineal excision may result in a number of
perineal wound issues in addition to the obligate
permanent stoma. Sphincter-sparing low anterior
resection routinely results in a significant change
in defecatory function that can even be disabling
[3]. Additionally, either operation or the adminis-
tration of radiotherapy may result in sexual dys-
function, urinary dysfunction, or chronic pelvic
pain [4]. Fortunately, these risks are at least in
part counterbalanced by vastly improved onco-
logic outcomes over the past century [1, 5–8].
Key breakthroughs allowing for these improve-
ments include surgical innovation (abdomino-
perineal excision, total mesorectal excision) in
addition to significant advances in chemotherapy
and radiation therapy. Consequently, the manage-
Q. M. Hatch
Department of Surgery, Madigan Army Medical
Center, Tacoma, WA, USA
E. K. Johnson (*)
Cleveland Clinic Foundation,
Cleveland, OH, USA
Department of Surgery, Division of Colorectal
Surgery, Hillcrest Hospital, Mayfield Heights,
OH, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_69
69
ment of rectal cancer has become a complex mul-
tidisciplinary endeavor for which a simple linear
algorithm does not exist. This chapter will
attempt to distill the nuances and complexity of
rectal cancer into a straightforward flow.
A. There is no “classic” presentation of rectal
cancer. This is in part due to relatively poor
screening rates, reluctance of patients to seek
early care for anorectal complaints, and the
lack of specificity regarding visceral pain and
gastrointestinal hemorrhage [9, 10]. Despite
the nonspecific nature of presenting com-
plaints, it is important to maintain a high
index of suspicion for malignancy as up to
two thirds of colorectal cancers will manifest
vague abdominal complaints or anemia prior
to diagnosis [10].
Because of the myriad presentations, we may
come in contact with rectal cancer patients at any
given point in the diagnostic evaluation. As such,
we must be able to pick up efficiently at any point
in the algorithm. Regardless of the point at which
we as surgeons encounter the patient, the history
and physical examination is a requisite first step
before further discussion can ensue. We must
rapidly decide if this is an acute presentation that
needs an immediate intervention (such as severe
bleeding or complete obstruction) or if there is
time for a thorough evaluation before initiating
treatment. A complete large bowel obstruction
275
276
secondary to a rectal cancer is a surgical emer-
gency necessitating colonic decompression. In
most cases, this may be accomplished with a loop
sigmoid colostomy or perhaps a rectosigmoid
stent. It is important to bear in mind that while an
endoluminal stent is an attractive tool as a bridge
to surgery, it must be proximal enough that the
distal extension does not impinge on the anorec-
tal ring [11]. In rare instances, the colon proximal
to the tumor may be compromised or perforated,
in which case a subtotal colectomy with end ile-
ostomy and a mucous fistula may be warranted.
Bleeding may be corrected by resuscitation and
stabilization, followed by radiation therapy [12].
An emergent proctectomy is rarely required,
although for hemodynamically compromising
bleeding refractory to endovascular treatments it
may be necessary.
The majority of rectal cancer referrals will
exhibit subacute or chronic symptoms such as
changes in bowel habits (74%), vague abdominal
pain (67%), or anemia (41%) [10]. These patients
are afforded the luxury of a complete evaluation.
A thorough assessment of preoperative sphincter
function must be performed. This is a critical step
as a restorative proctectomy will be particularly
morbid for a patient with questionable continence
at baseline. It is also essential to identify the
patient’s preoperative sexual function (erections,
ejaculation in men). The abdominal exam should
assess for distention or organomegaly which
would suggest obstruction or metastatic disease,
respectively. A digital rectal examination should
be performed, with particular attention paid to
the distance between the anal sphincter complex
and the distal aspect of the tumor, evidence of
tumor fixation, and anterior-posterior location.
Patients with tumor abutting the anal sphincters
should be counseled that an abdominoperineal
excision will likely be required. Anterior tumors
are inherently more likely to abut or invade adja-
cent structures such as the posterior vagina,
uterus, prostate, urethra, and bladder (in men or
women post-hysterectomy) as all reside within
millimeters of the anterior rectum.
An essential adjunct to the physical exam is
rigid proctoscopy in the office. This critical step
should be performed during surgical workup of
Q. M. Hatch and E. K. Johnson
any rectal cancer or left-sided colon cancer (as
flexible endoscopy is inaccurate when assessing
distance from the anus). This procedure allows
for precise tumor localization in relation to the
anus and thereby helps predict our ability to per-
form a sphincter-sparing surgery.
B. In cases where a minimally symptomatic or
asymptomatic rectal polyp is identified on
endoscopy, it is essential that the staging
workup not be compromised by poor diag-
nostic decision-making. Small sessile polyps
or pedunculated polyps may undergo polyp-
ectomy with near impunity, insofar as the
endoscopist feels confident of the ability to
perform complete polypectomy. However, in
cases where a complete endoscopic excision
cannot be ensured (as in large, sessile pol-
yps), it is best to proceed with staging prior to
tissue biopsy. Unfortunately, it is all too com-
mon that a large rectal polyp is “excised” and
returns with adenocarcinoma and a positive
margin. This sequence of events severely
compromises the ability of the surgeon to
adequately stage the cancer, as the tissue
planes are edematous and inflamed. This
error in judgment diminishes our ability to
accurately differentiate the T-stage. This is a
critical mistake as preoperative staging deter-
mines which patients will derive benefit from
neoadjuvant therapy. Regardless of the spe-
cific management of the polyp, endoscopic
“tattooing” adjacent to the lesion is essential,
as it allows for accurate identification later in
the workup.
C. Once the diagnosis of adenocarcinoma is
confirmed, the depth of invasion must be
assessed. In the case of cancer limited to a
polyp with a clear (>2 mm) resection margin,
endoscopic surveillance is appropriate [13,
14]. Notable exceptions are cases in which
the cancer is poorly differentiated, there is
lymphovascular invasion, or if the cells are
mucinous or signet-ring cell type [15]. If the
margin is in question or there is invasion into
the rectal wall proper, a complete staging
workup is required. If the diagnosis remains
in question after biopsies of a large polyp, a
69  Rectal Cancer
transanal excision or submucosal lift and
snare polypectomy may be performed [16].
D. Further evaluation after diagnosis of inva-
sive cancer necessitates assessment of
tumor markers (carcinoembryonic antigen
(CEA) and complete blood count (CBC)).
Liver function tests are routinely obtained
but are not essential. Clinical tumor, node,
metastasis (TNM) staging is entirely reliant
on imaging modalities. Depth of invasion
(T-stage) and regional nodal involvement
may be assessed using either transrectal
ultrasound (TRUS) or magnetic resonance
imaging (MRI) using a specific rectal cancer
protocol. Neither modality has proven supe-
riority, although TRUS may more accurately
stage early (T1 vs T2) tumors, while MR
may more accurately determine the tumor’s
distance from the sphincters and the distance
to the mesorectal fascia (threatened circum-
ferential resection margin) [17]. Computed
tomography of the chest, abdomen, and pel-
vis with oral and intravenous contrast is used
to rule out distant metastases. In cases where
axial imaging shows suspicious lesions
without definitive evidence of metastasis,
positron emission tomography (PET) scan-
ning may be helpful.
E. The staging of rectal cancer can be seen
in Tables 69.1 and 69.2 [18]. Stage 1 dis-
ease encompasses T1 and T2 lesions with-
out nodal involvement. For small (<3  cm,
<40% luminal circumference) T1 cancers,
a full-­thickness transanal excision is likely
appropriate [19]. This approach is limited
by the technical ability to perform the pro-
cedure without compromising the rectal
lumen. Additionally, patients must be thor-
oughly counseled that transanal excision
does not include lymphadenectomy, which
is essential for pathologic staging. This is a
critical point as up to 12% of T1 lesions may
have regional nodal involvement that would
upstage them to stage III [20]. Risk factors
for regional node involvement include poor
differentiation, lymphovascular invasion, or
adverse histologic subsets such as “muci-
nous” or signet-­ring cell type [15, 20]. If the
277
Table 69.1  American Joint Committee on cancer TNM
definitions for rectal cancer
Primary Tumor
Tx Primary tumor cannot be assessed
T0 No evidence of primary tumor
Tis Carcinoma in situ: intraepithelial or invasion of
lamina propria
T1 Tumor invades submucosa
T2 Tumor invades muscularis propria
T3 Tumor invades through the muscularis propria
into pericolorectal tissues
T4a Tumor penetrates to the surface of the visceral
peritoneum
T4b Tumor directly invades or is adherent to other
organs or structures
Regional Nodes
Nx Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1a Metastasis in one regional lymph node
N1b Metastasis in 2–3 regional lymph nodes
N1c Tumor deposit(s) in the subserosa, mesentery,
or nonperitonealized pericolic or perirectal
tissues without regional nodal metastasis
N2a Metastasis in 4–6 regional lymph nodes
N2b Metastasis in 7 or more regional lymph nodes
Distant Metastases
M0 No distant metastasis
M1a Metastasis confined to one organ or site (for
example, liver, lung, ovary,
nonregional node)
M1b Metastases in more than one organ/site or the
peritoneum
final pathology returns with these adverse
risk factors or if the pathologic T-stage is
higher than was previously expected, fur-
ther treatment is needed. While a number
of approved algorithms exist, we recom-
mend completion proctectomy with total
mesorectal excision (low anterior resection
versus abdominoperineal excision, depend-
ing on the distance from the sphincter), fol-
lowed by observation (if pathologic stage
returns T1-2, N0) or a combination of sys-
temic chemotherapy and chemoradiation
(if pathologic stage returns T3-4 or N1-2)
(Table  69.3). An alternative algorithm is to
proceed to chemoradiation (Table 69.3) fol-
lowed by either observation (if complete
response), completion proctectomy, or com-
bination chemotherapy [21].
278 Q. M. Hatch and E. K. Johnson

Table 69.2  American Joint Committee on cancer TNM Table 69.3  Definitions and types of combination che-
stages for rectal cancer motherapy and chemoradiation within NCCN guidelines
Stage T N M Chemoradiation: 50·4 Gy in 28 fractions of 1·8 Gy
0 Tis N0 M0 plus radiosensitizing radiation and interval surgery
1 T1 N0 M0 Capecitabine plus radiation
T2 N0 M0 Infusional 5-FU plus radiation
IIA T3 N0 M0 Bolus 5-FU/Leucovorin plus radiation
IIB T4a N0 M0 Short-course radiation: 25 Gy in five fractions of 5 Gy
IIC T4b N0 M0 and surgery within 7 days
IIIA T1–T2 N1/N1c M0 Combination chemotherapy
T1 N2a M0 FOLFOX
IIIB T3–T4a N1/N1c M0 CAPEOX
T2–T3 N2a M0 5-FU/Leucovorin or capecitabine
T1–T2 N2b M0
IIIC T4a N2a M0 Cancer Network (NCCN) recommends
T3–T4a N2b M0
against short-­course radiation in cases of T4
T4b N1–N2 M0
disease. Definitive proctectomy should follow
IVA Any T Any N M1a
IVB Any T Any N M1b radiation therapy by 4–12 weeks, though most
are waiting 8–12  weeks prior to undertaking
resection [24].
T2 lesions have a 22% risk of regional nodal
involvement [20]. Accordingly, T2 lesions should Interestingly, the benefit of neoadjuvant radia-
be managed with proctectomy/total mesorectal tion/chemoradiation in terms of local control has
excision (TME) (depending on sphincter involve- not definitively resulted in improved mortality in
ment and preoperative sphincter function. most cases [7, 8]. This is likely explained by our
Assuming complete excision and an adequate ongoing relative inability to control distant recur-
mesorectal dissection, additional chemotherapy rence, which remains roughly 30% for stage II
or radiation is not required. and III rectal cancer [8, 22]. These high rates of
metastatic recurrence have led many to adopt
F. Stage II rectal cancer includes T3 and T4
neoadjuvant combination chemotherapy fol-
tumors. It represents the formal stage at lowed by chemoradiation and ultimately defini-
which neoadjuvant therapy is recommended. tive resection. This algorithm front-loads
A number of studies have observed a benefit systemic therapy to treat subclinical metastases.
in local recurrence when surgery is preceded Further studies are needed to determine if this
by radiation therapy. The debate between the treatment strategy will yield improved survival.
benefit of short-course radiation (Table 69.3) It is important to understand that the current
and long-course radiation (in conjunction standard is to recommend preoperative chemora-
with radiosensitizing chemotherapy) rages diotherapy in extraperitoneal rectal adenocarci-
on, as randomized controlled trials have not nomas that are T3 or greater or node positive
shown oncologic superiority of either strategy. based on preoperative staging. This recommen-
However, the secondary outcome of negative dation may be called into question in the future
circumferential resection margin (CRM) seems based on outcomes as they relate to tumors with
to be improved with long-course chemora- and without threatened circumferential resection
diation, and this endpoint has been associated margin on MRI pending the results of ongoing
with lower local recurrence rates [22, 23]. It is studies [25].
this fact which has led many centers to pref-
erentially select chemoradiation in cases with G. Stage III rectal cancer is defined as regional
a threatened CRM by MRI.  In keeping with node-positive disease. Treatment algorithms
this concept, the National Comprehensive are the same as those for stage II disease, with
69  Rectal Cancer
neoadjuvant radiation conferring a 52% (9%
versus 19%) decrease in  local recurrence
when compared to resection alone. Long-­
term follow-up to the landmark Dutch ran-
domized controlled trial also suggests a
survival benefit in patients with stage III rec-
tal cancer treated with neoadjuvant radiation
(50% versus 40% at 10 years) [26].
H. The definition of resectable disease is in flux
and may change depending on tumor response
to neoadjuvant chemotherapy. Suffice it to
say that the old paradigm suggesting M1 dis-
ease is unresectable is no longer valid.
Patients with resectable liver metastases and
potentially extrahepatic metastases may be
considered resectable for cure [27]. In fact,
patients undergoing R0 resection of liver
metastases have 5-year survival as high as
71% in some series [28]. Clearly, this deci-
sion requires multidisciplinary discussion
with surgeons who routinely evaluate these
organ systems. The decision-making strategy
regarding the order in which to proceed with
chemoradiation, combination chemotherapy,
and surgery in cases of metastatic disease is
beyond the scope of this chapter, but all are
valid first options depending on the specific
clinical scenario.
In the case of unresectable disease (either
locally unresectable or metastases), palliative
chemotherapy is an option in appropriately fit
patients who desire to extend life. In rare cir-
cumstances, a robust response to chemotherapy
may actually convert the disease burden from
unresectable to resectable. Hepatic artery infu-
sion of chemotherapy may act as an adjunct
[29]. In these cases, additional multidisciplinary
discussion is warranted. There is also the situ-
279
ation where a patient presents with oligometa-
static disease. Most would not recommend
chemoradiation followed by resection up front
but would instead recommend a strategy of
employing palliative chemotherapy followed by
restaging after an appropriate period of time—
typically 3  months. If the metastatic disease is
stable or improved, then many would encourage
standard chemoradiation followed by palliative
resection after an appropriate wait (8–12 weeks
after completion of radiotherapy). While resec-
tion is not curative, it will prevent the suffering
associated with a locally invasive tumor in the
pelvis. It is the authors’ preference to perform
an abdominoperineal resection in this setting.
This offers a single stage procedure allowing
the patient to resume life-lengthening chemo-
therapy as soon as possible.
I. Surveillance begins after treatment for cura-
tive intent. This should include office history
and physical every 3–6  months for 2  years,
then every 6  months for a total surveillance
period of 5 years. In cases of stage II–IV dis-
ease treated only with transanal excision, the
office exam should be accompanied by rigid
proctoscopy and either transrectal ultrasound
or rectal MRI. CEA levels should be obtained
in conjunction with all clinic visits. Computed
tomography of the chest, abdomen, and pelvis
with oral and intravenous (IV) contrast should
be obtained every 6 to 12 months for a total of
5  years. Colonoscopy should be performed
1 year after surgery. If an advanced adenoma
is found, another colonoscopy should be per-
formed a year later. If an advanced adenoma
is not found, colonoscopy should be per-
formed 3 years after the first and every 5 years
thereafter [21].
280 Q. M. Hatch and E. K. Johnson

History and physical:

A rectal polyp or mass
digital rectal exam
rigid proctoscopy

Minimally
Obstructed?
symptomatic

Pedunculated or Site marking (tattoo)

Fecal diversion Sessile ³ 2cm
sessile < 2cm TRUS or MRI rectal protocol
Stent

Polypectomy Rigid proctoscopy

site marking biopsy

Adenocarcinoma

C
Margin Margin positive Pathology uncertain
negative Adenocarcinoma
or unclear

CEA
CBC
LFT EMR
transanal
Surveillance excision

D Stage?
• TRUS
• MRI Rectum
• CT Chest, Abdomen,
Pelvis

Algorithm 69.1
69  Rectal Cancer 281

E I
F II III
G IV
H

T1 £1/3 luminal T2, large T1, high

circumference risk T1 Short course
Chemoradiation Chemotherapy
radiation (not T4) Resectable
metastases?
• Liver
• Lung
TME Transanal TME • Inguinal
excision nodes
Chemoradiation

Chemotherapy TME TME

High risk? T1 Sort course
Chemoradiation Chemotherapy
LVI radiation (not T4)
Poor differentiation
Mucinous
Signet ring
³T2
Chemotherapy
Chemoradiation TME Chemoradiation

I
Chemotherapy TME
Surveillance

Algorithm 69.1 (continued)

Interview Survey. Cancer Epidemiol Biomark Prev.

References
10. Alexiusdottir K, Moller P, Snaebjornsson P, et  al.
1. Miles WE.  A method of performing abdomino-
perineal excision for carcinoma of the rectum and
of the terminal portion of the pelvic colon. Lancet.
1908;172:1812–3.
2. Whipple A.  Complications associated with major
proctectomy. Ann Surg. 1932;95(6):916–22.
3. Guren MG, et  al. Quality of life and functional
outcome following anterior or abdominoperi-
neal resection for rectal cancer. Eur J Surg Oncol.
2005;31(7):735–42.
4. Eveno C, Lamblin A, Mariette C, Pocard M. Sexual
and urinary dysfunction after proctectomy for rectal
cancer. J Visc Surg. 2010;147(1):e21–30.
5. Heald RJ.  The mesorectum in rectal cancer surgery.
Br J Surg. 1982;69:613–6.
6. Cedermark B, Dahlberg M, Glimelius B, et al. Improved
survival with preoperative radiotherapy in resectable
rectal cancer. N Engl J Med. 1997;336:980–7.
7. Kapiteijn E, Marijnen CA, Nagtegaal ID, et  al.
Preoperative radiotherapy combined with total meso-
rectal excision for resectable rectal cancer. N Engl J
Med. 2001;345(9):638–46.
8. Sauer R, Becker H, Hohenberger W, et al. Preoperative
versus postoperative chemoradiotherapy for rectal
cancer. N Engl J Med. 2004;351(17):1731–40.
9. Shapiro J, Seeff L, Thompson T, et  al. Colorectal
cancer test use from the 2005 National Health
2008;17(7):1623–30.
Association of symptoms of colon cancer patients
with tumor location and TNM tumor stage. Scand J
Gastroenterol. 2012;47:795–801.
11. Watson AJ, Shanmugam V, Mackay I, et al. Outcomes
after placement of colorectal stents. Color Dis.
2005;7:70–3.
12. Chia D, Lu J, Zheng H, et  al. Efficacy of palliative
radiation therapy for symptomatic rectal cancer.
Radiother Oncol. 2016;121(2):258–61.
13. Haggitt RC, Glotzbach RE, Soffer EE, Wruble
LD. Prognostic factors in colorectal carcinomas aris-
ing in adenomas: implications for lesions removed
by endoscopic polypectomy. Gastroenterology. 1985
Aug;89(2):328–36.
14. Kudo S.  Endoscopic mucosal resection of flat and
depressed types of early colorectal cancer. Endoscopy.
1993;25(7):455–61.
15. Ramirez M, Schierling S, Papaconstantinou HT,
Thomas JS. Management of the malignant polyp. Clin
Colon Rectal Surg. 2008;21(4):286–90.
16. Ferlitsch M, Moss A, Hassan C.  Colorectal pol-
ypectomy and endoscopic mucosal resection
(EMR): European Society of Gastrointestinal
Endoscopy (ESGE) Clinical Guideline. Endoscopy.
2017;49(03):270–97.
17. Al-Sukhni E, Milot L, Fruitman M, et al. Diagnostic
accuracy of MRI for assessment of T category, lymph
node metastases, and circumferential resection mar-
gin involvement in patients with rectal cancer: a sys-
282
tematic review and metaanalysis. Ann Surg Oncol.
2012;19:2212–23.
18. Hari DM, Leung AM, Lee JH, et  al. AJCC Cancer
Staging Manual 7th edition criteria for colon cancer:
do the complex modifications improve prognostic
assessment? J Am Coll Surg. 2013;217(2):181–90.
19. Nascimbeni R, Burgart LJ, Nivatvongs S, Larson
DR.  Risk of lymph node metastasis in T1 carci-
noma of the colon and rectum. Dis Colon Rectum.
2002;45(2):200–6.
20. Saraste D, Gunnarsson U, Martin J. Predicting lymph
node metastases in early rectal cancer. Eur J Cancer.
2013;49(5):1104–8.
21. National Comprehensive Cancer Network. Rectal
cancer (Version 3.2017). https://www.nccn.org/pro-
fessionals/physician_gls/PDF/rectal.pdf. Accessed 25
July 2017.
22. Bujko K, Nowackib MP, Nasierowska-Guttmejer A,
et  al. Sphincter preservation following preoperative
radiotherapy for rectal cancer: report of a randomised
trial comparing short-term radiotherapy vs. conven-
tionally fractionated radiochemotherapy. Radiother
Oncol. 2004;72:15–24.
23. Nagtegaal I, Quirke P.  What is the role for the cir-
cumferential margin in the modern treatment of rectal
cancer? J Clin Oncol. 2008;26(2):303–12.
Q. M. Hatch and E. K. Johnson
24. Garcia-Aguilar J, Smith DD, Avila K, et al. Optimal
timing of surgery after chemoradiation for advanced
rectal cancer: preliminary results of a multicenter,
nonrandomized phase II prospective trial. Ann Surg.
2011;254(1):97–102.
25. Taylor F, Quirke P, Heald RJ, et al. Preoperative high-­
resolution magnetic resonance imaging can identify
good prognosis stage I, II, and III rectal cancer best
managed by surgery alone: a prospective, multicenter,
European study. Ann Surg. 2011;253:711–9.
26. van Gijn W, Marijnen C, Nagtegaal I, et  al.
Preoperative radiotherapy combined with total meso-
rectal excision for resectable rectal cancer: 12-year
follow-up of the multicentre, randomised controlled
TME trial. Lancet Oncol. 2011;12:575–82.
27. Pawlik T, Schulick R, Choti M.  Expanding crite-
ria for resectability of colorectal liver metastases.
Oncologist. 2008;13(1):51–64.
28. Aloia TA, Vauthey JN, Loyer EM, et  al. Solitary
colorectal liver metastasis: resection determines out-
come. Arch Surg. 2006;141(5):460–6.
29. Kemeny N, Huitzil Melendez F, Capanu M, et  al.
Conversion to resectability using hepatic artery infu-
sion plus systemic chemotherapy for the treatment of
unresectable liver metastases from colorectal carci-
noma. J Clin Oncol. 2009;27(21):3465–71.
 Rectovaginal Fistula
70
John Kuckelman and Eric K. Johnson

Algorithmic Approach ment of these fistulas can be a significant

challenge for the consulted surgeon. There is a
Rectovaginal fistula is an inappropriate commu- relatively limited body of evidence that guides
nication between the rectum and the vaginal workup and treatment of these patients; however,
vault, most commonly caused by obstetrical the data that has been accumulated can effec-
trauma suffered during childbirth. Approximately tively guide clinically sound judgment and ulti-
1% of women who experience third- or fourth-­ mately successful resolution. The Clinical
degree perineal lacerations during vaginal birth Practice Guideline Committee of the American
will develop a rectovaginal fistula [1]. Midline Society of Colon and Rectal Surgeons has pro-
episiotomy has also been associated with rela- vided guidance based on the available evidence
tively high rates of fistula formation [2]. Incidence to help guide the physician in the surgical man-
is notably higher in developing countries with agement of rectovaginal fistulas [6]. This chapter
limited access to professional obstetric care and will attempt to provide a systematic approach to
sterility being contributing factors [3]. the patient with a rectovaginal fistula.
Inflammatory bowel disease, specifically Crohn’s
disease, is associated with rectovaginal fistula A. History and physical exam should be focused
with an incidence of 9–10% being reported [4, 5]. on symptoms as well as past medical and sur-
Infections after perineal repairs, complications gical history that would place the patient at
from low anterior resection, pelvic radiation, higher risk for fistula development. Symptoms
perianal or rectal abscess, and malignancies of can be influenced by the size and underlying
pelvic organs all carry a risk of rectovaginal fis- etiology. Patients may present with com-
tula development [6]. The discovery and treat- plaints of recurrent vaginal irritation, feculent
vaginal malodor, and passage of gas through-
J. Kuckelman out the vaginal canal. Passage of stool through
Department of General Surgery, Madigan Army the vagina may be present when the patient is
Medical Center, Tacoma, WA, USA experiencing loose or softer stools. Issues
Uniformed Services University of the Health with stooling urgency and symptoms of
Sciences, Bethesda, MD, USA incontinence may also be present if there is
E. K. Johnson (*) concomitant sphincter dysfunction. Personal
Cleveland Clinic Foundation, Cleveland, OH, USA history should focus on obstetrical history
Department of Surgery, Division of Colorectal elucidating number of vaginal births that
Surgery, Hillcrest Hospital, Mayfield Heights, required episiotomy and/or repair of
OH, USA

© Springer Nature Switzerland AG 2019 283

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_70
284
l­acerations. History of inflammatory bowel
disease, need for pelvic radiation, and any
other pelvic surgery histories should be eluci-
dated during the interview.
Physical exam that accurately locates recto-
vaginal fistulae can be very challenging but is
crucial to the decision-making process. Digital
rectal exam should focus on sphincter function
and may identify low fistulas with simple palpa-
tion. Speculum exam may identify stool in the
vagina. Direct visualization of a dimple or open-
ing may be seen on anoscopy and speculum
exam. Acute inflammation or vaginitis may be
present. Alternatively, placement of a tampon
with injection of methylene blue into the rectum
has also been described. After 1 h, the tampon is
removed, and blue discoloration confirms a rec-
tovaginal fistula.
An exam under anesthesia may be neces-
sary to make the diagnosis in more challenging
cases. Many methods of discovery have been
described. Beginning with positioning in the
lithotomy position, the vagina may be filled with
warm water and the rectum insufflated after the
placement of a proctoscope. Dual visualization
with a speculum exam may reveal the fistula
tract with evidence bubbles in the vaginal vault.
Other methods include a similar technique using
hydrogen peroxide. These methods provide the
benefit of discovering exact location of the fis-
tula which may ultimately be necessary if surgi-
cal repair is required.
B. Given the variable causes and presentations
of rectovaginal fistulae, the first step should
be determining whether the clinician is deal-
ing with an acute or an established fistula. In
the acute setting, definitive repair should be
postponed and the focus should be on optimal
management of the underlying cause. When
abscess or frank pelvic sepsis is present,
source control/drainage, resuscitation, and
antibiotic courses should be completed pri-
marily. In the case of Crohn’s disease, opti-
mal medical management should be the focus.
Metronidazole is the antibiotic of choice in
Crohn’s patients as it has been reliably shown
J. Kuckelman and E. K. Johnson
to decrease inflammation in this subset of
patients [7]. When malignancy is suspected,
appropriate workup and treatment should be
addressed first.
Management in the acute setting is not differ-
ent from other types of fistulae. Conservative
measures with a period of observation, sitz baths
and diet, and placement of a draining seton is
appropriate. Seton placement may aid in source
control, but importantly it will aid in the develop-
ment of a defined fibrotic tract, necessary for
eventual surgical repair.
C. Fistulae that are established, less than 5 mm
in width, low (just above dentate line or vagi-
nal fourchette), and simple (not involving
sphincter and not associated with Crohn’s)
may see spontaneous closure with conserva-
tive management [8]. There is no defined
period of observation that is appropriate, but
up to 50% may have complete resolution after
6–9  months—Though it may be difficult to
get many patients to wait this long [9]. The
authors would recommend a waiting period
of at least 12 weeks, ensuring adequate source
control, prior to attempting any surgical
repair. As mentioned above, watchful waiting
should also include patient education on the
benefits of a high fiber diet and sitz baths with
or without use of bulking agents.
When watchful waiting is unsuccessful, surgi-
cal treatment should be discussed. Further char-
acterization of the fistula is crucial to surgical
planning. If needed, this may be accomplished
using ancillary studies such as contrast enemas
and fistulography. Just as in the imaging of other
fistulas, pelvic MRI can help characterize the
location, tract, and evidence of additional fistulas
otherwise missed on physical exam [10].
Endorectal ultrasound with or without the instil-
ment of hydrogen peroxide can characterize the
fistula tract in addition to measuring the width of
the perineal body as well as the state of the anal
sphincter muscles [11, 12]. It is the authors’
experience that most fistulas can be localized by
simple exam under anesthesia allowing
70  Rectovaginal Fistula
d­ifferentiation between low and high fistulas
which are managed quite differently.
D. As previously mentioned, in patients who
have low, simple rectovaginal fistulas, con-
servative management may be attempted
prior to surgical intervention. However, when
operative repair is necessary, an endorectal
advancement flap is the preferred first surgi-
cal step. A repair on the rectal side is sup-
ported by the fact that the rectum is the
higher-pressure cavity and thus closure and
protection of the closure on the rectal side
have the best chance for long-term success.
This operation is accomplished through rais-
ing a partial thickness flap on the rectal side
of the fistula, closing the fistula primarily on
the rectal side and advancing the flap cau-
dally to the extent that healthy mucosa is cov-
ering the now closed fistula tract. The excess
distal mucosa is then excised. This operation
has the added advantage of anal sphincter
repair, when necessary with a sphinctero-
plasty. Success rates range from 78% to 100%
in patients who have simple fistulas due to
obstetrical injury [13–16]. These success
rates may drop to just below 50% in patients
who have Crohn’s disease or other complex
etiologies [14, 17–19]. Advancement flaps
have also been shown to have relatively high
rates of success in recurrence as well with
some studies reporting over 90% success in
cases where prior attempts have failed [15,
18, 20]. No studies have shown improved out-
comes with fecal diversion in conjunction
with endorectal advancement flaps [18, 20].
When fecal incontinence or sphincter dys-
function secondary to an anterior sphincter
defect is associated with rectovaginal fistula,
Tsang and colleagues showed that sphincter-
oplasty improves success rate with 84% of
women having successful repairs with sphinc-
teroplasty versus 33% in women who have
flaps created without sphincteroplasty [16].
Finally, continuous anal mucosal discharge
due to a flap that has been brought too low
over the anoderm is an avoidable complica-
tion of this operation. In cases when flap for-
285
mation is in danger of being created too low,
a reverse of the classic operation should be
performed cranially using the anoderm as the
flap [21].
E. If sphincter damage is extensive strictly due
to obstetrical trauma or prior abscess, then a
episioproctotomy may be beneficial. This
operation involves transperineal takedown of
the fistula tract and complete reconstruction
of the rectovaginal septum. Studies have
found that this operation results in high rates
of fistula closure as well as excellent func-
tional outcomes with appropriately selected
patients [22–25]. This approach is analogous
to a classically described sphincteroplasty for
fecal incontinence resulting from an anterior
sphincter defect. This approach is useful only
in low-lying rectovaginal fistulae. Anterior
sphincter disruption should be confirmed
based on physical exam and an imaging
modality—Typically endoanal ultrasound—
Prior to undertaking this procedure.
F. With recurrent rectovaginal fistulas or those
in complex situations such as those in patients
with prior radiation or Crohn’s disease, the
next best option is using tissue interposition
of either the gracilis muscle or the bulbocav-
ernosus (Martius flap). Studies of these meth-
ods are relatively limited to small retrospective
studies; however, the largest series available
evaluating 24 patients found the gracilis flap
to be successful in nearly 80% of patients
overall [26–28]. Similar results have been
shown for patients undergoing bulbocavern-
ousus flaps [29–31]. Studies completing these
operations in combination with fecal diver-
sion have shown the highest rates of success.
Unfortunately, for patients with Crohn’s dis-
ease, there is a wide range of reported success
from 30% to 100%. In Crohn’s disease related
fistulae, it is essential to have adequate medi-
cal control of disease locally. Any repair
undertaken in the setting of active Crohn’s-­
related inflammation will fail. Patients with
ongoing active Crohn’s disease related procti-
tis should be managed either nonoperatively
with a draining seton or via fecal diversion or
proctectomy based on severity of symptoms
286
and patient desire. If a gracilis or Martius flap
repair is being undertaken in the setting of a
recurrent fistula, it would be wise to perform
proximal fecal diversion prior to or as a part
of this procedure.
G. Patients are considered to have high recto-
vaginal fistulas if the vaginal opening of the
tract is near the cervix or vaginal cuff in the
setting of prior hysterectomy. High fistulas
can be very difficult to diagnose, but if they
are due to a benign etiology, it is typically
from a prior operation such as a hysterectomy
or proctectomy. In the setting of fistula for-
mation that is not associated with a colorectal
anastomosis, the first option is to perform a
fistula takedown through an abdominal
approach either using open or laparoscopic
technique. When the tissue planes are sepa-
rated and the tracts closed, interposition of
vascularized tissue, such as the omentum or
other biologic materials, can be placed
between the two tissues [32]. It is important
J. Kuckelman and E. K. Johnson
to debride the involved structures back to
healthy tissue prior to closure.
In some cases, repair of high fistulae may
require proctectomy with coloanal reconstruction.
If this is undertaken, the anastomosis should be
protected with a proximal stoma—typically a loop
ileostomy. These may be required for a patient
with complex causes for their rectovaginal fistula
to include prior radiation. Success in approxi-
mately 75% of patients has been reported for proc-
tectomy with coloanal anastamosis [33–35].
H. Rectovaginal fistulization resulting from
anastomotic leak may occur in up to 10% of
women who have a proctectomy with recon-
struction for any reason. This should be
treated with fecal diversion primarily as over
one third of patients may see resolution at
6  months [36]. If fecal diversion fails to
resolve the fistula, then previously discussed
options can be explored.
70  Rectovaginal Fistula 287

History and physical

-Vaginal malodor
-Fecal soiling
-Incontinence
-Vaginal passage of gas or stool
-Digital rectal exam
-Anoscopy
A. -Vaginal exam
-Exam under anesthesia

Observe
Small (5mm)
B. Acute Chronic
low
sitz baths
high fiber diet
C. simple

Ancillary studies
-Fistulography
Observe -Transrectal ultrasound
sitz baths -Pelvic MRI
High fiber diet
Treat underlying
cause

G.
Low
Draining seton High

No Abdominal approach
Sphincter sphincter
involved involvement
From colorectal
anastomosis
D. Fistula takedown

H.
E. Episioproctotomy Endorectal advancement
Observe Failure
flap w/wo sphincteroplasty
Sitz baths
High fiber diet
Treat underlying
cause Proctectomy
Recurrent
or
F. Complex
Seton

Reconstruction Fecal diversion

with muscle flap

Algorithm 70.1
288 J. Kuckelman and E. K. Johnson

References related rectovaginal fistula. J Gastrointest Surg.

2010;14(5):824–9.
20. Halverson AL, et  al. Repair of recurrent rectovagi-
1. Goldaber KG, et  al. Postpartum perineal morbid-
nal fistulas. Surgery. 2001;130(4):753–7. discussion
ity after fourth-degree perineal repair. Am J Obstet
757–8.
Gynecol. 1993;168(2):489–93.
21. Chew SS, Rieger NA.  Transperineal repair of

2. Homsi R, et  al. Episiotomy: risks of dehiscence
obstetric-­related anovaginal fistula. Aust N Z J Obstet
and rectovaginal fistula. Obstet Gynecol Surv.
Gynaecol. 2004;44(1):68–71.
1994;49(12):803–8.
22. Hull TL, et al. Multimedia article. Success of episio-
3. Wall LL, et  al. The obstetric vesicovaginal fistula:
proctotomy for cloaca and rectovaginal fistula. Dis
characteristics of 899 patients from Jos Nigeria. Am
Colon Rectum. 2007;50(1):97–101.
J Obstet Gynecol. 2004;190(4):1011–9.
23. Hull TL, et  al. Surgeons should not hesitate to per-
4. Radcliffe AG, et  al. Anovaginal and rectovagi-
form episioproctotomy for rectovaginal fistula sec-
nal fistulas in Crohn’s disease. Dis Colon Rectum.
ondary to cryptoglandular or obstetrical origin. Dis
1988;31(2):94–9.
Colon Rectum. 2011;54(1):54–9.
5. Das B, Snyder M. Rectovaginal Fistulae. Clin Colon
24. Khanduja KS, et  al. Reconstruction of rectovaginal
Rectal Surg. 2016;29(1):50–6.
fistula with sphincter disruption by combining rectal
6. Vogel JD, et  al. Clinical practice guideline for the
mucosal advancement flap and anal sphincteroplasty.
Management of Anorectal Abscess, Fistula-in-­
Dis Colon Rectum. 1999;42(11):1432–7.
Ano, and rectovaginal fistula. Dis Colon Rectum.
25. MacRae HM, et  al. Treatment of rectovaginal fistu-
2016;59(12):1117–33.
las that has failed previous repair attempts. Dis Colon
7. Nitzan O, et  al. Role of antibiotics for treatment of
Rectum. 1995;38(9):921–5.
inflammatory bowel disease. World J Gastroenterol.
26. Lefevre JH, et  al. Operative results and qual-

2016;22(3):1078–87.
ity of life after gracilis muscle transposition for
8. Rothenberger DA, Goldberg SM.  The manage-
recurrent rectovaginal fistula. Dis Colon Rectum.
ment of rectovaginal fistulae. Surg Clin North Am.
2009;52(7):1290–5.
1983;63(1):61–79.
27. Wexner SD, et al. Gracilis muscle interposition for the
9. Rahman MS, et  al. Surgical treatment of rectovagi-
treatment of rectourethral, rectovaginal, and pouch-­
nal fistula of obstetric origin: a review of 15 years’
vaginal fistulas: results in 53 patients. Ann Surg.
experience in a teaching hospital. J Obstet Gynaecol.
2008;248(1):39–43.
2003;23(6):607–10.
28. Hotouras A, et  al. Gracilis muscle interposition for
10. Sheedy SP, et al. MR imaging of perianal Crohn dis-
rectovaginal and anovaginal fistula repair: a system-
ease. Radiology. 2017;282(3):628–45.
atic literature review. Color Dis. 2015;17(2):104–10.
11. Sudol-Szopinska I, Jakubowski W, Szczepkowski

29. Pitel S, et al. Martius advancement flap for low rec-
M.  Contrast-enhanced endosonography for the
tovaginal fistula: short- and long-term results. Color
diagnosis of anal and anovaginal fistulas. J Clin
Dis. 2011;13(6):e112–5.
Ultrasound. 2002;30(3):145–50.
30. Songne K, et al. Treatment of anovaginal or rectovag-
1 2. Dwarkasing S, et  al. Anovaginal fistulas: evalu-
inal fistulas with modified Martius graft. Color Dis.
ation with endoanal MR imaging. Radiology.
2007;9(7):653–6.
2004;231(1):123–8.
31. Kniery KR, Johnson EK, Steele SR. Martius flap for
13. Lowry AC, et al. Repair of simple rectovaginal fistu-
repair of recurrent rectovaginal fistulas. Dis Colon
las. Influence of previous repairs. Dis Colon Rectum.
Rectum. 2015;58(12):1210.
1988;31(9):676–8.
32. van der Hagen SJ, et  al. Laparoscopic fistula exci-
14. Mazier WP, Senagore AJ, Schiesel EC.  Operative

sion and omentoplasty for high rectovaginal fistulas:
repair of anovaginal and rectovaginal fistulas. Dis
a prospective study of 40 patients. Int J Color Dis.
Colon Rectum. 1995;38(1):4–6.
2011;26(11):1463–7.
15. Sonoda LA, et al. Novel application of a fecal manage-
33. Nowacki MP.  Ten years of experience with Parks’
ment system for vaginal use in radiotherapy-­associated
coloanal sleeve anastomosis for the treatment of post-­
rectovaginal fistula. Palliat Med. 2013;27(1):91–3.
irradiation rectovaginal fistula. Eur J Surg Oncol.
16. Tsang CB, et al. Anal sphincter integrity and function
1991;17(6):563–6.
influences outcome in rectovaginal fistula repair. Dis
34. Patsouras D, Yassin NA, Phillips RK.  Clinical out-
Colon Rectum. 1998;41(9):1141–6.
comes of colo-anal pull-through procedure for com-
17. Mizrahi N, et  al. Endorectal advancement flap:

plex rectal conditions. Color Dis. 2014;16(4):253–8.
are there predictors of failure? Dis Colon Rectum.
35. Remzi FH, et al. Outcomes following Turnbull-Cutait
2002;45(12):1616–21.
abdominoperineal pull-through compared with colo-
18. Pinto RA, et al. Are there predictors of outcome fol-
anal anastomosis. Br J Surg. 2009;96(4):424–9.
lowing rectovaginal fistula repair? Dis Colon Rectum.
36. Kosugi C, et al. Rectovaginal fistulas after rectal can-
2010;53(9):1240–7.
cer surgery: incidence and operative repair by gluteal-­
19. El-Gazzaz G, et al. Analysis of function and predic-
fold flap repair. Surgery. 2005;137(3):329–36.
tors of failure in women undergoing repair of Crohn's
 Management of Hemorrhoids
Matthew Z. Wilson and Joseph R. Notaro
Algorithmic Approach
A. “Hemorrhoids” are a very common com-
plaint. Patients will relate varying symptoms
including rectal pain or pressure, prolapsing
tissue that reduces spontaneously or manu-
ally, difficulty maintaining hygiene (“seep-
age”), or general perineal discomfort.
Examination of the perineum includes a
visual inspection, digital rectal examination,
and anoscopy/rigid proctoscopy. Hemorrhoids
should be graded (I–IV), and other disease
processes such as abscess, fistula, or condy-
loma should be ruled out.
B. Classify hemorrhoids according to location.
Internal hemorrhoids are insensate and above
the anal verge. External hemorrhoids are dis-
tal to the anal verge and covered by squamous
epithelium. The former are responsible for
painless bleeding, whereas the latter for pain
and/or irritation.
C. Bleeding per rectum should not be primarily
ascribed to hemorrhoids without ruling out
other potential causes. Patients at low risk of
M. Z. Wilson (*)
Department of Surgery, Dartmouth Hitchcock
Medical Center, One Medical Center Drive,
Lebanon, NH, USA
e-mail: matthew.z.wilson@hitchcock.org
J. R. Notaro
Department of Surgery, Rutgers Robert Wood
Johnson Medical School, New Brunswick, NJ, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_71
71
colorectal malignancy may undergo office
flexible sigmoidoscopy and hemoccult test-
ing. Patients at higher risk (age, family his-
tory, genetic predisposition) should undergo
full colonoscopy.
After a trial of medical management,
patients should be reevaluated to assess for
symptomatic improvement. Patients who do
not improve should be considered for office-­
based treatments. Banding is the most effec-
tive and can be repeated. It is best to avoid
banding multiple internal hemorrhoids at the
same time, and patients should not be taking
aspirin or blood thinners at the time of the
procedure or for the following 7  days.
Sclerotherapy with 5% phenol in vegetable
oil and infrared coagulation can be useful in
patients who cannot be without anticoagula-
tion, though the efficacy is inferior to
banding.
D. External hemorrhoids may present with
thrombosis. This is exquisitely painful but
will resolve with time and nonsurgical man-
agement. In the early acute phase (24–72 h),
the clot may be excised under local anesthe-
sia in the office setting. After 96 h, the pain
has generally begun to reduce, and drainage
will be less effective. Erosion of clot through
the epithelium can occur in later stages, and
this should be excised under local anesthesia.
In the absence of thrombosis, excision of
external hemorrhoids should be avoided;
289
290
hygiene or local irritation or excoriation
concerns can be addressed with topical
­ stenosis, fissure, and even incontinence.
hydrocortisone, zinc-oxide-based cream, and
barrier gel or powder. Minimization of cof-
fee, spicy foods, hot showers, and harsh soaps
will help reduce the potential for irritation.
E. Surgical hemorrhoidectomy should only be
entertained when all other attempts at treat-
ment have failed due to the potentially severe
discomfort and protracted recovery period
M. Z. Wilson and J. R. Notaro
along with complications such as stricture,
Grade IV hemorrhoids are a surgical emer-
gency; use of hyaluronidase combined with
local anesthetic agents will allow reduction of
the prolapsed tissue; any external hemorrhoid
thrombosis can then be excised. Prolapsing
internal components can be banded.
Otherwise, excisional hemorrhoidectomy can
be performed in the operating room.
71  Management of Hemorrhoids 291

History: symptoms vary but frequently include (alone or in

A combination) bleeding, prolapsing tissue, pain, difficulty
maintaining hygiene, or general discomfort.

Exam: visual inspection, digital rectal examination, anoscopy and/or

proctoscopy looking for thrombosis or other disease processes
mistakenly ascribed to
“hemorrhoids”

B External
Internal or Internal
external

C
D Thrombosis? Bleeding
symptoms?
Yes

No
Endoscopy to
24–72 hrs, may Dietary modification
Excoriation and rule out
excise under local with increased fiber
induration may alternative
anesthesia to uptake, and avoidance
be treated with pathology
relieve symptoms. of straining with
topical therapy
defecation. May
>96 h, Abnormal Normal consider emollient or
supportive hydrocortisone
therapy suppositories for
Treat Symptoms symptomatic relief.
accordingly resolve
No improvement
Continue
conservative
therapy Consider office-based
Surgical hemorrhoidectomy should be reserved banding, sclerotherapy,
for patients with disease refractory to office or infrared coagulation
procedures, large external hemorrhoids, for grade I, II, or III
Continued symptoms
combined internal, and external hemorrhoids hemorrhoids
with grades III–IV prolapse. E

Excisional
hemorrhoidectomy
(open or closed)
useful for single
quadrant disease
Stapled hemorrhoidopexy (PPH)
useful for multiple quadrant
disease or circumferential
mucosal prolapse with minimal
external disease
Doppler-guided
hemorrhoidectomy/pexy,
particularly useful for
patients with predominant
symptoms of bleeding with
prolapsing hemorrhoids

Algorithm 71.1

Suggested Reading
Rivadeniera DE, et  al. Practice parameters for the man-
agement of hemorrhoids (Revised 2010). Dis Colon
Rectum. 2011;54:1059–64.
 Management of Anal Fissure
Matthew Z. Wilson and Kirsten Bass Wilkins
Algorithmic Approach
A. Patients with acute anal fissure present with
pain during and after defecation. They may
notice bleeding onto the toilet tissue.
Questions regarding bowel habits, specifi-
cally constipation or straining with defeca-
tion, will help to confirm the diagnosis. As
fissures can be exquisitely painful, it is
acceptable to do a limited perianal exam to
evaluate for other causes of anal pain such as
external thrombosed hemorrhoid or abscess.
Persistent pain despite medical therapy is a
reason for examination under anesthesia.
Treatment is targeted toward controlling
constipation, alleviating pain, and healing the
fissure. Fiber supplements and stool softeners
are crucial. Topical calcium channel com-
pounds or nitrates reduce spasm of the inter-
nal sphincter and encourage healing. Calcium
channel blockers (diltiazem or nifedipine) are
preferred due to lower incidence of head-
aches associated with their use. Systemic
absorption is minimal with topical use.
M. Z. Wilson (*)
Department of Surgery, Dartmouth Hitchcock
Medical Center, One Medical Center Drive,
Lebanon, NH, USA
e-mail: matthew.z.wilson@hitchcock.org
K. B. Wilkins
Department of Surgery, Rutgers Robert Wood
Johnson Medical School, New Brunswick, NJ, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_72
72
Emollient suppositories can help to soothe
inflamed tissue. Warm sitz baths and topical
lidocaine may also relieve pain.
Acetaminophen/nonsteroidal antiinflamma-
tory drugs (NSAIDS) are helpful.
B. Continue nonoperative treatment for 4 weeks
and reassess the patient. Patients with
improved symptoms may continue topical
therapy with fiber supplementation for an
additional 4  weeks with good results.
Persistent discomfort is an indication for
examination under anesthesia.
C. The purpose of an examination under anesthe-
sia is twofold: to determine whether the fis-
sure is typical or atypical and to render
appropriate therapy. Typical fissures are
located in the posterior midline in the majority
of cases. However, anterior midline fissures
and simultaneous anterior and posterior mid-
line fissures do occur. Atypical fissures are
located laterally in the anal canal. Multiple
simultaneous fissures are also considered
atypical. The presence of an atypical fissure
should prompt careful evaluation for Crohn’s,
tuberculosis, syphilis, human immunodefi-
ciency virus (HIV), or hematologic malig-
nancy. Regardless of location, the edges of the
fissure should be biopsied for pathological
evaluation.
Surgical treatment of fissure consists of
two approaches: botulinum toxin injection
and sphincterotomy. Botulinum toxin injec-
293
294
tion into the internal sphincter has similar
rates of healing compared to topical therapy
as a first line and shows slightly increased
rates of healing as a second line after a
course of topical therapy. Lateral internal
sphincterotomy is the standard treatment for
chronic fissures and is associated with higher
healing rates compared to any other therapy
but carries a risk of incontinence. Recently
“tailored” sphincterotomy, where the muscle
M. Z. Wilson and K. B. Wilkins
is divided into the proximal extent of the fis-
sure rather than into the dentate line as with
traditional sphincterotomy, has been advo-
cated. Healing rates with this approach are
slightly less than traditional sphincterotomy,
but the risk of incontinence is also less.
Patients with significant anal stenosis are
good candidates for sphincterotomy. Patients
with patulous anal tone may benefit from
flap procedures.
72  Management of Anal Fissure 295

A History: Primary symptom is anal pain with defecation. Pain

may last for several hours, +/– bleeding. The patient will often
relate a history of constipation and straining to defecate.

Exam: Acute fissure manifests as a linear tear in the anal mucosa, often just inside the anal verge.
Chronic fissures may have a hypertrophied papilla proximally, exposed internal sphincter at the
base and a skin tag distally. Frequently acute fissure will be exquisitely painful, and it is acceptable
to defer DRE until pain has improved. Persistent pain is an indication for exam under anesthesia.

First line therapy: Sitz baths (10 min in warm water) two times or more daily, psyllium fiber
supplementation (with plenty of water), and topical nitrates or calcium channel blockers. Emollient
suppositories may provide relief.

Continue topical Symptoms Symptoms

therapy for additional 4 RE-exam Examination under
weeks, long-term fiber in 4 weeks anesthesia
supplementation/diet
improve persist
modification

No Yes Treat internal sphincter

Typical
Biopsy with botox vs lateral
Fissure?
internal sphincterotomy
after assessing anal
tone. Debride edges of
lesion and biopsy.

Treat underlying cause

of fissure
Long-term fiber
supplementation/diet
modification

Algorithm 72.1

Suggested Reading
Stewart DB, et  al. Clinical practice guideline for the
management of anal fissures. Dis Colon and Rectum.
2017;60:7–14.
 Management of Perianal Abscess
and Fistula-in-Ano
Matthew Z. Wilson and Bertram T. Chinn
Algorithmic Approach
A. Perianal and ischiorectal abscesses are sig-
nificantly more common than intersphincteric
or supralevator abscesses. They are generally
amenable to drainage under local anesthesia
with a generous elliptical incision or catheter
drainage with a stab incision and a 10–14fr
Pezzer catheter. Incisions should be made as
close to the anal verge as possible without
injuring the sphincter complex; this will pro-
vide the shortest fistula tract possible should
one develop. Packing is generally unneces-
sary as it may impede drainage. Packing for
hemostasis is rarely required as a topical
hemostatic agent such as ferric subsulfate is
usually adequate to control raw surface bleed-
B. Following treatment of the acute abscess,
ing. Sitz baths twice daily will provide symp-
tomatic relief.
Due to pain, intersphincteric and suprale-
vator abscesses may best be addressed in the
operating room, likely with general anesthe-
sia. Transrectal drainage is advised for an
M. Z. Wilson (*)
Department of Surgery, Dartmouth Hitchcock
Medical Center, One Medical Center Drive,
Lebanon, NH, USA
e-mail: matthew.z.wilson@hitchcock.org
B. T. Chinn
Department of Colon and Rectal Surgery, Rutgers
Robert Wood Johnson Medical School,
Edison, NJ, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_73
73
intersphincteric abscess or a supralevator
abscess due to a proximal extension of an
intersphincteric abscess. Drainage of these
abscesses through the ischiorectal fossa may
result in a transsphincteric or suprasphinc-
teric fistula.
A supralevator abscess due to a proximal
extension of a transsphincteric abscess should
be drained from the ischiorectal fossa as tran-
srectal drainage may result in an extrasphinc-
teric fistula.
Drainage of a supralevator abscess not due
to a crypto-glandular source (e.g., abdominal
or pelvic) generally requires treatment of the
underlying source and possible operative or
interventional radiology (IR) drainage.
some patients will have persistent drainage
from the site of the previous abscess. The
acute inflammation will be resolved, but a
small amount of granulation tissue may be
present in the area, likely representing the
external opening of a fistula-in-ano. Probing
of these openings in the office setting is dis-
couraged due to significant patient discom-
fort and the possibility of disrupting the tract.
If evidence of abscess is present, this should
be treated again with drainage.
Examination under anesthesia is the best
way to delineate the course of a fistula tract
and determine appropriate treatment. Inability
to identify the internal opening in any fi­ stula
297
298
is reason to obtain a pelvic MRI to identify
the tract. Although most causes of an abscess/
fistula are due to a crypto-glandular source,
a full examination of the perianal skin, anal
canal, and rectum should be performed to
evaluate for alternative causes of abscess and
fistula such as malignancy or Crohn’s disease.
C. Superficial fistulae, particularly those in the
posterior midline, are amenable to fistulot-
omy; this is the most effective treatment for
fistulae. Complex fistulae are generally best
approached in a staged manner, primarily to
avoid major sphincter disruption. Placement
of a seton will allow the tract to drain and
reduce local inflammation. Frequently, the
presence of a seton will allow the fistula to be
M. Z. Wilson and B. T. Chinn
come more superficial, allowing for subse-
quent fistulotomy. If fistulotomy is not possi-
ble, then consider more advanced procedures
with the understanding that none are as effec-
tive as fistulotomy. These procedures include
ligation of intersphincteric fistula tract
(LIFT), plug procedures, and endorectal
advancement flaps. Setons can remain in
place indefinitely to control sepsis if a defini-
tive procedure cannot be performed or the
fistula is due to Crohn’s disease. Fistulotomy
in Crohn’s-associated fistulae can result in
prolonged or nonhealing wounds. In these
cases, evaluation by a surgeon with experi-
ence in treating inflammatory bowel disease
(IBD) is warranted.
73  Management of Perianal Abscess and Fistula-in-Ano 299

H&P: Varies, but may include fever, pain, tenderness,

erythema, draining sinus, a perianal mass or relatively normal
appearance but with deep seated pelvic pain.

Perianal or ischiorectal abscess will almost Intersphincteric and supralevator abscesses

always have a tender, fluctuant mass. A may have few external findings. It will
frequently have fluctuance on digital rectal
examination but pain may preclude DRE.

Incise and drain under local anesthesia with DRE, anoscopy or rigid sigmoidoscopy may
elliptical incision or stab incision with Pezzer be confirmatory and reveal internal opening.
(10–14Fr) catheter. Consider CT scan if diagnosis is unclear or
supralevator abscess suspected.

Antibiotics should be limited to patients with Exam under anesthesia (EUA) and
severe cellulitis, immune suppression, or transrectal drainage for intersphincteric
concomitant systemic illness (e.g., DM) abscess. Drainage of supralevator abscess
based upon etiology.

Fistula-in-ano

B Will often present as

persistent drainage
after treatment of
acute abscess

If fistula is intersphincteric
Simple Complex with diminished sphincter
Perform fistulotomy for EUA integrity, extrasphincteric,
superficial or
transsphincteric, proceed
intersphincteric fistula with
with a staged procedure.
minimal sphincter involved.

If tract is clearly identified with both internal and external openings,

If tract is unclear, consider place a non-cutting seton (silastic vessel loop or large (#1)
MRI fistulagram to polyester suture) to promote drainage and avoid recurrent abscess.
identify the tract.

After period of 6–16 weeks of seton in place, repeat EUA. If a

candidate, may perform a fistulotomy. Otherwise consider LIFT
D procedure, endorectal advancement flap, porcine or PTFE
plug procedures.

Algorithm 73.1

Suggested Reading
Steele SR, et al. Practice parameters for the management
of perianal abscess and Fistula-in-Ano. Dis Colon
Rectum. 2011;54:1465–74.
 Management of Anal Cancer
74
Matthew Z. Wilson and Kirsten Bass Wilkins

Algorithmic Approach sarily indicated at this time as continued

A. Patients with anal cancer present with various D. If a complete response is observed, perform
anorectal complaints. Symptoms vary, and
there are multiple risk factors. Detailed peri-
anal exam is necessary to delineate the extent
of the disease. Examination under anesthesia
may be required to obtain adequate tissue
biopsy and determine the location of the lesion.
B. The location of the lesion is imperative with
regard to treatment. T1N0M0 well-­ val (1  month). If the lesion appears stable,
differentiated anal margin lesions may be
locally excised with 1 cm margins. All other
stages of both anal canal and anal margin can-
cer should be evaluated for treatment with
chemoradiotherapy. Human immunodefi-
ciency virus (HIV) testing is important, as E. After confirmation of persistent or progres-
confirmation of appropriate CD4 counts is
necessary prior to initiation of therapy. CD4
counts <200 cells/mL are associated with
higher treatment toxicity.
C. Approximately 12 weeks after completion of
therapy, the patient should be reexamined to
determine the response. Biopsy is not neces-
M. Z. Wilson (*)
Department of Surgery, Dartmouth Hitchcock
Medical Center, One Medical Center Drive,
Lebanon, NH, USA
e-mail: matthew.z.wilson@hitchcock.org
K. B. Wilkins
Department of Surgery, Rutgers Robert Wood
Johnson Medical School, New Brunswick, NJ, USA
response to treatment is frequently observed.
digital rectal examination (DRE), anoscopy,
and inguinal node palpation at the prescribed
intervals. Annual imaging with computed
tomography (CT) of the chest, abdomen,
and pelvis is recommended to survey for
occult metastasis. Evidence of persistent
disease should be followed at a shorter inter-
then continue to observe and reevaluate at
3 months. At 6 months, any suspicious lesion
should be biopsied. If disease progresses
despite therapy, then biopsy the lesion and
repeat the staging workup.
sive disease after primary treatment, local
disease (including inguinal nodes) can be
treated with APR (with groin dissection if
necessary). Patients with metastatic disease
should be considered for systemic chemo-
therapy. Patients who develop metastatic dis-
ease after salvage abdominoperineal resection
(APR) for recurrent or persistent local disease
should also be considered for systemic che-
motherapy. Inguinal node recurrence (with-
out evidence of anal disease) can be treated
with groin dissection and radiation if previ-
ous radiation field did not include the groin.
Following surgery, surveillance continues as
prescribed above.

© Springer Nature Switzerland AG 2019 301

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_74
302 M. Z. Wilson and K. B. Wilkins

A
History: Patients will complain of a slow growing perianal mass, frequently mistaken for a “hemorrhoid”,
may be in the anal canal itself. Pain, puritis, and/or bleeding are common. Inguinal lymphadenopathy
may be present. Risk factors include history of other HPV-related disease, previous STD or HIV,
cigarette smoking, anoreceptive intercourse, history of solid organ transplant or
other immunosuppression.

Office exam: Anorectal examination and evaluation of inguinal nodes. Determine size of primary lesion
and location in relation to anal verge. May biopsy in office setting if patient will tolerate.
Gynecologic exam needed for female patients. Exam under anesthesia (if required): Biopsy of suspicious
lesions through anoscope or sigmoidoscope. Determine size of primary lesion.

Anal margin (anal verge

Anal canal B to 5cm circumference of
Location perianal skin)
of lesion

Obtain CT chest,
T2 or greater, any N, any M
abdomen and pelvis,
T/N/M
and pelvic MRI. PET-CT
stage
may be obtained. HIV
testing Primary treatment is T1N0M0
should be done. chemotherapy with
Local Well differentiated
radiation

Wide local excision

Evaluate 12 weeks after
completion of therapy Complete response
with exam + DRE and
anoscopy DRE and anoscopy q3-6mos
for 2yrs then q6mo up to 5
C years then annually. Annual
imaging for 5 years.
APR + groin dissection if
Persistent disease positive inguinal nodes

Continue to follow regularly,

Response biopsy suspicious lesions at
to 6mo E
therapy?
Local
Progressive disease disease
D
Rebiopsy, Restage Systemic chemotherapy
should be considered
for metastasis or
Metastatic disease
recurrence
following salvage
surgery

Algorithm 74.1

Suggested Reading
NCCN clinical practice guidelines in oncology anal carci-
noma version 2. 2017.
Steele SR, et  al. Practice parameters for anal squamous
neoplasms. Dis Colon Rectum. 2012;55:735–49.
 Management of Fecal
Incontinence 75
Matthew Z. Wilson and Suraj Alva

Algorithmic Approach atropine and opioids, while effective in slow-

ing intestinal transport, are associated with
A. Management of incontinence is multifactorial dependency and can cause constipation.
and should be individualized. Severity of fecal C. Anorectal physiology and endoanal ultrasound
incontinence can be measured with scoring testing will help to define the anatomic factors
instruments such as the Fecal Incontinence contributing to incontinence such as squeeze
Severity Index, St. Mark’s incontinence score, pressure and resting sphincter tone, rectal sensa-
and the Cleveland Clinic Florida Fecal tion, compliance, and capacity and evidence of
Incontinence Score. All are based on patient’s sphincter defect. Endoscopy should be performed
subjective experience, and none correlate to in patients who are presenting with specific
objective findings, and none are predictive of symptoms (diarrhea, bleeding, or obstruction) or
outcomes of the various treatment options. who meet general screening criteria. Magnetic
Given these limitations, the instruments are use- resonance imaging (MRI) defecography or fluo-
ful to measure response to treatment over time. roscopic examination is valuable to assess the
B. Initial management of incontinence begins coordination of pelvic floor musculature and elu-
with increasing fiber intake and reduction of cidate conditions such as paradoxical contraction
caffeine, sugar substitutes, lactose, and other of the puborectalis or pelvic descent.
bowel irritants. Skin care including barrier Biofeedback therapy is not invasive and should be
ointments and gentle soap can increase considered for failure of medical management
patient comfort. Medications may be useful in patients with voluntary sphincter contrac-
in instances of increased motility. Kaopectate tion. Sphincter reconstruction, performed by a
will absorb excess fluid, and cholestyramine colorectal surgeon, can improve continence in
will bind bile acids. Antidiarrheals such as the short term for patients with sphincter dis-
loperamide and diphenoxylate-atropine will ruption, but long-term improvement is not
slow intestinal motility. Diphenoxylate-­ assured. Sacral neuromodulation can be used in
patients with and without sphincter defects as
well as those with concomitant urinary and
M. Z. Wilson (*) fecal incontinence with good results. Patients
Department of Surgery, Dartmouth Hitchcock Medical
who have failed the above therapies or cannot
Center, One Medical Center Drive, Lebanon, NH, USA
e-mail: matthew.z.wilson@hitchcock.org pursue them due to personal preference or med-
ical comorbidities can have a stoma created.
S. Alva
Department of Surgery, Rutgers Robert Wood Patients who elect this option report improved
Johnson Medical School, Edison, NJ, USA quality of life in the majority of cases.
© Springer Nature Switzerland AG 2019 303
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_75
304 M. Z. Wilson and S. Alva

A History: Incontinence is defined as uncontrolled passage of feces or gas over

at least a 1-month duration in an individual at least 4 years of age who
previously achieved control. Common risk factors include: multiple
pregnancies, chronic diarrhea, previous anorectal surgery, neurologic disease,
obesity, rectal prolapse, and sphincter disruption due to birth or other trauma

Exam: External inspection and digital rectal exam; observe for signs of
patulous anus, fistulous opening or mucosal or full-thickness
prolapse. Assess rectovaginal septum for atrophy. Digital
examination may provide estimation of resting, squeeze pressure,
and/or pelvis floor coordination. Rule out impaction and overflow
incontinence. Use grading scale to determine severity of symptoms.

Dietary and medication

modification, Psyllium fiber
supplementation, and Kegel Improvement
exercises. Consider antimotility
agents.

No improvement

Worsening of Continue dietary

Anorectal physiology testing and modification and
ERUS based on risk factors and medication(s). No further
C clinical suspicion. +/– MRI or
symptoms
intervention
fluoro defecogram

No improvement

Refer to pelvic floor Improvement

physical therapy if dis-
coordination of pelvic
floor musculature

No improvement

Consider referral to colorectal

surgeon for evaluation for surgical Colostomy
intervention.

Algorithm 75.1

Suggested Reading
Paquette IM, et  al. The American Society of Colon and
Rectal Surgeons’ clinical practice guideline for
treatment of fecal incontinence. Dis Colon Rectum.
2015;58:623–36.
Part X
Liver
 Evaluation of Liver Nodule
Katelin A. Mirkin and Niraj J. Gusani
Algorithmic Approach
Diagnosis
A. History: In addition to a thorough history,
focus should be placed on symptoms such as
abdominal fullness or pain, early satiety, and
weight loss. The patient should be evaluated
for a history of anemia, rectal bleeding,
malignancy, or liver disease, including jaun-
dice, hepatitis, or cirrhosis. Patients should be
asked if they have used oral contraceptive
pills (OCPs) or anabolic steroids in the past
and how often they drink alcohol. Risk fac-
tors for viral hepatitis, including history of
blood transfusions, unprotected sex, and
intravenous drug use, should be assessed. It is
also important to inquire about family history
of liver diseases.
B. Physical exam: A full physical exam should
be performed with focused attention on the
abdominal exam. Particular attention should
be placed on stigmata of liver disease, such as
jaundice, a palpable liver mass, palmar ery-
thema, spider angiomata and other varices,
and fluid wave or other signs of ascites.
K. A. Mirkin · N. J. Gusani (*)
Department of Surgery, Program for Liver, Pancreas,
and Foregut Tumors, Penn State College of Medicine,
Penn State Cancer Institute, Hershey, PA, USA
e-mail: ngusani@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_76
76
C. Labs: In addition to liver function tests,
patients with a liver mass should have serum
alpha-fetoprotein drawn. If elevated, con-
cern for hepatocellular carcinoma grows. To
evaluate for common metastases to the liver,
serum carcinoembryonic antigen (CEA),
cancer antigen 19-9 (CA19-9), and chromo-
granin levels should be drawn. Additionally,
serologic testing for hepatitis B virus (HBV)
surface antigen and hepatitis C virus (HCV)
antibody should be drawn to evaluate for
hepatitis B virus and hepatitis C virus,
respectively.
D. Imaging: Typically, a tri-phasic abdominal
computed tomography (CT) scan with con-
trast is obtained to evaluate a solid nodule.
However, a patient may present with a mass
found incidentally on imaging for an unre-
lated workup. In the event that the CT is non-
diagnostic, a magnetic resonance imaging
(MRI) with gadolinium-­ based contrast is
recommended.
Etiology
E. Hepatocellular carcinoma (HCC): HCC is
primary liver cancer that typically occurs in
the setting of chronic liver disease. Patients
typically present with symptoms of chronic
liver disease such as ascites, jaundice,
encephalopathy, and/or a history of variceal
307
308
bleeds. The American Association for the
Study of Liver Diseases (AASLD) has pub-
lished an algorithm for evaluating liver nod-
ules based on underlying liver disease and
lesion size. A mass found in the setting of
hepatitis B or cirrhosis is more likely HCC
[1]. Nodules under 1 cm should be followed
by ultrasound (US) every 3–6  months. If,
after 2 years, there has been no growth, rou-
tine surveillance can commence. For nodules
>1 cm, MRI or contrast CT is needed for fur-
ther characterization. Tissue biopsy should
only be pursued when two diagnostic imag-
ing studies are inconclusive. On US, HCC
typically appears as a hyperechoic mass with
poorly defined, irregular margins. On CT,
HCC tumors demonstrate increased vascular-
ity during the hepatic arterial phase and
washout during the delayed phases. HCC
appears as a low-intensity lesion on
T1-weighted images and a high-intensity
lesion on T2-weighted images. LI-RADS
imaging criteria can help determine whether a H. Hepatic adenoma: Hepatic adenomas are
lesion is consistent with or suspicious for
HCC by CT or MRI.
F. Metastatic disease: Several malignancies
have a propensity to metastasize to the liver.
In fact, metastases are far more common in
Western countries than primary liver tumors
[2]. Metastatic disease from the colon, stom-
ach, and pancreas should be ruled out when
evaluating a liver nodule. On CT, metastatic
lesions typically demonstrate lower attenua-
tion relative to the liver parenchyma. Much
like HCC, metastatic lesions appear as low-­
intensity lesions on T1-weighted images and
high-intensity lesions on T2- weighted
images.
G. Focal nodular hyperplasia (FNH): FNH,
the second most common benign hepatic
mass, typically occurs in women and pres-
ents asymptomatically. It carries no malig-
nant potential and is often found incidentally.
FNH derives from a polyclonal proliferation
of all liver components, including Kupffer
cells. Classically, this lesion demonstrates
the pathognomonic central stellate scar. US is
often of limited use in the diagnosis of FNH,
K. A. Mirkin and N. J. Gusani
as it is difficult to distinguish the classic cen-
tral stellate scar and lesion itself can appear
hyper, hypo, or isoechoic [3]. On noncontrast
CT, FNH appears hypodense relative to the
surrounding tissue. The central stellate scar
is only identified in one third of patients [4].
Once contrast is injected, there is rapid tran-
sient enhancement in the arterial phase, and
then the lesion is isodense during the portal
phase. FNH appears as an isodense lesion on
T1-weighted images and can be hyperintense
on T2-weighted images. The central stellate
scar enhances on delayed images. Recently,
MR imaging using gadobentate dimeglu-
mine – eliminated via renal and hepatobiliary
excretion – has been used to differentiate FNH
from hepatic adenomas. FNH lesions, com-
prised of hepatic cells, appear isointense with
this substance. Because FNH derives from a
polyclonal proliferation of hepatic cells, FNH
lesions show equal or greater uptake of the
tracer on Tc-99 sulfur colloid scans.
classically found in the right lobe of young
women (20–40) and are associated with the
use of steroids and oral contraceptives
(OCPs). They tend to present with epigastric
or right upper quadrant abdominal pain.
Hepatic adenomas derive from monoclonal
proliferations of hepatocytes. Thus, they
carry the potential for malignant transforma-
tion in addition to a risk of bleeding and rup-
ture. Hepatic adenomas findings on ultrasound
are relatively nonspecific and can appear as
hyperechoic and well circumcised or hetero-
geneous. Hepatic adenomas appear as well-­
demarcated lesions on CT and may have
areas of intratumoral hemorrhage. On con-
trast CT, adenomas show peripheral enhance-
ment during early phase and centripetal flow
during the portal venous phase. It should be
noted that hepatic adenomas share many
diagnostic features, and it is important to dif-
ferentiate the two as they are managed differ-
ently. On MRI, adenomas appear well
demarcated and are usually hyperintense on
T1-weighted images. Adenomas have a small
number of nonfunctional Kupffer cells. Thus,
76  Evaluation of Liver Nodule
adenomas do not take up technetium Tc-99 m
sulfur colloid and produce a cold spot on the
liver during this scan.
I. Hepatic hemangioma: Hepatic hemangiomas
are the most common benign hepatic mass.
Most are asymptomatic and present inciden-
tally on imaging or laparoscopy for an unre-
lated condition. When they do produce
symptoms, they typically present with upper
abdominal pain and fullness. On ultrasound,
hepatic hemangiomas usually appear as well-­
demarcated homogenous lesions. They are
hyperechoic and blood flow can be demon-
strated with color Doppler, though this has
not been shown to improve diagnostic accu-
racy [5]. It is important to note that hepatocel-
lular carcinoma and hepatic metastases can
309
appear similar. Hepatic hemangiomas appear
as a well-demarcated hypodense lesion on
CT.  Contrast CT classically demonstrates
peripheral to central enhancement. On MRI,
hepatic hemangiomas typically appear as a
well-demarcated hypodense mass with a low
signal intensity on T1 and a high signal inten-
sity on T2. On tagged red blood cell (RBC)
studies, hepatic hemangiomas show an initial
hypoperfusion during arterial flow, followed
by retention of the tracer on delayed images.
Tagged RBC scans offer the greatest specific-
ity for diagnosing hepatic hemangiomas
(~100%) [6]. Fine-needle aspiration biopsy
(FNAB) is not currently recommended for
suspected hemangioma, as it poses severe
bleeding risks.
310 K. A. Mirkin and N. J. Gusani

A
History: history of fullness/pain, early satiety, weight loss,history of malignancy or hepatitis, anemia,
rectal bleeding, jaundice, cirrhosis, use of OCPs, alcohol use

B Physical exam: palpable liver mass, palmar erythema, spider angiomata, jaundice, and as cites

C Laboratory studies: CBC, chem, LFTs, serum AFP, CEA, CA19-9, chromogranin A, HBV, HCV

D Imaging: triphasic abdominal CT scan with contrast. If non-diagnostic, obtain MRI with gadolinium-
based contrast.

Risk factors Yes E

Concern for HCC
for HCC?

No

Elevated tumor
Yes Concern for metastatic F
makers, weight loss,
disease
history of
malignancy?

No
G

Central stellate Yes

FNH
scar on CT?
H
Hepatic adenoma:
peripheral enhancement
No during early phase,
centripetal flow during
portal venous phase
Enhancement
on CT?

I
Hepatic hemangioma:
peripheral to central
enhancement

Algorithm 76.1
76  Evaluation of Liver Nodule 311

References 4. Shamsi K, De Schepper A, Degryse H, Deckers

F.  Focal nodular hyperplasia of the liver: radiologic
findings. Abdom Imaging. 1993;18(1):32–8.
1. Bruix J, Sherman M. Management of hepatocellular
5. Perkins AB, Imam K, Smith WJ, Cronan JJ.  Color
carcinoma: an update. Hepatology (Baltimore Md).
and power Doppler sonography of liver hemangio-
2011;53(3):1020–2.
mas: a dream unfulfilled? J Clin Ultrasound : JCU.
2. Paley MR, Ros PR. Hepatic metastases. Radiol Clin N
2000;28(4):159–65.
Am. 1998;36(2):349–63.
6. Tamm EP, Rabushka LS, Fishman EK, Hruban
3. Cherqui D, Rahmouni A, Charlotte F, et  al.
RH, Diehl AM, Klein A.  Intrahepatic, extramed-
Management of focal nodular hyperplasia and hepa-
ullary hematopoiesis mimicking hemangioma on
tocellular adenoma in young women: a series of
technetium-­99m red blood cell SPECT examination.
41 patients with clinical, radiological, and patho-
Clin Imaging. 1995;19(2):88–91.
logical correlations. Hepatology (Baltimore Md).
1995;22(6):1674–81.
 Cystic Diseases of the Liver
Laura M. Enomoto and Niraj J. Gusani
Algorithmic Approach
A
Clinical Presentation
Cysts of the liver include hydatid cysts, simple
cysts, polycystic liver disease (PCLD), von
Meyenburg complexes, Caroli disease, cystade-
nomas, and cystadenocarcinomas [1, 2]. Most
patients with cystic liver disease are asymptom-
atic. Large cysts may cause abdominal pain, dis-
comfort, and distension, but this must be
diagnosed with caution only after other possible
causes of abdominal pain have been excluded.
Acute pain has been reported, largely related to
biliary obstruction due to large cysts. Patients
may also present with jaundice and pruritus, but
cholangitis is rare. Caroli disease may progress to
recurrent cholangitis and portal hypertension
with variceal bleeding or liver failure.
Etiology
1. Hydatid cysts: Form due to infection caused
by Echinococcus, a parasite carried by
sheep and dogs. Humans become infected
after eating contaminated food or by close
L. M. Enomoto · N. J. Gusani (*)
Department of Surgery, Program for Liver, Pancreas,
and Foregut Tumors, Penn State College of Medicine,
Penn State Cancer Institute, Hershey, PA, USA
e-mail: ngusani@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_77
77
contact with infected dogs. When the para-
site reaches human liver parenchyma, it
progresses to a cystic larval phase, which
can develop into a hydatid cyst within weeks
to months.
2. Simple cysts: Unknown. An association
between simple hepatic and renal cysts has
been reported but not well explained.
3. PCLD: Can be associated with autosomal
dominant polycystic kidney disease (ADPKD)
or occurs alone. Both are autosomal domi-
nant, however, and their clinical course is
identical [3].
4. Caroli disease: Dilation of the intrahepatic
bile ducts due to a long common pancreatico-
biliary channel that causes reflux of pancreatic
juice into the biliary tree leading to inflamma-
tion, ectasia, and dilation.
5. von Meyenburg complexes: Also known as
biliary hamartomas, they are due to abnor-
mal development of small intrahepatic bile
ducts.
6. Cystadenoma: Hypothesized that tumors form
due to ectopic ovarian cells migrating to the
liver during embryonic development, releas-
ing hormones and growth factors causing
endodermally derived epithelium to prolifer-
ate to form a tumor.
7. Cystadenocarcinoma: Unknown. It is usually
assumed to represent the malignant degenera-
tion of a cystadenoma. Risk of malignant
transformation is variable.
313
314
Diagnosis
Demographics  Simple cysts are uncommon
before age 40, and the incidence is higher in
women. von Meyenburg complexes are associ-
ated with PCLD, Caroli disease, and congenital
hepatic fibrosis but can be seen in 6% of normal
livers. Cystadenomas with an ovarian stromal
(OS) component are found almost exclusively in
women.
B
Labs  Liver function tests are generally normal
in all cystic disease. Alkaline phosphatase is ele-
vated in cystadenoma, helping to differentiate
from simple cysts. Increase in serum carcinoem-
bryonic antigen (CEA) and CA 19-9 in cystade-
nocarcinoma is rare.
Serologic testing  If the patient is in a region
where echinococcal disease is endemic, serologic
testing for parasitic infection should be per-
formed, with antibody testing being the method
of choice.
Genetic testing  PCLD associated with
ADPKD is linked to mutations in PKD1 or
PKD2. Isolated PCLD is associated with muta-
tions in PRKCSH, SEC63, or LRP5 genes. All
mutations have not yet been identified, however,
so genetic testing is not required for diagnosis.
There are no clinical guidelines to distinguish
PCLD from multiple simple cysts, but previous
case series have used five or six cysts or greater
than 50% involvement of the parenchyma, as
well as family history.
C
Cyst aspiration  Cystic fluid does not discrimi-
nate between cystadenoma and cystadenocarci-
noma, and thus aspiration is usually not indicated.
Malignant or atypical cells are infrequently
retrieved. CEA and CA 19-9 are increased in
L. M. Enomoto and N. J. Gusani
simple cysts, cystadenomas, and cystadenocarci-
nomas. Cyst aspiration should be performed with
caution as cystadenocarcinomas have a high pro-
pensity for peritoneal seeding.
D
 bdominal Imaging (table in algorithm 77.1)
A
1. Hydatid cysts:
(a). US: first-line imaging in endemic regions.
Cysts can be classified into six types
depending on the stage of growth. Early
stages are unilocular with thin cyst walls,
but as they progress through the lifecycle
they become heterogenous with thick-
ened walls and daughter cysts.
(b). CT: well circumscribed lesions with clear
membrane that do not invade surround-
ing liver tissue.
(c). MRI: low signal intensity rim on
T2-weighted images due to the collagen-­
rich outer-laminated membrane of the
cyst. Daughter cysts are hypointense rel-
ative to the parent cyst on T1-weighted
images and hyperintense on T2-weighted
images.
2. Simple cysts:
(a). US: best diagnostic modality; anechoic
circular or oval lesion with sharp, smooth
borders and posterior wall echoes, no
septations
(b). CT: water-dense lesions without
septations
(c). MRI: hypointense on T1-weighted
images and hyperintense on T2-weighted
images with homogenous cystic content
3. PCLD:
(a). US: multiple fluid-filled round or oval
cysts with sharp margins
(b). CT: cysts with −5 to +20 Houndsfield
units with distinct margins
(c). MRI: hypointense on T1-weighted
images and hyperintense on T2-weighted
images with homogenous cystic content
4. Caroli disease:
(a). US: hypoechoic intrahepatic biliary dila-
tions without septations
77  Cystic Diseases of the Liver
(b). CT: combine with intravenous (IV) chol-
angiography to identify contrast within
the cyst and identify a communication
with the bile ducts
(c). MRI: multiple unilobar or cysts arising
from segmental intrahepatic bile ducts.
Magnetic resonance cholangiopancrea-
tography (MRCP) is the gold standard
for imaging.
5. von Meyenburg complexes:
(a). US: range from hypoechoic to hyper-
echoic or heterogenous based on size,
associated biliary dilation, and fibrous
stroma
(b). CT: hypodense with no enhancement
(c). MRI: hypointense on T1-weighted
images, hyperintense on T2-weighted
images. Best seen on MRCP
6. Cystadenoma:
(a). US: anechoic mass with echogenic inter-
nal septations and papillary projections
into the cyst
(b). CT: multi-loculated hypodense mass
with well-defined wall, fine septal calcifi-
cations. CT is less accurate than US and
MRI as it may not visualize internal
septa.
(c). MRI: multi-loculated cyst with high sig-
nal intensity on T2-weighted images and
low signal intensity on T1-weighted
images. Contrast enhancement of thin
internal septa.
7. Cystadenocarcinoma:
(a). CT: larger septa, cystic debris, bile duct
dilation, coarse calcifications along the
wall or septa, and enhancement of mural
nodules
(b). MRI: hypointense cysts on T1-weighted
images and hyperintense on T2-weighted
images with cystic debris, calcifications,
and bile duct dilation
Management
Hydatid Cyst
Treatment is aimed at removing or destroying the
entire parasite and cavity as well as identifying
and treating any biliary fistula, depending on the
315
location, size, and number of cysts. In all cases,
spillage of cyst content should be avoided due to
the risk of anaphylaxis.
1. Radical surgery: Cysts are injected with an
ethanol and hypertonic saline solution, which
should remain in contact with the germinal
layer for at least 15 min. Cysts are then aspi-
rated, and partial hepatectomy is performed.
2. Cystectomy: It does not require transection of
liver parenchyma. All cysts are surrounded
with hypertonic saline-soaked packs and then
carefully aspirated, avoiding spillage.
Hypertonic saline is then injected into the
cysts, carefully monitoring for hypernatremia.
This is aspirated after several minutes, and the
process is repeated. After the second aspira-
tion, the cyst wall is resected and the entire
cavity washed with hypertonic saline.
3. Puncture, aspiration of cyst, injection of pro-
toscolicidal solution, reaspiration of fluid
(PAIR): Fine aspiration needle is inserted into
cysts under image guidance. As much fluid as
possible is aspirated, followed by injection of
a protoscolicidal solution. After 15  min of
dwell time, the fluid is aspirated and the nee-
dle withdrawn.
4. Medical management: For inoperable patients
with multiple cysts in two or more organs or
peritoneal cysts. Mebendazole and albenda-
zole are antihelminthic drugs that impair the
parasite’s glucose uptake. Albendazole is the
drug of choice due to its superior gastrointes-
tinal (GI) absorption. A 74% success rate has
been shown in patients with single cysts
treated 3–6 months.
Simple Cyst
1. Asymptomatic simple cysts: no treatment or
further surveillance
2. Symptomatic cysts [4]:
(a). Sclerotherapy: destroys the epithelial lin-
ing of the cyst by US-guided injection of
95% ethanol
(b). Fenestration: excision of the roof of the
cyst to establish a communication with
the peritoneal cavity causing cyst cavity
collapse
316
(c). Marsupialization: incision of the cyst
wall and suturing the wall open so the
cyst remains open and draining
PCLD
1. Medical Management
(a). Somatostatin analogs: There is limited
decrease in liver volume, and liver reverts
to baseline when treatment is stopped.
(b). Mammalian target of Rapamycin
Inhibitors: longterm efficacy and safety
studies still required.
(c). Arterial embolization: Cysts are largely
supplied by hepatic arteries and emboli-
zation target segments replaced by cysts.
2. Surgical Management
(a). Sclerotherapy: often ineffective because rigid
architecture of the cysts prevents collapse.
(b). Fenestration: excision of the roof of as
many cysts as possible.
(c). Partial hepatectomy: partial liver resec-
tion is possible if cysts are asymmetri-
cally distributed. The remnant liver is
widely fenestrated.
(d). Liver transplantation: only curative treat-
ment. May require simultaneous renal
transplant in patients with ADPKD and
requires special exceptions in (MELD)
scoring for those patients who do not
have concomitant liver failure.
L. M. Enomoto and N. J. Gusani
Caroli Disease
Treatment depends on the distribution of cysts.
If they are localized to one hepatic lobe or seg-
ment, hepatic resection with hepaticojejunos-
tomy is appropriate. If disease is diffuse, hepatic
transplantation offers the best chance of
survival.
von Meyenburg Complexes
No treatment is required. These are often found
incidentally during surgery for carcinoma of
another organ, causing the surgeon to biopsy for
frozen section. Pathologists must be aware of the
existence of these complexes to avoid mistaking
them for metastases.
Cystadenoma
Complete resection to prevent malignant trans-
formation or recurrence, with consideration of
intraoperative cholangiogram to exclude commu-
nication with the biliary tree.
Cystadenocarcinoma
Complete resection with wide margins, with
consideration of intraoperative cholangiogram
as some tumors communicate with the biliary
tree. Hepaticojejunostomy may be required if
the resection of the biliary confluence is
required. Care should be taken not to rupture
the cyst as peritoneal carcinomatosis has
been reported.
77  Cystic Diseases of the Liver 317

History:

• Most patients with cystic liver disease are asymptomatic.

• Large cysts may cause abdominal pain, discomfort and distension, but this must be
diagnosed with caution only after other possible causes of abdominal pain have
been excluded.
• Acute pain has been reported, largely related to biliary obstruction due to large
cysts. Patients may also present with jaundice and pruritis, but cholangitis is rare.
• Caroli disease may progress to recurrent cholangitis and portal hypertension with
variceal bleeding or liver failure.

Laboratory:

• Liver function tests are generally normal in all cystic disease.

• Alkaline phosphatase is elevated in cystadenoma, helping to differentiate from simple cysts.
• Increase in serum CEA and CA 19-9 in cystadenocarcinoma is rare.
• If the patient is in a region where ecchinococcal disease is endemic, serologic testing for parasitic infection
should be performed, with antibody testing being the method of choice.

Cyst Aspiration:

• Cystic fluid does not discriminate between cystadenoma and cystadenocarcinoma and thus aspiration is
usually not indicated.
• Malignant or atypical cells are infrequently retrieved.
• CEA and CA 19-9 are increased in simple cysts, cystadenomas, and cystadenocarcinomas.
• Cyst aspiration should be performed with caution as cystadenocarcinomas have a high propensity for
peritoneal seeding.

Algorithm 77.1
318 L. M. Enomoto and N. J. Gusani

D
Table: Abdominal imaging
Ultrasound
Hydatid cyst Early stages are unilocular
with thin cyst walls, but as
they progress through the
lifecycle they become
heterogenous with thickened
walls and daughter cysts
Simple cyst Best diagnostic modality;
anechoic circular or oval
lesion with sharp, smooth
borders and posterior wall
echoes, no septations
PCLD multiple fluid filled round or
oval cysts with sharp margins
Caroli disease hypoechoic intrahepatic
biliary dilations without
septations
von Meyenburg complexes range from hypechoic to
hyperechoic or heterogenous
based on size, associated
biliary dilation, and fibrous
stroma
Cystadenoma anechoic mass with
echogenic internal septations
and papillary projections into
the cyst
Cystadenocarcinoma
CT
Well circumscribed lesions
with clear membrane that do
not invade surrounding liver
tissue
water dense lesions without
septations
cysts with –5 to +20
Houndsfield units with
distinct margins
combine with IV
cholangiography to identify
contrast within the cyst and
identify a communication with
the bile ducts
hypodense with no
enhancement
multi-loculated hypodense
mass with well-defined wall,
fine septal calcifications. CT
is less accurate than US and
MRI as it may not visualize
internal septa
larger septa, cystic debris,
bile duct dilation, coarse
calcifications along thewall
or septa, and enhancement
of mural nodules
MRI
Low signal intensity rim on
T2-weighted images due to
the collagen-rich outer
laminated membrane of the
cyst. Daughter cysts are
hypointense relative to the
parent cyst on T1-weighted
images and hyperintense on
T2-weightedimages
hypointense on T1-weighted
images and hyperintense on
T2-weighted images with
homogenous cystic content
hypointense on T1-weighted
images and hyperintense on
T2-weighted images with
homogenous cystic content
multiple unilobar or cysts
arising from segmental
intrahepatic bile ducts.
MRCP is the gold standard
for imaging
hypointense on T1-weighted
images, hyperintense on T2-
weighted images. Best seen
on MRCP
multi-loculated cyst with high
signal intensity on T2-
weighted images and low
signal intensity on T1-
weighted images. Contrast
enhancement of thin internal
septa
hypointense cysts on T1-
weighted images and
hyperintense on T2-weighted
images with cystic debris,
calcifications, and bile duct
dilation

Algorithm 77.1 (continued)

3. Everson GT, Taylor MR, Doctor RB. Polycystic dis-

References
1. Jarnagin W, editor. Blumgart’s surgery of the liver,
biliary tract, and pancreas. 6th ed. Philadelphia:
Elsevier, Inc.
2. Hai S, Hirohashi K, Uenishi T, Yamamoto T, Shuto
T, Tanaka H, et  al. Surgical management of cystic
hepatic neoplasms. J Gastroenterol. 2003;38(8):759–
64. Epub 2003/09/25.
ease of the liver. Hepatology. 2004;40(4):774–82.
Epub 2004/09/24.
4. Furuta T, Yoshida Y, Saku M, Honda H, Muranaka
T, Oshiumi Y, et  al. Treatment of symptomatic non-­
parasitic liver cysts–surgical treatment versus alcohol
injection therapy. HPB Surg. 1990;2(4):269–77. dis-
cussion 77-9. Epub 1990/10/01.
 Management of Benign Liver
Masses
Katelin A. Mirkin and Niraj J. Gusani
Algorithmic Approach
A. Hepatic hemangioma: Hemangiomas are
common in the general population, and the
use of medical imaging has further illumi-
nated their prevalence. Hepatic hemangiomas
follow a benign course, and conservative non-
operative management should be followed in
most cases [1].
Asymptomatic: Per the American College of
Gastroenterology clinical guidelines, there
is no intervention required for asymptom-
atic hepatic hemangiomas regardless of
size [2].
Symptomatic: Symptomatic patients with
impaired quality of life should be offered
surgical resection once other potential causes
of symptoms have been excluded [1].
Arterial embolization: In the event of acute
bleeding, arterial embolization is a viable
treatment option. It can also be used to
reduce the size of the lesion preoperatively
or control symptoms.
Surgical resection: Surgical management
ranges from enucleation to liver
transplantation.
K. A. Mirkin · N. J. Gusani (*)
Department of Surgery, Program for Liver, Pancreas,
and Foregut Tumors, Penn State College of Medicine;
Penn State Cancer Institute, Hershey, PA, USA
e-mail: ngusani@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_78
78
B. Hepatic adenoma: Hepatic adenomas harbor
a malignant potential, in addition to a poten-
tial for hemorrhagic rupture. Hemorrhagic
events most commonly occur in lesions ≥
5 cm. Thus, surgical resection should be con-
sidered in large lesions.
Symptomatic: Symptomatic patients should
undergo surgical resection.
Arterial embolization: There is some evidence
that preoperative arterial embolization may
control hemorrhage and reduce mortality
[3]. Alternatively, in high-risk patients
unable to tolerate resection, arterial embo-
lization may offer a viable option [2].
Surgical resection: Surgical management
ranges from enucleation to resection to
liver transplantation.
Asymptomatic: Oral contraceptive pills
(OCPs), anabolic steroids, and hormone
containing intrauterine devices (IUDs)
should be avoided per the American
College of Gastroenterology [2].
Pregnancy is not contraindicated. For
small adenomas <5 cm, discontinuation of
OCPs or steroid use can be considered,
with a follow-up with repeat imaging (CT
or MRI) in 6–12 months. If the lesion does
not resolve or increases in size after medi-
cation changes have been made, surgical
resection should be considered. For
asymptomatic lesions ≥5 cm, surgical
resection should be considered to reduce
319
320 K. A. Mirkin and N. J. Gusani

the risk of hemorrhage and malignant
degeneration [2, 4, 5].
C. Focal nodular hyperplasia: FNH is the sec-
ond most common benign hepatic lesion. It
tends to follow a benign course, and nonop-
erative management should be followed in
most lesions [2].
Observation: Because FNH does not carry a
malignant potential, this lesion should be
managed nonoperatively. For women with
FNH who continue to use OCPs, they
should undergo annual ultrasound for
2–3  years [5]. Follow-up imaging is not
necessary in patients not using OCPs.

A B C

Focal nodular
Hepatic adenoma Hepatic hemangioma hyperplasia

Yes
Yes Consider surgical Use of
Sympto
resection or Annual ultrasound OCPs?
matic?
arterial for 2–3 years
embolization

No
No
Yes

Yes Consider surgical

Sympto-
resection or arterial
≥5cm? matic?
embolization

No No

Discontinuation of OCPs and

steroids No intervention or follow-up No intervention or follow-up
Repeat imaging (CT or MRI) in necessary necessary
6-12 months

Algorithm 78.1
78  Management of Benign Liver Masses 321

References 3. Ault GT, Wren SM, Ralls PW, Reynolds TB, Stain
SC. Selective management of hepatic adenomas. Am
Surg. 1996;62(10):825–9.
1. Deneve JL, Pawlik TM, Cunningham S, et  al. Liver
4. Terkivatan T, de Wilt JH, de Man RA, et  al.
cell adenoma: a multicenter analysis of risk fac-
Indications and long-term outcome of treatment for
tors for rupture and malignancy. Ann Surg Oncol.
benign hepatic tumors: a critical appraisal. Arch Surg
2009;16(3):640–8.
(Chicago, Ill : 1960). 2001;136(9):1033–8.
2. Marrero JA, Ahn J, Rajender RK. ACG clinical guide-
5. Dokmak S, Paradis V, Vilgrain V, et al. A single-center
line: the diagnosis and management of focal liver
surgical experience of 122 patients with single and
lesions. Am J Gastroenterol. 2014;109(9):1328–47.
multiple hepatocellular adenomas. Gastroenterology.
quiz 1348.
2009;137(5):1698–705.
 Hepatic Abscess
Jasvinder Singh and Niraj J. Gusani
Algorithmic Approach
Epidemiology
The overall incidence of liver abscess in the
United States is estimated to be 3.6 per 100,000
population per year. Although the incidence and
mortality from liver abscess have gone down sig-
nificantly over the last century, its incidence
appears to be increasing in recent years [1, 2].
Amoebic liver abscess is the most common type
of liver abscess worldwide, whereas in western
series, pyogenic liver abscess predominates.
A present with multiple abscesses, especially
Clinical Presentation and Diagnosis
The most common symptoms include fever
(90%) and chills (50%), respectively, right upper
quadrant pain and hepatomegaly with or without
jaundice [2, 3]. Diagnosis is usually made after
radiologic studies, e.g., ultrasound (US) abdo-
men or computed tomography (CT) scan.
J. Singh · N. J. Gusani (*)
Department of Surgery, Program for Liver, Pancreas,
and Foregut Tumors, Penn State College of Medicine,
Penn State Cancer Institute, Hershey, PA, USA
e-mail: ngusani@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_79
79
Patients may have prodromal symptoms of
weight loss, fatigue, malaise, fever, and anorexia
for many days before more specific symptoms
like right upper quadrant pain localize the pro-
cess. Patient may even present with bacteremia of
unclear etiology.
Etiology
1. Pyogenic: Biliary, portal, arterial, or traumatic
origin. The etiology has changed over the last
100  years, with the biliary route replacing
portal route as the most common cause of
pyogenic liver abscess [3]. Patients usually
when biliary in origin.
(a). Biliary: Result of biliary obstruction and
cholangitis from gallstones, biliary stric-
ture or malignancy.
(b). Portal: Spread of infection from the gas-
trointestinal tract to the liver via the por-
tal vein. Examples include appendicitis,
diverticulitis, perforated ulcers, perfo-
rated cancers, etc.
(c). Arterial: Hematogenous spread of infec-
tion from a distant site, e.g., infectious
endocarditis.
(d). Traumatic: Secondary infection of a trau-
matic liver hematoma.
2. Amoebic: Usually solitary and in the right
lobe but can be multiple. It is uncommon in
323
324
the United States but is important to consider
if there is history of travel to the tropical
region, immunosuppression, human immuno-
deficiency virus (HIV), and corticosteroids.
3 . Malignant: Historically, malignant tumors
accounted for approximately 3% of liver
abscess cases [4]. But with the increased use
hepatic arterial interventions like transarterial
chemoembolization (TACE) and transarterial
radioembolization (TARE) with yttrium mic-
roparticles, it is not uncommon to see hepatic
abscess in patients with malignant tumors in
the present era.
Diagnosis
B prompt evaluation for this [7].
Right upper quadrant US  It can identify liver
abscess, gallstones, biliary dilation from com-
mon bile duct (CBD) stones.
CT scan  Compared to ultrasound, CT scan has
slightly increased sensitivity (95% vs 90%) and
better anatomic localization for complex biopsies
and drainage procedures. The characteristics sug-
gestive of pyogenic liver abscess include contrast
enhancement in the periphery as opposed to non-
enhancement of the central portion during the
portal venous phase [5].
MRI  Magnetic resonance imaging (MRI) is a
reasonable cross-sectional imaging modality but
does not have any advantage over CT for diagno-
sis or management of liver abscess.
C chloroquine (600  mg daily for 2 days,
Labs  Elevated white blood cell (WBC) count,
anemia, elevated liver enzymes, hyperbilirubine-
mia, hypoalbuminemia
J. Singh and N. J. Gusani
D
Serologic diagnosis  Serologic testing for anti-
bodies to Entamoeba histolytica using indirect
hemagglutination and gel diffusion precipitation is
the best way to confirm diagnosis of amoebic liver
abscess (85–95% sensitivity and specificity) [6].
Culture  The most commonly isolated organ-
isms in those with positive blood culture include
Streptococcus species (29.5%) and E. coli
(18.1%) with polymicrobial cultures noted in
16.3% [1]. Presence of Streptococcus faecalis
may indicate underlying colon cancer and should
Stool for ova and parasites  The cysts of
Entamoeba histolytica are found in the stool in
about 1/4th of the patients [6].
Management
E
 moebic Liver Abscess
A
(a). Medical Treatment
–– Metronidazole is the mainstay of treat-
ment. Dosage is 750 mg three times daily
for 7–10 days.
–– Metronidazole treatment needs to be fol-
lowed with paromomycin (25–35 mg/kg/
day in three divided doses for 7 days) or
diloxanide furoate (500  mg three times
daily for 10 days) to eradicate amoeba in
the intestine.
–– Alternatives for metronidazole include
followed by 300  mg daily for 3 weeks)
with or without dehydroemetine.
–– Role of antibiotics: Antibiotics may be
needed in case of secondary infection of
amoebic liver abscess. Secondary infec-
79  Hepatic Abscess
tion should be suspected if patient doesn’t
respond to metronidazole within a few
days; usually aspiration of abscess would
be required to confirm this.
( b). Drainage
–– Abscess drainage: Routine drainage of
abscess is not needed. When needed, per-
cutaneous needle aspiration (PNA) usu-
ally provides relief, and catheter
placement may be avoided. Indications
for drainage include left-lobe abscess,
impending rupture, multiple abscesses,
or abscess that does not respond to medi-
cal therapy within three to 5 days, unclear
diagnosis [8].
F success rate and reduced time to achieve
 yogenic Liver Abscess
P of the affected liver is required.
(a). Antibiotics: Initially start with parenteral
broad spectrum antibiotics (polymicrobial
infection is common), with adjustments per
culture reports. Usually 4–6 weeks of antibi-
325
otic therapy is needed, but duration of anti-
biotic treatment should be individualized
based on clinical response, etiology, and
number/extent of abscesses [3]. If there is
significant clinical improvement, patients
can be transitioned to oral antibiotics after
2–3  weeks of intravenous antibiotics with
equivalent results [9].
(b). Drainage (percutaneous or internal):
Drainage is essential to control sepsis and
may be needed to confirm diagnosis. Usually
percutaneous needle aspiration (PNA) alone
is sufficient especially when the size of the
abscess is <5  cm. Percutaneous catheter
drainage (PCD) should be done in abscesses
>5 cm or those that fail to resolve with PNA
alone [10]. PCD generally is more effective
than PNA for large abscesses, with a higher
clinical relief [11]. Occasionally, operative
intervention including drainage or resection
(c). Primary source control: Treatment of the
primary cause (e.g., appendicitis, diverticu-
litis, biliary obstruction, etc.) is essential.
326 J. Singh and N. J. Gusani

Typical symptoms: fever, chills, right upper quadrant pain, and hepatomegaly with or without jaundice
Prodromal symptoms: Weight loss, fatigue, malaise, fever, and anorexia (may be the only symptoms)
Imaging findings: Fluid collection in liver (Single or multiple)

A
Clinical history
Pyogenic abscess: h/o gallstones/CBD stones, septic focus in GI tract (appendicitis,
diverticulitis etc.), h/o liver trauma, h/o HPB malignancy/ liver metastasis
Amoebic liver abscess: recent travel to the tropical region, immunosuppressed

B C
Imaging: US abdomen, CT scan (more sensitive), MRI
Labs: elevated WBC count, deranged liver function tests,
Findings: fluid collection (single or multiple)
hypoalbuminemia, amoebic serology
Associated pathology: gallstones, CBD stones, malignantlesion in liver

D Amoebic serology

Positive
Negative

F Pyogenic liver abscess

Amoebic liver abscess E

Send blood cultures - Metronidazole (750 mg thrice daily for 7-10 days).
- Followed with paromomycin (25-35 mg/kg/day in 3
divided doses for 7 days) or diloxanide furoate (500 mg
thrice daily for 10 days) to eradicate amoeba in intestine.
Start broad-spectrum antibiotics early – Antibiotics: may be needed if secondary infection.
Change later per antibiotic sensitivity

Drainage of abscess Drainage: No need for routine drainage.

<5 cm: PNA Indications: left-lobe abscess, impending rupture, multiple
>5 cm: PCD abscesses, or abscess that does not respond to medical therapy
Send for culture and sensitivity within 3–5days, unclear diagnosis

Treatment of primary cause

- Relieve biliary obstruction: ERCP or PTC, surgical drainage
- Appendicitis, diverticulitis, other infectious
intra-abdominal pathology

Algorithm 79.1

6. Haque R, Huston CD, Hughes M, Houpt E, Petri WA,

References
1. Meddings L, Myers RP, Hubbard J, Shaheen AA,
Laupland KB, Dixon E, et  al. A population-based
study of pyogenic liver abscesses in the United States:
incidence, mortality, and temporal trends. Am J
Gastroenterol. 2010;105(1):117–24.
2. Huang CJ, Pitt HA, Lipsett PA, Osterman FA Jr,
Lillemoe KD, Cameron JL, et  al. Pyogenic hepatic
abscess. Changing trends over 42 years. Ann Surg.
1996;223(5):600–7. discussion 7–9.
3. Pitt HA. Surgical management of hepatic abscesses.
World J Surg. 1990;14(4):498–504.
4. Trump DL, Fahnestock R, Cloutier CT, Dickman MD.
Anaerobic liver abscess and intrahepatic metastases:
a case report and review of the literature. Cancer.
1978;41(2):682–6.
5. Benedetti NJ, Desser TS, Jeffrey RB.  Imaging of
hepatic infections. Ultrasound Q. 2008;24(4):
267–78.
Amebiasis J. N Engl J Med. 2003;348(16):1565–73.
7. Teitz S, Guidetti-Sharon A, Manor H, Halevy
A. Pyogenic liver abscess: warning indicator of silent
colonic cancer. Report of a case and review of the lit-
erature. Dis Colon Rectum. 1995;38(11):1220–3.
8. Sharma MP, Ahuja V.  Amebiasis. N Engl J
Med. 2003;349:307–8. https://doi.org/10.1056/
NEJM200307173490323.
9. Ng FH, Wong WM, Wong BC, Kng C, Wong SY, Lai KC,
et al. Sequential intravenous/oral antibiotic vs. continuous
intravenous antibiotic in the treatment of pyogenic liver
abscess. Aliment Pharmacol Ther. 2002;16(6):1083–90.
10. Zerem E, Hadzic A.  Sonographically guided percu-
taneous catheter drainage versus needle aspiration in
the management of pyogenic liver abscess. AJR Am J
Roentgenol. 2007;189(3):W138–42.
11. Cai YL, Xiong XZ, Lu J, Cheng Y, Yang C, Lin YX, et al.
Percutaneous needle aspiration versus catheter drainage
in the management of liver abscess: a systematic review
and meta-analysis. HPB (Oxford). 2015;17(3):195–201.
 Malignant Liver Tumors
(Metastatic Liver Disease)
Neal M. Mineyev, Karla M. Chaffee,
and Joyce Wong
Algorithmic Approach
A. Many patients with metastatic liver disease
are identified because of staging imaging or
imaging obtained to evaluate specific con-
cerns, such as elevated liver function enzymes
or elevated tumor markers. Staging imaging
typically involves computed tomography
(CT) scan, magnetic resonance imaging
(MRI), or positron emission tomography
(PET)/CT, depending on the primary tumor.
Hepatic disease should be noted, whether
identified during initial staging of a cancer
(i.e., synchronous hepatic disease) or during
surveillance for a cancer (metachronous).
Dedicated liver imaging should be obtained
to determine hepatic burden of disease, i.e.,
triple phase CT of the liver or MRI of the
abdomen. The presence of extrahepatic dis-
ease must also be considered.
B. The tumor burden within the liver should be
defined: solitary metastasis vs. multiple
metastases, single lobe vs. bilobar distribu-
tion, and proximity to the hepatic veins, main
portal veins, or biliary tree. Resectability
should be determined based on the functional
liver remnant and quality of liver remaining.
N. M. Mineyev · K. M. Chaffee · J. Wong (*)
Department of General Surgery, Lenox Hill Hospital,
New York, NY, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_80
80
If the anticipated functional liver remnant is
inadequate, portal vein embolization can be
offered to allow for hypertrophy of the rem-
nant [1].
C. If the primary lesion is not symptomatic, sys-
temic chemotherapy should be offered. In
colorectal cancer with an intact colorectal pri-
mary cancer, for example, the majority of
patients will not require palliative resection
of the primary tumor during chemotherapy
[2]. These patients can be offered resection,
either in a combined or staged manner, if they
do not demonstrate disease progression fol-
lowing short-course systemic therapy. If the
patient has resectable hepatic metastases and
primary lesion, other options also include
combined resection of the primary tumor
with hepatic metastasectomy, followed by
adjuvant systemic treatment, or even staged
resection with resection of the primary tumor
followed by hepatic metastasectomy [3]. This
approach is generally reserved for patients
with oligometastatic hepatic disease or single
hepatic metastasis. Resection of the hepatic
metastasis(es) is considered the treatment of
choice and offers improved outcome vs. abla-
tion [4]. In patients with unresectable liver
metastases, systemic chemotherapy should
be offered as initial treatment, followed by
restaging imaging. In patients with extrahe-
patic disease in addition to the primary tumor,
systemic therapy is typically offered. Further
327
328
treatment would be predicated upon disease
response to chemotherapy.
D. In those with persistent unresectable hepatic
disease, without extrahepatic disease, liver
directed therapies should be considered,
including radioembolization (i.e., yittrium-
90), transarterial chemoembolization, or
­ cross-sectional imaging. If disease progression
hepatic artery infusion pump [5, 6].
E. If the disease burden progresses following
systemic chemotherapy, change to an alter-
nate systemic chemotherapy regimen should
N. M. Mineyev et al.
be offered [3]. Interval follow-up with restag-
ing imaging should be performed.
F. If patients are rendered disease free, they should
complete the recommended systemic chemo-
therapy and be followed in surveillance with
interval physical examination, bloodwork and
is demonstrated, third-­ line chemotherapy or
clinical trial should be considered. Surveillance
should be continued for 5 years [3].
80  Malignant Liver Tumors (Metastatic Liver Disease) 329

Hepatic mass identified on routine surveillance imaging

A Detected on workup for symptoms such as abdominal pain
Detected during staging for primary cancer, i.e., colon cancer

Obtain vital signs, and blood work and perform physical examination
Review imaging, obtain dedicated imaging, i.e. MRI, as needed
Status of primary malignancy must be defined

Solitary or mulitple
hepatic lesions?
B
Status of primary
cancer?

Resectable hepatic disease Resectable hepatic disease

Primary tumor intact, Multiple hepatic lesions,
Primary tumor intact,
symptomatic not resectable
asymptomatic

Consider resecting primary

tumor. Systemic therapy (i.e.,
If solitary liver lesion, may chemotherapy)
C perform metastasectomy in
same setting.

Restage with cross-sectional imaging

Multiple hepatic lesions, still

Resectable hepatic disease, unresectable
Progressive disease
stable or regressed

If primary tumor controlled,

E Surgical Resection of hepatic
Systemic therapy
consider liver-directed
metastases therapy:
(second line) D
Resect primary tumor if intact Y-90 radioembolization
TACE
Hepatic artery infusion pump

Algorithm 80.1
330 N. M. Mineyev et al.

References 4. Abdalla EK, Vauthey JN, Ellis LM, et al. Recurrence

and outcomes following hepatic resection, radio-
frequency ablation, and combined resection/abla-
1. Covey AM, Brown KT, Jarnagin WR, et al. Combined
tion for colorectal liver metastases. Ann Surg.
portal vein embolization and neoadjuvant chemo-
2004;239:818–25.
therapy as a treatment strategy for resectable hepatic
5. Van Hazel GA, Heinemann V, Sharma NK, et  al.
colorectal metastases. Ann Surg. 2008;247:451–5.
SIRFLOX: randomized phase III trial comparing first-­
2. Poultsides GA, Servais EL, Saltz LB, et al. Outcome
line mFOLFOX6 (plus or minus bevacizumab) versus
of primary tumor in patients with synchronous stage
mFOLFOX6 (plus or minus bevacizumab) plus selec-
IV colorectal cancer receiving combination chemo-
tive internal radiation therapy in patients with meta-
therapy without surgery as initial treatment. JCO.
static colorectal cancer. JCO. 2016;34:1723–31.
2009;27(20):3379–84.
6. Zacharias AJ, Jayakrishnan TT, Rajeev R, et  al.
3. NCCN Clinical Practice Guidelines in Oncology,
Comparative effectiveness of hepatic artery based
Colon Cancer. Version 2.2017  – March 13, 2017.
therapies for unresectable colorectal liver metastases:
NCCN.org.
a meta-analysis. PLoS One. 2015;10:e0139940.
 Diagnosis and Management
of Hepatocellular Carcinoma
Neal M. Mineyev, Karla M. Chaffee,
and Joyce Wong
Algorithmic Approach
A.
Patients with hepatocellular carcinoma
(HCC) are typically male, between 50 and
60 years of age, with a liver mass identified
on routine imaging for surveillance in hepati-
tis B/C, with evaluation of cirrhosis, or found
incidentally. Patients may present with unex-
plained weight loss, nausea, lethargy, or right
upper quadrant pain with/without a palpable
mass. Evaluation of these symptoms includes
routine laboratory studies including a liver
function panel and alpha-fetoprotein (AFP).
Although AFP has a low sensitivity and spec-
ificity for HCC, it is useful in monitoring
treated patients for possible recurrence.
Dedicated liver imaging should be obtained
to determine hepatic burden of disease with a
triple phase CT of the liver or MRI of the
abdomen [1].
B. Once radiologic evidence of HCC is con-
firmed by arterial hypervascularity and venous
or delayed phase washout, the presence of
extrahepatic metastasis must be carefully
evaluated. Additionally, the extent of tumor
burden within the liver should be defined:
number of tumors, lobar distribution, and
proximity to the hepatic veins, main portal
N. M. Mineyev · K. M. Chaffee · J. Wong (*)
Department of General Surgery, Lenox Hill Hospital,
New York, NY, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_81
81
veins, or biliary tree. Resectability is deter-
mined based on the primary tumor character-
istics, functional liver remnant and quality of
liver remaining as well as tumor location, lack
of portal hypertension, and bilirubin level [2].
C. If extrahepatic metastasis is identified, patients
will generally receive palliative treatment with
sorafenib or other systemic therapy, regardless
of liver function or Child-Pugh class. If no
extrahepatic metastasis is identified, then the
treatment of choice is complete excision of
HCC by resection or liver transplantation.
Selection of the appropriate patients for resec-
tion is crucial as the mortality after liver resec-
tion can be as high as 20%, depending on the
patient’s preoperative liver function [3].
D. Liver volumetry and Child-Pugh classification
are key elements to determine if the patient
will tolerate resection. Patients with Child-
Pugh class B or C cirrhosis or those with portal
hypertension typically do not tolerate resec-
tion. Taking location of tumor into account,
there is no general consensus on tumor size for
selection of patients for resection, although
generally eligibility for resection is restricted
to tumors that are ≤5  cm in diameter.
Locoregional therapies can be used for a vari-
ety of patients with complex disease and those
who are not eligible for resection or transplan-
tation. Radiofrequency ablation (RFA) is typi-
cally used for unresectable Child-Pugh class A
or B, for tumors <4  cm, and as a bridge to
331
332
transplant. According to current National
Comprehensive Cancer Network (NCCN)
guidelines, RFA plus TACE (transarterial che-
moembolization) has been recommended for
intermediate-sized HCC from 3 to 5  cm.
Radioembolization with yttrium-90 (Y-90)
particles has shown great success in recent tri-
als; however, its efficacy compared to other
ablative therapies has yet to be thoroughly
studied. Although controversial, small tumors
in Child-Pugh class B patients with no portal
hypertension, favorable peripheral location,
and adequate functional status may be able to
tolerate resection or ablative therapy (RFA/
TACE/Y-90/etc.) [4].
E. Patients who are unresectable due to underly-
ing severe liver dysfunction (Child-Pugh
class B/C) or with portal hypertension are
N. M. Mineyev et al.
treated with orthotopic liver transplantation
(OLTx). An established guideline for OLTx
evaluation is the Milan criteria. However,
some intuitions will apply the University of
California San Francisco (UCSF) criteria
(single tumor ≤6.5 cm, or 2–3 lesions, none
exceeding 4.5  cm, with total tumor diame-
ter  ≤8  cm, and no vascular invasion) as an
extended version of Milan criteria. For those
patients whose disease falls within the crite-
ria, OLTx is the only treatment with or with-
out adjuvant “bridging” ablation therapy.
Patients whose disease extends beyond the
confines of the guidelines are treated with
palliative care and sorafenib. In recent stud-
ies, a new systemic agent, regorafenib, has
shown survival benefit in HCC patients who
have previously received sorafenib [5].
81  Diagnosis and Management of Hepatocellular Carcinoma 333

Liver mass identified on routine

imaging or detected on workup for
abdominal pain

Obtain vital signs, blood work, including AFP and physical exam
A Review imaging, obtain dedicated imaging i.e., triple-phase
contrast CT and/or MRI of abdomen

HCC identified

B
Staging of disease and
liver
functionality/cirrhosis

Select Child-Pugh class B

Resection if adequate functional
C Extrahepatic liver remnant
metastasis? +/–ablation, TACE, Y–90
Yes No

Palliative care Child-Pugh class

+/–sorafenib A/B/C
Child-Pugh class A Child-Pugh class B/C E

Resection if adequate functional

Liver transplant
D liver remnant
evaluation
+/–ablation, TACE, Y–90

Within milan F
Milan criteria* criteria?*

1 lesion ≤ 5 cm Yes No
3 lesions ≤ 3 cm
No extrahepatic metastatic invasion
Liver transplant listing Palliative Care
No evidence of vascular invasion +/–Sorafenib
+/–Neoadjuvant RFA/TACE/Y-90

Algorithm 81.1
334 N. M. Mineyev et al.

References 4. Bruix J, et  al. Prognostic prediction and treatment

strategy in hepatocellular carcinoma. Hepatology.
2002;35:519.
1. Townsend CR, Beauchamp MB, Evers M, Mattox
5. Bruix J, et  al. Regorafenib for patients with hepa-
K.  Sabiston textbook of surgery. 20th ed. Elsevier:
tocellular carcinoma who progressed on sorafenib
Philadelphia, PA. 2016. p. 1458–63.
treatment (RESORCE): a randomized, double-­
2. Xavier A, et  al. Usefulness of staging systems and
blind, placebo-controlled, phase 3 trial. Lancet.
prognostic scores for HCC treatments. World J
2017;389(10064):56–66.
Hepatology. 2016;8(17):703–15.
3. National Comprehensive Cancer Network, HCC;
v.1.2016.
 Diagnosis and Management
of Primary Sclerosing Cholangitis 82
Neal M. Mineyev, Karla M. Chaffee,
and Joyce Wong

Algorithmic Approach rubinemia is warranted, as ultrasound is not

A. The first step in the evaluation of a patient
with primary sclerosing cholangitis (PSC) is
a thorough history and physical. Patients may
experience varying degrees of symptoms,
often long-standing, from 12 to 24  months
that can include fatigue, jaundice with or D. Liver biopsy is not routinely performed in the
without pruritus, choluria, steatorrhea, and
acute cholangitis.
B. Evaluation of these symptoms includes rou-
tine laboratory studies including a liver func-
tion panel. Marked elevation in bilirubin,
gamma-glutamyl transferase (GGT), and/or
aspartate aminotransferase (AST)/liver func-
tion tests (LFTs) will generally prompt an
ultrasound of the right upper quadrant that
may or may not show dilation of intrahepatic
or extrahepatic bile ducts. If PSC is sus- E. ERCP is the preferred route for cholangiogra-
pected, autoantibodies such as antinuclear,
antismooth muscle, anticardiolipin, and IgG4
may be obtained, although they are of uncer-
tain significance. Intrahepatic saccular dila-
tions and signs of portal hypertension may be
visualized in long-standing disease or end-­
stage PSC [1].
C. If no abnormalities are observed on ultra-
sound, further investigation of the hyperbili-
F. Medical treatment of PSC has shown little to
N. M. Mineyev · K. M. Chaffee · J. Wong (*)
Department of General Surgery, Lenox Hill Hospital,
New York, NY, USA
the most sensitive diagnostic modality for
intrahepatic biliary pathology and is very
operator dependent. MRCP or ERCP should
be performed at this point; however, ERCP
will yield better results from both diagnostic
and therapeutic perspectives [2].
diagnosis of PSC. It is indicated when visual-
ization of the biliary ducts by MRCP has not
yielded any abnormal findings and other
causes of cholestatic liver disease need to be
investigated. Liver biopsy tends to show an
“onion-skin” appearance of concentric peri-
ductal fibrosis in PSC.  As the disease pro-
gresses, the periductal fibrosis advances to
necrosis, periportal fibrosis, and eventually
biliary cirrhosis [3].
phy and can demonstrate the characteristic
appearance of PSC: multifocal, diffusely dis-
tributed dilations, and strictures of the intra-
hepatic and extrahepatic biliary system. The
classic pattern is described as “beading,”
resembling the arrangement of beads on a
string. Cholangioscopy is currently being
investigated and may play a role in directed
tissue biopsy; however, it is not considered to
be a standard of care in PSC [4].
no lasting effects. Dominant intrahepatic
strictures are best managed endoscopically

© Springer Nature Switzerland AG 2019 335

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_82
336
with balloon dilation and/or stenting. Biliary
reconstruction is an option for a select group
of patients with dominant extrahepatic stric-
tures only and minimal intrahepatic disease.
With the high risk of developing cholangio-
carcinoma in PSC, as well as increased suc-
cess of orthotopic liver transplantation
(OLTx), the use of biliary reconstruction pro-
cedures has decreased.
. If no dominant strictures are identified during
G 5- and 10-year survival rates for PSC after OLTx
ERCP and no endoscopic interventions per-
N. M. Mineyev et al.
formed, the patient must continue to be sur-
veilled. Both the American Association for
the Study of Liver Disease (AASLD) and the
European Association for the Study of the
Liver (EASL) recommend having quarterly
blood work evaluation and yearly MRCP and
CA19-9 tumor markers [5].
H. OLTx is the only curative option for patients
with progressive liver disease due to PSC. The
have been reported between 75% and 87%.
82  Diagnosis and Management of Primary Sclerosing Cholangitis 337

History and presentation:

Vague abdominal/RUQ pain,
fatigue, jaundice, pruritis

Obtain vital signs and blood work,

A and perform physical exam

Elevated alkaline phosphatase,

total bilirubin, GGT, AST/ALT

Right upper
B quadrant ultrasound

E F

Dilated Diffuse biliary Endoscopic

Yes Yes
intrahepatic ERCP strictures and brush Dominant dilation and/or
bile ducts? cytology +/– biopsy stricture? stenting
confirm PSC

No No

Surveillance:
C MRCP Labs Q3 months
CA19–9 Q1 Year
MRCP Q1 Year

H
Dilated Yes
intrahepatic
bile ducts? Yes
Severe liver
G disease?
Liver transplant

No

Liver biopsy No

Continue
surveillance +/–
D ERCP for further
interventionsif
necessary
Characteristic
Yes
onion-skin
periductal
fibrosis?

No

Further
investigation

Algorithm 82.1
338 N. M. Mineyev et al.

References 3. Eaton J, et  al. Pathogenesis of primary sclerosing

cholangitis and advances in diagnosis and manage-
ment. Gastroenterology. 2013;145(3):521–36.
1. Townsend CR, Beauchamp MB, Evers M, Mattox K.
4. Srinivasan N, et al. Diagnosis and treatment: ERCP
Sabiston textbook of surgery. 20th ed. Philadelphia:
in PSC; endoscopy in inflammatory bowel disease.
Elsevier; 2016. p. 1508–9.
Switzerland: Springer International Publishing; 2014.
2. Kovac J, et al. Primary biliary cirrhosis and primary
p. 309–22.
sclerosing cholangitis: an update on MR imaging
5. Lutz H, et  al. PSC: diagnosis and treatment. Dtsch
findings with recent developments. J Gastrointestin
Arztebl Int. 2013;110(51–52):867–74.
Liver Dis. 2016;25(4):517–24.
 Portal Hypertension and Shunting
Neal M. Mineyev, Karla M. Chaffee,
and Joyce Wong
Algorithmic Approach
A. The diagnosis of portal hypertension typi-
cally occurs with imaging demonstrating cir-
rhosis or secondary signs such as
hypersplenism, ascites, and/or bleeding from
varices. It is important to perform a history
and physical examination, obtain blood work,
and perform dedicated liver imaging. Portal
hypertension is broadly categorized as related
to cirrhosis or noncirrhosis etiologies.
B. Noncirrhotic etiologies are classified into
three general groups: pre-hepatic, intrahe-
patic, and posthepatic. Prehepatic causes
include splenic vein thrombosis or portal vein
thrombosis. Left-sided portal hypertension
(sinistral hypertension) may be related to
severe pancreatitis with splenic vein thrombo-
sis or postsurgical splenic vein ligation. In
patients with varices and bleeding, splenec-
tomy should be considered; asymptomatic
patients can be monitored [1]. Portal vein
thrombosis can be classified as acute or
chronic and may be related to malignancy, cir-
rhosis, or a hypercoagulable state. In noncir-
rhotic patients, early anticoagulation is
important to prevent varices from forming [2].
N. M. Mineyev · K. M. Chaffee · J. Wong (*)
Department of General Surgery, Lenox Hill Hospital,
New York, NY, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_83
83
C. Intrahepatic causes of portal hypertension
include schistosomiasis, a parasitic disease
caused by trematode flukes, particularly S.
japonicum and S. mansoni. Because of the
immune response to parasite egg antigens,
extensive fibrosis and hepatosplenic disease
with periportal fibrosis can occur. Praziquantel
is the treatment of choice, although oxam-
niquine is also effective [3]. Other intrahe-
patic causes include biliary disease such as
biliary cirrhosis, neoplastic occlusion of the
intrahepatic portal veins, developmental
abnormalities such as polycystic liver disease
or congenital hepatic fibrosis, and acquired
diseases such as nonalcoholic fatty liver dis-
ease or inflammatory viral hepatitis. There
are a multitude of intrahepatic etiologies;
treatment generally centers on the prevention
of severe complications such as variceal
bleeding.
D. Posthepatic etiologies include Budd-Chiari
syndrome or hepatic vein outflow obstruc-
tion. Treatment options include anticoagula-
tion, short segment angioplasty, or
transjugular intrahepatic portosystemic shunt
(TIPS) in patients not in liver failure. If the
inferior vena cava is patent and there is not a
significant pressure gradient between the
infrahepatic and suprahepatic portions, sur-
gical shunting can also be offered, such as
portacaval, splenorenal, or mesocaval shunts.
339
340
In patients with symptoms of liver failure,
liver transplantation is offered [4].
E. Care of the patient with portal hypertension
is often directed toward management of
symptoms. Patients with cirrhosis or plate-
let count <150,000 should undergo screen-
ing endoscopy. Prophylaxis of bleeding
with a nonselective beta-blocker or endo-
scopic variceal ligation should be consid-
ered. Those with upper gastrointestinal
bleeding from esophageal varices should
undergo endoscopy with sclerotherapy,
which controls bleeding in more than 90%
of patients. If sclerotherapy fails, balloon
tamponade can be used for temporary con-
trol, up to 24 h, followed by repeat endos-
copy or TIPS [5].
N. M. Mineyev et al.
F. For patients with ascites, paracentesis should
be performed to evaluate cell count and dif-
ferential, total protein, and serum-ascites
albumin gradient. Typical management starts
with sodium restriction (2gm/day) and diuret-
ics (spironolactone, furosemide). For those
with refractory ascites, serial paracenteses
can be offered. For ongoing refractory asci-
tes, liver transplantation should be considered
[6].
G. For patients with refractory symptoms or
development of end-stage liver disease, hepa-
torenal syndrome, or hepatopulmonary syn-
drome, liver transplantation is an important
option, and referral to transplantation should
be done, unless there is an underlying psychi-
atric or medical contraindication.
83  Portal Hypertension and Shunting 341

Diagnosed with portal hypertension

Incidentally found
Symptoms such as bleeding, elevated LFTs
A

Obtain vital signs, and blood work and perform a physical examination
Review imaging, obtain dedicated imaging, i.e., MRI, as needed

Cirrhosis Non cirrhosis

C D
B
Pre hepatic Intra hepatic Post hepatic
Symptoms from
portal hypertension?

Splenic vein Portal vein Budd-Chiari

Schistosomiasis Other causes
thrombosis thrombosis* syndrome*

Praziquantel
Splenectomy Anticoagulation
oxamniquine
Liver failure?

D Budd-Chiari syndrome or chronic portal vein

thrombosis*
No Yes

Symptomatic TIPS/stent

Follow-up Liver transplant

If IVC open, consider
mesocaval or portacaval
shunt

Algorithm 83.1
342 N. M. Mineyev et al.

Symptoms from portal

hypertension?

Yes No Follow-up
E F

Esophageal varices
Ascites Liver failure
Bleeding

Endoscopic banding
Diuretics Yes No
Beta-blocker therapy

Follow-up Follow-up

Supportive care
Follow-up

G Liver failure?

No Yes

Supportive care Not a candidate Liver transplant

Algorithm 83.1 (continued)

4. Valla DC. Budd-Chiari syndrome/hepatic venous out-

References flow tract obstruction. Hepatol Int, 2017; Jul 6 [Epub
ahead of print].
1. Loftus JP, Nagorney DM, Ilstrup D, et  al. Sinistral 5. Hwang JH, Shergill AK, Acosta RD, et  al. The
portal hypertension. Splenectomy or expectant man- role of endoscopy in the management of vari-
agement. Ann Surg. 1993;217(1):35–40. ceal hemorrhage. J Gastrointestinal Endoscopy.
2. Manzano-Robleda Mdel C, Barranco-Fragoso B, 2014;80(2):221–7.
Uribe M, et al. Portal vein thrombosis: what is new? 6. Runyon BA.  Management of adult patients with
Ann Hepatol. 2015;14(1):20–7. ascites due to cirrhosis: update: AASLD Practice
3. Colley DG, Bustinduy AL, Secor WE, Guideline; Alexandria, VA. 2012.
et  al. Human schistosomiasis. Lancet.
2014;383(9936):2253–64.
Part XI
Biliary
 Acute Cholecystitis and Biliary
Colic
Chanak J. Chantachote and Samer Sbayi
Algorithmic Approach
Acute calculous cholecystitis (ACC) represents
about 1/3 of surgical admissions and is the most
frequent complication of cholelithiasis [1]. Risk
of complications such as gallstone pancreatitis
and choledocholithiasis is 1–4% per year [1].
ACC is commonly caused by an impacted gall-
stone in the infundibulum or cystic duct that
causes an inflammatory process within the gall-
bladder wall [2]. This can lead to serosal edema,
mucosal sloughing, and venous and lymphatic
congestion. It can further be complicated by bac-
terial infection from the bile duct entering via the
portal system [3]. Diagnosis of ACC typically
requires clinical and imaging studies. Grading
systems to qualify severity are available by the
American Association for the Surgery of Trauma
(AAST) [4] and the Tokyo Guidelines.
A & B: Ultrasound is typically the first-line
imaging if ACC is suspected. It can help to
diagnose lumen distention, gallstones,
Murphy’s sign, and hyperemia [3]. The posi-
C. J. Chantachote (*)
Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA
e-mail: CHANAK.CHANTACHOTE@
STONYBROOKMEDICINE.EDU
S. Sbayi
Department of General Surgery, Stony Brook
University Hospital, Stony Brook, NY, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_84
84
tive findings of gallstones, gallbladder wall
thickness, and Murphy’s sign have a 95% pre-
dictive value for ACC [5]. Signs of acute cho-
lecystitis on ultrasound are sonographic
Murphy sign (tenderness elicited by pressing
the gallbladder with the ultrasound probe),
thickened gallbladder wall (>4  mm, if the
patient does not have chronic liver disease and/
or ascites or right heart failure), enlarged gall-
bladder (long axis diameter >8 cm, short axis
diameter >4 cm), incarcerated gallstone, debris
echo, pericholecystic fluid collection, sonolu-
cent layer in the gallbladder wall, striated
intramural lucencies, and Doppler signals [6].
C. Computed tomography (CT) can aid in the
diagnosis of complicated ACC and may help
differentiate between other intra-abdominal
processes [7, 8]. Abnormal liver function tests
such as presence of abnormal transaminases
(e.g., total serum bilirubin >1.5 and/or aspar-
tate aminotransferase >60) and mild hyper-
bilirubinemia may be indicative of worsening
disease, inflammation of the liver, and wors-
ening infection [9, 10].
With regard to common bile duct stones
(CBDS), a Cochrane metaanalysis compared
magnetic resonance cholangiopancreatogra-
phy (MRCP) and endoscopic ultrasound
(EUS) and concluded that both are highly
accurate and can determine the presence of
CBDS with high sensitivity and specificity
(95%) [11].
345
346
D. The choice of treatment in concomitant CBDS
and ACC ranges from open common bile duct
exploration (CBDE), laparoscopic cholecys-
tectomy with laparoscopic common bile duct
exploration, preoperative endoscopic retro-
grade cholangiopancreatography (ERCP), or
postoperative ERCP.  A systematic review of
randomized controlled trials has shown that
open cholecystectomy (OC) with CBDE has
the lowest incidence of retained stones but is
associated with high morbidity and mortality,
especially in elderly patients [12].
Treatment of choice remains a laparoscopic
cholecystectomy (LC) which carries a smaller
influence on the immune response reflected in
lowered levels of cytokines yielded and a lesser
systemic inflammatory response severity. This
has improved outcomes [13]. A systematic
review concluded that, when a difficult gall-
bladder is encountered during LC, laparoscopic
partial cholecystectomy (LPC) can be a safe
alternative to conversion and closing of the cys-
tic duct, gallbladder remnant, or both [14, 15].
Another systematic review assessed the
associated factors linked to the conversion of
C. J. Chantachote and S. Sbayi
LC to OC.  The results showed that male
patients, ages 60–65 years, sclerotic gallblad-
der or wall thickness (>4 mm) and acute cho-
lecystitis, were significant risk factors for
conversion [16, 17].
E. Biliary colic is the most common form of
symptomatic gallbladder disease [18]. It is
often used to describe gallbladder pain expe-
rienced by patients without any obvious
signs of gallbladder infection. It develops in
at least one third of patients with cholelithia-
sis over a 10-year period of follow-up [18].
It is usually caused by transient gallstone
obstruction of the cystic duct or edema
caused by the passage of a stone [18]. Colic
refers to the type of pain that “comes and
goes” typically after eating a meal that
causes contraction of the gallbladder.
Cholecystectomy is considered to be the
gold standard treatment [17]. However, the
timing of cholecystectomy may be on the
index admission or on an elective basis.
Elective cholecystectomy may include pain
control and in some cases a “low-fat” diet
prior to elective surgery.
84  Acute Cholecystitis and Biliary Colic 347

H&P RUQ pain

A

B LFTs and U/S of the RUQ

Normal LFTs;
C Increasing LFTs; cholelithiasis;
+GB thickening normal GB wall
+ Murphys sign no Murphy's Sign

Biliary colic
Acute cholecystitis
On index
admission
E

D
Laparoscopic Pain control and
cholecystectomy low fat diet

Elective

Algorithm 84.1

NT. Measuring anatomic severity of disease in emer-

References
1. National Institutes of Health consensus devel-
opment conference statement on gallstones
and laparoscopic cholecystectomy. Am J Surg.
1993;165:390–8.
2. Shaffer EA.  Gallstone disease: epidemiology of
gallbladder stone disease. Best Pract Res Clin
Gastroenterol. 2006;20:981–96.
3. Riall TS, Zhang D, Townsend CM, Kuo YF, Goodwin
JS.  Failure to perform cholecystectomy for acute
cholecystitis in elderly patients is associated with
increased morbidity, mortality, and cost. J Am Coll
Surg. 2010;210:668–79.
4. Shafi S, Aboutanos M, Brown CV, Ciesla D, Cohen
MJ, Crandall ML, Inaba K, Miller PR, Mowery
gency general surgery. J Trauma Acute Care Surg.
2014;76:884–7.
5. Ralls PW, Colletti PM, Lapin SA, Chandrasoma P,
Boswell WD, Ngo C, Radin DR, Halls JM.  Real-­
time sonography in suspected acute cholecystitis.
Prospective evaluation of primary and secondary
signs. Radiology. 1985;155:767–71.
6. Hirota M, Takada T, Kawarada Y, Nimura Y, Miura
F, Hirata K, Mayumi T, Yoshida M, Strasberg S,
Pitt H, Gadacz TR, de Santibanes E, Gouma DJ,
Solomkin JS, Belghiti J, Neuhaus H, Büchler MW,
Fan S-T, Ker C-G, Padbury RT, Liau K-H, Hilvano
SC, Belli G, Windsor JA, Dervenis C. Diagnostic cri-
teria and severity assessment of acute cholecystitis:
Tokyo guidelines. J Hepato-Biliary-Pancreat Surg.
2007;14:78–82.
348
7. Buonamico P, Suppressa P, Lenato GM, Pasculli G,
D’Ovidio F, Memeo M, Scardapane A, Sabbà C. Liver
involvement in a large cohort of patients with heredi-
tary hemorrhagic telangiectasia: echo-color-Doppler
vs multislice computed tomography study. J Hepatol.
2008;48:811–20.
8. Reginelli A, Mandato Y, Solazzo A, Berritto D,
Iacobellis F, Grassi R.  Errors in the radiological
evaluation of the alimentary tract: part II.  Semin
Ultrasound CT MR. 2012;33:308–17.
9. Brooks KR, Scarborough JE, Vaslef SN, Shapiro
ML. No need to wait: an analysis of the timing of cho-
lecystectomy during admission for acute cholecysti-
tis using the American College of Surgeons National
Surgical Quality Improvement Program database. J
Trauma Acute Care Surg. 2013;74:167.
10. Cameron JL, Cameron AM, editors. Current surgical
therapy. 11th ed. Philadelphia: Elsevier Saunders; 2014.
11. Giljaca V, Gurusamy KS, Takwoingi Y, Higgie D,
Poropat G, Štimac D, et al. Endoscopic ultrasound ver-
sus magnetic resonance cholangiopancreatography for
common bile duct stones. Cochrane Database Syst Rev.
2015;2:CD011549. https://doi.org/10.1002/14651858.
CD011549.
12. Hong DF, Xin Y, Chen DW.  Comparison of laparo-
scopic cholecystectomy combined with intraoperative
endoscopic sphincterotomy and laparoscopic explora-
C. J. Chantachote and S. Sbayi
tion of the common bile duct for cholecystocholedo-
cholithiasis. Surg Endosc. 2006;20:424–7.
13. Di Saverio S. Emergency laparoscopy: a new emerg-
ing discipline for treating abdominal emergencies
attempting to minimize costs and invasiveness and
maximize outcomes and patients’ comfort. J Trauma
Acute Care Surg. 2014;77:338–50.
14. Henneman D, da Costa DW, Vrouenraets BC, van
Wagensveld BA, Lagarde SM.  Laparoscopic partial
cholecystectomy for the difficult gallbladder: a sys-
tematic review. Surg Endosc. 2013;27:351–8.
15. Gomes CA, Junior CS, Di Saveiro S, et al. Acute cal-
culous cholecystitis: review of current best practices.
World J Gastrointest Surg. 2017;9(5):118–26.
16. Philip Rothman J, Burcharth J, Pommergaard HC,
Viereck S, Rosenberg J. Preoperative risk factors for
conversion of laparoscopic cholecystectomy to open
surgery  - a systematic review and meta-analysis of
observational studies. Dig Surg. 2016;33:414–23.
17. Tiderington E, Lee SP, Ko CW.  Gallstones: new
insights into an old story. F1000Res. 2016;5.:
F1000 Faculty Rev-1817. https://doi.org/10.12688/
f1000research.8874.1.
18. Warren KW, EGC T. Surgical approach to disease of
the biliary system. In: Schiff L, Schiff ER, editors.
Diseases of the liver. 7th ed. Philadelphia: Lippincott;
1993. p. 448–86.
 Acalculous Cholecystitis
Chanak J. Chantachote and Samer Sbayi
Algorithmic Approach
A. Acute acalculous cholecystitis (AAC), repre-
senting only 5–10% of all cases of cholecysti-
tis, is inflammation of the gallbladder which is
not associated with the presence of gallstones
[1, 2]. This pathology was described initially
in critically ill patients who underwent major
surgery or in the setting of extensive burns [1].
Ischemia is the most likely underlying cause
of acute acalculous cholecystitis [1]. Clinical
findings of AAC can be difficult to distinguish
from calculous cholecystitis. Oftentimes, the
clinical signs and laboratory workup are non-
specific [3].
Treatment of acute acalculous cholecystitis
consists of early radiologic imaging and effec-
tive management. The three most common
treatments are open cholecystectomy, laparo-
scopic cholecystectomy, or percutaneous cho-
lecystostomy [4], depending on severity of
disease.
C. J. Chantachote (*)
Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA
e-mail: CHANAK.CHANTACHOTE@
STONYBROOKMEDICINE.EDU
S. Sbayi
Department of General Surgery, Stony Brook
University Hospital, Stony Brook, NY, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_85
85
B, C. Imaging plays a major role in the accuracy
of diagnosis and management. Which study to
begin with, an ultrasound, a CT scan, or a
HIDA scan, is debatable [5]. Sonographic fea-
tures of abdominal circumference (AC)
include an abnormally distended GB, wall
thickening, pericholecystic fluid (without
ascites), and sludge (in the absence of choleli-
thiasis) [6].
D. Patients who are deemed clinically stable for a
laparoscopic cholecystectomy should undergo
surgery early in the disease process. If the
patient is critical with multiple comorbidities
or a poor surgical candidate, then percutane-
ous cholecystostomy tube placement is a safer
choice. In some papers, there is a higher inci-
dence of gangrenous cholecystitis of 31%
compared to calculous cholecystitis of 5.6%
[7]. Mortality from acute acalculous cholecys-
titis is at least 30% because of the association
of gangrene and the rapid disease progression
in critically ill patients [8, 9].
349
350 C. J. Chantachote and S. Sbayi

References
H&P RUQ Pain
A
1. Poddighe D, Tresoldi M, Licari A, Marseglia
GL.  Acalculous acute cholecystitis in previously
healthy children: general overview and analysis of
pediatric infectious cases. Int J Hepatol. 2015;2015
Article ID 459608, 6 pages.
B LFTs U/S RUQ 2. Prashanth GP, Angadi BH, Joshi SN, Bagalkot PS,
Maralihalli MB. Unusual cause of abdominal pain in
pediatric emergency medicine. Pediatr Emerg Care.
2012;28(6):560–1.
3. Hermiz SJ, Diegidio P, Garimella R, Ortiz-Pujols S,
Yu H, Isaacson A, Mauro MA, Cairns BA, Hultman
– Increasing LFTs
CS.  Acalculous cholecystitis in burn patients. Clin
C – US: No cholelithiasis,
GB wallthickening Plast Surg. 2017;44(3):567–71.
4. Treinen C, Lomelin D, Krause C, et  al. Acute acal-
culous cholecystitis in the critically ill: risk factors
and surgical strategies. Langenbeck's Arch Surg.
2015;400:421.
Acalculous 5. Taoka H.  Experimental study on the pathogenesis
cholecystitis
of acute acalculous cholecystitis, with special refer-
ence to the roles of microcirculatory disturbances,
free radicals and membrane-bound phospholipase A2.
Gastroenterol Jpn. 1991;26:633–44.
6. Smith EA, Dillman JR, Elsayes KM, Menias CO,
Is the patient clinically
D Bude RO.  Cross-sectional imaging of acute and
stable for surgery?
chronic gallbladder inflammatory disease. Am J
Roentgenol. 2009;192:188–96.
Yes No 7. Gu M, Kim TN, Song J, Nam YJ, Lee JY, Park
JS.  Risk factors and therapeutic outcomes of acute
acalculous cholecystitis. Digestion. 2014;90:75–80.
Laparoscopic Percutaneous 8. Barie PS, Eachempati SR. Acute acalculous cholecys-
cholecystectomy cholecystostomy
titis. Gastroenterol Clin N Am. 2010;39(2):343–57.
tube
9. Huffman JL, Schenker S.  Acute acalculous cho-
lecystitis: a review. Clin Gastroenterol Hepatol.
Algorithm 85.1 2010;8(1):15–22.
 Postcholecystectomy
Chanak J. Chantachote and Samer Sbayi
Algorithmic Approach
A.  B. In the case of a patient presenting to the
emergency department status postcholecys-
tectomy with abdominal pain, suspicion for a
bile leak should be considered as it can occur
in 0.3–27% of patients [1]. The bile leak can
arise from an injury to the common bile,
hepatic duct, cystic duct stump, or duct of
Luschka [2]. These leaks can present as a bili-
ary fistula, subhepatic/subphrenic collection,
or even peritonitis. The principle in manage-
ment of a bile leak is drainage of the leak [1].
Postcholecystectomy syndrome includes a
heterogeneous group of disease-manifested
findings, characterized as abdominal symp-
toms. The most common symptoms in
descending order include right upper quadrant
pain or epigastric pain, nausea/vomiting, and
fever. Total bilirubin can be elevated above
1.5 mg/dl in almost 30% of patients, elevated
LFTs in over 50%, and elevated white blood
cells in over 60% of patients [3, 4].
C. J. Chantachote (*)
Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA
e-mail: CHANAK.CHANTACHOTE@
STONYBROOKMEDICINE.EDU
S. Sbayi
Department of General Surgery, Stony Brook
University Hospital, Stony Brook, NY, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_86
86
Initial assessment is done by transabdomi-
nal ultrasound and liver function tests some-
times followed by endoscopic retrograde
cholangiopancreatography (ERCP) [5].
Transabdominal ultrasound allows rapid
detection and can differentiate between
obstructive and nonobstructive jaundice [6].
Endoscopic retrograde cholangiography
(ERCP) and magnetic resonance cholangiog-
raphy (MRC) examinations are likely to dem-
onstrate the presence of biliary leak and often
provide the level of duct laceration or transac-
tion [6, 7]. ERCP in addition provides a thera-
peutic option in this scenario when
sphincterotomy and endobiliary stenting may
be considered; other therapeutic intervention
commonly used includes percutaneous tran-
shepatic cholangiography, transhepatic biliary
drainage, and percutaneous drainage of intra-
abdominal collection [8].
C. A common bile duct (CBD) diameter less than
10 mm was normal and greater than or equal
to 10 mm was abnormal. Direct evidence of a
stone in the bile duct is considered abnormal
irrespective of the size of the duct.
MRCP is able to demonstrate the level and
presence of biliary obstruction with a sensitiv-
ity of 95% and a specificity of 97%, being less
sensitive for detecting stones, especially less
than 6 mm in size [9].
351
352
D. Sphincter of Oddi dysfunction (SOD) is a syn-
drome of chronic biliary pain or recurrent pan-
creatitis due to functional obstruction of
pancreaticobiliary flow at the level of the
sphincter of Oddi [10]. Symptoms attributable
to SOD can be seen in three clinical scenarios:
(1) postcholecystectomy syndrome, (2) acal-
culous biliary pain with an intact gallbladder,
and (3) recurrent idiopathic pancreatitis. The
current gold standard for diagnosis is manom-
etry to detect elevated sphincter pressure,
which correlates with outcome of
sphincterotomy.
E. Endoscopic treatment at ERCP with stent and
sphincterotomy is usually the first line of
treatment with success rate greater than 90%
C. J. Chantachote and S. Sbayi
[11]. The median time for resolution of the
leak was 3  days (range 1–39  days) [11].
Kaffes and colleagues reported that stent
insertion alone for postcholecystectomy bile
leak is superior to sphincterotomy alone,
because fewer patients required additional
intervention (particularly surgery) to control
the leak [11].
F.  For clinically benign presentations with no
abnormal lab value and found to have a biloma
that was treated with drainage, conservative
treatment may be sufficient. A biloma can be
managed by percutaneous catheter drainage
placed under imaging guidance. If the leak is
small, it will resolve spontaneously in a few
days [12–15].
86 Postcholecystectomy 353

A H&P RUQ pain (post

cholecystectomy)

LFTs/CBC/ultrasound

B C Inc LFTs
Inc LFTs
US: dilated CBD
(+) US: collection
F

Drain collection MRCP

HIDA/MRCP Eovist

+ Positive – Negative
Retained
stone?
D
No
Bile leak Conservative Rx
ERCP/stent Abx Yes

E
Dysfunctional sphincter
of Oddi syndrome

ERCP/sphincterotomy/
stenting

Algorithm 86.1

5. Machado NO.  Biliary complications post laparo-

References
1. Ahmad F, Saunders RN, Lloyd GM, Lloyd DM,
Robertson GS. An algorithm for the management of
bile leak following laparoscopic cholecystectomy.
Ann R Coll Surg Engl. 2007;89:51–6.
2. De Palma GD, Galloro G, Iuliano G, Puzziello
A, Persico F, Masone S, et  al. Leaks from laparo-
scopic cholecystectomy. Hepato-Gastroenterology.
2002;49:924–5.
3. Woods MS, Shellito JL, Santoscoy GS, et al. Cystic
duct leaks in laparoscopic cholecystectomy. Am J
Surg. 1994;168(6):560–3.
4. Eisenstein S, Greenstein AJ, Kim U, Divino
CM. Cystic duct stump leaks after the learning curve.
Arch Surg. 2008;143(12):1178–83.
scopic cholecystectomy: mechanism, preventive
measures, and approach to management: a review.
Diagn Ther Endosc. 2011;2011 Article ID 967017, 9
pages.
6. Rogoveanu I, Gheonea DI, Saftoiu A, Ciurea T. The
role of imaging methods in identifying the causes of
extrahepatic cholestasis. J Gastrointestin Liver Dis.
2006;15:265–71.
7. Schmidt SC, Langrehr JM, Hintze RE, Neuhaus
P. Long-term results and risk factors influencing out-
come of major bile duct injuries following cholecys-
tectomy. Br J Surg. 2005;92(1):76–82.
8. Sandha GS, Bourke MJ, Haber GB, Kortan
PP. Endoscopic therapy for bile leak based on a new
classification: results in 207 patients. Gastrointest
Endosc. 2004;60(4):567–74.
354
9. Tse F, Barkun JS, Romagnulo J, Friedman G,
Bornstein JD, Barkun AN.  Nonoperative imaging
techniques in suspected biliary tract obstruction. HPB
(Oxford). 2006;8:409–25.
10. Bistritz L, Bain VG. Sphincter of Oddi dysfunction:
managing the patient with chronic biliary pain. World
J Gastroenterol: WJG. 2006;12(24):3793–802.
11. Kaffes AJ, Hourigan L, De Luca N, Byth K, Williams
SJ, Bourke MJ. Impact of endoscopic intervention in
100 patients with suspected postcholecystectomy bile
leak. Gastrointest Endosc. 2005;61(2):269–75.
12. Festekjian JH, Hassantash SA, Taylor EW. Abdominal
wall biloma: an unusual complication of laparoscopic
cholecystectomy. JSLS. 1997;1:353–5.
C. J. Chantachote and S. Sbayi
13. Nunez D Jr, Becerra JL, Martin LC.  Subhepatic
collections complicating laparoscopic cholecystec-
tomy: percutaneous management. Abdom Imaging.
1994;19:248–50.
14. Sammak BM, Yousef BA, Gali MH, al Karawi MA,
Mohamed AE.  Case report: radiological and endo-
scopic management of bile leak following laparo-
scopic chole-cystectomy. J Gastroenterol Hepatol.
1997;12:34–8.
15. Pavlidis TE, Atmatzidis KS, Papaziogas BT, et  al.
Biloma after laparoscopic cholecystectomy. Ann
Gastroenterol. 2002;15:178–80.
 Management
of Postcholecystectomy Cholangitis 87
Joel VanderVelde and Ross F. Goldberg

Algorithmic Approach ment. Distal obstructions are usually amena-

A. Fever, jaundice, and right upper quadrant
pain are classic signs and symptoms of acute
cholangitis. The diagnosis is also more likely
given a history of recent cholecystectomy.
Initial evaluation should include vitals, a
physical exam, and laboratory values includ-
ing white blood cell count, which may indi-
cate active inflammation and/or infection,
and liver function tests, which may indicate
cholestasis [1, 2].
B. The patient should be immediately resusci-
tated, and broad-spectrum antibiotics should
be started. An abdominal ultrasound should
be obtained. A common bile duct diame-
ter  >6  mm may be indicative of biliary
obstruction [3].
C. An emergent ERCP should be performed for
biliary drainage and possible definitive treat-
ble to ERCP [4].
D. A PTC should be attempted if ERCP is unsuc-
cessful or contraindicated.
E. If attempts with ERCP and PTC are unsuc-
cessful, the patient should undergo open
drainage. Distal obstructions should be man-
aged with choledochotomy and placement of
a tympanostomy tube (T-tube). Surgical man-
agement should focus on drainage alone
especially in the setting of instability [1, 2].
Following decompression of the biliary tree, the
patient should undergo treatment of the underly-
ing cause where appropriate. A secondary com-
mon bile duct stone is often definitively managed
with removal of the stone alone, whether by
ERCP or open surgical management. Definitive
management should be performed on an elective
basis [1, 2].

J. VanderVelde
Department of Surgery, Maricopa Integrated Health
System, Phoenix, AZ, USA
R. F. Goldberg (*)
Creighton University School of Medicine,
Phoenix, AZ, USA
University of Arizona College of Medicine –
Phoenix, Phoenix, AZ, USA
e-mail: ross_goldberg@dmgaz.org

© Springer Nature Switzerland AG 2019 355

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_87
356 J. VanderVelde and R. F. Goldberg

History and physical exam:

A Right upper quadrant pain,
fever, jaundice s/p
cholecystectomy

Obtain vital signs and labs, perform physical exam

Leukocytosis, elevated
B LFTs and bilirubin

Fluid resuscitation, antibiotic therapy, abdominal ultrasound

ERCP

Yes
C
ERCP successful?
No

PTC

Yes
PTC successful? Definitive management
D after stabilization
No
F
E OR for open drainage

Algorithm 87.1

3. Surviving Sepsis Campaign Guidelines Committee.

References
1. Cameron J, Cameron A.  Current surgical therapy.
11th ed. Philadelphia: Elsevier; 2014.
2. Townsend C, Beauchamp R, Evers B, Mattox
K. Sabiston textbook of surgery. 19th ed. Philadelphia:
Elsevier; 2012.
Surviving Sepsis Campaign: international guide-
lines for management of sepsis and septic shock:
2016. Crit Care Med. 2017;45(3):486–552.
4. Hou LA, Laine L, Motamedi N, Sahakian A, Lane C,
Buxbaum J. Optimal timing of endoscopic retrograde
cholangiopancreatography in acute cholangitis. J Clin
Gastroenterol. 2017;51(6):534–8.
 Management
of Choledocholithiasis
Joel VanderVelde and Ross F. Goldberg
Algorithmic Approach
A. A history and physical exam is the first step in
evaluating a patient with choledocholithiasis.
Right upper quadrant pain is nonspecific to
choledocholithiasis and can be attributed to
other etiologies such as biliary colic, chole-
cystitis, and cholangitis, so a thorough history
including onset and associated symptoms is
important [1, 2].
B. Initially differentiating choledocholithiasis
from other disease processes usually starts
with initial laboratory values which may
show a cholestatic pattern. Liver function
tests, direct bilirubin, and alkaline phospha-
tase may be elevated. Lab findings of elevated
lipase and leukocytosis plus fever lend suspi-
cion to gallstone pancreatitis and acute chol-
angitis, respectively, which may also be
present with choledocholithiasis. If no chole-
static pattern is shown on initial laboratory
values, then another etiology should be
sought [1, 2].
J. VanderVelde
Department of Surgery, Maricopa Integrated Health
System, Phoenix, AZ, USA
R. F. Goldberg (*)
Creighton University School of Medicine,
Phoenix, AZ, USA
University of Arizona College of Medicine –
Phoenix, Phoenix, AZ, USA
e-mail: ross_goldberg@dmgaz.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_88
88
C. An abdominal ultrasound is the most com-
mon initial imaging study obtained due to
low cost, noninvasive nature, and speed at
which it may be obtained. Ultrasound has a
relatively high sensitivity but low specificity
[3]. Stones within the common bile duct or a
dilated common bile duct may be seen.
D. If no stone is seen on ultrasound, then a mag-
netic resonance cholangiopancreatography
(MRCP) should be obtained. MRCP has high
sensitivity and specificity for diagnosis of
choledocholithiasis [4]. This also allows eval-
uation of the entire biliary tree to rule out
other possible causes of biliary obstruction.
E. A common bile duct stone may be identified by
ultrasound or MRCP.  A preoperative endo-
scopic retrograde cholangiopancreatography
(ERCP) may be obtained at this point.
Preoperative ERCP can be effective in the hands
of an experienced endoscopist but does add an
additional procedure. Laparoscopic cholecys-
tectomy with common bile duct exploration can
also be chosen and has the benefit of offering
the patient only one procedure. However, it is
not a commonly performed procedure among
most general surgeons. Both options are avail-
able to the surgeon and should be decided with
utility and patient’s benefit in mind.
F. If a stone is removed with preoperative ERCP
or no stone is seen on MRCP (indicating pas-
sage of a stone), then a laparoscopic
­cholecystectomy should be performed during
the admission.
357
358 J. VanderVelde and R. F. Goldberg

History and physical exam:

Right upper quadrant/epigastric pain
A Nausea and vomiting
+/– jaundice

Obtain vital signs and labs,

perform physical exam

No
Elevated LFTs,
B Pursue other diagnosis
bili, alk phos?

Yes

C Obtain abdominal ultrasound

Equivocal

MRCP CBD stone?

Yes Yes E

CBD stone? Preoperative ERCP

No
ERCP successful? Lap chole with CBDE

No Yes

Cholecystectomy during admission

Algorithm 88.1

3. Qiu Y, et  al. An analysis of the factors related to

References
1. Cameron J, Cameron A.  Current surgical therapy.
11th ed. Philadelphia: Elsevier; 2014.
2. Townsend C, Beauchamp R, Evers B, Mattox
K. Sabiston textbook of surgery. 19th ed. Philadelphia:
Elsevier; 2012.
missed diagnosis of choledocholithiasis by preopera-
tive ultrasound. BM Gastroenterol. 2015;15:158.
4. Yaghoobi M, et  al. Diagnostic accuracy of EUS
compared with MRCP in detecting choledocho-
lithiasis: a meta-analysis of diagnostic test accu-
racy of head-to-head studies. Gastrointest Endosc.
2017;86(6):986–93.
 Acute Cholangitis
89
Joel VanderVelde and Ross F. Goldberg

Algorithmic Approach drainage. If no end-organ dysfunction is evi-

A. Acute cholangitis presents classically with
fever, jaundice, and right upper quadrant pain D. The location of the obstruction within the
(Charcot’s triad). The presence of altered
mental status and hypotension (Reynold’s
pentad) indicates a more severe form of the
disease. Initial evaluation should include
vitals, a physical exam, and laboratory values
including liver function tests and white blood E. If ERCP and PTC are unsuccessful at biliary
cell count [1, 2].
B. Resuscitation with intravenous fluids should
be started immediately as well as initiation
of antibiotic therapy, usually with a third-­
generation cephalosporin such as ceftriax-
one [3].
C. Evidence of end-organ dysfunction includes
altered mental status and hypotension
(included in Reynold’s pentad) as well as
elevated lactate, decreased urinary output,
and acute kidney injury. The presence of end-­
organ dysfunction necessitates urgent biliary
denced, then definitive management of the
underlying cause may be sought [4].
biliary tree dictates the method of drainage if
drainage is necessary. Distal obstructions are
usually amenable to ERCP [5]. Proximal
obstructions are not as amenable to ERCP
and may require PTC drainage [6].
drainage, then the patient should be taken for
open surgical drainage with choledochotomy.
Laparoscopic drainage may be performed as
well but is contraindicated if there is evidence
of hemodynamic instability [7].
F. If biliary drainage is successful with the
above measures, then definitive management
of the underlying obstructive etiology should
be performed. If the obstruction is due to gall-
stones, a cholecystectomy should be per-
formed during the same admission.

J. VanderVelde
Department of Surgery, Maricopa Integrated Health
System, Phoenix, AZ, USA
R. F. Goldberg (*)
Creighton University School of Medicine,
Phoenix, AZ, USA
University of Arizona College of Medicine –
Phoenix, Phoenix, AZ, USA
e-mail: ross_goldberg@dmgaz.org

© Springer Nature Switzerland AG 2019 359

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_89
360 J. VanderVelde and R. F. Goldberg

History:
Fever, jaundice, RUQ pain
+/– AMS, hypotension

Obtain vital signs and labs,

A
perform physical exam

Leukocytosis, elevated
LFTs, bili, alk phos

B
Fluid resuscitation, antibiotic therapy with 3rd
generation cephalosporin

No
Evidence of end
C
organ dysfunction?

Yes
D Urgent biliary drainage

Proximal Distal
obstruction obstruction

PTC No ERCP

Successful? Successful?
Yes

Yes
No

Surgical management Definitive management

E F

Algorithm 89.1

5. Hou LA, Laine L, Motamedi N, Sahakian A, Lane C,

References
1. Cameron J, Cameron A.  Current surgical therapy.
11th ed. Philadelphia: Elsevier; 2014.
2. Townsend C, Beauchamp R, Evers B, Mattox
K. Sabiston textbook of surgery. 19th ed. Philadelphia:
Elsevier; 2012.
3. Gomi H, et  al. Tokyo guidelines 2018: antimicro-
bial therapy for acute cholangitis and cholecystitis. J
Hepatobiliary Pancreat Sci. 2018;25:3–16.
4. Surviving Sepsis Campaign Guidelines Committee.
Surviving Sepsis Campaign: international guidelines
for management of sepsis and septic shock: 2016. Crit
Care Med. 2017;45(3):486–552.
Buxbaum J. Optimal timing of endoscopic retrograde
cholangiopancreatography in acute cholangitis. J Clin
Gastroenterol. 2017;51(6):534–8.
6. Qureshi WA.  Approach to the patient who has sus-
pected bacterial cholangitis. Gastroenterol Clin N
Am. 2006;35(2):409–23.
7. SAGES guidelines – guidelines for the clinical appli-
cation of laparoscopic biliary tract surgery. https://
www.sages.org/publications/guidelines/guidelines-
for-the-clinical-application-of-laparoscopic-biliary-
tract-surgery/. Accessed 2017.
 Cholangiocarcinoma
Zachary J. Senders, John B. Ammori,
and Jeffrey M. Hardacre
Algorithmic Approach
A. The presenting signs and symptoms of a
patient with cholangiocarcinoma will depend
on the anatomical location of the tumor.
Extrahepatic tumors, representing approxi-
mately 90% of all cholangiocarcinomas, most
often present with sequelae of biliary obstruc-
tion, including jaundice, pruritis, clay-­colored
stool, and dark urine. Serum bilirubin and
alkaline phosphatase are often elevated,
though aspartate aminotransferase (AST) and
alanine aminotransferase (ALT) may initially
be normal. Benign causes of biliary obstruc-
tion must be considered in a patient present-
ing with obstructive jaundice, especially if
clinical suspicion for malignancy is low.
Intrahepatic tumors (10% of all cholangiocar-
cinomas) are much less likely to present with
jaundice. These patients may have a history
of dull right upper quadrant pain, fever, or
weight loss and may have elevated alkaline
phosphatase. Intrahepatic cholangiocarci-
noma may also be discovered incidentally in
an asymptomatic patient during the workup
of abnormal LFTs [1].
Z. J. Senders · J. B. Ammori · J. M. Hardacre (*)
Department of Surgery, University Hospitals
Cleveland Medical Center, Cleveland, OH, USA
e-mail: jeffrey.hardacre@uhhospitals.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_90
90
B. If cholangiocarcinoma is suspected, patients
should undergo either multidetector, multipha-
sic, contrast-enhanced abdominal/pelvic com-
puted tomography (CT) or magnetic resonance
imaging (MRI) with magnetic resonance chol-
angiopancreatography (MRCP). Tumor mark-
ers cancer antigen 19-9 (CA 19-9) and
carcinoembryonic antigen (CEA) should be
obtained as a baseline measurement in patients
with cholangiocarcinoma, though they are nei-
ther sensitive nor specific for the diagnosis.
AFP should be obtained if intrahepatic cholan-
giocarcinoma is suspected, as an elevated level
is suggestive of hepatocellular carcinoma.
C. Cholangiocarcinoma is classified by the ana-
tomical location of the tumor. Intrahepatic
cholangiocarcinoma appears as an intrahe-
patic mass on cross-sectional imaging.
Intrahepatic biliary ductal dilation in both
hepatic lobes is suggestive of an extrahepatic
hilar (Klatskin) tumor, which constitutes
60–70% of all extrahepatic cholangiocarcino-
mas. Intra- and extrahepatic biliary ductal
dilation in the absence of a pancreatic head
mass or choledocholithiasis suggests distal
extrahepatic cholangiocarcinoma [2]. Tissue
diagnosis is not needed to proceed with sur-
gery for resectable disease, although endo-
scopic retrograde cholangiopancreatography
(ERCP)/endoscopic ultrasound (EUS) can
aid in diagnosis and staging of distal lesions
and should be considered [3].
361
362
D. Chest CT scan is recommended as part of the
staging workup to detect disseminated dis-
ease. Esophagogastroduodenoscopy (EGD)
and colonoscopy are mandatory in the setting
of an intrahepatic tumor to rule out metastatic
disease from a distant primary. Criteria for
resectability depend on the anatomical loca-
tion of the tumor. Distant liver metastasis or
disseminated disease precludes resection.
Invasion of the main portal vein, hepatic
artery, or extrahepatic adjacent organs is a
relative contraindication. An intrahepatic
tumor is considered unresectable if there
would not be an adequate future liver remnant
after resection. [4]
E. There are few treatment options for patients
with metastatic or unresectable disease,
though a regimen of gemcitabine plus cispla-
tin has been shown in a phase III trial to
improve survival. [5] Biliary drainage should
be considered in patients with unresectable
extrahepatic cholangiocarcinoma for symp-
tomatic relief. [1] Orthotopic liver transplan-
tation, most notably combined with
neoadjuvant chemoradiation, has shown
promise as a treatment modality for highly
selected patients with hilar cholangiocarci-
noma. As such, referral to a transplant center
Z. J. Senders et al.
can be considered. Percutaneous biliary
drainage, biopsy, or EUS with fine-needle
aspiration (FNA) can be contraindications to
transplant; therefore, consultation should be
obtained before proceeding with these proce-
dures in potential transplant candidates [6].
Locoregional therapies such as ablation and
transarterial chemoembolization (TACE)
have been shown to increase progression-free
survival in unresectable intrahepatic cholan-
giocarcinoma and can be considered.
F. Surgical management of intrahepatic cholan-
giocarcinoma involves hepatic resection, with
the goal of achieving negative margins. There
is no evidence that lymphadenectomy
improves survival; however, it can be consid-
ered for its prognostic value. Approach to the
resection of hilar tumors is based on the
Bismuth-­Corlette classification and Blumgart
staging system. This includes resection of the
involved biliary tract usually with en bloc
hepatic resection. Distal cholangiocarcinoma
is treated with pancreaticoduodenectomy.
Various regimens of adjuvant chemotherapy
and chemoradiation have shown modest sur-
vival benefit in phase II trials. Patients should
undergo postoperative surveillance at regular
intervals [1].
90 Cholangiocarcinoma 363

Patients may present with jaundice, pruritis, clay-colored stool, dark urine, abnormal
LFTs, dull RUQ pain, and/or weight loss

Obtain right upper No benign etiology of

No
High suspicion of quadrant ultrasound biliary obstruction found
malignancy?

Yes

B Obtain MRI/MRCP or MDCT, tumor markers (CA 19-9, CEA, AFP)

Intrahepatic No Intrahepatic biliary No No Alternative

Extrahepatic biliary diagnosis likely
mass on ductal dilation and/or
ductal dilation on
imaging? perihilar mass on
imaging?
imaging?

Yes Yes
C
Suggests hilar
cholangiocarcinoma
Pancreatic head Yes
No mass or
Positive AFP? Suggests intrahepatic choledocholithiasis
cholangiocarcinoma seen?

Yes No

Suggests HCC or Suggests distal extrahepatic Consider

mixed HCC/CCA cholangiocarcinoma EUS/ERCP

Options include
Yes
chemotherapy, clinical
trial, best supportive care,
biliary drainage if
indicated.
Options include
chemotherapy, clinical trial,
best supportive care, biliary
drainage if indicated.
No
Consider locoregional
therapy for intrahepatic
cholangiocarcinoma.
Consider referral to
transplant center. Biopsy
after transplant evaluation.
D
Metastatic Complete staging workup and evaluate resectability of tumor
disease?
Intrahepatic cholangiocarcinoma
Surgical management includes hepatic E
No resection. Consider staging
laparoscopy, portal lymphadenectomy.
Supportive care,
Hilarcholangiocarcinoma surveillance,
Yes
Resectable Surgical management includes consider
tumor? resection of involved biliary tract adjuvant therapy
usually withen bloc liver resection.
Consider staging laparoscopy.
Distal extrahepatic cholangiocarcinoma
Surgical management includes F
pancreaticoduodenectomy.

Algorithm 90.1
364 Z. J. Senders et al.

References 4. Jarnagin WR, Fong Y, DeMatteo RP, Gonen M, Burke

EC, Bodniewicz BSJ, et al. Staging, resectability, and
outcome in 225 patients with hilar cholangiocarci-
1. Benson AB III. NCCN guidelines: hepatobiliary can-
noma. Ann Surg. 2001;234(4):507–17. discussion
cers. NCCN Clin Pract Guidel Oncol. 2017;2:39–47.
517-9.
2. DeOliveira ML, Cunningham SC, Cameron JL,
5. Valle J, Wasan H, Palmer DH, Cunningham D,
Kamangar F, Winter JM, Lillemoe KD, et  al.
Anthoney A, Maraveyas A, et al. Cisplatin plus gem-
Cholangiocarcinoma. A spectrum of intrahe-
citabine versus gemcitabine for biliary tract Cancer. N
patic, perihilar, and distal tumors. Ann Surg.
Engl J Med. 2010;362(14):1273–81.
2007;245(5):755–62.
6. Rosen CB, Heimbach JK, Gores GJ.  Liver trans-
3. Abu-Hamda EM, Baron TH.  Endoscopic manage-
plantation for cholangiocarcinoma. Transpl Int.
ment of cholangiocarcinoma. Semin Liver Dis.
2010;23(7):692–7.
2004;24(2):165–75.
 Diagnosis and Management
of Gallbladder Cancer
Joshua L. Lyons, John B. Ammori,
and Jeffrey M. Hardacre
Algorithmic Approach
While uncommon with less than 5000 diagnoses
per year in the United States, gallbladder cancer
(GC) is the most frequently diagnosed cancer of
the biliary tract. It has a high mortality rate due to
its frequently advanced stage at diagnosis [1]. Its
incidence increases with age, and it is more com-
mon in women and blacks [2]. Risk factors
include cholelithiasis, gallbladder polyps, obesity,
and chronic infections of the gallbladder [3, 4].
Diagnosis of GC is made in one of three ways:
preoperatively, intraoperatively, or postopera-
tively. Due to the asymptomatic nature of early
GC, approximately 50% of diagnoses are inci-
dentally discovered postoperatively on pathology
[5]. The course of treatment and treatment goals
are different for the varying presentations and
therefore will be discussed separately.
A. Gallbladder cancer can be suspected preopera-
tively on various imaging modalities.
Ultrasonography is the most common modal-
ity used for evaluation of the gallbladder and
findings that suggest GC include an intralumi-
nal or fixed mass, no discernable plane between
the liver and gallbladder, and/or mural calcifi-
cations. While small lesions (<1 cm) can rep-
J. L. Lyons · J. B. Ammori · J. M. Hardacre (*)
Department of Surgery, University Hospitals
Cleveland Medical Center, Cleveland, OH, USA
e-mail: jeffrey.hardacre@uhhospitals.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_91
91
resent a variety of benign lesions, any lesion
>1 cm is an indication for surgery as it carries
a higher likelihood of malignancy [6]. Cross-
sectional imaging with CT scan of the chest,
abdomen, and pelvis or magnetic resonance
imaging (MRI)/magnetic resonance cholangi-
opancreatography (MRCP) with chest com-
puted tomography (CT) should be performed
preoperatively to evaluate for metastatic spread
and local invasion. Positron emission tomogra-
phy (PET)/CT is done selectively. Endoscopic
ultrasound can further differentiate between
benign and malignant lesions and also has the
ability to stage the tumor, although it is not
commonly used. While there is no laboratory
value that has sufficient specificity or sensitiv-
ity in the diagnosis of GC, an elevated CA
19-9 can be useful. After the workup is com-
pleted, the patient is deemed appropriate for
surgery if the mass is locally resectable with-
out metastatic spread. At surgery, diagnostic
laparoscopy is performed to rule out distant
metastases followed by resection at the same
setting. If the gallbladder mass or polyp is
between 1 and 2 cm without evidence of inva-
sion, then a laparoscopic cholecystectomy
with intraoperative frozen section is appropri-
ate. Care must be taken to avoid entry into the
gallbladder or bile spillage. Conversion to
open surgery is warranted if findings suggest
malignancy or there is no clear plane between
the gallbladder and liver bed. If frozen section
365
366
is positive, then oncologic surgery is under-
taken at the same setting. If the gallbladder
mass or polyp is greater than 2  cm, then an
oncologic surgery should be undertaken from
the outset. The operation of choice in GC is
an extended cholecystectomy which involves
resection of the gallbladder and hepatic bed
to a negative margin (usually liver segments
IVb and V but may require a more extensive
hepatectomy), regional lymphadenectomy,
and cystic/bile duct excision to a negative mar-
gin (if cystic margin is positive, a bile duct
resection with subsequent reconstruction is
necessary).
B. If a suspicious mass is encountered intraopera-
tively, it is recommended that the operation be
converted to open in order to have better tactile
feedback and minimize the risk of entering the
gallbladder. It is also accepted to stop the oper-
ation at this point and refer the patient to a high-
volume center. An open cholecystectomy
should then be performed without bile spillage
and the mass sent for frozen section exam. If
the mass is adherent to the liver bed, it is impor-
tant to resect a portion of the liver in order to
avoid violating the tumor and seeding the peri-
toneum. If the frozen section exam is positive
for malignancy and the surgeon is comfortable
with proceeding, an extended cholecystectomy
and lymphadenectomy should be done. If the
surgeon is not comfortable proceeding, closing
the patient with referral to a high-volume cen-
ter is the preferred course.
C. Gallbladder cancer is diagnosed most com-
monly on pathologic exam of a cholecystec-
tomy specimen done for benign biliary
disease. Management is dependent on the
tumor staging. If the tumor is Tis or T1a with
negative margins, no further resection is nec-
essary, as this does not convey a survival ben-
efit [7]. If the tumor is T1b or greater,
cross-sectional imaging of the chest, abdo-
men, and pelvis should be performed preop-
eratively to evaluate for metastatic spread and
local invasion. If no metastatic spread is
found, then diagnostic laparoscopy followed
by potentially curative hepatic resection,
lymphadenectomy, and cystic/bile duct exci-
J. L. Lyons et al.
sion should be performed. This second proce-
dure is required due to the high incidence of
residual disease and therefore does convey a
survival benefit [8].
D. Surgery is the only potentially curative ther-
apy for GC.  Five-year survival for stage IA
carcinoma is 50% compared to 2% in stage IV
carcinoma [9]. If an R0 resection is achieved
on final pathology with no lymph node
involvement, observation or adjuvant chemo-
radiation versus chemotherapy is reasonable.
There are no historical randomized controlled
trials (RCT) to guide adjuvant therapy for bili-
ary tract malignancies. However, a recent
RCT of 447 patients with biliary tract malig-
nancies (18% were GC) showed a survival
benefit with single agent capecitabine in the
adjuvant setting [10]. While further studies
are needed to compare capecitabine with cur-
rent adjuvant therapy regimes (gemcitabine
and cisplatin [11]), it emphasizes the need for
multidisciplinary care. In addition, there have
been retrospective studies that have shown a
survival advantage with radiation alone and
chemoradiation [12, 13]. There are no data
with regard to surveillance, but a reasonable
schedule could include repeat imaging every
6  months for 2  years and then annually for
5 years. If the resection has a positive margin
or there is gross residual disease or regional
lymph node involvement, the patient should
be referred for adjuvant chemoradiation ver-
sus chemotherapy. There is no role for pallia-
tive, debulking, or repeat resections as these
procedures do not convey a survival or pallia-
tive benefit. If the patient has obstructive jaun-
dice, endoscopic or percutaneous stenting is
preferred over biliary bypass. Multidisciplinary
cancer care teams are important to guide the
management of this disease.
Gallbladder cancer is an uncommon yet often
fatal malignancy. However, in selected patients,
surgical intervention can be curative. It is
­therefore prudent for surgeons to develop a sys-
tematic management plan in the event that GC is
diagnosed on pathologic review or during routine
cholecystectomy.
91  Diagnosis and Management of Gallbladder Cancer 367

Gallbladder cancer

Gallbladder mass on imaging Gallbladder cancer Gallbladder cancer diagnosed

A (US or EUS)
B C
suspected intraoperatively on pathology

MRI/MRCP with Chest CT

OR
Chest/Abd/Pelvis CT scan
Tis or T1a?

No
<1 cm 1–2 cm >2 cm

Yes
Yes MRI/MRCP with Chest CT
Concerning Frozen section exam OR
features? Chest/Abd/Pelvis CT scan
Observe

No

Mass is resectable
Laparoscopic with no evidence of
cholecystectomy metastatic spread?

Yes

Extended cholecystectomy with

lymphadenectomy and possible No
biliary tract
resection/reconstruction

No
R0 resection and
no lymph node Chemoradiation, chemotherapy,
involvement? or clinical trial

Yes

Consider adjuvant chemotherapy ± radiation vs observation

Algorithm 91.1
368
References
1. Carriaga MT, Henson DE.  Liver, gallbladder,
extrahepatic bile ducts, and pancreas. Cancer.
1995;75(S1):171–90.
2. Scott TE, Carroll M, Cogliano FD, Smith BF, Lamorte
WW. A case-control assessment of risk factors for gall-
bladder carcinoma. Dig Dis Sci. 1999;44(8):1619–25.
3. Okamoto M, Okamoto H, Kitahara F, Kobayashi
K, Karikome K, Miura K, Matsumoto Y, Fujino
MA.  Ultrasonographic evidence of association of
polyps and stones with gallbladder cancer. Am J
Gastroenterol. 1999;94(2):446–50.
4. Dutta U, Garg PK, Kumar R, Tandon RK.  Typhoid
carriers among patients with gallstones are at
increased risk for carcinoma of the gallbladder. Am J
Gastroenterol. 2000;95(3):784–7.
5. Duffy A, Capanu M, Abou-Alfa GK, Huitzel D,
Williams P, Jarnagin W, Fong Y, Kelsen DP, O’Reilly
EM. Gallbladder cancer (GBC): 10-year experience at
memorial Sloan-Kettering Cancer Centre (MSKCC).
J Clin Oncol. 2007;25(18_suppl):4648.
6. Toda K, Souda S, Yoshikawa Y, Momiyama T,
Ohshima M.  Significance of laparoscopic excisional
biopsy for polypoid lesions of the gallbladder. Surg
Laparosc Endosc Percutan Tech. 1995;5(4):267–71.
7. Taner CB, Nagorney DM, Donohue JH.  Surgical
treatment of gallbladder cancer. J Gastrointest Surg.
2004;8(1):83–9.
J. L. Lyons et al.
8. Shoup M, Fong Y. Surgical indications and extent of
resection in gallbladder cancer. Surg Oncol Clin N
Am. 2002;11(4):985–94.
9. Fong Y, Wagman L, Gonen M, Crawford J, Reed
W, Swanson R, Pan C, Ritchey J, Stewart A,
Choti M.  Evidence-based gallbladder cancer stag-
ing: changing cancer staging by analysis of data
from the National Cancer Database. Ann Surg.
2006;243(6):767.
10. Primrose JN, Fox R, Palmer DH, Prasad R, Mirza
D, Anthoney DA, Corrie P, Falk S, Wasan HS, Ross
PJ, Wall LR.  Adjuvant capecitabine for biliary tract
cancer: the BILCAP randomized study. J Clin Oncol.
2017;35(suppl; abstr 4006):4006.
11.
Malik IA, Aziz Z, Zaidi MS, Sethuraman
G.  Gemcitabine and cisplatin is a highly effec-
tive combination chemotherapy in patients with
advanced cancer of the gallbladder. Am J Clin Oncol.
2003;26(2):174–7.
12. Nakeeb A, Tran KQ, Black MJ, Erickson BA,
Ritch PS, Quebbeman EJ, Wilson SD, Demeure
MJ, Rilling WS, Dua KS, Pitt HA.  Improved sur-
vival in resected biliary malignancies. Surgery.
2002;132(4):555–64.
13. Kresl JJ, Schild SE, Henning GT, Gunderson LL,
Donohue J, Pitot H, Haddock MG, Nagorney
D.  Adjuvant external beam radiation therapy with
concurrent chemotherapy in the management of gall-
bladder carcinoma. Int J Radiat Oncol Biol Phys.
2002;52(1):167–75.
 Choledochal Cysts
Shreya Gupta, Jeffrey M. Hardacre,
and John B. Ammori
Algorithmic Approach
Five types of CC are described in this classifica-
tion. Type I CC (80–90% of all CC) is a fusiform
dilation of the common bile duct. Type II CC is a
true diverticula of the common bile duct (CBD).
Type III CC is an intraduodenal dilation of the
common channel also known as choledochocele.
Type IVA CC (15–20% of all CC) is multiple dila-
tions of the intra- and extrahepatic biliary tree,
whereas type IV B CC is multiple extrahepatic
dilations only. Type V CC or Caroli’s disease is
intrahepatic biliary tree dilation only. Symptoms
of CC include abdominal pain, jaundice, and
often a palpable abdominal mass if presenting at
the age of <10 years. About 20% of patients are
older than 20 years of age with the most common
symptom of abdominal pain. Untreated CC com-
plications include cholangitis, pancreatitis, and
obstructive jaundice. Cancer has been associated
with all subtypes of biliary cysts but is most com-
monly found in type I and type IV CC.
A. Vague patient presentation is often mislead-
ing and leads to delayed diagnosis. The most
common presenting symptom is abdominal
pain [1]. Even though these cysts are congen-
S. Gupta · J. M. Hardacre (*) · J. B. Ammori
Department of Surgery, University Hospitals
Cleveland Medical Center, Cleveland, OH, USA
e-mail: jeffrey.hardacre@uhhospitals.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_92
92
ital, they often present in adult years with
vague right upper quadrant symptoms, often
leading to cholecystectomy for presumed
gallbladder disease. Neonates with obstruc-
tive jaundice and palpable abdominal mass
are usually diagnosed promptly [2].
B. Ultrasound is often obtained to evaluate for
right upper quadrant pain or jaundice. An
ultrasound finding of a common bile duct dila-
tion >10  mm should alert the physician to
investigate for choledochal cyst [2]. Ultrasound
findings suggestive of CC should be investi-
gated with magnetic resonance cholangiopan-
creatography (MRCP), which is considered to
be a gold standard of diagnosing all types of
CC. Endoscopic retrograde cholangiopancrea-
tography (ERCP) is unnecessary for diagnosis
as it is more invasive and increases the risks of
cholangitis or pancreatitis [3, 4].
C. The type of CC dictates the surgical manage-
ment. Type II requires diverticulectomy or
simple excision. Type III CC or choledocho-
cele, on the other hand, requires ERCP with
sphincterotomy. The risk of malignancy is
reported to be very low in both type II and III
CC [2].
D. Type I and IVB CC warrant surgery including
complete cyst excision and Roux-en-Y hepat-
icojejunostomy for restoration of biliary con-
tinuity. Some surgeons suggest the use of
intraoperative frozen sections to rule out
­dysplasia or malignancy. However, malignancy
369
370 S. Gupta et al.

can develop anywhere in the biliary tract
including the gallbladder [5]. The literature
suggests a 0.7–6% post-excisional malig-
nancy rate in patients with remnant cyst tissue
or subclinical malignant disease that is not
detected during surgery [2].Type IVA and V
(Caroli’s disease) CC involve the intrahepatic
biliary and may require partial hepatectomy
[6, 7].
E. Type V may require liver transplantation for
pan-liver involvement. The risk of neoplasia
is <7%, but surgical intervention or liver
transplant is warranted secondary to cholan-
gitis and liver dysfunction/failure [2]. Given
the risk of malignancy in type I and IV CCs,
postoperative surveillance is performed with
ultrasonography or cross-sectional imaging
as well as liver enzymes to detect early can-
cer. The risk of malignancy is approximately
0.7–6% even in complete excision, primarily
due to undetectable cancerous lesions before
or at the time of surgery [1, 3, 4].

A Patient presents with vague right upper quadrant pain, jaundice,

nausea and vomiting

B Ultrasound of the right upper quadrant abdomen/MRCP

Type II Choledochocele-
Type III ERCP and
Simple Type of choledochal cyst
excision Sphincterotomy,
C if symptomatic

Type I/IV B
Type IV A/V

Hepatectomy for excision of the cyst,

D and reconstruction with wide hilar Complete excision with Roux-en- Y Hepaticojejunostomy
Roux-en-Y hepaticojejunostomy.

Follow up with surveillance ultrasonography and liver

E Possible liver transplant
enzymes

Algorithm 92.1
92  Choledochal Cysts 371

References 4. Martin RF.  Biliary cysts. Surg Clin N Am.

2014;94(2):219–32. https://doi.org/10.1016/j.
suc.2014.01.011. ISSN 0039-6109.
1. Todani T, Tabuchi K, Watanabe Y, Kobayashi
5. Singham J, Yoshida EM, Scudamore CH. Choledochal
T.  Carcinoma arising in the wall of congenital bile
cysts: Part 2 of 3: diagnosis. Can J Surg.
duct cysts. Cancer. 1979;44(3):1134–41.
2009;52(6):506–11.
2. Soares KC, Arnaoutakis DJ, Kamel I, Rastegar N,
6. Singham J, Yoshida EM, Scudamore CH. Choledochal
Anders R, Maithel S, Pawlik TM. Choledochal cysts:
cysts: Part 3 of 3: management. Can J Surg.
presentation, clinical differentiation, and manage-
2010;53(1):51–6.
ment. J Am Coll Surg. 2014;219(6):1167–80. https://
7. Roukounakis N, Manolakopoulos S, Tzourmakliotis
doi.org/10.1016/j.jamcollsurg.2014.04.023. ISSN
D, Bethanis S, Mccarty TM, Cuhn J.  Biliary tract
1072-7515.
malignancy and abnormal pancreaticobiliary junc-
3. Ohashi T, Wakai T, Kubota M, et  al. Risk of sub-
tion in a Western population. J Gastroenterol Hepatol.
sequent biliary malignancy in patients undergoing
2007;22(11):1949–52.
cyst excision for congenital choledochal cysts. J
Gastroenterol Hepatol. 2013;28(2):243–7.
 Cholecystectomy of the Pregnant
Patient
Avi Hameroff and Jaimey M. Pauli
Algorithmic Approach
A. Gallbladder disease (GD) is a wide spectrum
of disorders of the gallbladder and biliary
tract. Increased levels of sex steroid hor-
mones in pregnancy and the postpartum
period contribute to biliary stasis, with gall-
stones occurring in 7% of nulliparous women
and 19% of multiparous women [1, 2].
Complicated GD (CGD; cholecystitis, chol-
angitis, gallstone pancreatitis) is the third
most common cause of rehospitalization
within 60  days of delivery, and compared
with women who deliver vaginally, Cesarean
section increases the risk of CGD [3].
B. Initial evaluation of a pregnant patient sus-
pected to have GD includes history and phys-
ical exam. Symptoms of cholecystitis include
fever, nausea, and ill appearance, whereas
cholangitis is described as presenting with
Charcot’s triad of fever, right upper quadrant
(RUQ) pain, and jaundice but is only seen in
about 50% of cases [4]. Labs may be drawn to
evaluate serum bilirubin, alkaline phospha-
tase, aspartate aminotransferase (AST), ala-
nine aminotransferase (ALT), and amylase.
Bile salts may also help in the assessment.
A. Hameroff · J. M. Pauli (*)
Maternal-Fetal Medicine, Department of Obstetrics
and Gynecology, Penn State Health Milton S.
Hershey Medical Center, Hershey, PA, USA
e-mail: jpauli@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_93
93
Additionally, ultrasound should be consid-
ered first line as part of the workup for RUQ
pain [5].
C. Although cholecystectomy may be performed
via open or laparoscopic approaches depend-
ing on surgeon preference and experience,
laparoscopic cholecystectomy is safe and
effective at treating GD during pregnancy and
may decrease the frequency of antepartum
and postpartum admissions of affected patient
[6–8]. The laparoscopic approach has been
found to have shorter operative times,
decreased hospital length of stay, and reduced
complications with similar risk of antenatal
complications compared to the open tech-
nique [9, 10]. It has additionally been found
to be safe in any trimester, and significant
maternal and/or fetal morbidity, including
fetal loss, may result from delay in surgical
management [11].
D. Practitioners should have a low threshold to
recommend surgical intervention, although
medical management with ursodeoxycholic
acid is an option and is generally considered
safe during pregnancy. Consultation with an
obstetrician is recommended to assist with
monitoring and delivery planning of the fetus,
as well as coordination of surgery if Cesarean
section is indicated.
E. Strategies to minimize the effect of surgery
(open or laparoscopic) on the pregnancy
include the following: early diagnosis,
373
374 A. Hameroff and J. M. Pauli

­ inimal uterine manipulation, continuous

m matic compression devices, fetal and uterine
urinary catheterization and gastric emptying, activity monitoring during and after surgery,
open entry for laparoscopy, alternative entry consideration of tocolytic therapy, and ante-
sites to avoid the gravid uterus, left lateral natal steroid administration for gestational
recumbent positioning, maintaining intraab- age >23–24 weeks [12].
dominal pressure <12 mm Hg, use of pneu-

History:
A Right upper quadrant pain (especially in relation to eating
and/or cyclic throughout day), anorexia, chills

B Exam:
Vital signs to assess temperature, heart rate, blood pressure
Labs:
CBC, AST/ALT, alk phos, total bilirubin, bile acids, amylase
Ultrasound:
Presence of gallstones, biliary sludge, dilation of biliary tracts

Complicated Uncomplicated
C gallbladder disease? gallbladder disease?

Consultation with OB for fetal monitoring, Consultation with OB for fetal monitoring,
delivery planning delivery planning

Proceed to cholecystectomy (laparoscopy

preferred)

Conservative or medical management Proceed to cholecystectomy

D
with ursodeoxycholic acid (laparoscopy preferred)

Ensure close follow-up with OB (+/– antenatal

surveillance)
E Develop plan for cholecystectomy if symptoms
worsen
Plan elective cholecystectomy postpartum

Algorithm 93.1
93  Cholecystectomy of the Pregnant Patient 375

References stone disease in pregnancy is associated with recur-

rent postpartum symptoms. J Gastrointest Surg.
2013;17(11):1953–9.
1. Gilat T, Konikoff F. Pregnancy and the biliary tract.
8. Muench J, Albrink M, Serafini F, Rosemurgy A,
Can J Gastroenterol. 2000;14(Suppl D):55D–9D.
Carey L, Murr MM. Delay in treatment of biliary dis-
2. Pataia V, Dixon PH, Williamson C.  Pregnancy and
ease during pregnancy increases morbidity and can be
bile acid disorders. Am J Physiol Gastrointest Liver
avoided with safe laparoscopic cholecystectomy. Am
Physiol. 2017;313(1):G1–6.
Surg. 2001;67(6):539–42. discussion 542–543.
3. Lydon-Rochelle M.  Association between method
9. Cox TC, Huntington CR, Blair LJ, Prasad T,
of delivery and maternal rehospitalization. JAMA.
Lincourt AE, Augenstein VA, et  al. Laparoscopic
2000;283(18):2411.
appendectomy and cholecystectomy versus open:
4. Avegno J, Carlisle M.  Evaluating the patient with
a study in 1999 pregnant patients. Surg Endosc.
right upper quadrant abdominal pain. Emerg Med
2016;30(2):593–602.
Clin North Am. 2016;34(2):211–28.
10. Corneille MG, Gallup TM, Bening T, Wolf SE,

5. Revzin MV, Scoutt LM, Garner JG, Moore CL. Right
Brougher C, Myers JG, et al. The use of laparoscopic
upper quadrant pain: ultrasound first!: RUQ Pain:
surgery in pregnancy: evaluation of safety and effi-
Ultrasound first! J Ultrasound Med [Internet]. 2017
cacy. Am J Surg. 2010;200(3):363–7.
Jun 6 [cited 2017 Aug 18]; Available from: http://doi.
11. Jackson H, Granger S, Price R, Rollins M, Earle

wiley.com/10.1002/jum.14274.
D, Richardson W, et  al. Diagnosis and laparo-
6. Jorge AM, Keswani RN, Veerappan A, Soper NJ,
scopic treatment of surgical diseases during preg-
Gawron AJ.  Non-operative management of symp-
nancy: an evidence-based review. Surg Endosc.
tomatic cholelithiasis in pregnancy is associated
2008;22(9):1917–27.
with frequent hospitalizations. J Gastrointest Surg.
12. Weiner E, Mizrachi Y, Keider R, Kerner R, Golan
2015;19(4):598–603.
A, Sagiv R.  Laparoscopic surgery performed in
7. Veerappan A, Gawron AJ, Soper NJ, Keswani
advanced pregnancy compared to early pregnancy.
RN. Delaying cholecystectomy for complicated gall-
Arch Gynecol Obstet. 2015;293:1063–108.
 Part XII
Pancreas
 Acute Pancreatitis
Kayla M. Hartz and Jennifer Maranki
Algorithmic Approach
A. A diagnosis of acute pancreatitis (AP)
requires two of the following criteria: acute
onset of persistent, severe, upper abdominal
pain; elevation in serum lipase to three times
the upper normal limit; and imaging (ultra-
sound (US), computed tomography (CT),
magnetic resonance imaging (MRI)) demon-
strating characteristic findings [1].
B. AP is classified based on three levels of sever-
ity. Mild acute pancreatitis is characterized
by the lack of organ failure and local and sys-
temic complications. Moderately severe pan-
creatitis includes transient organ failure (less
than 48 h) and/or local or systemic complica-
tions without persistent organ failure. Severe
acute pancreatitis is characterized by persis-
tent organ failure in one or more organs.
C. On physical exam, there may be a range of
tenderness to palpation of the epigastrium, as
well as abdominal distention and hypoactive
bowel sounds. In severe cases, patients may
be febrile, hypotensive, tachypnic, and
hypoxemic. Jaundice or scleral icterus may
K. M. Hartz (*)
Edward Via College of Osteopathic Medicine,
Blacksburg, VA, USA
J. Maranki
Department of Gastroenterology and Hepatology,
Penn State Milton S. Hershey Medical Center,
Hershey, PA, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_94
94
be present. Cullen’s sign (periumbilical
ecchymosis) or Grey Turner sign (flank
ecchymosis) occurs in the setting of retroperi-
toneal hematoma and pancreatic necrosis.
D. Lipase is more sensitive than amylase in pan-
creatitis. Sensitivity and specificity for AP
range from 82% to 100% [2]. Elevations in
lipase occur earlier and last longer compared
with elevations in amylase.
E. Patients with moderately severe or severe AP,
sepsis, or clinical deterioration 72 h after ini-
tial presentation should undergo contrast-­
enhanced CT scan to assess for necrosis or
local complications.
F. Severity of AP should be evaluated via exam
to assess for fluid losses, organ failure, acute
physiology and chronic health evaluation
(APACHE) II score, and systemic inflamma-
tory response syndrome (SIRS) score.
G. Indications for admission to a monitored set-
ting or ICU care include hemodynamic or
respiratory instability, electrolyte dysregula-
tion, hyperglycemia, anuria, or changes in
mental status and, additionally, those with
SIRS >48 h, age >60 years, APACHE II >8 at
24 h, hematocrit >44%, creatinine >1.8 mg/
dL, BUN >20  mg/dL, or coexisting cardio-
pulmonary disease [3].
H. Main goals of initial management consist of
fluid resuscitation, pain control, and nutri-
tional support.
379
380
(a). Intravenous hydration with lactated
Ringer’s (LR) solution or normal saline
at a rate of 5–10 mL/kg/h. Avoid LR in
hypercalcemic patients. Some data sug-
gest LR may decrease the SIRS response.
Frequently assess adequacy of fluid
resuscitation. Goals are MAPs
65–85 mmHg, urine output >0.5 to 1 cc/
kg/h, hematocrit reduced to 35–44%,
heart rate  <120  bpm, and reductions in J. In patients with gallstone pancreatitis who
blood urea nitrogen (BUN) [4]. Limit
fluid resuscitation to the first 24–48 h.
(b). Intravenous opioids are effective at pro-
viding pain control. Frequently patient-­
controlled analgesia (PCA) pumps are
used. Patients should be closely moni-
tored for side effects.
(c). Nutritional support is required for
patients who are unable to tolerate on K. Cholecystectomy should be performed after
oral diet within 7 days. Nasojejunal tube
feeding is preferred to total parenteral
nutrition and is recommended for those
with moderately severe and severe AP
who cannot tolerate an oral diet.
I. Local and systemic complications may
develop and include acute peripancreatic
fluid collections, pseudocysts, acute necrotic
K. M. Hartz and J. Maranki
collections, and walled-off necrosis.
Pseudocysts and walled-off necrosis occurs
typically greater than 4 weeks after the initial
presentation. Infected necrosis should be sus-
pected in patients who clinically deteriorate
(elevated white count, fevers, sepsis-like clin-
ical picture) or fail to improve after 7–10 days.
Management of fluid collections and necrosis
is discussed elsewhere.
develop cholangitis, ERCP with sphincterot-
omy should be performed within 24 h. If clin-
ical suspicion for biliary obstruction is
present without overt cholangitis, an endo-
scopic ultrasound (EUS) or a magnetic reso-
nance cholangiopancreatography (MRCP)
should be performed for the evaluation of
common bile duct stones.
recovery in all patients with gallstone pancre-
atitis. For those with mild AP, it should be
performed during the index hospitalization
[5]. Failure to perform a cholecystectomy is
associated with a 25–30% risk of recurrent
AP, cholangitis, or cholecystitis within
6–18 weeks [6].
94  Acute Pancreatitis 381

Symptoms of persistent upper abdominal pain

plus serum lipase >3 x ULN and/or cross-sectional
A imaging demonstrating findings characteristic of
pancreatic inflammation

Diagnosis of acute pancreatitis (AP)

B
Organ failure or No
local/systemic Mild AP
complications?

Yes, transient Yes, persistent

Moderately severe
Severe AP
AP

Physical exam/labs: TTP epigastrium, distention,

C, D, G hypoactive bowel sounds, febrile, hemodynamic
instability, jaundice, Cullen’s/Grey Turner signs;
elevated lipase/amylase; elevated glucose,WBC;
elevated BUN/Cr, Hct; electrolyte abnormalities
Assess for ICU monitoring

Treat with LR or NS, 5–10 ml/kg/h

Goal MAP 65-85 mmHg, urine output >0.5 to 1
H cc/kg/h, hematocrit reduced to 35-44%,
heart rate < 120 bpm, reductions in BUN
Pain control
Nutritional support if >7 days with no POs

Algorithm 94.1
382 K. M. Hartz and J. Maranki

E,F
Clinical deterioration
or failure to improve
after 72 h?

CT scan with contrast to assess for necrosis or

local complications

I
Fluid collection or
necrosis and fever,
leukocytosis, or sepsis
physiology?

Treat with IV abx for infected collection (typically

occurs 7–10 days after initial presentation; if no
improvement, debridement via necrosectomy
(wait 4 weeks if possible for wall to form)

If gallstone pancreatitis and cholangitis, ERCP with

J, K sphincterotomy within 24 h;
cholecystectomy within index hospitalization if
mild AP; wait for recovery in other cases

Algorithm 94.1 (continued)

4. Working Group IAP/APA Acute Pancreatitis

References
1. Banks PA, Bollen TL, Dervenis C, et al. Classification
of acute pancreatitis  – 2012: revision of the Atlanta
classification and definitions by international consen-
sus. Gut. 2013;62:102.
2. Yadav D, Agarwal N, Pitchumoni CS. A critical eval-
uation of laboratory tests in acute pancreatitis. Am J
Gastroenterol. 2002;97:1309.
3. Wu BU, Banks PA.  Clinical management of
patients with acute pancreatitis. Gastroenterology.
2013;144:1272.
Guidelines. IAP/APA evidence-based guidelines for
the management of acute pancreatitis. Pancreatology.
2013;13:e1.
5. Aboulian A, Chan T, Yaghoubian A, et al. Early cho-
lecystectomy safely decreases hospital stay in patients
with mild gallstone pancreatitis: a randomized pro-
spective study. Ann Surg. 2010;251:615.
6. Hernandez V, Pascual I, Almela P, et  al. Recurrence
of acute gallstone pancreatitis and relationship with
cholecystectomy or endoscopic sphincterotomy. Am J
Gastroenterol. 2004;99:2417.
 Chronic Pancreatitis
Kayla M. Hartz and Jennifer Maranki
Algorithmic Approach
A. Chronic pancreatitis is characterized by epi-
gastric abdominal pain, often radiating to the
back, and frequently postprandial. Early in
the disease process, pain episodes may be
discrete, whereas the pain may become con-
tinuous later in the course. In over 20% of
patients with chronic pancreatitis, pain is not
a feature of their disease.
B. Pancreatic insufficiency results from exocrine
function that is severely compromised; clini-
cally significant deficiencies occur when 90%
of exocrine function is lost. Fat malabsorp-
tion presents with greasy, foul-smelling stools
and results in losses of vitamins A, D, E, K,
and B12. Glucose intolerance is common,
and diabetes occurs late in the disease, par-
ticularly in patients with calcific pancreatitis.
C. Patients may develop benign biliary strictures
as a result of chronic pancreatitis, as well as
duodenal stenosis, splenic vein thrombosis,
pseudocysts, gastric outlet obstruction, pleu-
ral effusions and pancreatic ascites, and pan-
creatic cancer.
K. M. Hartz (*)
Edward Via College of Osteopathic Medicine,
Blacksburg, VA, USA
J. Maranki
Department of Gastroenterology and Hepatology,
Penn State Milton S. Hershey Medical Center,
Hershey, PA, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_95
95
D. A diagnosis of chronic pancreatitis may be
difficult. Pancreatic calcifications identified
on imaging is diagnostic; other findings
include beading and irregularity of the pan-
creatic duct with enlarged side branches and
an abnormal secretin study.
E. Serum amylase and lipase may be normal in
chronic pancreatitis. Complete blood count
(CBC) and basic metabolic panel (BMP) may
be normal. Elevations in LFTs may signify
biliary compression through the intrapancre-
atic portion. Elevations in immunoglobulin
G4 (IgG4), antinuclear antibody (ANA),
rheumatoid factor (RF), erythrocyte sedimen-
tation rate (ESR), anti-Smith (anti-Sm) anti-
body may indicate an autoimmune process.
Increased fecal fat excretion or fecal elastase
may also aid in the diagnosis.
F. MRCP is the preferred diagnostic imaging
test since it can show irregularities of the pan-
creatic duct (beading and ectatic side
branches) as well as calcifications. EUS is
also helpful in making the diagnosis, particu-
larly in early disease. In addition to stones,
suggestive findings include lobularity, cysts,
hyperechoic foci and strands, ductal dilation,
and hyperechoic duct walls [1].
G. General treatment includes alcohol and
smoking cessation, hydration, small, low-fat
meals. Pancreatic enzyme supplementation
may be helpful in pain control. Pain control
should follow a step-up pattern, starting with
383
384
TCAs (amitriptyline or nortriptyline).
NSAIDs may be used in the short-term in
conjunction with TCAs. Pregabalin may also
provide pain control. Chronic opioids may be
needed for those with persistent significant
pain. Long-acting agents such as MS Contin
or fentanyl patches may be beneficial. An opi-
ate contract should be maintained by the pre-
scribing physician, and a pain management
consultation may be beneficial. [2]
H. Additional therapies such as celiac plexus
block, pancreatic duct stenting, and extracor-
K. M. Hartz and J. Maranki
poreal shock wave lithotripsy. Surgical
approaches may achieve decompression or
drainage, denervation, or resections.
Decompression procedures, such as Frey or
Puestow, are suited for those with pancre-
atic duct dilation and may achieve pain con-
trol in 60–80% of patients. Resection
procedures are reserved for those with a
nondilated duct and localized disease.
Autologous islet cell transplantation may be
beneficial in post-resection patients with
pancreatic insufficiency.
95  Chronic Pancreatitis 385

History: persistent epigastric abdominal pain, often radiating to the back.

A Pain episodes may initially be episodic but become continuous as the
disease progresses. Pain is not a feature in around 20%

Check 72-h fecal fat or fecal elastase; vitamins A,D,E,K, and B12 may become
B, C, E deficient; assess for glucose intolerance/diabetes; amylase and lipase may be
normal; LFTs may be elevated if biliary obstruction

D Obtain imaging such as RUQ U/S, CT, or MRI to assess for biliary
dilation/stricture, panc calcifications, duodenal stricture/GOO,
effusions/ascites, pancreatic cancer, and pseudocysts

Findings
concerning
chronic
pancreatitis?

Check MRCP to assess for ductal irregularities; perform EUS to exclude

F pancreatic cancer and to assess for parenchymal and ductal characteristics of
chronic pancreatitis

Tx: smoking/EtOH cessation, hydration, low-fat diet, pancreatic enzyme

G supplementation (use PPI if non-enteric coated), TCAs, NSAIDs for short term. If
opiates are needed, rec narcotic contract

If sxs persist: ERCP with PD stenting, CBD stenting if benign biliary

H stricture; celiac plexus block, ESWL for PD stones; surgical drainage
or resection, autologous islet cell transplantation

Algorithm 95.1

atitis: interobserver agreement among experienced

References ultrasonographers. Gastrointest Endosc. 2001;53:294.
2. Braganza JM, Lee SH, McCloy RF, McMahon
1. Wallace MB, Hawes RH, Durkalski V, et al. The reli- MJ. Chronic pancreatitis. Lancet. 2011;377:1184.
ability of EUS for the diagnosis of chronic pancre-
 Pancreas Divisum
Kayla M. Hartz and Jennifer Maranki
Algorithmic Approach
A. The first step in the evaluation of a patient
with suspected pancreas divisum is obtaining
a thorough history and physical examination.
Key aspects of the history include recurrent
pancreatobiliary pain, mild acute pancreatitis,
recurrent idiopathic pancreatitis, or the pres-
ence of chronic pancreatitis. While pancreas
divisum may be present in up to 10% of the
population, less than 5% of these individuals
will become symptomatic. However, in
patients with idiopathic pancreatitis, pancreas
divisum may be present in up to 50% [1].
B. Diagnosis is usually made via cross-sectional
imaging, including CT scan or MRCP. If the
pancreatic duct is visualized on CT scan,
axial images demonstrate the dorsal duct
coursing superiorly and anteriorly to the dis-
tal common bile duct and draining at the
minor papilla. The presence of a fat plane
between the dorsal and ventral segments is
suggestive of pancreas divisum.
K. M. Hartz (*)
Edward Via College of Osteopathic Medicine,
Blacksburg, VA, USA
J. Maranki
Department of Gastroenterology and Hepatology,
Penn State Milton S. Hershey Medical Center,
Hershey, PA, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_96
96
C. From the embryologic foregut, the dorsal
and ventral anlages fuse to form the pan-
creas. Pancreas divisum occurs when the
dorsal and ventral duct systems fail to fuse.
Classic or complete pancreas divisum is
when the dorsal duct (Santorini) becomes
enlarged and drains the body and tail through
the minor papilla. The ventral duct (Wirsung)
is disconnected from the main duct and often
drains the uncinate. Incomplete pancreas
divisum is when a small branch of the ventral
duct communicates with the dorsal duct.
Reverse divisum may occur if the dorsal duct
is isolated from the main duct. This is clini-
cally significant in the setting of gallstone
pancreatitis, which may cause a more severe
pancreatitis than would have occurred in a
pancreas with typical anatomy.
D. Additional evaluation and/or treatment is
dependent on whether the patient is symp-
tomatic or not. For asymptomatic individu-
als, no further additional evaluation should
be pursued. In symptomatic patients, a
secretin-­enhanced MRCP and/or endoscopic
ultrasound provides additional information
about the pancreas and improves ductal
visualization.
E. ERCP is reserved for endoscopic therapy of
pancreas divisum but may also provide diag-
nostic information. Features of pancreas divi-
sum on ERCP are a thin, short ventral duct
and, when cannulating the dorsal duct, the
387
388 K. M. Hartz and J. Maranki

filling of the entire dorsal duct to the tail.
Other suggestive findings are delayed drain-
age of the dorsal duct, a santorinicele, and the
presence of pain during dorsal ductography.
F. For patients with minimal symptoms, con-
servative treatment is recommended. This
consists of a low-fat diet, analgesics, and
pancreatic enzyme supplementation. For
patients with severe or recurrent symp-
toms, minor papillotomy may be per-
formed, particularly in patients with two or
more bouts of acute pancreatitis with no
other etiology [2].

History and physical exam: recurrent

A pancreatobiliary pain, mild acute
pancreatitis, recurrent idiopathic
pancreatitis, chronic pancreatitis

Obtain cross-sectional imaging (CT or MRCP). Dorsal duct will

B course superiorly and anteriorly to the distal common bile duct
and drain at minor papilla

Assess type of pancreas divisum based on features of the ventral duct. Classic pancreas
divisum occurs when Wirsung is disconnected from Santorini, whereas incomplete pancreas
C divisum describes the presence of a small branch of Wirsung communicating with the
dorsal duct

No
D Is the patient
symptomatic? No further workup is needed

Yes

E Secretin-enhanced MRCP and/or EUS

Minimal Sxs: conservative tx with low-fat diet, analgesics, pancreatic enzymes

F Severe/recurrent Sxs: ERCP with minor papillotomy

Algorithm 96.1
96  Pancreas Divisum 389

References 2. Lehman GA, Sherman S, Nisi R, Hawes RH. Pancreas

divisum: results of minor papilla sphincterotomy.
Gastrointest Endosc. 1993;39(1):1–8.
1. Bernard JP, Sahel J, Giovannini M, Sarles H. Pancreas
divisum is a probable cause of acute pancreatitis: a
report of 137 cases. Pancreas. 1990;5:248.
 Walled-Off Pancreatic Fluid
Collections
Kayla M. Hartz and Jennifer Maranki
Algorithmic Approach
A. Symptoms of PC and WOPN may include
abdominal pain, fever/infection, gastric outlet
obstruction, biliary obstruction, venous
thrombosis or pseudoaneurysm, or fistulas,
hemosuccus pancreaticus, pancreatic ascites,
or pleural effusions.
B. Walled-off pancreatic fluid collections con-
sist of pseudocysts (PC) and walled-off pan-
creatic necrosis (WOPN) [1].
(a) Both typically become mature at least
4  weeks after the onset of acute
pancreatitis.
(b) PC have a well-defined wall and consist
of only liquid (no solid component or
necrosis).
(c) WOPN is an encapsulated collection of
necrosis that contains liquid and solid
components.
C. For diagnosis, a history suggestive of pancre-
atitis or pancreatic trauma, plus imaging (CT
or MRI), and sometimes fluid sampling is
required.
K. M. Hartz (*)
Edward Via College of Osteopathic Medicine,
Blacksburg, VA, USA
J. Maranki
Department of Gastroenterology and Hepatology,
Penn State Milton S. Hershey Medical Center,
Hershey, PA, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_97
97
(a) History of pancreatitis or pancreatic
trauma
(b) PC: round or oval, well-defined fluid col-
lection with a clear “rind” or wall around
the collection; homogenous fluid density;
usually extrapancreatic
(c) WOPN: well-defined wall around a het-
erogenous collection with solid and liq-
uid components; may be multiloculated
(d) If diagnosis is uncertain, EUS- or CT-­
guided sampling of fluid is helpful. Fluid
analysis will show an elevated amylase
and low CEA levels; gram stain and cul-
ture may be helpful in directing antibiot-
ics for infected collections.
D. Treatment depends on the presence of symp-
toms or complications. Options for drainage
include endoscopic, percutaneous, or surgical
approaches.
(a) Endoscopic cystgastrostomy or cystduo-
denostomy is suitable for collections
abutting the gastrointestinal (GI) lumen
and accessible with EUS. Placement of a
lumen-apposing metal stent or two
double-­pigtail stents will provide drain-
age of the liquid component. If necrosis
or solid debris is found, necrosectomy
may be needed. Nasocystic drainage tube
placement is also an option. Endoscopic
retrograde cholangiopancreatography
(ERCP) with pancreatic duct stenting
may help heal leak and resolve fluid
391
392 K. M. Hartz and J. Maranki

­collection [2]. Multiple procedures may
be required. It is not appropriate in the
case of pseudoaneurysm.
(b) Percutaneous (via interventional radiol-
ogy) approach is done with CT-guided
placement of drains. It requires multiple
procedures and may cause a cutaneous
fistula.
(c) Surgical creation of a cystgastrostomy or
cystenterostomy: left-sided pancreatec-
tomy may be needed in the case of dis-
connected pancreatic tail.
(d) If pseudoaneurysm is suspected, emboli-
zation is recommended prior to
drainage.
E. Follow-up imaging in patients with expectant
management every 3 months until resolution.
Sooner imaging based on symptoms and
interventions.

In a patient with acute or chronic pancreatitis or pancreatic

A trauma, assess for symptoms of walled-off collections, including
fever/infection, nausea/vomiting/inability to tolerate PO,
jaundice, worsening abdominal pain, GI bleeding, ascites, or
symptoms of pleural effusion

Obtain CT or MRI: walled-off collections at least 4 weeks after

onset of pancreatitis
B Pseudocysts: round or oval, thin walls and liquid contents only
WOPN: encapsulated collection with liquid and solid
debris/necrosis, may be multiloculated

Yes
Is diagnosis Obtain EUS- or CT-guided fluid
C in analysis
question? Expect low CEA, very high amylase,
Gram stain and cx may be helpful

No

No Expectant management;
Is patient
symptomatic?
consider CT in 3 months E
and follow until resolution

Yes

Endoscopic treatment: EUS-guided cystgastrostomy, cystduodenostomy; necrosectomy;

D nasocystic drain, ERP with PD stent
Percutaneous: CT-guided drain placement; gradual upsizing to allow for debris removal
Surgical: cystgastrostomy, cystenterosotomy, pancreatic resection
If pseudoaneurysm, then IR for treatment first

Algorithm 97.1
97  Walled-Off Pancreatic Fluid Collections 393

References 2. Baron TH, Harewood GC, Morgan DE, Yates

MR. Outcome differences after endoscopic drainage
of pancreatic necrosis, acute pancreatic pseudocysts,
1. Banks PA, Bollen TL, Dervenis C, et al. Classification
and chronic pancreatic pseudocysts. Gastrointest
of acute pancreatitis  – 2012: revision of the Atlanta
Endosc. 2002;56:7.
classification and definitions by international consen-
sus. Gut. 2013;62:102.
 Periampullary Carcinoma
Heidi N. Overton and Matthew J. Weiss
Algorithmic Approach
Periampullary adenocarcinoma (PAC) is a clin-
icopathologic entity comprised of four distinct
subtypes in one high-density anatomic region.
Formally defined as tumors arising ≤2 cm from
the ampulla of Vater, PAC can originate from
the pancreatic head, duodenum, distal bile
duct, or ampulla of Vater [1]. Pancreatic ductal
adenocarcinoma (PDAC) is the most common
PAC with a recent longitudinal study demon-
strating its occurrence at 66% compared to
16%, 12%, and 6% for ampullary, biliary, and
duodenal adenocarcinomas, respectively [2].
Though not a common tumor type, PAC has
low overall survival rates that differ signifi-
cantly by location of origination [3]. To illus-
trate, one series reported primary site-specific
5-year PAC survival rates of only 17% for pan-
creas, 23% for bile duct, 37% for ampulla, and
51% for duodenum [4]. The high and variable
mortality of PAC is likely attributable to stage
at presentation and inherent biologic differ-
ences in pancreatobiliary versus intestinal his-
tology [1, 5].
H. N. Overton · M. J. Weiss (*)
Department of Surgery, Johns Hopkins Hospital,
Baltimore, MD, USA
e-mail: mweiss5@jhmi.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_98
98
Diagnosis and Preoperative
Evaluation
A. Patients most frequently present with obstruc-
tive jaundice possibly accompanied by vague
abdominal pain, nausea, and weight loss [6].
PAC should always be considered when eval-
uating a patient with obstructive jaundice,
and basic workup of laboratory studies
including liver function tests (LFTs), cancer
antigen 19-9 (CA 19-9), carcinoembryonic
antigen (CEA), and cross-sectional imaging
should be obtained [6–8]. A multidetector
spiral computed tomography scan with intra-
venous contrast performed in both the arterial
and portal venous phase (pancreas protocol
CT) is ideal to evaluate for a periampullary
mass [7]. Findings on pancreas protocol CT
are critically important to determining the
next steps in the patient’s management.
B. Recent advances in radiographic technology
now facilitate assessment of many preopera-
tive staging factors necessary to determine
resectability of a periampullary mass, includ-
ing involvement of mesenteric vessels [9].
395
396
Resection and Clinicopathologic
Staging
As surgical resection remains the best chance of
cure for PACs, the time from identification of the
mass to operation should be optimized [2].
Proceeding to surgery based on pancreas proto-
col CT findings alone is acceptable, but the clini-
cal scenario may require further workup [7].
C. Biliary drainage procedures are typically rec-
ommended only in cases of cholangitis, sub-
stantially elevated bilirubin, or prolonged
period of elevated bilirubin [10, 11].
Preoperative tissue diagnosis is not necessary
if there is a high index of suspicion for cancer
on cross-sectional imaging and immediate
operative intervention is planned. However,
tissue diagnosis is necessary if neoadjuvant
therapy is considered, as is frequently the
case for PDAC [12, 13].
H. N. Overton and M. J. Weiss
D. The standard procedure for PAC is pancreati-
coduodenectomy (PD) with the goal of com-
plete tumor resection with negative oncologic
margins [2]. Full descriptions of the opera-
tive technique and complications of PD are
out of the scope of this chapter.
Clinicopathologic staging is based on the
American Joint Committee on Cancer
(AJCC) Cancer Staging Manual for each
location of PC origination [14]. Key factors
are resection margins, nodal involvement,
microvascular invasion, and perineural inva-
sion [14].
E. As chemotherapy and immunotherapy con-
tinue to improve for PAC, further important
features are histomolecular markers such as
KRAS and DPAC that are more prevalent in
PDAC and offer opportunity for targeted
therapy [15]. Multidisciplinary oncologic
care is essential along the continuum of treat-
ment [16].
98  Periampullary Carcinoma 397

Patient presents with

A obstructive jaundice

Labs: CBC, CMP, LFTs, Ca 19-9, CEA

Imaging:
o pancreas protocol CT scan

No EUS/ERCP for tissue diagnosis

Periampullary
B mass Refer to medical oncology for possible
resectable? neoadjuvant therapy
Reevaluate for resectability after completion of
neoadjuvant therapy

Yes

Consider preoperative biliary stenting:

Biliary Yes o ERCP with biopsy and stent
C obstruction o PTC/PBD if unable to decompress biliary
present? tree with ERCP

No
Legend:
CBC: complete blood count
CMP: complete metabolic panel
LFTs: liver function tests
CEA: carcinoembryonic antigen
Pancreas protocol CT scan: a multidetector
Neoadjuvant therapy (chemo +/– radiation) should be spiral computed tomography scan with
considered by multidisciplinary oncologic team intravenous contrast performed in both the
D arterial and portal venous phase
Proceed to OR for pancreaticoduodenectomy
EUS: endoscopic ultrasound
o Complete resection with negative margins
ERCP: endoscopic retrograde
Adjuvant therapy dependent on pathologic staging cholangiopancreatography
E PTC: percutaneous transhepatic
cholangiography
PBD: percutaneous biliary drainage
OR: operating room

Algorithm 98.1
398
Conclusion
PAC consists of pancreatic, biliary, ampullary,
and duodenal carcinoma which all present with
similar symptoms but have variable survival
References
1. Sarmiento JM, Nagorney DM, Sarr MG, Farnell
MB.  Periampullary cancers: are there differences?
Surg Clin North Am. 2001;81(3):543–55.
2. He J, Ahuja N, Makary MA, Cameron JL, Eckhauser
FE, Choti MA, et  al. 2564 resected periampullary
adenocarcinomas at a single institution: trends over
three decades. HPB [Internet]. 2014;16(1):83–90.
Available from: 10.1111/hpb.12078.
3. Siegel R, Miller K, Jemal A. Cancer statistics, 2015.
CA Cancer J Clin [Internet]. 2015;65(1):29. Available
from: http://onlinelibrary.wiley.com/doi/10.3322/
caac.21254/pdf.
4. Riall TS, Cameron JL, Lillemoe KD, Winter JM,
Campbell KA, Hruban RH, et al. Resected periampul-
lary adenocarcinoma: 5-year survivors and their 6- to
10-year follow-up. Surgery. 2006;140(5):764–72.
5. WestgaardA, Tafjord S, Farstad IN, Cvancarova M, Eide
TJ, Mathisen O, et al. Pancreatobiliary versus intesti-
nal histologic type of differentiation is an independent
prognostic factor in resected periampullary adeno-
carcinoma. BMC Cancer [Internet]. 2008;8(1):170.
Available from: http://bmccancer.biomedcentral.com/
articles/10.1186/1471-2407-8-170.
6. Godellas CV.  In: Saclarides TJ, Millikan KW,
Godellas CV, editors. Surgical oncology: periam-
pullary malignancies. New  York: Springer; 2003.
p. 282–99.
7. Cooper M, Newman NA, Ibrahim AM, Lam E, Herman
JM, Singh VK, et  al. Unnecessary tests and proce-
dures in patients presenting with solid tumors of the
pancreas. J Gastrointest Surg. 2013;17(7):1218–23.
8. Gloor B, Todd KE, Reber HA. Diagnostic workup of
patients with suspected pancreatic carcinoma. Cancer.
1997;79(9):1780–6.
H. N. Overton and M. J. Weiss
rates depending on site and specific histology.
Pancreas protocol CT scan is the most useful
imaging modality, and surgical resection with
pancreaticoduodenectomy offers the best chance
for cure.
9. House MG, Yeo CJ, Cameron JL, Campbell KA,
Schulick RD, Leach SD, et al. Predicting resectabil-
ity of periampullary cancer with three-­dimensional
computed tomography. J Gastrointest Surg.
2004;8(3):280–8.
10. Scheufele F, Schorn S, Demir IE, Sargut M, Tieftrunk
E, Calavrezos L, et  al. Preoperative biliary stenting
versus operation first in jaundiced patients due to
malignant lesions in the pancreatic head: A meta-­
analysis of current literature. Surg (United States).
2017;161(4):939–50.
11. Moole H, Bechtold M, Puli SR. Efficacy of preopera-
tive biliary drainage in malignant obstructive jaundice:
a meta-analysis and systematic review. World J Surg
Oncol [Internet]. 2016;14(1):182. Available from:
http://wjso.biomedcentral.com/articles/10.1186/
s12957-016-0933-2.
12. Hartwig W, Schneider L, Diener MK, Bergmann
F, Büchler MW, Werner J.  Preoperative tissue
diagnosis for tumours of the pancreas. Br J Surg.
2009;96(1):5–20.
13. Clarke DL, Clarke BA, Thomson SR, Garden OJ,
Lazarus NG. The role of preoperative biopsy in pan-
creatic cancer. HPB. 2004;6(3):144–53.
14. Egner JR.  AJCC cancer staging manual. JAMA.
2010;304:1726.
15. Chandrasegaram MD, Chiam SC, Chen JW, Khalid
A, Mittinty ML, Neo EL, et  al. Distribution and
pathological features of pancreatic, ampullary, bili-
ary and duodenal cancers resected with pancreati-
coduodenectomy. World J Surg Oncol [Internet].
2015;13(1):85. Available from: http://www.wjso.
com/content/13/1/85.
16. Kumar R, Herman JM, Wolfgang CL, Zheng
L.  Multidisciplinary management of pancreatic can-
cer. Surg Oncol Clin N Am. 2013;22:21231.
 Management of Intraductal
Papillary Mucinous Neoplasms
Jonathan G. Sham and Matthew J. Weiss
Algorithmic Approach
A. The diagnosis of intraductal papillary muci-
nous neoplasm (IPMN) of the pancreas most
often stems from the workup of nonspecific
clinical symptoms or as an incidental finding
on medical imaging. The most common clini-
cal symptoms leading to evaluation for IPMN
are epigastric discomfort (70–80%), nausea/
vomiting (11–21%), backache (10%), weight
loss (20–40%), diabetes, and jaundice [1].
B. Any cystic structure of the pancreas greater
than 5 mm in size should be further character-
ized with either computed tomography (CT)
or magnetic resonance imaging (MRI) with
magnetic resonance cholangiopancreatogra-
phy (MRCP) in order to evaluate the cyst for
“high-risk stigmata” or “worrisome features”
for malignancy [2]. In general, symptomatic
cysts have a higher overall risk of invasive
carcinoma and high-grade dysplasia than do
asymptomatic cysts [3].
C. “High-risk stigmata” of malignancy include
obstructive jaundice in patients with a cystic
lesion in the pancreatic head, enhancing
mural nodules of greater than 5  mm, or a
main pancreatic duct (MPD) size of greater
than 10  mm. If surgically fit, these patients
J. G. Sham · M. J. Weiss (*)
Department of Surgery, Johns Hopkins Hospital,
Baltimore, MD, USA
e-mail: mweiss5@jhmi.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_99
99
should undergo resection without additional
testing given the high rate of malignancy in
these cysts [2, 4].
D. Features on imaging concerning for malig-
nant transformation include cyst size of
≥3 cm, presence of an enhancing mural nod-
ule <5 mm, thickened or enhanced cyst walls,
MPD measuring 5–9  mm, abrupt change in
MPD caliber with distal pancreatic atrophy,
lymphadenopathy, elevated serum CA19-9,
and cyst growth rate of >5  mm/2  years [2,
5–7].
E. Should any of the aforementioned features be
present, endoscopic ultrasound (EUS) can be
a useful adjunct in delineating cyst anatomy,
invasion, and other malignant characteristics
[8]. It is important to note that biochemical
analysis of amylase and carcinoembryonic
antigen (CEA) can differentiate between
mucinous and non-mucinous, but not benign
from malignant cysts [9]. A cyst fluid CEA of
≥192–200 ng/ml has been shown to be ~80%
accurate in diagnosing a cyst as mucinous [9,
10]. Cytologic evaluation of cyst fluid can be
useful for confirming the diagnosis of malig-
nancy; however, sensitivity is limited [11],
and its use should be circumscribed to high-­
volume centers with expertise in this
technique.
F. If no concerning features are present or EUS
evaluation of the cyst is reassuring, surveil-
lance of IPMN is recommended as long as the
399
400 J. G. Sham and M. J. Weiss

patient remains fit for surgery. Several sur-
veillance schemes have been suggested, with
the most recent Fukuoka consensus guide-
lines summarized at the terminus of the
attached algorithm. MRI and EUS are recom-
mended for use when frequent surveillance is
required, given the carcinogenic effects of
ionizing radiation associated with
CT.  Particularly with larger cysts, resection
should be strongly considered in younger
patients who will require long-term surveil-
lance, as the risk of malignant progression
does not decrease over time [2]. When evalu-
ating a patient’s appropriateness for surgical
resection, any family history of pancreas can-
cer (PDAC) should be thoroughly explored.
The risk of developing PDAC in the setting of
IPMN rises dramatically—2.3-, 6.4-, and
32-fold—with one, two, and three affected
first-degree relatives, respectively [12, 13].

Clinical symptoms: Epigastric/back pain, nausea, weight loss, diabetes, jaundice,

A or Incidental imaging finding of pancreatic cyst

B Pancreas protocol CT or MRI/MRCP

C Any “high-risk stigmata” present?

Enhancing mural nodule ≥5 mm, main pancreatic duct ≥10 mm, obstructive jaundice

No

D Yes Any “worrisome features” present?

Cyst ≥3cm, enhancing mural nodules <5 mm, thickened/enhancing cyst walls, abrupt caliber change of pancreatic
duct, main duct size 5–9mm, lymphadenopathy, elevated serum CA19-9, cyst growth rate ≥5mm/2 yrs, pancreatitis

Yes

Perform EUS: Are any of these present?

Consider surgical Yes Definite mural nodules ≥5 mm, main duct features suspicious E No
resection for involvement, cytology suspicious or positive for malignancy

No
F

What is the size of the largest cyst?

<2 cm: CT/MRI every 6 months x 1 year, yearly thereafter

2–3 cm: EUS in 3–6 months, consider q6 month CT/MRI for 2 years and then yearly thereafter if no change, consider surgery in young pts with need
for prolonged surveillance

Algorithm 99.1

pancreatic cysts: clinicopathologic characteristics and

References
1. Machado NO, Al Qadhi H, Al Wahibi K. Intraductal
papillary mucinous neoplasm of pancreas. N Am J
Med Sci. 2015;7(5):160–75.
2. Tanaka M, Fernández-Del Castillo C, Kamisawa T,
Jang JY, Levy P, Ohtsuka T, et al. Revisions of inter-
national consensus Fukuoka guidelines for the man-
agement of IPMN of the pancreas. Pancreatology.
2017;17(5):738–53.
3. Fernández-del Castillo C, Targarona J, Thayer SP,
Rattner DW, Brugge WR, Warshaw AL.  Incidental
comparison with symptomatic patients. Arch Surg.
2003;138(4):427–3. discussion 33–4.
4. Kim TH, Song TJ, Hwang JH, Yoo KS, Lee WJ, Lee
KH, et  al. Predictors of malignancy in pure branch
duct type intraductal papillary mucinous neoplasm
of the pancreas: a nationwide multicenter study.
Pancreatology. 2015;15(4):405–10.
5. Bassi C, Crippa S, Salvia R.  Intraductal papillary
mucinous neoplasms (IPMNs): is it time to (some-
times) spare the knife? Gut. 2008;57(3):287–9.
6. Kwong WT, Lawson RD, Hunt G, Fehmi SM,
Proudfoot JA, Xu R, et  al. Rapid growth rates of
99  Management of Intraductal Papillary Mucinous Neoplasms
s­ uspected pancreatic cyst branch duct intraductal pap-
illary mucinous neoplasms predict malignancy. Dig
Dis Sci. 2015;60(9):2800–6.
7. Brounts LR, Lehmann RK, Causey MW, Sebesta
JA, Brown TA. Natural course and outcome of cystic
lesions in the pancreas. Am J Surg. 2009;197(5):619–
22. discussion 22–3.
8. Ohno E, Hirooka Y, Itoh A, Ishigami M, Katano
Y, Ohmiya N, et  al. Intraductal papillary muci-
nous neoplasms of the pancreas: differentiation
of malignant and benign tumors by endoscopic
ultrasound findings of mural nodules. Ann Surg.
2009;249(4):628–34.
9. Park WG, Mascarenhas R, Palaez-Luna M, Smyrk
TC, O'Kane D, Clain JE, et  al. Diagnostic perfor-
mance of cyst fluid carcinoembryonic antigen and
amylase in histologically confirmed pancreatic cysts.
Pancreas. 2011;40(1):42–5.
401
10. Cizginer S, Turner BG, Turner B, Bilge AR, Karaca
C, Pitman MB, et  al. Cyst fluid carcinoembryonic
antigen is an accurate diagnostic marker of pancreatic
mucinous cysts. Pancreas. 2011;40(7):1024–8.
11. Pitman MB, Deshpande V.  Endoscopic ultrasound-­
guided fine needle aspiration cytology of the pan-
creas: a morphological and multimodal approach
to the diagnosis of solid and cystic mass lesions.
Cytopathology. 2007;18(6):331–47.
12. Klein AP, Brune KA, Petersen GM, Goggins M,
Tersmette AC, Offerhaus GJ, et  al. Prospective risk
of pancreatic cancer in familial pancreatic cancer kin-
dreds. Cancer Res. 2004;64(7):2634–8.
13. He J, Cameron JL, Ahuja N, Makary MA, Hirose
K, Choti MA, et al. Is it necessary to follow patients
after resection of a benign pancreatic intraductal
papillary mucinous neoplasm? J Am Coll Surg.
2013;216(4):657–65. discussion 65–7.
 Pancreatic Necrosis
Ammar Asrar Javed and Matthew J. Weiss
Algorithmic Approach
Acute pancreatitis is one of the most common
gastrointestinal disorders requiring hospitaliza-
tion with an incidence of 4.5 to 35 per 100,000
people [1, 2]. It is often a sequela of gallstones,
alcoholism, or endoscopic retrograde cholangio-
pancreatography (ECRP). Approximately 20% of
pancreatitis patients will develop pancreatic
necrosis, which can lead to a systemic inflamma-
tory response, multi-organ system failure, and
death [1]. Early intervention is essential to avoid
poor outcomes. Pancreatic necrosis can be either
sterile or infected, and the outcomes between the
two are significantly different. The mortality
associated with sterile necrosis is 10%, while that
of infected necrosis is 30%, which increases to
over 40% when presenting with multi-organ sys-
tem failure [3, 4]. In the absence of clinical sep-
sis, the distinction between sterile and infected
necrosis can be made based on computed tomog-
raphy (CT) findings and/or ultrasound-guided
biopsy with gram stain and culture. Distinguishing
between the two is perhaps the most vital step in
the management of pancreatic necrosis.
Open necrosectomy has historically been the
treatment of choice for pancreatic necrosis; how-
ever, it is associated with high morbidity and
A. A. Javed · M. J. Weiss (*)
Department of Surgery, Johns Hopkins Hospital,
Baltimore, MD, USA
e-mail: mweiss5@jhmi.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_100
100
mortality [5]. In recent times, a step-up approach
has become more common [2, 5]. This entails ini-
tial stabilization of the patient and management
using less invasive approaches, such as percuta-
neous or endoscopic drainage followed by video-­
assisted retroperitoneal debridement (VARD) or
laparoscopic drainage. In the event of clinical
deterioration, surgical interventions such as mini-
mally invasive retroperitoneal necrosectomy or
open necrosectomy are recommended. Using this
approach has been shown to improve patient out-
comes [2]. This chapter discusses the step-up
approach, which is depicted in the subsequent
algorithm.
Management of Pancreatic Necrosis
A. Evaluation should begin with a detailed his-
tory and physical examination. A history
should include details regarding symptoms
including abdominal pain (onset, duration,
intensity, and radiation), persistent fever, nau-
sea, and vomiting. Past history of chronic
pancreatitis, gallstones, and alcohol use
should be elucidated [1]. On physical exami-
nation, these patients might have abdominal
guarding and rebound tenderness. Positive
Grey-Turner or Cullen signs are suggestive of
pancreatitis, but these are infrequently posi-
tive in clinical practice.
403
404
B. Vital signs, blood work, and imaging can pro-
vide important information to determine the
type of necrosis. Elevated serum amylase and
lipase are suggestive of pancreatitis, the latter
being more sensitive and specific. Currently,
abdominal CT is the standard imaging modal-
ity used to identify and assess pancreatic
necrosis. Lack of contrast uptake is represen- D. If the patient has sterile necrosis, then medi-
tative of tissue necrosis, and gas in the pan-
creas is pathognomonic for infected
pancreatic necrosis. Magnetic resonance
imaging (MRI) and magnetic resonance chol- E. Patients demonstrating evidence of infected
angiopancreatography (MRCP) can also
assess the extent of necrosis and identifica-
tion of gallstones. Elevated white cell count,
persistent fever, gas in the pancreas on imag-
ing, adynamic ileus, and progressive multi-­
organ system failure are suggestive of infected
pancreatic necrosis. It is important to distin-
guish between sterile and infected necrosis
because the management differs significantly
and placement of drain in a sterile necrosis
can induce infection.
C. The aim of initial management is to stabilize
the patient, which consists of aggressive
intravenous (IV) fluid replacement and nutri-
tional support in the setting of an intensive
care unit. The prophylactic use of antibiotics
is not recommended; however, if there are
signs suggestive of infected necrosis, then
antibiotics should be administered [1].
Surgical intervention within 48–72 h of pre-
sentation has been associated with a high
mortality [2]. This risk decreases significantly
if the surgical intervention can be pushed
beyond 28–30 days from initial presentation.
A. A. Javed and M. J. Weiss
Therefore, appropriate initial management
can help delay the need for surgical interven-
tion and help stabilize patients to avoid high-
mortality procedures. However, in patients
with worsening clinical condition and multi-
organ system failure, early surgical interven-
tion may be necessary [6].
cal management via administration of IV flu-
ids and nutritional support should be
continued.
pancreatic necrosis, i.e., persistent fever, wors-
ening condition, or multi-organ system failure,
will require intervention. Interventions are per-
formed using a step-up approach [2]. The ini-
tial intervention should include evacuation of
necrotic tissue and infected fluid collection by
percutaneous or endoscopic (transgastric)
drain placement. This can result in a resolution
in approximately 35% of the patients [2]. If the
patient does not show improvement within
72 h of the procedure, they should be reevalu-
ated using imaging, and a second drainage pro-
cedure should be performed. When there is an
increase in the extent of necrosis based on
imaging or if the patient continues to deterio-
rate, surgical resection/debridement should be
adopted [6]. This can be performed via VARD,
minimally invasive retroperitoneal necrosec-
tomy, or an open necrosectomy based on the
experience of the surgeon [7]. The aim of sur-
gical resection should be the removal of all
necrotic tissue, unroofing of all cavities in the
retroperitoneal spaces, and placement of a
large-bore catheter for drainage and irrigation.
100  Pancreatic Necrosis 405

Detailed history and physical exam

 Sharp abdominal pain, persistent fever, nausea, and vomiting
A History of chronic pancreatitis, gallstones, alcoholism, or ERCP

 Abdominal guarding and rebound tenderness on physical examination

Vital signs, blood work, and imaging

 Tachycardia and persistent pyrexia
B  Elevated serum amylase, lipase, and WBC on labs
 CT scan showing pancreatic necrosis. Lack of contrast uptake is representative of
tissue necrosis, and gas in the pancreas is pathognomonic for infected pancreatic necrosis

Initial management and stabilization

 Aggressive intravenous fluid replacement and nutritional support
 Antibiotics to be used only in case of infected pancreatic necrosis
C
 Aimed at pushing surgical intervention beyond 30 days from initial presentation. Surgical
intervention only recommended in patients with worsening clinical conditions or multi-organ
system failure

Development of E
Sterile necrosis
infection
 Continue medical management via
D intravenous fluids and nutritional
support Infected necrosis
 Intervention using a step-up approach

Surgical resection
Disease escalation
 Minimally invasive retroperitoneal
necrosectomy or open necrosectomy

Drainage of necrosis
No improvement

 Evacuation of necrotic tissue and

infected fluid collection by
in 72 h

percutaneous or endoscopic
(transgastric) drainage
Improvement

Re-evaluation of disease
No improvement in
 Re-evaluation of disease using imaging
72 h
 If a fluid collection is identified, a
second drainage procedure should be
performed
Medical management
Improvement  Continue medical management via
intravenous fluids and nutritional
support

Algorithm 100.1
406 A. A. Javed and M. J. Weiss

References pancreatic necrosis as determinants of mortality in

patients with acute pancreatitis. Gastroenterology.
2010;139(3):813–20.
1. Donald G, Donahue T, Reber HA, Hines OJ.  The
5. Working Group IAPAPAAPG.  IAP/APA evidence-­
evolving management of infected pancreatic necro-
based guidelines for the management of acute pancre-
sis. Am Surg. 2012;78(10):1151–5. Pubmed Central
atitis. Pancreatology. 2013;13(4 Suppl 2):e1–15.
PMCID: 3678520.
6. Uhl W, Warshaw A, Imrie C, Bassi C, McKay CJ,
2. van Santvoort HC, Besselink MG, Bakker OJ, Hofker
Lankisch PG, et  al. IAP guidelines for the surgical
HS, Boermeester MA, Dejong CH, et  al. A step-up
management of acute pancreatitis. Pancreatology.
approach or open necrosectomy for necrotizing pan-
2002;2(6):565–73.
creatitis. N Engl J Med. 2010;362(16):1491–502.
7. Alverdy J, Vargish T, Desai T, Frawley B, Rosen
3. Dugernier T, Dewaele J, Laterre PF. Current surgical
B.  Laparoscopic intracavitary debridement of peri-
management of acute pancreatitis. Acta Chir Belg.
pancreatic necrosis: preliminary report and descrip-
2006;106(2):165–71.
tion of the technique. Surgery. 2000;127(1):112–4.
4. Petrov MS, Shanbhag S, Chakraborty M, Phillips
AR, Windsor JA.  Organ failure and infection of
Part XIII
Spleen
 Management of Splenic Abscess
101
Andrew T. Bates and Michael G. Svestka

Algorithmic Approach neous drainage, or deep or hilar abscess or

Splenic abscess is a relatively rare entity with
autopsy reports ranging in incidence from
0.145% to 0.7% [1]. Sources of infection are typ-
ically either hematogenous spread from endocar-
ditis, superinfection of splenic infarction, tumors
or cysts, or trauma, especially in the setting of
immunocompromised states [2, 3]. Though rare,
splenic abscess carries a mortality rate of 15–20% C. Once percutaneous access is obtained, abscesses
in healthy patients and 70–80% in immunocom-
promised patients [4].
A. Ultrasound imaging is a reasonable first-line
diagnostic tool given its speed and cost-­
effectiveness; however, computed tomogra-
phy (CT) scan remains the diagnostic method
of choice as it can better delineate abscess
position, attenuation, and loculation [1, 5].
B. After diagnostic imaging, it is reasonable to
begin broad-spectrum, empiric antibiotics. The
most common causative organisms include D. A post-procedure ultrasound should be per-
Streptococcus, Klebsiella, Staphylococcus, and
E. coli [1, 5–7]. Given the risk of post-splenec-
tomy sepsis, the decision to perform splenec-
tomy should be reserved for patients over the
age of 18, hemodynamically stable patients,
abscesses where phlegmon prohibits percuta-
E. A total antibiotic course of 8 weeks is suffi-
A. T. Bates · M. G. Svestka (*)
Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA
e-mail: michael.svestka@stonybrookmedicine.edu
when more than two abscesses are present.
Alternatively, percutaneous drainage is pre-
ferred in the pediatric population, critically ill
patients who are unable to tolerate surgery,
and unilocular or bilocular liquid collections
without phlegmon that are anatomically ame-
nable to percutaneous access, such as those in
the middle and lower poles [3, 6, 7].
less than 3 cm may be successfully aspirated;
however, a drain should be left in place other-
wise. An 8 French catheter is recommended;
however, if drainage if unsuccessful, Seldinger
replacement with a 10 French catheter is rea-
sonable. Historically, splenectomy has been the
treatment of choice for abscesses; however,
with the advent of image-guided access, percu-
taneous aspiration and catheter drainage have
grown increasingly popular with effective
results in selected populations [3, 8, 9].
formed at 24  h post-drainage to rule out
hematoma and verify successful collection
drainage. Hemorrhage following drainage is
rare and is reported to be between 0% and 2%
[10–12]. The drain may be left in position
until output decreases to 3 ml daily.
cient to clear most infections. If percutaneous
drainage fails, salvage splenectomy is accept-
able and does not increase mortality [2].

© Springer Nature Switzerland AG 2019 409

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_101
410 A. T. Bates and M. G. Svestka

A CT-diagnosed splenic abscess

Begin empiric antibiotics

>18 years old <18 years old

No contraindications to surgery Critically ill/unable to tolerate
surgery
Hemodynamically stable
B Unilocular/bilocular liquid
Phlegmonous changes collection
>2 loculations or septations
Anatomically amenable to
Deep or hilar abscess percutaneous access

Percutaneous drainage
C Splenectomy

>3cm <3cm

Leave drain Aspirate

D Post-splenectomy vaccines

Post-procedure ultrasound

Remove drain once <3 ml daily

E If recurrent, salvage splenectomy 8 weeks of targeted antibiotics

Algorithm 101.1

5. Lee W, Choi ST, Kim KK. Splenic abscess: a single

References
1. Chun CH, Raff MJ, Contreras L.  Splenic abscess.
Medicine. 1980;59:50–65.
2. Ooi L, Leong S. Splenic abscesses from 1987 to 1995.
Am J Surg. 1997;174:87–93.
3. Kang M, Kalra N, Gulati M, et  al. Image guided
percutaneous splenic interventions. Euro J Radiol.
2007;64:140–6.
4. Wiesel O, Fisichella PM. The management of cysts,
tumors and abscesses of the spleen. In: Cameron JL,
Cameron AM, editors. Current surgical therapy. 12th
ed. Philadelphia, PA: Elsevier, Inc; 2016.
institution study and review of the literature. Yonsei
Med J. 2011;52(2):288–92.
6. Smyrniotis V, Kehagias D, Voros D, et  al. Splenic
abscess. Dig Surg. 2000;17:354–7.
7. Llenas-Garcia J, Fernandes-Ruiz M, Caurcel
L.  Splenic abscess: a review of 22 cases in a single
institution. Euro J Intern Med. 2009;20:537–9.
8. Chou Y, Tiu C, Chiou H, et  al. Ultrasound-guided
interventional procedures in splenic abscesses. Euro
J Radiol. 1998;28:167–70.
9. Thanos L, dailiana T, Papaioannou G, et  al.
Percutaneous CT-guided drainage of splenic abscess.
Am J Radiol. 2002;179:629–32.
101  Management of Splenic Abscess 411

10. Quinn SF, vanSonnenberg E, Cassola G, et  al.

12.
Lucey BC, Boland GW, Maher MM, et  al.
Interventional radiology in the spleen. Radiology. Percutaneous nonvascular splenic interven-
1986;161:289–91. tion: a 10-year review. AJR Am J Roentgenol.
11. Caraway NP, Fanning CV. Use of fine needle aspira- 2002;179:1591–6.
tion biopsy in the evaluation of splenic lesions in a
cancer center. Diagn Cytopathol. 1997;16:312–6.
 Atraumatic Indications
for Splenectomy 102
Maria S. Altieri and Andrew T. Bates

Algorithmic Approach glucose-­6-phosphate dehydrogenase

Indications for splenectomy for atraumatic rea-
sons can be divided into several categories:
benign, malignant, and others.
Algorithm 102.1. Benign conditions include
red blood cell (RBC) disorders (A), hemoglobin-
opathies (B), and platelet disorders (C). Malignant
conditions include white blood cell (WBC) disor-
ders and bone marrow disorders, while other con-
ditions include infectious and other lesions.
A. RBC disorders can be divided into congenital
(hereditary spherocytosis [HS], enzyme defi-
ciencies, such as pyruvate kinase and glucose-­
6-­phosphate dehydrogenase deficiencies) and
acquired such as warm-antibody autoimmune
hemolytic anemia. Among these, indications
for splenectomy include recurrent transfu-
sions and intractable leg ulcers in HS and
recurrent transfusions in pyruvate kinase defi-
ciencies. Failure of medical therapy is an
indication for splenectomy in condition such
as warm-antibody autoimmune hemolytic
anemia. Splenectomy is not indicated in
deficiencies.
Algorithm 102.2. Hemoglobinopathies include
sickle cell anemia (SCA) and thalassemia, and
indications for splenectomy are shown in
Algorithm 102.2.
A. In case of SCA, restoration of RBC volume is
important. If patient is refractory, then sple-
nectomy is needed.
B. Transfusions and iron chelation are the treat-
ment therapy for thalassemia. Splenectomy is
indicated in case of refractory symptoms.
Algorithm 102.3. Platelet disorders include
idiopathic thrombocytopenic purpura (ITP),
which is the most common indication for elective
splenectomy, and thrombotic thrombocytopenic
purpura (TTP).
A. When platelets are <30,000/mm3, medical
therapy is the first step.
B. Indications for splenectomy in case of ITP
include failure of medical therapy and recur-
rent disease.

M. S. Altieri (*) Algorithm 102.4.

Department of General Surgery, Stony Brook
University Hospital, Stony Brook, NY, USA

A .
First-line treatment for TTP is
A. T. Bates plasmapheresis.
Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA

© Springer Nature Switzerland AG 2019 413

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_102
414 M. S. Altieri and A. T. Bates

B. Excessive plasma exchange requirements can
be an indication for splenectomy.
Malignant conditions include white blood cell
(WBC) disorders and bone marrow disorders.
WBC disorders include non-Hodgkin’s lym-
phoma (NHL), Hodgkin’s disease, hairy cell leu-
kemia, and chronic lymphocytic leukemia.
Indications for surgery for NHL include symp-
tomatic splenomegaly and cytopenia. Bone mar-
row disorders include acute myeloid leukemia,
chronic myeloid leukemia, chronic myelomono-
cytic leukemia, polycythemia vera, myelofibro-
sis, and essential thrombocythemia. Indications
for splenectomy in these conditions are usually
due to symptomatic splenomegaly.
Other conditions include splenic abscesses,
cysts, and metastasis. Splenectomy is the therapy
of choice for abscesses and symptomatic para-
sitic cysts, while symptomatic nonparasitic cysts
can be treated with partial splenectomy or
unroofing.

Benign

A B C
Red blood
Platelet
cell
disorders
disorders

Hemoglobino-
pathies

PK ITP
HS TTP AIHA
deficiency

Sickle cell
anemia Thalassemia

Algorithm 102.1
102  Atraumatic Indications for Splenectomy 415

Sickle cell anemia Thalassemia

B
A
Autoinfarction
splenic abscess
splenic sequestration

Restoration of RBC Transfusions

volume iron chelation therapy

No Observation
Refractory?

Yes

Splenectomy

Algorithm 102.2
416 M. S. Altieri and A. T. Bates

ITP

A Platelets <30,000/mm3

Prednisone for 2– 4
weeks, followed by
a taper

B No
Refractory? Observation

Yes

Splenectomy

Algorithm 102.3

TTP
Suggested Reading
Cameron JL, Cameron AM. Current surgical therapy. 12th
ed. St. Louis: B.C. Decker; 2017.
A Plasmapharesis

Refractory? Observation

Splenectomy

Algorithm 102.4
 Part XIV
Thyroid/Parathyroid
 Hypothyroidism
Lukasz Czerwonka
Algorithmic Approach
A. Primary hypothyroidism is the most common
form of hypothyroidism and is characterized
by a combination of low thyroid-stimulating
hormone (TSH) and low T4. The most com-
mon cause is chronic autoimmune
(Hashimoto’s) thyroiditis, which is mediated
by both cellular (cytotoxic T-cells) and
humoral (thyroglobulin and thyroid peroxi-
dase antibodies) mechanisms. The gland can
be enlarged or atrophic. Antibody testing to
confirm Hashimoto’s thyroiditis is not rou-
tinely required, but measuring thyroperoxi-
dase (TPO) antibodies may be useful in
postpartum/painless thyroiditis or subclinical
hypothyroidism to predict likelihood of pro-
gression to permanent hypothyroidism. Other
etiologies of hypothyroidism to consider
include iatrogenic (surgery, radio active
iodoine (RAI), external beam radiation
(XRT)), medication-induced (methimazole,
propylthiouracil (PTU), lithium, amiodarone,
interferon alfa, immune checkpoint inhibitors,
tyrosine kinase inhibitors, cholestyramine,
phenytoin, carbamazepine), and iodine defi-
ciency (most common cause worldwide) or
L. Czerwonka (*)
Department of Surgery, Division of
Otolaryngology – Head and Neck Surgery, Stony
Brook University Hospital, Stony Brook, NY, USA
e-mail: Lukasz.Czerwonka@stonybrookmedicine.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_103
103
excess (Wolff–Chaikoff effect) [1]. Regardless
of cause, all patients with overt primary hypo-
thyroidism require treatment with thyroid hor-
mone, and synthetic thyroxine (T4,
levothyroxine) is the treatment of choice [2].
B. Subclinical hypothyroidism is defined by ele-
vated TSH and normal free T4. Most patients
are asymptomatic. The prevalence in the US
population is 4% when primary hypothyroid-
ism is excluded [3]. It is more prevalent
worldwide in areas of iodine deficiency. The
etiologies are the same as overt primary hypo-
thyroidism. Annual progression to overt pri-
mary hypothyroidism is 2–4% per year [4].
C. Subclinical hypothyroidism can increase risk
of cardiovascular disease. A meta-analysis
from 7 prospective studies including >25,000
participants showed an increased risk of coro-
nary heart disease events from 20.3 to 38.4
events/100 person-years in patients with TSH
≥10 [5]. Therefore, it is recommended to start
levothyroxine if TSH ≥10. Treatment of
patients aged <65–70 with lower TSH levels
is controversial and not recommended in
older individuals [2].
D. Several viral illnesses can cause transient
subacute thyroiditis, and these patients should
be treated symptomatically and monitored for
resolution [1].
E. Less than 1% of patients with hypothyroidism
have central hypothyroidism from secondary
(TSH deficiency) or tertiary (thyrotropin-
releasing hormone [TRH] d­ eficiency) causes.
419
420 L. Czerwonka

Secondary hypothyroidism is most commonly
the result of a pituitary micro- or macroade-
noma. Other causes of secondary and tertiary
hypothyroidism include pituitary necrosis
(Sheehan syndrome), trauma, radiation,
hypophysitis, other cranial tumors or infiltra-
tive diseases, and TSH or TRH gene mutations.
TSH may be low, normal, or slightly elevated.
Evaluation begins with magnetic resonance
imaging (MRI) to rule out a sellar mass fol-
lowed by biochemical testing if a mass is pres-
ent. All patients should undergo testing for
secondary adrenal insufficiency prior to initiat-
ing levothyroxine, as failure to administer glu-
cocorticoids along with levothyroxine in
patients with adrenal insufficiency can precipi-
tate acute adrenal crisis. Patients with sellar
masses require neurosurgical evaluation [6].

Presentation: fatigue, weight gain, slow movement and speech, constipation, cold
intolerance, bradycardia, HTN, coarse hair, nonpitting edema, periorbital edema
and/or
abnormal thyroid function tests

B
No High Yes No
Low fT4 Low fT4 Subclinical hypothyroidism
TSH

Yes Yes

E Central hypothyroidism A Primary hypothyroidism

MRI brain ACTH stimulation test Identify cause:

· Thyroidectomy
· RAI/XRT
· Drugs that affect thyroid
hormone synthesis or
No clearance
Adrenal
· History of iodine
deficiency or excess
Yes

Levothyroxine Measure TPO

+ antibodies if goiter,
glucocorticoid painless thyroiditis or
subclinical thyroiditis
C

Sellar mass Measure: Yes

gonadotropins, Levothyroxine TSH 10
testosterone, estradiol,
prolactin, IGF1
and
consult neurosurgery D No
Acute nonthyroidal illness
Repeat TSH and fT4 in 4–6 weeks

Follow-up: TSH q6–12 months

Algorithm 103.1
103 Hypothyroidism 421

References Nutrition Examination Survey (NHANES III). J Clin

Endocrinol Metabol. 2002;87(2):489–99.
4. Vanderpump MP, Tunbridge WM, French JM,
1. Sweeney LB, Stewart C, Gaitonde DY. Thyroiditis:
Appleton D, Bates D, Clark F, Grimley Evans J, Hasan
an integrated approach. Am Fam Physician. 2014;
DM, Rodgers H, Tunbridge F, et al. The incidence of
90(6):389–96.
thyroid disorders in the community: a twenty-year
2. Jonklaas J, Bianco AC, Bauer AJ, Burman KD,
follow-up of the Whickham Survey. Clin Endocrinol.
Cappola AR, Celi FS, et al. Guidelines for the treat-
1995;43(1):55–68.
ment of hypothyroidism: prepared by the American
5. Rodondi N, Den Elzen WP, Bauer DC, Cappola AR,
Thyroid Association task force on thyroid hormone
Razvi S, Walsh JP, et al. Subclinical hypothyroidism
replacement. Thyroid. 2014;24(12):1670–751.
and the risk of coronary heart disease and mortality.
3. Hollowell JG, Staehling NW, Flanders WD, Hannon
JAMA. 2010;304(12):1365–74.
WH, Gunter EW, Spencer CA, et  al. Serum TSH,
6. Persani L. Central hypothyroidism: pathogenic, diag-
T4, and thyroid antibodies in the United States
nostic, and therapeutic challenges. J Clin Endocrinol
population (1988 to 1994): National Health and
Metabol. 2012 Sep;97(9):3068–78.
 Hyperthyroidism
Ewen Chao and Lukasz Czerwonka
Algorithmic Approach
A. On physical exam, there may be findings
associated with Graves’ disease, such as
exophthalmos or pretibial myxedema.
Children and the elderly may present with
alternate symptoms, such as apathetic hyper-
thyroidism in the elderly, which primarily
consists of apathy and depression, along
with weight loss, congestive heart failure,
tachycardia, muscle weakness, dry skin, or
ptosis [1].
B. If the thyroid-stimulating hormone (TSH)
level is normal or elevated, then one should
consider non-thyroidal causes. Elevated T4
levels in the setting of normal TSH may be
due to abnormally elevated levels of thyroid
hormone-binding proteins, drugs that inhibit
T4 to T3 conversion such as amiodarone or
high-dose propranolol, acute psychosis, high
altitude, or amphetamine abuse [2].
C. The incidence of subclinical hyperthyroidism
(TSH <0.1  mU/L) is 0.7% in the United
States and leads to an increased risk of overall
mortality, cardiovascular mortality, atrial
E. Chao · L. Czerwonka (*)
Department of Surgery, Division of Otolaryngology –
Head and Neck Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA
e-mail: Lukasz.Czerwonka@stonybrookmedicine.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_104
104
fibrillation, and a decrease in bone mineral
density. The American Thyroid Association
recommends repeating TSH and free T4 lev-
els if subclinical hyperthyroidism is persis-
tent (TSH <0.1 mU/L). It should be treated in
patients ≥65  years old, particularly those
with cardiac risk factors, heart disease, or
osteoporosis, in postmenopausal women not
on estrogens or bisphosphonates, and in
patients who have symptoms of hyperthy-
roidism [2].
D. Thyroid storm is a clinical diagnosis and may
be due to infection, intravenous (IV) contrast
exposure, diabetic ketoacidosis (DKA), or
surgery. It may be scored with the Burch-­
Wartofsky scale [3].
E. Both radioactive iodine uptake and thyroid
hormone receptor antibody (TRAb) are
acceptable tests to differentiate causes of
hyperthyroidism. One model showed a 46%
faster time to diagnosis and 47% cost savings
when using TRAb testing [4].
F. Radioactive iodine (RAI) ablation, antithy-
roidal medications, and surgery are all
acceptable treatments for Graves’ disease,
but surgery is the most effective [5]. RAI
and surgery are most effective for toxic mul-
tinodular goiter or toxic solitary adenoma,
but antithyroidals may be used to achieve
euthyroidism prior to surgery. If surgery is
chosen as treatment for Graves’ disease,
423
424 E. Chao and L. Czerwonka

total thyroidectomy is the most effective of permanent hypocalcemia/hypoparathy-

procedure for reducing risk of recurrent roidism with total vs subtotal thyroidectomy,
hyperthyroidism. In a recent Cochrane but no difference in p­ermanent recurrent
review, some studies showed increased risk laryngeal nerve palsy [6].

Presentation:
A Heat intolerance, increased sweating and thirst,
weight loss, diarrhea, palpitations, tremors, fatigue

Obtain thyroid function tests: TSH, free T4, total T3

C
Yes High Low/Normal
Subclinical Normal Normal Yes
TSH Euthyroidism
hyperthyroidism T4/T3 T4/T3

No
No B
D Fever, agitation, nausea/vomiting, • TSH-secreting pituitary
diarrhea, tachycardia, signs of CHF: adenoma
“Thyroid storm”→beta blockers, • Pituitary resistance to
Lugol’s iodine, PTU, corticosteroids thyroid hormone
• Euthyroid
hyperthyroxinemia
E

Diffuse high uptake Positive

RAIU Graves’ disease TRAb

Negative
• Radioactive iodine
F • Antithyroidals
• Surgery

Focal high uptake • Toxic multinodular goiter Nodules

US
• Toxic solitary adenoma

Low uptake No nodules

Thyroiditis

Follow-up TSH q4–12 months or change in symptoms

Algorithm 104.1
104 Hyperthyroidism 425

References 4. McKee A, Peyerl F. TSI assay utilization: impact on

costs of Graves’ hyperthyroidism diagnosis. Am J
Manag Care. 2012;18(1):e1–14.
1. Arnold BM, Casal G, Higgins HP.  Apathetic thyro-
5. Genovese BM, Noureldine SI, Gleeson EM, Tufano
toxicosis. Can Med Assoc J. 1974;111(9):957–8.
RP, Kandil E. What is the best definitive treatment for
2. Ross DS, Burch HB, Cooper DS, Greenlee MC,
Graves’ disease? A systematic review of the existing
Laurberg P, Maia AL, et al. 2016 American Thyroid
literature. Ann Surg Oncol. 2013;20(2):660–7.
Association Guidelines for diagnosis and manage-
6. Liu ZW, Masterson L, Fish B, Jani P, Chatterjee
ment of hyperthyroidism and other causes of thyro-
K. Thyroid surgery for Graves’ disease and Graves’
toxicosis. Thyroid. 2016;26(10):1343–421.
ophthalmopathy. Cochrane Database Syst Rev.
3. Burch HB, Wartofsky L.  Life-threatening thyrotoxi-
2015;11:CD010576.
cosis. Thyroid storm. Endocrinol Metab Clin N Am.
1993;22(2):263–77.
 Thyroiditis
105
Lukasz Czerwonka

Algorithmic Approach through four stages: first, a hyperthyroid

phase which may require β-blockers if symp-
A. Infections of the thyroid are exceedingly rare tomatic; second, a euthyroid phase; third, a
due to its iodine content, encapsulation, lym- hypothyroid phase in 20–30% of patients
phatic drainage, and blood supply. They which may require thyroid hormone replace-
occur via distant seeding, direct spread from ment; and fourth, a resolution phase to a
persistent pyriform sinus fistulas or thyro- euthyroid state in over 90% of patients.
glossal duct cysts, or penetrating trauma and Treatment is symptomatic with high-dose
are more common in children, patients with aspirin for pain relief and steroids in severe
preexisting thyroid disease, and those who cases. Thyroidectomy is reserved for persis-
are immunocompromised. Streptococcus, tent refractory disease or to rule out malig-
Staphylococcus, or anaerobes account for the nancy [2–5].
majority of cases. Patients present with fever, C. Several drugs can cause painless thyroiditis
neck pain, odynophagia, and dysphonia. including interferon alfa, interleukin 2, amio-
Some patients develop thyrotoxicosis. Fine-­ darone, lithium, kinase inhibitors, and
needle aspiration (FNA) should be performed immune checkpoint inhibitors. Some of these
for culture, and computed tomography (CT) agents result in hyperthyroidism and some
can be obtained to delineate the extent of hypothyroidism [4, 5].
infection including sinus tracts and drainable D. Painless thyroiditis is a sporadic variant of
collections. Treatment consists of parenteral chronic autoimmune thyroiditis, which is
antibiotics, percutaneous or open drainage of characterized by transient hyperthyroidism,
abscesses, and thyroidectomy for patients sometimes followed by hypothyroidism and
who fail more conservative management [1]. then recovery [4, 5].
B. De Quervain’s thyroiditis or subacute non-­ E. Postpartum thyroiditis is painless thyroiditis
suppurative thyroiditis is thought to result occurring within 1  year after pregnancy. It
from a viral infection and is characterized by occurs in 8–10% of pregnancies when tested
a tender enlarged gland that progresses for with thyroid antibodies; however, much
fewer women develop symptoms of hyper- or
L. Czerwonka (*) hypothyroidism [4, 5].
Department of Surgery, Division of Otolaryngology – F. Lymphocytic or Hashimoto’s thyroiditis is the
Head and Neck Surgery, Stony Brook University most common cause of hypothyroidism with
Hospital, Stony Brook, NY, USA an annual incidence of 0.3–1.5 cases per 1000
e-mail: Lukasz.Czerwonka@stonybrookmedicine.edu
persons. Most cases present with a nontender
© Springer Nature Switzerland AG 2019 427
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_105
428 L. Czerwonka

goiter, but it can also present in atrophic forms.
Rarely patients can present with hyperthyroid-
ism. Diagnosis can be confirmed with thyroid
autoantibodies (90% of patients have TPO
antibodies), although not usually necessary.
Treatment consists of thyroid replacement in
clinically hypothyroid patients. Surgery is
reserved for compressive symptoms [4–6].
. Riedel’s thyroiditis is a rare variant of chronic
G of the isthmus. More extensive resection is
thyroiditis that is characterized by replace-
ment of thyroid parenchyma and surrounding
tissue by essentially scar. This leads to a firm
“woody” thyroid gland which can cause com-
pression including dysphagia, dysphonia, and
dyspnea. Diagnosis usually requires open
biopsy. The disease can respond to steroids,
but surgery is usually required to decompress
the trachea by performing a wedge excision
not advised due to the fibrosis [4].

Presentation: Thyroid enlarged, +/– firm, +/– tender, TFTs

Clinically hyperthyroid TFTs, Clinically hypothyroid

bB, antithyroidals Levothyroxine
symptoms TSH >10

Yes No
Painful

B C
Subacute Subacute
Timing De Quervain’s thyroiditis Drug-induced thyroiditis Timing

No
Acute Chronic
A
High-dose ASA, No Yes
<1 yr
Suppurative thyroiditis Steroids if severe
parturition

D Painless thyroiditis E Postpartum thyroiditis

FNA culture,
IV antibiotics,
CT neck
No
Firm
F
Fistula Surgery once
Abscess acute inflammation Hashimoto’s thyroiditis Yes
resolves

Stable G Reidel’s thyroiditis

Airway Percutaneous drainage

Compromised
Compressive symptoms Open biopsy,
Urgent I&D or thyroidectomy decompression steroids

Follow-up: TSH q4–12 months or change in symptoms

Algorithm 105.1
105 Thyroiditis 429

References 4. Pearce EN, Farwell AP, Braverman LE. Thyroiditis. N

Engl J Med. 2003;348(26):2646–55.
5. Sweeney LB, Stewart C, Gaitonde DY.  Thyroiditis:
1. Paes JE, Burman KD, Cohen J, Franklyn J, McHenry
an integrated approach. Am Fam Physician.
CR, Shoham S, et al. Acute bacterial suppurative thy-
2014;90(6):389–96.
roiditis: a clinical review and expert opinion. Thyroid.
6. Jonklaas J, Bianco AC, Bauer AJ, Burman KD,
2010;20(3):247–55.
Cappola AR, Celi FS, et al. Guidelines for the treat-
2. Fatourechi V, Aniszewski JP, Fatourechi GZE,
ment of hypothyroidism: prepared by the American
Atkinson EJ, Jacobsen SJ. Clinical features and out-
Thyroid Association Task Force on thyroid hormone
come of subacute thyroiditis in an incidence cohort:
replacement. Thyroid. 2014;24(12):1670–751.
Olmsted County, Minnesota, study. J Clin Endocrinol
Metabol. 2003;88(5):2100–5.
3. Ranganath R, Shaha MA, Xu B, Migliacci J,
Ghossein R, Shaha AR. de Quervain’s thyroiditis: a
review of experience with surgery. Am J Otolaryngol.
2016;37(6):534–7.
 Goiter
Lukasz Czerwonka
Algorithmic Approach
A. Toxic multinodular goiter is characterized by
hyperthyroidism in the setting of an enlarged
multinodular thyroid gland with hot nodules
on thyroid radioactive iodine uptake scan
(RAIU). It usually presents in older individu-
als with history of nontoxic multinodular goi-
ter where one or several nodules have
developed autonomous hormone production.
Treatment begins with antithyroidal medica-
tions to control signs and symptoms followed
by definitive treatment ideally total or near-
total thyroidectomy. In patients at high opera-
tive risk, radioactive iodine can be used but
can cause swelling which may worsen any
airway compromise [1, 2].
B. Nontoxic goiter has multiple etiologies rang-
ing from iodine deficiency in areas with
endemic goiters to enzyme defects or medica-
tion side effects. Goiters can be diffuse or
multinodular. Dominant, enlarging, or tender
nodules should undergo fine-needle aspira-
tion (FNA) biopsy to rule out malignancy.
Patients with clinical hypothyroidism should
be treated with thyroid hormone [2]. Thyroid
hormone can also be used in euthyroid
L. Czerwonka (*)
Department of Surgery, Division of
Otolaryngology – Head and Neck Surgery, Stony
Brook University Hospital, Stony Brook, NY, USA
e-mail: Lukasz.Czerwonka@stonybrookmedicine.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_106
106
patients to decrease or stabilize the size of the
goiter but is effective in less than half of
patients with modest decrease in size of about
25% and likely rebound after discontinuation
of treatment [3, 4].
C. Surgery for nontoxic goiter is indicated in
patients with concern for malignancy, com-
pressive symptoms, persistent enlargement,
or significant cosmetic deformity [4]. Patients
should be at reasonable surgical risk. Elderly
patients with stable asymptomatic goiters do
not require surgical treatment.
D. Prior to undertaking surgery for goiter with
possible substernal extension, a computed
tomography (CT) of the neck down to the
carina or a CT of the chest should be obtained
to rule out significant substernal extension, so
appropriate arrangements can be made for
possible sternotomy [4].
E. Patients who do not undergo surgery should
be monitored with thyroid function tests
(TFTs), ultrasound, and/or CT for enlarge-
ment and thyroid hypo- or hyperfunction.
Patients who undergo surgery will require
thyroid hormone replacement and monitoring
with first thyroid-stimulating hormone (TSH)
checked 6–8 weeks postoperatively. Patients
who undergo radioactive iodine (RAI) for
toxic multinodular goiter will require contin-
ued monitoring for possible recurrence [1, 2].
431
432 L. Czerwonka

Presentation: enlarged thyroid, +/– compressive symptoms

TSH TSH /nml

T3/T4 T3/T4 /nml
A Toxic TFTs Nontoxic B

Clinically hyperthyroid Clinically hypothyroid

βB, Antithyroidals Levothyroxine

RAIU Ultrasound

Yes Yes
Low Dominant
Thyroiditis FNA
uptake nodule

No C
No
Graves’ or toxic Concern for No
multinodular malignancy
goiter

Yes Yes Compressive

symptoms

Airway
compromise No
Yes

Yes Persistent
No
growth

Antithyroidals RAI
No

D Substernal Obtain Yes Cosmetic

chest CT preop Thyroidectomy deformity

No

E Follow-up: TSH, US/CT q6–12 months

Algorithm 106.1
106 Goiter 433

References Association Guidelines task force on thyroid nod-

ules and differentiated thyroid cancer. Thyroid.
2016;26(1):1–133.
1. Ross DS, Burch HB, Cooper DS, Greenlee MC,
3. Wesche MF, Tiel-v Buul MM, Lips P, Smits NJ,
Laurberg P, Maia AL, et al. 2016 American Thyroid
Wiersinga WM. A randomized trial comparing levo-
Association Guidelines for diagnosis and manage-
thyroxine with radioactive iodine in the treatment of
ment of hyperthyroidism and other causes of thyro-
sporadic nontoxic goiter. J Clin Endocrinol Metabol.
toxicosis. Thyroid. 2016;26(10):1343–421.
2001;86(3):998–1005.
2. Haugen BR, Alexander EK, Bible KC, Doherty GM,
4. Chen AY, Bernet VJ, Carty SE, Davies TF, Ganly I,
Mandel SJ, Nikiforov YE, et  al. 2015 American
Inabnet WB, et  al. American Thyroid Association
Thyroid Association Management Guidelines for
Statement on optimal surgical management of Goiter.
adult patients with thyroid nodules and differ-
Thyroid. 2014;24(2):181–9.
entiated thyroid cancer: The American Thyroid
 Thyroid Nodule
Melissa Boltz
Algorithmic Approach
A. Evaluation of a patient with a thyroid nodule
begins with a thorough history assessing risk
factors for malignancy. Questions regarding
compressive symptoms such as voice
changes, dysphagia, choking, shortness of
breath, coughing, a general feeling of pres-
sure and tightness, as well as sudden increase
in size are important. Additionally, the patient
should be asked about family history of thy-
roid disorders, other endocrinopathies, and
personal exposure to ionizing radiation to the
head or neck region [1].
B. Biochemical assessment of thyroid function
(serum TSH, free T4, free T3) is required as
clinical assessment will not reliably indicate
thyroid status. If the patient is euthyroid or
hypothyroid, a fine-needle aspiration (FNA)
biopsy should be done to assess the cytology
of the nodule. A suppressed TSH indicates
hyperthyroidism. In general, FNA is not done
in this situation as it may cause thyrotoxicosis.
Neck ultrasonography (US) can be performed
to identify additional nodules not palpable on
exam. Some US characteristics may indicate a
higher risk of malignancy (irregular nodule
borders, hypervascular, hypoechoic, internal
M. Boltz (*)
Department of Surgery, Penn State Hershey Medical
Center, Hershey, PA, USA
e-mail: mboltz2@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_107
107
calcifications). Additionally, ultrasound may
yield information on the overall vascularity of
the gland suggestive of Graves’ disease versus
a dominant toxic nodule if the patient is hyper-
thyroid [2].
C. Hyperthyroid patients more commonly have
either Graves’ disease or a toxic hyperfunc-
tioning nodule. A thyroid-stimulating immu-
noglobulin (TSI) level can be checked and if
high indicates Graves’ disease. If US reveals
a dominant nodule, a radionuclide scan can
be done to determine if it is hyperfunctional
(hot nodule). If the US and radionuclide scan
are concordant, FNA is not necessary as the
incidence of malignancy is low (5%). Both
causes of hyperthyroidism can be treated with
either medication, radioactive iodine abla-
tion, or total thyroidectomy with life-long
thyroid supplementation afterward [1].
D. Patients with normal thyroid function but
with compressive symptoms should have
either a lobectomy or total thyroidectomy.
E. Patients with normal thyroid function who do
not have compressive symptoms with nod-
ules >1  cm meet biopsy criteria with
ultrasound-­guided FNA [2].
F. The Bethesda system for reporting thyroid
FNA cytopathology is used to recommend
clinical management based on implied risk of
malignancy. Patients with nondiagnostic
cytology should have a repeat FNA 3 months
after the initial biopsy. Waiting 3  months
435
436 M. Boltz

reduces the likelihood of having the second
FNA return as inadequate. If it is, then lobec-
tomy can be done for definitive pathology.
Benign cytology should be followed yearly
with US versus repeating the FNA if the nod-
ule grows or surgery if compressive symp-
toms develop. Atypia of undetermined
significance has a 5–15% risk of malignancy;
thus a repeat FNA is done, and if the cytology
remains the same, definitive operation is
offered. A report of suspicious follicular neo-
plasm harbors a 15–30% risk of malignancy,
and diagnostic surgery of either lobectomy or
total thyroidectomy is indicated. A diagnosis
of follicular cancer is supported by pathology
demonstrating capsular and vascular inva-
sion. Suspicion for malignancy has a 60–80%
risk of malignancy, and malignant cytology
has a near 100% risk. Both of those cytology
results warrant total thyroidectomy [2].
Of note, a thyroid mass in the setting of ele-
vated calcitonin levels is pathognomonic for
medullary thyroid cancer. Medullary thyroid can-
cer involves the calcitonin-producing parafollicu-
lar C cells and is the most common initial
presentation of multiple endocrine neoplasia
(MEN) IIa and MEN IIb syndromes. It is neces-
sary to rule out a pheochromocytoma (and treat if
present) and hyperparathyroidism prior to per-
forming a total thyroidectomy and central lymph
node dissection. A modified radical neck dissec-
tion is required if lymph nodes are positive for
disease. RET proto-oncogene mutations should
be investigated as it predicts the prognosis and
aggressiveness of the disease.

Thyroid nodule

A
History and physical exam

B Diagnostic evaluation/imaging Hyperthyroid C

• Thyroid function tests
• Neck ultrasonography
D
Graves’ disease Toxic nodule

Compressive symptoms Normal E

• Medication Radionuclide scan

Surgery • Radioactive iodine
ablation
• Definitive surgery

FNA F

Follicular neoplasm/
Nondiagnostic/ Atypia/follicular lesion of Suspicious for
Benign suspicious for Malignant
unsatisfactory undetermined significance malignancy
follicular neoplasm

Repeat FNA • Repeat US annually Diagnostic surgery

• Repeat FNA vs. • Lobectomy
surgery in case of growth, • Total thyroidectomy Total thyroidectomy
Inadequate compressive symptoms

Repeat FNA
Lobectomy vs. FNA Abbreviations: AUS, Atypia of undetermined
Benign AUS/FLUS significance; FNA, Fine needle aspiration; FLUS,
Follicular lesion of undetermined significance

Algorithm 107.1
107  Thyroid Nodule 437

References SI, Sosa JA, Steward DL, Tuttle RM, Wartofsky L.

2015 American Thyroid Association Management
Guidelines for adult patients with thyroid nodules
1. Suliburk J, Delbridge L.  Thyroid nodule. In Morita
and differentiated thyroid cancer: The American
SY, Dackiw APB, Zeiger MA, editors. McGraw-­
Thyroid Association Guidelines task force on thyroid
Hill manual endocrine surgery. 1st ed. New  York.
nodules and differentiated thyroid cancer. Thyroid.
McGraw-Hill; 2009.
2016;26(1):1–133.
2. Haugen BR, Alexander EK, Bible KC, Doherty GM,
Mandel SJ, Nikiforov YE, Pacini F, Randolph GW,
Sawka AM, Schlumberger M, Schuff KG, Sherman
 Thyroid Cancer
Melissa Boltz
Algorithmic Approach
A. Papillary, follicular, medullary, and anaplas-
tic make up the majority of thyroid cancers
with papillary thyroid cancer (PTC) being the
most common. Patients referred with a diag-
nosis of biopsy-proven PTC should have a
history obtained paying attention to past his-
tory of radiation exposure, family history of
thyroid malignancy, and symptoms of inva-
sive disease such as voice changes or hemop-
tysis. Physical exam is done to assess for
local metastasis with palpable cervical lymph
nodes [1].
B. At the very least, patients with PTC undergo
total thyroidectomy, but preoperative staging
is necessary to determine additional concom-
itant surgical interventions. Neck ultrasonog-
raphy is essential to assess for possible
metastases to lateral cervical lymph nodes
(LN). Pathologic-appearing nodes should be
biopsied to aid in operative planning. If his-
tory is suggestive of invasion of the recurrent
laryngeal nerve (RLN) trachea or esophagus,
then laryngoscopy, bronchoscopy, and/or
endoscopy should be performed [2].
C. In general, the treatment for thyroid malig-
nancies is multifaceted and involves removal
M. Boltz (*)
Department of Surgery, Penn State Hershey Medical
Center, Hershey, PA, USA
e-mail: mboltz2@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_108
108
of the primary tumor with total thyroidec-
tomy and appropriate lymph node dissection
to allow accurate staging and guide postop-
erative treatment. If during thyroidectomy a
suspicious-appearing central neck node is
encountered, it is sent for frozen section, and
if positive for PTC, an ipsilateral central neck
dissection (CND) is done. Patients with
biopsy-proven lateral neck nodes identified
preoperatively should have an ipsilateral
CND and selective lateral neck dissection
(LND) of level II, III, and IV lymph nodes
during the initial thryoidectomy [2].
D. Vocal cord paralysis on preoperative laryn-
goscopy indicates tumor involvement of the
RLN.  An R0 resection should still be
attempted with potential sacrifice of the RLN
if necessary [2].
E. Invasion of the aerodigestive tract on preop-
erative staging warrants further assessment
for distant metastases and functional status.
Patients with poor performance status should
not undergo extensive surgical intervention.
Those with good performance status and
regional disease may have a shave resection
of the tumor for tracheal or esophageal wall
invasion. Luminal invasion involves laryngo-
tracheal or full-thickness esophageal resec-
tion. While these procedures can be
excessively morbid, it may be appropriate in
highly selective patients when combined with
439
440 M. Boltz

multimodal therapy along with radiation and
chemotherapy [1].
F. For situations where local invasion is identi-
fied intraoperatively, the RLN should be pre-
served or reconstructed while tumors invading
the tracheal or esophageal walls can be
shaved or segmentally resected [2].
G. Postoperative follow-up includes thyroid
stimulating hormone (TSH) suppression,
ultrasound surveillance of the neck, and mon-
itoring thyroglobulin levels. Depending on
the stage, pathology, and extent of disease,
radioactive iodine ablation, external beam
radiation therapy, or chemotherapy may be
used as adjuvant therapies [1, 2].

Biopsy-proven PTC

A
History and physical exam
• Fixed nodule, rapid growth
• Symptoms of invasion (hoarseness, hemoptysis)
• Palpable cervical LN

B Preoperative staging
• Neck US: assess cervical LN
• FNA-suspicious LN
• Laryngoscopy/bronchoscopy/endoscopy if suspicious
for involvement of RLN/trachea/esophagus

Operation: total thyroidectomy

C D E F

Intraop-suspicious Biopsy-proven PTC Vocal cord paralysis on Invasion of aerodigestive Introp finding of
central LN in lateral cervical preop laryngoscopy tract on preop staging local invasion
neck node(s)

Send frozen section Attempt R0 resection, Evaluate for distant RLN Tracheal/esophageal
Ipsilateral CND and with involved segment of metastases, assess invasion wall invasion
selective LND RLN if necessary performance status
Ipsilateral CND
Preserve nerve if Shave/segmental
Resectable local Palliative care for possible or resection
disease, good multiple metastases, resect/reconstruct
performance status poor performance status

Tracheal/esophageal Tracheal/esophageal
wall invasion lumen invasion

Abbreviations: CND, central neck dissection; Shave/segmental Laryngotracheal resection

FNA, fine needle aspiration; LN, lymph node; resection or full-thickness
LND, lymph node dissection; PTC, papillary esophageal resection
thyroid cancer; RLN, recurrent laryngeal
nerve; US, ultrasound G Follow-up

Algorithm 108.1
108  Thyroid Cancer 441

References oncology handbook. 4th ed. Philadelphia: Lippincott

Williams & Wilkins; 2012.
2. Elaraj DM, Sturgeon C.  Papillary thyroid Cancer.
1.
Thoas RM, Habra MA, Perrier ND, Grubbs
In: Morita SY, Dackiw APB, Zeiger MA, editors.
EG.  Well-­
differentiated carcinoma of the thyroid
McGraw-hill manual endocrine surgery. 1st ed.
and neoplasms of the parathyroid gland. In: Feig
New York: McGraw-Hill; 2009.
BW, Ching CD, editors. The MD Anderson surgical
 Hyperparathyroidism
Melissa Boltz
Algorithmic Approach
A. The recognition of primary hyperparathy-
roidism (pHPT) increased in the 1970s with
the introduction of routine automated cal-
cium testing, and the incidence continues to B. When pHPT is biochemically confirmed, the
rise today [1]. Although pHPT secondary to a
parathyroid adenoma is the most common
cause of hypercalcemia in the outpatient set-
ting, the evaluation of a patient referred for
hypercalcemia begins with consideration of
other non-parathyroid causes. The diagnosis
of pHPT is biochemical. Initial laboratory
evaluation should include concomitant serum
calcium and intact parathyroid hormone
(PTH). In classic pHPT, patients present with
an elevation of both calcium and PTH and a
negative history of multiple endocrine neo-
plasia (MEN) syndromes. A chloride-to-­
phosphate (Cl/PO4) ratio  >33 also suggests
pHPT.  An X-ray of the hands or skull may
demonstrate cystic formations due to resorp-
tion of Ca. A 25-hydroxyvitamin D level is
necessary to assess for a correctable second-
ary HPT due to vitamin D deficiency. C. Imaging is performed for operative planning
Additionally, a 24-h urine calcium (24-h
UCa) measurement should be obtained to rule
out benign familial hypocalciuric hypercalce-
M. Boltz (*)
Department of Surgery, Penn State Hershey Medical
Center, Hershey, PA, USA
e-mail: mboltz2@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_109
109
mia (FHH), which is an autosomal dominant
disorder of the renal calcium-sensing recep-
tor that can mimic pHPT. The urine calcium
levels in FHH patients are usually less than
50 mg/24 h [1].
patient can be classified as either symptom-
atic or asymptomatic. Parathyroidectomy is
recommended for all patients with objective
symptoms of nephrolithiasis or fragility frac-
tures. Although neurocognitive symptoms are
subjective, there is strong evidence to support
parathyroidectomy, as observational studies
suggest improved symptoms of muscle
strength and functional capacity after surgery.
Surgical treatments in asymptomatic individ-
uals are guided by the National Institutes of
Health criteria and include age younger than
50 years, significant hypercalcemia >1 mg/dL
over the reference range, 24-h UCa > 400 mg/
dL, renal insufficiency with creatinine clear-
ance reduced by 30%, osteoporosis with
t-score of the spine < −2.5, and patient desire
for surgical intervention [2].
after deciding whether or not a patient is a
surgical candidate, as it has no utility in con-
firming or excluding the diagnosis of
pHPT.  Neck ultrasonography is recom-
mended to localize parathyroid disease as it is
noninvasive and the least costly. It can also
assess for concomitant thyroid disease, which
443
444
should be addressed during the parathyroid-
ectomy if appropriate. If ultrasound is incon-
clusive, then technetium Tc 99  m sestamibi
scan or 4D-CT of the neck can be performed
depending on surgeon and institution prefer-
ence [1].
D. In cases where imaging does not localize a
parathyroid adenoma or is discordant, a bilat-
eral neck exploration should be performed.
All four parathyroid glands are identified
with removal of the abnormal-appearing or
enlarged gland(s). Intraoperative parathyroid
hormone monitoring (IOPM) may or may not
be used as an adjunct to assess cure [2]. All
specimens removed should be sent to pathol-
ogy for frozen section to confirm the presence
of parathyroid tissue.
E. Focused or unilateral parathyroidectomy with
IOPM may be done with a localized parathy-
roid adenoma. A baseline PTH is drawn prior
to excision of the abnormal parathyroid
gland, and the gland is excised and sent for
frozen section to confirm parathyroid tissue.
Another PTH is drawn 10 min post-excision.
The post-excision PTH should drop by at
least 50% from the baseline PTH and into the
normal range to predict cure or postoperative
M. Boltz
eucalcemia. If the PTH fails to decrease,
hypersecreting parathyroid tissue remains
present and requires further bilateral neck
exploration [2].
F. Oral calcium supplementation is typically
provided for 2  weeks postoperatively to
prevent symptomatic transient hypocalce-
mia. Patients who are vitamin D deficient
should receive vitamin D supplementation
as well. Serum calcium, PTH, and vitamin
D levels should be checked 6 months post-
operatively to assess for cure or persistent
disease.
Of note, secondary hyperparathyroidism
occurs in the setting of chronic renal failure. Low
levels of calcium lead to elevated PTH and
increased calcium resorption from the bone and
hyperplastic parathyroid glands. Biochemical
evaluation demonstrates an elevated PTH and
decreased calcium levels. Three-and-a-half-gland
or four-­gland resection with autotransplantation
is a treatment of choice. Tertiary hyperparathy-
roidism occurs in renal transplant patients. Both
PTH and calcium are elevated. Treatment is
either three-and-a-half-gland or four-gland resec-
tion with autotransplantation.
109 Hyperparathyroidism 445

Referral for hypercalcemia

Suspicious for primary hyperparathyroidism
A

Consider other causes: medications (Thiazides, lithium, bisphosphonates, vitamin D), FHH,
malignancy, sarcoidosis
Confirm biochemical dx: serum calcium, intact PTH, vitamin D, 24-h urine calcium

B
Asymptomatic Symptomatic

Age < 50 years Nephrolithiasis

Ca > 1mg/dL above reference range Fragility fractures
24-hr UCa > 400 mg/dL Neurocognitive symptoms (short-
term memory loss, difficulty
Renal insufficiency
concentrating), irritability, anxiety
Osteoporosis (t-score < –2.5)
Fatigue, myalgias, arthralgias
Patient prefers surgery
Constipation, polyuria, polydipsia

No Yes Surgical candidate

Non-operative management Pre-operative localization C

Ultrasound
Sestamibi (parathyroid scan)
4D-CT (neck/upper chest)

D Non-localized Localized E

Bilateral neck exploration Focused parathyroidectomy vs. bilateral

IOPM neck exploration
IOPM

PTH ¯50% and into normal range

Abbreviations: 4D-CT, four dimensional

computed tomography; Ca, calcium; FHH,
F End surgery/Follow-up familial hypocalciuric hypocalcemia; IOPM,
intraoperative parathyroid hormone monitoring;
PTH, parathyroid hormone; UCa, urine calcium

Algorithm 109.1
446 M. Boltz

References p­rimary h­ yperparathyroidism. JAMA Surg.

2016;151(10):959–68.
2. Sneider MS, Solorzano CC, Lew JI.  Primary hyper-
1. Wilhelm SM, Wang TS, Ruan DT, et  al. The
parathyroidism. In: Morita SY, APB D, Zeiger MA,
American Association of Endocrine Surgeons
editors. McGraw-Hill manual endocrine surgery. 1st
guidelines for definitive management of
ed. New York: McGraw-Hill; 2009.
 Part XV
Endocrine
 Cushing’s Syndrome and Disease
Edwina Moore and Vikram D. Krishnamurthy
Algorithmic Approach
A. The signs and symptoms associated with
Cushing’s syndrome and disease include cen-
tral obesity, impaired glucose tolerance,
hypertension, fluid retention, dermatologic
changes (abdominal striae, acne, hirsutism,
easy bruising), musculoskeletal decline
(proximal muscle weakness, osteopenia), and
poor wound healing/immunosuppression [1].
B. The first step in diagnosis is establishing
hypercortisolism, which can accurately be
assessed with a 24-h urine collection for cor-
tisol and creatinine. Late-night salivary corti-
sol levels on two to three separate evenings, if
elevated, demonstrate the loss of normal diur-
nal variation [2].
C. The second step involves distinguishing
between Cushing’s syndrome and Cushing’s
disease or ectopic ACTH secretion by obtain-
ing a serum ACTH measurement. If the ACTH
level is normal or suppressed, then autono-
mous secretion of cortisol from the adrenal
should be suspected. If the ACTH level is ele-
vated, then either a pituitary adenoma or ecto-
pic secretion from a neuroendocrine tumor
should be suspected. A high-dose dexametha-
sone suppression test will differentiate
E. Moore · V. D. Krishnamurthy (*)
Department of Endocrine Surgery, The Cleveland
Clinic, Cleveland, OH, USA
e-mail: krishnv3@ccf.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_110
110
between pituitary and ectopic etiology. Serum
cortisol levels will not suppress after high-
dose dexamethasone intake when the excess
ACTH secretion is ectopic in origin [3].
D. Once the biochemical diagnosis has been made,
imaging is obtained to identify the source.
Cushing’s syndrome may be caused by a solitary
adrenal adenoma, bilateral adrenal hyperplasia,
or adrenocortical carcinoma. All three can be
identified on computed tomography of the abdo-
men, especially “adrenal protocol” when avail-
able. Cushing’s disease from a pituitary adenoma
is identified by magnetic resonance imaging of
the pituitary and/or inferior petrosal sinus sam-
pling. Neuroendocrine tumors secreting ectopic
ACTH can be found throughout the body and
identification should be directed at the lung,
mediastinum, gastrointestinal tract, retroperito-
neum, pancreas, and neck.
E. Surgery is the first-line treatment option for
most causes of Cushing’s syndrome, such as
unilateral adrenalectomy for adrenal adeno-
mas and carcinomas, transsphenoidal selec-
tive adenectomy for pituitary adenomas, and
resection of tumor secreting ectopic ACTH
[4]. Bilateral adrenalectomy is reserved as a
palliative measure in severe, debilitating
hypercortisolism from occult, refractory, or
metastatic ectopic ACTH secretion [5].
F. After surgery, glucocorticoid replacement
may be necessary until the patient’s
hypothalamic-­pituitary-adrenal axis recov-
449
450 E. Moore and V. D. Krishnamurthy

ers. Lifelong follow-up and treatment of necessary. Depending on the etiology,

­comorbidities such as hypertension, glu- patients also may need to be followed up
cose intolerance, and bone loss may be for recurrence [4, 6].

Suspicion for hypercortisolism based on phenotype, hypertension, glucose

A intolerance, weight gain, fluid retention, easy bruising, abdominal striae

Obtain a 24-h urine collection for cortisol and creatinine and repeated late-
B night salivary cortisol measurements

Obtain a serum ACTH level, and if elevated, perform a high-dose dexamethasone

C suppression test

D
If Cushing’s syndrome, obtain CT adrenal protocol

If Cushing’s disease, obtain MRI pituitary and/or

inferior petrosal sinus sampling

If ectopic, image chest, mediastinum, abdomen,

neck and/or endoscopy

Treatment is unilateral adrenalectomy for adrenal adenomas and carcinomas,

E trans-sphenoidal selective adenectomy for pituitary adenomas, and resection of
tumor secreting ectopic ACTH

Postoperatively, screen for adrenal insufficiency, treat comorbidities, and

F monitor for recurrence

Algorithm 110.1
110  Cushing’s Syndrome and Disease 451

References a consensus statement. J Clin Endocrinol Metab.

2008;93(7):2454–62.
4. Nieman LK, Biller BM, Findling JW, Murad MH,
1. Dekkers OM, Horvath-Puho E, Jorgensen JO,
Newell-Price J, Savage MO, et  al. Treatment of
Cannegieter SC, Ehrenstein V, Vandenbroucke
Cushing’s syndrome: an endocrine society clini-
JP, et  al. Multisystem morbidity and mortality in
cal practice guideline. J Clin Endocrinol Metab.
Cushing’s syndrome: a cohort study. J Clin Endocrinol
2015;100(8):2807–31.
Metab. 2013;98(6):2277–84.
5. Findling JW, Raff H.  Cushing’s syndrome: impor-
2. Nieman LK, Biller BM, Findling JW, Newell-Price
tant issues in diagnosis and management. J Clin
J, Savage MO, Stewart PM, et  al. The diagnosis of
Endocrinol Metab. 2006;91(10):3746–53.
Cushing’s syndrome: an endocrine society clini-
6. Mitchell J, Barbosa G, Tsinberg M, Milas M,
cal practice guideline. J Clin Endocrinol Metab.
Siperstein A, Berber E. Unrecognized adrenal insuf-
2008;93(5):1526–40.
ficiency in patients undergoing laparoscopic adrenal-
3. Biller BM, Grossman AB, Stewart PM, Melmed
ectomy. Surg Endosc. 2009;23(2):248–54.
S, Bertagna X, Buchfelder M, et  al. Treatment of
adrenocorticotropin-dependent Cushing’s syndrome:
 Primary Hyperaldosteronism
(Conn’s Syndrome)
Iuliana Bobanga, Cassandre Bénay,
and Vikram D. Krishnamurthy
Algorithmic Approach
A. Primary hyperaldosteronism is the most com-
mon cause of secondary hypertension and C. After establishing the diagnosis of hyperaldo-
should be suspected in patients with hyper-
tension that is diagnosed earlier than age 35,
severe (BP < 160/100), persistent despite >3
medications, and present along with hypoka-
lemia and/or an adrenal incidentaloma [1].
B. The first diagnostic assessment in patients
with Conn’s syndrome requires demonstra-
tion of aldosterone excess along with sup-
pressed plasma renin activity. Before
measuring serum aldosterone levels and
plasma renin activity, medications that can
affect these measurements (e.g., angiotensin-­ D. The laterality of aldosterone hypersecretion is
converting enzyme inhibitors, angiotensin
receptor blockers, aldosterone receptor antag-
onists, and beta-blockers) are replaced with
others (e.g., calcium channel blockers or
alpha-adrenergic blockers) for several weeks.
The aldosterone-to-renin ratio (ARR) is then
calculated, with a ratio >20–40:1 along with
an aldosterone level >15 ng/dL being sugges-
tive of primary hyperaldosteronism (further-
more, an ARR  >35 is 100% sensitive and
92% specific). If the ARR is equivocal but the
diagnosis is still suspected, confirmatory test-
I. Bobanga · C. Bénay · V. D. Krishnamurthy (*)
Department of Endocrine Surgery, The Cleveland
Clinic, Cleveland, OH, USA
e-mail: krishnv3@ccf.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_111
111
ing may be performed (e.g., oral sodium
loading, saline infusion, or captopril chal-
lenge testing) [1, 2].
steronism by biochemical studies, the next step
is localizing the production to either a unilateral
adenoma or bilateral hyperplasia. The imaging
modality of choice is an “adrenal protocol” thin-
cut computed tomography (CT) scan, which
can demonstrate normal adrenal glands, thick-
ened glands, or a unilateral adrenal mass [3]. An
aldosterone-­producing adenoma should be sus-
pected in younger patients with hypertension
whose CT scan reveals a unilateral adrenal mass
and a contralateral normal adrenal gland.
then confirmed by bilateral adrenal venous
sampling (AVS), which is the gold standard for
distinguishing between unilateral and bilateral
disease. The acquisition of AVS in every
patient with primary hyperaldosteronism is
controversial; however, many centers perform
this routinely. Reliance on CT findings alone is
questionable for two reasons: (1) aldosterono-
mas are typically small and may be missed
(false negatives) and (2) non-­ aldosterone-­
secreting/nonfunctional adrenal adenomas
increase with age (false positives). During
AVS, aldosterone levels are obtained from the
SVC, IVC, and adrenal veins. Cortisol levels
are also obtained, with an adrenal vein to IVC
cortisol ratio  >2:1 confirming successful
453
454 I. Bobanga et al.

c­ annulation of the adrenal veins. The aldoste-
rone-to-cortisol ratio between both adrenal
veins is then compared. A ratio of more than
4:1 lateralizes unilateral hypersecretion and
identifies the gland to be removed [4, 5].
E. Hyperaldosteronism is typically cured by
laparoscopic adrenalectomy; however, blood
pressure may remain elevated secondary to
the vascular damage caused by the prior long-­
standing, severe hypertension. Factors pre-
dictive of the resolution of hypertension
include female sex, body mass index
(BMI)  ≤25, hypertension lasting ≤6  years,
prescription of ≤2 antihypertensive medica-
tions, and decline in plasma aldosterone by
10 ng/dL on postoperative day 1 [6, 7].

Suspect primary hyperaldosteronism in patients when:

Age <35
Severe hypertension (BP>160/100)
>3 antihypertensive medications required
A
Hypokalemia
Adrenal incidentaloma

Obtain Plasma Aldosterone Concentration (PAC)

B and Plasma Renin Activity (PRA)

Unlikely primary
PAC/PRA >20? hyperaldosteronism
No

Y es

C Obtain adrenal CT scan

D Obtain adrenal venous sampling

Lateralization?

No Yes

E
Medical management Unilateral adrenalectomy

Algorithm 111.1
111  Primary Hyperaldosteronism (Conn’s Syndrome) 455

References of Endocrine Surgeons medical guidelines for the

management of adrenal incidentalomas. Endocr
Pract. 2009;15(Suppl 1):1–20.
1. Harvey AM.  Hyperaldosteronism: diagnosis, lat-
5. Chao CT, Wu VC, Kuo CC, Lin YH, Chang CC,
eralization, and treatment. Surg Clinic N Am.
Chueh SJ, et  al. Diagnosis and management of pri-
2014;94(3):643–56.
mary aldosteronism: an updated review. Ann Med.
2. Yin G, Zhang S, Yan L, et  al. One-hour upright
2013;45(4):375–83.
posture is an ideal position for serum aldosterone
6. Aranova A, Gordon BL, Finnerty BM, Zarnegar
concentration and plasma renin activity ­measuring
R, Fahey TJ.  Aldosterone resolution score pre-
on primary aldosteronism screening. Exp Clin
dicts long-term resolution of hypertension. Surgery.
Endocrinol Diabetes. 2012;120(7):388–94.
2014;156(6):1387–92.
3. Bobanga ID, McHenry CR.  Chapter 6. Imaging
7. Swearingen AJ, Kahramangil B, Monteiro R,
modalities for adrenal cortical tumors. In: Kebebew
Krishnamurthy VD, Jin J, Shin JJ, et  al. Analysis
E, editor. Management of adrenal masses in children
of postoperative biochemical values and clinical
and adults. 1st ed. Switzerland: Springer; 2017.
outcomes after adrenalectomy for primary aldoste-
4. Zeiger MA, Thompson GB, Duh Q-Y, Hamrahian AH,
ronism. Surgery. 2017. https://doi.org/10.1016/j.
Angelos P, Elaraj D, et  al. American Association of
surg.2017.10.045.
Clinical Endocrinologists and American Association
 Glucagonoma
112
Talia Burneikis and Vikram D. Krishnamurthy

Algorithmic Approach C. Initial treatment is supportive and involves

A. When suspected, the diagnosis is established
by an elevated fasting glucagon level >500 pg/
mL (normal reference range  <50  pg/mL).
Additional findings include normocytic ane-
mia and secondary elevations of neuroendo-
crine markers (gastrin, somatostatin,
vasoactive intestinal peptide, serotonin, and
pancreatic polypeptide) [1].
B. Once the diagnosis is confirmed, imaging is
obtained to localize primary tumors and
stage for distant disease, as glucagonomas D. For patients with unresectable disease and/or
are almost always malignant. Computed
tomography (CT) and magnetic resonance
imaging (MRI) are sensitive initial imaging
modalities to detect primary tumors, as most
glucagonomas are >3 cm [2]. If CT does not
demonstrate an obvious pancreatic lesion,
endoscopic ultrasound (EUS) can detect E. Subsequent follow-up is dependent on stage at
tumors as small as 2–3  mm [3]. Extra-­
pancreatic disease can be detected with
somatostatin-­receptor scintigraphy (octreo-
tide scan) or gallium Ga-68 DOTATATE-
PET scan [4].
glycemic control and improving nutritional
status. When disease burden is amenable,
resection of the primary tumor and debulking
of metastases are indicated. Even for local-
ized disease, laparotomy is generally the rec-
ommended surgical approach due to the
generally large tumor size and need for
lymphadenectomy [5]. Liver metastasis can
be addressed by anatomic hepatectomy, mul-
tiple “wedge” resections, and/or radiofre-
quency and microwave ablation [6].
overwhelming tumor burden, debulking, hepatic
artery embolization (with or without doxorubi-
cin, cisplatin, streptozocin, drug-­eluting beads),
and somatostatin analogs can be palliative.
Systemic therapies include streptozocin, temo-
zolomide, everolimus, and sunitinib [7].
presentation, as well as multiple endocrine neo-
plasia syndrome type 1 (MEN1) status. Generally,
guidelines recommend evaluation every
3–12  months with history and physical exam,
serum glucagon measurement, and imaging [7].

T. Burneikis · V. D. Krishnamurthy (*)

Department of Endocrine Surgery, The Cleveland
Clinic, Cleveland, OH, USA
e-mail: krishnv3@ccf.org

© Springer Nature Switzerland AG 2019 457

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_112
458 T. Burneikis and V. D. Krishnamurthy

Suspect glucagonoma with weight loss, rash,

A
glucose intolerance, diabetes, diarrhea,
venous thrombosis and serum glucagon
measurement >500 pg/mL.

Imaging and staging with triple-phase contrast CT

B (or MRI). EUS, octreotide scan, and dotatate-PET
may further characterize tumor burden.

C Provide nutritional
support, optimize
glycemic control, and
determine resectability.

Localized or metastatic
disease with >90% Unresectable disease or
resectable and unacceptable operative risk.
acceptable operative risk.

Pancreatic resection with Palliative procedures:

or without cytoreductive surgery,
resection/ablation of radiofrequency ablation,
D
liver metastases cryoablation, hepatic artery
embolization (+/–
chemotherapy) and/or liver
transplantation and/or
systemic therapies:
somatostatin analogues,
molecular-targeted
(everolimus, sunitinib), and/or
chemotherapy (temozolomide,
stretozocin).

E
Surveillance and follow-up:
H&P, glucagon levels, axial imaging (CT or MRI)

Algorithm 112.1
112 Glucagonoma 459

References 4. Nauck C, Ivancevic V, Emrich D, Creutzfeldt W.

111In-pentetreotide (somatostatin analogue) scin-
tigraphy as an imaging procedure for endocrine
1. Wermers RA, Fatourechi V, Wynne AG, Kvols LK,
gastro-entero-pancreatic tumors. Z Gastroenterol.
Lloyd RV.  The glucagonoma syndrome. Clinical
1994;32(6):323–7.
and pathologic features in 21 patients. Medicine
5. Fraker DL, Norton JA.  The role of surgery in the
(Baltimore). 1996;75(2):53.
management of islet cell tumors. Gastroenterol Clin
2. Dromain C, de Baere T, Baudin E, Galline J, Ducreux M,
N Am. 1989;18(4):805.
Boige V, Duvillard P, Laplanche A, Caillet H, Lasser P,
6. Karabulut K, Akyildiz HY, Lance C, Aucejo F,
Schlumberger M, Sigal R. MR imaging of hepatic metas-
McLennan G, Agcaoglu O, Siperstein A, Berber
tases caused by neuroendocrine tumors: comparing four
E.  Multimodality treatment of neuroendocrine liver
techniques. AJR Am J Roentgenol. 2003;180(1):121.
metastasis. Surgery. 2011;150(2):316–25.
3. Khashab MA, Yong E, Lennon AM, Shin EJ, Amateau
7. National Comprehensive Cancer Network (NCCN).
S, Hruban RH, Olino K, Giday S, Fishman EK,
NCCN Clinical practice guidelines in oncology.
Wolfgang CL, Edil BH, Makary M, Canto MI. EUS
http://www.nccn.org/professionals/physician_gls/f_
is still superior to multidetector computerized tomog-
guidelines.asp. Accessed on 27 Feb 2016.
raphy for detection of pancreatic neuroendocrine
tumors. Gastrointest Endosc. 2011;73(4):691.
 Management
of Pheochromocytoma
Hadley E. Ritter and Benjamin C. James
Algorithmic Approach
A. Pheochromocytomas are rare catecholamine-­
secreting tumors of the medullary adrenal
chromaffin cells. They represent roughly 0.1–
0.6% of patients with hypertension (HTN)
and occur in 3–7% of patients with an inci-
dentally found adrenal mass.
Pheochromocytomas generally occur in the
third to fifth decade, and about 10% are malig-
nant. Genetic syndromes associated with
pheochromocytomas include von Hippel-
Lindau disease, neurofibromatosis type 1, and
multiple endocrine neoplasia type 2. In addi-
tion, mutations in any of the succinate dehy-
drogenase complex subunit genes, including
SDHA, SDHB, SDHC, and SDHD, may lead
to pheochromocytomas with variable pene-
trance [1]. Genetic testing may be considered
in all patients diagnosed with a pheochromo-
cytoma but should always be performed when
bilateral, present in children or adults <45,
and when they exist in multiple family mem-
B. Biochemical evaluation is most sensitive and
H. E. Ritter
Department of Surgery, Indiana University,
Indianapolis, IN, USA
B. C. James (*)
Department of Surgery, Harvard Medical School,
Boston, MA, USA
Department of Surgery, Beth Israel Deaconess
Medical Center, Boston, MA, USA
e-mail: bjames1@bidmc.harvard.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_113
113
bers or co-exist with other endocrine syn-
dromes [2]. Presenting symptoms are related
to the catecholamine excess and tend to be
paroxysmal, although hypertension can be
sustained or exhibit severe lability with ortho-
static hypotension. Symptoms of tremors, pal-
pitations, diaphoresis, dyspnea, headache,
panic episodes, chest pain, and a sense of
impending death are typical of e­ pisodic spells
and may be spontaneous or exacerbated by
postural change, increased abdominal pres-
sure, exercise, and ­medications. Chronic over-
production of catecholamines can lead to
weight loss, cardiomyopathy, fatigue, consti-
pation, chronic headaches, and sequelae of
chronic uncontrolled hypertension. Screening
for a pheochromocytoma should be done in
patients with recalcitrant hypertension, hyper-
tension diagnosed <20 years of age, hyperad-
renergic spells, pressor response during
procedures, and family history of paragangli-
oma, pheochromocytoma, or related syn-
dromes or in patients with an adrenal mass.
specific with 24-h urine collection of fraction-
ated metanephrines and catecholamines and
should include dopamine in addition to creati-
nine for adequacy of sample. Plasma testing
has a higher false-positive rate but is a useful
screening test in children and patients where
reliable urine collection is difficult. Clinical
circumstances must be considered regarding
461
462
the timing of testing as illness, psychiatric
medications, and physical stress can confound
the interpretation of elevated levels.
C. Computed tomography (CT) imaging with
and without intravenous (IV) contrast is rec-
ommended for localization of an adrenal
tumor once a biochemical diagnosis has been
made. Pheochromocytomas are usually inho-
mogeneous tumors with smooth edges and
have marked contrast enhancement, which
differentiates them from adenomas. Although
they may be of any size, they are usually
greater than 3  cm. Imaging should also be
reviewed for concerning features of malig-
nancy including local invasion, enhancing
lymphadenopathy, and extra-adrenal pheo-
chromocytomas, referred to as paraganglio-
mas. Magnetic resonance imaging (MRI) is
useful in patients who are unable to receive
radiation exposure and may better detail local
invasion. Iodine 123 metaiodobenzylguanidine
(123I-MIBG) localization is useful when abdom-
inal imaging is negative, when metastatic dis-
ease is suspected, or when a paraganglioma
is identified. F­ luorodeoxyglucose-positron
emission tomography (FDG-PET) is useful
in  localizing both primary and metastatic
tumors with succinate dehydrogenase (SDH)
mutations [1, 3].
H. E. Ritter and B. C. James
Adrenal vein sampling and biopsy of a
suspected pheochromocytoma are not recom-
mended and can be detrimental by precipitat-
ing a hyperadrenergic crisis.
D. Medical management is not recommended
but may be needed for treating unresectable
or diffusely metastatic disease.
E. Surgical management with minimally invasive
adrenalectomy is recommended for most
pheochromocytomas. Consideration should
be given to open adrenalectomy for tumors
>6 cm and for any tumor with concerning fea-
tures of malignancy to ensure complete resec-
tion and avoid tumor seeding [4].
Preoperative preparation targeting sympa-
thetic blockade is essential prior to proceeding
with surgical intervention to avoid intraopera-
tive labile hypertension. Patients should be
started on alpha-blockade until rendered
orthostatic. After adequate alpha-blockade,
some patients may develop rebound tachycar-
dia and should be started on beta-blockade.
High-sodium diet and adequate fluid intake
are recommended for volume expansion.
Intraoperative and postoperative management
with an experienced team is necessary and
should include arterial monitoring, adequate
IV access, and pharmacologic preparation for
rapid cardiovascular shifts.
113  Management of Pheochromocytoma 463

History and physical exam:

-Hypertension: paroxysmal, sustained or with severe lability
A
-Tremors, palpitations, diaphoresis, dyspnea, headache, panic episodes,
chest pain and a sense of impending death

Laboratory evaluation:
B -Screening with plasma metanephrines
-Confirmatory testing with 24-h urine catecholamines

Tumor localization:
-Non-contrast CT or MRI
Preoperative management:
C
-Alpha-blockade until adequate hypertension control. Addition of beta-blockade
if rebound tachycardia occurs
-High sodium diet and adequate fluid intake for volume expansion

Tumor >6 cm, evidence of

Adenoma concerning features of
malignancy

Consideration for open

D, E Laparoscopic adrenalectomy D, E
adrenalectomy

Algorithm 113.1
464 H. E. Ritter and B. C. James

References in pheochromocytoma and paraganglioma. J Nucl

Med. 2014;55:1253–9.
4. Lenders JWM, Duh Q-Y, Eisenhofer G, Giminez-­
1. Assadiour Y, Sadowski SM, Alimchandani M,
Roqueplo A-P, Grebe SKG, Murad MH, Naruse
Quezado M, Steinberg SM, Nilubol N, Patel D,
M, Pacak K, Young WF Jr. Pheochromocytoma
Prodanov T, Pacak K, Kebebew E.  SDHB muta-
and paraganglioma: an endocrine society clini-
tion status and tumor size but not grade are
cal practice guideline. J Clin Endocrinol Metab.
important predictors of clinical outcome in pheo-
2014;99(6):1915–42.
chromocytoma and abdominal paraganglioma.
Surgery. 2017;161:230–9.
2. Melmed S, Polonsky KS, Larsen PR, Kronenberg
HM. Chapter 16 endocrine hypertension. In: Williams Suggested Reading
textbook of endocrinology. 13th ed. Philadelphia:
Elsevier; 2016. p. 566–88.
Clark OH, Duh Q-Y, Gosnell JE, Shen W.  Textbook of
3. Van Berkel A, Rao JU, Kusters B, et al. Correlation
endocrine surgery. 3rd ed. New Delhi: Jaypee Brothers
between in  vivo 18F-FDG PET and immunohisto-
Medical Publishers; 2014.
chemical markers of glucose uptake and metabolism
 Management of Aldosteronoma
Hadley E. Ritter and Benjamin C. James
Algorithmic Approach
A. Primary hyperaldosteronism, also known as
Conn’s syndrome, is defined as the excess
production of aldosterone from an adrenal
source. It may be caused by a single adenoma
or from idiopathic hyperplasia of the adrenal
glands. Although once considered a rare
cause of hypertension, it is now thought to be
the cause of hypertension in 5–10% of
patients. The majority of patients present
without symptoms. However, patients may
endorse symptoms of muscle weakness,
cramping, headaches, polydipsia, and poly-
uria as a result of hypokalemia. Screening for
hyperaldosteronism should be considered in
patients diagnosed with hypertension at a
young age, in those with hypokalemia, and in
patients with medically recalcitrant disease
on three or more antihypertensive agents.
Additionally, biochemical evaluation for
hyperaldosteronism should be considered in
any patient with an adrenal mass [1, 2].
H. E. Ritter
Department of Surgery, Indiana University,
Indianapolis, IN, USA
B. C. James (*)
Department of Surgery, Harvard Medical School,
Boston, MA, USA
Department of Surgery, Beth Israel Deaconess
Medical Center, Boston, MA, USA
e-mail: bjames1@bidmc.harvard.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_114
114
B. Biochemical evaluation should include a
plasma aldosterone concentration (PAC),
plasma renin activity (PRA), and a metabolic
panel. Patients may occasionally have hypo-
kalemia and hypernatremia but are more
commonly within the normal range. A PAC
>15  ng/dl, PRA <1.0  ng/ml, and PAC/PRA
>20 are suggestive of a primary hyperaldoste-
ronism [1]. A PAC/PRA greater than 35 is
highly sensitive and specific for primary
hyperaldosteronism. Confirmatory testing
with aldosterone suppression tests can be
considered if results are equivocal and in
patients over 40 years of age, as the incidence
of both non-functioning adenomas and idio-
pathic adrenal hyperplasia (IAH) is higher in
this population [3]. Biochemical evaluation
should be performed after cessation of miner-
alocorticoid receptor antagonists for at least
2  weeks. If possible, angiotensin-converting
enzyme inhibitors and angiotensin receptor
blockers should be discontinued prior to eval-
uation as these medications may falsely ele-
vate the PRA [4].
C. Adrenal masses are often identified inciden-
tally. If no prior imaging has been performed,
evaluation should include a non-contrasted
CT scan. Aldosteronomas are generally small,
1–3  cm, and should have low Hounsfield
units (HU) (>10) indicative of a benign ade-
noma. If multiple or bilateral small nodules
are identified or if the adrenal glands have a
465
466 H. E. Ritter and B. C. James

thickened or micronodular appearance, a oversecretion and may include mineralocorti-

diagnosis of IAH is more likely. Biopsy
should not be performed [2]. If imaging is
unclear, adrenal vein sampling (AVS) should
be done to lateralize aldosterone hypersecre-
tion. AVS should also be considered in
patients >40 to exclude IAH. The presence of
adrenocortical carcinoma in the setting of pri-
mary hyperaldosteronism is rare [4].
D. Medical management is the preferred treat-
ment in patients with bilateral aldosterone
coid receptor antagonists such as spironolac-
tone and eplerenone. Treatment with medical
therapy may also be considered in patients
with unilateral disease who are not surgical
candidates.
E. For patients with clear unilateral disease, sur-
gical resection with laparoscopic adrenalec-
tomy is recommended and may result in a
reduction in the number of required antihy-
pertensives [1, 2, 4].

History and physical exam:

-Hypertension: early onset, severe or medically recalcitrant
A
-Occasional muscle weakness, cramping, headaches,
polydipsia, polyuria

Laboratory evaluation:
B -May have hypokalemia and slight hypernatremia
-Elevated PAC >15ng/ml and decreased PRA <1.0 ng/ml per hour
-PAC/PRA >20
If needed confirmatory aldosterone suppression test

Tumor localization, staging, and tissue diagnosis

-Non-contrast CT
If needed: adrenal vein sampling

Idiopathic adrenal
Adenoma
hyperplasia

-Unilateral adrenalectomy
-Mineralocorticoid
D -Mineralocorticoid suppression D, E
suppression
if poor operative candidate

Algorithm 114.1
114  Management of Aldosteronoma 467

References treatment of patients with primary aldosteronism. Eur

J Endocrinol. 2010;162:435–8.
4. Montori VM, WF Y.  Use of plasma aldosterone
1. Melmed S, Polonsky KS, Larsen PR, Kronenberg
concentration-­to-plasma renin activity ratio as a
HM.  Chapter 16: Endocrine hypertension. In:
screening test for primary aldosteronism. A system-
Williams textbook of endocrinology. 13th ed.
atic review of the literature. Endocrinol Metab Clin N
Philadelphia: Elsevier; 2016. p. 566–88.
Am. 2002;31:619–32.
2. Funder JW, Carey RM, Fardella C, Gomez-Sanchez
CE, Mantero F, Stowasser M, Young WF Jr, Montori
V. Case detection, diagnosis, and treatment of patients
with primary aldosteronism: an Endocrine Society Suggested Reading
clinical practice guideline. J Clin Endocrinol Metab.
2008;93(9):3266–81. Clark OH, Duh Q-Y, Gosnell JE, Shen W.  Textbook of
3. Arlt W. A detour guide to the Endocrine Society clini- endocrine surgery. 3rd ed. New Delhi: Jaypee Brothers
cal practice guideline on case detection, diagnosis and Medical Publishers; 2014.
 Management of Gastrinoma
Rachel E. Simpson and Benjamin C. James
Algorithmic Approach
A. Gastrinoma is the second most common func-
tional pancreatic neuroendocrine tumor [1].
The first step in diagnosis is a full history and
physical exam. The most common clinical
presentation includes symptoms of abdomi-
nal pain, diarrhea, and reflux [2]. These
symptoms are vague with a broad differential.
Zollinger-Ellison syndrome (ZES) is charac-
terized by gastrin-producing tumors stimulat-
ing marked gastric acid production, with
resultant refractory peptic ulcer disease [3].
Around 75% of gastrinomas are sporadic,
while 25% are associated with multiple endo-
crine neoplasia type 1 (MEN 1) [1].
B. Multiple tests are utilized to prove that a
patient not only has elevated serum gastrin
levels but also hypersecretion of gastric acid.
The first test is a fasting serum gastrin level,
which is usually markedly elevated in patients
with a gastrinoma (10 times normal
or >1000 pg/mL) [4].
R. E. Simpson
Department of Surgery, Indiana University,
Indianapolis, IN, USA
B. C. James (*)
Department of Surgery, Harvard Medical School,
Boston, MA, USA
Department of Surgery, Beth Israel Deaconess
Medical Center, Boston, MA, USA
e-mail: bjames1@bidmc.harvard.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_115
115
C. Once hypergastrinemia has been established,
other causes of hypergastrinemic state (gas-
tric outlet obstruction, prior vagotomy, renal
failure, and atrophic gastritis, among others)
should be ruled out [1]. A fasting gastric
pH  <2 is seen in 99% of patients with ZES
[4]. After discontinuation of proton-pump
inhibitor therapy for 2  weeks, gastric acid
secretion should measure <15 mEq/h. values
greater than this suggest hypersecretion of
gastric acid [2].
D. When results are equivocal, a secretin stimu-
lation test can be performed. On a fasting
patient, 2 IU/kg secretin is administered, and
gastrin levels are measured at 0, 2, 5, 10, 15,
20, and 30 min. An increase in serum gastrin
level of 200 ng/L or greater within 15 min is
considered a positive result for the diagnosis
of gastrinoma [5].
E. Once the biochemical diagnosis is made,
cross-sectional imaging with pancreas proto-
col computed tomography (CT) scan or mag-
netic resonance imaging (MRI) is used to
localize the tumor and determine extent of
disease and presence of metastases. Ninety
percent of tumors will be within the gastri-
noma triangle, bordered by the cystic duct,
the junction of the second and third portion of
the duodenum, and the junction of the neck
and body of the pancreas. Most gastrinomas
have somatostatin receptors, so somatostatin
469
470
receptor scintigraphy may be useful for fur-
ther localization [1].
F. If imaging fails to localize the tumor, more
invasive testing may be employed, including
endoscopic ultrasound or operative explora-
tion. A reported 24–30% of masses are located
by performing open duodenotomy [1].
G. All patients regardless of tumor burden
J. The approach for patients with MEN 1 is less
should be treated with a proton-pump inhibi-
tor [1], with or without the addition of a hista-
mine-­2 receptor blocker [3].
H. For sporadic, isolated gastrinoma, surgical
resection is recommended [4].
I. Fifty percent of patients will have metastatic
disease at the time of diagnosis [1]. The most
significant predictor of survival is the presence
of liver metastases. Twenty-year survival is near
95% with isolated disease versus 15% 10-year
survival in the presence of metastases [3].
R. E. Simpson and B. C. James
Tumor debulking surgery may be ­considered
for locoregional and symptomatic control along
with other methods including hepatic artery
embolization, radiofrequency ablation, or selec-
tive internal radiation. Systemic therapies such
as octreotide, interferon, or chemotherapy may
also be employed [3].
clear. Many of these patients have ­multiple, small
duodenal tumors [2]. Pancreaticoduodenectomy
(PD) has been shown in some studies to
improve the length of disease-free period com-
pared to non-PD resections [6] and may have
a higher rate of cure [7]. However, because of
the morbidity associated with PD, some recom-
mend this treatment modality only for patients
with larger tumors as patients with tumors less
than 2  cm have excellent survival rates when
­managed nonoperatively [4].
115  Management of Gastrinoma 471

History and physical exam:

A
Abdominal pain, diarrhea, reflux, peptic ulcer disease. Consider ZES and
association with MEN1.

B No Not ZES
Hypergastrinemia?

Yes

Gastric acid No
C Not ZES
hypersecretion?

Yes

Secretin Stimulation Test

No
D for confirmatory testing Not ZES
or equivocal results

Yes

E,F Localization:
Cross-sectional imaging, endoscopic ultrasound, exploration

MEN 1?

No Yes

Metastases -PPI
G,J
Yes -Possible resection
No

-PPI
-PPI; systemic therapies;
-Resection locoregional therapies; G,I
tumor Debulking
G,H

Algorithm 115.1
472 R. E. Simpson and B. C. James

References Fordtran’s gastrointestinal and liver disease. 10th ed.

Philadelphia: Elsevier; 2016. p. 501–41.
5. McPherson RA, Pincus MR. Chapter 22: Laboratory
1. Townsend CM Jr, Beauchamp RD, Evers BM, Mattox
diagnosis of gastrointestinal and pancreatic disor-
KL.  Chapter 38: Endocrine pancreas. In: Sabiston
ders. In: Henry’s clinical diagnosis and management
textbook of surgery. 20th ed. Philadelphia: Elsevier;
by laboratory methods. St. Louis: Elsevier; 2017.
2017. p. 941–62.
p. 306–23.
2. Melmed S, Polonsky KS, Larsen PR, Kronenberg
6. Lopez CL, Falconi M, Waldmann J, Boninsegna L,
HM.  Chapter 39: Multiple endocrine neoplasia.
Fendrich V, Goretzki PK, Langer P, Kann PH, Partelli
In: Williams textbook of endocrinology. 13th ed.
S, Bartsch DK.  Partial pancreaticoduodenectomy
Philadelphia: Elsevier; 2016. p. 1723–61.
can provide cure for duodenal gastrinoma associated
3. Jameson JL, De Groot LJ, de Kretser DM, Giudice
with multiple endocrine neoplasia Type 1. Ann Surg.
LC, Grossman AB, Melmed S, Potts JT, Weir
2013;257(2):308–14.
GC. Chapter 148: Multiple endocrine neoplasia Type
7. Tonelli F, Fratini G, Falchetti A, Nesi G, Brandi
1. In: Endocrinology: adult and pediatric. 7th ed.
ML.  Surgery for gastroenteropancreatic tumours in
Elsevier Saunders: Philadelphia; 2016. p. 2566–93.
multiple endocrine neoplasia type 1: review and per-
4. Feldman M, Friedman LS, Brandt LJ.  Chapter
sonal experience. J Intern Med. 2005;257(1):38–49.
33: Neuroendocrine tumors. In: Sleisenger and
 Management of Insulinoma
Rachel E. Simpson and Benjamin C. James
Algorithmic Approach
A. The history and physical exam are key to
diagnosis of insulinoma. The classic
“Whipple’s triad” of insulinoma includes
symptoms of hypoglycemia (neuroglycope-
nic symptoms including confusion, seizures,
coma, tachycardia, palpitations, diaphoresis),
concomitant blood glucose <60, and resolu-
tion with glucose administration [1]. The
patient may note a history of weight gain due
to frequent meals to maintain blood glucose.
Timing of symptoms can help differentiate
insulinoma from other causes of hypoglyce-
mia. Symptoms most commonly occur after
periods of fasting, in the early morning, or
during exercise. However, 25% of patients
will also have postprandial symptoms, so this
history should be used in concert with addi-
tional workup [2]. Though only 5% of insuli-
nomas are associated with multiple endocrine
neoplasia 1 (MEN1) syndrome, this diagnosis
should be considered [1].
R. E. Simpson
Department of Surgery, Indiana University,
Indianapolis, IN, USA
B. C. James (*)
Department of Surgery, Harvard Medical School,
Boston, MA, USA
Department of Surgery, Beth Israel Deaconess
Medical Center, Boston, MA, USA
e-mail: bjames1@bidmc.harvard.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_116
116
B. Patients acutely hypoglycemic should be
treated with supportive care and glucose
administration [3].
C. The gold standard for the diagnosis of an
insulinoma is a 72-h supervised fasting
period, during which blood glucose and
symptoms are monitored every 6 h until blood
glucose drops below 60, after which glucose,
insulin, proinsulin, and c-peptide levels are
checked at 1–2-h intervals [1]. Between 60%
and 75% of patients will become symptom-
atic within the first 24 h, and by 72 h, 85–95%
of patients will be symptomatic [1, 4].
D. After obtaining a biochemical diagnosis of insu-
linoma, cross-sectional imaging with dual-phase
CT or MRI should be used for localization,
which has a sensitivity of 40–80% for tumors
over 1  cm [4]. Other less common modalities
include functional imaging with radionuclide-
labeled glucagon-like peptide (GLP-1), which
utilizes the high expression of GLP-1 receptors
present within insulinomas [5].
E. Invasive localization may be necessary when
cross-sectional imaging fails to localize the
tumor. Endoscopic ultrasound (EUS) is highly
sensitive (93%) and specific (95%) and can
detect tumors as small as 2–3 mm [4, 5]. Calcium
arteriography involves cannulation of the arterial
supply via the celiac and superior mesenteric
branches to the head and neck of the pancreas
and splenic artery branches to the body and tail
of the pancreas. Calcium ­ gluconate is then
infused while monitoring serum insulin levels in
473
474 R. E. Simpson and B. C. James

the right hepatic vein. A two-fold increase in
insulin in response to calcium gluconate sug-
gests the presence of insulinoma in this location,
which can guide surgical resection [4].
F. The mainstay of treatment is surgical resec-
tion. Enucleation should be attempted if pos-
sible, as 90% of insulinomas are solitary,
small, and benign. Intraoperative ultrasound
can help localize the lesion, as well as direct
inspection and palpation [1]. Insulinomas
associated with MEN1 tend to be more
aggressive and multifocal, so full assessment
of the pancreas is imperative [1, 5].
G. When metastatic disease is present, patients can
be managed non-operatively with ­ diazoxide,
calcium channel blockers, and small frequent
meals to avoid hypoglycemia. Tumor debulking
should be considered if 90% of tumor mass can
be excised and the patient is a proper surgical
candidate [2]. A number of modalities exist for
loco-regional control of metastases that are not
amenable to surgical resection and include, but
are not limited to, selective chemoembolization
and radiofrequency or microwave ablation to
control symptoms [5]. Prognosis is overall good
for insulinomas after resection. Cure rate after
complete excision of a sporadic insulinoma is
95% [4]. Median survival for metastatic insuli-
noma is 5 years [1].

A History and physical exam:

“Whipple’s Triad,” neuroglycopenic symptoms, consider MEN 1

B Immediate treatment of hypoglycemia when discovered

72-h supervised fast:

C Assessment of symptoms, serum glucose, insulin/
proinsulin/c-peptide levels

Localized w/ cross-
D sectional imaging or
functional imaging? No

Invasive
Localization: EUS,
Yes E
calcium
arteriography

Metastatic
disease?

No Yes

-Medical therapies
Surgical resection
F -Small, frequent meals G
-Locoregional therapies
-Tumor Debulking

Algorithm 116.1
116  Management of Insulinoma 475

References Fordtran’s gastrointestinal and liver disease.

10th ed. Philadelphia: Elsevier Saunders; 2016.
p. 501–41.
1. Townsend CM Jr, Beauchamp RD, Evers BM, Mattox
4. Lennard TWJ.  Chapter 5: Endocrine tumours of the
KL.  Chapter 38: Endocrine pancreas. In: Sabiston
pancreas. In: Endocrine surgery. 5th ed. Edinburgh:
textbook of surgery. 20th ed. Philadelphia: Elsevier;
Elsevier; 2014. p. 125–46.
2017. p. 941–62.
5. Jameson JL, De Groot LJ, de Kretser DM, Giudice
2. Melmed S, Polonsky KS, Larsen PR, Kronenberg
LC, Grossman AB, Melmed S, Potts JT, Weir
HM. Chapter 38: Gastrointestinal hormones and gut
GC.  Chapter 150: Neuroendocrine tumor syn-
endocrine tumors. In: Williams textbook of endo-
dromes. In: Endocrinology: adult and pediatric.
crinology. 13th ed. Philadelphia: Elsevier; 2016.
7th ed. Philadelphia: Elsevier Saunders; 2016.
p. 101–1722.
p. 2606–14.
3. Feldman M, Friedman LS, Brandt LJ.  Chapter
33: Neuroendocrine tumors. In: Sleisenger and
 Management of Somatostatinoma
Rachel E. Simpson and Benjamin C. James
Algorithmic Approach
A. Somatostatinoma is an extremely rare neuro-
endocrine tumor [1]. The constellation of
signs and symptoms on presentation varies
but may include hyperglycemia, cholelithia-
sis, steatorrhea, and hypochlorhydria [2].
Many are discovered while evaluating for
more nonspecific complaints, such as abdom-
inal pain, weight loss, or obstructive jaundice
related to mass effect [3].
B. On laboratory evaluation, patients may have
hyperglycemia secondary to the inhibited
release of insulin, hypochlorhydria, hyper-
bilirubinemia, or evidence of malnutrition [2,
3]. Fasting somatostatin levels >160  pg/mL
suggest the diagnosis of somatostatinoma [1].
C. Cross-sectional imaging and endoscopic
ultrasound with fine-needle aspiration biopsy
are commonly used modalities to localize
tumors [3, 4]. Somatostatinomas tend to be
solitary, large tumors, most often measuring
>2 cm in diameter. Sixty percent are found in
R. E. Simpson
Department of Surgery, Indiana University,
Indianapolis, IN, USA
B. C. James (*)
Department of Surgery, Harvard Medical School,
Boston, MA, USA
Department of Surgery, Beth Israel Deaconess
Medical Center, Boston, MA, USA
e-mail: bjames1@bidmc.harvard.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_117
117
the head of the pancreas, with the remainder
generally located in the periampullary duode-
num or proximal small intestine [1, 3].
Pancreatic somatostatinomas tend to be more
aggressive. Over 70% of patients will have
metastatic disease at the time of diagnosis,
and the 5-year survival is poor at less than
50% [5]. Somatostatinomas localized to the
small intestine carry a much better prognosis,
with 5-year survival over 80% [5]. These
individuals should undergo genetic testing for
neurofibromatosis 1, as 48% of duodenal
somatostatinomas have been found to be
associated with this genetic disorder [6].
D. Somatostatin analogs have been shown to
decrease fasting serum somatostatin levels
and improve the severity of symptoms [3].
E. For patients with localized disease, surgical
resection is recommended, as this is the only
chance for cure [7].
F. Patients with metastatic disease may be
treated with systemic chemotherapy [4].
Some have also supported surgical debulking
or hepatic artery embolization in the setting
of metastatic disease to help with symptom-
atic control [6, 8].
477
478 R. E. Simpson and B. C. James

History and physical exam:

A -Obstructive symptoms, jaundice, weight loss, abdominal pain
-Diabetes, cholelithiasis, steatorrhea

Laboratory evaluation:
B -Hyperglycemia, hyperbilirubinemia, hypoalbuminemia, hypochlorhydria
-Fasting somatostatin level >160 pg/mL

Tumor localization, staging, and tissue diagnosis

C -Cross sectional imaging, endoscopic ultrasound with FNA biopsy

Metastatic
disease?

-Somatostatin analogues
-Surgical resection -Systemic chemotherapy
D, E D, F
-Somatostatin analogues -Surgical debulking/hepatic artery
embolization

Algorithm 117.1
117  Management of Somatostatinoma 479

References 4. Melmed S, Polonsky KS, Larsen PR, Kronenberg

HM.  Chapter 38: Gastrointestinal hormones and gut
endocrine tumors. In: Williams textbook of endo-
1. Townsend CM Jr, Beauchamp RD, Evers BM, Mattox
crinology. 13th ed. Philadelphia: Elsevier; 2016.
KL.  Chapter 38: Endocrine pancreas. In: Sabiston
p. 1701–22.
textbook of surgery. 20th ed. Philadelphia: Elsevier;
5. Goldman L, Schafer AI. Chapter 195: Pancreatic neu-
2017. p. 941–62.
roendocrine tumors. In: Goldman-cecil medicine.
2. Jameson JL, De Groot LJ, de Kretser DM, Giudice
25th ed. Philadelphia: Elsevier; 2016. p. 1334–9.
LC, Grossman AB, Melmed S, Potts JT, Weir
6. Anderson CW, Bennett JJ.  Clinical presentation and
GC.  Chapter 42: Hyperglycemia secondary to non-
diagnosis of pancreatic neuroendocrine tumors. Surg
diabetic conditions and therapies. In: Endocrinology:
Oncol Clin N Am. 2016;25(2):363–74.
adult and pediatric. 7th ed. Philadelphia: Elsevier;
7. Yeo CJ.  Chapter 94: Neuroendocrine tumors of
2016. p. 737–51.
the pancreas. In: Shackelford’s surgery of the ali-
3. Feldman M, Friedman LS, Brandt LJ.  Chapter
mentary tract. 7th ed. Philadelphia: Elsevier; 2013.
33: Neuroendocrine tumors. In: Sleisenger and
p. 1206–16.
Fordtran’s gastrointestinal and liver disease. 10th ed.
8. Azimuddin K, Chamberlain RS.  The surgical man-
Philadelphia: Elsevier; 2016. p. 501–41.
agement of pancreatic neuroendocrine tumors. Surg
Clin N Am. 2001;81(3):511–25.
 Management of VIPoma
Rachel E. Simpson and Benjamin C. James
Algorithmic Approach
A. Tumors that secrete vasoactive intestinal pep-
tide (VIP), or “VIPomas,” are exceedingly
rare with an incidence of 0.01/1,000,000
person-­years and tend to be located in the
body and tail of the pancreas [1, 2]. Diagnosis
starts with a careful history and physical
examination. The most common symptom is
high volume (>1 L/day), watery diarrhea that
persists despite fasting [3]. Patients may also
experience a flushing rash, hypotension, and
dehydration [2]. Other common causes of
secretory diarrhea should be considered and
ruled out. Most VIPomas are sporadic, but
around 5% are associated with multiple endo-
crine neoplasia 1 (MEN1) [4].
B. The classic biochemical finding is hypochlore-
mic, hypokalemic metabolic acidosis [2].
Clinically patients present with watery diarrhea,
hypokalemia and achlorhydria. This is referred
to as Watery diarrhea with hypokalemia and
achlorhydria (WDHA) syndrome. Fasting VIP
R. E. Simpson
Department of Surgery, Indiana University,
Indianapolis, IN, USA
B. C. James (*)
Department of Surgery, Harvard Medical School,
Boston, MA, USA
Department of Surgery, Beth Israel Deaconess
Medical Center, Boston, MA, USA
e-mail: bjames1@bidmc.harvard.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_118
118
levels >200  pg/mL are considered diagnostic,
though individuals with VIPoma tend to have
levels >1000 pg/mL [5]. In the acute setting, flu-
ids and electrolytes are replaced [2].
C. Tumor localization begins with cross-­sectional
imaging with CT or MRI, proceeding to
octreotide scan if these modalities fail to iden-
tify the tumor. More invasive means including
endoscopic ultrasound are also commonly
employed [5]. The use of gallium-­ labeled
radioligands to the somatostatin receptors
commonly found on VIPomas has led to the
development of other functional studies
such as the Gadolinium-labeled 1,4,7,10-
tetraazacyclododecane-1,4,7, 10-tetraacetic
acid octreotide Ga-DOTANOC scan that has a
sensitivity of 78.3% and specificity of 92.5%
for localizing primary gastrointestinal and
pancreatic neuroendocrine tumors, and even
better sensitivity and specificity for detecting
metastatic disease approaching 100% [6].
VIPomas tend to be large (2  cm or greater),
solitary, and located in the body or tail of the
pancreas [5]. In rare instances they are found
in the adrenal gland or sympathetic chain [2].
D. Medical treatment to relieve the symptoms of
VIPoma includes somatostatin inhibitors,
which inhibit the release and circulating lev-
els of VIP and also directly decrease diarrhea
[5]. Somatostatin inhibits motilin and slows
intestinal motility [7]. Through these various
mechanisms, long-acting somatostatin ana-
481
482 R. E. Simpson and B. C. James

logs have been found to control symptoms in
78–100% of patients [3].
E. For patients with isolated disease, surgical
resection is recommended. Of all patients that
undergo surgical resection, surgical cure is
achieved in approximately 30% [3].
F. Around 75% of patients have regional lymph
node or liver metastases at the time of diagno-
sis [2]. In these cases, somatostatin analogs or
systemic chemotherapy is the mainstay of
treatment. Surgical resection is rarely cura-
tive but may help relieve symptoms [8]. Some
consider cytoreductive surgery if at least 90%
of disease burden can be resected [3].
However, others do not support tumor deb-
ulking surgery [4].

History and physical

A
-Watery diarrhea, flushing, dehydration

Laboratory evaluation:
B -Hypokalemia, hypochloremia, metabolic acidosis.
-VIP level >200 pg/mL

Tumor localization:
C
-Cross-sectional imaging (CT/MRI), octreotide scan, endoscopic ultrasound

Metastatic
disease?

No Yes

-Somatostatin analogues
-Somatostatin analogues -Systemic chemotherapy
D,E -Surgical resection -Consideration for cytoreductive D,F
therapy

Algorithm 118.1
118  Management of VIPoma 483

References 5. Jameson JL, De Groot LJ, de Kretser DM, Guidice

LC, Grossman AB, Melmed S, Potts JT, Weir
GC.  Chapter 150: Neuroendocrine tumor syn-
1. James BC, Aschebrook-Kilfoy B, Cipriani N,
dromes. In: Endocrinology: adult and pediatric.
Kaplan EL, Angelos P, Grogan RH.  The incidence
7th ed. Philadelphia: Elsevier Saunders; 2016.
and survival of rare cancers of the thyroid, para-
p. 2606–14.
thyroid, adrenal, and pancreas. Ann Surg Oncol.
6. Maxwell JE, O’Dorisio TM, Howe JR. Biochemical
2016;23(2):424–33.
diagnosis and preoperative imaging of gastroentero-
2. Melmed S, Polonsky KS, Larsen PR, Kronenberg
pancreatic neuroendocrine tumors. Surg Oncol Clin
HM.  Chapter 38: Gastrointestinal hormones and gut
N Am. 2016;25(1):171–94.
endocrine tumors. In: Williams textbook of endocrinol-
7. O’Dorisio TM, Gaginella TS, Mekhjian HS, Rao
ogy. 13th ed. Philadelphia: Elsevier; 2016. p. 1701–22.
B, O’Dorisio MS.  Somatostatin and analogues
3. Feldman M, Friedman LS, Brandt LJ.  Chapter 33:
in the treatment of VIPoma. Ann N Y Acad Sci.
Neuroendocrine tumors. In: Sleisenger and Fordtran’s
1988;527:528–35.
gastrointestinal and liver disease. Philadelphia:
8. Niederhuber JE, Armitage JO, Doroshow JH, Kastan
Elsevier; 2016. p. 501–41.
MB, Tepper JE.  Chapter 71: Cancer of the endo-
4. Townsend CM Jr, Beauchamp RD, Evers BM, Mattox
crine system. In: Abeloff’s clinical oncology. 5th ed.
KL.  Chapter 38: Endocrine pancreas. In: Sabiston
Philadelphia: Elsevier; 2014. p. 1112–42.
textbook of surgery. 20th ed. Philadelphia: Elsevier;
2017. p. 941–62.
Part XVI
Pediatric
 Congenital Diaphragmatic Hernia
Christopher J. McLaughlin, Rachel E. Hanke,
and Robert E. Cilley
Algorithmic Approach
A. Congenital diaphragmatic hernia (CDH) is a
common congenital abnormality (1  in 2500
live births) [1]. With advances in prenatal
ultrasound, the majority of CDH is diagnosed
prenatally, with mean detection time of
24 weeks. Delivery should be planned at an
experienced tertiary care center to optimize
outcome [2]. Prenatal care of the mother
should be optimized to prolong gestation to
decrease mortality and the need for extracor-
poreal membrane oxygenation (ECMO) [3].
CDH is typically a posterolateral diaphragm
defect (Bochdalek hernia), 80% occurring on
the left, 15% on the right, and 5% bilateral.
B. CDH is usually diagnosed before or at birth.
Two to three percent of CDH is diagnosed
after birth, occasionally long after (see Chap.
121, Other Diaphragmatic Hernias) [4].
Symptoms include respiratory distress (espe-
cially around feedings) and feeding difficul-
ties including intestinal obstruction. The
abdomen may appear scaphoid. Respiratory
distress, cyanosis, sternal retractions, dis-
placed heart sounds, and absent breath sounds
on the affected side provide additional clues.
C. J. McLaughlin (*) · R. E. Hanke · R. E. Cilley
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: cmclaughlin4@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_119
119
The diaphragm defect disrupts the mechanics
of respiration.
C. For infants born with confirmed or suspected
CDH, initial stabilization includes the
following:
(i) Intubation and gentle, non-injurious
ventilation (note: bag-valve mask venti-
lation is avoided due to risk of gastric
distension)
(ii) Nasogastric (NG) tube insertion for gas-
tric decompression
(iii) Arterial and venous cannulation, typi-
cally via the umbilicus
(iv) Monitoring of pre-ductal (right radial)
and post-ductal (lower extremity) oxy-
gen saturations, temperature, glucose
level, volume status/urine output
(v) Pharmacologic support of cardiac func-
tion and treatment of pulmonary
hypertension
D. After stabilization, diagnosis can be con-
firmed through identification of abdominal
contents (liver, bowel, stomach) above the
hemidiaphragm on a plain chest radiograph,
with a gastric bubble and/or distal nasogastric
tube tip found in the chest being pathogno-
monic. Subsequently, echocardiography, cra-
nial ultrasounds, and renal ultrasounds should
be performed to assess for concurrent devel-
opmental abnormalities and to characterize
the extent of disease. Echocardiography
487
488
should further characterize right ventricular
function and pulmonary artery pressures.
E. Following these diagnostic steps, ongoing
physiologic optimization should occur. Goals G. A recent meta-analysis shows all infants with
of ventilatory support should be to avoid lung
injury while maintaining a pre-ductal
PO2  >60  mm Hg (with corresponding pre-­
ductal SaO2 90–95%) and tolerating relative
hypercapnia. High-frequency oscillatory ven-
tilation and nitric oxide may be useful.
Pulmonary hypoplasia and pulmonary hyper-
tension ultimately determine the severity of
respiratory failure and outcome [5].
F. Respiratory failure may progress and become
life-threatening as a result of uncorrectable
pulmonary hypertension. ECMO is an appro-
priate treatment unless pulmonary hypoplasia
incompatible with life is present. Predictive
indices assist with these difficult decisions
C. J. McLaughlin et al.
[6]. During ECMO, treatment is focused on
improving pulmonary hypertension and
avoiding further lung injury.
CDH benefit from definitive surgical repair
[7]. For infants not requiring ECMO, the dia-
phragm defect should be repaired after stabi-
lization and reversal of pulmonary
hypertension. For infants requiring ECMO,
surgical repair after decannulation decreases
the risk of hemorrhagic complications.
Laparoscopic, thoracoscopic, or open
approach can be used with equal effective-
ness of repair, though open repair is recog-
nized as most effective for prevention of
recurrence [8]. Biologic and synthetic patches
may be used if native tissues are inadequate.
Recurrence is more likely with prosthetic
patches [9].
119  Congenital Diaphragmatic Hernia 489

A B

Prenatal detection of CDH: Symptoms of CDH at birth:

-Delivery near term, experienced CDH center Respiratory distress, scaphoid abdomen

Delivery and initial management:

C Intubation, NG tube, pre and post-ductal sat
monitoring, umbilical cannulation

Confirm CDH: CXR, ECHO, U/S Alternative

D Determine extent of disease or concurrent abnormalities diagnoses

Monitoring and goals

E Pre-ductal PaO2 >60, non-injurious ventilation

ECMO
required?
Yes No
F

Monitor pulmonary hypertension,

optimize cardiac function, Ongoing resuscitation and
decannulate prior to repair pre-operative optimization

Operative repair: native tissue

G superior to prosthetic patch

Algorithm 119.1
490 C. J. McLaughlin et al.

References 6. Le LD, Keswani SG, Biesiada J, Lim FY, Kingma PS,

Haberman BE, Frischer J, Habli M, Crombleholme
TM.  The congenital diaphragmatic hernia compos-
1. Zani A, Zani-Ruttenstock E, Pierro A.  Advances
ite prognostic index correlates with survival in left-­
in the surgical approach to congenital dia-
sided congenital diaphragmatic hernia. J Pediatr Surg.
phragmatic hernia. Semin Fetal Neonatal Med.
2012;47(1):57–62.
2014;19(6):364–9.
7. Harting MT, Hollinger L, Tsao K, Putnam LR, Wilson
2. Nasr A, Langer JC. Influence of location of delivery
JM, Hirschl RB, Skarsgard ED, Tibboel D, Brindle
on outcome in neonates with congenital diaphrag-
ME, Lally PA, Miller CC. Aggressive surgical man-
matic hernia. J Pediatr Surg. 2011;46(5):814–6.
agement of congenital diaphragmatic hernia: worth
3. Odibo AO, Najaf T, Vachharajani A, Warner B,
the effort? A multicenter, prospective, cohort study.
Mathur A, Warner BW.  Predictors of the need for
Ann Surg. 2018;267(5):977–82.
extracorporeal membrane oxygenation and survival
8. Putnam LR, Tsao K, Lally KP, Blakely ML,
in congenital diaphragmatic hernia: a center’s 10-year
Jancelewicz T, Lally PA, Harting MT, Group
experience. Prenat Diagn. 2010;30(6):518–21.
CD. Minimally invasive vs open congenital diaphrag-
4. Kitano Y, Lally KP, Lally PA.  Late-presenting
matic hernia repair: is there a superior approach? J
congenital diaphragmatic hernia. J Pediatr Surg.
Am Coll Surg. 2017;224(4):416–22.
2005;40(12):1839–43.
9. Moss RL, Chen CM, Harrison MR.  Prosthetic
5. Dillon PW, Cilley RE, Mauger D, Zachary C, Meier
patch durability in congenital diaphragmatic her-
A. The relationship of pulmonary artery pressure and
nia: a long-term follow-up study. J Pediatr Surg.
survival in congenital diaphragmatic hernia. J Pediatr
2001;36(1):152–4.
Surg. 2004;39(3):307–12.
 Tracheoesophageal Fistula
Rachel E. Hanke, Morgan K. Moroi,
and Robert E. Cilley
Algorithmic Approach
A. Tracheoesophageal fistula (TEF) and esopha-
geal atresia (EA) can occur separately or in
several combinations with an incidence of
1 in 3000 live births [1]. There are five EA/
TEF anomalies:
• Type A: EA without TEF (pure esophageal
atresia).
• Type B: EA with proximal TEF.
• Type C: EA with distal TEF (most
common).
• Type D: EA with proximal and distal TEF.
• Type E: TEF without esophageal atresia
(commonly called “H” or “N” fistula).
The most common is type C, found in
about 85% of patients. Patients with EA
may be detected prenatally, with ultra-
sound evidence of polyhydramnios and a
small or absent stomach bubble [2]. All
except type E present shortly after birth
with some combination of excessive drool-
ing, choking, regurgitation, and/or respira-
tory distress [3]. If distal TEF is present,
R. E. Hanke · M. K. Moroi · R. E. Cilley (*)
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: rcilley@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_120
120
the abdomen may become distended as air
fills the stomach. Only with high clinical
suspicion will the more rare, isolated TEF
(type E) be diagnosed after patients pres-
ent with choking when eating or unex-
plained cyanotic episodes [3].
B. If there is suspicion for EA/TEF in a new-
born, diagnosis often starts by placing an
esophageal tube. In EA, a chest radiograph
will show the tube coiled in the blind-ending
esophageal pouch within the chest. If there is
stomach/intestinal gas on radiograph, this
confirms distal TEF. Preoperative esophageal
pouch studies may also be used to determine
EA/TEF type and length of esophageal
pouch, an important consideration for even-
tual surgical repair [1].
C. Initially, management should be focused on
decreasing risk of aspiration and respiratory
issues by maintaining the esophageal drain-
age catheter on suction. Perioperative antibi-
otics are indicated. Long antibiotic courses
are reserved for the treatment of specific
infection or infection risk [4]. Positive-­
pressure ventilation is avoided, if possible,
and used with THE lowest possible pressures
if needed. Vascular access is obtained using
umbilical or peripheral sites [4].
D. A thorough physical exam may reveal associ-
ated anomalies. Echocardiography evaluates
structural heart disease, which occurs in
about 35% of patients. The position of the
491
492
aortic arch may influence the surgical
approach [2]. Studies have shown that for
patients with EA/TEF, two-thirds had at least
one other anomaly [1]. A renal ultrasound
and genetic testing identify other anomalies.
EA/TEFs are seen in or associated with many
syndromes, including VACTERL and
CHARGE [3].
Surgical division and repair of TEF with
repair of the esophagus is the mainstay of
treatment. In patients with severe respiratory
distress, urgent thoracotomy with clip liga-
tion of the TEF may be life-saving. Patients
with progressive gastric distention may
require emergent trans-abdominal needle
decompression followed by urgent gastros-
tomy. Primary one-stage repair is preferred.
Gastrostomy is rarely required. However, if
definitive correction is delayed due to serious
concurrent disease such as congenital heart
disease or extreme prematurity, a gastros-
tomy may be performed. Although not per-
formed by all surgeons, direct visualization
with diagnostic bronchoscopy can evaluate
for multiple fistulas [1, 3]. In pure atresia
(type A) and when the esophageal gap is too
long for primary repair, esophageal lengthen-
ing and staged repairs are performed [3, 5].
Many pediatric surgeons have abandoned
esophageal replacement. Colon interposition,
gastric “pull-up,” or reversed gastric tubes are
R. E. Hanke et al.
rarely, if ever, needed [3]. Repair within the
first few days of life allows for full evaluation
of the patient. Thoracoscopic repair and open
thoracotomy (using either trans-pleural or
extra-pleural approaches) are used for TEF
division/repair and EA repair, with the choice
based on surgeon preference [2, 3].
E. Post-operatively, antibiotics are discontin-
ued [4]. Parenteral nutrition, gastrostomy
feeds, or trans-anastomotic feeding tubes
are used to support nutrition [3]. An esopha-
gram is performed post-operatively to eval-
uate the integrity of the esophageal repair.
Recent data indicate that the study may be
performed safely as early as 5  days after
surgery [4]. Most leaks, found in up to 23%
of patients, are contained and will heal
without further surgery [1]. Narrowing and
strictures occur in up to 40% of patients and
usually respond to dilation [1].
Gastroesophageal reflux is common. Acid
suppression previously was standard practice
in all patients; however, recent data indicate
that acid suppression does not reduce stric-
ture rate [4]. Antireflux surgery is avoided if
possible. All patients have some degree of
esophageal dysmotility. Recurrent TEF is
rare and requires intervention (“re-do sur-
gery” or fibrin glue plugging). Airway insta-
bility/tracheomalacia usually responds to
supportive care [3].
120  Tracheoesophageal Fistula 493

A Newborn noted to have excessive salivation

and regurgitation/choking after feeding

Perform thorough physical exam, place esophageal tube, obtain

PA/lateral CXR

B CXR shows coiling of tube in chest

C Air in
Yes No
stomach?

Esophageal atresia with TEF Pure esophageal atresia

D Obtain echocardiogram Work up per EA/TEF. Plan staged/delayed

repair using lengthening techniques *

E Severe respiratory No Further evaluation:

distress with gastric renal ultrasound and genetic testing
distension (consider
gastric decompression/
gastrostomy
first)
Thoracoscopy vs thoracotomy to
divide/repair of TEF
Yes

Urgent thoracotomy and

ligation/clipping of TEF
Yes Long gap EA?
Repair after clinical improvement No

Primary repair
* Esophageal lengthening and/or
of EA
staged repair of EA

F Post-operative esophagram and surveillance

Algorithm 120.1
494 R. E. Hanke et al.

References 4. Lal DR, Gadepalli SK, Downard CD, Ostlie DJ,

Minneci PC, Swedler RM, Chelius TH, Cassidy L,
Rapp CT, Billmire D, Bruch S, Burns RC, Deans
1. Lal DR, Gadepalli SK, Downard CD, Ostlie DJ,
KJ, Fallat ME, Fraser JD, Grabowski J, Hebel F,
Minneci PC, Swedler RM, Chelius T, Cassidy L,
Helmrath MA, Hirschl RB, Kabre R, Kohler J,
Rapp CT, Deans KJ, Fallat ME, Finnell ME, Helmrath
Landman MP, Leys CM, Mak GZ, Raque J, Rymeski
MA, Hirschl RB, Kabre RS, Leys CM, Mak G, Raque
B, Saito JM, St. Peter SD, von Allmen D, Warner
J, Rescorla FJ, Saito JM, St. Peter SD, von Allmen D,
BW, Sato TT.  Challenging surgical dogma in the
Warner BW, Sato TT. Perioperative management and
management of proximal esophageal atresia with
outcomes of esophageal atresia and tracheoesopha-
distal Tracheoesophageal fistula: outcomes from the
geal fistula. J Pediatr Surg. 2017;52(8):1245–51.
Midwest Pediatric Surgery Consortium. J Pediatr
2. Slater BJ, Rothenberg SS. Tracheoesophageal fistula.
Surg. 2018;53(7):1267–72.
Semin Pediatr Surg. 2016;25(3):176–8.
5. Foker JE, Krosch TCK, Catton K, Munro F, Khan
3. Harmon C, Coran A. Pediatric surgery. In: Coran AG,
KM. Long-gap esophageal atresia treated by growth
Adzick NS, Krummel TM, Laberge JM, Shamberger
induction: the biological potential and early follow-up
RC, Caldamone AA, editors. Congenital anomalies of
results. Semin Pediatr Surg. 2009;18:23–9.
the esophagus. 7th ed. Philadelphia: Saunders; 2012.
 Other Diaphragmatic Hernias:
Late-Presenting Bochdalek Hernia,
Morgagni Hernia, and Giant Hiatal
Hernia of Infancy
Morgan K. Moroi, Christopher J. McLaughlin,
and Robert E. Cilley
Algorithmic Approach
A. Congenital diaphragmatic hernias (CDH) are
classically posterolateral diaphragm defects
(Bochdalek hernia) that present in early
infancy [1]. CDH clinical algorithms are
found in Chap. 119, Congenital Diaphragmatic
Hernia. A smaller number of CDH (10–20%)
patients may present later in life, even as
adults [1, 2]. These late-presenting patients
most often have a posterolateral defect with a
well-formed hernia sac containing viscera.
Morgagni hernias, on the other hand, are cen-
trally located anterior diaphragm defects with
similar contents [3]. Rarely, an infant with
feeding or respiratory symptoms will be
found to have an “intrathoracic stomach,”
consistent with giant hiatal hernia, where a
significant portion of the stomach has herni-
ated through a large opening in the esopha-
geal hiatus. Regardless of location,
late-presenting patients do not have pulmo-
nary hypoplasia or pulmonary hypertension
[1, 2].
M. K. Moroi · C. J. McLaughlin · R. E. Cilley (*)
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: rcilley@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_121
121
B. These unusual diaphragmatic hernias are
associated with a wide spectrum of symptoms
ranging from mild respiratory problems to
intestinal obstruction. The rarity of late-­
presenting diaphragmatic hernias and their
diverse clinical presentation can delay diag-
nosis. Diaphragm hernia should be consid-
ered in the differential diagnosis of a child
with dysphagia, decreased appetite, vomiting,
constipation, abdominal pain, recurrent respi-
ratory infections, dyspnea, cough, cyanosis,
or tachypnea [1–3]. Patients may also be
asymptomatic. There are rarely clues on the
physical exam, such as abnormal breath
sounds or a scaphoid abdomen. Diagnosis is
most often suggested by an abnormal chest
radiograph.
C. The initial step in the evaluation is to obtain
an anterior-posterior and lateral chest radio-
graph. Gastrointestinal contrast studies are
also diagnostic. Occasionally, body imaging
may be necessary to understand the anatomy.
Presence of abdominal contents above the
diaphragm confirms diagnosis. Other con-
genital abnormalities may be present and
should be evaluated [1–3]. Echocardiography
should be considered to evaluate for struc-
tural heart disease.
D. Intestinal obstruction, caused by incarcerated
intestine or gastric volvulus, may require
emergency operation. For all of these dia-
phragmatic defects, correction is performed
495
496
promptly. Late-presenting CDH may be
repaired traditionally via laparotomy or tho-
racotomy. Thoracoscopic repair is gaining
popularity [1, 2]. For Morgagni hernias, lapa-
roscopic repair is the method of choice [3].
For giant hiatal hernias of infancy with an
intrathoracic stomach, open or laparoscopic
methods may be used. An antireflux proce-
dure and a gastrostomy are also typically
included after the reduction of the stomach,
resection of the hernia sac, and closure of the
hiatal defect [4]. In all of these diaphragmatic
hernia defects, a hernia sac will be encoun-
tered. Resection of the hernia sac likely
reduces recurrence, although this customary
M. K. Moroi et al.
practice is not well supported by outcome
studies [3, 4].
E. Post-operative imaging requirements are lim-
ited to chest radiographs for most procedures.
Gastrointestinal contrast studies may help
assess for recurrence. Hernia recurrence rates
are low, and prognosis for patients with late-­
presenting diaphragmatic hernia is excellent
when compared to those who present as neo-
nates [1, 2]. Postoperative complications are
extremely rare after Morgagni hernia repair
[3]. Giant hiatal hernia patients do well,
although they may experience typical prob-
lems associated with antireflux surgery and
gastrostomies.
121  Other Diaphragmatic Hernias: Late-Presenting Bochdalek Hernia, Morgagni Hernia, and Giant Hiatal… 497

A 15 month-old, recurrent respiratory infections, respiratory distress, vomiting

Obtain vital signs and blood work.

Perform a thorough physical examination.

B 37.1°C, HR 120, RR 30, BP 90/60, WBC 11,000

Possible decreased breath sounds at left lung base

Presentation concerning for late-presenting diaphragmatic hernia.

C Obtain a chest radiograph.

Yes Diaphragmatic
No
hernia identified?

Intestinal Continue workup for

incarceration or alternative diagnoses
gastric volvulus?
Yes No

Imaging for preoperative planning (GI contrast, possibly CT) and

evaluation of other congenital abnormalities (consider
echocardiography)

Emergent operative D Prompt surgical repair

repair
E

Repair via thoracic or abdominal

approach, open or video-endoscopic Post-operative imaging
procedure and surveillance

Algorithm 121.1
498 M. K. Moroi et al.

References 3. Golden J, Barry WE, Jang G, Nguyen N, Bliss

D.  Pediatric Morgagni diaphragmatic hernia: a
descriptive study. Pediatr Surg Int. 2017;33(7):771–5.
1. Stolar C, Dillon P.  Pediatric surgery. In: Coran AG,
4. Kohn GP, Price RR, Demeester SR, Zehetner J,
Adzick NS, Krummel TM, Laberge JM, Shamberger
Muensterer OJ, Awad Z, Mittal SK, Richardson
RC, Caldamone AA, editors. Congenital diaphrag-
WS, Stefanidis D, Fanelli RD.  Guidelines for
matic hernia and eventration. 7th ed. Philadelphia:
the management of hiatal hernia. Surg Endosc.
Saunders; 2012.
2013;27(12):4409–28.
2. Kitano Y, Lally KP, Lally PA.  Late-presenting
congenital diaphragmatic hernia. J Pediatr Surg.
2005;40(12):1839–43.
 Duodenal Obstruction
in Newborns
Abdulraouf Y. Lamoshi, Sophia Abdulhai,
and Todd A. Ponsky
Algorithmic Approach
A. Prenatal diagnosis of duodenal atresia is usu-
ally achieved in more than 70% of the cases
[1] where antenatal ultrasound can show
polyhydramnios and a distended stomach [2].
B. Signs and symptoms: Bile-stained emesis
(occurs in 90% of the infants) without abdom-
inal distension and failure to pass meconium
are the main presenting symptoms [3]. Pre-
ampullary duodenal atresia, which occurs in
10% of patients, can be differentiated from
the other causes of non-bilious vomiting
using the patient history (i.e., prenatal, age,
and gender of the patient) and using abdomi-
nal X-ray, by placing a nasogastric (NG) tube
and injecting about 50 ml of air into the stom-
ach which can work as a contrast medium and
makes the double-bubble sign clearer [3].
C. Initial resuscitation includes starting intrave-
nous (IV) fluids, keeping the patient NPO,
and inserting an NG tube to correct the elec-
trolyte abnormalities and fluid balance and to
stop vomiting. Workup for associated anoma-
lies, such as cardiac defects, is of utmost
importance during the preoperative time [2].
D. Abdominal plain X-ray should first be per-
formed, and a double-bubble sign with no air
distal to the ligament of Treitz is sufficient to
A. Y. Lamoshi · S. Abdulhai · T. A. Ponsky (*)
Division of Pediatric Surgery, Akron Children’s
Hospital, Akron, OH, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_122
122
diagnose a duodenal atresia and mandates sur-
gical intervention [3]. Presence of air distal to
the ligament of Treitz could mean malrotation
with or without volvulus, so urgent surgery is
required. Duodenal web can also present with
duodenal obstruction but with presence of distal
air in the stable newborn [3]. Pneumoperitoneum
on the abdominal X-ray also demands urgent
surgery. Echocardiogram is the most important
test that should be conducted preoperatively.
Other work-up, such as renal and spinal ultra-
sounds, should also be performed during the
hospitalization to diagnose potential associated
renal or spinal abnormalities [3].
E. Treatment: Laparoscopic or open duodeno-
duodenostomy is the most common surgical
approach to repair this anomaly, and this
should be carefully performed to avoid injury
to the ampulla of Vater in the second portion
of the duodenum. The same procedure or web
excision can be used to treat a duodenal web.
This same surgery may also be used to bypass
an annular pancreas [3].
F. Postoperatively: Consider starting feeds when
the gastric drainage is decreasing in amount,
becoming lighter in color, when the patient has
return of bowel function or after a leak negative
upper GI contrast study postoperative day 5 [3].
Potential long-term complications to evaluate
for are intestinal obstruction, gastroesophageal
reflux, peptic ulcer, megaduodenum, duodeno-
gastric reflux, gastritis, delayed gastric empty-
ing, and blind-­loop syndrome [3].
499
500 A. Y. Lamoshi et al.

Antenatal
Diagnosis
made?
A
Yes
No

B Will present with early bilious vomiting

Open or Lap
Duodeno-duodenostomy
Obtain V/S and physical exam

C NPO, NG tube, & IVF

D KUB (AXR)

Free air
Double-bubble with No free air

Urgent surgery
With air distal to the
ligament of Treitz
No air distal to the
ligament of Treitz

Duodenal atresia
Urgent surgery for
possible malrotation
+/- volvulus
Echo

Surgery (Duodeno-duodenostomy)
E Duodeno-duodenostomy
or web-excision) if no then likely
duodenal web

F Follow-up care

Algorithm 122.1

ECR 2016 / C-0486 / Final Year Radiography Students’

References
1. Burjonrappa S, Crete E, Bouchard S.  Comparative
outcomes in intestinal atresia: a clinical outcome
and pathophysiology analysis. Pediatr Surg Int.
2011;27(4):437–42.
2. Elsayed M, et  al. “Abnormal Neonatal Bowel Gas
Patterns on Plain Radiography - Back to the Basics”.
Perception of Stressors in Clinical Placement.  -
EPOS™, European Congress of Radiology 2016. 2013.
posterng.netkey.at/esr/viewing/index.php?module=
viewing_poster&doi=10.1594/ecr2013/C-1059.
3. Ashcraft KW, et  al. Ashcraft’s pediatric surgery.
London/New York: Saunders; 2014.
 Small Intestinal Atresia
Abdulraouf Y. Lamoshi, Sophia Abdulhai, and
Todd A. Ponsky
Algorithmic Approach
A. Antenatal diagnosis can be established in
41% of the patients [1], where polyhydram-
nios and dilated bowels together are highly
suggestive of the diagnosis [2]. Postnatally,
bilious vomiting, upper abdominal disten-
sion, and failure to pass meconium are the
main presenting signs and symptoms. Rarely,
the patient will pass normal meconium, and
about 10% of patients present with meconium
peritonitis, which requires urgent surgical
intervention [3].
B. Initial resuscitative measures include starting
IV fluids, inserting a nasogastric (NG) tube,
and keeping the patient NPO to correct hypo-
volemia, electrolyte abnormalities, and mini-
mize vomiting. Antibiotics are needed when
there is suspicion for intestinal perforation.
C. Diagnosis: Abdominal plain X-ray is the ini-
tial imaging study. Multiple dilated loops of
bowel and the absence of distal air are highly
suggestive of small bowel atresia, and most
pediatric surgeons would take patients to the
operating room (OR) based on these findings
alone. Presence of distal air requires a con-
trast enema, which can diagnose other poten-
tial causes such as Hirschsprung disease,
A. Y. Lamoshi · S. Abdulhai · T. A. Ponsky (*)
Division of Pediatric Surgery, Akron Children’s
Hospital, Akron, OH, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_123
123
meconium ileus, meconium plug syndrome,
or colonic atresia [3]. A meconium pseudo-
cyst may occur in the case of intrauterine
intestinal perforation, and intraluminal calci-
fications of meconium have also been docu-
mented with intestinal atresia [3].
D. Treatment: The operative technique is based
on the site, type, the intraoperative findings,
and the length of the intestine. End-to-end
anastomosis with tapering of the proximal
bowel, when needed, and resection of the
dilated and hypertrophied proximal bowel is
the most common approach. Checking for
another atresia by passing a small catheter
and instilling saline is of utmost importance
before performing the anastomosis [2].
E. Follow-up care should include watching the
amount and color of NG tube output and
bowel function, which should be used to
decide when to initiate feeds [3]. Clear fluids
or breast milk is usually introduced before
any formula. After discharge, follow-up care
is a crucial measure, especially when there is
loss of a considerable amount of small bowel
length. The nutritional status and signs of
intestinal obstructions should always be eval-
uated [3]. Temporary gastrointestinal dys-
function is a common observation in these
newborns [3].
501
502 A. Y. Lamoshi et al.

A Antenatal
Diagnosis
made? Yes

No

Will present with early bilious vomiting Resection and

anastomosis

Obtain V/S and physical exam

Peritonitis: Yes Peritonitis: No

Urgent Surgery
B NPO, NGT, and IVF

C KUB (AXR)

Dilated bowels
Double-bubble (consider
other pathologies)

Distal loops of bowel distal

to the ligament of Treitz
Dilated loops of bowel proximal
to the ligament of Treitz
Contrast Enema

Proximal small bowel atresia

Yes Micro-colon
Distal small bowel with no
atresia/other surgical meconium
pathologies
Surgery
D
No

Follow-up care Consider other pathologies

E

Algorithm 123.1
123  Small Intestinal Atresia 503

References 2. Adams SD, Stanton MP.  Malrotation and intestinal

atresias. Early Human Dev. 2014;90(12):921–5.
3. Holcomb GW, Murphy JD, Ostlie DJ. Ashcraft’s pedi-
1. Burjonrappa S, Crete E, Bouchard S.  Comparative
atric surgery e-book. Philadelphia: Elsevier Health
outcomes in intestinal atresia: a clinical outcome
Sciences; 2014.
and pathophysiology analysis. Pediatr Surg Int.
2011;27(4):437–42.
 Management of Malrotation
Sophia Abdulhai, Abdulraouf Y. Lamoshi,
and Todd A. Ponsky
Algorithmic Approach
A. Malrotation, which has an incidence of about
1  in 500 patients, classically presents as a
full-term infant with bilious emesis [1]. Up to
89% of patients present with symptoms by
the age of 1  year, and full-term infants are
more likely to have malrotation compared to
preterm children. Bilious emesis presents in
48% of patients, followed by abdominal dis-
tention (21%) [2]. Any pediatric patient that
presents with bilious emesis should be
assumed to have midgut volvulus until proven
otherwise. Initial evaluation of these patients
should include vital signs and abdominal
examination.
B. If there is evidence of peritonitis or hemody-
namic instability, then intestinal ischemia
from malrotation with midgut volvulus
should be considered and NG tube place-
ment, fluid resuscitation, broad-spectrum
antibiotics, and immediate operative explora-
tion should be performed. If the patient has a
benign abdominal examination, then further
work-up with an abdominal X-ray (AXR)
should be performed.
C. An AXR has limited utility in diagnosing
malrotation, but it should be performed first
S. Abdulhai · A. Y. Lamoshi · T. A. Ponsky (*)
Division of Pediatric Surgery, Akron Children’s
Hospital, Akron, OH, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_124
124
to evaluate for proximal or distal bowel
obstructions, free air, or pneumatosis [3]. If
there are no significant abnormalities seen on
the AXR that require emergent exploration
and the patient is clinically stable, an upper
gastrointestinal (GI) contrast study should be
performed next.
(a) Free air/pneumatosis: Ischemic bowel
may occur from a malrotation with mid-
gut volvulus. Pneumatosis, portal venous
gas, and/or free air may be seen in these
patients, and they should be taken to the
operating room (OR) for immediate
exploration. If malrotation is identified,
surgery would include counterclockwise
detorsion of the volvulus and performing
a Ladd’s procedure. Necrotizing entero-
colitis should also be considered with
these X-ray findings.
(b) Proximal obstruction: Although duode-
nal atresia and duodenal web commonly
present as a double-bubble sign on AXR,
this sign cannot be used to definitively
rule out malrotation, since Ladd’s bands
or midgut volvulus can also present this
way. So any patient with proximal bowel
obstruction and evidence of air past the
duodenum should go to the OR emer-
gently. Additionally, duodenal atresia and
web are the most common congenital
anomaly associated with malrotation,
occurring in up to 11% of patients [2].
505
506
(c) Distal obstruction: Distal obstruction
may occur with Hirschsprung disease,
colonic obstruction, etc. or may occur
from malrotation with a distal volvulus.
A contrast enema should be performed
next, and if it is positive for distal pathol-
ogy, then consider other diagnoses. If the
contrast enema is negative and the patient
is clinically stable, then obtain an upper
GI contrast study.
D. An upper GI contrast study is the current gold
standard for diagnosing malrotation. The key
feature to look for is the location of the
duodenal-­jejunal junction (DJJ).
E. Location of the DJJ:
(a) Normal position: If the DJJ is in the nor-
mal anatomical position, which is left of
midline and at the level of the gastric
antrum, then the diagnosis is unlikely
malrotation and other etiologies should
be considered.
S. Abdulhai et al.
(b) Equivocal: If the results are equivocal,
then consider a repeat UGI after 1 month
if the patient is asymptomatic now. If the
patient continues to have bilious emesis,
then consider laparoscopy.
(c) If the DJJ is in the abnormal position,
then malrotation should be considered
and treated with an NGT and an open or
laparoscopic Ladd’s procedure.
F. Follow-up care: Outcomes depend on pres-
ence of volvulus with intestinal ischemia and
extent of bowel resection. Most common
complication after a Ladd’s procedure is
adhesive bowel obstruction, occurring in
5.6% of patients. Although rare and occurring
in less than 1% of patients, recurrent volvulus
should also be considered in patients who
present with obstructive symptoms [1].
124  Management of Malrotation 507

A History and Physical

Infant with bilious emesis.

Obtain vital signs and perform physical examinations

B Peritonitis,
hemodynamic
YES
instability?

OR
NO

Abdominal
C X-ray

Free Air/Pneumatosis Distal Obstruction

or Proximal Obstruction
Unremarkable

OR
Contrast
Enema with
NO Distal
Pathology?
Upper GI
D Contrast
Study

Equivocal Normal DJJ YES

Abnormal DJJ position
position
E

Repeat UGI in 1 Malrotation

month or
Laparoscopy if still Consider other
symptomatic pathology

Ladd’s Procedure

F Follow-up Care

Algorithm 124.1
508 S. Abdulhai et al.

References 2. Ford EG, Senac MO, Srikanth MS, Weitzman

JJ. Malrotation of the intestine in children. Ann Surg.
1992;215(2):172–8.
1. El-Gohary Y, Alagtal M, Gillick J.  Long-term com-
3. Langer JC. Intestinal rotation abnormalities and mid-
plications following operative intervention for intes-
gut volvulus. Surg Clin North Am. 2017;97(1):147–
tinal malrotation: a 10-year review. Pediatr Surg
59. https://doi.org/10.1016/j.suc.2016.08.011.
Int. 2010;26(2):203–6. https://doi.org/10.1007/
s00383-009-2483-y.
 Management of Imperforate Anus
Sophia Abdulhai and Aaron Garrison
Algorithmic Approach
A. Anorectal malformations (ARMs), or imper-
forate anus, should be diagnosed during the
newborn examination. A fistula may be more
difficult to diagnose immediately, as it can
take 16–24 h after birth for meconium to pass
through the fistula.
B. ARMs are commonly associated with other
congenital anomalies, and appropriate work-
­up should be performed within the first 24 h.
(a) Cardiovascular defects: Up to 27% of
patients with imperforate anus also have
cardiovascular defects [1], so an echocar-
diogram should be performed prior to
any surgical intervention.
(b) Urologic defects: About 50% of all ARM
patients also have some type of urologi-
cal defect, and incidence of urologic
abnormalities is highest with cloaca.
Renal ultrasound (US) should be per-
formed on every patient.
(c) Gastrointestinal defects: Esophageal
atresia occurs in 5–10% of all ARMs [1,
2] and duodenal atresia in about 4% [1].
This should be ruled out using a nasogas-
tric tube and abdominal X-ray.
S. Abdulhai · A. Garrison (*)
Division of Pediatric Surgery, Akron Children’s
Hospital, Akron, OH, USA
e-mail: agarrison@chmca.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_125
125
(d) Musculoskeletal: Tethered cord, which
occurs in about 25% of anorectal malfor-
mations and is associated with worse
future bowel function, should be evaluated
using US or magnetic resonance imaging
(MRI) of the spine prior to 3  months of
age [3]. Anterior-Posterior (AP) and lat-
eral films of the sacrum should also be
performed to evaluate for other sacral
anomalies, such as hemisacrum and hemi-
vertebrae. This information can also be
used to calculate the sacral ratio.
(e) In females with cloaca, pelvic US should
be performed to rule out hydrocolpos.
C. Males:
(a) Perineal fistula: This presents as an ori-
fice anterior to the sphincter complex.
(b) Flat perineum: If there is meconium in
the urine, then this indicates a recto-­
urethral fistula. This is the most common
type of fistula in males. Eventually, a
contrast study through the mucous fistula
should be performed to evaluate the anat-
omy and/or level of the fistula.
(c) Undefined: A cross-table lateral film
should be performed 24  h after birth to
evaluate the rectal gas pattern.
(d) There will be times where the definitive
anatomy is not known until a contrast
study through the mucous fistula is per-
formed after the colostomy.
509
510
D. Females:
(a) Perineal fistula: This is an orifice anterior
to the sphincter but posterior to the
introitus.
(b) Vestibular fistula: This is diagnosed by
finding an orifice within the introitus,
typically distal to the hymen in the poste-
rior wall of the vagina.
(c) Single perineal orifice/cloaca: Imperforate
anus in a female with a single perineal
opening is a cloaca, which varies in com-
plexity based on common channel length.
This evaluation requires cystoscopy, vagi-
noscopy, and in some centers an MRI.
(d) No fistula: This occurs in less than 10%
of patients.
E. Treatment:
(a) Perineal and sub-epithelial fistulas in males
and perineal or vestibular fistulas in females
may be managed with anoplasty without
diversion. Some may choose to perform
colostomy prior to posterior sagittal ano-
rectoplasty (PSARP), and some surgeons
may choose to dilate the fistula and perform
anoplasty later if needed. Fistula dilation
and referral to a colorectal center should be
considered by inexperienced surgeons.
S. Abdulhai and A. Garrison
(b) Recto-urethral fistulas in males and
­cloacas in females should be managed
with a colostomy initially. Definitive
repair with a posterior sagittal anorecto-
plasty or posterior sagittal anorectovag-
inourethroplasty should be performed
about 1–2  months later after work-up
for additional anomalies has been com-
pleted and the patient is exhibiting nor-
mal growth patterns. Management of
obstructive urologic issues can be an
emergency in females with cloaca, and
hydrocolpos should be drained if
present.
(c) If the fistula is undefined in males, or if
there is no fistula in a female, then a
cross-table lateral film should be per-
formed to evaluate the distance between
the dilated gas and the skin.
(i) If the rectal gas is below the coccyx,
anoplasty should be performed with
or without a colostomy (depending
on surgeon preference).
(ii) If the rectal gas is above the coccyx,
then a colostomy should be per-
formed, and definitive repair deferred
to a later date.
125  Management of Imperforate Anus 511

History and Physical

A Newborn child with lack of anal opening, evaluate for potential fistulas. May need to wait 16-24 hours for meconium to pass
through a separate orifice.

In first 24 hours, work up for other congenital anomalies.

B Echocardiogram, Renal US, r/oesophageal and duodenal atresia using NGT and abdominal X-ray film,
AP and lateral films of the sacrum In females, if cloaca, also obtain pelvic US.

C Male D Female

Perineal fistula Flat Perineum

No Fistula Perineal or Single Perineal
vestibular Opening (Cloaca)
fistula
Meconium
in Urine
Anoplasty (or No Anoplasty (or Colostomy and
fistula dilation) fistula dilation) drainage of
Yes Hydrocolpos (if
Undefined/
No fistula present)
E

Colostomy
Cross Table
Lateral Film Fistulogram

Rectal Gas Rectal Gas

Fistulogram ABOVE coccyx BELOW coccyx < 3 cm common > 3 cm common
channel channel

Colostomy Anoplasty (with

PSARP or without
PSARVUP Transfer to
Colostomy)
colorectal center
PSARP for PSARVUP

Algorithm 125.1

2. Peña A, Hong AR.  In: Mattei P, editor. Anorectal

References
1. Cho S, Moore SP, Fangman T.  One hundred three
consecutive patients with anorectal malformations
and their associated anomalies. Arch Pediatr Adolesc
Med. 2001;155(5):587. https://doi.org/10.1001/
archpedi.155.5.587.
malformation. Philadelphia: Lippincott Williams &
Wilkins; 2003.
3. Tsuda T, Iwai N, Kimura O, Kubota Y, Ono S, Sasaki
Y.  Bowel function after surgery for anorectal mal-
formations in patients with tethered spinal cord.
Pediatr Surg Int. 2007;23(12):1171–4. https://doi.
org/10.1007/s00383-007-2025-4.
 Hirschsprung Disease
126
Rachel E. Hanke, Morgan K. Moroi,
and Kathryn Lynn Martin

Algorithmic Approach associated enterocolitis (HAEC). HAEC is

characterized by fever, abdominal distension,
A. Hirschsprung disease (HD) is characterized and diarrhea. It can be life-threatening and is
by incomplete migration of ganglion cells the most common cause of death in children
within the myenteric and submucosal with HD [1].
plexuses to the distal bowel leading to C. Initial evaluation includes abdominal radio-
­
aganglionosis and functional obstruction.
­ graphs which demonstrate obstruction.
Approximately 75% of cases involve a transi- Contrast enema reveals proximal distended
tion point within the rectosigmoid region, bowel that tapers through the transition zone
while 15% have long-segment colonic dis- to a decompressed distal rectum. Anorectal
ease, 5–10% have total colonic disease, manometry may be helpful in documenting
and <5% have total intestinal disease [1]. the recto-anal inhibitory reflex, which is
B. HD is typically diagnosed in early infancy, absent in HD [1].
with a small proportion of cases presenting D. Definitive diagnosis is made by tissue biopsy.
later in childhood. Neonates present with In infants, suction rectal biopsy is performed
abdominal distension, bilious vomiting, feed- at the bedside without the need for anesthe-
ing intolerance, and failure to pass meconium sia. The yield of suction rectal biopsy
within the first 48 h of life [1]. Rectal exami- decreases with age; thus full-thickness rectal
nation causes explosive decompression of gas biopsy is required in older children. The
and stool. HD diagnosed beyond the neonatal pathognomonic findings are the absence of
period presents with chronic abdominal dis- ganglion cells with hypertrophied nerve fibers
tension, constipation, overflow incontinence, [1]. Additional staining may assist with diag-
encopresis, and failure to thrive. Ten percent nosis including stains demonstrating
of patients will present with Hirschsprung-­ increased acetylcholinesterase uptake and
absent calretinin [2].
E. HD is associated with several other congeni-
R. E. Hanke · M. K. Moroi
Department of Surgery, Penn State Milton S. Hershey tal anomalies including malrotation, congeni-
Medical Center, Hershey, PA, USA tal heart disease, genitourinary abnormalities,
K. L. Martin (*) and several syndromes, the most common of
Department of Surgery, Division of Pediatric Surgery, which is Trisomy 21 [1]. Preoperatively,
Penn State Milton S. Hershey Medical Center, patients should be stabilized and screened for
Hershey, PA, USA associated anomalies.
e-mail: kmartin15@pennstatehealth.psu.edu

© Springer Nature Switzerland AG 2019 513

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_126
514
F. Initial management is dictated by the stability
of the patient. With signs of peritonitis, intes-
tinal perforation, or HAEC, the first priority
is resuscitation with intravenous fluids,
broad-spectrum antibiotics, gastric decom-
pression, and colonic irrigations, followed by
emergent surgical intervention. The goal of
surgery in this setting involves control of per-
foration, if present, and leveling stoma. A lev-
eling stoma involves determination of the
level of aganglionosis with stoma creation
proximal to this point [1].
G. Definitive treatment of HD is surgical.
Surgery involves removal of the aganglionic
bowel segment followed by anastomosis of
the normally innervated proximal bowel to
the distal rectum just above the dentate line.
This may be done as a single stage or in mul-
tiple stages. Historically, all patients received
leveling stomas prior to definitive repair.
Presently, surgical correction depends on the
patient’s level of disease, comorbidities, and
R. E. Hanke et al.
age [3]. Surgical techniques differ in the
method used to bring the proximal ganglion-
ated bowel through the pelvis to the dentate
line and include the Swenson extra-rectal
pull-through, Soave endo-rectal pull-through,
and Duhamel rectal sparing pull-through.
Laparoscopic and transanal approaches are
gaining popularity with a trend toward one-­
stage repair in newborns [4]. In total colon
HD, a staged approach is preferred, with ini-
tial leveling stoma and subsequent pull-­
through [4]. In total intestinal aganglionosis,
patients require a stoma to decompress the
gastrointestinal (GI) tract with total paren-
teral nutrition (TPN) for nutritional support
and possible intestinal transplantation.
H. Post-operatively, patients are assessed for
stricture and followed closely as the risk of
HAEC persists. Long-term complications
include stricture and stooling dysfunction,
which may present as constipation, soiling, or
fecal incontinence.
126  Hirschsprung Disease 515

A
3 day-old with abdominal distension and 2-year-old with chronic severe constipation
failure to pass meconium and abdominal distension
B

Plain Radiograph
C Contrast Enema

Concerning
for HD
No

Yes
Alternative
diagnoses

Positive rectal No
D biopsy

Yes

E Evaluate for other

congenital abnormalities

F
Plan for surgical
intervention

Unstable patient +/-peritonitis Long segment, total colon or Long segment or recto-sigmoid
Stabilization and urgent OR delayed diagnosis. OR for leveling disease in stable patient. OR for
for leveling stoma stoma with delayed pull-through pull-through without colostomy

Post-operative surveillance for HAEC, stooling

H dysfunction (fecal incontinence,constipation)

Algorithm 126.1
516 R. E. Hanke et al.

References staining in Hirschsprung disease. J Pediatr Surg.

2016;51(12):2005–9.
3. Bradnock TJ, Knight M, Kenny S, Nair M, Walker
1. Langer JC.  Pediatric surgery. In: Coran AG, Adzick
GM. The use of stomas in the early management of
NS, Krummel TM, Laberge JM, Shamberger RC,
Hirschsprung disease: findings of a national, prospec-
Caldamone AA, editors. Hirschsprung disease. 7th
tive cohort study. J Pediatr Surg. 2017;52(9):1451–7.
ed. Philadelphia: Saunders; 2012.
4. Langer JC.  Laparoscopic and transanal pull-through
2. Tran VQ, Lam KT, Truong DQ, Dang MH, Doan
for Hirschsprung disease. Semin Pediatr Surg.
TT, Segers V, Butler MW, Robert A, Goyens P,
2012;21(4):283–90.
Steyaert H.  Diagnostic value of rectal suction
biopsies using calretinin immunohistochemical
 Pediatric Inguinal Hernia
Afif N. Kulaylat and Kathryn Lynn Martin
Algorithmic Approach
A. Primary goals in the evaluation of patients
with inguinal hernias are to confirm the pres-
ence of the inguinal hernia, excluding other
etiologies of groin swelling, and to determine
whether the hernia is incarcerated with the
potential for visceral injury. An inguinal her-
nia should be suspected in any infant or child
with a “bulge” in the groin, labia, or scrotum.
This bulge may be accentuated during times
of increased intra-abdominal pressure such as
crying or straining. Primary differential diag-
noses include hydrocele, undescended testi-
cles, inguinal adenopathy, and testicular
torsion.
B. In the pediatric population, inguinal hernias
are typically indirect secondary to a patent
processus vaginalis. Inguinal hernias com-
monly present during the first year of life,
with nearly one-third of cases presenting
before 6 months of age [1]. The incidence is
higher in premature infants. There is a 3:1
male-to-female preponderance. Incarceration
is most common in the first 6 months of life.
In older children and adolescents, in whom
the risk of incarceration is low, hernia repair
A. N. Kulaylat · K. L. Martin (*)
Department of Surgery, Division of Pediatric Surgery,
Penn State Milton S. Hershey Medical Center,
Hershey, PA, USA
e-mail: kmartin15@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_127
127
can be performed electively. In young infants
a wait time for surgery of more than 14 days
is associated with a doubling of the risk of
incarceration, and thus repair should be pur-
sued in a time-sensitive fashion [2]. Premature
infants with asymptomatic inguinal hernias
may benefit from delayed repair to allow co-
morbid lung disease to improve prior to
surgery.
C. If the inguinal hernia is incarcerated, all
attempts should be made to reduce the hernia
before it progresses to strangulation. This
may require sedation to permit adequate
manipulation and reduction of contents. If
bowel is incarcerated in the hernia, the patient
may present with signs of bowel obstruction
such as pain, distension, vomiting, obstipa-
tion, and even peritonitis. If there is concern
for strangulation or if peritoneal findings are
present, urgent exploration is mandated.
While the intestine is the most commonly
incarcerated visceral component, the omen-
tum, ovary, mesosalpinx, or bladder may also
become entrapped within a hernia sac.
D. If the diagnosis is unclear on physical exam,
ultrasound can be a useful adjunct [3]. If the
hernia cannot be reproduced at the time of
examination, follow-up examination may be
helpful. Many surgeons will still proceed to
elective hernia repair if the appropriate his-
tory is given or appropriate images are pro-
vided by the family.
517
518
E. If the inguinal hernia is not incarcerated,
elective repair can be scheduled with the fam-
ily appropriately educated regarding the risk
of incarceration and strangulation.
F. If the hernia is initially incarcerated but
maneuvers to reduce it are successful, a brief
period of observation allows for resuscitation,
resolution of tissue edema, and confirmation
of a normal abdominal exam prior to pro-
ceeding with operative repair.
G. For those with truly incarcerated hernias with
concerns for strangulation or peritonitis,
expeditious arrangements are made for the
operating room (OR) following appropriate
and often parallel resuscitative efforts includ-
ing intravenous fluids and antibiotics.
Nasogastric tube should be considered on the
basis of obstructive symptoms.
H. In males, open operative repair involves an
inguinal incision with identification of the
cord structures followed by isolation of the
hernia sac away from the vas deferens and
testicular vasculature. After reduction of its
contents and confirmation that the sac is
A. N. Kulaylat and K. L. Martin
empty, the hernia sac is ligated at the level of
the internal ring. In females, the sac is simi-
larly mobilized and ligated at the level of the
internal ring which may then be sutured
closed. While many surgeons still prefer open
inguinal hernia repair [4], laparoscopic
approaches are becoming increasingly com-
mon with some evidence suggesting lower
recurrence rates [5–8].
I. Investigation of the contralateral side remains
a controversial topic. Traditionally, the high
likelihood of contralateral patent processus
vaginalis (PPV) was cited as an indication for
routine exploration. However, the progres-
sion of PPV to symptomatic inguinal hernia
is lower than previously believed. Recent
studies have suggested PPV occurs in ~10–
45% of patients, [5, 6, 9] but of those with
PPV, only 10% develop an inguinal hernia [9,
10]. One study estimated that 21 contralateral
PPV would need to be closed to prevent one
metachronous inguinal hernia [8]. As such,
there has been a trend away from routine con-
tralateral exploration [8–10].
127  Pediatric Inguinal Hernia 519

History:
A 2 year old male, intermittent right groin bulge with crying and straining

Obtain vital signs and perform physical examination.

Make note of the location of the swelling/bulge, ability to
transilluminate, presence and location of testes, presence
of inguinal adenopathy

Reducible Unclear exam

B hernia
No Yes
Consider
ultrasound D
Incarcerated Schedule for elective
hernia E hernia repair

Attempt Obstructive symptoms? Open or Laparoscopic

C reduction +/- IV resuscitation, + Antibiotics, + Hernia Repair +/-
sedation Nasogastric tube as clinically contralateral
appropriate exploration

Reducible
hernia
No Yes

F
G Expedite OR Observe 24-48 hours to allow
edema to decrease

Open or Laparoscopic
Hernia Repair
+/-resection via
inguinal/midline/laparoscopic
approach per surgeon
H I
preference

Algorithm 127.1
520 A. N. Kulaylat and K. L. Martin

References 6. Miyake H, Fukumoto K, Yamoto M, et al. Risk fac-

tors for recurrence and contralateral inguinal her-
nia after laparoscopic percutaneous extraperitoneal
1. Lao OB, Fitzgibbons RJ Jr, Cusick RA.  Pediatric
closure for pediatric inguinal hernia. J Pediatr Surg.
inguinal hernias, hydroceles, and undescended tes-
2017;52(2):317–21.
ticles. Surg Clin North Am. 2012;92(3):487–504, vii.
7. Gause CD, Casamassima MG, Yang J, et  al.
2. Zamakhshary M, To T, Guan J, Langer JC.  Risk of
Laparoscopic versus open inguinal hernia repair in
incarceration of inguinal hernia among infants and
children </=3: a randomized controlled trial. Pediatr
young children awaiting elective surgery. CMAJ.
Surg Int. 2017;33(3):367–76.
2008;179(10):1001–5.
8. Zhao J, Chen Y, Lin J, et  al. Potential value of rou-
3. Sameshima YT, Yamanari MG, Silva MA, Neto MJ,
tine contralateral patent processus vaginalis repair in
Funari MB.  The challenging sonographic ingui-
children with unilateral inguinal hernia. Br J Surg.
nal canal evaluation in neonates and children: an
2017;104(1):148–51.
update of differential diagnoses. Pediatr Radiol.
9. Centeno-Wolf N, Mircea L, Sanchez O, et al. Long-­
2017;47(4):461–72.
term outcome of children with patent processus vagi-
4. Zani A, Eaton S, Hoellwarth M, et al. Management of
nalis incidentally diagnosed by laparoscopy. J Pediatr
pediatric inguinal hernias in the era of laparoscopy:
Surg. 2015;50(11):1898–902.
results of an international survey. Eur J Pediatr Surg.
10. Weaver KL, Poola AS, Gould JL, Sharp SW, St

2014;24(1):9–13.
Peter SD, Holcomb GW 3rd. The risk of developing
5. Esposito C, Escolino M, Cortese G, et al. Twenty-year
a symptomatic inguinal hernia in children with an
experience with laparoscopic inguinal hernia repair in
asymptomatic patent processus vaginalis. J Pediatr
infants and children: considerations and results on
Surg. 2017;52(1):60–4.
1833 hernia repairs. Surg Endosc. 2017;31(3):1461–8.
 Meconium Ileus
Kathryn Lynn Martin and Afif N. Kulaylat
Algorithmic Approach
A. Meconium ileus is characterized by newborn
bowel obstruction secondary to inspissated
meconium impacted within the distal small
bowel. Over 75% of children with meconium
ileus will have cystic fibrosis [1]. Meconium
ileus is the initial presentation of cystic fibro-
sis in 15–27% of affected individuals [1].
There may be a positive family history lead-
ing to increased suspicion of the diagnosis.
Prenatal diagnosis may be suggested in the
setting of sonographic evidence of polyhy-
dramnios, dilated bowel, a calcified mass, or
echogenic intra-abdominal cyst. These find-
ings are variable and nonspecific [1, 2].
Postnatally, the history of early-onset abdom-
inal distension, bilious emesis, and delayed
passage of meconium, with palpable loops of
bowel and/or an abdominal mass, is highly
suggestive of meconium ileus [2, 3].
Malrotation with volvulus should be ruled out
in any neonate presenting with bilious
emesis.
B. Infants with uncomplicated meconium ileus
present with progressive abdominal disten-
sion in the first 24–48  h of life. Abdominal
K. L. Martin (*) · A. N. Kulaylat
Department of Surgery, Division of Pediatric Surgery,
Penn State Milton S. Hershey Medical Center,
Hershey, PA, USA
e-mail: kmartin15@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_128
128
exam reveals a distended but soft abdomen
with palpable, doughy bowel loops.
Abdominal x-rays in uncomplicated meco-
nium ileus demonstrate loops of dilated bowel
typically without air-fluid levels with a clas-
sic “ground glass” or “soap bubble” appear-
ance [3]. Infants with complicated meconium
ileus due to atresia, volvulus, meconium peri-
tonitis, or meconium pseudocyst often pres-
ent with abdominal distension at birth [1].
This may be associated with signs of fetal
distress and peritonitis. Abdominal x-rays in
complicated meconium ileus classically dem-
onstrate calcifications suggestive of in utero
perforation with a possibility of meconium
peritonitis with or without a well-formed
pseudocyst [3].
C. Contrast enema in meconium ileus will dem-
onstrate a microcolon secondary to disuse
with outlining of meconium pellets in the dis-
tal small bowel. Use of a water-soluble hyper-
osmolar contrast agent such as Gastrografin®
can be diagnostic and therapeutic [1–3].
D. Initial treatment of uncomplicated meconium
ileus is non-surgical with solubilizing ene-
mas. Hyperosmolar enemas are effective but
can cause significant fluid shifting and dehy-
dration; thus concurrent IV fluid administra-
tion is required [1–3]. Gastrografin® is the
most commonly used agent [3]. The addition
of N-acetylcysteine can be helpful as it has
been shown to aid in the dissolution of inspis-
521
522 K. L. Martin and A. N. Kulaylat

sated meconium in animal studies [2]. stoma formation versus anastomosis. If an

­Enemas can be repeated until the meconium atresia is present, the proximal dilated seg-
obstruction clears as long as the infant ment is resected, the distal bowel cleaned of
remains clinically well without worsening meconium, and a decision made regarding
obstruction or signs of intestinal compromise stoma formation versus anastomosis [1–3]. In
[1, 2]. cases of perforation with meconium peritoni-
E. Operation is required for infants with uncom- tis or a meconium pseudocyst, abdominal
plicated meconium ileus that fails to improve washout with debridement of the cyst fol-
with solubilizing enemas to evacuate the lowed by resection and stoma formation is
inspissated meconium and relieve their preferred [3].
obstruction before complications develop. A G. A diet may started once the infant is stabi-
wide variety of surgical options exist includ- lized and stooling. Work-up for cystic fibrosis
ing enterotomy with irrigation or stoma cre- should be initiated. Diagnostic modalities
ation. Classically described stomas for include genetic analysis and sweat chloride
meconium ileus include the Mikulicz double-­ testing [1, 2]. Genetic testing assesses for an
barreled stoma, Bishop-Koop (distal “chim- array of causative mutations, with the most
ney”) stoma, or Santulli (proximal “chimney”) common being ΔF508 [1]. Sweat chloride
stoma [1–3]. Resection is rarely required in testing can be done after 48  h of life; how-
uncomplicated disease. ever, it may be difficult to obtain the volume
F. Complicated meconium ileus is managed for sweat needed in children less than 2 weeks
operatively. If volvulus is present, the bowel of age [1, 2]. Long-term complications of
should be detorted and assessed for viability. meconium ileus associated with cystic fibro-
If viable, the distal bowel is cleaned of meco- sis include failure to thrive, pancreatic insuf-
nium as described earlier. If the bowel is non-­ ficiency, constipation, rectal prolapse, and
viable, then resection should be completed distal intestinal obstruction syndrome (DIOS)
after which the distal bowel is cleaned of also known as meconium ileus equivalent
meconium and a decision is made regarding syndrome [1, 3].
128  Meconium Ileus 523

Newborn with progressive abdominal distension, emesis and failure to

A pass meconium +/- Family history of cystic fibrosis

Place NG tube
Initiate fluid resuscitation

38 C, HR 200, BP 70/40, RR 50,

Sats 99% Perform physical examination
Obtain abdominal radiographs

Peritonitis or meconium
pseudocyst on AXR?

No Yes

Exam - distension, palpable, doughy, bowel loops. Exam - distension, rigidity, tenderness +/- palpable
AXR - Distension with air fluid levels, ground mass AXR – Signs of bowel obstruction with
glass/soap-bubbles in terminal ileum suggestion of cystic mass and scattered calcifications

Obtain contrast enema

OR F
C
Enema - micro-colon with meconium pellets
in the distal small bowel and proximal colon
Initiate diet when appropriate
Complete work-up for cystic fibrosis
G
D Non-surgical management
with solubilizing enemas

Enemas
successful?

Yes No

Initiate diet OR E
G Complete work-up for
cystic fibrosis

Initiate diet when appropriate

Complete work-up for cystic fibrosis G

Algorithm 128.1
524 K. L. Martin and A. N. Kulaylat

References 2. Carlyle BE, Borowitz DS, Glick PL.  A review of

pathophysiology and management of fetuses and neo-
nates with meconium ileus for the pediatric surgeon. J
1. Boczar M, Sawicka E, Zybert K. Meconium ileus in
Pediatr Surg. 2012;47:772–81.
newborns with cystic fibrosis – results of treatment in
3. Rescirka FJ, Grosfeld JL. Contemporary management
the group of patients operated on in the years 2000–
of meconium ileus. World J Surg. 1993;17:318–25.
2014. Dev Period Med. 2015;XIX(1):32–40.
 Pediatric Intussusception
Afif N. Kulaylat and Kathryn Lynn Martin
Algorithmic Approach
A. Intussusception in children is typically ileo-
colic in nature. It is a common source of
bowel obstruction which results from the
telescoping of bowel onto itself.
Intussusception should be suspected in any
patient with episodic abdominal pain, which
may be accompanied by emesis, an abdomi-
nal mass, and rectal bleeding. Ninety percent
of patients with intussusception are between
the ages of 3 months and 3 years (peak inci-
dence, 5–9  months) [1]. Infants are more
likely to present with emesis than older chil-
dren. Rectal bleeding is classically a mucous-
like texture described as “red-currant jelly”
and is often a late finding. Ileal lymphade-
nopathy, including hypertrophic Peyer’s
patches, is thought to be the lead point for
ileocolic intussusception. Non-ileocolic
intussusception is rare in children and typi-
cally presents with a pathologic lead point, of
which Meckel’s diverticulum and small
bowel tumors are the most common.
B. The presentation of intussusception includes
severe, acute, and intermittent abdominal
pain which is episodic in nature, often lasting
A. N. Kulaylat · K. L. Martin (*)
Department of Surgery, Division of Pediatric Surgery,
Penn State Milton S. Hershey Medical Center,
Hershey, PA, USA
e-mail: kmartin15@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_129
129
a few minutes, with intervening periods of
remission and normal behavior typically
about 30 min apart. Fifteen percent of patients
present with atypical symptoms, such as pale-
ness or lethargy, suggestive of advanced dis-
ease [2]. Fever, tachycardia, hypotension,
and/or peritonitis are also suggestive of
advanced disease with risk of bowel ischemia
or perforation.
C. The workup of patients with suspected intus-
susception begins with plain radiographs
which will show signs of bowel obstruction.
Ultrasound should follow [2]. Ultrasound
classically demonstrates a target sign and,
when present, may also identify a lead point.
If intussusception is not present, ultrasound
may reveal other etiologies of the patient’s
symptoms such as appendicitis, ovarian tor-
sion, or urinary tract abnormalities. In suspi-
cious clinical presentations, a negative
ultrasound study should not exclude repeat
ultrasound or progression to air/contrast
enema if deemed clinically indicated. Of
note, small bowel-small bowel intussuscep-
tion without signs of obstruction or a patho-
logic lead point is a common finding in
patients with abdominal pain and is typically
self-limited.
D. On the basis of clinical examination and labo-
ratory studies, the child or infant should be
treated with intravenous fluids and correction
of electrolyte abnormalities. Placement of a
525
526
nasogastric tube and antibiotic coverage
should also be considered. Children who are
unstable or have peritonitis should be taken
directly to the operating room. If ileocolic
intussusception is present and the child is
stable without peritonitis, then air/contrast
enema should be pursued. In the hands of an
experienced radiologist, enema reduction is
successful in over 80% of cases [3].
E. If enema reduction is successful, patients
should be observed for signs of recurrence.
Historically, recurrence rates were cited as
5–15% after enema reduction with the major-
ity occurring within the first few days of ini-
tial presentation and up to one-third in the
first 24 h [2]. Recent meta-analysis suggests
24- and 48-h recurrence rates of less than 3%
following fluoroscopic-guided air enema
reduction [4]. Accordingly, select patients
may be safely discharged from the emergency
department after reduction with proper edu-
cation and follow-up [5].
F. If abdominal pain recurs ultrasound should be
repeated to assess for recurrence. If recur-
rence is confirmed then air/contrast enema is
repeated. Air/contrast enemas can be repeated
as often as necessary, as long as each reduc-
A. N. Kulaylat and K. L. Martin
tion proceeds easily and the child does not
demonstrate signs of peritonitis or clinical
deterioration. This strategy decreases the rate
of bowel resection and reduces mean length
of stay and costs [6]. If enema reduction is
unsuccessful, the child is taken to the operat-
ing room.
G. Once the decision has been made to operate,
the approach, laparoscopic or open, should be
dictated by the clinical stability of the patient
and surgeon preference [7]. Initial open
maneuvers include attempted reduction by
gently pulling on the bowel just proximal to
the intussusception while applying pressure
distally (traction-pulsion technique).
Laparoscopically a traction-traction technique
is used with gentle pulling on the involved
bowel to allow reduction. Once reduced the
bowel should then be assessed for viability. If
intestinal ischemia or perforation is present,
or if reduction is unsuccessful, then bowel
resection is completed. If a pathologic lead
point is identified, the patient should undergo
resection with primary anastomosis.
Pathologic small bowel-small bowel intussus-
ceptions cannot be reduced with air enemas
and thus require operative intervention.
129  Pediatric Intussusception 527

History:
2 year old male, episodic abdominal pain, emesis, red-currant jelly stools

Obtain vital signs, blood work and

perform physical examination

37.1 C, HR 100, RR 14, BP 90/50, WBC 11,000

Na 140, Cl 110, HCO3 24
RUQ/epigastric tenderness + palpable mass

Presentation concerning for intussusception in otherwise stable

C patient AXR suggest obstruction. Obtain an ultrasound

Intussusception
identified
No
Alternative
diagnosis on U/S? Yes
Continue workup
for other etiologies
D Air/contrast enema

E Failure to reduce intussusception Intussusception reduced

Repeat
Operating room Observe Ultrasound

Operative
G reduction
F
+/-resection Discharge Recurrent pain

Algorithm 129.1
528 A. N. Kulaylat and K. L. Martin

References 4. Gray MP, Li SH, Hoffmann RG, Gorelick

MH.  Recurrence rates after intussusception
enema reduction: a meta-analysis. Pediatrics.
1. Savoie KB, Thomas F, Nouer SS, Langham MR
2014;134(1):110–9.
Jr, Huang EY.  Age at presentation and manage-
5. Raval MV, Minneci PC, Deans KJ, et  al. Improving
ment of pediatric intussusception: a Pediatric
quality and efficiency for intussusception manage-
Health Information System database study. Surgery.
ment after successful enema reduction. Pediatrics.
2017;161(4):995–1003.
2015;136(5):e1345–52.
2. Columbani PM, Scholz S.  Intussusception. In:
6. Lautz TB, Thurm CW, Rothstein DH. Delayed repeat
Coran AG, Adzick NS, Krummel TM, Laberge J,
enemas are safe and cost-effective in the manage-
Shamberger RC, Calamone AA, editors. Pediatric sur-
ment of pediatric intussusception. J Pediatr Surg.
gery, vol. 2. 7th ed. Philadelphia: Elsevier Saunders;
2015;50(3):423–7.
2012.
7. Apelt N, Featherstone N, Giuliani S.  Laparoscopic
3. Sadigh G, Zou KH, Razavi SA, Khan R, Applegate
treatment of intussusception in children: a systematic
KE. Meta-analysis of air versus liquid enema for intus-
review. J Pediatr Surg. 2013;48(8):1789–93.
susception reduction in children. Am J Roentgenol.
2015;205(5):W542–9.
 Pyloric Stenosis
Dan W. Parrish, Jonathan H. DeAntonio,
and David A. Lanning
Algorithmic Approach
A. The typical patient presenting with pyloric
stenosis is between 2 and 8 weeks of age with
a male/female (M/F) ratio of 4:1. Patients ini-
tially tolerate feeds well with gradual
increases in episodes of emesis which eventu-
ally occur with every feed. The emesis is non-
bilious in color and is forceful or “projectile.”
In a relaxed and calm infant, the enlarged
pylorus will feel like an olive in the upper
abdomen in 72–89% of patients. The physical
exam is performed by palpating the infant’s
liver edge and sliding the examiner’s finger-
D. W. Parrish
Department of Pediatric Surgery, Batson Children’s
Hospital, University of Mississippi Medical Center,
Jackson, MS, USA
J. H. DeAntonio
Division of Pediatric Surgery, Department of General
Surgery, Virginia Commonwealth University Health,
Richmond, VA, USA
Department of Surgery, Virginia Commonwealth
University School of Medicine, Richmond, VA, USA
D. A. Lanning (*)
Division of Pediatric Surgery, Department of General
Surgery, Virginia Commonwealth University Health,
Richmond, VA, USA
Department of Surgery and Pediatrics, Children’s
Hospital of Richmond, Richmond, VA, USA
Department of Surgery, Virginia Commonwealth
University School of Medicine, Richmond, VA, USA
e-mail: david.lanning@vcuhealth.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_130
130
tips underneath the liver in the midline; the
fingertips are pulled back and down, trying to
trap the “olive.” [1]
B. These patients can present with mild-to-­
severe dehydration depending on the duration
and severity of symptoms. The levels of
severity have been largely based on bicarbon-
ate levels and are defined as slight
(<25 mEq/L), moderate (26–35 mEq/L), and
severe (>35 mEq/L) [2]. Other abnormal lab
values seen in these patients are the tradi-
tional hypokalemic, hypochloremic meta-
bolic alkalosis with possible decreased urine
output and a paradoxical aciduria. If the phys-
ical exam and lab values are unrevealing, an
ultrasound or upper gastrointestinal series
may be performed. Positive ultrasound find-
ings include a pyloric muscle thickness of
≥4 mm and a pyloric channel length ≥16 mm.
Stopping feeds is necessary. As these infants
are typically able to tolerate their gastric
secretions, a nasogastric tube is not a require-
ment, but it may be necessary in severe cases
[1, 3].
C. This condition is not a surgical emergency.
The primary emphasis needs to be placed on
resuscitation and correcting electrolyte
abnormalities. If the patient were taken to the
operating room prior to resuscitation, it could
precipitate difficulty weaning from the venti-
lator due to postoperative apnea secondary to
metabolic alkalosis. Correction of dehydra-
529
530
tion is traditionally started with an ­intravenous
(IV) fluid bolus with normal saline at 20 cc/
kg followed by continuous IV fluids at 1.25–
2x maintenance rate of D5 ½ normal saline
with 20–30 mEq KCl/L. [1] Historical teach-
ing was to delay potassium replacement until
urine output returns or increases, but this
E. Two schools of thought exist for post-­
unnecessarily delays needed replacement. We
recommend monitoring of urine output and
rechecking labs every 6–8 h until electrolytes
normalize [1, 3].
D.
Once the lab values are normalized
(CO2  <  30  mEq/L, Cl  >  100, K  >  4), the
patient is deemed resuscitated and is taken to
the operating room for a pyloromyotomy. The
two traditional approaches are open and lapa-
D. W. Parrish et al.
roscopic. The open approach utilizes a right
upper quadrant transverse or umbilical inci-
sion, while the laparoscopic approach uses an
umbilical port for the camera and two stab
incisions lateral to the umbilicus to follow the
same principles as the open incision [1, 3].
pyloromyotomy feeding schedule with no
significant differences in length of stay
being observed. An ad lib feeding schedule
has been associated with more episodes of
emesis but a shorter time to full feeds. A
typical regimented feeding schedule con-
sists of pedialyte followed by increasing
amounts of formula or breast milk every few
hours [1].
130  Pyloric Stenosis 531

History and Physical Exam:

· Previously healthy baby now intolerant of feeds
A · History of nonbilious, forceful emesis
· Possible “olive-shaped” enlarged pylorus is palpable in the upper abdomen
in 75% of patients

Obtain vital signs, including urine output (uop), blood work

(including BMP); if physical exam is unrevealing, obtain
ultrasound; place nasogastric tube

B
· Decreased urine output, nonbilious emesis, positive US
findings of thickened pylorus
· Typical lab values: CO 2 > 30, Cl < 100, K < 3
· Typical lab values: CO2 > 25

· Bolus with NS @ 20cc/kg

C · Begin fluid resuscitation with D5 ½ NS 20 KCl @ 1.25-2x
maintenance rate until uop 1 cc/kg/hr
· Monitor urine output, recheck abnormal labs every
6 hours

· Lab recheck: CO 2 > 30, Cl < 100, K < 3 · Lab recheck: CO 2 < 30, Cl > 100, K > 4

D
· Continue resuscitation, recheck labs
in 8 hours Proceed with
Pyloromyotomy
· Once labs normalize

Post-pyloromyotomy Feeding Schedule:

E
· Regimented feeding schedule
· Ad lib feeding

Algorithm 130.1
532 D. W. Parrish et al.

References 2. Schwartz M. Hypertrophic pyloric stenosis. In: Coran

A, et  al., editors. Pediatric surgery. 7th ed. London:
Elsevier Inc; 2012.
1. Koontz C, Wulkan M.  Lesions of the stomach. In:
3. Benson C, Alpern E.  Preoperative and postoperative
Holcomb III G, Murphy J, Ostlie D, editors. Ashcraft’s
care of congenital pyloric stenosis. AMA Arch Surg.
pediatric surgery. 6th ed. London: Elsevier Inc; 2014.
1957;75(6):877–9.
 Necrotizing Enterocolitis
Jonathan H. DeAntonio, Dan W. Parrish,
and David A. Lanning
Algorithmic Approach
A. Necrotizing enterocolitis (NEC) typically
occurs in preterm, low-birth-weight infants
and has an increasing incidence due to
advances in neonatal intensive care. It is asso-
ciated with hypoxia, infections, cyanotic
heart defects, and initiation of enteral nutri-
tion [1]. Less than 10% of cases occur in term
infants; these infants will commonly have an
insult, such as cyanotic heart defects, leading
to hypoxia [1]. NEC’s pathophysiology
J. H. DeAntonio
Division of Pediatric Surgery, Department of General
Surgery, Virginia Commonwealth University Health,
Richmond, VA, USA
Department of Surgery, Virginia Commonwealth
University School of Medicine, Richmond, VA, USA
D. W. Parrish
Department of Pediatric Surgery, Batson Children’s
Hospital, University of Mississippi Medical Center,
Jackson, MS, USA
D. A. Lanning (*)
Division of Pediatric Surgery, Department of General
Surgery, Virginia Commonwealth University Health,
Richmond, VA, USA
Department of Surgery, Virginia Commonwealth
University School of Medicine, Richmond, VA, USA
Department of Surgery and Pediatrics, Children’s
Hospital of Richmond, Richmond, VA, USA
e-mail: david.lanning@vcuhealth.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_131
131
remains largely unknown but is believed to be
due to the immature epithelial gastrointesti-
nal lining of neonates, leading to transloca-
tion of bacteria resulting in an inflammatory
response that may eventually cause perfora-
tion [2]. NEC often presents with lethargy,
feeding intolerance (vomiting, high gastric
residuals), bloody stools, respiratory distress,
or hypoperfusion. Physical exam findings
consist of a tender, erythematous, and dis-
tended abdomen with more advanced disease
demonstrating systemic symptoms such as
hemodynamic instability (hypotension,
shock), respiratory distress (apnea, respira-
tory acidosis), or decreased peripheral perfu-
sion (metabolic acidosis) [1, 3].
B. Evaluation continues with laboratory assess-
ments including complete blood count
(CBC), chemistry panel (basic metabolic
panel—BMP), arterial blood gas (ABG), and
cultures. These labs, depending on severity of
disease, may demonstrate a leukocytosis or
leukopenia, thrombocytopenia, metabolic or
respiratory acidosis, hypoxia, and bactere-
mia. Abdominal radiographs can be used to
look for radiographic signs such as pneuma-
tosis intestinalis, portal venous gas, free air,
or a “fixed” portion of small bowel (multiple
x-rays with a portion of small bowel in same
position) [1]. Ultrasound is highly user
dependent but may be used as well.
Differential diagnosis includes sepsis, ileus,
533
534
small bowel obstruction, and bacterial or viral
enteritis.
C. The Modified Bell’s Staging Criteria is often
used to clinically and radiographically diag-
nose and stage NEC [1, 4]. Management of
suspected or confirmed NEC begins with gas-
tric decompression with nasogastric or oro-
gastric tube (NGT, OGT) placement, stopping
enteral nutrition, broad IV antibiotics, and
correction of respiratory and metabolic
derangements as needed (IV fluid resuscita-
tion, ventilation, or vasopressors). Fifty per-
cent of infants with NEC require surgical
intervention [1].
D. The only absolute surgical indication for
NEC is pneumoperitoneum. However, rela-
tive indications include hemodynamic insta-
bility or failure of medical management,
portal venous gas, abdominal mass, “fixed”
J. H. DeAntonio et al.
bowel loop, abdominal wall erythema, and
bacteria positive paracentesis [1]. A patient
can become an operative candidate due to
failure of medical management or develop-
ment of the above indications.
E. If a patient meets criteria for surgical inter-
vention and is >1500  g, then may proceed
with laparotomy. If <1500  g and hemody-
namically unstable, a percutaneous drain may
be placed in the right lower quadrant in the
NICU to help stabilize the patient; however,
if hemodynamically stable, then the patient
may proceed with exploratory laparotomy.
The goal at laparotomy is removal of all
necrotic bowel (source control) while pre-
serving as much intestinal length as possible.
Mortality rate ranges from 10% to 50% but
increases toward 100% with panintestinal
disease [1].
131  Necrotizing Enterocolitis 535

History and Physical Exam:

· Preterm/Low Birth Weight Infant OR Term with insult (10%- listed below)
· Association: Hypoxia, Bacterial infection, Cyanotic heart defects, and Initiation of
enteral nutrition
A
· Presentation: Lethargy, Feeding intolerance, Bloody stools, Respiratory distress, or
Hypoperfusion
· VS: Bradycardia, Apnea, or Temp. instability. Distended, tense, and erythematous
abdomen. Advanced: Hemodynamic (HD) instability, Respiratory collapse, Sepsis, Shock
· Advanced Disease: Systemic Signs of Seps

Testing/Evaluation:
B · Labs: CBC, BMP, ABG, and Cultures
· Imaging: Abdominal XR (supine and left lateral decubitus) Pneumatosis intestinalis,
Portal venous gas, Free air, and a “Fixed” bowel loop

Suspect or Confirm
NEC? (Modified Bell’s
Staging) No

Evaluate Diff. Diagnoses

Yes
C
Medical Management:
· OGT/NGT placement, Stop enteral feeding, Broad
spectrum IV antibiotics
· Correct respiratory & metabolic derangements

· HD stability · Pneumoperitoneum
· · HD instability
D No pneumoperitoneum OR Relative
surgical indications · Relative surgical indications

Yes
Failure
Continue Medical Management Weight < 1500g Weight > 1500g
E
HD Instability HD Stable

No Improvement
RLQ Percutaneous Laparotomy
Drainage

Algorithm 131.1
536 J. H. DeAntonio et al.

References rotizing enterocolitis: modeling the innate immune

response. Am J Pathol. 2015;185(1):4–16.
3. Neu J.  Necrotizing enterocolitis. World Rev Nutr
1. Castle SL, Speer AL, Grikscheit TC, Ford
Diet. 2014;110:253–63.
H. Necrotizing enterocolitis. In: Ziegler MM, Azizkhan
4. Walsh MC, Kliegman RM. Necrotizing enterocolitis:
RG, Dv A, Weber TR, editors. Operative pediatric sur-
treatment based on staging criteria. Pediatr Clin N
gery. New York: McGraw-Hill Education; 2014.
Am. 1986;33(1):179–201.
2. Tanner SM, Berryhill TF, Ellenburg JL, Jilling T,
Cleveland DS, Lorenz RG, et al. Pathogenesis of nec-
 Omphalocele and Gastroschisis
Jonathan H. DeAntonio, Dan W. Parrish,
and David A. Lanning
Algorithmic Approach
A. Gastroschisis involves an abdominal wall
defect (usually 2–5  cm in size), typically to
the right of the umbilical cord, with eviscer-
ated abdominal contents that are not sur-
rounded by a membranous sac. The bowel is
usually thickened and edematous. Believed to
be caused by embryological failure, the lat-
eral body wall folds to migrate to the midline
[1]. Occurs earlier in embryonic development
than omphaloceles with possible causative
J. H. DeAntonio
Division of Pediatric Surgery, Department of General
Surgery, Virginia Commonwealth University Health,
Richmond, VA, USA
Department of Surgery, Virginia Commonwealth
University School of Medicine, Richmond, VA, USA
D. W. Parrish
Department of Pediatric Surgery, Batson Children’s
Hospital, University of Mississippi Medical Center,
Jackson, MS, USA
D. A. Lanning (*)
Division of Pediatric Surgery, Department of General
Surgery, Virginia Commonwealth University Health,
Richmond, VA, USA
Department of Surgery, Virginia Commonwealth
University School of Medicine, Richmond, VA, USA
Department of Surgery and Pediatrics, Children’s
Hospital of Richmond, Richmond, VA, USA
e-mail: david.lanning@vcuhealth.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_132
132
factors including environmental exposures
(tobacco), lower maternal age or socioeco-
nomic status [1]. Classically, not associated
with other congenital defects; however,
recently a few cases are suggestive of rare
genetic causes. Intestinal atresia is also noted
in 10–12% of patients [1]. Gastroschisis inci-
dence was noted to be 5.2 out of 1000 live
births in a recent US database study [2].
Omphaloceles are considered midline
abdominal wall defects (usually 4–10 cm in
size) with a peritoneal membrane covering
the abdominal contents and the umbilical
cord coming directly off the defect. It is
believed to result from the intestinal loops not
returning to the abdomen after the tenth week
of gestation. Omphalocele occurs embryo-
logically after gastroschisis and is not sus-
pected to be associated with teratogen
exposure [1]. Omphaloceles are classically
associated with numerous congenital anoma-
lies including cardiac, renal, chromosomal,
and genetic syndromes (i.e., Beckwith–
Wiedemann and Pentalogy of Cantrell). The
incidence of omphaloceles has decreased in
developed countries due to prenatal diagnosis
and termination of some pregnancies, cur-
rently 1–2 out of 1000 live births in the United
States [1, 2].
Both are typically diagnosed on prenatal
ultrasound (U/S) in developed countries.
Elevated maternal serum α-fetoprotein should
537
538 J. H. DeAntonio et al.

be evaluated with diagnostic pre-natal ultra- transparent film dressing, after reducing the
sound due to its correlation with gastroschisis bowel into the abdomen, can avoid the need
[1]. If an omphalocele is diagnosed prena- for surgical closure in the perinatal period but
tally, then chromosome evaluation by amnio- may lead to the development of an umbilical
centesis is typically offered to parents, as well hernia.
as more extensive evaluation for associated Omphalocele repair is more complex and
anomalies by U/S or MRI. varies by size and associated congenital mal-
B. Gastroschisis and omphalocele diagnosed formations. The repairs can be described as
prenatally may be delivered vaginally if there immediate (small to medium), staged
are no fetal or obstetric concerns. For gastros- (medium to large), or delayed (giant) [1]. If
chisis, the bowel is assessed looking for sus- the defect is small or medium sized and there
pected areas of dilatation, atresia, or necrosis, are no other congenital concerns, attempts at
then contents are covered with saline-­ an immediate closure may proceed. If
moistened gauze, and infant is placed inside a medium to large, a staged closure with a
plastic bag-like device, which covers the modified silo and gradual reduction with
lower limbs to above the defect. This cover- eventual primary closure are attempted. Some
ing prevents evaporative and heat losses. omphaloceles are too large (giant) to be
Intravenous fluid resuscitation, antibiotics, closed, or the neonate has other congenital
and gastric decompression should begin. malformations that prevent repair during this
Omphaloceles with an intact sac are covered period; these can be closed in a delayed fash-
with petroleum or saline-moistened gauze. ion (6 months to 1 year). Ruptured omphalo-
U/S evaluation for associated congenital celes will require resuscitation, plastic
defects is performed and karyotype analysis covering, and antibiotics, as in gastroschisis,
is sent if not done previously. than usually staged or delayed closure.
C. Surgical management of gastroschisis con- D. Post-op management for gastroschisis consists
sists of placing abdominal contents within a of antibiotics, bowel rest with parenteral nutri-
silo and slowly reducing them back into the tion (proper intestinal motility delayed by sev-
abdomen over usually several days or, if able, eral weeks), and close monitoring (HD status
closing the defect primarily after safely and abdominal compartment syndrome).
reducing the contents and no resultant
changes in hemodynamic status (evaluating For omphalocele, postoperative management
peak/mean airway pressures and vitals). If depends on time frame of repair but also is con-
there is ischemic bowel, perforation, or cerned with evaluation and management of other
hemodynamic (HD) instability, immediate congenital defects. Abdominal compartment syn-
exploration in the NICU or operating room drome (ACS) should be a concern, like gastros-
for further evaluation may be necessary. A chisis, for immediate repairs, but these patients
newer technique for closure of applying a typically have improved intestinal motility.
132  Omphalocele and Gastroschisis 539

History and Physical Exam:

· Abdominal wall defect on prenatal ultrasound (most likely) or at birth
· Evaluate for maternal risk factors: tobacco, socioeconomic, low maternal age
· Elevated maternal serum -fetoprotein evaluate for Gastroschisis
· Vaginal delivery appropriate unless fetal of obstetric concerns

Gastroschisis Omphalocele
A · Abdominal wall defect-Right of · Midline abdominal wall defect
umbilical cord · Sac covering eviscerated contents
· No sac covering eviscerated contents · Associated with cardiac, renal, genetic
defects

B · Evaluate bowel for dilatation, atresia, or

necrosis
· If intact sac over contents, cover with
· Cover contents with saline soaked gauze
petroleum or saline soaked gauze
and place plastic covering to above defect.
· U/S evaluation for associated anomalies and
karyotype sent if not done prenatally

Evidence of Size and Other

perforation, mal- Congenital
YES Abnormalities
rotation, necrosis
and HD instability?

Exploration,
Source Control,
Immediate-
NO & Staged Closure Staged
Primary
Closure
Closure

Immediate- Silo with daily Delayed

Primary Fails/Unable reduction & Closure
closure delayed fascial
closure

Postoperative Management
D · Depends significantly on Immediate (ACS) vs Staged (Silo management) vs Delayed
(Wound care) closure
· Gastroschisis => TPN for intestinal Dismotiliy
· Omphalocele => Evaluation/Management of Congenital Malformations

Algorithm 132.1
540 J. H. DeAntonio et al.

References New York: McGraw-Hill Education; 2014.

2. Allman R, Sousa J, Walker MW, Laughon MM,
Spitzer AR, Clark RH. The epidemiology, prevalence
1. Islam S.  Abdominal wall defects: omphalocele and
and hospital outcomes of infants with gastroschisis. J
gastroschisis. In: Ziegler MM, Azizkhan RG, Dv
Perinatol. 2016;36(10):901–5.
A, Weber TR, editors. Operative pediatric surgery.
 Biliary Atresia
Dan W. Parrish, Jonathan H. DeAntonio,
and David A. Lanning
Algorithmic Approach
A. Neonatal jaundice may be present in 50–60%
of newborns in the first week of life [1]. More
than 50% of patients with biliary atresia may
present with passage of meconium and col-
ored stools for the first few days of life.
Typical symptoms of biliary atresia are per-
sistently elevated conjugated bilirubin, jaun-
dice, acholic stools, and possibly
hepatomegaly. Once jaundice has persisted
for >2  weeks or the hyperbilirubinemia is
D. W. Parrish
Department of Pediatric Surgery, Batson Children’s
Hospital, University of Mississippi Medical Center,
Jackson, MS, USA
J. H. DeAntonio
Division of Pediatric Surgery, Department of General
Surgery, Virginia Commonwealth University Health,
Richmond, VA, USA
Department of Surgery, Virginia Commonwealth
University School of Medicine, Richmond, VA, USA
D. A. Lanning (*)
Division of Pediatric Surgery, Department of General
Surgery, Virginia Commonwealth University Health,
Richmond, VA, USA
Department of Surgery, Virginia Commonwealth
University School of Medicine, Richmond, VA, USA
Department of Surgery and Pediatrics, Children’s
Hospital of Richmond, Richmond, VA, USA
e-mail: david.lanning@vcuhealth.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_133
133
caused primarily by elevated conjugated
bilirubin, an investigation into the cause
­
needs to begin [2].
B. There is no definitive test to diagnose biliary
atresia, so the workup consists of ruling out
other diseases. Lab tests to be obtained are
liver function tests, including GGT. One will
typically see elevated transaminases and
GGT, in addition to the hyperbilirubinemia.
Cultures and biochemical studies to evaluate
for TORCH (Toxoplasmosis, Other (syphilis,
varicella-zoster, parvovirus B19), Rubella,
Cytomegalovirus (CMV), and Herpes infec-
tion) infections, hepatitis, alpha 1-antitrypsin
deficiency, should be obtained. An ultrasound
allows for the evaluation of the liver contour
and biliary anatomy. A HIDA scan or intraop-
erative cholangiogram can demonstrate the
biliary anatomy and can rule out biliary atre-
sia if contrast is seen in the intestines. A liver
biopsy should be performed to evaluate the
presence of bile ducts and ductular prolifera-
tion [2, 3].
C. Once the diagnosis of biliary atresia is made,
operative timing is key. More favorable out-
comes are seen when the definitive procedure
is performed within 60 days of age, as cirrho-
sis begins to develop by 3–4 months of age.
Preoperative steps to take are to maintain
good hydration with intravenous fluid resus-
citation, broad-spectrum antibiotic coverage,
541
542
and fat-soluble vitamin supplementation with
IM vitamin K, if needed [2, 3].
D. The operation of choice for biliary atresia is
the Roux-en-Y hepatic portoenterostomy  —
the Kasai procedure. It has been modified
many times, including open and minimally
invasive techniques. The principal steps of
the procedure continue to be excision of the
extrahepatic biliary tree, transection of the
portal plate near the hilum of the liver, and
biliary drainage with bilioenteric limb [4]. If
a choledochal cyst is noted, the cysts are
excised and a Roux-en-Y hepaticojejunos-
tomy is performed.
E. There is a large discrepancy in the morbidity
and mortality rates that are presented in the
literature, but successful postoperative out-
comes after Roux-en-Y hepatic portoenter-
D. W. Parrish et al.
ostomy are traditionally divided into thirds.
One-third of patients will have successful
long-term biliary drainage, one-third will
have temporary drainage but will be older
and more able to withstand a liver transplant,
and one-third will receive no relief and will
progress to liver failure requiring transplan-
tation [3]. Cholangitis is the most common
postoperative complication following a
Kasai procedure.
F. Controversy exists regarding the use of corti-
costeroids postoperatively to decrease scarring
and subsequent obstruction at the anastomosis.
Antibiotics, choleretic agents, and fat-soluble
vitamin supplementation are commonly used.
The most common complications after porto-
enterostomy are cholangitis (33–60%) and
portal hypertension (34–76%) [2, 3].
133  Biliary Atresia 543

History and physical exam:

· Infant typically >2 weeks old
A · Persistent conjugated hyperbilirubinemia, jaundice, acholic stools,
hepatomegaly
· Begin workup to rule out other conditions

· Lab tests: CMP (including GGT), cultures to rule out

perinatal infections
· Ultrasound: evaluate liver contour and presence of
gallbladder, bile ducts, or choledochal cysts
B
· HIDA: evaluate passage of contrast into intestines
· Liver Biopsy: evidence of ductular proliferation
· Intraoperative cholangiogram and liver biopsy

C · Intravenous fluid resuscitation as needed

· Preoperative antibiotics
· Oral fat-soluble vitamin supplementation or IM vitamin K

D Proceed with
Roux-en-Y hepatic
portoenterostomy

1/3 of patients will 1/3 of patients will 1/3 of patients will

E have successful long have temporary have no relief from
term biliary drainage biliary drainage but the operation and
will ultimately will progress to
require a transplant liver failure

Complications: Cholangitis, Decreased bile flow, Portal

F Hypertension, Essential Fatty Acid deficiency, Intrahepatic cysts
544 D. W. Parrish et al.

References 2. Koontz C, Wulkan M.  Lesions of the stomach. In:

Holcomb III G, Murphy J, Ostlie D, editors. Ashcraft’s
pediatric surgery. 6th ed. London: Elsevier Inc; 2014.
1.
Practice parameter: management of hyperbiliru-
3. Schwartz M. Hypertrophic pyloric stenosis. In: Coran A,
binemia in the healthy term newborn. American
et al. Pediatric surgery. 7th. London. Elsevier Inc; 2012.
Academy of Pediatrics. Provisional Committee
4. Nio M, Ohi R.  Biliary atresia. Semin Pediatr Surg.
for Quality Improvement and Subcommittee on
2000;9:177–86.
Hyperbilirubinemia. Pediatrics. 1994;94(4 Pt
1):558–65.
Part XVII
Vascular
 Carotid Artery Stenosis
Ian Bailey and Faisal Aziz
Algorithmic Approach
A. Introduction: Stroke is among the most com-
mon causes of disability in the world. In the
United States, over 85% of the strokes are
considered to be ischemic in origin [1]. The
most common cause of ischemic stroke is
extracranial carotid artery disease.
Management of extracranial carotid disease
is the cornerstone of ischemic stroke preven-
tion. In majority of the cases, ischemic stroke
is preceded by episodes of transient ischemic
attacks (TIA). Typical symptoms of TIA
include dysarthria, amaurosis fugax, and
hemiparesis. North American Symptomatic
Carotid Endarterectomy Trial (NASCET)
showed that in patients presenting with TIAs
and ipsilateral carotid stenosis of >70%,
I. Bailey
Division of Vascular Surgery, Penn State Heart and
Vascular Institute, Pennsylvania State University
College of Medicine, Hershey, PA, USA
Penn State Health Milton S. Hershey Medical Center,
Hershey, PA, USA
F. Aziz (*)
Division of Vascular Surgery, Penn State Heart and
Vascular Institute, Pennsylvania State University
College of Medicine, Hershey, PA, USA
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: faziz@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_134
134
carotid endarterectomy (CEA) reduced the
incidence of stroke from 26% to 9% [2].
B. Evaluation/ Physical Examination: Key ele-
ments of the physical examination include a
neurologic exam, cardiac exam, neck auscul-
tation, as well as an ocular exam. The neuro-
logic exam may reveal signs of stroke such as
cranial nerve deficits, pronator drift, and
motor or sensory deficits. An ocular exam
may demonstrate Hollenhorst plaques in the
setting of transient blindness as a result of
retinal artery emboli. Neck auscultation may
reveal carotid bruits. Finally, a cardiac exam
may point against a carotid source of stroke if
an arrhythmia is detected or if a cardiac mur-
mur is transmitted through the carotid
circulation.
C. Imaging: Carotid artery duplex ultrasound is
often the first-choice modality which displays
increased peak systolic velocities, diastolic
velocities, and spectral widening with hemo-
dynamically significant lesions.
D. Indications for Surgery: Surgical intervention
is recommended for patients presenting with
TIAs and  >50% ipsilateral carotid stenosis
and for asymptomatic patients with >80%
carotid stenosis.
E. Management: Management options for suit-
able patients include carotid endarterectomy
(CEA) and carotid artery stenting (CAS).
CREST trial [3] showed that CEA was asso-
ciated with 4.7% risk of stroke and death
547
548 I. Bailey and F. Aziz

while CAS was associated with 6.4% risk of
these complications. Carotid shunt is placed
if there is evidence of cerebral ischemia on
electroencephalogram (EEG) or if stump
pressure is below 50  mm Hg. These differ-
ences were statistically significant. Generally,
CEA is the preferred treatment of choice for
suitable candidates. Patients who are deemed
high risk for CEA (previous neck radiation,
previous carotid surgery, and unfit for general
anesthesia) are best treated with CAS.
F. Postoperative Complications: Postoperative
complications for CEA include stroke and
cranial nerve injuries. CAS is associated with
stroke and access site complications.
G. Long-term Follow-up: Generally, a carotid
duplex is performed at 6  weeks and subse-
quently 6 months to determine patency of the
carotid and to monitor the contralateral
carotid stenosis. Most surgeons recommend
lifelong follow-up with carotid duplex scans.

A History of TIAs and Carotid Bruit on

neck examination

Thorough physical examination: assessment

B of systemic vascular disease, neurologic
examination, ocular examination

Duplex ultrasound: Degree of carotid

C stenosis

D Symptomatic Carotid Stenosis Asymptomatic Carotid Stenosis

>50% >80%

CEA
(Carotid Shunting, if
indicated)

E Contra indications to CEA (previous

neck radiation, previous carotid
surgery, unfit for general anesthesia)

CAS

Postoperative Care
F

Algorithm 134.1
134  Carotid Artery Stenosis 549

References 3. Brott TG, Hobson RW 2nd, Howard G, Roubin

GS, Clark WM, Brooks W, Mackey A, Hill MD,
Leimgruber PP, Sheffet AJ, Howard VJ, Moore WS,
1. Grysiewicz RA, Thomas K, Pandey DK. Epidemiology
Voeks JH, Hopkins LN, Cutlip DE, Cohen DJ, Popma
of ischemic and hemorrhagic stroke: incidence,
JJ, Ferguson RD, Cohen SN, Blackshear JL, Silver
prevalence, mortality, and risk factors. Neurol Clin.
FL, Mohr JP, Lal BK, Meschia JF, Investigators
2008;26(4):871–95.
CREST.  Stenting versus endarterectomy for treat-
2. North American Symptomatic Carotid
ment of carotid-artery stenosis. N Engl J Med.
Endarterectomy Trial Collaborators, HJM B, Taylor
2010;363(1):11–23.
DW, Haynes RB, Sackett DL, Peerless SJ, Ferguson
GG, Fox AJ, Rankin RN, Hachinski VC, Wiebers DO,
Eliasziw M.  Beneficial effect of carotid endarterec-
tomy in symptomatic patients with high-grade carotid
stenosis. N Engl J Med. 1991;325(7):445–53.
 Abdominal Aortic Aneurysm
Erin K. Greenleaf and Faisal Aziz
Algorithmic Approach
A. Definitions: An aneurysm is defined as a focal
dilatation of an artery to a diameter of at least
1.5 times larger than the expected normal
diameter. As this pertains to the infrarenal
abdominal aorta, a diameter of 3 cm or greater
typically qualifies as aneurysmal.
B. Evaluation/history: With the widespread use
of cross-sectional imaging, many abdominal
aortic aneurysms are discovered incidentally.
Others are found on screening exams, as the
US Preventative Services Task Force recom-
mends that men aged 65–75 years who have
ever smoked undergo screening ultrasound
[1]. A small proportion of patients present
with symptomatic AAA, with abdominal and/
or back pain and a palpable pulsatile abdomi-
E. K. Greenleaf
Division of Vascular Surgery, Penn State Heart and
Vascular Institute, Pennsylvania State University
College of Medicine, Hershey, PA, USA
Penn State Milton S. Hershey Medical Center,
Hershey, PA, USA
F. Aziz (*)
Division of Vascular Surgery, Penn State Heart and
Vascular Institute, Pennsylvania State University
College of Medicine, Hershey, PA, USA
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: faziz@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_135
135
nal mass, which is widely believed to repre-
sent an impending aneurysmal rupture [2].
C. Evaluation/physical examination: Risk fac-
tors for development of AAA include
advanced age, male gender, and a history of
smoking. The positive predictive value of
physical exam for detection and diagnosis of
AAA is only 15% [3]. Physical examination
should also focus on identifying factors that
may impact intervention, such as surgical
scars on the abdominal wall, hernias, and
body habitus.
D. Imaging: Screening and monitoring of
AAA typically use duplex ultrasonography
as it is low risk and the least invasive. In
the setting of preoperative planning, com-
puted tomographic angiography (CTA)
provides greater accuracy and more reli-
able measurements.
E. Indications and management: Any patient
with a reasonable life expectancy and an
AAA >5 cm, or aortic expansion of 1 cm or
more in 1 year, is a candidate to be considered
for surgical repair. Surgical operations for the
treatment of AAA include open surgical
repair (OSR) and endovascular aortic repair
(EVAR). The character of the aortic neck
bears great influence over the suitability for
endovascular repair, as length, angulation,
diameter, and shape will impact the ability to
obtain an adequate proximal seal. Both OSR
and EVAR must remain in the ­armamentarium
551
552
of the vascular surgeon as conversion to open
repair may be necessary when safe execution
of EVAR is not possible; moreover, long-term
outcomes demonstrate that no differences in
long-term mortality exist between the two
modalities [4].
F. Postoperative complications: Depending on
the circumstances of the presentation and of
the repair, common complications following
AAA repair include cardiac ischemia, renal
failure, and ischemia of the sigmoid colon,
lower extremities, or spinal cord. Graft-
related complications following EVAR
include endoleaks. Ischemic colitis can pres-
ent with bloody diarrhea, abdominal pain,
distension, fever, leukocytosis, or metabolic
acidosis.
G. Long-term follow-up: Following EVAR, con-
trast-enhanced CT scanning should be under-
taken at 1 and 12  months; alternatively,
E. K. Greenleaf and F. Aziz
duplex ultrasound combined with non-con-
trast CT serves as a viable option in patients
with renal insufficiency. An endoleak, a com-
plication unique to EVAR, occurs due to per-
sistent blood flow into the aneurysmal sac
and if seen at 1  month would necessitate a
CTA at 6  months to determine need for re-
intervention. There are five types of endole-
aks: Type 1 (incomplete seal between the
stent and native vessel  – Immediate repair
required), type 2 (blood flow into aneurysm
sac via branch vessels of the intrarenal
abdominal aorta), type 3 (blood flow between
the separate components of the graft), type 4
(blood flow through the graft fabric), and type
5 (persistently elevated pressure within the
aneurysm sac). Thereafter, surveillance fol-
lowing EVAR should be continued at least on
an annual basis. Following open repair, imag-
ing should be obtained at least every 5 years.
135  Abdominal Aortic Aneurysm 553

A Presence of risk factors for development of aortic

aneurysm (AAA)

Physical examination reveals pulsatile aortic

B mass

Duplex ultrasound: AAA diagnosis. Infrarenal

C AAA >5.5cm.
Weigh the risks and benefits of surgery. For
patients deemed to be appropriate for surgery,
obtain CTA to delineate anatomy.

Acceptable landing zones and

D access vessels: Feasible for EVAR

Yes No

EVAR Open AAA Repair

E Post-operative Evaluation: Post-operative Evaluation: ischemica

Endoleaks of the colon, lower extremities, or
spinal cord, cardiac ischemia, and
renal failure

Algorithm 135.1

3. Beede SD, Ballard DJ, James EM, Ilstrup DM, Hallet

References
1. US Preventive Services Task Force: Abdominal
Aortic Aneurysm. Web address: https://www.
uspreventiveservicestaskforce.org/Page/Document/
UpdateSummaryFinal/abdominal-aortic-aneurysm-
screening. Accessed 25 Aug 2017.
2. Sullivan CA, Rohrer MJ, Cutler BS. Clinical manage-
ment of symptomatic but unruptured abdominal aortic
aneurysm. J Vasc Surg. 1990;11(6):799–803.
JW Jr. Positive predictive value of clinical suspicion
of abdominal aortic aneurysm. Implications for effec-
tive use of abdominal ultrasonography. Arch Intern
Med. 1990;150(3):549–51.
4. Schermerhorn M, Dominique B, O’Malley J, Curran
T, McCallum J, Darling J, Landon BE.  Long term
­outcomes of abdominal aortic aneurysm in the medi-
care population. N Engl J Med. 2015;373:328–38.
 Ruptured Abdominal Aortic
Aneurysm
Faisal Aziz
Algorithmic Approach
A. Definitions: Rupture is the most feared com-
plication of an abdominal aortic aneurysm
(AAA). It is a catastrophe associated with
mortality rates in excess of 80% [1]. It is the
15th leading cause of death. Elective repair of
AAA to prevent rupture is the best strategy
for dealing with aneurysms.
B. Evaluation/history: The blood loss from rup-
tured AAA (rAAA) is massive and majority
of patients do not make it to the hospital. The
classic description of patients presenting with
rAAA is severe abdominal pain, abdominal
distension, and hypotension. Previous history
of a known AAA or a family history of AAAs
are useful clues to make a prompt diagnosis.
C. Evaluation/physical examination: a clinician
should look for hypotension with tachycar-
dia. Majority of patients in older age groups
are on beta-blockers, and this may mask
tachycardia. Abdominal examination reveals
firm distension. Timely diagnosis and prompt
operation is the only strategy to save lives of
persons presenting with this fatal diagnosis.
F. Aziz
Division of Vascular Surgery, Penn State Heart and
Vascular Institute, Pennsylvania State University
College of Medicine, Hershey, PA, USA
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: faziz@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_136
136
D. Imaging: Computed tomography ­angiography
(CTA) is the standard imaging technology to
diagnose rAAA and to determine the feasibil-
ity of endovascular repair (EVAR). However,
it should only be utilized for patients with
stable hemodynamics. Patients presenting
with hemodynamic instability should be
rushed to the operating room, where on-table
angiography can be used to determine land-
ing zones required for EVAR placement.
E. Management: Ruptured AAA can be repaired
with either open surgical operation or endo-
vascular repair (EVAR). For patients who
present with relatively stable hemodynamics,
CTA is used to determine the choice of opera-
tion. For patients who are unstable, a percuta-
neous sheath can be placed in the common
femoral artery on the operating room table
and a diagnostic aortogram is performed to
determine suitability for EVAR.  The basic
principles for open surgical repair and EVAR
for ruptured AAA patients are essentially the
same as those for elective repair. The key dif-
ference in patients presenting with ruptured
AAA is the importance of obtaining quick
inflow control to stop active hemorrhage. In
patients undergoing EVAR, an occlusion bal-
loon inserted via femoral access can be used
for inflation in aorta and in patients undergo-
ing open surgical repair, a supraceliac clamp
can be used to stop active hemorrhage.
555
556 F. Aziz

F. Postoperative complications: Overall mortal-
ity for patients with rAAA remains high, with
majority of patients dying even before reach-
ing a hospital. Thirty-day mortality for
patients treated with EVAR is significantly
better than those treated with open surgical
repair (21% vs. 44%) [2]. New-onset postop-
erative acute renal failure after rAAA surgery
is the biggest predictor of mortality, and inci-
dence of acute renal failure in patients treated
with EVAR is significantly lower than those
treated with open surgical repair [3].
G. Long-term Follow-up: Long-term follow-up
for patients who survive an operation for
rAAA is not different from those who require
elective repair. Patients who have undergone
EVAR require a close follow-up with CTA at
6 months to determine endoleaks, and patients
who have stable sac size require less frequent
follow-ups.

Triad of Abdominal Pain, Abdominal Distension

A and Hypotension

High Suspicion for rAAA. Determine

B feasibility of getting CTA

Unstable hemodynamics: Directly

C to OR, on table angiography to Stable hemodynamics: Obtain CTA and
determine if candidacy for EVAR determine if candidacy for EVAR
(Landing zone length of at least
D 15mm, neck angulation of <60
degrees)

Suitable for EVAR: EVAR Unsuitable for EVAR: Open

Surgical Repair

E
Key Step: Hemorrhage Control
by using supra celiac aortic
occlusion balloon
Key Step: Hemorrhage Control
by supra celiac aortic clamp
Ligate IMA if no back bleeding or
pulsatile back bleeding

F G Postoperative Care

Algorithm 136.1
136  Ruptured Abdominal Aortic Aneurysm 557

References 2. Mehta, et  al. Endovascular repair of ruptured infra-

renal AAA is associated with lower 30 day mortal-
ity and better 5 year survival rates than open surgical
1. Kantonen I, Lepantalo M, Brommels M, et  al.
repair. J Vasc Surg. 2013;57(2):368–75.
Mortality in ruptured abdominal aortic aneurysms.
3. Aziz F, Azab A, Schaefer E, Reed AB. Endovascular
TheFinnvasc study group. Eur J Vasc Endovasc Surg.
repair of ruptured abdominal aortic aneurysm is asso-
1999;17:208–12.
ciated with lower incidence of post-operative acute
renal failure. Ann Vasc Surg. 2016;35:147–55.
 Aortic Dissection
Katelynn Ferranti and Faisal Aziz
Algorithmic Approach
A. Definitions: Acute aortic dissection or a
“tear” in the aortic wall is among the most
lethal catastrophes affecting the aortic wall. If
left untreated, almost 50% of patients will die
within 24  h [1]. Of those who survive the
acute phase of this pathology, few survive
beyond 5 years due to aneurysmal degenera-
tion and rupture of the weakened wall of false
lumen [2].
B. Evaluation/history: Most patients will present
with acute onset of severe chest or abdominal
pain, radiating to the back. It is pertinent to
ask about history of previous, family history
of aortopathies and history of hypertension.
C. Evaluation/physical examination: A thorough
physical examination is key to making an
K. Ferranti
Division of Vascular Surgery, Penn State Heart and
Vascular Institute, Pennsylvania State University
College of Medicine, Hershey, PA, USA
Department of Vascular Surgery, Penn State Health,
Milton S. Hershey Medical Center,
Hershey, PA, USA
F. Aziz (*)
Division of Vascular Surgery, Penn State Heart and
Vascular Institute, Pennsylvania State University
College of Medicine, Hershey, PA, USA
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: faziz@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_137
137
accurate diagnosis of aortic dissection and to
determine its extent. Patients presenting with
extremely high blood pressure should receive
immediate treatment of HTN. Cardiac exami-
nation should include auscultation for mur-
murs. The abdominal examination should
focus on identifying clinical signs of bowel
ischemia. Pulses should be palpated in all
four extremities to determine involvement of
one or more peripheral blood vessels as well
as a motor and sensory exam in each
extremity.
D. Laboratory testing: Blood work should be
obtained and include a CBC, CMP, troponin,
and lactic acid. This will help to identify signs
of end-organ malperfusion such as cardiac,
liver, kidney, or intestinal ischemia.
E. Imaging: Emergent computed tomography
angiography (CTA) should be obtained
including the chest, abdomen, and pelvis.
Emergent transthoracic echocardiogram
should be obtained to determine the involve-
ment of aortic valve, pericardial effusion, and
proximal extent of dissection.
F. Indications: Indications for emergent surgical
treatment include type A aortic dissection
(involving the ascending aorta) and involve-
ment of visceral arteries (celiac artery, supe-
rior mesenteric artery, and renal arteries) and
iliac arteries.
G. Management: Surgical management of aortic
dissection is complicated and requires sound
559
560
clinical judgment. Type A dissections need
emergent surgical repair by aortic arch
replacement. Type B dissections involving
mesenteric blood vessels are treated with
endovascular repair (TEVAR), fenestrations, I. Long-term follow-up: Patients surviving
or mesenteric bypasses. Type B dissections
compromising lower extremity arterial flow
are managed by TEVAR, fenestrations, extra-­
anatomic bypasses, or iliac stenting.
H. Postoperative complications: Operations
for aortic dissections are associated with
K. Ferranti and F. Aziz
significantly high risk of mortality and
postoperative complications including
damage to the bowels and kidneys and
limb loss.
acute aortic dissections need to be followed
for the rest of their lives with serial CTAs to
monitor for development of aneurysmal
degeneration, which may require further
intervention.
137  Aortic Dissection 561

Clinical scenario:
60 y.o. Man with PMHx of HTN presents with severe stabbing
chest pain that radiates to back.

Vital signs, Physical exam

Laboratories: CBC, BMP, Lactic Acid, Troponin
EKG

VS: Tachycadia? HTN?

PE: New Murmur? Abdominal pain or

tenderness? Lower extremity pain,
tenderness, pulses, palor?

Labs:Leukocytosis? Elevated Creatinine?

Lactic acidosis? Elevated Troponin?

CTA Chest/Abdomen/Pelvis

Stanford type A dissection Stanford type B dissection

Surgical emergency!
Consult cardiac surgery
OR
562 K. Ferranti and F. Aziz

Stanford type B dissection

Anti-impulse therapy:
Blood pressure control: Goal SBP 100-120
Heart rate control: Goal HR <60 bpm

Absence of Lower extremity

Bowel ischemia ischemia
malperfusion

Malperfusion?

1st line: Labetalol drip

OR for revascularization OR for revascularization
or esmolol drip
2nd line: Nicardipine drip
3rd line: Nitroprusside
drip (after beta blocker)

Unilateral ischemia:
Arterial Line Surgical options: · Fem-Fem
· TEVAR · Iliac stent
Admit to ICU · Endovascular aortic
fenestration Bilateral ischemia:
Serial abdominal and · Open aortic · Endovascular aortic
lower extremity exams fenestration fenestration
· Mesenteric bypass · Open aortic
fenestration

Algorithm 137.1
137  Aortic Dissection 563

References
1. Khan IA, Nair CK.  Clinical, diagnostic, and man-
agement perspectives of aortic dissection. Chest.
2002;122(1):311–28.
2.
Crawford ES, Crawford JL, Safi HJ, Coselli
JS, Hess KR, Brooks B, Norton HJ, Glaeser
DH.  Thoracoabdominal aortic aneurysms: preopera-
tive and intraoperative factors determining immediate
and long-term results of operations in 605 patients. J
Vasc Surg. 1986;3(3):389–404.
 Acute Lower Extremity Ischemia
Afsha Aurshina and Anil Hingorani
Algorithmic Approach
A. Acute limb ischemia (ALI) must be recog-
nized rapidly in order to limit the skeletal
muscle damage. A comprehensive history is
necessary in order to determine the cause of
thrombosis/embolization. Possible causes
include atrial fibrillation, left ventricular
thrombus, aortic dissection, trauma, hyperco-
agulable state, thrombosis, history of MI,
CHF or possible endocarditis, history of DVT
with patent foramen ovale, or a family history
of thrombosis.
B. Medical therapy for ALI: In all patients, sys-
temic anticoagulation with IV unfractionated
heparin is recommended unless contraindi-
cated, as it limits thrombus propagation. If
history of heparin-induced thrombocytopenia
is suspected, a direct thrombin inhibitor is
recommended.
C. Revascularization using catheter-directed
thrombolysis (CDT) or surgical thromboem-
bolectomy has demonstrated similar limb sal-
vage rates but better survival with CDT [1–5].
A. Aurshina
Department of Vascular Surgery, Vascular Institute
of New York, Brooklyn, NY, USA
A. Hingorani (*)
Division of Vascular Services, NYU Langone
Hospital-Brooklyn, Brooklyn, NY, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_138
138
D. In the setting of profound ischemia >6–8  h,
there is an unlikely potential for limb salvage
(nonviable limb). The risk of multi-organ fail-
ure and cardiovascular collapse is also high
with reperfusion and circulation of ischemic
metabolites. However, if pain can be con-
trolled and there is no evidence of infection,
amputation may be deferred to meet patient
needs.
E. Follow-up schedule: Patient should follow
up at 4–6 weeks, 6 months, and 12 months in
the first year and yearly thereafter. Clinical
evaluation of cardiovascular risk factors,
functional status, adherence to medical ther-
apy and smoking cessation should be reas-
sessed at each subsequent visit. For patients
with revascularization, reassess limb symp-
toms and interval change in functional sta-
tus, pulse examination, and ABI. Change in
ABI >0.15 is clinically significant. Duplex
ultrasound for routine surveillance of
infrainguinal, autogenous vein bypass grafts
or after endovascular revascularization is
recommended.
565
566 A. Aurshina and A. Hingorani

A Definition: Acute (<2 week), severe hypoperfusion of the limb characterized by

features: pain, pallor, pulselessness, poikilothermia, paresthesia and paralysis. (6P’s)

Patient History to assess symptom duration, pain intensity, sensory and motor nerve deficit. Physical exam:
Vascular exam of pulses/ bruit. Assess for signs and symptoms of myonecrosis. Clinical bedside assessment:
arterial and venous exam with hand held Doppler. (Class I)

Audible arterial Inaudible arterial Inaudible arterial

Audible venous Audible venous Inaudible venous

Assess motor Category III: Irreversibly

Category I: Viable limbs3 function non-viable3
Normal sensory/motor function Absent capillary Refill Complete
Intact Capillary Refill Sensory Loss Complete motor
function loss

Category IIa: Category IIb:

Marginally threatened3 Immediately threatened3
Slow to normal capillary Refill Slow to absent capillary Refill
Sensory Loss limited to toes Sensory loss more than toes with D
No motor weakness ischemic rest pain
B Mild/Moderate motor weakness

Anticoagulation first, then Primary amputation (Class I)

revascularization (urgent: Salvageable if treated Salvageable if treated
within 6-24 h), unless promptly emergently
contraindicated (Class I)

Anticoagulation followed by revascularization

(Emergency, within 6 h), unless contraindicated
(Class I)1
C

Revascularization options: Catheter-Directed Thrombolysis (Class I), Percutaneous mechanical

thrombectomy with/without TPA (Class IIa) & Open Surgical Revascularization (Class IIa)4, 5

Monitor and Treat for compartment syndrome after revascularization with fasciotomy for elevated
pressures (Symptoms: Increased pain, muscle tenderness, tense muscle, pain on passive flexion,
nerve Injury)

Follow-up care E

Algorithm 138.1
138  Acute Lower Extremity Ischemia 567

References ACC guideline on the management of patients with

lower extremity peripheral artery disease: a report of
the American College of Cardiology/American Heart
1. Berridge DC, Kessel D, Robertson I.  Surgery ver-
Association Task Force on clinical practice guide-
sus thrombolysis for acute limb ischaemia: ini-
lines. Circulation. 2017;135(12):e726–e79.
tial management. Cochrane Database Syst Rev.
4. Norgren L, Hiatt WR, Dormandy JA, Nehler MR,
2000;4:CD002784.
Harris KA, Fowkes FG.  Inter-society consensus
2. Ouriel K, Veith FJ, Sasahara AA.  Thrombolysis or
for the Management of Peripheral Arterial Disease
peripheral arterial surgery: phase I results. TOPAS
(TASC II). J Vasc Surg. 2007;45(Suppl S):S5–67.
investigators. J Vasc Surg. 1996;23(1):64–73. discus-
5. Rutherford RB, Baker JD, Ernst C, Johnston KW,
sion 4-5.
Porter JM, Ahn S, et  al. Recommended standards
3. Gerhard-Herman MD, Gornik HL, Barrett C, Barshes
for reports dealing with lower extremity ischemia:
NR, Corriere MA, Drachman DE, et al. 2016 AHA/
revised version. J Vasc Surg. 1997;26(3):517–38.
 Chronic Lower Extremity Ischemia
139
Afsha Aurshina and Anil Hingorani

Algorithmic Approach C. The goal of surgical or endovascular revascu-

A. After proper history and physical examina-
tion, the ankle brachial index is the best initial
test to diagnose chronic lower extremity isch-
emia and evaluate the next steps in
management.
B. In patients with chronic limb ischemia, timely
diagnosis and treatment are essential to pre-
serve tissue viability; therefore, invasive
angiography and expeditious revasculariza-
tion are most effective to avoid delay due to
additional noninvasive imaging (Class I rec-
ommendation) [1, 2].
larization should be to provide blood flow
through at least one patent artery, help
decrease ischemic pain, and allow healing of
ulcers while preserving a functional limb and
minimizing tissue loss and need for major
amputation. The decision of open or endovas-
cular procedure is based on a patient-focused
approach after proper cardiovascular risk
assessment [3].

A. Aurshina
Department of Vascular Surgery, Vascular Institute of
New York, Brooklyn, NY, USA
A. Hingorani (*)
Division of Vascular Services, NYU Langone
Hospital-Brooklyn, Brooklyn, NY, USA

© Springer Nature Switzerland AG 2019 569

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_139
570 A. Aurshina and A. Hingorani

Definition: Chronic (>2 week) ischemic rest pain, non-healing wound/ulcers, or

gangrene in 1 or both legs attributable to objectively proven arterial occlusive disease.

History and Physical exam of lower extremity including: Inspection of legs/feet

A for signs of PAD, non-healing wound/ulcer or gangrene.

Initial Test: Ankle Brachial Index

(ABI) (Class I)3

Abnormal ABI: <0.90 Borderline ABI: 0.91–0.99 Non-compressible arteries

Normal ABI: 1.00–1.40 ABI >1.40

Assess for local perfusion

especially if ABI <0.70 Non-healing ulcer or gangrene + Toe Brachial Index
(TBI)

YES NO

Pulse volume Abnormal Normal

recordings (PVR) (TBI <0.7) (TBI >0.7)

B
Abnormal
Normal Search for
alternate diagnosis

Further anatomical
assessment: Endovascular
Cardiovascular revascularization
· Duplex ultrasound risk assessment
· CTA or MRA C
· Invasive angiography
(Class I)
Open procedure

Algorithm 139.1
139  Chronic Lower Extremity Ischemia 571

References 3. Gerhard-Herman MD, Gornik HL, Barrett C, Barshes

NR, Corriere MA, Drachman DE, et al. 2016 AHA/
ACC guideline on the management of patients with
1. Norgren L, Hiatt WR, Dormandy JA, Nehler MR,
lower extremity peripheral artery disease: a report of
Harris KA, Fowkes FG.  Inter-society consensus for
the American College of Cardiology/American Heart
the management of peripheral arterial disease (TASC
Association task force on clinical practice guidelines.
II). J Vasc Surg. 2007;45(Suppl S):S5–67.
Circulation. 2017;135(12):e726–e79.
2. Rutherford RB, Baker JD, Ernst C, Johnston KW,
Porter JM, Ahn S, et  al. Recommended standards
for reports dealing with lower extremity ischemia:
revised version. J Vasc Surg. 1997;26(3):517–38.
 Intermittent Claudication
140
Afsha Aurshina and Anil Hingorani

Algorithmic Approach dorsalis pedis (DP) or posterior tibial (PT) pres-

sure by the higher of the right- or left-arm blood
A. To diagnose patients at increased risk of
pressure for each leg. Segmental blood pressures
peripheral arterial disease (PAD), a proper and Doppler waveforms (pulse volume record-
history and physical exam is necessary. ings) can be used to further localize the anatomi-
Table 1 summarizes the common risk factors cal segments of disease (e.g., aortoiliac,
for PAD (Table 140.1). femoropopliteal, or infrapopliteal) [2, 3].
B. It is essential rule out other causes of lower D. Supervised exercise program for 6  weeks
extremity pain which may mimic claudica- and conservative medical management are
tion. Table  2 summarizes the differential the first steps in management. However, if
diagnosis for leg pain/claudication [1] claudication persists, consider revascular-
(Table 140.2). ization [4].
C. Ankle-brachial index (ABI) is the best initial test
and is calculated by dividing the higher of the
Table 140.2  Differential diagnosis for leg pain/claudica-
tion (Non-PAD related with normal ABI)
Symptomatic Increases with Present at rest
Table 140.1  Patient at increased risk for PAD Bakers cyst exercise
Age >65 years Venous Increases after Subsides
Claudication walking slowly,
Age 50–64 years with Risk Factors for atherosclerosis
improves with
(DM, HTN, smoking, hyperlipidemia, family Hx of
elevation
PAD)
Chronic After much Subsides very
Age <50 years with DM and one additional RF for
Compartment exercise (Jogging) slowly
atherosclerosis
Syndrome
Individual with known atherosclerotic disease
Spinal Stenosis Mimics Variable, relief
(Coronary, Carotid, renal, Mesenteric, AAA)
claudication; by spinal
onset with flexion
variable distance
Nerve Root Induced by Present at rest,
A. Aurshina Compression sitting, standing improved by
Department of Vascular Surgery, Vascular Institute of or walking change in
New York, Brooklyn, NY, USA position
A. Hingorani (*) Hip/ Foot/Ankle After variable Improves
Division of Vascular Services, NYU Langone Arthritis degree of exercise when
Hospital-Brooklyn, Brooklyn, NY, USA non-weight
bearing

© Springer Nature Switzerland AG 2019 573

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_140
574 A. Aurshina and A. Hingorani

Definition: Pain or cramping of vascular origin in the muscles of lower extremity that is
induced by walking consistently at fixed distance & relieved by rest (within 10 minutes)
A

A thorough lower extremity vascular examination including:

· Inspection of legs/feet for signs of peripheral artery disease
· Assessment of LE pulse: DP, PT, Fem, Pop – Abnormal/Absent
B

Initial Test: Resting Ankle Brachial Index (ABI) with or without segmental
pressures and waveforms (Grade IA recommendation)2, 4
· <0.90: Diagnostic for PAD
· 0.91–0.99: Borderline C
· 1–1.4: Normal. No further testing needed.
· >1.4: Non-compressible likely due to arterial calcification

IF PAD+: ABI <0.90 If borderline/normal If ABI>1.4: non-

in suspected PAD compressible artery
Noninvasive BP in both arms patients:
to rule out subclavian artery Exercise Treadmill
stenosis/ UE PAD. ABI

Toe Brachial Index TBI >0.7, Search

Exercise Treadmill ABI or (TBI) <0.7 is for alternative
Symptoms not diagnostic of PAD diagnosis
6 minute walk test very suggestive
of PAD

Supervised Exercise Search for

Program (SEP) for 6 alternative
weeks. diagnosis
D

Medical Management:
Cilostazol
Antiplatelet drugs Anatomic Assessment (Class I):
Statin therapy If claudication persistent
Duplex Ultrasound with SEP, consider
CTA/MRA based on availability revascularization
(Grade 1B)2
No response to conservative
management Invasive Angiography (Class II)

Algorithm 140.1
140  Intermittent Claudication 575

References asymptomatic disease and claudication. J Vasc Surg.

61(3):2S–41S.e1.
3. Shishehbor MH, Hammad TA, Zeller T, Baumgartner
1. Gerhard-Herman MD, Gornik HL, Barrett C, Barshes
I, Scheinert D, Rocha-Singh KJ.  An analysis of
NR, Corriere MA, Drachman DE, et al. 2016 AHA/
IN.PACT DEEP randomized trial on the limitations of
ACC guideline on the management of patients with
the societal guidelines-recommended hemodynamic
lower extremity peripheral artery disease: a report of
parameters to diagnose critical limb ischemia. J Vasc
the American College of Cardiology/American Heart
Surg. 2016;63(5):1311–7.
Association Task Force on clinical practice guide-
4. Gerhard-Herman MD, Gornik HL, Barrett C, Barshes
lines. Circulation. 2017;135(12):e726–e79.
NR, Corriere MA, Drachman DE, et al. 2016. AHA/
2. Conte MS, Pomposelli FB, Clair DG, Geraghty PJ,
ACC guideline on the management of patients with
McKinsey JF, Mills JL, et  al. Society for vascular
lower extremity peripheral artery disease: executive
surgery practice guidelines for atherosclerotic occlu-
summary. Vasc Med. 2017;22(3):Np1–np43.
sive disease of the lower extremities: management of
 Acute Deep Venous Thrombosis
Afsha Aurshina and Anil Hingorani
Algorithmic Approach
A. The first step in the evaluation of acute deep
vein thrombosis (DVT) is a proper history and
physical examination. The Modified Wells
score (Table 141.1) should be used to evaluate
the risk and next step in management.
B. Unprovoked DVT is defined as no idenfiable
provoking event for DVT. In contrast, provoked
DVT is due to a known risk factor. The tran-
sient major risk factors include major surgery,
hospitalization, or immobility >3 days. Minor
risk factors include minor surgical procedures,
pregnancy, or estrogen therapy. Persistent risk
factors include reversible risk factors (malig-
nancy or inflammatory bowel disease) and irre-
versible risk factors (inherited thrombophilia,
CHF, and metastatic cancer) [2].
C. Proximal DVT has higher risk of complica-
tion and includes thrombus in popliteal,
­femoral, or iliac veins. Isolated distal DVT is
confined to the calf veins.
D. Anticoagulation is the mainstay treatment of
choice for acute DVT with the primary objec-
tive of prevention of further thrombosis and
A. Aurshina
Department of Vascular Surgery, Vascular Institute of
New York, Brooklyn, NY, USA
A. Hingorani (*)
Division of Vascular Services, NYU Langone
Hospital-Brooklyn, Brooklyn, NY, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_141
141
early/late complications including extension,
pulmonary embolism, major bleeding, and
death. Late complications include recurrent
clot and post-thrombotic syndrome [3].
Assess for bleeding risk and hepatic/renal
insufficiency especially with use of direct
oral anticoagulants (DOACs).
E. Patients with phlegmasia cerulea dolens (ilio-
femoral DVT) should be considered for more
aggressive management, usually catheter-­
directed thrombolysis and/or surgical or
mechanical thrombectomy. Intravenous (IV)
unfractionated heparin should be initiated
early with no delay prior to procedure [4].
Table 141.1  Modified wells criteria [1]
Active cancer 1
Bedridden recently >3 days or major surgery 1
within 4 weeks
Calf swelling >3 cm compared to the other leg 1
Measured 10 cm below tibial tuberosity 1
Collateral (nonvaricose) superficial veins present 1
Entire leg swollen 1
Localized tenderness along the deep venous 1
system
Pitting edema, confined to symptomatic leg 1
Paralysis, paresis, or immobilization of the lower 1
extremity
Previously documented DVT 1
Alternative diagnosis to DVT as likely or more −2
likely
Score of 0 or less, DVT is unlikely
Score or 1–2, risk of DVT is moderate
Score of >2, risk of DVT is likely
577
578 A. Aurshina and A. Hingorani

Patient presents with signs and symptoms of acute DVT: pain, swelling, tenderness,
inflammatory signs of warmth and redness

Excluding other causes

A based on H&P

Clinical suspicion of DVT

B Determine Pretest probability using Modified Wells Score1

Assess for known risk factors of DVT

Low Intermediate or High

Perform D-Dimer assay Perform compression ultrasonography

Negative Positive Negative Positive

DVT excluded Perform compression DVT excluded DVT confirmed
ultrasonography
C

Contraindication to anticoagulation? Proximal DVT Distal DVT

Yes No contraindication High risk Low risk /

D contraindicated
anticoagulation

Phlegmasia No phlegmasia No contraindication

IVC filter cerulea dolens to anticoagulation
cerulean dolens
Retrievable or
Permanent filter; follow OBSERVE, repeat
for 3-6 months with proximal compressive
anticoagulation when Consider ultrasound in 1–2
Initial Anticoagulation weeks
contraindication resolves thrombolytics or Heparin/Warfarin or
thrombectomy LMWH for 3–6 months
Alternative: DOAC3

E
DVT extension Stable, no
Consider long-term Provoked DVT into or towards extension,
Unprovoked proximal DVT/ with identified continue
indefinite anticoagulation the proximal
Recurrent DVT/ Persistent DVT risk factors: STOP surveillance
Follow-up with risk- veins, patient
benefit assessment anticoagulation at risk of
after 3–6 months extension

Algorithm 141.1
141  Acute Deep Venous Thrombosis 579

References 3. Kearon C, Akl EA, Ornelas J, Blaivas A, Jimenez

D, Bounameaux H, et al. Antithrombotic therapy for
VTE Disease: CHEST guideline and expert panel
1. Wells PS, Anderson DR, Rodger M, Forgie M, Kearon
report. Chest. 2016;149(2):315–52.
C, Dreyer J, et al. Evaluation of D-dimer in the diag-
4. Meissner MH, Gloviczki P, Comerota AJ, Dalsing
nosis of suspected deep-vein thrombosis. N Engl J
MC, Eklof BG, Gillespie DL, et  al. Early thrombus
Med. 2003;349(13):1227–35.
removal strategies for acute deep venous thrombosis:
2. Kearon C, Ageno W, Cannegieter SC, Cosmi B,
clinical practice guidelines of the Society for Vascular
Geersing GJ, Kyrle PA. Categorization of patients as
Surgery and the American Venous Forum. J Vasc
having provoked or unprovoked venous thromboem-
Surg. 2012;55(5):1449–62.
bolism: guidance from the SSC of ISTH.  J Thromb
Haemost. 2016;14(7):1480–3.
 Management of Acute Mesenteric
Ischemia
Josh Radtka
Algorithmic Approach
A. The first step in the management of a patient
with acute mesenteric ischemia is the history
D. An emergent operative intervention will be
and physical exam. The diagnosis of acute
mesenteric ischemia requires a high index of
suspicion. These patients usually develop
sudden onset of acute abdominal pain. The
physical exam is classically characterized by
abdominal pain that is more severe than
would be expected; however, this classic
description of abdominal pain may be absent
in 20–25% of individuals [1]. The patients
can have leukocytosis or an elevated lactic
acid level. The prompt diagnosis of this con-
dition is important as there is only a 30% sur-
vival rate when the diagnosis is delayed more
than 24 h [2].
B. When acute mesenteric ischemia is suspected,
the first test that should be performed is a
computed tomography angiogram (CTA) of
the abdomen and pelvis. This is a rapid study
that can provide information regarding the
diagnosis and cause of acute mesenteric isch-
emia, as well as the viability of the bowel [2].
C. The etiology of the patient’s symptoms could
be secondary to NOMI, or another source, if
the CTA fails to show evidence of an arterial
J. Radtka ()
Division of Vascular Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: jradtka@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_142
142
occlusion. NOMI occurs in 20% of cases and
is typically due to a low flow start due to
shock or vascocontstrictors [3].
required if the CTA demonstrates an arterial
occlusion. The patient should receive intrave-
nous fluids, antibiotics, and a heparin drip.
Restoration of blood flow should be attempted
by an embolectomy/thrombectomy of the SMA.
E. If an embolectomy is unsuccessful, the patient
may require an open bypass. This can be per-
formed in a retrograde fashion originating
from either the aorta or iliac artery. Another
option would be retrograde stenting of the
superior mesenteric artery (SMA) occlusion
through the previous embolectomy incision.
F. Once arterial flow has been restored, any non-­
viable bowel should be resected. The patient’s
abdomen should be left open and transported
to the ICU for further resuscitation. In
24–48 h after the initial procedure, the patient
should return to the operating room for a re-­
exploration. At this time, any non-viable
bowel should be removed. Once all non-­
viable bowels have been resected, the abdo-
men can be closed. An echocardiogram with
agitated saline and a CTA of the chest should
be performed to determine a potential source
of the vascular occlusion if an embolism is
believed to be the source of the acute mesen-
teric ischemia.
581
582 J. Radtka

History:
Sudden onset of severe diffuse abdominal pain

A
Obtain vital signs, blood work, perform a physical exam,

Vital Signs: May demonstrate fever, tachycardia, hypotension

Labs: May demonstrate leukocytosis and elevated lactic acid
PE: Abdominal pain that is more severe then would be expected

No arterial
CTA of occlusion, possible C
B Abdomen and NOMI, or another
Pelvis diagnosis

Arterial occlusion
D Start heparin drip, ABX, IVF, Exploratory Laparotomy
SMA embolectomy/thrombectomy

Arterial Flow
Restored?

No

E Bypass or Retrograde Yes

stenting

F Bowel Resection and Second look

Laparotomy

Follow-up Care: Echo with agitated saline;

and CTA of the chest

Algorithm 142.1
142  Management of Acute Mesenteric Ischemia 583

References 3. Cheng CC, Choi L, Cheema Z, Silva MB Jr. Acute

mesenteric ischemia. Current surgical therapy. In:
Cameron JL, Cameron AM, editors. Current surgi-
1. Jimenez, Quinones-Baldrich. Mesenteric vascular dis-
cal therapy. 11th ed. Philadelphia: Elsevier; 2014.
ease: general considerations. In: Cronenwett J, editor.
p. 939–46.
Rutherford’s vascular surgery. Philadelphia: Elsevier;
2010. p. 2260–1.
2. Wyers. Mesenteric vascular disease: acute ischemia.
In: Cronenwett J, editor. Rutherford’s vascular sur-
gery. Philadelphia: Elsevier; 2010. p. 2292–4.
 Management of Chronic
Mesenteric Ischemia
Josh Radtka
Algorithmic Approach
A. The first step in the management of a patient
with chronic mesenteric ischemia is the his-
tory and physical exam. The classic descrip-
tion of a patient with chronic mesenteric
ischemia is mid-epigastric abdominal pain
15–45 min after a meal due to the inability of
the vascular supply to meet metabolic
demands of the visceral organs [1]. The
underlying etiology of this inadequate blood
supply is arterial stenosis of the mesenteric
vessels. These patients tend to experience a
significant weight loss and present with a
cachectic appearance. Weight loss is typically
due to “food fear” or an avoidance of eating
in order to limit their postprandial abdominal
pain. Similar to arterial occlusive disease
patients, a history of smoking is common.
Although these patients tend to have abdomi-
nal pain, they do not usually have peritoneal
signs. A mid-epigastric bruit may be
appreciated.
B. The majority of these chronic mesenteric
ischemia (CMI) patients are initially referred
to a gastroenterologist. Patients commonly
undergo an extensive work-up which may
include x-rays, computed tomography (CT)
J. Radtka (*)
Division of Vascular Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: jradtka@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_143
143
scans, and endoscopies. If another diagnosis
is suspected, it should be investigated and
treated prior to the treatment of CMI.
C. After ruling out other possible etiologies, the
patient should be evaluated for chronic mes-
enteric ischemia. The diagnosis of CMI
requires that two of the three mesenteric ves-
sels have severe stenosis or occlusion and one
of these vessels needs to be the superior mes-
enteric artery. The work-up begins with a
duplex of the mesenteric arteries. This modal-
ity has minimal patient risk and provides
dynamic information about the degree of ste-
nosis within the mesenteric vessels. Bowel
gas and patient body habitus may obscure the
visualization of the vessels. A computed
tomography angiogram (CTA) of the abdo-
men and pelvis provides anatomic informa-
tion about the extent and degree of stenosis in
the mesenteric vessels. The gold standard
method of diagnosis is an aortogram. Though
an aortogram is invasive, it allows for imme-
diate therapeutic intervention.
D. After the diagnosis of chronic mesenteric
ischemia has been made, the treatment
options are either an endovascular interven-
tion or an open bypass. Medical management
is not successful as it does not treat the under-
lying etiology. The stenosis of the mesenteric
arteries occurs most commonly at the orifice
of the artery. This allows for the endovascular
stenting of the origins of the celiac and
585
586 J. Radtka

s­uperior mesenteric arteries as a possible in many institutions. Open bypass options

treatment option. A balloon expandable stent include an antegrade aorto-mesenteric, a ret-
is often utilized during endovascular treat- rograde aorto-mesenteric, or an ileo-mesen-
ments. Currently, endovascular techniques teric artery bypass [2].
for revascularization are the first-line therapy

History:
A Patients typically present with complaints of abdominal pain
30 minutes after meals, food fear, and weight loss

Obtain Vital Signs, blood work, and perform a

physical exam

Due to chronicity, vital signs are often normal

PE: Patient with diffuse mild abdominal pain and mid-epigastric
bruit Patient is Cachectic

Positive
B Standard GI Treat Other
Workup Pathology

Negative

Evaluate for Negative

C Continue to evaluate
Mesenteric
for other etiologies
Stenosis

Positive

D Revascularization Procedure:
Endovascular or Open

Algorithm 143.1
143  Management of Chronic Mesenteric Ischemia 587

References 2. Schwartz, et al. Diagnosis and surgical management

of the visceral ischemic syndromes. In: Moore W, edi-
tor. Vascular and endovascular surgery. Philadelphia:
1. Huber, Lee. Mesenteric vascular disease: chronic isch-
Elsevier; 2013. p. 423–35.
emia. In: Cronenwett J, editor. Rutherford’s vascular
surgery. Philadelphia: Elsevier; 2010. p. 2274–5.
 Thoracic Outlet Syndrome
Tarik Z. Ali and Josh Radtka
Algorithmic Approach
A. Thoracic outlet syndrome (TOS) is a constel-
lation of upper extremity symptoms resulting
from compression of the brachial plexus, sub-
clavian artery, and subclavian vein as they
pass between the clavicle and the first rib. The
majority of patients are between 20 and
50  years of age and about 70% are females
[1]. There are three types of TOS: neurogenic,
arterial, and venous. The history and physical
exam are important in differentiating the dif-
ferent types of thoracic outlet syndromes.
Neurogenic is the most common type and is
usually a diagnosis of exclusion. Common
symptoms are pain, paresthesia, and weak-
ness in the affected extremity without local-
ization to a particular nerve distribution [2].
Arterial TOS occurs when compression of the
subclavian artery creates an aneurysm distal
to the site of compression. This could cause
embolization distally, leading to ischemic
symptoms. Venous TOS or Paget-von
Schrotter syndrome occurs when repetitive
movement in the compressed vein results in
endothelial damage and can lead to subcla-
vian and axillary vein thrombosis. This leads
to swelling, pain, and possible cyanosis.
T. Z. Ali · J. Radtka (*)
Division of Vascular Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: jradtka@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_144
144
B. In order to determine if the extremity swell-
ing is secondary to venous thrombosis, a
venous duplex should be performed. If there
is no thrombus present, then an alternative
diagnosis for the upper extremity swelling
should be sought. A chest X-ray should be
obtained to determine if cervical ribs or
anomalous first ribs are present. If the patient
is suspected to have neurogenic TOS, the
Adson test, elevated arm stress test, or the
Elvey test are maneuvers that may be helpful
in establishing a diagnosis.
C. If a subclavian-axillary vein thrombosis is
discovered, patient should be considered for
pharmaco-mechanical thrombolysis. Long-­
term anticoagulation alone has been associ-
ated with significant disability [3]. Prior to
thrombolytic therapy, the patient’s history
should be reviewed to ensure that there are no
any absolute contraindications to treatment.
After successful thrombolysis, definitive
treatment includes venous stent placement in
the offending vessel.
D. Once the thrombus is removed and the venous
narrowing is identified, extrinsic compression
needs to be corrected with a first rib resection.
The timing of this intervention is controver-
sial and has been recommended to occur from
immediate to 3 months post thrombolysis [3].
After the first rib is removed, venous stenosis
requires treatment with either open or endo-
vascular methods.
589
590 T. Z. Ali and J. Radtka

History:
The presentation can be variable based on the type of TOS. Neurogenic symptoms may be
chronic while the vascular symptoms may be acute.

Obtain vital signs, perform a physical exam

A

Physical Exam
Findings

Pain without vascular

Embolic/Ischemic Event Arm Swelling
compromise

CXR
B Arterial and Venous Duplex
Arterial Duplex,
Venous Duplex of RUE
CT Angiogram
MRI

Thrombolysis of
C Physical Therapy Revascularization Axillary and
Subclavian Veins

D First Rib Resection First Rib Resection

First Rib Resection Possible Arterial Possible Venous
Reconstruction Reconstruction

Follow-up Care

Algorithm 144.1
144  Thoracic Outlet Syndrome 591

References 2. Thompson, Driskill. Thoracic outlet syndrome: neuro-

genic. In: Cronenwett J, editor. Rutherford’s vascular
surgery. Philadelphia: Elsevier; 2010. p. 1878–98.

1. Sanders. Thoracic outlet syndrome: general con-
3. Schanzer, Messina. Thoracic outlet syndrome: general
siderations. In: Cronenwett J, editor. Rutherford’s
considerations. In: Cronenwett J, editor. Rutherford’s
vascular surgery. Philadelphia: Elsevier; 2010.
vascular surgery. Philadelphia: Elsevier; 2010.
p. 1865–77.
p. 1907–17.
 AV Shunt Complications
Josh Radtka
Algorithmic Approach
A. It is important to take a good history and
physical exam in a patient with an arterial
venous (AV) shunt problem. Vital informa-
tion includes the following: is the access a
fistula or graft, when it was created, when
was the last dialysis session, and if any prob-
lems were occurring with the access (i.e., par-
esthesia in the digits could represent steal,
and a prolonged time prior to hemostasis after
dialysis could represent venous stenosis).
During the physical exam, it is important to
assess the access for a thrill and a bruit. A
vascular exam of the affected extremity
should also be performed. If you are unable to
determine if the access is patent, a duplex
should be obtained.
B. Blood work should be obtained and include a
basic metabolic panel and a complete blood
count. It is important to determine if the
patient requires emergent dialysis prior to any
intervention on the dialysis access. Common
reasons to perform emergent dialysis are ure-
mia, fluid overload, acidosis, and
hyperkalemia.
C. If the patient requires hemodialysis and the
access is occluded, then a temporary hemodi-
J. Radtka ()
Division of Vascular Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: jradtka@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_145
145
alysis catheter should be placed preferentially
in the right internal jugular vein [1]. Following
hemodialysis the occluded dialysis access
should be de-clotted.
D. The occluded dialysis access should be de-­
clotted with either open or endovascular sur-
gical techniques [2].
E. Following a successful procedure to re-­
establish blood flow through the access, it is
important to evaluate the access for the cause
of failure. This can be performed best with a
fistulagram. This procedure will be both diag-
nostic and therapeutic. It will allow for treat-
ment of common causes of dialysis access
occlusion such as arterial anastomotic steno-
sis, venous anastomotic stenosis, and central
vein stenosis. After the cause of failure is dis-
covered and corrected, the access can again
be used for dialysis.
F. If the dialysis access cannot be de-clotted,
then a long-term dialysis catheter should be
placed. This catheter should be placed prefer-
entially in the right internal jugular vein. The
patient will then require a work-up for place-
ment of a new hemodialysis access. This may
require ultrasound-guided vein mapping or
moving the site of access creation to another
extremity.
593
594 J. Radtka

History:
A Patient had dialysis 1 day ago through a left AV Graft, which
now no longer has a thrill

Obtain Vital Signs, blood work, perform

a physical exam,

PE: No Thrill in Graft on exam.

Is emergent
B hemodialysis
required?
Yes

C Place Temporary Dialysis

No
Catheter

Surgical intervention to
D restore blood flow to
access successful?

Yes No

Evaluate for cause of failure Place a permanent catheter

E Evaluate for other permanent F
Use for Hemodialysis
dialysis options

Algorithm 145.1

2. Meier G.  Hemodialysis access: failing and throm-
References bosed. In: Cronenwett J, editor. Rutherford’s vascular
surgery. Philadelphia: Elsevier; 2010. p. 1132–6.
1. Macasta, Sidawy. Hemodialysis access: general con-
siderations. In: Cronenwett J, editor. Rutherford’s vas-
cular surgery. Philadelphia: Elsevier; 2010. p. 1105–6.
 Part XVIII
Genitourinary
 Management of the Renal Mass
146
J. Chris Riney, Neil J. Kocher, and Matthew Kaag

Algorithmic Approach tain internal septa, solid components, or cal-

A. A history and physical examination is the ini-
tial step in renal mass evaluation. Patients
may exhibit nonspecific symptoms including
gross or microscopic hematuria, flank pain,
weight loss, fever, or diaphoresis. Physical
signs are uncommon but may include hyper-
tension, palpable flank mass, and/or ipsilat-
eral varicocele. The majority of renal masses D. The differential diagnosis for a solid renal
(up to 70%) are incidental findings and other-
wise asymptomatic [1].
B. Dedicated imaging is necessary to further
characterize the renal mass as cystic or solid.
A three-phase abdominal computed tomogra-
phy (CT) scan with/without intravenous (IV)
contrast (“renal mass protocol”) is considered
the gold standard cross-sectional study.
Abdominal magnetic resonance imaging
(MRI) with gadolinium and ultrasonography
are additional imaging modalities for renal
mass characterization [2].
C. The Bosniak classification system defines
cystic renal masses based on their contrast-­
enhanced CT imaging characteristics. Simple E. If RCC is suspected after imaging, obtain
renal cysts (Bosniak I) do not enhance or con-
J. Chris Riney and Neil J. Kocher contributed equally to metastases. Additional studies include a
this work.
J. C. Riney · N. J. Kocher · M. Kaag (*)
Division of Urology, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: mkaag@pennstatehealth.psu.edu
cifications. Bosniak I and II cysts are benign
and do not require follow-up. Increasingly
complex features are useful in predicting risk
of malignancy. Management strategies for
more complex cysts are based on AUA guide-
lines which recommend routine surveillance
(Bosniak IIF) versus surgical resection
(Bosniak III and IV) [3].
mass includes malignant and non-malignant
entities. Macroscopic fat (HU –20 to −80) is
virtually diagnostic for angiomyolipoma
(AML). Asymptomatic patients with small
(<4  cm) AML are monitored with serial
imaging. The risk of spontaneous rupture
increases with AML size >4 cm. Significant
active bleeding necessitates embolization or
open surgical control for life-threatening
hemorrhage [4]. Renal mass biopsy should be
considered when a mass is suspected to be
metastatic [5]. Enhancing solid renal masses
are usually malignant and most commonly
renal cell carcinoma (RCC).
CBC, CMP, and UA. Chest imaging (CXR or
CT) is performed to rule out pulmonary
nuclear medicine bone scan and/or brain MRI
if patients present with bone pain or neuro-
logic symptoms, respectively [6].

© Springer Nature Switzerland AG 2019 597

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_146
598 J. C. Riney et al.

F. Treatment of suspected RCC is based on nephrectomy. Select medium-sized masses

tumor size, location, and characteristics.
Other considerations include patient’s age,
comorbidities, presence of lymphadenopathy,
venous tumor thrombus, and invasiveness of
tumor. Small renal masses are managed with
active surveillance, ablation, or partial
(T1b 4–7  cm) amenable to nephron-sparing
surgery are managed with partial nephrec-
tomy. Large tumors are managed with radical
nephrectomy [5]. Locally advanced tumors
may invade the vena cava and require cavot-
omy and reconstruction.

Perform focused history and physical exam

A · Nonspecific symptoms
· Physical signs uncommon

Obtain 3-phase abdominal CT scan with/without IV

B contrast (“renal mass protocol”)

C Cystic D Solid

Bosniak I or II Bosniak IIF Bosniak III or IV Enhancing Concern for Fat present
>15HU metastasis or
lymphoma

No follow-up Surveillance Surgical

AML
necessary imaging removal
Consider
biopsy

Obtain CBC, CMP, and UA.

Imaging: CXR or CT chest, bone scan if pathologic fracture or bone pain, elevated calcium
or alkaline phosphatase; MRI of brain if neurologic signs/symptoms; biopsy in select patients

Small renal mass

F 4 cm(T1a) Select T1b (4-7cm) Large mass or not amendable
to nephron sparing

Active Partial Radical

Ablation Nephrectomy
Surveillance Nephrectomy

Algorithm 146.1
146  Management of the Renal Mass 599

References 4. Nelson CP, Sanda M.  Contemporary diagnosis and

management of renal angiomyolipoma. J Urol.
2002;168:1315.
1. Chen DY, Uzzo RG. Evaluation and management of the
5. National Comprehensive Cancer Network (NCCN)
renal mass. Med Clin North Am. 2011;95(1):179–89.
clinical practice guidelines in oncology: kidney can-
2. Kang SK, Chandarana H. Contemporary imaging of
cer. V.1.2018, 2018. www.nccn.org.
the renal mass. Urol Clin North Am. 2012;39:161–70.
6. Campbell S, Uzzo RG, Allaf ME, et  al. Renal mass
3. Israel GM, Bosniak MA.  An update of the
and localized renal cancer: AUA guideline. J Urol.
Bosniak renal cyst classification system. Urology.
2017 Sep;198(3):520–9.
2005;66(3):484.
 Prostate Cancer
Rosa Park and Matthew Kaag
Algorithmic Approach
A. Prostate cancer is the most common malig-
nancy in US males after skin cancer, but the
mortality rate in this usually unaggressive
cancer is low [1]. Most patients present with-
out symptoms, and the question of appropri-
ate screening is addressed below. Patients
with locally advanced disease complain of
obstructive or irritative voiding symptoms
and hematuria. Metastatic prostate cancer
may manifest as hydronephrosis or bone pain.
Pathologic fractures are possible [2].
B. Screening of asymptomatic men was preva-
lent in the United States until 2012 and con-
sists of a prostate-specific antigen (PSA)
blood test and digital rectal exam (DRE). In
2012 the US Preventative Services Task Force
(USPSTF) identified a lack of data support-
ing prostate cancer screening, driven by the
historic over-treatment of men with low-risk
disease who were unlikely to die of their can-
cer regardless of therapy [3]. Prostate cancer
screening was given a D grade, with the
USPSTF recommending against its use.
C. The American Urological Association revised
recommendations include narrowing the age
range for screening to men 55–69, unless the
R. Park · M. Kaag (*)
Division of Urology, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: mkaag@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_147
147
patient is at higher risk due to positive family
history or African American descent. Patients
over the age of 70 or with less than 10-year
life expectancy should not be screened.
Recommendations also include an increased
interval between screening visits (2  years)
and involving the patient in shared decision-­
making when deciding whether to embark on
screening [4].
D. In most cases an abnormal DRE will prompt
a prostate needle biopsy. PSA is assessed
based on temporal trends and normal ranges
that are dependent on the patient’s age.
Normal fluctuation as well as inflammation
and local trauma may increase the PSA in the
absence of malignancy, and an isolated ele-
vated level should prompt a repeat test [5].
E. Definitive diagnosis of prostate cancer is via
transrectal ultrasound-guided prostate needle
biopsy. Typically, a single dose of fluoroqui-
nolone antibiotic prophylaxis is recom-
mended at least 1  h prior to biopsy. Rectal
cultures can be obtained prior to biopsy in
patients with increased risk of resistant bacte-
ria. Expected sequelae include gross hematu-
ria, hematochezia, and hematospermia. Risk
of sepsis is 0.3–3.1%, and the risk of post-­
biopsy urinary retention is 0.2–2.6% [6].
F. If there is cancer present on biopsy, staging
work-up may be indicated. Obtain a bone
scan for Gleason score ≥8, PSA >20 ng/mL,
T2 and PSA >10 ng/mL, and clinical T3 and
601
602
T4 or if symptomatic. Pelvic CT or MRI is
considered for T3 and T4 disease, or T1–T2 if
nomogram indicates >10% lymph node
involvement [7].
G. Risk stratification of clinically localized
disease guides therapy. Patients deemed to
be at low risk (low volume of cancer on
biopsy, low-grade disease, low PSA) may
be offered active surveillance using one of a
number of accepted protocols. Patients
desiring active treatment and those at high
R. Park and M. Kaag
risk of progression may be offered radical
prostatectomy or radiotherapy. Androgen
deprivation therapy may be combined with
radiation to increase survival rates in men
with intermediate- or high-risk disease.
Patients with disseminated disease are man-
aged via a therapeutic algorithm that is
structured around depriving tumor cells of
their androgen source but also may include
immunotherapy and conventional chemo-
therapy [7].
147  Prostate Cancer 603

History and physical exam:

· Most are asymptomatic
A · Family History
· Perform DRE

Normal DRE Abnormal DRE

B
Does the patient meet PSA
based screening criteria?

D No Yes Check PSA

Normal PSA Elevated PSA

No further work-up
C Follow up as indicated
May repeat PSA

E Prostate needle biopsy

No further work-up
Repeat DRE and Normal biopsy Prostate cancer
PSA as appropriate

F Imaging by risk category: MRI pelvis, CT, or bone scan

Metastatic
G Clinically localized disease Regional disease
disease

Active Radical prostatectomy ± Androgen

Radiation Refer to oncology
surveillance pelvic lymph node deprivation
dissection

Algorithm 147.1
604 R. Park and M. Kaag

References 5. Eastham JA, Riedel E, Scardino PT, Shike M, Fleisher

M, Schatzkin A, Lanza E, Latkany L, Begg CB, Polyp
Prevention Trial Study Group. Variation of serum
1. Siegel RL, Miller KD, Jemal A.  Cancer statistics,
prostate-specific antigen levels: an evaluation of year-­
2015. CA Cancer J Clin. 2015;65(1):5–29.
to-­year fluctuations. JAMA. 2003;289(20):2695–700.
2. Loeb S, Eastham JA. Chapter 111, Diagnosis and stag-
6. Liss MA, Ehdaie B, Loeb S, Meng MV, Raman JD,
ing of prostate cancer. In: Campbell-Walsh urology.
Spears V, Stroup SP.  An update of the American
11th ed. Philadelphia: Elsevier; 2016. p. 2601–8.
Urological Association White Paper on the pre-
3. Moyer VA, U.S.  Preventive Services Task Force.
vention and treatment of the more common com-
Screening for prostate cancer: U.S. preventive services
plications related to prostate biopsy. J Urol. 2017
task force recommendation statement. Ann Intern
Aug;198(2):329–34.
Med. 2012;157(2):120–34.
7. National Comprehensive Cancer Network, Inc.
4. Carter HB, Albertsen PC, Barry MJ, Etzioni R,
NCCN clinic practice guidelines in oncology: pros-
Freedland SJ, Greene KL, Holmberg L, Kantoff
tate cancer. Version 1.2018. [Internet]. 2018. [cited
P, Konety BR, Murad MH, Penson DF, Zietman
2018 Feb 14]. Available from: https://www.nccn.org/
AL.  Early detection of prostate cancer: AUA guide-
professionals/physician_gls/pdf/prostate.pdf.
line. J Urol. 2013;190(2):419–26.
 Management of Scrotal/Testicular
Mass
Brian M. Blair and Matthew Kaag
Algorithmic Approach
A. Initial evaluation of a scrotal or testicular
mass requires a thorough history and focused
physical examination, including genital,
abdominal, lymph node, breast, and neuro-
logical exams. The examiner should attempt
to distinguish intratesticular from paratesticu-
lar lesions. The causes of scrotal masses may
be classified as follows: benign/malignant,
infectious/noninfectious, and emergent/non-
emergent. Consultation of a urologist is often
necessary [1].
B. Scrotal ultrasound should be obtained early to
confirm diagnosis. The urgency in which to
obtain the ultrasound will be determined
upon the patient presentation and suspected
diagnosis [2].
C. Testicular torsion results when the testicle
twists on its blood supply causing loss of
blood flow to the testicle. The testicle may be
enlarged or present in an abnormal position.
Exam findings include abnormal testicular
lie, loss of cremasteric reflex, swelling/edema
with exquisite tenderness, and Prehn sign. It
is accompanied by acute, severe pain with
nausea/vomiting. Incidence is distributed in a
bimodal fashion with torsion seen most com-
B. M. Blair · M. Kaag (*)
Division of Urology, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: mkaag@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_148
148
monly in the neonatal period and at puberty.
Cryptorchidism is a predisposing factor.
Testicular torsion is a urologic emergency as
testicular loss can occur if blood flow is not
restored within 6  h. Immediate surgical
exploration with detorsion of the testicle and
fixation via orchiopexy is required [3].
D. Trauma to the scrotum/testicle is a common
cause of testicular enlargement or irregular-
ity. A scrotal mass may be noted, secondary
to hematoma. Penetrating injury of the scro-
tum requires surgical exploration and repair.
Blunt scrotal trauma may result in rupture of
the tunica albuginea, requiring prompt surgi-
cal repair. Eighty to ninety percent of testicles
are salvaged when surgery is performed
within 72 h of injury, whereas only 32–45%
are salvageable after 72 h [1].
E. Epididymo-orchitis is an infectious/inflam-
matory cause for testicular mass that may
involve outpatient management with NSAIDs
± oral antibiotics. However if significant
infection is present, admission to the hospital
may be required for intravenous (IV) antibi-
otics ± surgical drainage/orchiectomy if
abscess develops.
F. Benign cystic masses of the epididymis or
spermatic cord include spermatocele, epidid-
ymal head cyst, and varicocele. These entities
are classified as paratesticular and are gener-
ally benign. Observation is usually appropri-
ate unless symptomatic. Varicoceles may be
605
606
associated with infertility, prompting repair.
While left-sided varicoceles are fairly com-
mon, right-sided varicoceles are rare and may
indicate the presence of a mass compressing
the gonadal vein. CT of the abdomen/pelvis is
warranted in this setting [4]. Paratesticular
sarcomas may be mistaken for one of these
benign cystic entities on palpation but are
solid on ultrasound and very rare.
G. A solid testicular mass on exam is concerning
for testicular neoplasm. These are often painless
but may be painful if infarcted. Testicular ultra-
sound demonstrates a hypoechoic vascular
intratesticular lesion. Obtain testicular tumor
markers including α-fetoprotein, quantitative
β-human chorionic gonadotropin, and lactate
dehydrogenase. Additional labs to include are a
CBC, BMP, LFTs, and a PT/INR. Sperm bank-
ing should be discussed. Metastatic work-up
must be obtained and should include a CT of the
abdomen/pelvis with IV and oral contrast and a
chest X-ray. In patients at higher risk of pulmo-
nary metastasis, a chest CT is warranted [5].
B. M. Blair and M. Kaag
H . All suspected testicular tumors should be
resected through an inguinal incision. The
scrotum should not be violated. High liga-
tion of the spermatic cord is required and
assists in future surgery if a retroperito-
neal lymph node dissection becomes
necessary.
I. Further management of testicular cancers is
predicated on tumor subtype (seminoma vs.
nonseminoma). Patients without clinical
evidence of retroperitoneal metastasis and
normal post-orchiectomy tumor markers
may be observed, though some patients may
opt for prophylactic radiation, chemother-
apy, or RPLND.  Patients with seminoma
who have low-volume metastasis are eligi-
ble for low-­dose chemotherapy or radiation
to the retroperitoneum, whereas patients
with low-volume seminoma may opt for
RPLND or low-dose chemotherapy. The
mainstay of treatment for disseminated dis-
ease is platinum-­based multi-drug chemo-
therapy [1, 5].
148  Management of Scrotal/Testicular Mass 607

History of Present Illness and Vitals/Physical Exam

A (genitals, abdomen, lymph nodes, breasts, neuro)

Painful and
Scrotal or
suspect
Painless/painful testicular
testicular
mass and torsion trauma?
torsion?
not suspected?

Scrotal Scrotal
B Ultrasound Scrotal Ultrasound
STAT Ultrasound STAT
E

No blood
C flow?
Epididymo-
Hydrocele
Evidence of D
orchitis testicular
rupture?

Immediate
No Observe or
exploration Abscess
Abscess elective
and
orchiopexy repair Scrotal
exploration
Antibiotics and repair
IV antibiotics,
surgical and/or Epididymal/Spermatic
drainage or NSAIDS Cord Mass
orchiectomy

Spermatocele,
Varicocele
F Solid Testicular Mass Epididymal cyst

· Obtain labs (CBC, BMP, PT/INR, LFTs)and tumor markers (AFP, quantitative b-HCG, LDH)
· Discuss sperm banking
· Staging with CT abdomen/pelvis with PO and IV contrast and either chest X-ray or CT chest

Radical inguinal orchiectomy with high

G spermatic cord ligation

Algorithm 148.1
608 B. M. Blair and M. Kaag

References 4. Rybenstein R, Dogra V, Seftel A, Resnick M. Benign

intrascrotal lesions. J Urol. 2004;171(5):1765–72.
5. NCCN Clinical Practice Guidelines in Oncology  –
1. Wein A, Kavoussi L, Partin A, Peters C.  Campbell-­
Testicular Cancer  – Version 2.2017 [Internet]. www.
Walsh urology. 11th ed. Philadelphia: Elsevier; 2016.
nccn.org. 2017 [cited 8 Oct 2017]. Available from:
2. Montgomery J, Bloom D.  The diagnosis and man-
https://www.nccn.org/professionals/physician_gls/
agement of scrotal masses. Med Clin North Am.
pdf/testicular.pdf.
2011;95(1):235–44.
3. Rabinowitz R, Hulbert W.  Acute scrotal swelling.
Urol Clin North Am. 1995;22(1):101–5.
 Diagnosis and Management
of Fournier’s Gangrene 149
Augustyna Gogoj and Matthew Kaag

Algorithmic Approach Radiographs may show swelling or subcuta-

A. Fournier’s gangrene is a necrotizing infection
involving the genitals. Patients often present
with, or rapidly develop signs of, sepsis, and
this condition may be progressive and life-­
threatening. Treatment hinges on the rapid
initiation of broad-spectrum antibiotics and
aggressive local debridement with/without
urinary and fecal diversion.
B. Diagnosis of Fournier’s gangrene starts with D. Broad-spectrum parenteral antibiotic therapy
clinical findings on physical exam including
fluctuance, localized tenderness, and wounds
of the genitalia and perineum [1]. Crepitus or
evidence of tissue necrosis differentiates
Fournier’s gangrene from genital cellulitis
and scrotal abscess. Vital signs and blood
work may be used as predictors for mortality.
Patients older than 50 with diabetes mellitus
(in 20–70% of patients) or an alcohol abuse
history (in 20–50% of patients) are at greatest
risk and should be thoroughly examined.
Other predisposing factors include poor
hygiene, malnutrition, malignancy, steroid E. Aggressive and timely surgical debridement
use, or an immunocompromised state [2, 3].
C. Imaging is not necessary unless disease
extent or diagnosis is not clear and should
never prolong time to surgical management. F. Fecal diversion is indicated with anal sphinc-
A. Gogoj · M. Kaag (*)
Division of Urology, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: mkaag@pennstatehealth.psu.edu
neous emphysema. Ultrasound can demon-
strate a thickened, edematous scrotal wall
containing hyperechoic foci or paratesticular
fluid. Computed tomography can be used to
guide surgical management and visualize
asymmetric fascial thickening, fluid collec-
tions, abscess formation, fat stranding, and
subcutaneous emphysema. Computed tomog-
raphy has greatest specificity [4].
is to be started immediately upon diagnosis.
Antibiotics must cover staphylococcal, strep-
tococcal, and gram-negative bacteria, coli-
forms, Pseudomonas, Bacteroides, and
Clostridium. Adequate coverage typically
includes a broad-spectrum penicillin with
third-generation cephalosporin or aminogly-
coside and metronidazole or clindamycin.
Expansion to include vancomycin or line-
zolid may be necessary based on the clinical
situation. Culture results can guide eventual
narrowing of antibiotic coverage [3].
is imperative for decreased mortality. All
devitalized tissues must be resected. Serial
debridement is often necessary [5].
ter involvement, fecal incontinence, or con-
tinued fecal contamination of the wound’s
margins [6]. In the event of extensive penile

© Springer Nature Switzerland AG 2019 609

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_149
610
or urethral involvement, suprapubic urinary
diversion may be necessary; however, ure-
thral catheterization is often sufficient [1].
G. Post-operatively wounds are managed with
dressing changes or negative-pressure wound
therapy and continued antibiotics [7]. Adjunct
hyperbaric oxygen therapy may enhance
patient survival, but reported results have
been inconsistent [8].
A. Gogoj and M. Kaag
H. Reconstruction may be necessary for skin
coverage of wounds, cosmesis, and preserva-
tion of genital function. Primary closure of
wounds shows the best functional and cos-
metic results. Closure of wounds through sec-
ondary intention increases healing time and
scrotum deformity [9]. Large defects may
require myocutaneous or fasciocutaneous
flaps [10, 11]. Follow-up may include further
reconstruction.
149  Diagnosis and Management of Fournier’s Gangrene 611

Physical exam:
fluctuance, crepitus, localized tenderness,
wounds of the genitalia and perineum

A Obtain vital signs, blood work, assess risk factors

Yes
B Disease extent Obtain imaging
or diagnosis CT is most specific: fascial thickening,
unclear? fluid collections, paratesticular fluid

No

C Start broad-spectrum IV antibiotics

D Aggressive surgical debridement

Fecal diversion through colostomy or Flexi-seal

E Need for
fecal management system
fecal/urinary
urinary diversion through cystostomy,
diversion? Yes catheterization, or suprapubic diversion

No

F Open wound care with sterile dressings or negative-pressure wound therapy

Hyperbaric oxygen therapy used as adjunct

G Reconstruction: closure of wounds through primary or secondary intention, full

thickness or split thickness skin grafts, myocutaneous or fasciocuteous flaps

Follow-up care

Algorithm 149.1
612 A. Gogoj and M. Kaag

References 6. Ozturk E, Sonmez Y, Yilmazlar T. What are the indi-

cations for a stoma in Fournier’s gangrene? Color Dis.
2011;13:1044–7.
1. Chennamsetty A, Khourdaji I, Burks F, Killinger
7. Ozkan O, Koksal N, Altinli E, Celik A, Uzun M,
K.  Contemporary diagnosis and manage-
Cikman O, Akbas A, Ergun E, Kiraz HA, Karaayvaz
ment of Fournier’s gangrene. Ther Adv Urol.
M.  Fournier’s gangrene current approaches. Int
2015;7(4):203–15.
Wound J. 2011;15(5):713–6.
2. Clayton M, Fowler J, Sharifi R, Pearl R. Causes, pre-
8. Jallali N, Withey S, Butler P.  Hyperbaric oxygen as
sentation and survival of fifty-seven patients with nec-
adjuvant therapy in the management of necrotizing
rotizing fasciitis of the male genitalia. Surg Gynecol
fasciitis. Am J Surg. 2005;189(4):462–6.
Obstet. 1990;170:49–55.
9. Maguina P, Palmieri T, Greenhalgh D. Split thickness
3. Mallikarjuna M, Vijayakuma A, Patil V, Shivswamy
skin grafting for recreation of the scrotum following
B. Fournier’s gangrene: current practices. ISRN Surg.
Fournier’s gangrene. Burns. 2003;29:857–62.
2012;942437.
10. Lee S, Rah D, Lee W. Penoscrotal reconstruction with
4. Levenson R, Singh A, Novelline R. Fournier gangrene:
gracilis muscle flap and internal pudendal artery per-
role of imaging. Radiographics. 2008;28:519–28.
forator flap transposition. Urology. 2012;79:1390–6.
5. Sorenson M, Krieger J, Rivara F, Klein M, Wessells
11. Chen S, Fu J, Wang C, Lee T, Chen S. Fournier gan-
H.  Fournier’s gangrene: management and mortal-
grene: a review of 41 patients and strategies for recon-
ity predictors in a population based study. J Urol.
struction. Ann Plast Surg. 2010;64:765–9.
2009;182:2742–7.
Part XIX
Trauma
 Hypotension and Blunt Abdominal
Trauma 150
Cheyenne C. Sonntag and Steven R. Allen

Algorithmic Approach crystalloid solution given. Patients will often

A. On patient arrival, a brief history provided by
transporting EMS may identify blunt mecha-
nism. The first steps in evaluation of patients
with blunt traumatic injury is the primary sur-
vey (ABCs) to identify and intervene for life-­ C. In the setting of persistent hypotension, it is
threatening conditions [1]. The airway is
assessed for patency, with maintenance of
spinal precautions. Bilateral chest is auscul-
tated for presence of breath sounds, oxygen
saturation obtained, chest wall inspected, and
oxygen therapy initiated. Interventions such
as obtaining definitive airway and needle
decompression are performed as indicated if
life-threatening condition is found during air-
way and breathing assessment.
B. In continuation of the primary survey, circu-
latory assessment consists of blood pressure, D. DPA is considered positive if gross blood is
heart rate evaluation, and assessment of
peripheral pulses. Sources of large external
blood loss are controlled. Two large-bore IVs
should be obtained preferentially and, in
patients found to be hemodynamically unsta-
ble, a bolus of 1–2 liters of warm isotonic
C. C. Sonntag
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
S. R. Allen (*)
Department of Surgery, Penn State Health Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: sallen4@pennstatehealth.psu.edu
have IV access and fluids initiated in the field
by EMS, and this volume should be consid-
ered. If hypotension does not correct with
crystalloid bolus, early transition to blood
products is warranted.
inappropriate to transport the patient for com-
puted tomography (CT) scan, and other diag-
nostic modalities must be considered to
evaluate for internal hemorrhage. For abdom-
inal evaluation, these include diagnostic peri-
toneal aspirate (DPA), diagnostic peritoneal
lavage (DPL), and focused assessment sonog-
raphy in trauma (FAST) and are equally
appropriate and dependent on provider/insti-
tution capabilities. Thoracic and pelvic
trauma are elsewhere covered.
found on aspiration (10 mL); DPL is positive
if microscopic analysis reveals >100 K/mm3
red blood cells and >500 K/mm3 white blood
cells or lavage shows bile or particulate mat-
ter [2, 3]. It should be remembered that false-­
positive DPL may occur in the setting of
pelvic fractures, when retroperitoneal hema-
toma may unintentionally be sampled [3].
Positive DPA/DPL in a hemodynamically
unstable patient warrants emergent operative
exploration.
E. Exploratory laparotomy is indicated in
patients who are hemodynamically unstable

© Springer Nature Switzerland AG 2019 615

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_150
616
with positive intraabdominal fluid found on
FAST exam. FAST is sensitive in detecting a
minimum of 200 mL of fluid in experienced
hands; however, sensitivity may vary with
operator ultrasound experience and patient
body habitus [4, 5].
F. Hypotensive patients with negative FAST
exam should have continued resuscitation,
and alternate sources of shock should be eval-
uated. DPA/DPL may be considered as well
C. C. Sonntag and S. R. Allen
as repeat FAST.  Negative FAST should not
delay exploratory laparotomy in unstable
patients with clear physical findings on
examination.
G. As with negative FAST, persistent hypoten-
sion in a patient with negative DPA and DPL
should trigger further investigation for other
sources of shock. Repeat procedure may be
considered.
150  Hypotension and Blunt Abdominal Trauma 617

Patient arrival & EMS report

A
Primary survey
E

Airway

Breathing

Circulation
B · Assess BP, HR, peripheral
pulses
· IV access and fluid bolus

Persistent Continue
No
hemodynamic primary
instability survey

C YES

· Transfuse blood products

· DPA/DPL or FAST

DPA positive? FAST positive?

· aspirate 10mL gross blood

or
DPL positive?
E No F
· RBC>100 K/mm3 YES
· WBO >500 K/mm3
· Bile or particulates D

YES · Continue resuscitation

G No
· Investigate other sources
of shock
· Consider DPA/DPL
· Continue resuscitation
Exploratory
· Investigate other sources laparotomy
of shock

Algorithm 150.1
618 C. C. Sonntag and S. R. Allen

References for the evaluation of blunt abdominal trauma: the

East practice management guidelines work group. J
Trauma. 2002;53(3):602–15.
1. Initial Assessment and Management. Advanced
4. Branney SW, Wolfe RE, Moore EE, Albert NP, Heinig
trauma life support ATLS: student course manual. 9th
M, Mestek M, et al. Quantitative sensitivity of ultra-
ed. Chicago: American College of Surgeons; 2012.
sound in detecting free intraperitoneal fluid. J Trauma.
p. 6–13.
1995;39(2):375–80.5.
2. Root HD, Hauser CW, McKinley CR, Lafave JW,
5. Carter JW, Falco MH, Chopko MS, Flynn WJ Jr,
Mendiola RP Jr. Diagnostic peritoneal lavage.
Wiles Iii CE, Guo WA. Do we really rely on fast for
Surgery. 1965;57:633–7.
decision-making in the management of blunt abdomi-
3. Hoff WS, Holevar M, Nagy KK, Patterson L, Young
nal trauma? Injury. 2015;46(5):817–21.
JS, Arrillaga A, et al. Practice management guidelines
 Traumatic Brain Injury
Shannon R. Kotch and Steven R. Allen
Algorithmic Approach
A. In a patient who has sustained significant
trauma, especially if there is high suspicion
for a head injury based on the mechanism of
injury, advanced trauma life support (ATLS)
protocol should be followed [1].
B. After calculating the Glasgow Coma Score
(GCS), traumatic brain injury (TBI) can be
classified into mild, moderate, and severe.
Patients with mild TBI have a GCS of 13–15
upon arrival to the emergency department,
those with moderate TBI have a GCS of 9–12,
and those with severe TBI have a GCS of 8 or
less [2].
C. In a patient with a GCS of 13–15, a complete
neurological and mental status exam should
be performed. If there is any report of loss of
consciousness or amnesia reported, a com-
puted tomography (CT) scan should be
obtained to rule out a more significant brain
injury. It is common for patients with moder-
ate or severe TBI to present with a lucid inter-
val, as seen with epidural hematoma, and
subsequently decompensate rapidly [1].
S. R. Kotch
Department of General Surgery, Penn State Health
Milton S. Hershey Medical Center, Hershey, PA, USA
S. R. Allen (*)
Department of Surgery, Penn State Health Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: sallen4@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_151
151
D. If the CT scan is negative for further injury,
the patient with a normal neuro exam who has
been observed for 4–6 h and without further
concerns for neurologic injury can be dis-
charged with instructions on symptoms which
would prompt a return visit. If there are con-
cerns for the patient despite a normal exam,
12–24 h of continued observation prior to dis-
charge is appropriate [1].
E. A patient with a GCS of 9–12 on presentation
to the emergency department has a moderate
TBI.  These patients should also undergo a
complete neurological and mental status
exam along with a CT scan. These patients
warrant admission to an intensive care unit
for frequent neurological and mental status
exams [1].
F. If there is improvement in the patient’s condi-
tion, the patient may be downgraded and
neuro exams performed with less frequency.
If the patient does not show any signs of
improvement within 6–12 h, a CT scan should
be repeated to rule out worsening of known
lesions or the formation of new lesions [1].
G. Nearly all patients with a moderate TBI will
need some sort of rehab. Patients who have a
severe TBI will need extensive rehab, assum-
ing they recover from the inciting insult [1].
H. Patients with a GCS of 8 or less have a
severe TBI. Based on GCS alone, these
patients are unable to properly protect their
airway and should be intubated immediately.
619
620
­ yperventilation can be considered in the
H tract from the ABCDEs. A CT scan should be
acute setting, maintaining PaCO2 between 30
and 35 mm Hg. Patients also need to be ade-
quately resuscitated, and the patient should
also be properly assessed for any sources of
ongoing bleeding which may lead to a hypo-
volemic state. It is critical to avoid hypoten-
sion (systolic blood pressure  <90  mm Hg)
and hypoxia (oxygen saturation  <90%) to
prevent further ischemic insult to the brain.
Early neurosurgical consultation is advisable
[1, 2].
I. If possible, prior to intubation, a complete
neurological and mental status exam should
be performed. This should not, however, dis-
S. R. Kotch and S. R. Allen
performed as soon as the patient is stable
enough to undergo the test. These patients
also prompt an intensive care unit (ICU)
admission with frequent neurological exami-
nations [1].
J. Intracranial pressure (ICP) monitoring should
be performed in patients with severe TBI. If
ICP is found to be elevated (≥25 mm Hg), the
patient can be managed medically with man-
nitol (0.5–1 g/kg) or hypertonic saline. If an
epidural hematoma or subdural hematoma is
responsible for the elevated ICP, surgical
management with a decompressive craniec-
tomy is necessary [1].
151  Traumatic Brain Injury 621

History:
Teenager who fell from trampoline, hit head on concrete wall
Brief loss of consciousness, remembers event

A ABCDEs –ATLS protocol

Mild TBI: Moderate TBI: Severe TBI:

B GCS 13-15 GCS 9-12 GCS 8

C Complete neurological Complete neurological Intubate, resuscitate H

and mental status exam and mental status exam

Complete neurological
Positive loss of CT scan and mental status exam
consciousness or amnesia

Admission to ICU, I
CT scan
E frequent neuro exams
CT scan

D F
Admission to ICU,
frequent neuro exams
Observation 4–6 h, Observation 4–6 h, Improvement No
normal exam, no normal exam, improvement
concerns concerns
ICP monitoring J
Downgrade
level of care Repeat CT
Discharge Observe in 6–12 h Elevated ICP
12–24 h

Rehab likely
Medical Surgical
management management
G

G Rehab

Algorithm 151.1

2. Chesnut RM. Care of central nervous system injuries.

References Surg Clin North Am. 2007;87(1):119–56., vii. https://
doi.org/10.1016/j.suc.2006.09.018.
1. Decuypere M, Klimo P Jr. Spectrum of traumatic
brain injury from mild to severe. Surg Clin North Am.
2012;92(4):939–57., ix. https://doi.org/10.1016/j.
suc.2012.04.005.
 Penetrating Neck Trauma
Alexis Lauria and Steven R. Allen
Algorithmic Approach
A. Initial resuscitation and wound assessment:
Initial resuscitation of a patient with PNT
should follow the Advanced Trauma Life
Support (ATLS) guidelines [1]. Dependent
upon the location of injury, airway manage-
ment may be a challenge. Orotracheal intuba-
tion is the preferred method of securing the
airway and should be performed immediately
if any hard signs are present (table in
Alogrithm 152.1). If orotracheal intubation is
contraindicated (extensive midface trauma,
significant upper airway distortion, or inabil-
ity to visualize the glottis), an emergent crico-
thyroidotomy should be performed.
Once ATLS resuscitation has been com-
pleted, the wound should be assessed more
carefully. Spine immobilization, which may
hinder a full examination or rapid manage-
ment of the neck injury, is not recommended
if there are no neurological deficits in a con-
scious patient with isolated penetrating neck
trauma (PNT) [2]. Without probing, the sur-
geon should assess whether the injury pene-
A. Lauria
Department of Surgery, Walter Reed National
Military Medical Center, Bethesda, MD, USA
S. R. Allen (*)
Department of Surgery, Penn State Health Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: sallen4@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_152
152
trates the platysma, requiring further work-up
according to the algorithm. If no platysmal
violation is present, the trauma team should
continue with secondary and tertiary surveys.
In follow-up care, the wound should be fre-
quently monitored for signs of occult dam-
age. While injuries to the neck can be
significant and require prioritization, it is also
important not to overlook potential concomi-
tant injuries in a patient with PNT.
B. Hard signs of vascular or tracheoesophageal
injury: Listed are commonly accepted hard
signs of vascular (hemorrhage, hematoma,
thrills or bruits, unresponsive shock, dimin-
ished pulses, and neurological deficits) and
aerodigestive (air bubbling from the wound,
hemoptysis or hematemesis, and respiratory
distress) injuries. If any of these signs are
present, or the patient is clinically deteriorat-
ing, the patient should be taken immediately
to the operating room (OR). The airway
should be secured, if this had not been indi-
cated during the initial resuscitation. Pressure
should be applied to the wound to tamponade
any active bleeding. For significant bleeding
not amendable to tamponade, Foley balloon
catheterization may be considered [3, 4]. Soft
signs of injury (wounds within 1–2  cm of a
major vessel, minor hemorrhage, non-­
expanding hematoma, fluid responsive mild
hypotension, minor hemoptysis or
­hematemesis, and dysphonia or dysphagia)
623
624
should prompt more frequent and close moni-
toring of the patient.
Operative management for a rapidly decom-
pensating patient should focus on source con-
trol of bleeding and repair of vital structures.
The standard operative approach is a vertical
incision along the anterior border of the sterno-
cleidomastoid, extending from the angle of the
mandible to the sternoclavicular junction, with
variations by zone, as described below [5].
C. Zone III injury: Important structures within
Zone III include the vertebral arteries, distal
internal carotid arteries, jugular veins, phar-
ynx, spinal cord, sympathetic chain, and cra-
nial nerves IX, X, XI, and XII. Structures in
Zone III can be challenging to reach due to the
bony structures of the jaw. As such, endovas-
cular management, when possible, may be
more appropriate for more distal Zone III inju-
ries. For an open approach, the vertical inci-
sion [B] is extended with a horizontal limb
extending to the mastoid on the appropriate
side [5]. More invasive measures such as sub-
luxation, dislocation, or resection of the man-
dible may be necessary to reach more distal
structures [6].
D. CTA—indications and findings: For patients
who are hemodynamically stable, but with an
injury violating the platysma, or any soft signs
of injury, further imaging should be obtained.
Computed tomography angiography (CTA)
can allow quick, noninvasive visualization of
major vascular and aerodigestive structures in
the neck. Most trauma centers today have CT
capabilities within feet of the trauma bay.
Positive findings on CTA include notable dis-
ruption or abnormality in the lumen of any
vascular or aerodigestive structures or a
“blush” indicating active bleeding. If CTA is
positive, surgical, endoscopic, or endovascu-
lar management should be considered based
on the location and type of identified injury.
E. Zone II injury: Zone II is the largest and thus
most commonly injured area of the neck.
Important structures within Zone II include
the common carotid and its internal and exter-
A. Lauria and S. R. Allen
nal branches, vertebral arteries, jugular veins,
trachea, esophagus, larynx, pharynx, spinal
cord, and the vagus and recurrent laryngeal
nerves. The standard incision described in B
should allow access to most structures in
Zone II. However, additional horizontal inci-
sions may be used to provide maximum
access as necessary [5].
F. Zone I injury: Zone I, the most caudal zone,
includes the thoracic inlet structures (subcla-
vian arteries and veins and internal jugular
veins), proximal carotid arteries, vertebral
arteries, trachea, esophagus, spinal cord, tho-
racic duct, thyroid gland, and apices of the
lungs. A lower neck injury should increase
suspicion for mediastinal injury or pneumo-
thorax. For Zone I injuries, the standard inci-
sion [B] may be modified with horizontal
limbs along the superior aspect of the clavicle
for full exposure [5]. Furthermore, if medias-
tinal vessels are injured, a median sternot-
omy, disarticulation of the sternoclavicular
joint, or anterolateral thoracotomy may be
necessary [5].
G. Suspicion for T/E injury: If there is clinical
(hemoptysis, hematemesis, dysphonia, dys-
phagia, or subcutaneous or mediastinal air) or
radiographic concern for tracheoesophageal
injury, more invasive studies should be per-
formed. These may include swallow studies
or esophagoscopy for concern for esophageal
injury and/or bronchoscopy for concern for
airway disruption. Operative or interventional
endoscopy/bronchoscopy should be per-
formed based on findings here.
H. Follow-up care: Patients who underwent pro-
cedures involving the neck require close mon-
itoring for the formation of a hematoma,
which may compromise the airway. If an
expanding hematoma is seen, the wound
should be immediately opened to avoid air-
way compromise. Clinicians should continue
to monitor all patients for signs of decompen-
sation, development of hard or soft signs,
wound infection, or any other indications for
further management.
152  Penetrating Neck Trauma 625

Resuscitate patient according to ATLS

A Assess wound (without probing)

Proceed with secondary and tertiary survey

Platysma No Continue to monitor for hard signs or
violated? worsening exam

Yes

Hard Yes Straight to OR

signs? Secure airway
B Apply direct pressure to tamponade wound

No

(+) OR
D Endo/embo
Zone III Injury
C (above angle of mandible)
CTA

(-)

H
OR
Symptomatic Endo/embo Follow-up care
Bronchoscopy
Zone II Injury
E (cricoid cartilage to angle of
mandible No
Asymptomatic (-)
Suspicion
for T/E
CTA
Injury?
Yes
Zone I Injury G
(between clavicles and cricoid (+)
F cartilage)
Swallow study
EGD
Bronchoscopy

OR
Endo/embo
Bronchoscopy
EGD

Table Hard signs of vascular (1-6) or aerodigestive

(7-9) Injury
1. Significant uncontrolled hemorrhage
2. Large, expanding or pulsatile hematoma
3. Thrill or bruits
4. Shock unresponsive to fluid resuscitation
5. Absent or diminished radial pulse
6. Neurologic deficits consistent with cerebral ischemia
7. Air bubbling from wound
8. Massive hemoptysis or hematemesis
9. Respiratory distress

Algorithm 152.1
626 A. Lauria and S. R. Allen

References 4. Navsaria P, Thoma M, Nicol A.  Foley catheter

balloon tamponade for life-threatening hemor-
rhage in penetrating neck trauma. World J Surg.
1. American College of Surgeons Committee on Trauma.
2006;30(7):1265–8.
Advanced trauma life support for doctors. 8th ed.
5. Bagheri SC, Khan HA, Bell RB.  Penetrating neck
Chicago: American College of Surgeons; 2012.
injuries. Oral Maxillofac Surg Clin North Am.
2. Stuke LE, Pons PT, Guy JS, Chapleau WP, Butler FK,
2008;20(3):393–414.
McSwain NE. Prehospital spine immobilization for pen-
6. Sperry JL, Moore EE, Coimbra R, Croce M, Davis
etrating trauma—review and recommendations from the
JW, Karmy-Jones R, McIntyre RC Jr, Moore FA,
Prehospital Trauma Life Support Executive Committee.
Malhotra A, Shatz DV, Biffl WL.  Western Trauma
J Trauma Acute Care Surg. 2011;71(3):763–70.
Association critical decisions in trauma: pen-
3. Van Waes OJ, Cheriex KC, Navsaria PH, Van Riet PA,
etrating neck trauma. J Trauma Acute Care Surg.
Nicol AJ, Vermeulen J.  Management of penetrating
2013;75(6):936–40.
neck injuries. Br J Surg. 2012;99(S1):149–54.
 Penetrating Chest Trauma
Melissa Linskey and Steven R. Allen
Algorithmic Approach
A. The first step in evaluating a patient that has
suffered a penetrating injury to the chest is to
assess for pulses. Cardiopulmonary arrest or
severe hemodynamic instability may neces-
sitate a prompt resuscitative thoracotomy
through a left anterolateral thoracotomy to
control life-threatening hemorrhage [1].
B. Patients with pulses should be evaluated for
life-threatening injuries quickly through
advanced trauma life support protocols and
should receive appropriate resuscitative flu-
ids, blood products, and tube thoracostomy
for treatment of hemothorax and pneumotho-
rax. Chest x-ray (CXR) and focused assess-
ment sonography in trauma (FAST) can aid in
identifying transmediastinal injuries or those
with laterality [2]. Possible findings seen on
physical exam in penetrating chest trauma
can include distended neck veins, tracheal
deviation, subcutaneous emphysema, bub-
bling from wound, absent breath sounds,
muffled heart sounds, and absence of upper
extremity pulse.
C. Unstable patients not responding to fluid,
blood products, and chest tube placement
should be taken to the operating room emer-
M. Linskey · S. R. Allen (*)
Department of Surgery, Penn State Health Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: sallen4@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_153
153
gently with incision planned based on the
location of injury [3]. The anatomy of the
thoracic cavity and the trajectory of the pen-
etrating injury should be considered when
determining the structures possibly injured
and how they are best approached
operatively.
D. Emergent anterolateral thoracotomy should
be performed in unstable patients with lateral
or posterior wounds and with massive hemo-
thorax [2].
E. Anterior or central injuries (those between
the midclavicular lines), or patients with pos-
itive FAST consistent with cardiac tampon-
ade, should undergo median sternotomy [2].
F. In stable patients, further diagnostic testing
can be performed to identify specific struc-
tures that have been injured. Diagnostic test-
ing can include computed tomography (CT)
scans, CT angiography, esophagogastroduo-
denoscopy (EGD), and bronchoscopy [2, 3].
G. Median sternotomy is the approach of choice
for cardiac, ascending aorta, innominate
artery, right and left carotid arteries, and right
subclavian artery injuries. Extension of this
incision to the neck or supraclavicular inci-
sion can be performed based on the injury [4].
H. In penetrating chest trauma, 14% of stab
wounds and 15–20% of gunshot wounds will
require thoracotomy [3]. Posterolateral thora-
cotomy is appropriate for the intrathoracic
trachea, intrathoracic esophagus, and retained
627
628 M. Linskey and S. R. Allen

hemothorax. Left thoracotomy is specifically phragm injuries. Because of the variability in

helpful for descending aorta, intrathoracic
left subclavian artery, and left mainstem
bronchus injuries [4].
I. Video-assisted thoracoscopy or laparoscopy
can be utilized on an urgent basis for dia-
diaphragmatic excursion, low thoracic inju-
ries should raise suspicion for intraabdominal
injury [2].

A History and physical exam

Penetrating injury to chest (i.e. stabbing or gunshot wound)

No Pulses?

Resuscitative
thoracotomy
Yes

B Initial ATLS assessment and resuscitation

CXR, FAST

C No
Stable?
Yes F

Proceed to OR
Diagnostic tests/procedures: CT,
CTA, EGD, Bronchoscopy

Posterior/Lateral wound Anterior/Central wound

massive hemothorax tamponade

Cardiac/Great Trachea/ Diaphragm

vessel bronchus

Esophagus
G
D E I
H

Anterolateral Median Posterolateral VATS/

thoracotomy sternotomy thoracotomy laparoscopy

Algorithm 153.1
153  Penetrating Chest Trauma
References
1. Seamon MJ, Haut ER, Van Arendonk K, Barbosa RR,
Chiu WC, Dente CJ, et al. An evidence-based approach
to patient selection for emergency department thora-
cotomy: a practice management guideline from the
Eastern Association for the Surgery of Trauma. J
Trauma Acute Care Surg. 2015;79(1):159–73.
2. Karmy-Jones R, Namias N, Coimbra R, Moore EE,
Schreiber M, McIntyre R Jr, et  al. Western Trauma
629
Association critical decisions in trauma: pen-
etrating chest trauma. J Trauma Acute Care Surg.
2014;77(6):994–1002.
3. DuBose JA, O’Connor JV, Scalea TM. Lung, trachea,
and esophagus. In: Mattox KL, Moore EE, Feliciano
DV, editors. Trauma. 7th ed. New York: McGraw-Hill
Medical; 2013. p. 468–84.
4. Mattox KL, Wall MJ, Tsai P.  Trauma thoracotomy:
principles and techniques. In: Mattox KL, Moore EE,
Feliciano DV, editors. Trauma. 7th ed. New  York:
McGraw-Hill Medical; 2013. p. 461–7.
 ED Thoracotomy
Nathan R. Manley and George O. Maish III
Algorithmic Approach
Any patient presenting to the emergency depart-
ment (ED) in extremis should be quickly evalu-
ated to ascertain whether they have a blunt or
penetrating mechanism of injury.
A. In the patient with blunt injury, the first step is
to evaluate for presence of vital signs (defined
as pupillary response, spontaneous ventila-
tion, presence of carotid pulse, measurable or
palpable blood pressure, extremity movement
or cardiac electrical activity).
A1. If the patient had no vital signs en route
and has no vital signs on arrival, the
patient should be pronounced with no
further resuscitation.
A2. If the patient lost vital signs en route,
then cardiopulmonary resuscitation
(CPR) should be temporarily stopped
and vital signs reassessed while a car-
diac ultrasound is performed.
B. Cardiac ultrasound is used to assess the need
for further resuscitative efforts.
B1. If there is no cardiac activity on ultra-
sound, then the patient should be pro-
nounced, and no further efforts at
resuscitation should be performed.
N. R. Manley · G. O. MaishIII (*)
Department of Surgery, University of Tennessee
Health Science Center, Memphis, TN, USA
e-mail: gmaish@uthsc.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_154
154
B2. If the patient has cardiac activity, then
consider placement of resuscitative
endovascular balloon occlusion of the
aorta (REBOA).
B3. If the patient has cardiac activity and
there is evidence of tamponade, proceed
directly to ED thoracotomy to evacuate
blood from the pericardial space.
C. In the patient with penetrating trauma, there
should be a much lower threshold for perform-
ing ED thoracotomy due to higher salvage rates
in comparison to blunt traumatic cardiac arrest.
C1. If the patient never had vital signs in the
prehospital setting or if CPR has been
ongoing for more than 20  min, the
patient should be pronounced and fur-
ther resuscitative efforts stopped after
pulse check on arrival to the ED.
D. If the patient had loss of vital signs en route to
the hospital or in the ED, aggressive interven-
tion should be performed depending upon
whether there is obvious penetrating trauma
to the chest or abdomen.
D1. If there is obvious penetrating trauma to
the chest, then ED thoracotomy should
be performed without hesitation to cor-
rect any obvious injury to the heart,
lungs, or great vessels.
D2. If there is obvious penetrating trauma to
the abdomen, consider placing a REBOA
or proceeding with ED thoracotomy and
cross-clamping the aorta to prevent fur-
ther truncal hemorrhage.
631
632 N. R. Manley and G. O. Maish

If REBOA or ED thoracotomy is performed, the as soon as possible. ATLS and ACLS should
patient should go immediately to the operating guide resuscitative interventions if REBOA or
room to definitively address destructive injuries ED thoracotomy is not pursued immediately.

Mechanism of injury

A C
Blunt Penetrating
D
A1. No vital C1. No vital Loss of vital
A2. Loss of
signs en route signs or CPR signs en route or
vital signs en
or in ED > 20 min in ED
route

B
Pronounce Pronounce D2.
D1. Chest
Abdominal
Cardiac Injury
injury
ultrasound

B1. No B3. + Fluid

cardiac B2. + (Tamponade)
activity Cardiac Consider
Emergent
activity REBOA
thoracotomy
Emergent
thoracotomy
Consider
REBOA

Abbreviations: CPR: cardiopulmonary resuscitation; ED: emergency department;

REBOA: resuscitative endovascular balloon occlusion of the aorta.

Algorithm 154.1

endovascular occlusion of the aorta as an alterna-

Suggested Readings
American College of Surgeons. Advanced trauma life sup-
port. 9th ed. Chicago: American College of Surgeons;
2012. 336 p.
American Heart Association. Advanced cardiac life sup-
port. Dallas: American Heart Association; 2015. 183 p.
Burlew CC, Moore EE, Moore FA, Coimbra R, McIntyre
RC, Davis JW, et al. Western Trauma Association criti-
cal decisions in trauma: resuscitative thoracotomy. J
Trauma Acute Care Surg. 2012;73(6):1359–63.
Moore LJ, Brenner M, Kozar RA, Pasley J, Wade CE,
Baraniuk MS, et  al. Implementation of resuscitative
tive to resuscitative thoracotomy for noncompress-
ible truncal hemorrhage. J Trauma Acute Care Surg.
2015;79(4):523–30.
Seamon MJ, Haut ER, Van Arendonk K, Barbosa RR, Chiu
WC, Dente CJ, et al. An evidence-based approach to
patient selection for emergency department thora-
cotomy: a practice management guideline from the
Eastern Association for the Surgery of Trauma. J
Trauma Acute Care Surg. 2015;79(1):159–73.
Western Trauma Association [Internet]. Resuscitative
Thoracotomy. 2012 [cited 2017 Aug 13]. Available from:
http://westerntrauma.org/algorithms/WTAAlgorithms_
files/gif_8.htm
 Blunt Chest Wall Trauma
Nathan R. Manley and George O. Maish III
Algorithmic Approach
All patients presenting with blunt chest wall
trauma and history of significant mechanism A. In the stable patient with significant mecha-
should initially be assessed following ATLS pro-
tocols, including airway, breathing, circulation,
disability, and exposure (ABCDE). Any threat to
ABCDE should be addressed immediately. Next,
screening imaging should be performed, includ-
ing focused assessment with sonography for
trauma (FAST) exam and chest x-ray. Immediate
life-threatening injuries include pneumothorax,
hemothorax, and pericardial effusion and should
be treated as they are found. A chest tube should
be placed for pneumothorax or hemothorax (with
hemothorax, note how much came out of chest
tube on placement, and if it is >1500 mL, then the
patient should go to the OR for immediate thora-
cotomy). A pericardial effusion can be managed
in the emergency department (ED) with pericar-
diocentesis, although we recommend going to the
OR for subxiphoid pericardial window if these
resources are available. If the patient loses vital
signs, consider an ED thoracotomy (see separate
Algorithm). A high degree of suspicion for intra-­
thoracic or intra-abdominal injury should be
maintained if scapula fracture, flail chest, sternal
fracture, or posterior sternoclavicular dislocation
N. R. Manley · G. O. Maish III (*)
Department of Surgery, University of Tennessee
Health Science Center, Memphis, TN, USA
e-mail: gmaish@uthsc.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_155
155
is found. Further management will be dictated by
whether the patient is stable or unstable.
nism and evidence of blunt chest wall trauma
on history and physical exam, a CT scan with
contrast should be performed to rule out
injury to the heart, lungs, and great vessels. If
there is any concern for blunt cardiac injury,
perform a 12-lead electrocardiography (EKG)
and send troponins.
• Severe injuries include blunt aortic injury,
flail chest, sternal fracture, and severe pul-
monary contusions. Blunt aortic injury
should be managed with a vascular surgery
consult, angiography, and possible open
versus endovascular management of aortic
injury. With flail chest, sternal fracture, and
severe pulmonary contusions, there should
be a low threshold for intubating the patient
if they are in respiratory distress.
Management for these conditions is mostly
conservative (i.e., mechanical ventilation,
pain control, and aggressive pulmonary
toilet). Rib plating for flail chest or multi-
ple rib fractures will be dictated by existing
institutional protocols, as there are no con-
clusive guidelines at this time.
• Mild to moderate injuries include rib frac-
tures, mild pulmonary contusions, soft tis-
sue injury, thoracic spine fractures, and
clavicle fractures. Rib fractures and mild
633
634
pulmonary contusions can be managed
with pain control, incentive spirometry,
and early ambulation. Repeat chest x-rays
can be performed as needed to assess
respiratory status and resolution of injury.
Local wound care will generally suffice
for soft tissue injury. Any thoracic spine
fractures should be evaluated by the spine
service for specific management. Clavicle
fractures should be managed by the ortho-
pedic service, and general management is
a sling for comfort.
B. In the unstable patient, continue resuscitation
with fluid and close monitoring of any life-­
threatening injuries found on the primary sur-
vey. Special attention should be paid to
N. R. Manley and G. O. Maish III
amount of blood from the chest tube placed
for hemothorax: if greater than 1500 mL ini-
tially or more than 250 mL/h for 4 h, then OR
thoracotomy should be performed. If the
patient responds to resuscitation, then CT
angiography should be performed and spe-
cific injuries managed as in the stable patient.
If the patient does not respond to further
resuscitation and remains unstable, re-­
evaluate for life-threatening injury—includ-
ing blunt cardiac injury—before sending the
patient to the CT scanner. Any arrhythmia
should be managed by ACLS protocols. If the
patient remains unstable or loses vital signs,
an emergent thoracotomy should be strongly
considered.
155  Blunt Chest Wall Trauma 635

Patient with blunt chest wall trauma

ATLS

Screening
Imaging:
FAST, CXR

Management of life-threatening injuries:

· HTX/PTX: Chest tube
· Pericardial effusion: OR for
pericardial window
· Loss of VS: Consider ED
thoracotomy

A B

Stable Unstable

Chest CT Continued
Angiography Resuscitation

Severe Mild or No
Injury Moderate Responds
response
Injury

Manage per
etiology Manage per · Reassess for
etiology life-threatening
injury
· Consider Blunt
Abbreviations: ACLS: Advanced cardiac life support; ATLS: Advanced
Cardiac Injury
trauma life support; CXR: Chest x-ray; ED: Emergency department; FAST:
· ACLS
Focused assessment with sonography in trauma; HTX: Hemothorax; OR:
Operating room; PTX: Pneumothorax; VS: Vital signs

Algorithm 155.1

rib fractures after blunt trauma: a practice manage-

Suggested Reading
American College of Surgeons. Advanced trauma life sup-
port. 9th ed. Chicago: American College of Surgeons;
2012. 336 p.
American Heart Association. Advanced cardiac life support.
Dallas: American Heart Association; 2015. 183 p.
Galvagno SM, Smith CE, Varon AJ, Hasonboehler EA,
Sultan S, Shaefer G, et al. Pain management for blunt
thoracic trauma: A joint practice management guide-
line from the Eastern Association for the Surgery
of Trauma and Trauma Anesthesiology Society. J
Trauma Acute Care Surg. 2016;81(5):936–51.
Kasotakis G, Hasenboehler EA, Streib EW, Patel N,
Patel MB, Alarcon L, et  al. Operative fixation of
ment guideline from the Eastern Association for
the Surgery of Trauma. J Trauma Acute Care Surg.
2017;82(3):618–26.
Legome E, Hammel JM.  Initial evaluation and man-
agement of chest wall trauma in adults. Up to Date
[Internet]. 2016 Sep [cited 2017 Aug 14]. Available
from: https://www.uptodate.com/contents/initial-
evaluation-and-management-of-chest-wall-trauma-
in-adults.
Simon B, Ebert J, Bokhari F, Capella J, Emhoff T,
Hayward T, et  al. Management of pulmonary con-
tusion and flail chest: an Eastern Association for
the Surgery of Trauma practice management guide-
line. J Trauma Acute Care Surg. 2012;73(5 Suppl
4):S351–61.
 Blunt Cardiac Injury
Nathan R. Manley and George O. Maish III
Algorithmic Approach
Any patient presenting to the emergency depart-
ment (ED) with blunt trauma to the anterior chest
should be worked up for blunt cardiac injury
(BCI). In addition to routine trauma labs (e.g.,
CBC, BMP, lactate, PT/INR, PTT, ABG) and
imaging (e.g., portable chest), a 12-lead EKG
should be done, and cardiac troponins should be
sent to assess baseline level. It is also important
to obtain a thorough past medical history (PMH)
if possible to put the patient’s current injuries into
context. Pertinent PMH to BCI includes any pre-­
existing cardiac abnormality (e.g., murmur or C. In the hemodynamically unstable patient, fol-
pacemaker), current medications (especially car-
diac meds and anticoagulants), previous myocar-
dial infarction, previous cardiac catheterizations
and any stents placed, baseline functional status,
and any past cardiac surgeries (e.g., coronary
artery bypass surgery [CABG]). Always consider
myocardial infarction as the inciting event that
led to the trauma, especially in the elderly.
A. In the patient with normal EKG and normal
troponin, blunt cardiac injury (BCI) is effec-
tively ruled out. Continue with trauma work-
­up per chief complaint and mechanism of
injury.
N. R. Manley · G. O. Maish III (*)
Department of Surgery, University of Tennessee
Health Science Center, Memphis, TN, USA
e-mail: gmaish@uthsc.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_156
156
B. In the patient with abnormal EKG and normal
troponin, consult cardiology for further work-
up. Consider cardiac ECHO.  If injury is
­
found, manage per specific etiology and con-
sider ICU admission for cardiac monitoring.
Continue full trauma work-up as indicated. In
the patient with abnormal troponin and nor-
mal EKG, consult cardiology for further
work-up. Again, consider cardiac ECHO.  If
injury is found, manage per specific etiology
and consider ICU admission for cardiac mon-
itoring. Continue with full trauma work-up as
appropriate.
low ATLS protocols in the trauma bay and
ensure ABCs are secure. Even if BCI is high
on the differential diagnosis for instability,
assume tachycardia is secondary to hemor-
rhage until proven otherwise. Any arrhyth-
mias should be managed with ACLS
protocols. Echocardiogram should be done to
assess for structural defects; if any valve, sep-
tum, or ventricular wall injuries are found,
cardiothoracic surgery should be consulted
immediately for possible operative interven-
tion. Consider inserting a pulmonary artery
catheter (PAC) to guide fluid resuscitation
when cardiac abnormalities are present, as it
is important to avoid fluid overload in these
patients. Once trauma work-up is complete,
these patients require ICU admission, con-
tinuous telemetry, and close observation.
637
638 N. R. Manley and G. O. Maish III

Patient with blunt trauma to

anterior chest and concern for BCI

· EKG: New arrhythmia, ST

changes, heart block,
ischemia, etc.
· Troponin: Baseline and trend
· PMH: Pre-existing cardiac
abnormality, meds, previous
stents, functional capacity, etc.

Abnormal EKG or abnormal Hemodynamically

A Normal EKG B troponin; hemodynamically
C unstable
and Troponin
stable

· No BCI · ATLS & ACLS

· Continue · Cardiology · ICU admit
trauma consult · Cardiology
work up · Consider consult
ECHO · ECHO
· Specific · Consider PAC
management · Specific
per etiology[1] management per
etiology[1]

1. Specific Management:
· Valve, septum or ventricular wall injury: Cardiothoracic surgery consult
· Acute coronary syndrome: ACLS protocols, cardiology consult, possible
catheterization with stent, avoid thrombolytics
· Cardiac dysfunction: Cardiology consult and ECHO
· Arrhythmias: ACLS protocols. If patient tachycardic, assume hemorrhage until
proven otherwise in the setting of trauma

Abbreviations: ACLS: Advanced cardiac life support; ATLS: Advanced trauma life
support; BCI: Blunt cardiac injury; EKG: Electrocardiogram; ECHO: Echocardiogram;
ICU: Intensive care unit; PAC: Pulmonary artery catheter; PMH: Past medical history

Algorithm 156.1
156  Blunt Cardiac Injury 639

Suggested Reading Clancy K, Velopulos C, Bilaniuk JW, Collier B, Crowley

W, Kurek S, et al. Screening for blunt c­ ardiac injury:
An Eastern Association for the Surgery of Trauma
American College of Surgeons. Advanced trauma life sup-
practice management guide. J Trauma Acute Care
port. 9th ed. Chicago: American College of Surgeons;
Surg. 2012;73(5 Suppl 4):S301–6.
2012. 336 p.
Legome E, Kadish H. Cardiac injury from blunt trauma.
American Heart Association. Advanced cardiac life
Up to Date [Internet]. 2017 Jul [cited 2017 Aug 13].
Support. Dallas: American Heart Association; 2015.
Available from: http://www.uptodate.com/contents/
183 p.
cardiac-injury-from-blunt-trauma.
 Deceleration Injury: Blunt Aortic
Injury
Nathan R. Manley and George O. Maish III
Algorithmic Approach
A. Blunt aortic injury should be suspected in any
patient involved in high-speed motor vehicle
crash or fall from a great height. The follow-
ing algorithm should be followed in the stable
patient.
B. Initial management of any trauma patient pre-
senting to the trauma bay should follow
advanced trauma life support (ATLS) proto-
cols. It is especially important in patients
with a high degree of suspicion for blunt aor-
tic injury to have two large-bore IVs placed
for administration of fluid and medications to
control heart rate and blood pressure. Baseline
labs (CBC, BMP, PT/INR, PTT, lactate and
ABG) should be sent.
C. Initial work-up for suspected blunt aortic
injury is done with an anterior-posterior por-
table chest x-ray. Common features indicat-
ing aortic injury include widened
mediastinum, abnormal-appearing aortic
arch, left “apical cap” (i.E., blood above apex
of left lung), left hemothorax, displacement
of the left main stem bronchus, deviation of
trachea to the right, and wide left paraverte-
bral stripe. Next, if the patient is stable
N. R. Manley · G. O. Maish III (*)
Department of Surgery, University of Tennessee
Health Science Center, Memphis, TN, USA
e-mail: gmaish@uthsc.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_157
157
enough, a CT of the chest with contrast
should be obtained.
D. If an aortic injury is found on CT, urgent vascu-
lar and/or thoracic surgery consultation is rec-
ommended, depending on location of injury.
Heart rate should be maintained below 100
beats per minute and blood pressure less than
100  mmHg by using medication. Esmolol, a
beta-blocker, is recommended, given its short
half-life. If a beta-blocker is contraindicated,
diltiazem, a calcium channel blocker, can be
used. If esmolol is insufficient in controlling
blood pressure, Nicardipine is another option
and can be easily titrated. Nitroglycerin or nitro-
prusside can be added to achieve target blood
pressure as second-line agents. Please be aware
that nitroprusside can cause reflex tachycardia
and, therefore, increase ventricular contractility
(dP/dt). Vascular and/or thoracic surgery may
elect to pursue an arch angiogram prior to repair.
Both endovascular and open approaches to aor-
tic injury are possible, although current recom-
mendations favor the endovascular approach
unless the patient is hemodynamically unstable
and the patient has other obvious injuries requir-
ing operative exploration. Aortic injuries based
on CT findings and general management guide-
lines are as follows:
• Type I: Intimal tear. Typically managed
conservatively with heart rate (<100 BPM)
and blood pressure (<100 mmHg) control,
as well as serial imaging (although there is
641
642
not currently any standard timing for fol-
low-­up imaging—use clinical judgment).
• Type II: Intramural hematoma. Endovascular
or operative intervention is recommended.
• Type III: Pseudoaneurysm. Endovascular
or operative intervention is recommended.
A Patient with suspected blunt aortic injury
B ATLS
C Chest x-ray
CT chest
D Positive
· Control BP < 100 mm
Hg & HR < 100 BPM
· Vascular and/or thoracic
surgery consult
· Consider arch angiogram
· Possible open vs
endovascular surgery
Grade of aortic injury on CT:
· Type I: Intimal tear Non-
operative management
· Type II: Intramural hematoma
Endovascular or operative
management
· Type III: Pseudoaneurysm
Endovascular or operative
management
· Type IV: Rupture
Endovascular or operative
management
Abbreviations: ATLS: Advanced trauma life support; BP: Blood pressure; BPM:
Beats per minute; CT: Computed tomography.
Algorithm 157.1
N. R. Manley and G. O. Maish III
• Type IV: Rupture. Endovascular or opera-
tive intervention is recommended.
E. If the chest CT is negative for blunt aortic
injury, the trauma work-up should proceed
based on history, physical exam, and mecha-
nism of injury.
Negative E
Continue work
up for other
injuries
Recommended medications
for HR and BP control:
· Esmolol: Rapid acting beta
blocker with short half-life
· Diltiazem: Can be used if beta
blocker contraindicated
· Nicardipine: Easily titratable
· Nitroglycerin: Can be added if
esmolol not controlling BP alone
· Nitroprusside: Can be added if
esmolol not controlling BP alone
157  Deceleration Injury: Blunt Aortic Injury 643

Suggested Reading blunt traumatic aortic injury: a practice manage-

ment guideline from the Eastern Association for
the Surgery of Trauma. J Trauma Acute Care Surg.
American College of Surgeons. Advanced trauma life sup-
2015;78(1):136–46.
port. 9th ed. Chicago: American College of Surgeons;
Neschis DG.  Blunt thoracic aortic injury. Up to
2012. 336 p.
Date [Internet]. 2017 May [cited 2017 Aug 14].
Fox N, Schwartz D, Salazar JH, Haut ER, Dahm P,
Available from: https://www.uptodate.com/contents/
Black JH, et  al. Evaluation and management of
blunt-thoracic-aortic-injury.
 Penetrating Abdominal Trauma
Michael Smith and Fausto Vinces
Algorithmic Approach
A. Under most circumstances, patients with
penetrating abdominal trauma are brought
to the emergency room as a leveled trauma.
Immediately, the patient should have his or
her vital signs measured. Initial evaluation
should begin by obtaining a history from the
patient, if able, and additional information
from emergency medical transport. The
advanced trauma life support (ATLS) algo-
rithm should be followed and chest tubes
placed as needed. The most critical infor-
mation that needs to be obtained from the
history is the type of penetration (high or
low energy), the location of the wounds, the
approximate time that has passed since the
injury, and the hemodynamic stability of the
patient.
B. If hemodynamic instability is encountered in
penetrating abdominal injury, the patient
should be immediately transported to the
operating room for emergent laparotomy.
C. During ATLS work-up of the patient, con-
comitant thoracic trauma should be evaluated
for. Hemodynamically stable patients should
M. Smith
Department of Surgery, Westchester Medical Center,
Valhalla, NY, USA
F. Vinces (*)
Department of Surgery, Vassar Brothers Medical
Center, Poughkeepsie, NY, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_158
158
have careful but rapid evaluation of the abdo-
men; patients with peritoneal signs or signs of
fascial penetration should be taken to the
operating room. In patients without these
clear signs, a focused assessment sonography
for trauma (FAST) exam should follow; those
patients with free fluid should be taken to the
operating room for exploration. In isolated
penetrating abdominal injury, the area of pen-
etration should be marked with a radio-­
opaque marker such as a paper clip. Upright
chest x-ray (CXR) will demonstrate the pres-
ence of free air. Abdominal and pelvic roent-
genograms should be taken to identify foreign
bodies, noting their location to the radio-­
opaque markers.
D. Patients who sustained high-energy penetrat-
ing abdominal trauma (gunshot wounds) and
are hemodynamically stable, without free
fluid on FAST, warrant computerized tomog-
raphy to further elucidate the path of the bul-
let and any associated injuries. It is not
uncommon, especially in the obese patient,
that a bullet track is seen in the soft tissues
without fascial violation. Wound irrigation
and light packing of the bullet wound sites
should occur. It should also be noted that bul-
lets may cause thermal injury to the surround-
ing structures and blast injury from the
temporary cavitation that occurs; therefore, it
is not unwise to admit these patients for over-
night observation on NPO status while
645
646
p­erforming serial abdominal exams. Any
intra-abdominal path of the bullet warrants
immediate exploration.
E. In patients that have sustained low-energy
penetrating abdominal trauma (knife wounds,
glass lacerations, etc.), local wound explora-
tion is indicated. This may be performed with
local anesthesia and by lengthening the lac-
eration by one to two centimeters at each end.
If no fascial penetration is identified, hemo-
stasis, irrigation, and wound closure may be
performed, based upon the level of contami-
nation of the wound. In grossly contaminated
M. Smith and F. Vinces
wounds, it may be beneficial to irrigate and
debride these in the operating room as well as
place a drain and provide additional IV anti-
biotics during an overnight observation
period. If fascial violation is identified, at this
point, diagnostic peritoneal aspiration (DPA)
and diagnostic peritoneal lavage (DPL) may
be beneficial to determine if the patient
requires further exploration. Positive DPA/
DPL should then undergo either diagnostic
laparoscopy or exploratory laparotomy based
upon the comfort level of the performing
surgeon.
158  Penetrating Abdominal Trauma 647

A Penetrating abdominal injury

Vital signs
History and physical exam

Hemodynamically No
B stable?

Yes

Evisceration or Yes
peritoneal? Exploratory
laparotomy

Yes
C CXR –free air?

Positive
FAST exam

High energy Low energy

Local wound
exploration E
D Computerized
tomography

Fascial
Intraperitoneal penetration?
Extraperitoneal
injury injury
Yes No

Observation and Laparotomy / Wound management

discharge laparoscopy and discharge

Algorithm 158.1
648 M. Smith and F. Vinces

Suggested Reading Gonzalez RP, Turk B, Famlimirski M, Holevar

M.  Abdominal stab wounds: diagnostic peritoneal
lavage criteria for emergency room discharge. J
American College of Surgeons. ATLS student course
Trauma Inj Infect Crit Care. 2001;51:939–43.
manual: advanced trauma life support. 9th ed.
Zajtchuk R, Jenkins DP, Bellamy RF, Quick CM, editors.
Chicago: American College of Surgeons; 2012.
Warfare, weaponry, and the casualty. In: Textbook of
Biffl WL, Leppaniemi A.  Management guideline for
military medicine. Office of the Surgeon General,
penetrating abdominal trauma. World J Surg.
Department of the Army, United States of America;
2015;39:1373–80.
1991.
 Blunt Abdominal Trauma
Michael Smith and Fausto Vinces
Algorithmic Approach
A. Management of suspected blunt abdominal
trauma begins immediately upon viewing the
patient. The patient that is lying still and
extremely tenuous to move has either a sig-
nificant intra-abdominal injury or an injury of
the lower extremity. However, even in those
patients who appear comfortable, careful
evaluation is required. The patient’s vital
signs should be immediately measured and
with routine repeated measurements. A thor-
ough history should be taken. Stabilization of
all patients should be performed in accor-
dance with advanced trauma life support
algorithm (airway, breathing, circulation,
etc.). Large-bore intravenous access should
be established, and blood should be drawn for
analysis, including a type and cross, if the
need arises for blood transfusion. Upright
chest x-ray (CXR) should be performed to
rule out associated thoracic trauma and free
intra-abdominal air.
B. Physical exam should follow. A careful and
systematic examination of the abdomen must
be undertaken. All ecchymosis or markings
M. Smith
Department of Surgery, Westchester Medical Center,
Valhalla, NY, USA
F. Vinces (*)
Department of Surgery, Vassar Brothers Medical
Center, Poughkeepsie, NY, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_159
159
should be noted and recorded. Careful per-
cussion and palpation of the abdomen noting
any areas of fullness or tenderness should be
undertaken.
C. A focused abdominal sonography for trauma
(FAST) should be performed. Fluid is identi-
fiable on FAST exam when 250 mL has accu-
mulated. A FAST exam should not take more
than 60  s. A caveat is in the patient with
underlying cirrhosis and ascites. If the history
taken suggests this and the patient has a large
amount of free fluid, while hemodynamically
stable, the patient should be taken for a com-
puterized tomography (CT) with intravenous
contrast.
D.
The hemodynamically unstable patient
should have packed red blood cell and fresh
frozen plasma transfused and the operating
room should be notified. The hemodynami-
cally stable patient should be transported with
physician escort to computerized tomography
(CT) scan. CT scan with arterial phase and
delayed phase contrast should be performed.
If an arterial blush is seen on the computer-
ized tomographic injury, the hemodynami-
cally stable patient should undergo
angiography and embolization. The patient
should then be observed, serial hemoglobin
and hematocrit should be monitored, and
serial abdominal exams should be performed.
If the patient continues to hemorrhage or if
the serial abdominal exams demonstrate
649
650 M. Smith and F. Vinces

p­ eritoneal signs, the patient should be taken
for laparotomy or laparoscopy (with low
threshold to open conversion) based upon the
comfort of the surgeon.
E. If the CT scan demonstrates no injury, the
patient may be observed and discharged if
they remain hemodynamically stable. If CT
scan demonstrates free fluid without obvious
solid organ injury (FFWOSOI), the patient
must be observed carefully. In the hemody-
namically stable patient, observation, serial
hematocrits, and serial abdominal exam may
be performed with a low threshold for emer-
gent laparoscopy converted to laparotomy.
Diagnostic peritoneal aspiration (DPA) or
diagnostic peritoneal lavage (DPL) can be
performed; if positive, the patient should be
prepared for laparotomy. If the DPA/DPL is
negative, the patient may be discharged.

Vital signs History

Suspected abdominal trauma 25 year-old as possible Initial
female ejected from a motor vehicle complaining A stabilization Initial B
of back and low abdominal pain Abdominal Exam

Focused
C abdominal
sonography

Free fluid No free fluid

No
Exploratory Hemodynamically
D stable?
D
laparotomy

Yes

CT scan E

Active Free fluid

extravasation No injury without
extravasation

or

Hemodynamically
stable? DPA /
No DPL
Yes (+)
(-)
Angiography Laparoscopy /
and laparotomy
embolization

Observation,
Failure serial Discharge
abdominal
exams

Algorithm 159.1
159  Blunt Abdominal Trauma
Suggested Reading
Carter JW, Falco MH, Chopko MS, Flynn WJ, Wiles CE,
Guo WA.  Do we really rely on FAST for decision-­
making in the management of blunt abdominal
trauma? Injury. 2014; https://doi.org/10.1016/j.
injury.2014.11.023.
2. Chereau N, Wagner M, Tresallet C, Lucidarme O,
Raux M, Menegaux F. CT scan and diagnostic peri-
toneal lavage: towards a better diagnosis in the area
of operative management of blunt abdominal trauma.
Injury. 2016;47:2006–11.
Dammers D, El Moumni M, Hoogland II, Veeger N,
ter Avest E.  Should we perform a FAST exam in
hemodynamically stable patient presenting after
blunt abdominal injury: a retrospective cohort study.
Scand J Trauma Resus Em Med. 2017; https://doi.
org/10.1186/s13049-016-0342-0.
Harris HW, Morabito DJ, Mackersie RC, Halvorsen RA,
Schecter WP. Leukocytosis and free fluid are impor-
tant indicators of isolated intestinal injury after blunt
trauma. J Trauma Inj Infec Crit Care. 1999;46:656–9.
Jones EL, Stovall RT, Jones TS, Bensard DD, Burlew
CC, Johnson JL, Jurkovich GJ, et al. Intra-abdominal
651
injury following blunt trauma becomes clinically
apparent within 9 hours. J Trauma Acute Care Surg.
2014;76:1020–3.
Kelley SR, Tsuei BJ, Bernard AC, Boulanger BR,
Kearney PA, Chang PK. The effectiveness of focused
assessment with sonography for trauma in evaluating
blunt abdominal trauma with a seatbelt mark sign. J
Curr Surg. 2014;4:17–22.
Moore FA, Davis JW, Moore EE, Cocanour CS, West MA,
McIntyre RC.  Western Trauma Association (WTA)
critical decisions in trauma: management of adult
blunt splenic trauma. J Trauma. 2008;65:1007–11.
Ng AKT, Simons RK, Torreggiani WC, Ho SG,
Kirkpatrick AW, Brown DRG.  Intra-abdominal free
fluid without solid organ injury in blunt abdominal
trauma: an indication for laparotomy. J Trauma Inj
Infec Crit Care. 2002;52:1134–40.
Robinson JD, Sandstrom CK, Lehnert BE, Gross
JA. Imaging of blunt abdominal solid organ trauma.
Sem Roentgen. 2016;51:215–29.
Rodriguez C, Barone JE, Wilbanks TO, Rha C-K, Miller
K. Isolated free fluid on computed tomographic scan
in blunt abdominal trauma: a systematic review of
incidence and management. J Trauma Inj Infect Crit
Care. 2002;53:79–85.
 Management Algorithm for Acute
and Chronic Diaphragmatic
Injuries
Elif Onursal and Fausto Vinces
Algorithmic Approach
A. Diagnosis of diaphragmatic injury in the
acute setting presents a unique challenge to
many clinicians as these injuries are often
asymptomatic or masked by other concomi-
tant injuries. As such, the most important tool
in the initial assessment of the patient with
diaphragmatic injury is a high index of suspi-
cion [1]. Primary and secondary surveys
should be completed as outlined by advanced
trauma life support (ATLS) protocol [2].
After establishing that the patient is hemody-
namically stable, additional history should
include questions regarding the mechanism
of injury, severity of impact, and trajectory of
any missile-related injuries [3].
B. Once hemodynamic stability has been estab-
lished, adjuncts to history and physical may
include the focused abdominal sonography
for trauma (FAST) exam (may detect large
ruptures associated with blunt force), plain
chest radiographs (intra-abdominal contents
may be seen in the left hemithorax), or helical
computed tomography (CT) scan of the chest,
abdomen, and pelvis with 3D reconstructions
E. Onursal
Department of General Surgery, St. Barnabas
Hospital Health System, Bronx, NY, USA
F. Vinces (*)
Department of Surgery, Vassar Brothers Medical
Center, Poughkeepsie, NY, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_160
160
[3]. It is important to note that these imaging
studies are intended more to rule in a dia-
phragmatic injury rather than to rule one out.
C. If clinical suspicion of a diaphragmatic injury
persists after imaging studies, operative inter-
vention to establish a diagnosis is mandated
[4]. Operative approach for management of
diaphragmatic injury is stratified based upon
chronicity of injury, the presence of concomi-
tant injuries, and the hemodynamic stability
of the patient [3].
D. For acute injuries in which there is no other
indication for laparotomy, a minimally inva-
sive technique may be employed with prefer-
ence given to thoracoscopy over laparoscopy
due to an increased risk of precipitating ipsi-
lateral tension pneumothorax during estab-
lishment of pneumoperitoneum [3]. For acute
diaphragmatic injuries associated with con-
comitant injury, operative approach is via
laparotomy with trans-diaphragmatic explo-
ration of the ipsilateral thoracic cavity to rule
out further hemorrhage or injury [1].
E. In the event that a damage control laparotomy
in a hemodynamically unstable patient
reveals a diaphragmatic injury, it is consid-
ered acceptable to temporarily pack any
defect found with laparotomy pads and return
for definitive repair once the patient is stabi-
lized [3].
F. For chronic injuries, many favor thoracot-
omy due to tendency of dense pleural
653
654
adhesions to form in this setting requiring
extensive lysis.
G. Intraoperative technique in all settings is
dependent upon size of defect and degree of
contamination from associated injury or per-
foration of a strangulated viscus [5].
H. Because of the natural progression of dia-
phragmatic defects toward herniation, stran-
gulation, and obstruction or perforation of
intra-abdominal viscera, all defects should be
repaired regardless of size [3]. All non-viable
tissue should be debrided. Primary repairs
should be conducted using non-absorbable
suture due to an increased risk of recurrence
when absorbable sutures are utilized [1].
I. Defects less than 8 cm in size can be repaired
primarily. Defects larger than this size favor
prosthetic synthetic mesh repair or transposi-
E. Onursal and F. Vinces
tion and re-implantation of the diaphragm
cephalad by 1–2 interspaces [1].
J. In the event of gross spillage of intestinal
contents, a washout of the thoracic cavity
should be done using saline irrigation con-
taining antibiotics [3]. The use of synthetic
mesh should be avoided in these cases in
favor of autologous tissue (latissimus dorsi,
rectus abdominis, or external oblique muscle
flaps) or biologic mesh (that is replaced with
synthetic mesh at a later date) [1].
K. Postoperatively, the clinician should be mind-
ful of complications such as breakdown of
repair, iatrogenic injuries to the phrenic nerve
leading to hemiparesis of the diaphragm, atel-
ectasis, empyema, pneumonia, and morbidity
related to concomitant injuries [3].
160  Management Algorithm for Acute and Chronic Diaphragmatic Injuries 655

Traumatic injury to thoraco-

abdominal region A

Damage control No
laparotomy with Perform
temporary packing of Patient HD stable? primary
any diaphragmatic survey
injury found
C
Yes

Proceed to chronic Secondary survey

including imaging No
diaphragmatic injury Findings concerning for or Manage other injuries
algorithm (CXR, CT scan or
diagnostic of diaphragm present
FAST exam)
injury?

F B E
Yes

Minimally invasive
techniques: No Indications for
thoracoscopy > laparotomy present?
laparoscopy

D Yes

Perform exploratory laparotomy

Explore ipsilateral thorax

through defect to rule out G
Primary repair with non- hemorrhage and further injury
absorbable suture

Yes H

Washout thorax with saline Yes

I Defect < 8 cm in antibiotic irrigation + avoid use
Gross contamination
present?
size? of synthetic mesh for repair

No J No

Prosthetic biologic mesh repair OR

autologous tissue repair OR transposition Yes
and re-implantation of diaphragm cephalad I Defect < 8 cm in
Primary repair with non-
absorbable suture
size?

No

Prosthetic
synthetic mesh
repair

Algorithm 160.1
656 E. Onursal and F. Vinces

Perform history &

physical exam
A

Obtain adjunctive imaging

studies: CXR, US, CT scan B

Perform thoracotomy and lysis

of adhesions and reduction of F
abdominal contents

Washout thorax with saline Yes

Gross contamination
H antibiotic irrigation + avoid use
present?
G
of synthetic mesh for repair

No

Yes Defect <8

Primary repair with non-
absorbable suture
cm in
size?
I Defect <8 Yes Primary repair with non-
cm in
absorbable suture
size?

No
No

Prosthetic biologic mesh repair or Prosthetic synthetic

autologous tissue repair OR transposition mesh repair
and re-implantation of diaphragm cephalad

Algorithm 160.2

3. Cameron J, Cameron A. Cameron current surgical ther-

References
1. Mattox K, Moore E, Feliciano D.  Trauma. 7th
ed. New  York: McGraw-Hill Medical; 2013.
p. 901–17.
2. American College of Surgeons. Advanced trauma
life support. 9th ed. Chicago: American College of
Surgeons; 2013.
apy. 11th ed. Philadelphia: Saunders; 2014. p. 2692–9.
4. Brunicardi F, Anderson D, Billiar T, Dunn D, Hunter
J, Matthews J, Pollock R. Schwartz’s principles of sur-
gery. 9th ed. New York: McGraw-Hill; 2010. p. 324.
5. Townsend C, Beauchamp R, Evers B, Mattox
K. Sabiston textbook of surgery: the biological basis
of modern surgical practice. 19th ed. Philadelphia:
Saunders; 2012. p. 454–5.
 Management of Traumatic Liver
Injuries
Melissa Amberger and Fausto Vinces
Algorithmic Approach
A. As with all trauma patients, initial evaluation
of the patient with a traumatic injury concern-
ing for hepatic injury should be taken accord-
ing to the advanced trauma life support
(ATLS) algorithm [1]. This should include an
immediate primary survey assessing airway
(A), breathing (B), circulation (C), disability
(D), and exposure (E). Once a patient is ini-
tially stabilized during the primary survey, a
further history is elicited and can be taken
from emergency medical personnel or
bystanders if the patient is obtunded or intu-
bated and unable to provide history. A focused
history should include allergies, medications,
past medical history, last meal, and events or
mechanism of injury (AMPLE). A complete
head to toe physical should then occur inves-
tigating for any signs of traumatic injury. Any
decompensation in clinical status should
prompt a re-evaluation of the primary
survey.
D. Angioembolization of the proper hepatic
M. Amberger
Department of Surgery, St. Barnabas Health System,
Bronx, NY, USA
F. Vinces (*)
Department of Surgery, Vassar Brothers Medical
Center, Poughkeepsie, NY, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_161
161
B. As part of the primary survey, circulation or
hemodynamic (HD) stability should be
assessed. Tachycardia and hypotension are
hallmarks of intravascular depletion and
should prompt investigation for source of
hemorrhage in the traumatically injured
patient. This includes a focused assessment
with sonography in trauma (FAST) exam or a
diagnostic peritoneal lavage (DPL) to evaluate
for intra-abdominal source of hemorrhage.
Any study positive for intra-abdominal source
of hemorrhage in a HD-unstable patient
should prompt emergent laparotomy [2].
C. In patients who are HD stable with a mecha-
nism concerning for solid organ injury,
including hepatic injury, a computed tomog-
raphy (CT) scan [2] should be completed
with intravenous contrast administration to
evaluate for injuries with active hemorrhage.
Hepatic injury is graded using a radiographi-
cally or clinically based system [3] developed
by the American Association for the Surgery
of Trauma (AAST). Increasing grade of
injury is associated with higher likelihood of
need for angioembolization or operative man-
agement [4].
artery or segmental branches can be per-
formed to control hepatic hemorrhage. This is
particularly useful in the traumatically injured
patient who is HD stable, but with active
extravasation of contrast (a blush) on CT
657
658
scans [5]. Angioembolization can be used as
an adjunct to operative intervention for
­further control of hemorrhage. Additionally it
can be used in the patient admitted and man-
aged non-operatively with ongoing transfu-
sion requirements as a primary intervention
for control of hemorrhage [6].
E. Patients with hepatic injury who are HD sta-
ble without a blush on CT scan or who are
HD stable with a blush on CT scan who have
undergone angioembolization should be
admitted for observation. Serial monitoring
of hemoglobin or hematocrit should be under-
taken. The patient should receive serial
abdominal examinations, initially be kept nil
per os (NPO), be placed initially on bed rest,
and be closely HD monitored. If clinical
decompensation occurs or there are ongoing
transfusion requirements, the patient should
undergo angioembolization. If this has
already been performed and is deemed unsuc-
cessful, operative exploration is mandated.
F. Operative exploration should proceed via
exploratory laparotomy. Packing should be
M. Amberger and F. Vinces
placed in all four quadrants of the abdomen.
The decision to pursue definitive repair ver-
sus damage control measures should be made
early so as to minimize risk of progression to
the lethal triad (hypotension, acidosis, and
coagulopathy) [6]. If packing does not suc-
cessfully obtain hemostasis of liver injury
then a Pringle maneuver (intermittent clamp-
ing of the hepatoduodenal ligament and its
contained structures) can be employed [7].
This is successful for many liver injuries with
the exception of a retrohepatic caval injury.
This particular injury has been treated with
cavo-atrial shunting but is often fatal [8].
G. After successful management of hepatic
injury, the practitioner should remain wary
for complications of hepatic injury such as a
liver abscess, biloma (which may require
ERCP for management) [8], biliary ascites, or
hemoperitoneum. These entities can be man-
aged with a combination of interventional
radiology or laparoscopically placed drainage
catheters. In the case of hemobilia, repeated
angioembolization may be required [9].
161  Management of Traumatic Liver Injuries 659

A Initial assessment of trauma

patient w/ suspected Hepatic Injury

HD unstable or Yes FAST exam or

B peritonitis? DPL

No

C Positive? No
CT scan demonstrating liver injury

Continue resuscitation
Consider other sources of
No instability
Blush Yes Repeat FAST/DPL

Yes

No Emergent
Continued laparotomy/damage F
HD stability? control surgery

Yes

No Previous IR
D Angioembolization w/ embolization
interventional radiology ??

No

Admission for serial abdominal exams, Continued HD

E serial hemoglobin measurements, HD Stability?
monitoring

Yes

G Follow up Care

Algorithm 161.1
660 M. Amberger and F. Vinces

References 5. East.org. Blunt hepatic injury, selective nonopera-

tive management of  – practice management guide-
line. 2012. [online] Available at: http://www.east.org/
1. American College of Surgeons. Advanced trauma
education/practice-management-guidelines/blunt-
life support. 9th ed. Chicago: American College of
hepatic-injury%2c-selective-nonoperative-manage-
Surgeons; 2013.
ment-of [Accessed 30 Oct 2017].
2. East.org. Blunt abdominal trauma, evaluation of  –
6. Kozar R.  WTAAlgorithms. n.d. [online]
practice management guideline. [online] East.
Westerntrauma.org. Available at: http://www.western-
org. Available at: http://www.east.org/education/
trauma.org/algorithms/WTAAlgorithms_files/gif_3.
practice-management-guidelines/blunt-abdominal-
htm [Accessed 30 Oct 2017].
trauma%2c-evaluation-of [Accessed 30 Oct 2017].
7. Kozar R.  WTAAlgorithms. [online] Westerntrauma.
3. Moore E, Cogbill T, Malangoni M, Jurkovich G,
org. n.d. Available at: http://www.westerntrauma.
Champion H.  Injury scoring scales  – the American
org/algorithms/WTAAlgorithms_files/gif_5.htm.
Association for the Surgery of Trauma. [online]
[Accessed 30 Oct 2017].
Aast.org. 1994. Available at: http://www.aast.org/
8. Hirshberg A, Mattox K.  Top knife. Nr Shrewsbury:
Library/TraumaTools/InjuryScoringScales.aspx#liver
TFM; 2005. p. 83–98.
[Accessed 30 Oct 2017].
9. Baillie J.  Hemobilia. Gastroenterol Hepatol.
4. Mattox K, Moore E, Feliciano D.  Trauma. 7th ed.
2012;8(4):270–2.
New York: McGraw-Hill Medical; 2013.
 Management of Pancreatic Trauma
Shreya Jammula and Eric H. Bradburn
Algorithmic Approach
A. Mechanism of injury (MOI) is important to
discern as it can provide valuable information
on patient presentation. Blunt pancreatic
injury can be notoriously difficult to diagnose
but presence of concurrent abdominal injuries
can result in distinct physical exam findings,
including shock and peritonitis. Initial workup
with positive findings on focused assessment
with sonography in trauma (FAST) and/or
diagnostic peritoneal lavage (DPL) can also
help aid diagnosis and provide clear indica-
tions for exploratory laparotomy.
B. For blunt MOI, it is important to maintain a high
index of suspicion in order to accurately diag-
nose pancreatic injury as physical exam and ini-
tial imaging can frequently be negative [1].
(a) It is important to obtain additional imag-
ing such as an abdominal computed
tomography (CT) scan as well as serum
lipase and amylase levels.
(i) It should be noted that elevated serum
lipase/amylase levels are not diagnos-
tic of pancreatic injury as elevations
can occur secondary to other sources
of injury.
S. Jammula · E. H. Bradburn (*)
Department of Trauma and Acute Care Surgery, Penn
Medicine Lancaster General Health,
Lancaster, PA, USA
e-mail: ebradburn3@lghealth.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_162
162
(b) It is important to serially follow levels of
enzymes. Repeat abdominal CT scan
may be warranted.
(c) In the event of positive findings on abdom-
inal CT and/or rising enzyme levels,
exploratory laparotomy may be indicated.
C. In the absence of CT findings and normal levels
of enzymes, additional diagnostic imaging may
be warranted. Magnetic resonance cholangio-
pancreatography (MRCP) is a non-­ invasive
diagnostic imaging modality that can help diag-
nose injury to the pancreatic duct. Visualization
of a normal duct indicates preserved pancreatic
duct and likely does not require surgery.
(a) MRCP should only be attempted on
hemodynamically stable patients and
does not offer any therapeutic value.
D. The presence of extravasation on MRCP indi-
cates ductal injury and likely warrants surgi-
cal exploration. The degree of extravasation
and location of ductal injury (proximal vs.
distal) can affect decision to preserve/resect
portions of the pancreas.
E. Penetrating pancreatic injury typically war-
rants surgical exploration. The presence of
non-specific physical exam findings such as
shock and peritonitis as well as positive find-
ings on initial diagnostic imaging makes it
easier to diagnose. In addition, certain mech-
anisms of injury themselves can prompt an
automatic exploratory laparotomy i­ rrespective
of presence of other findings.
661
662
F. Once the appropriate surgical exposure has
been achieved, a thorough inspection of the
entire pancreas must be performed.
(a) Pancreatic injury can be graded on a scale
from I to V, with Grades I–II indicating
preservation of pancreatic duct and
majority of pancreatic tissue.
(b) Once the pancreatic tissue has been exam-
ined, direct inspection of the pancreatic
duct should also be performed. In addi-
tion, a fluoroscopic cholecystocholan-
giography can be performed for definitive
knowledge regarding status of the duct.
Blunt
mechanism
of injury
A B
Findings: shock, peritonitis, + FAST, +
DPL
Exploratory
laparotomy
F, G, H
Exploratory
laparotomy
Algorithm 162.1
S. Jammula and E. H. Bradburn
G. Negative findings on cholecystocholangiog-
raphy warrant conservative therapy with pres-
ervation of pancreatic tissue. A surgical drain
(closed suction) is indicated.
H.
Extravasation indicates ductal injury.
Location of ductal injury is important as
proximal injury can be managed with a surgi-
cal drain without pancreatic resection. Distal
ductal injury requires pancreatectomy.
(a) It should be noted that extensive pancre-
atic injury with or without ductal involve-
ment may warrant pancreatectomy and/or
splenectomy [2, 3].
Minimal/no physical exam findings,
normal FAST
Enzyme assays,
abdominal CT
scab
+ –
MRCP (stable
C
patient)
Extravasation –
D Ductal injury Conservative management
Exploratory
laparotomy
H
162  Management of Pancreatic Trauma 663

Penetrating
mechanism of
injury

Non-specific indications: shock, peritonitis, Mechanism of injury (transperitoneal

+ FAST, + DPL, + abdominal CT scan gunshot wound)

Exploratory laparotomy

Fluoroscopic
F ERCP optional
cholecystocholangiography

Extravasation –

Conservative therapy (closed

H Ductal injury
suction drainage) G

Proximal Distal

Closed suction Distal

drainage pancreatectomy

Algorithm 162.2
664 S. Jammula and E. H. Bradburn

References 2. Jacobs LM, Gross RI, Luk SS. Advanced trauma oper-

ative management. Woodbury: Cine-Med, Inc; 2004.
3. Maggio PM, Clark D. Management of duodenal and pan-
1. Debi U, Kaur R, Prasad KK, Sinha SK, Sinha A,
creatic trauma in adults. In: Post TW, editor. UpToDate.
Singh K. Pancreatic trauma: A concise review. World
Waltham: UpToDate. Accessed on 29 Nov 2017.
J Gastroenterol. 2013;19(47):9003–11.
 Management of Traumatic Splenic
Injuries
Eric H. Bradburn, Kameron Durante,
and Shreya Jammula
Algorithmic Approach
A. Splenic injury is commonly encountered in
the setting of blunt abdominal trauma, of
which motor vehicle collisions (MVCs)
account for roughly 75% [1]. Initial trauma
evaluation follows the principles established
by advanced trauma life support (ATLS) in
order to rapidly identify life-threatening inju-
ries and provide appropriate resuscitation [1,
2]. Following primary assessment, a thorough
history and physical examination are essen-
tial. Acute trauma to left thoracic/abdomen/
flank areas should prompt special consider-
ation of splenic injury. Physical findings can
include left upper quadrant pain, referred
pain to the left shoulder (Kehr’s sign), abdom-
inal wall contusion, and peritonitis [2]. It is
vital to remember that some patients with sig-
nificant splenic injuries can present without
any remarkable physical exam findings.
B. Along with physical examination, vital signs,
diagnostic imaging, and laboratory values
can be helpful in detecting injury and guiding
subsequent management. Abdominal trauma
patients typically undergo focused assess-
ment with sonography in trauma (FAST). A
E. H. Bradburn (*) · K. Durante · S. Jammula
Department of Trauma and Acute Care Surgery, Penn
Medicine Lancaster General Health,
Lancaster, PA, USA
e-mail: ebradburn3@lghealth.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_163
163
positive FAST in the setting of hemodynamic
instability is an absolute indication for emer-
gent exploratory laparotomy. Diffuse perito-
nitis and decreasing hemoglobin suspected to
be secondary to splenic bleeding also warrant
prompt operative care [2].
C. In patients who did not initially require emer-
gent surgical intervention, computed tomog-
raphy (CT) scan with intravenous (IV)
contrast is indicated as it can provide infor-
mation regarding the grade of injury [2].
Grades I–III are classified as injuries to the
spleen up to lacerations greater than 3-cm
parenchymal depth or involving trabecular
vessels as well as subscapular hematoma
greater than 50% surface area/intraparenchy-
mal equal to or greater than 5-cm or expand-
ing [2, 3]. Grades IV–V include laceration
involving segmental or hilar vessels resulting
in major devascularization (>25%) up to
complete devascularization or shattered
spleen [2, 3]. Grades I–III can be managed
non-operatively, while grades IV–V are typi-
cally managed surgically [3]. For grades I–
III, in the setting of a large hemoperitoneum
or ongoing bleeding, angiography could be
an alternative to laparotomy.
D. Angiography with or without embolization
has been useful for patients managed non-­
operatively. A negative result can avoid
unnecessary surgery, and a positive result can
be treated with embolization. A retrospective
665
666
analysis of blunt splenic injuries at a Level I
trauma center determined that embolization
in non-operative patients was associated with
salvage rates of 92% [4]. Angioembolization
is not without risks as evidenced by incidence
of complications in 20% of patients including
failure to control bleeding [5].
E. All patients managed non-operatively should
be monitored closely for changes in vitals
(tachypnea, tachycardia, hemodynamic insta-
bility). Patients should also receive a secondary
CT scan with IV contrast 48 h post-trauma [3].
F. Twenty to forty percent of patients with
splenic injury warrant surgical intervention,
E. H. Bradburn et al.
with open approach regarded as the standard
of care [6]. Grades IV–V spleen typically
necessitate surgery [3].
G. Patients with splenic injuries are advised to
refrain from participating in contact sports
and other high-risk activities for 3  months
following trauma [3]. While delayed rupture
of splenic pseudoaneurysm is a documented
complication in patients managed non-­
operatively, repeat CT imaging is not per-
formed routinely, though there may be an
indication in select patients to lift activity
restrictions.
163  Management of Traumatic Splenic Injuries 667

History and physical examination

Blunt abdominal trauma and/or left upper quadrant abdominal tenderness
A

Obtain vital signs, physical examination

B
Hemodynamically
unstable?
peritonitis?

No Yes
F

CT scan abdomen with IV contrast to identify splenic Immediate

injury grade laparotomy

Grade I-III Grade IV-V

Ongoing splenic Consider

bleeding, moderate to angiography
Small hemoperitoneum large hemoperitoneum

F
E
If unsuccessful or
unable, immediate
laparotomy
Manage non-operatively, monitor closely, repeat CT
with IV contrast 48 h post trauma/symptoms

G Follow up care

Algorithm 163.1
668 E. H. Bradburn et al.

References 4. Haan J, Scott J, Boyd-Kranis RL, Ho S, Kramer M,

Scalea TM. Admission angiography for blunt splenic
injury: advantages and pitfalls. J Trauma Acute Care
1. Diercks DB, Clarke S.  Initial evaluation and man-
Surg. 2001;51(6):1161–5.
agement of blunt abdominal trauma in adults. In:
5. Stassen NA, Bhullar I, Cheng JD, Crandall ML,
UpToDate, Post TW, editors. UpToDate, Waltham,
Friese RS, Guillamondegui OD, Jawa RS, Maung
Accessed via https://www.uptodate.com/contents/ini-
AA, Rohs TJ, Sangosanya A, et  al. Selective non-
tial-evaluation-and-management-of-blunt-abdominal-
operative management of blunt splenic injury: an
trauma-in-adults on 7 July, 2017.
Eastern Association for the Surgery of trauma practice
2. Maung AA, Kaplan LJ. Management of splenic injury
management guideline. J Trauma Acute Care Surg.
in the adult trauma patient. In: UpToDate, Post TW,
2012;73(5.4):S294–300.
editors. UpToDate, Waltham. Accessed via https://
6. Maung AA, Kaplan LJ.  Surgical management of
www.uptodate.com/contents/management-of-splenic-
splenic injury in the adult trauma patient In: UpToDate,
injury-in-the-adult-trauma-patient on 7 July, 2017.
Post TW, editors. UpToDate, Waltham. Accessed via
3. Watson GA, Hoffman MK, Peitzman AB. Nonoperative
https://www.uptodate.com/contents/surgical-manage-
management of blunt splenic injury: what is new? Eur
ment-of-splenic-injury-in-the-adult-trauma-patient on
J Trauma Emerg Surg. 2015;41(3):219–28.
7 July, 2017.
 Management of Kidney and Ureter
Injuries
Eric H. Bradburn, Madison Morgan,
and Danielle Von Nieda
 lgorithmic Approach: Kidney
A of kidney injury, a CT scan of the abdomen
Injuries
A. First, when performing an evaluation of a
patient with an acute kidney injury (AKI), the
physician should recount the history and per-
form a physical examination. AKI is defined
by a sudden decline in kidney function. The
major indicators of AKI are flank or abdomi-
nal pain and tenderness. Abdominal bruising
and skin rashes are also indicators of AKI, as
well as reported decreased urine output if the
evaluation does not immediately follow the
injury [1].
B. Vital signs, blood work, and a physical exam-
ination can provide essential information,
which may raise suspicion for an acute kid-
ney injury. An increase in blood urea nitro-
gen, an electrolyte imbalance, and hematuria
are all concerns for AKI.  An increase in
serum creatinine levels, a 50% or greater
decrease in globular filtration rate, and a urine
output less than 0.5  ml/kg/h over 12  h are
additional concerns for kidney injury [2].
C. If the patient is determined to be hemody-
namically stable but presents with indicators
E. H. Bradburn (*) · M. Morgan · D. Von Nieda
Department of Trauma and Acute Care Surgery, Penn
Medicine Lancaster General Health,
Lancaster, PA, USA
e-mail: ebradburn3@lghealth.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_164
164
should be obtained. If an AKI is suspected by
radiology, the injury should be graded in
order to determine the next steps in treating
the injury [3].
D. If the patient is determined to be hemody-
namically unstable upon initial examination,
immediate surgical intervention is suggested.
This intervention may include a laparotomy
to explore the abdomen to determine the
mechanism and severity of injury, allowing
the physician to decide what further actions
are necessary [4].
E. Grade I injuries are likely microscopic contu-
sions or subcapsular hematomas. Grade II
injuries are nonexpanding perirenal hemato-
mas or less than 1.0 cm parenchymal depth of
renal cortex lacerations without urinary extrav-
agation [4]. Grade I and II AKIs should be
managed with clinical observation, necessary
antibiotics, and a repeat of the blood work [2].
F. Grade III injuries are lacerations less than
1.0  cm parenchymal depth of renal cortex
without collecting system rupture or urinary
extravagation [4]. Grade III AKIs may or may
not require surgical intervention. It is to the
physician’s discretion as to whether or not
surgery is required, in which case the injury
will follow grade IV protocol [2].
G. Grade IV injuries are parenchymal lacera-
tions that extend through the renal cortex,
medulla, and collecting system, or vascular
669
670 E. H. Bradburn et al.

main renal artery or vein injuries with con-
tained hemorrhage. Grade V injuries include
lacerations that completely shatter the kidney
and vascular injuries with the avulsion of
renal hilum which devascularizes the kidney
[4]. Grade IV or V AKIs require immediate
surgical intervention [2].
H. Follow up care should be obtained when
appropriate.

History and Physical Exam:

A Flank or abdominal pain and bruising
Decreased urine output

B Obtain vital signs, blood work and perform a physical examination

Is the patient
hemodynamically
stable?

Yes No

C Analyze blood work further Immediate surgical intervention D

Increased Creatinine x2 or GFR decrease > 50%,Urine

Output < .5 ml/kg/h × 12 h, electrolyte imbalance, and
hematuria are concerns for kidney injury.Obtain
a CT scan

What grade of
kidney injury
does CT show?
G
Grade 4-5
Grade 1-2
E
Grade 3
Observation, antibiotics, and
repeat labs
F

No

Do the
associated Yes
injuries require
a laparotomy? H

Follow-up

Algorithm 164.1
164  Management of Kidney and Ureter Injuries
 lgorithmic Approach: Ureter
A nosed by surgical exploration due to the
Injuries
A. When evaluating a patient with a suspected
ureter injury, the first step should be obtain-
ing the history and performing a physical
exam. A major sign of a ureter injury is flank
pain. Penetrating injury near the ureter or a
recent surgical procedure should also be
taken into consideration during evaluation.
Ureter injuries are very uncommon. They
make up less than 1% of genitourinary inju-
ries. Ureter injuries are to be suspected if
there is a multisystem injury, specifically if
there is a penetrating injury near the ureter
[5]. Most damage to the ureter occurs during
surgery, with the most commonly occurring
during gynecological surgeries or a surgical
pelvic procedure [6].
B. If the injury is detected initially, and the
patient appears to be hemodynamically sta-
ble, a CT scan with delayed contrast should
be performed [5]. If the CT is normal, no fur-
ther treatment is necessary. However, if the
CT is nondiagnostic, retrograde pyelography
should be done [7]. If either the CT or the
retrograde pyelography shows extravasation,
surgical exploration/stenting should be com-
pleted. Many ureter injuries are first diag-
671
traumatic nature of the injuries [8]. A normal
retrograde pyelography also requires no
treatment.
C. If the injury is detected initially and the
patient is not hemodynamically stable, imme-
diate surgical intervention is necessary. The
principles of repair include spatulation, lack
of tension, stenting, postoperative drainage,
debridement, and a water-tight anastomosis
with fine nonreactive absorbable suture [6].
D. A delay in diagnosis is the biggest factor con-
tributing to morbidity in ureter injuries [6]. If
the ureter injury is not detected initially,
ultrasound (US), intravenous pyelogram
(IVP), and/or CT should be done to diagnose
the delayed injury. If an abscess or urinoma is
present, percutaneous nephrostomy and peri-
ureteral drainage should be performed. In the
case of an incomplete urethral injury, retro-
grade ureteral stenting should be considered
[5].
E. If symptoms still persist following these pro-
cedures, surgical exploration should be
considered.
F. No further treatment is necessary if the symp-
toms are resolved.
G. Follow-up should be done in ureter injuries
requiring surgical intervention.
672 E. H. Bradburn et al.

A History and Physical Exam:

Flank pain, penetrating injury to the abdomen, or recent surgical procedure

Is the ureter
injury detected
initially?
hemodynamically
D
Yes No

US, IVP, and/or CT

Is the patient
hemodynamically
Urinoma drainage and/or Urinary
stable?
diversion by stent or PCN
B Yes No C

Immediate surgical intervention Are

CT with delayed contrast
symptoms
persisting?
Not diagnostic
E No Yes F

Retrograde
Pyelography

Surgical
Extravasation Normal No treatment required
exploration

Surgical
exploration Follow-up
/stent
G

Algorithm 164.2
164  Management of Kidney and Ureter Injuries 673

References 5. Zinman LN, Vanni AJ.  Surgical Management of

Urologic Trauma and Iatrogenic Injuries. Surg Clin
North Am. 2016;96(3):425–39.
1. Moore EE, Cogbill TH, Malangoni M, Jurkovich GJ,
6. Teber D, Egey A, Gozen AS, Rassweiler J.  Ureteral
Champion HR.  Injury scoring scale: a resource for
injuries. Diagnostic and treatment algorithm. Urologe
trauma care professionals: The American Association
A. 2005;44(8):870–7.
for the Surgery of Trauma; 2017. http://www.aast.org/
7. Asali MG, Romanowsky I, Kaneti J. External ureteral
Library/TraumaTools/InjuryScoringScales.aspx
injuries. Harefuah. 2007;146(9):686–9, 734.
2. Khwaja A. KDIGO clinical practice guideline for acute
8. Siram SM, Gerald SZ, Greene WR, Hughes K,
kidney injury. Nephron Clin Pract. 2012;120(4):179–84.
Oyetunji TA, Chrouser K.  Ureteral trauma: patterns
3. Kalantarinia K. Novel imaging techniques in acute kid-
and mechanisms of injury of an uncommon condition.
ney injury. Curr Drug Targets. 2009;10(12):1184–9.
Am J Surg. 2010;199(4):566–70.
4. Rahman M, Shad F, Smith M.  Acute kidney injury:
a guide to diagnosis and management. Am Fam
Physician. 2012;86(7):631–9.
 Urethral Trauma
Cheyenne C. Sonntag and Susan MacDonald
Algorithmic Approach
A.  On arrival, the first step in the evaluation of
patients with blunt trauma is the primary sur-
vey (ABCs) to identify and treat life-­ eter drainage of the bladder (suprapubic or
threatening conditions.
B. Adjuncts and secondary survey are performed.
Urethral injury is strongly suspected if there is
blood at the urethral meatus, gross hematuria,
or a high-riding, ballotable prostate on rectal
examination, especially if these findings are in
conjunction with a pelvic fracture. While D. In males, urethral injury is categorized by the
female urethral injury is rare and almost
exclusively associated with pelvic fracture, it
should be suspected in cases of vaginal bleed-
ing, severe pelvic fracture, labial edema, gross
hematuria, or external genitalia injury [1–4].
If urethral injury is suspected, blind insertion
of a catheter should not be performed as it
risks conversion of partial laceration to a com-
plete urethral disruption.
C. If suspicion of urethral injury exists, a retro-
grade urethrogram should be performed.
Contrast is instilled through a catheter placed
C. C. Sonntag
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
S. MacDonald (*)
Division of Urology, Department of Surgery, Penn
State Milton S. Hershey Medical Center,
Hershey, PA, USA
e-mail: smacdonald@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_165
165
at the meatus to opacify the urethra while
oblique X-rays are obtained. Extravasation of
contrast confirms urethral injury. The immedi-
ate primary goal of treatment is to obtain cath-
urethral). A secondary goal of treatment may
be placement of a urethral catheter over a wire
placed into the bladder using a cystoscope by
the urology team in so-called primary realign-
ment to reduce future scarring or urethral
stricture disease.
segment of the urethra it occurs in: the poste-
rior urethra (at or above membranous urethra)
vs. the anterior urethra (penile or bulbar ure-
thra). Pelvic fracture urethral injury (PFUI) is
an injury of the posterior urethra which occurs
in 1.5–10% of pelvic fractures and can occur
with concomitant bladder injury in up to 15%
of cases [5, 6]. If PFUI is confirmed on retro-
grade urethrogram, an evaluation of the blad-
der should also be considered with a CT
cystogram or filling through a catheter at the
time of open exploration to identify any
lacerations.
E. Anterior injury may result from blunt (straddle
injury), penetrating injury or penile fracture.
F. Penetrating injury to the anterior urethra should
be immediately surgically repaired, as long as
there is no major tissue loss or other major
injuries [4]. Devitalized tissue is debrided, and
the edges of the remaining urethra are
675
676
r­eapproximated over a catheter that will
remain in place for 3–4 weeks postoperatively.
A peri-­catheter retrograde urethrogram is then
performed to assess for appropriate healing
prior to removing the catheter.
G. Straddle injury to the anterior urethra is treated
with suprapubic or urethral catheter drainage
and is associated with a high risk of future ure-
thral stricture.
H. and I. Posterior urethral/PFUI injury is tradi-
tionally managed with suprapubic catheter
drainage and reconstruction in a delayed fash-
ion 3–6  months later. Straddle injuries typi-
cally result in anterior urethral stricture disease
C. C. Sonntag and S. MacDonald
months after the initial injury and thus require
referral to a urologist for follow-up and possi-
ble future intervention. Primary realignment of
the posterior urethral injury, where a catheter is
placed across the region of disruption, is
increasingly common with advancements in
urethroscopic equipment; however, it should
only be performed by experienced providers.
Following primary realignment, a pericatheter
retrograde urethrography is performed at
3–4 weeks.
J.  All patients should be followed for at least
1  year to monitor for stricture, erectile dys-
function or incontinence [4].
165  Urethral Trauma 677

Primary survey, adjuncts, secondary survey

A

No
Signs of
Continue with
B urethral
standard trauma
trauma?
assessment and care

Yes

Retrograde
C urethrogram

D Posterior/ PFUI Injury Anterior E

location?

Evaluation for Straddle Penetrating

concomitant
bladder injury
G F

I H

Primary realignment: Traditional:

1. Catheter placement 1. Immediate reconstruction
1. Experienced/specialist 1. Suprapubic catheter (suprapubic or urethral) 2. Pericatheter Retrograde
2. Pericatheter Retrograde 2. Reconstruction delayed 2. Remove catheter in Urethrogram in
Urethrogram in 3-4 weeks 3-6 months 3-4 weeks 3-4 weeks

J All: Follow-up at least 1 year

Algorithm 165.1

4. Morey AF, Brandes S, Dugi DD 3rd, Armstrong JH,

References
1. Venn SN, Greenwell TJ, Mundy AR. Pelvic fracture inju-
ries of the female urethra. BJU Int. 1999;83(6):626–30.
2. Goldman HB, Idom CB Jr, Dmochowski RR. Traumatic
injuries of the female external genitalia and their associa-
tion with urological injuries. J Urol. 1998;159(3):956–9.
3. Perry MO, Husmann DA.  Urethral injuries in
female subjects following pelvic fractures. J Urol.
1992;147(1):139–43.
Breyer BN, Broghammer JA, et al. Urotrauma: AUA
guideline. J Urol. 2014;192(2):327–35.
5. Bjurlin MA, Fantus RJ, Mellett MM, Goble
SM.  Genitourinary injuries in pelvic fracture mor-
bidity and mortality using the National Trauma Data
Bank. J Trauma. 2009;67(5):1033–9.
6. Brandes S, Borrelli J Jr. Pelvic fracture and associated
urologic injuries. World J Surg. 2001;25(12):1578–87.
 Pelvic Fractures
166
Ryan M. Staszak and Lacee Jay Laufenberg

Algorithmic Approach ture include an abdominal seatbelt sign, ten-

A. Pelvic ring injuries in the setting of high-­
energy trauma can be life threatening and are
often associated with a significant risk of
morbidity and mortality [1]. Evaluation
begins with adherence to advanced trauma
life support (ATLS) protocols for primary and
secondary survey. Pelvic instability with
compression on physical exam is highly spe-
cific for unstable pelvic ring fractures (99%).
However, according to retrospective reviews, B. As part of the primary survey, it is imperative
physical examination has 26% sensitivity for
detecting unstable fractures and 8% for stable
fractures [1]. Repeated compression should
be avoided due to the risk of iatrogenic dis-
placement of fractures. Associated injuries
may include but are not limited to blunt chest
trauma; hollow viscus or other abdominal, C. An unstable patient with suspected pelvic frac-
neurologic, long bone fractures; hemorrhagic
shock; and urologic, gynecologic, or rectal
injury [2]. Other physical exam findings that
should raise the suspicion for a pelvic frac-
R. M. Staszak · L. J. Laufenberg (*)
Department of Surgery, Division of Trauma, Acute
Care, and Critical Care Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: llaufenberg@pennstatehealth.psu.edu
derness of pelvis, ecchymosis to perineum,
and evidence of other pelvic injuries. Also
consider the mechanism of injury when eval-
uating for possible pelvic fractures. A fall
from standing may be sufficient to generate a
clinically severe fracture in an osteoporotic
patient. A younger patient would likely need
a larger transfer of energy to sustain severe
pelvic fractures, such as a motor vehicle col-
lision at highway speeds.
to determine if the patient is hemodynamically
stable. If the patient is unstable and pelvic frac-
ture is suspected, immediate interventions are
indicated. If the patient is stable, then he or she
can undergo additional imaging with CT scan
prior to any interventions.
tures should immediately undergo resuscita-
tion with balanced blood products, utilizing a
massive transfusion protocol if one is avail-
able. Chest X-ray and pelvic X-rays should be
obtained. If an anterior posterior compression
fracture is present, a pelvic binder should be
placed to minimize pelvic expansion and hem-
orrhage. A binder should not be left in place
for >48  h [3]. The patient should also be
prepped for resuscitative endovascular balloon
occlusion of the aorta (REBOA), if this is
available at your institution.

© Springer Nature Switzerland AG 2019 679

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_166
680
D. Focused assessment with sonography for
trauma (FAST) should be performed in the
workup of the unstable patient as well. This
can help identify any intra-abdominal hemor-
rhage contributing to the instability [4].
E. If the FAST is positive for intra-abdominal
bleeding, one should proceed to the operating
room for exploratory laparotomy. If pelvic
fracture is present, consider hemorrhage con-
trol with preperitoneal packing, external fixa-
tion, REBOA, pelvic arteriography and
embolization, or a combination of approaches.
F. If the FAST is negative, for intra-abdominal
hemorrhage, but the patient remains unstable
and has evidence of pelvic trauma, procced to
the operating room (OR) for preperitoneal
packing, external fixation of fractures, pelvic
arteriography and embolization, or a combi-
nation of these approaches.
G. If the patient is hemodynamically stable,
obtain further imaging with pelvic X-rays
(anterior-posterior and inlet-outlet) and with
CT scan [2]. Remember the associated risk of
other injuries, and perform a thorough ter-
R. M. Staszak and L. J. Laufenberg
tiary survey after initial stabilization, looking
for evidence of gynecologic, urologic, or rec-
tal trauma not previously identified [4].
H. If there is evidence of pelvic fracture with
active extravasation and arterial injury noted
on CT scan, the patient requires intensive
care unit (ICU) admission or serial exams.
Additionally, the patient requires immediate
consultation with orthopedic surgery and
consideration for pelvic fixation, arteriogra-
phy, or a combination of approaches. If there
is no evidence of active hemorrhage, the
patient may still need ICU admission and
serial exams with serial CBCs to follow for
new hemorrhage. Typical management of
pelvic fractures is a combination of opera-
tive and nonoperative management, with
weight bearing as tolerated. Orthopedic sur-
gery should be involved early in the stabili-
zation of pelvic fractures and for
recommendations for or against operative
fixation and weight-­ bearing status of the
affected limbs [3].
166  Pelvic Fractures 681

Patient involved in an accident/traumatic injury suspected

A
Trauma evaluation ->ATLS guidelines & ABCDE
Obtain vital signs, lab work, establish 2 large bore IV’s

B Is the patient
hemodynamically stable?

No Yes

Immediate interventions:
C CT scan of abd/pelvis with
-Activate MTP
signs of bleeding from the F
-CXR & Pelvis, Pelvic binder (if
pelvis or major pelvic
amendable) -Femoral Arterial
injury?
catheter for possible REBOA

Yes No

D FAST
G -Obtain immediate
Admission with serial
surgical/ortho
re-examinations
consultation
orthopedics
- Pelvic arteriography
Positive Negative consultation as
or other intervention
indicated

-Control extra-abdominal
hemorrhage
-To operating room:
-Control pelvic hemorrhage
Control intra-abdominal
E hemorrhage
- Pelvic
stabilization/fixation ICU admission
-Control any pelvic follow
-Preperitoneal packing if
hemorrhage (pelvic CBC & exam
uncontrolled bleeding
fixation, preperitoneal
Consider Pelvic
packing, arteriography,
arteriography, REBOA
REBOA)

* REBOA –Resuscitative
endovascular balloon occlusion
ICU admission of the aorta
follow
CBC & exam

Algorithm 166.1
682 R. M. Staszak and L. J. Laufenberg

References [Internet]. Waltham, MA: UpToDate; 2017.

Available from: https://www.uptodate.com/contents/
pelvic-trauma-initial-evaluation-and-management.
1. Coccolini F, et al. Pelvic trauma: WSES classification
4. Cullinane DC, et al. Eastern Association for the sur-
and guidelines. World J Emerg Surg. 2017;12(5):1–18.
gery of trauma practice management guidelines for
2. Mattox KL, Moore EE, Feliciano DV. Trauma: pelvis.
hemorrhage in pelvic fractures – update and systemic
7th ed. New York: McGraw-Hill; 2013. p. 655–68.
review. J Trauma. 2011;71(6):1850–68.
3. Fiechtl J, et  al. Pelvic trauma: initial evaluation
and management. In: Post T, editor. UpToDate.
 Bladder Injuries
Ryan M. Staszak and Lacee Jay Laufenberg
Algorithmic Approach
A. The bladder is a hollow organ that is normally
protected by pelvic rami. As the bladder is
distended with urine it rises above the pelvic
rim, exposing itself to injury during compres-
sive or shear forces. An appropriate mecha-
nism and sufficient force can still result in
pelvic fracture and bladder injury. Bladder
injuries occur in 1.6% of blunt abdominal
trauma cases [1]. Of all bladder injuries,
60–80% are from blunt trauma and 15–40%
are from penetrating [2]. Injuries associated
with high risk of bladder injuries include pel-
vic fractures, blunt trauma to the lower abdo-
men, abdominal seatbelt sign, or penetrating
injuries to the lower abdomen or pelvis.
Bladder injuries can also occur iatrogenically
during pelvic surgery.
B. Evaluation for a suspected bladder injury fol-
lowing a traumatic mechanism should begin
with an advanced trauma life support (ATLS)
workup. If the patient is hemodynamically
stable and concern for a bladder injury exists,
R. M. Staszak · L. J. Laufenberg (*)
Department of Surgery, Division of Trauma, Acute
Care, and Critical Care Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: llaufenberg@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_167
167
workup should proceed without delay. An
unstable patient should first be stabilized
before proceeding with a bladder injury
workup.
The cardinal sign for traumatic injury to
the bladder is gross hematuria, found in about
95% of the cases [3]. All pelvic fractures or
patients with concern for bladder injury need
a genitourinary exam and should have urine
evaluated for gross hematuria. Rule out ure-
thra injury by exam or retrograde urethro-
gram prior to insertion of a Foley.
C. Stress cystography should be performed; one
of the most sensitive is CT cystogram. A
proper study requires an initial image, fol-
lowed by filling the bladder with 300–400 ml
of contrast. The pelvic CT is then repeated
when the bladder is distended with contrast.
After emptying the bladder, delayed images
are also obtained. Clamping the Foley just
prior to a CT with IV contrast will not pro-
vide sufficient distention of the bladder and
will result in a high rate of false negatives [4].
Cystoscopy can also be performed to evaluate
for bladder injury.
D. Extraperitoneal injuries with urine leak lim-
ited to the perivesical space are often associ-
ated with pelvic fracture. Eighty-three percent
of patients with bladder ruptures have pelvic
fractures, but less than 10% of patients with
pelvic fracture have bladder ruptures [5].
683
684
E. For uncomplicated extraperitoneal injuries,
the bladder catheter is left in place for
10–14 days. Usually >85% of injuries will be
healed by this point.
At times an extraperitoneal injury will need
to be repaired due to concurrent injury. These
are often repaired by making an anterior cys-
totomy cephalad to the pelvic hematoma. The
laceration is then repaired from the inside in a
single-layer full-thickness closure followed
by drainage with a catheter for 5–10 days.
F. Intraperitoneal injuries occur when the peri-
toneal surface has been disrupted with con-
comitant urinary extravasation. These
bladder injuries often occur when blunt trau-
matic forces are applied to a distended
bladder.
G. For intraperitoneal injuries open repair of the
bladder is undertaken after debridement and
evaluation of the interior of the bladder. This
helps to verify that there are no other injuries
R. M. Staszak and L. J. Laufenberg
and that there is clear efflux from both ure-
teral orifices. The bladder should always be
repaired with heavy absorbable suture in two
layers. The bladder is then drained for
5–10 days with a Foley catheter.
H. After the designated drainage period, a repeat
cystogram is performed, whether the injury
was repaired operatively or non-operatively.
The Foley is removed if there is no evidence
of leak. If a leak persists, the Foley is left in
place for an additional 7–10 days.
I. Combined injuries are often associated with
major pelvic trauma or penetrating injuries
and could have urethral, bladder, rectal, and
vaginal involvement. Injuries may also be
associated with cystoscopic procedures, usu-
ally during resection of a bladder tumor or
during biopsies. Injury can also occur during
other surgical procedures in the pelvis.
Complex injuries, i.e., bladder neck or trigone,
require expert consultation.
167  Bladder Injuries 685

History and physical exam:

(Lower abdominal trauma or pelvic fractures)
A

Obtain vital signs, blood work, physical examination, and

B Urine for gross blood (r/o urethral trauma before placing a
Foley)
Consult urology

Complex
No injury I
Gross blood or
Treat other injuries significant
concern for
Bladder injury? Yes
CT
cystogram C
or
cystoscopy
No injury

F Intraperitoneal
bladder injury Extraperitoneal
bladder injury D

OR for repair
G –2 layered closure
–Foley 5–10 days
Foley 10–14 days E

Repeat cystogram prior to

H removing foley

Algorithm 167.1

3. Carroll PR, McAninch JW.  Major bladder trauma:

References
1. Iverson AJ, Morey AF.  Radiographic evaluation of
suspected bladder rupture following blunt trauma:
critical review. World J Surg. 2001;25(12):1588–91.
2. Cass AS, Luxenberg M. Features of 164 bladder rup-
tures. J Urol. 1987;138(4:743–5.
mechanisms of injury and a unified method of diagno-
sis and repair. J Urol. 1983;132:254.
4. Peng MY, Parisky YR, Cornwell EE, et al. CT cystog-
raphy versus conventional cystography in evaluation
of bladder injury. Am J Roentgenol. 1999;173:1269.
5. Zacharias C, Robinson JD, Linnau KF, et  al. Blunt
urinary bladder trauma. Curr Probl Diagn Radiol.
2012;41(4):140–1.
 Rectal Injuries
Amanda E. Lee, Karima Fitzgerald,
and Lacee Jay Laufenberg
Algorithmic Approach
A. The first step in the evaluation of any trauma
patient is a systematic, thorough evaluation
utilizing the advanced trauma life support
(ATLS) protocol, with a primary and second-
ary survey to exclude life-threatening injuries
[1]. There are both blunt and penetrating
mechanisms by which rectal injuries can
occur. Blunt injuries to the rectum are uncom-
mon due to protection from bony pelvis but
can be seen with severe pelvic fractures [2].
Penetrating injuries can result from transpel-
vic gunshot wounds, perineal impalement,
iatrogenic processes, foreign body insertion,
or sex-related injuries [3].
B. The patient’s physical exam findings (abdom-
inal tenderness, seat belt sign, ecchymosis, or
blood at the perineum) can be suggestive of
injury to the rectum [4]. If any concern for a
rectal injury is present, a digital rectal exam
(DRE) could be performed, which assesses
anal tone, position of the prostate, gastrointes-
A. E. Lee
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
K. Fitzgerald · L. J. Laufenberg (*)
Department of Surgery, Division of Trauma, Acute
Care, and Critical Care Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: llaufenberg@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_168
168
tinal bleeding, potential pelvic fractures, and
presence of foreign bodies. Although DRE
has traditionally been part of the secondary
survey in ATLS protocol, it has been found to
have poor sensitivity for diagnosis of spinal
cord, urethral, small bowel, colon, and rectal
injuries [5]. It does not cause physical harm to
patient, but is also unlikely to affect immedi-
ate management of the patient, so perfor-
mance of a DRE should be based on clinical
judgment and presentation of the patient [6].
C. If concern for a rectal injury exists, the next
step is to confirm the presence of the injury
and then determine if it is intraperitoneal ver-
sus extraperitoneal. If there are any concern-
ing findings on the initial evaluation that
require immediate operative intervention, the
patient should proceed to the operating room
(OR). However, if the patient is stable and
appropriate to undergo further workup, a
computerized tomography (CT) scan should
be performed (with intravenous and water-­
soluble rectal contrast, if appropriate). The
CT scan can show bowel injury, extraluminal
air, contrast extravasation, or intestinal dis-
continuity [7].
D. Whether the patient went immediately to the
OR for another reason (but suspicion of rectal
injury remains) or had a rectal injury found on
imaging, the patient should then undergo rigid
proctoscopy or sigmoidoscopy which is con-
sidered the gold standard for detection and
687
688
localization of rectal injuries [8–10]. This will
serve to determine if the injury is intraperito-
neal or extraperitoneal. If the injury is to the
intraperitoneal portion of the rectum, then fur-
ther management should be as a distal colonic
injury with exploratory laparotomy [11].
E. If the rectal injury is extraperitoneal, the type
of intervention will be determined by the
extent of injury and presence of fecal con-
tamination. Historically, the gold standard
treatment for extraperitoneal rectal injuries is
proximal diversion [12, 13]. However, if the
injury is easily accessible and only partial
thickness, it can safely be managed with pri-
mary repair only [4, 14].
F. Any rectal injury that is either inaccessible or
more severe should undergo proximal diver-
sion. If the injury is nondestructive (<25%
loss of circumference), diversion alone is sat-
isfactory [15].
A. E. Lee et al.
G. If there is significant fecal contamination, the
patient should undergo pre-sacral drainage in
addition to diversion [4]. If the injury is
destructive, one should consider distal rectal
washout in addition to diversion and pre-­
sacral drainage [15]. Ultimately, management
of injury to the rectum should be handled on
an individualized patient basis.
H. Once the acute phase of the injury has passed,
the patient can be evaluated for stoma rever-
sal. The area of injury needs to be assessed
with a rectal contrast study (CT or X-ray) to
ensure that the injury has healed without
stricture formation. Furthermore, sphincter
integrity must be assessed to ensure the
patient will not have fecal incontinence or
significant pelvic floor dysfunction. This can
be done with physical exam, anoscopy, endo-
anal ultrasound, anal manometry, or pudendal
nerve studies [4].
168  Rectal Injuries 689

A Evaluate patient using ATLS protocol. Identify mechanism (blunt vs

penetrating) and determine if the patient is hemodynamically stable.

Is the patient
hemodynamically stable?
Yes No

Treat life
Perform thorough physical exam, making note of findings indicative threatening
of possible rectal injury injuries

Physical exam findings: abdominal

Consider DRE (digital rectal
tenderness, pelvic tenderness/pain,
exam)
seat belt sign, ecchymosis or blood at
the perineum

CT scan findings:
Obtain CT scan with IV and rectal free intraperitoneal
C air, intraperitoneal
contrast or rigid proctoscopy
free fluid,
intraperitoneal
bowel injury

Rigid proctoscopy
findings:
Intraperitoneal
injury
Is there evidence of
either
D
extraperitoneal or
intraperitoneal
rectal injury?

Exploratory laparotomy;
see management of colon
injuries

Algorithm 168.1
690 A. E. Lee et al.

CT scan findings:
extra luminal
extraperitoneal air,
contrast
extravasation,
extraperitoneal bowel
wall discontinuity

Rigid proctoscopy
findings:
Extraperitoneal injury

G
Injury is full
thickness, not easily
accessible,
Rigid proctoscopy if not significant fecal
already done contamination,
>25% circumference

E
Injury is
F
partial Fecal diversion with colostomy,
Injury is full
thickness and pre-sacral drainage, distal rectal
thickness, not easily
easily washout
accessible, <25%
accessible
circumference

Fecal diversion with

Primary repair diverting colostomy
only

Evaluate for reversal with rectal

contrast study and functional H
sphincter/pelvic floor analysis
Is there evidence of
stricture, leak,
incontinence or pelvic
floor dysfunction?

No
Yes

Elective colostomy reversal

Colorectal surgery referral

Algorithm 168.1 (continued)
168  Rectal Injuries 691

References 9. Shlamovitz G, Mower W, Bergman J, Crisp J, DeVore

H, Hardy D, et al. Poor test characteristics for the dig-
ital rectal examination in trauma patients. Ann Emerg
1. Committee on Trauma, American College of Surgeons.
Med. 2007;50:25–33.
ATLS: advanced trauma life support program for doc-
10. Ferraro F, Livingston D, Odom J, Swan K, McCormack
tors. 8th ed. Chicago: American College of Surgeons;
M, Rush B Jr. The role of sigmoidoscopy in the man-
2008.
agement of gunshot wounds to the buttocks. Am Surg.
2. Wei R, Cao X, Tu D. Clinical treatment of open pelvic
1993;59:350–2.
fractures associated with perineal injury. Zhongguo
11. Pasquale M, Fabian T.  Practice management guide-
Xiu Fu Chong Jian Wai Ke Za Zhi. 2012;25:550–3.
lines for trauma from the Eastern Association for the
3. Duncan A, Phillips T, Scalea T, Maltz S, Atweh
Surgery of Trauma. J Trauma. 1998;44:941–56.
N, Sclafani S.  Management of transpelvic gunshot
12. Grasberger R, Hirsch E.  Rectal trauma: a retrospec-
wounds. J Trauma. 1989;29:1335–40.
tive analysis and guidelines for therapy. Am J Surg.
4. Cheong J, Keshava A.  Management of colorectal
1983;145:795–9.
trauma: a review. ANZ J Surg. 2017;87:547–53.
13. Gonzalez R, Falimirski M, Holevar M.  The role of
5. Docimo S Jr, Diggs L, Crankshaw L, Lee Y.  No
pre-sacral drainage in the management of penetrating
evidence supporting the routine use of digital rec-
rectal injuries. J Trauma. 1998;45:656–61.
tal examinations in trauma patients. Indian J Surg.
14. Ahern D, Kelly M, Courtney D, Rausa E, Winter
2015;77:265–9.
D.  The management of penetrating rectal and anal
6. Ahl R, Riddez L, Mohseni S.  Digital rectal exami-
trauma: a systematic review. Injury. 2017;48:1133–8.
nation for initial assessment of the multi-injuried
15. Bosarge P, Como J, Fox N, Falck-Ytter Y, Haut E,
patient: can we depend on it? Ann Med Surg (Lond).
Dorion H, et al. Management of penetrating extraperi-
2016;9:77–81.
toneal rectal injuries: an Eastern Association for the
7. Greer L, Gillern S, Vertrees A. Evolving colon injury
Surgery of Trauma practice management guideline. J
management: a review. Am Surg. 2013;79:119–27.
Trauma Acute Care Surg. 2016;80:546–51.
8. Mangiante E, Graham A, Fabian T.  Rectal gunshot
wounds: management of civilian injuries. Am Surg.
1986;52:37–40.
 Extremity Compartment
Syndrome
Karima Fitzgerald, Amanda E. Lee,
and Lacee Jay Laufenberg
Algorithmic Approach
A. In the setting of extremity trauma, acute
extremity compartment syndrome should be
considered after the patient has been other-
wise evaluated and stabilized. Extremity
compartment syndrome can develop after
blunt or penetrating injury, with or without
fractures [1]. Up to 75% of extremity com-
partment syndrome is due to tibia fractures,
with the incidence of extremity compartment
syndrome in tibia fractures reported from 1%
to 10% [2]. Vascular injuries should be identi-
fied promptly, as they can be associated with
compartment syndrome due to lack of arterial
inflow, lack of venous outflow, or both [3].
Other patients at significant risk for extremity
compartment syndrome are those with a sig-
nificant crush injury or motor vehicle colli-
sion with entrapment. Recreational use of
injection drugs, infiltrated IV sites, burns, and
prolonged compression due to poor OR posi-
tioning are other risk factors, as is acute arte-
K. Fitzgerald · L. J. Laufenberg (*)
Department of Surgery, Division of Trauma, Acute
Care, and Critical Care Surgery, Penn State Milton
S. Hershey Medical Center, Hershey, PA, USA
e-mail: llaufenberg@pennstatehealth.psu.edu
A. E. Lee
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_169
169
rial ischemia due to peripheral vascular
disease [2]. The diagnosis of extremity com-
partment syndrome is nebulous and requires a
high index of suspicion; the consequences of
delay to diagnosis or delay to treatment are
severe and include loss of function, loss of
limb, and renal failure if rhabdomyolysis
accompanies the compartment syndrome [4].
It is suggested that functional impairment of
muscle becomes permanent after 4–12 h, and
nerve damage becomes irreversible after
12–24 h [5].
B. In addition to obtaining the details of the
inciting event, key symptoms of extremity
compartment syndrome to elicit are pain out
of proportion to exam; a persistent, deep, ach-
ing pain or burning pain; and paresthesias.
These symptoms may indicate ischemic
changes of the muscles and nerves. The “6
Ps” of arterial ischemia (pain, pallor, pulsel-
essness, paresthesia, pressure, poikilother-
mia) are associated with, but not diagnostic
of, extremity compartment syndrome. When
present, they have a high specificity, but the
sensitivity is lacking [5]. Pain, particularly
pain out of proportion to exam or to apparent
injury, is the most common and consistent
finding [2].
C. The physical exam should consist of gross
examination of the extremity observing for
pallor or mottling. Pain with palpation and
with passive stretch should be evaluated. A
693
694
full neuromuscular exam should be
­performed, noting strength and sensation in
all the affected muscle groups and derma-
tomes. Make note of the size of the extremity.
Circumferential measurements of the affected
and contralateral extremity should be
obtained when able. Tense, tight extremities,
with shiny-appearing skin and a woody feel-
ing on palpation, have a high likelihood of
extremity compartment syndrome. Distal
pulses should be palpated or Doppler signals
obtained. Pulselessness is uncommon in
extremity compartment syndrome as it
requires the extremity pressure to exceed the
arterial blood pressure but can occur given
the right combination of a hypotensive
patient, severe compartment syndrome, and/
or a vascular arterial injury [4]. If the patient
is awake, alert, and able to be examined,
serial examinations should be performed
every hour as compartment syndrome pro-
gresses rapidly. Sedated or obtunded patients
who cannot undergo serial exams should
undergo evaluation of compartment pressures
[4] with consideration given for prophylactic
or empiric fasciotomy if suspicion is high for
extremity compartment syndrome.
D. There are a few accepted methods of measur-
ing compartment pressures. The simplest and
most common is a pressure monitoring nee-
dle, such as the one made by Stryker. Other
methods include transducing the pressure
using a needle and arterial line setup and the
slit catheter technique [4]. Compartment
pressures vary depending on the compart-
ment, and even vary within a single compart-
ment, necessitating multiple measurements in
multiple areas [5].
E. There is no agreed-upon value for diagnosis
of extremity compartment syndrome.
Commonly used values are compartment
pressure of >/=30 mmHg or delta pressure of
</=30 mmHg [6]. (Delta pressure is the dif-
ference between the diastolic pressure and the
compartment pressure.)
F. Clinical suspicion must be high, and the diag-
nosis must be made with a combination of
physical exam findings and compartment
K. Fitzgerald et al.
pressures. A patient with risk factors and pro-
gressive signs and symptoms of pain, pares-
thesias, and decreased sensation or motor
function has sufficient indications for fasci-
otomy. Fasciotomy should not be delayed
while awaiting the Stryker needle to reach the
designated reading [6]. There is no consensus
as to the specific indications for fasciotomy,
and the diagnosis of extremity compartment
syndrome is “capricious and elusive” [6].
G. Emergent fasciotomy as soon as the diagnosis
has been made is the mainstay of treatment
for extremity compartment syndrome.
Adjunct maneuvers to improve flow include
relieving any external forces causing
increased compartment pressure such as
dressings, splints, or casts. Reduction of frac-
tures or dislocations can often restore blood
flow to the affected extremity. The limb
should remain in neutral position so as to
avoid changes in blood flow that can either
increase vascular congestion or cause further
reduction in arterial blood flow. If the patient
is noted to be hypotensive, resuscitation with
either crystalloid or colloid should be imple-
mented to avoid hypoperfusion and further
tissue injury [4]. Fasciotomy should be per-
formed promptly to prevent permanent dam-
age. Although there is evidence to support
that irreversible muscle damage begins as
early as 4 h after onset of ischemia, the gener-
ally accepted timeframe is 6 h to fasciotomy
to preserve muscle [4–6].
The key to fasciotomy is complete release
of all involved compartments. There are two
procedures that will allow for release of com-
partments. There are four compartments in
the leg: anterior, lateral, superficial posterior,
and deep posterior. These are most commonly
released via two incisions (medial and lat-
eral). The anterior and lateral compartments
are released via the lateral incision, and the
superficial and deep posterior compartments
are released through the medial incision. The
anterior compartment of the leg is the most
common site of extremity compartment syn-
drome [2].
169  Extremity Compartment Syndrome
In the thigh there are three compartments:
anterior, posterior, and medial. Typically
extremity compartment syndrome in the thigh
can be managed with a long lateral incision to
release the anterior and posterior compart-
ments, as compartment syndrome in the
medial adductors is rare [4]. The forearm has
four compartments: deep volar, superficial
volar, dorsal compartment, and lateral com-
partment [2]. Fasciotomy is performed
through volar and dorsal incisions, with
access to the lateral compartment (aka the
“mobile wad”) via the dorsal incision [1].
There are only the anterior and posterior
components which must be released in the
arm [2]. This is accomplished with a lateral
695
incision and release of the fascial planes of
the biceps brachii and triceps brachii.
H. Wound closure should not be attempted prior
to resolution of tissue edema, due to the
inherent risk of repeat tissue ischemia [4].
Patients should return to the operating room
(OR) for attempted closure on postoperative
days 3–5. Delayed primary closure is pre-
ferred, but if necrosis persists, further
debridement should be undertaken prior to
closure. Similarly, if tissue edema remains
too high to allow skin coverage, the wounds
should be allowed to heal via secondary
intention. Once an adequate bed of granula-
tion tissue has formed, a split-thickness skin
graft should be used for coverage [4].
696 K. Fitzgerald et al.

Patient with risk factors for extremity compartment syndrome:

A extremity trauma, injection drug abuse, reperfusion of ischemic
limb

History: Pain out of proportion to exam/injury, persistent deep

B ache or burning pain, paresthesias

Physical exam: pain with passive stretch, tense compartments,

C pallor, decreased sensation, weakness, paralysis, pulselessness

Findings positive for

compartment syndrome?

Yes No

Evaluation of compartment pressure: Continued observation

Stryker Quick Pressure Monitor with hourly exams.
D
Instrument, manometric IV pump
method, slit catheter technique

No

F
Compartment pressure No
>/=30mmHg or delta High clinical
E P</=30mmHg? suspicion?

Yes Yes

G Immediate fasciotomy

H Delayed primary closure or healing by secondary

intention and skin graft

Algorithm 169.1
169  Extremity Compartment Syndrome 697

References hand surgery. Philadelphia: WB Saunders; 1986.

p. 1–18.
4. Olson SA, Glasgow RR.  Acute compartment syn-
1. Morin RJ, Swan KG, Tan V.  Acute forearm com-
drome in lower extremity musculosketal trauma. J Am
partment syndrome secondary to local arterial injury
Acad Orthop Surg. 2005;13(7):436–44.
after penetrating trauma. J Trauma. 2009;66(4):
5. Ivatury RR.  Pressure, perfusion and compartments:
989–93.
challenges for the acute care surgeon. J Trauma Acute
2. Stracciolini A, Hammerberg EM. Acute compartment
Care Surg. 2014;76(6):1341–8.
syndrome of the extremities. In: Moreira ME, Bachur RG,
6. Kosir R, Moore FA, Selby JH, Cocanour CS, Kozar
editors. UpToDate. [Internet]. 2018 Feb 12. Retrieved
RA, Gonzalez EA, Todd SR.  Acute lower extrem-
from UpToDate: https://www.uptodate.com/contents/
ity compartment syndrome (ALECS) screening
acute-compartment-syndrome-of-the-extremities.
protocol in critically ill trauma patients. J Trauma.
3. Urbaniak JR, Roth JH. Arterial injuries of the upper
2007;63(2):268–75.
extremity. In: Boswisk J, editor. Complications in
 Part XX
Critical Care
 Management of Intracranial
Hemorrhage
Ariel P. Santos
Algorithmic Approach
Intracranial hemorrhage (ICH) is a devastating
condition that carries a significant morbidity and
mortality but can be mitigated by proper medical
care. Early assessment and diagnosis using CT
scan is imperative.
A. A cardinal sign of increased intracranial pres-
sure (ICP) is decreased level of consciousness
and may be associated with headache, nausea,
vomiting, hypertension, focal neurologic defi-
cit, and sudden progression of symptoms.
B. Whether it is in the pre-hospital or hospital
situation, the primary objective is to secure
airway management if needed, provide ade-
quate cardiovascular support, and transfer to
the closest facility where patient can defini-
tively be managed with the full complement
of neuro-radiologist, neurologist, neurosur-
geon, and intensivist. Primary survey will
help identify life-threatening condition.
Detailed history will help identify risk factors
and possible etiology of the ICH.
C. Early referral to neurologist, neurosurgeon,
and intensivist facilitates early treatment of
the patient avoiding risk of early neurological
deterioration.
A. P. Santos ()
Department of Surgery, Texas Tech University Health
Sciences Center, Lubbock, TX, USA
e-mail: ariel.santos@ttuhsc.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_170
170
D. According to the American Heart Association/
American Stroke Association (AHA/ASA)
Guidelines, rapid neurologic imaging with CT
scan or magnetic resonance imaging (MRI) is
recommended to distinguish ischemic stroke
from ICH [1]. CT scan is considered the gold
standard considering performance of a MRI
can be precluded by time, cost, patient’s clini-
cal status, and its availability. CT angiography
(CTA) and contrast-­enhanced imaging may be
considered to help identify patients at risk for
hematoma expansion. CTA, CT venography,
magnetic resonance angiogram (MRA), and
catheter angiography can also be useful to
evaluate for underlying lesions including vas-
cular malformations and tumors when there is
clinical or radiological suspicion [1].
E. Baseline severity score should be performed
as part of the initial evaluation of patients
with ICH [1]. ICH score is the most widely
used and externally validated severity scoring
[2] (table in Algorithm 170.1).
F. The Neurocritical Care Society recommends
an efficient, standardized, and integrated
management of patients with acute intracra-
nial hemorrhage, and this should be initiated
as soon as possible.
(a) Admission to neurocritical care unit:
Intracranial hemorrhage may be
associated with depressed sensorium;
­
for this reason, oxygen supplementation
and securing the airway is of utmost
701
702
importance. It is highly recommended to
admit a patient with intracranial hemor-
rhage to the stroke or neuroscience
intensive care unit managed by intensiv-
ist and nurse experts. Prolonged stay in
the emergency department may lead to
worse outcome [3], but early neurocriti-
cal care management in the ED may
ameliorate its effect [4].
(b) Blood pressure monitoring and control:
Uncontrolled high systolic blood pres-
sure is associated with intracranial hema-
toma expansion, neurological
deterioration, higher mortality, and poor
clinical outcome [5]. Intensive Blood
Pressure Reduction in Acute Cerebral
Hemorrhage 2 (INTERACT-2) trial, the
largest randomized clinical trial evaluat-
ing the efficacy of intensive blood pres-
sure lowering treatment to a SBP level
<140 mm Hg, found this management to
be safe and effective in improving func-
tional outcome [6].
(c) Correction of coagulopathy:
Anticoagulation taken by the patient
must be stopped. Measurement of coagu-
lation profile and elastography can help
guide the correction of the coagulopathy.
Accurate account of the medication taken
by the patient will guide the appropriate
antidote or reversal agent.
(d) Deep vein thrombosis (DVT) prophy-
laxis: Patients with ICH have an increased
risk of thromboembolic disease. The
CLOTS 3 trial (Clots in Legs Or sTock-
ings after Stroke) showed that intermittent
pneumatic compression started as early as
the day of hospital admission reduced the
occurrence of proximal DVT [7]. Once
cessation of intracranial bleed is docu-
mented, early use of low molecular
weight heparin or unfractionated heparin
(day 1 to 6 after admission) showed
reduction of pulmonary embolism and
non-significant reduction in mortality but
no difference in DVT or intracranial
hematoma enlargement [8]. Systemic
anticoagulation or IVC filter placement is
A. P. Santos
probably indicated in ICH patients with
symptomatic DVT or PE but should take
into account time from hemorrhage onset,
hematoma stability, cause of hemorrhage,
and overall patient condition [1, 9].
(e) EEG monitoring if needed and seizure
treatment. Cortical involvement of the
ICH is the most important risk factor for
early seizure which can occur as high as
16% [10]. As per AHA/ASA recommen-
dations, clinical seizure should be treated
with antiseizure drugs; continuous EEG
monitoring should be considered in ICH
with depressed mental status that is dis-
proportionate to the degree of brain
injury; and there is no data to suggest that
prophylactic antiseizure medication is
effective [1].
(f) Fever management after ICH is reason-
able as per AHA/ASA guidelines.
Therapeutic cooling may reduce perihe-
matomal edema but is considered investi-
gational in ICH at this time [11].
(g) Glycemic monitoring and control to
avoid hypoglycemia and hyperglycemia.
(h) Head of bed elevation. Keep the head of
bed elevated to help reduce ICP as well
as preventing aspiration.
(i) ICP monitor and control if indicated.
Increasing intracranial pressure and
decreasing cerebral perfusion pressure
(CPP) are associated with increased mor-
tality. AHA/ASA recommends that
patients with Glasgow (GCS) score of <8,
clinical evidence of transtentorial hernia-
tion, or significant IVH or hydrocephalus
be considered for ICP monitoring and
treatment; ventricular drainage as treat-
ment for hydrocephalus is reasonable
especially in patient with decreased level
of consciousness; and corticosteroids
should not be administered for treatment
of elevated ICP in ICH [1]. Medical treat-
ment includes head e­ levation, ventilation,
sedation, analgesia, use of paralytics,
mannitol, loop diuretics, hypertonic
saline, hypothermia, and barbiturates.
Randomised Evaluation of Surgery with
170  Management of Intracranial Hemorrhage
Craniectomy for Uncontrollable Elevation
of Intracranial Pressure (RESCUEicp)
trial showed that decompressive craniec-
tomy in patients with severe and refrac-
tory intracranial hypertension after
traumatic brain injury resulted in lower
mortality and higher rate of vegetative
state than medical management [12].
703
(j) Joint physical, occupational, and speech
therapy evaluation and treatment as early
as possible.
G. Multidisciplinary rehabilitation is recom-
mended including education of the patient,
family members, and caretaker regarding sec-
ondary prevention of stroke and prevention of
sequelae and complications of ICH.
704 A. P. Santos

A patient presents with severe headache, nausea, vomiting, focal neurologic

A
deficit, decreased level of consciousness and elevated blood pressure.

Causes of intracranial bleed

Hypertension
Primary survey: Coagulopathy, use of anticoagulant
A- Airway protection with C-spine immobilization in trauma Trauma
B- Breathing
B C- Circulation, avoid hypotension, control bleeding
Arteriovenous malformation
Intracranial aneurysm
D- Assess GCS and any neurologic deficit Cavernous angioma
E- Exposure Cerebral amyloid angiopathy
Secondary survey: History, PE, PMH, medications, family and Vasculitis
social history; Check for history of dementia, trauma, and illicit drug. Dural venous sinus thrombosis
Ancillary tests: CBC, CMP, UA, Coagulation profile, Troponin, Intracranial neoplasm
Glucose level and toxicology screen Dural arteriovenous fistula
Hemorrhagic conversion of infarct
Alcoholism
Cocaine abuse
C Consult: Neurosurgery, Neurology, Neuroradiology and Recreational drugs

NO

CT Scan findings of ICH? Re-evaluate

D

YES

Determination of the ICH score

Component ICH score points

GCS Score
3–4 2
5 – 12 1
13 – 15 0
ICH volume, cm3
E >30 1
< 30 0
Intraventricular hemorrhage
Yes 1
No 0
Infratentorial origin of ICH
Yes 1
No 0
Age in Years
 80 1
< 80 0
Total ICH score 0–6
GCS score indicates GCS score on initial presentation (or after resuscitation); ICH volume, volume on initial
CT calculated using ABCI method; and IVH, presence of any IVH on initial CT.
Hemphill JC III, Bonovich DC, Besmertis L, et al. The ICH score: a simple, reliable grading scale for intracerebral hemorrhage. Stroke
2001; 32:891-897.

Algorithm 170.1
170  Management of Intracranial Hemorrhage 705

A – Admit to Stroke, Neurocritical Care or Specialized Intensive Care Unit

F
B – Blood pressure control

C – Correct coagulopathy if present.

Vitamin K antagonist (VKA) – Withhold VKA, Vitamin K IV, FFP, PCC
Direct Oral Anticoagulants (DOACs) – PCC, FEIBA, FFP, activated charcoal if taken < 2 hours
Dabigatran – Idarucizumab (Praxbind)
Heparin – Protamine 1 mg per 100 unit of heparin
Factor deficiency – Factor transfusion
Thrombocytopenia – platelet transfusion
D – DVT control using intermittent pneumatic compression device and early DVT prophylaxis

E – EEG monitoring if depressed mental status and seizure treatment

F – Fever control

G – Glycemic monitoring and control

H – Head of bed elevation and hematoma evacuation if needed

I – ICP monitoring and control if needed

Ventilation control
Hypertonic saline solution
Mannitol
Diuretics
Sedation
Paralytics
Barbiturates
Decompressive Craniectomy
J – Joint physical, occupational and speech therapy evaluation and treatment and family support.

Constant re-evaluation
G Secondary prevention
Rehabilitation

Algorithm 170.1 (continued)
706 A. P. Santos

References 7. Dennis M, Sandercock P, Reid J, et al. CLOTS Trial

Collaboration. Effectiveness of intermittent pneu-
matic compression in reduction of risk of deep vein
1. Hemphill JC III, Greenberg SM, Anderson CS, et  al.
thrombosis in patients who have had a stroke (CLOTS
Guidelines for the management of spontaneous intra-
3): a multicenter randomized controlled trial. Lancet.
cerebral hemorrhage: a guideline for healthcare profes-
2013;382:516–24.
sionals from the American Heart Association/American
8. Paciaroni M, Agnelli G, Venti M, et al. Efficacy and
Stroke Association. Stroke. 2015;46:2032–60.
safety of anticoagulants in the prevention of venous
2. Hemphill JC III, Bonovich DC, Besmertis L, et  al.
thromboembolism in patients with acute cerebral
The ICH score: a simple, reliable grading scale for
hemorrhage: a meta-analysis of controlled studies. J
intracerebral hemorrhage. Stroke. 2001;32:891–7.
Thromb Haemost. 2011;9:893–8.
3. Rincon F, Mayer SA, Rivolta J, et al. Impact of delayed
9. Kelly J, Hunt BJ, Lewis RR, Rudd A. Anticoagulation
transfer of critically ill stroke patients from the emer-
or inferior vena cava filter placement for patient with
gency department to the Neuro-ICU. Neurocrit Care.
primary intracerebral hemorrhage developing venous
2010;13:75–81.
thromboembolism? Stroke. 2003;34:2999–3005.
4. Elmer J, Pallin DJ, Liu S, et al. Prolonged emergency
10. Beghi E, D’Alessandro R, Beretta S, et al. Incidence
department length of stay is not associated with worse
and predictors of acute symptomatic seizure after
outcomes in patients with intracerebral hemorrhage.
stroke. Neurology. 2011;77:1785–93.
Neurocrit Care. 2012;17:334–42.
11. Kollmar R, Juettler E, Huttner HB, et al. Cooling in
5. Sakamoto Y, Koga M, Todo K, et  al. Relative sys-
intracerebral hemorrhage (CINCH) trial: protocol of
tolic blood pressure reduction and clinical out-
a randomized German-Austrian clinical trial. Int J
comes in hyperacute intracerebral hemorrhage: the
Stroke. 2012;7:168–73.
SAMURAI-ICH observational study. J Hypertens.
12. Hutchinson PJ, Kolias AG, Timofeev EA, et  al.

2015;33(5):1069–73.
Trial of decompressive craniectomy for trau-
6. Anderson CS, Heeley E, Huang Y, et al. Rapid blood-­
matic intracranial hypertension. N Engl J Med.
pressure lowering in patients with acute intracerebral
2016;375(12):1119–30.
hemorrhage. N Engl J Med. 2013;368:2355–65.
 Airway Management
Robert S. Schoaps and Sprague W. Hazard III
Algorithmic Approach
A. Prior to any airway manipulation, evaluate
the patient. This includes assessment of perti-
nent medical history for findings which may
influence your plan or ability to perform dif-
ferent airway procedures (e.g., heart disease,
chronic kidney disease, head/neck radiation
or surgery, hospital course), performance of a
focused physical exam (mouth opening, C. Attempt first laryngoscopy. Consider the use
Mallampati classification, cervical spine
range of motion), review of nil per os (NPO)
status and recent labs, and review of prior air-
way intervention records if available. During
the initial evaluation, continually monitor for
hemodynamic instability and acute worsen-
ing of hypoxemia. Do not hesitate to call for
assistance if any difficulty is anticipated.
B. Ensure all appropriate equipment is available
and functioning; this includes, but is not lim-
ited to, a bag-valve-mask (BVM) apparatus,
suction with large-bore rigid catheter (e.g., D. If oxygenation is adequate with mask ventila-
Yankauer catheter), appropriately sized endo-
tracheal tubes (ETT) and laryngoscopes, ETT
introducer (e.g., gum elastic bougie), and
supraglottic airway devices. Assume the
sniffing position (neck flexion, atlanto-­
R. S. Schoaps · S. W. Hazard III (*)
Department of Anesthesiology and Perioperative
Medicine, Penn State Hershey Medical Center,
Hershey, PA, USA
e-mail: shazard@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_171
171
occipital extension) if possible; if patient
cannot tolerate the sniffing position or is
­
obese, elevate the head of bed to 20–30
degrees. Pre-­oxygenate with 100% FiO2 for
2 min if the patient is stable; if more expedi-
ent intervention is indicated, attempt four
inspiratory-­expiratory cycles at near-vital
capacity. Administer an appropriate sedative
and adequate neuromuscular blockade.
of video laryngoscopy or other adjuncts in
order to maximize the chance for success on
first attempt, as the chance of successful intu-
bation declines with each subsequent attempt
[1]. If successful, confirm placement by direct
visualization, observation of symmetric chest
rise, bilateral auscultation, and capnography.
Continuous quantitative capnography
remains the gold standard for confirmation of
ETT placement [1]. If unsuccessful, attempt
to mask ventilate.
tion, oxygenate and attempt up to two addi-
tional laryngoscopies. Consider the addition
of video laryngoscopy or other adjuncts in
order to improve likelihood of success with
subsequent attempts. If unable to achieve
adequate oxygenation with mask ventilation,
attempt insertion of a supraglottic airway
(SGA) device.
E. If SGA insertion is successful, continue oxy-
genation and consider options for the next step.
707
708
This may include intubating through the SGA
with a fiberoptic bronchoscope, utilization of
video laryngoscopy if not already attempted,
use of additional adjunctive devices if avail-
able, or procession to surgical airway interven-
tion (e.g., tracheotomy, cricothyroidotomy).
Appropriate consultant services should be noti-
fied of the situation (e.g., anesthesiology, air-
way surgical team, etc.). If you are unable to
oxygenate via the SGA, it is reasonable to
make one final attempt at mask ventilation.
F.
“Cannot intubate, cannot oxygenate”
(CICO) indicates at least one failed attempt
at laryngoscopy, at least one failed attempt
R. S. Schoaps and S. W. Hazard III
at mask ventilation, and failed SGA inser-
tion. CICO situations necessitate emergent
surgical airway intervention in order to
achieve adequate oxygenation. In such an
emergency setting, cricothyroidotomy is the
procedure of choice as it allows the fastest
reliable tracheal access [1].
Cricothyroidotomy is not recommended in
children due to a high incidence of subglot-
tic stenosis. If critical hypoxemia is
observed, consider inserting a 14-gauge nee-
dle through the cricothyroid membrane in
order to initiate passive oxygenation while
preparations for the procedure are made.
171  Airway Management 709

Assess patient
A Pertinent medical history, recent labs, NPO status, prior airway interventions, etc.

Prepare equipment, position, and pre-oxygenate with 100% FiO2

B
Induce with appropriate sedation and adequate neuromuscular blockade

Attempt first direct laryngoscopy (DL)

Successful?

No Yes

C Mask ventilate Confirm ETT placement:

Chest rise, auscultation, ETCO2

Oxygenating?

Yes
No

Insert supraglottic Oxygenate and attempt additional DL

D airway device Consider video laryngoscopy or other adjunct

Successful?

Yes
No

Oxygenate and consider options:

E Final attempt to Intubate through SGA, other adjunct, or
mask ventilate proceed to surgical airway

CICO

F Emergent surgical airway

(cricothyroidotomy)

Algorithm 171.1
710 R. S. Schoaps and S. W. Hazard III

Reference
1. Frerk C, et al. Difficult Airway Society 2015 guide-
lines for management of unanticipated difficult intu-
bation in adults. Br J Anesth. 2015;115(6):827–48.
 Intubation and Extubation
Ariel P. Santos
Algorithmic Approach
Intubation
A. The need for emergent intubation is one of
the most stressful situations any clinician can
potentially encounter. But awareness of the
indications, readiness, preparation, and prac-
tice can render this daunting task seamless.
B. Early identification of patients at risk for dif-
ficult intubation is imperative. Findings on
external airway examination like decreased
cervical mobility and increased distance
between the thyroid cartilage and tip of chin
or thyromental distance of less than 7 cm are
predictive of potentially difficult intubation.
De Jong et al. devised the MACOCHA scor-
ing system which correlates with intubation
difficulty [1] (see table in Algorithm 172.1).
C. According to Jaber et al., use of the ten-step
bundle could lower life-threatening compli-
cations, i.e., death, cardiac arrest, severe
hypotension, and severe hypoxemia from
34% to 21%. Other complications, such as
aspiration, dysrhythmia, and esophageal intu-
bation, could also be lowered from 21% to
9% [2]. Proper airway positioning is impor-
tant to achieve adequate oxygenation. Patient
A. P. Santos (*)
Department of Surgery, Texas Tech University Health
Sciences Center, Lubbock, TX, USA
e-mail: ariel.santos@ttuhsc.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_172
172
should be placed in sniffing position which
can be achieved by placing the back of the
bed at 30 degrees angle and placing a shoul-
der roll. However, in the presence of a possi-
ble or suspected cervical injury, cervical
stabilization will be required.
The most common induction agents used for
intubation are ketamine, propofol, and etomidate.
Propofol should be avoided in a hemodynami-
cally unstable patient. In addition, paralytics are
also administered during the rapid sequence intu-
bation. The two most common paralytics used are
succinylcholine and rocuronium. Succinylcholine
should be avoided in patients with renal failure,
hyperkalemia, crush injuries, neuromuscular
pathologies, and myopathies.
It is imperative to have a working laryngo-
scope (either a Miller or a Macintosh blade)
depending on the operator’s preference. Recently
direct laryngoscope was supplanted by video
laryngoscope as the preferred method of intuba-
tion. Griesdale et al. showed that the latter allows
for improved glottis visualization, faster intuba-
tion, and higher success rate [3].
After intubation, placement should be verified by
physical examination, auscultation, and capnog-
raphy. The American Heart Association (AHA)
International Consensus on Cardiopulmonary
Resuscitation (CPR) and Emergency
Cardiovascular Care (ECC) recommended rou-
tine use of waveform capnography for
711
712
e­ ndotracheal verification [4]. It is considered the
gold standard for verification of proper endotra-
cheal tube placement and carries a 100% sensi-
tivity and specificity even in low perfusion state
such as cardiac arrest [5]. The endotracheal tube
should be properly secured and an orogastric tube
A. P. Santos
placed to decompress the stomach. Chest X-ray
should be requested to evaluate placement of the
endotracheal tube. Complications of inappropri-
ate placement of endotracheal tube are clinically
significant that post-intubation chest X-rays are
deemed necessary [6].
172  Intubation and Extubation 713

A Indications of Intubation:
1. Respiratory Failure
2. Relief of airway obstruction
3. Airway protection
4. Shock
5. Low GCS < 8
6. Severe maxilla-facial injury
7. Reduction of work of breathing
8. Facilitation of pulmonary toilet

Any of the above No

indication exists? Continue to Monitor

Yes

Table 172.1 Examine the patient using the MACOCHA Scoring

B
POINTS
Factors related to patient
Mallampati Score III or IV 5
Obstructive sleep apnea Syndrome 2
Reduced mobility of cervical Spine 1
Limited mouth opening < 3 cm 1
Factors related to pathology
Coma 1
Severe Hypoxemia < 80% 1
Factor related to operator
Non-Anesthesiologist 1
Total 12
Definition of Abbreviation: MACOCHA= Mallampati score III or IV, Apnea syndrome
(obstructive), Cervical spine limitation, Opening mouth < 3 cm, Coma, Hypoxia,
Anesthesiologist non-trained. Coded 0 to 12: 0 = easy;12 = very difficult

Reprinted with permission of the American Thoracic Society. Copyright © 2017 American
Thoracic Society.
De Jong A, Molinari N, Terzi N et al. Early identification of patients at risk for difficult
intubation in the intensive care unit: development and validation of the MACOCHA
score in a multicenter cohort study. Am J Respir Crit Care Med. 2013 187(8): 837.
The American Journal of Respiratory and Critical Care Medicine is an official journal of the
American Thoracic Society
714 A. P. Santos

Difficult Intubation Cart (table 2)

Possible Yes
Difficult Call Anesthesiologist on call
Intubation?
Notify Surgery Team for possible
surgical airway

No

Intubation Protocol

Pre-intubation
C 1. Presence of intensivist, respiratory therapist, bedside RN, and intubation cart
2. Preparation for long term sedation
3. Procedure time-out
4. Positioning and Pre-oxygenation for at least 3 minutes

Intubation

5. Rapid Sequence intubation technique:

a. Induction agents: ketamine, propofol or etomidate
b. Paralytics:Succinylcholine 1.5-2.0 mg/kg or Rocuronium 1.0-1.2 mg/kg
6. Application of cricoid pressure
7. Visualization of glottic opening and intubation

Post-intubation

8. Immediate confirmation with capnography/capnometry

9. Confirmation with auscultation and chest x-ray
10. Secure the tube, place oro-gastric tube

Endotracheal intubation

Algorithm 172.1
172  Intubation and Extubation
Extubation
A. Extubation or removal of the endotracheal
tube is the final step of liberation from
mechanical ventilator. Prior to extubation, it
is important to review the indication for intu-
bation and ensure that the reason for intuba-
tion has been resolved.
B. Intubated patients should be assessed daily
for possible extubation. The patient must be
hemodynamically stable and on minimal
pressor support with appropriate and ade-
quate gas exchange. Sedation should be dis-
continued and the patient must pass a
spontaneous breathing trial. The patient
should be awake and be able to support their
airway with adequate respiratory drive and
muscle and cough strength to clear one’s
secretions. Patients with cough peak flow
(CPF) of less than 60 ml/min and secretions
of more than 2.5 ml/hour and those unable to
complete four simple tasks (open one’s eyes,
tracking with one’s eyes, hand grasping, and
stick out tongue) are at high risk for extuba-
tion failure [7]. Traditionally, we prefer to
have a respiratory rate of less than 35 per
715
minute, vital capacity of >10 ml/kg, negative
inspiratory force (NIF)  >−20, tidal volume
(TV) >5 ml/kg, and rapid shallow breathing
index (RSBI) less than 100.
C. If airway edema is suspected, cuff-leak test
can be done by deflating cuff and occluding
the endotracheal tube to ascertain whether
patient can breathe around the tube.
Administration of steroids can help amelio-
rate the edema. A failed cuff-leak test does
not always lead to failed extubation particu-
larly when inappropriately sized tube was
used.
D. Diligence must be observed prior to endo-
tracheal extubation especially if intubation
was noted to be difficult. Caution must be
taken in extubating patient with obstructive
sleep apnea, maxillofacial trauma, general-
ized edema, postoperative procedure like
thyroid and ENT surgeries, and cervical
spine procedures. Informing the anesthesia
or surgical team prior to extubating a previ-
ously difficult intubation patient is not
unreasonable. Reintubation has been asso-
ciated with higher mortality (see table in
Algorithm 172.2).
716 A. P. Santos

Criteria for Extubation:

1. Patient is awake and can support airway

A 2. Adequate respiratory drive and muscle strength
3. Adequate oxygenation and ventilation
4. Passed spontaneous breathing trial
5. (+) Cough reflex and able to clear secretions

Indication for the Do not Extubate

intubation
resolved? No Re-assess again

Yes

Spontaneous Breathing Trial Do not Extubate

B for 30 minutes or more
No Re-assess again

Yes

Yes

IV Steroids
C Cuff Leak?
No Re-assess again
172  Intubation and Extubation 717

Yes

Previous Difficult
Intubation? Prepare to extubate
No

D
Yes

Call anesthesiology

Difficult airway cart (Table 2)

Call Surgery: preparation for surgical airway

Table 172.2 Contents of Difficult Intubation Cart

Bag-and-mask Ventilation System

Nasopharyngeal airway in various sizes
Oral airway in various sizes
Yankauer suction, tubing and machine
Video laryngoscope
Laryngoscope: Macintosh and Miller in various blade sizes
Endotracheal tubes in various sizes
ET stylets
Eschmann stylet
Bougie
Magill forceps
Ventilating tube exchange catheters
Carbon dioxide detectors
Fiberoptic scope
Supraglottic airway devices like laryngeal mask airway
Cricothyroidotomy kit
Emergency Surgical Airway Kit
Algorithm 172.2

4. Neumar RW, Otto CW, Link M, et  al. Part 8: adult

References
1. De Jong A, Molinari N, Terzi N, et al. Early iden-
tification of patients at risk for difficult intuba-
tion in the intensive care unit: development and
validation of the MACOCHA score in a multi-
center cohort study. Am J Respir Crit Care Med.
2013;187(8):832–9.
2. Jaber S, Jung B, Corne P, et  al. An intervention to
decrease complications related to endotracheal intuba-
tion in the intensive care unit: a prospective, multiple-­
center study. Intensive Care Med. 2010;36(2):248–55.
3. Griesdale DE, Chau A, Isac G, Canadian Critical Care
Trial Group, et  al. Video-laryngoscopy versus direct
laryngoscopy in critically ill patients: a pilot random-
ized trial. Can J Anaesth. 2012 Nov;59(11):1032–9.
advanced cardiovascular life support: 2010 American
Heart Association guidelines for cardiopulmonary
resuscitation and emergency cardiovascular care.
Circulation. 2010;122:S729–67.
5. Silvestri S, Laddle J, Brown J, et  al. Endotracheal
tube placement confirmation: 100% sensitivity and
specificity with sustained four-phase capnographic
waveforms in a cadaveric experimental mode.
Resuscitation. 2017;115:192–8.
6. Hossein-Nejad H, Payandemehr P, Bashiri S, et  al.
Chest radiography after endotracheal tube place-
ment: is it necessary or not? Am J Emerg Med.
2013;31(8):1181–2.
7. Salam A, Tilluckdharry L, Amoateng-Adjepong Y,
et al. Neurologic status, cough, secretions and extuba-
tion outcomes. Intensive Care Med. 2004;30:1334–9.
 Acute Respiratory Distress
Syndrome (ARDS) 173
Dan A. Galvan

Algorithmic Approach D. Additional therapeutic measures may be

A. If one should have a patient developing new-­
onset or worsening respiratory compromise
within 1  week of exposure to relevant risk
factors, one should be aware that the patient E. Measurement of driving pressure [9] and
could be developing ARDS [1]. This syn-
drome is underrecognized in 40% of all cases
[2] and has a mortality rate of greater than
40% in moderate-to-severe disease [3].
B. Once you suspect ARDS, apply the criteria
cited in the Berlin definition of ARDS [1].
Recognition of a patient with ARDS and stag-
ing (mild, moderate, severe) of the syndrome
clarifies the mortality risk and drives treat- G. To optimize care of the ARDS patient, the
ment efforts maximizing survival. (see table
in Algorithm 173.1)
C. Patients meeting ARDS criteria must have
lung protective strategies initiated. These
strategies include low tidal volume ventila-
tion, elevated positive end-expiratory pres-
sure (PEEP), and diminished plateau
pressures [4]. PEEP strategy should be deter-
mined by the ARDS stage [5, 6].
undertaken for patients with moderate-to-­
severe ARDS including the use of neuro-
muscular blockade agents [7] and prone
positioning [8].
trans-pulmonary pressure [10] may impede
injury to the lung in the form of volutrauma,
barotrauma, atelectrauma, and biotrauma.
F. Recruitment maneuvers to open collapsed
alveoli [11] and utilization of a directed fluid
management strategy for specific subpheno-
types of ARDS [12] may benefit certain
ARDS patients.
ABCDEF [13] bundle must be employed.
H. Presently, there is no compelling evidence to
support the routine use of extracorporeal
membrane oxygenation [14], high-frequency
oscillatory ventilation [15], inhaled nitric
oxide [16], or glucocorticoids [17] in the
treatment of ARDS patients.

D. A. Galvan (*)
Geisinger Holy Spirit Hospital, Harrisburg, PA, USA
e-mail: dgalvan@geisinger.edu

© Springer Nature Switzerland AG 2019 719

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_173
720 D. A. Galvan

A young blunt trauma patient on the ventilator develops increasing

hypoxemia 4 days following a damage control laparotomy. The abdomen
is still open. Chest film reveals bilateral opacities and an echocardiogram
does not demonstrate cardiac contusion or fluid overload.

Risk Factors for ARDS:

Pneumonia
Non-pulmonary sepsis
Aspiration of gastric contents
Major trauma
A Is this ARDS? Pulmonary contusions
Pancreatitis
Inhalational injury
Severe burns
Non-cardiogenic shock
Drug overdose
Multiple transfusions or transfusion-
associated acute lung injury
Pulmonary vasculitis
Drowning

The Berlin Definition of Acute Respiratory Distress Syndrome

Acute Respiratory Distress Syndrome
Timing Within 1 week of a known clinical insult or new or worsening respiratory
symptoms
Chest imaginga Bilateral opacities—not fully explained by effusions, lobar/lung collapse, or
nodules
Origin of edema Respiratory failure not fully explained by cardiac failure or fluid overload
Need objective assessment (eg, echocardiography) to exclude hydrostatic
edema if no risk factor present
Oxygenationb
B Mild 20 mmHg < PaO2/FIO2 ≤300 mmHg with PEEP or CPAP ≥ 5 cmH2OC
Moderate 100 mmHg < PaO2/FIO2 ≤ 200 mmHg with PEEP ≥ 5 cmH2O
Severe PaO2/FIO2 ≤ 100 mmHg with PEEP ≥ 5 cmH2O
Abbreviations: CPAP, continuous positive airway pressure; FIO2, fraction of inspired oxygen; PaO2, partial pressure of arterial oxygen;
PEEP, positive end-expiratory pressure.
aChest radiograph or computed tomography scan.
bIf altitude is higher than 1000 m, the correction factor should be calculated as follows: [PaO /FIO x (barometric pressure/760)].
2 2
cThis may be delivered noninvasively in the mild acute respiratory distress syndrome group.

From Ranieri VM, Rubenfeld GD, Thompson BT, et al. The ARDS Definition Task
Force. Acute respiratory distress syndrome: the Berlin Definition. JAMA
2012;307(23):2526–2533; with permission from the American Medical Association.

Timing: worsening respiratory symptoms within one week of

major trauma
Chest imaging: bilateral opacities not explained by effusions or
lung collapse
Origin of edema: not explained by cardiac failure or fluid
overload as proven on echocardiography

Oxygenation: ABGs - PaO2 of 60; on an FIO2 of 1.0 and

PEEP 10 PaO2 /FIO2 of 60 mm Hg consistent with severe ARDS

Algorithm 173.1
173  Acute Respiratory Distress Syndrome (ARDS) 721

Begin lung protective strategies including low tidal volume ventilation

(4-6 mL/kg predicted body weight), elevated PEEP while keeping plateau
C pressures ≤ 30 cm H2O. Utilize low PEEP for mild ARDS and high PEEP
for moderate-to-severe ARDS.

Utilizing appropriate sedation, begin a continuous infusion of Cisatracurium

D for 48 hours. Then initiate proning of the patient for at least 16 consecutive
hours per day until desired improvement in oxygenation is achieved.

Initiate measurement of driving pressure and transpulmonary pressure as

E described in the referenced articles.

Utilize recruitment maneuvers; obtain plasma levels of IL-8, bicarbonate and

F tumor necrosis factor receptor-1 levels to accurately classify the patient’s
subphenotype and appropriately direct fluid management.

Assess, prevent and manage pain (particularly in the presence of significant

pain) utilizing numerical rating scales.

Both spontaneous awakening trials and spontaneous breathing trials should be

employed daily to liberate the patient from the ventilator in a timely fashion.

Choice of analgesia and sedation strategy should utilize numerical rating

scales and be deliberate and judicious; avoid benzodiazepines.

Delirium should be assessed utilizing numerical rating scales, prevented and

managed. Delirium leads to prolonged mechanical ventilation, increased
G
length of ICU and hospital stay as well as long-term cognitive impairment and
elevated mortality.

Early mobility decreases delirium and improves functional outcomes.

Family engagement is a critical foundational support needed by every

intensive care unit patient.
From Marra A, Ely EW, Pandharipande PP, Patel MB. The ABCDEF bundle in critical care. Crit Care Clin
2017;33(2):225-43; with permission from Elsevier.

Algorithm 173.1 (continued)
722 D. A. Galvan

References acute respiratory distress syndrome. N Engl J Med.

2013;368(23):2159–68.
9. Amato MB, Meade MO, Slutsky AS, et  al. Driving
1. Ranieri VM, Rubenfeld GD, Thompson BT, et  al.
pressure and survival in acute respiratory distress syn-
The ARDS definition task force. Acute respiratory
drome. N Engl J Med. 2015;372(8):747–55.
distress syndrome: the Berlin definition. JAMA.
10. Talmor D, Sarge T, Malhotra A, et al. Mechanical ven-
2012;307(23):2526–33.
tilation guided by esophageal pressure in acute lung
2. Bellani G, Laffey JG, Pham T, LUNG SAFE
injury. N Engl J Med. 2008;359(20):2095–104.
Investigators; ESICM Trials Group, et  al.
11. Constantin JM, Godet T, Jabaudon M, Bazin JE, Futier
Epidemiology, patterns of care, and mortality for
E.  Recruitment maneuvers in acute respiratory dis-
patients with acute respiratory distress syndrome
tress syndrome. Ann Transl Med. 2017;5(14):290–5.
in intensive care units in 50 countries. JAMA.
12. Famous KR, Delucchi K, Ware LB, et al. Acute respi-
2016;315(8):788–800.
ratory distress syndrome subphenotypes respond dif-
3. Villar J, Blanco J, Kacmarek RM. Current incidence
ferently to randomized fluid management strategy.
and outcome of the acute respiratory distress syn-
Am J Respir Crit Care Med. 2017;195:331–8.
drome. Curr Opin Crit Care. 2016;22(1):1–6.
13. Marra A, Ely EW, Pandharipande PP, Patel MB. The
4. The Acute Respiratory Distress Syndrome Network.
ABCDEF bundle in critical care. Crit Care Clin.
Ventilation with lower tidal volumes as compared
2017;33(2):225–43.
with traditional tidal volumes for acute lung injury
14. Abrams D, Brodie D. Extracorporeal membrane oxy-
and the acute respiratory distress syndrome. N Engl J
genation for adult respiratory failure 2017 update.
Med. 2000;342(18):1301–8.
Chest. 2017;152(3):639–49.
5. Briel M, Meade M, Mercat A, et al. Higher vs lower
15. Meade MO, Young D, Hanna S, et  al. Severity of
positive end-expiratory pressure in patients with
hypoxemia and effect of high-frequency oscillatory
acute lung injury and acute respiratory distress syn-
ventilation in acute respiratory distress syndrome. Am
drome systematic review and meta-analysis. JAMA.
J Respir Crit Care Med. 2017;196(6):727–33.
2010;303(9):865–73.
16.
Gebistorf F, Karam O, Wetterslev J, Afshari
6. Chiumello D, Cressoni M, Carlesso E, et al. Bedside
A.  Inhaled nitric oxide for ARDS in children and
selection of positive end-expiratory pressure in mild,
adults. Cochrane Database Syst Rev. 2016;(6). Art.
moderate and severe acute respiratory distress syn-
No.:CD002787.
drome. Crit Care Med. 2013;42(2):1–13.
17. The National Heart, Lung, and Blood Institute Acute
7. Papazian L, Forel JM, Gacouin A, ACURASYS Study
Respiratory Distress Syndrome (ARDS) Clinical
Investigators, et al. Neuromuscular blockers in early
Trials Network. Efficacy and safety of corticosteroids
acute respiratory distress syndrome. N Engl J Med.
for persistent acute respiratory distress syndrome. N
2010;363(12):1107–16.
Engl J Med. 2006;354(16):1671–84.
8. Guérin C, Reignier J, Richard JC, PROSEVA
Study Group, et  al. Prone positioning in severe
 Management of Sepsis
Jacklyn Engelbart and Luis J. Garcia
Algorithmic Approach
A. Sepsis is a life-threatening organ dysfunction
due to dysregulated response infection. Septic
shock occurs when underlying circulatory,
metabolic, and cellular abnormalities occur
including lactate >2.0 mmol/L and refractory
hypotension despite sufficient IV fluid resus-
citation and vasopressor requirement to main-
tain MAP >65  mmHg [1]. The first step in
evaluation of a patient with sepsis is the his-
tory and physical. Questions regarding the
onset of infection and concern for organ dys-
function are essential. Findings may include
altered mental status, tachycardia, hypoten-
sion, and tachypnea. Others include fever or
hypothermia, substantial edema or positive
fluid balance, hyperglycemia in absence of
diabetes mellitus, leukocytosis, leukopenia,
or normal white count with >10% bands, ele-
vated CRP, hypotension, elevated mixed
venous oxygen saturations, and elevated car-
diac index [2].
B. Signs of organ dysfunction include acute
hypoxemia, acute oliguria, increase in creati-
nine, coagulopathy, ileus, thrombocytopenia,
hyperbilirubinemia. Signs of decreased tissue
J. Engelbart · L. J. Garcia (*)
Department of Surgery, University of Iowa Hospitals
and Clinics, Iowa City, IA, USA
e-mail: luis-garcia@uiowa.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_174
174
perfusion, elevated lactate, and decreased
capillary refill or mottling [2].
C. Establish IV access and start fluid resuscita-
tion. Obtain cultures and then start empiric
broad-spectrum intravenous antibiotics as
soon as possible [1]. Trend labs including
lactate and ScVO2, frequently reassess fluid
responsiveness while providing fluid resus-
citation. Patients requiring surgical explora-
tion or intervention for emergent source
control should be identified with manage-
ment as soon as medically possible after
diagnosis [1].
D. Initial resuscitation for sepsis-induced hypo-
perfusion or lactate >4  mmol/L includes
30  mL/kg of IV crystalloid fluid within the
first 3  h with initial mean arterial pressure
goal of 65  mmHg. Complete reassessments
of volume status and tissue perfusion with
focused exam and/or with at least two of the
following: measure CVP, measure ScvO2,
bedside echocardiography, or dynamic
assessment of fluid responsiveness with pas-
sive leg raise or fluid challenge [3–5].
E. Vasopressors may be used for patients in sep-
tic shock with hypotension refractory to ade-
quate fluid bolus [1].
F. Antimicrobial therapy should be started
within 1  h of diagnosis. Narrow antibiotics
once pathogen is identified and sensitivities
are determined. Typically a treatment dura-
tion of 7–10 days, though longer courses may
723
724
be appropriate with slow clinical response,
bacteremia, undrainable source of infection,
immunologic deficiencies, and certain bacte-
rial, viral, and fungal infections [1, 6].
G. Supplemental oxygen or mechanical ventila-
tion may be required for patients with sepsis.
A large trial of pressure- and volume-limited
strategy showed 9% absolute decrease in mor-
tality in ARDS patients ventilated with tidal
volume of 6 mL/kg compared with 12 mL/kg
in adult patients with sepsis-­induced ARDS
and goal of plateau pressure ≤ 30 cm H2O [7].
Spontaneous breathing trials and weaning
protocol should be attempted in patients who
are ready for wean [1].
J. Engelbart and L. J. Garcia
H. Continuous or intermittent sedation should
be minimized in patients with sepsis,
though adequate sedation and analgesia
must be maintained when neuromuscular
blockade is in place. Neuromuscular block-
ade should be avoided in patients without
ARDS [1].
I. Continue supportive intensive care unit thera-
pies including glucose control and deep vein
thrombosis prophylaxis. Blood product
administration is appropriate in symptomatic
patients with hemoglobin <7.0  g/dL in the
absence of extenuating circumstances includ-
ing myocardial ischemia or infarction, acute
hemorrhage, or severe hypoxemia [1, 8].
174  Management of Sepsis 725

H&P:Temp > 38.3°C or < 36.0°C, HR >100, RR > 20, WBC > 12,000
A or < 4,000 or > 10% bands, hypotension altered mental status, edema
or positive fluid balance, hyperglycemia in absence of diabetes,
infection

Findings: signs of organ dysfunction (sepsis), SBP <90 mmHg after

B sufficient IV fluid resuscitation with vasopressor requirement to
maintain MAP > 65 mmHg, lactate > 2 mmol/L (septic shock)

Trend vital signs, frequent physical exams, cardiac and hemodynamic

C monitoring, pulse oximetry, obtain labs including cultures, ScVO2, and
lactate, obtain arterial and venous access and give fluid bolus

Initial resuscitation & fluid therapy

Administer 30 mL/kg crystalloid for hypotension or lactate 4 mmol/L
D within the first 4–6 hours.
Reassess volume status and tissue perfusion

Vasoactive medications
E Use vasopressors for hypotension that does not respond to IV fluid
resuscitation to maintain a mean arterial pressure (MAP) ≥65 mmHg

Antimicrobial therapy & source control

Start broad-spectrum IV antibiotics as soon as possible within 1 hr
F of identifying sepsis. Deescalate when culture data is available.
Pursue source control or surgical intervention as soon as possible

Supplemental O2 or mechanical ventilation

Ventilate with pressure and volume limited ventilation such as 6
G mL/kg tidal volumes in the setting of ARDS/ALI and plateau pressure
≤ 30 cm H2O in patient with sepsis-induced ARDS

Sedation & analgesia

Appropriate sedation and analgesia must be maintained if
H neuromuscular blockade is used in sepsis, avoid NMBA in patients
without ARDS due to risk of prolonged blockade

Supportive management
I Glucose control, DVT prophylaxis, blood product administration,
goals of care, communication of prognosis

Algorithm 174.1

4. Yealy DM, Kellum JA, Huang DT, et al. A random-

References
1. Rhodes A, et al. Surviving sepsis campaign: interna-
tional guidelines for management of severe sepsis and
septic shock: 2016. Crit Care Med. 2017;45:486–552.
2. Angus DC, Van der Poll T. Severe sepsis and septic
shock. N Engl J Med. 2013;369(9):840–51.
3. Mouncey PR, for the ProMISe Trial Investigators,
et  al. Trial of early, goal-directed resuscitation for
septic shock. N Engl J Med. 2015;372(14):1301–11.
ized trial of protocol-based care for early septic
shock. N Engl J Med. 2014;370(18):1683–93.
5. Peake SL, Delaney A, Bailey M, et al. Goal-directed
resuscitation for patients with early septic shock. N
Engl J Med. 2014;371(16):1496–506.
6. Ferrer R, Martin-Loeches I, Phillips G, et al. Empiric
antibiotic treatment reduces mortality in severe sepsis
and septic shock from the first hour: results from a
guideline-based performance improvement program.
Crit Care Med. 2014;42:1749–55.
726
7. Brower RG, Matthay MA, Morris A, et al. Ventilation
with lower tidal volumes as compared with tradi-
tional tidal volumes for acute lung injury and the
acute respiratory distress syndrome. N Engl J Med.
2000;342(18):1301–8.
J. Engelbart and L. J. Garcia
8. Holst LB, Haase N, Wetterslev J, TRISS Trial
Group; Scandinavian Critical Care Trials Group,
et  al. Lower versus higher hemoglobin threshold
for transfusion in septic shock. N Engl J Med.
2014;371:1381–91.
 Management of Shock
Jacklyn Engelbart and Luis J. Garcia
Algorithmic Approach
A. Shock can be described as a failure of the cir-
culatory system to adequately deliver blood,
oxygen, and nutrients to vital organs, prefer-
entially the heart and brain. Patients may
present with tachypnea, altered mental status,
and hypotension.
B. Initial stabilization of the patient’s airway,
breathing, and circulation should be estab-
lished first. This includes securing an airway
through intubation if necessary, establishing
IV access, and administering an initial intra-
venous fluid bolus while considering the eti-
ology of shock. Total volume of fluid
resuscitation is determined by the type of
shock. Patients with cardiogenic shock due to
infarction of the left ventricle or obstructive
shock due to pulmonary embolism may
require only small volumes for fluid resusci-
tation, whereas those with hemorrhagic
shock, sepsis, or infarction of the right ven-
tricle often require larger volumes for fluid
resuscitation. Patients with massive hemor-
rhage will require blood products. Patient
with shock may require vasopressors and ino-
tropes in addition to resuscitation, and hemo-
dynamic monitoring should be established
J. Engelbart · L. J. Garcia (*)
Department of Surgery, University of Iowa Hospitals
and Clinics, Iowa City, IA, USA
e-mail: luis-garcia@uiowa.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_175
175
with central venous access, pulmonary artery
catheters, and arterial lines. Occasionally
echocardiograms are necessary for visualiza-
tion. Necessary laboratory studies and imag-
ing may include basic metabolic panel
(BMP), complete blood count (CBC), coagu-
lation studies, serum lactate, renal function
tests, liver function tests, electrocardiogram
(ECG), chest X-ray (CXR), arterial blood gas
(ABG), or blood cultures with more targeted
studies depending on clinical presentation. At
this time, any early interventions should be
attempted depending on the etiology of
shock.
C. Distributive shock occurs in the setting of
anaphylaxis, adrenal crisis, neurogenic shock,
and sepsis. Adrenal insufficiency or crisis
presents as an acute cardiovascular collapse
unresponsive to fluids and vasopressors.
Treatment with IV dexamethasone is first line
and can be given empirically with suspicion
of adrenal crisis as it does not interfere with
the corticotrophin stimulation test used for
diagnosis. Neurogenic shock occurs as a
result of a spinal or head injury leading to loss
of the sympathetic tone. This results in
decrease in systemic vascular resistance,
decrease in blood pressure, decrease in heart
rate, and warm extremities. Initial treatment
is intravascular fluid resuscitation followed
by phenylephrine. Anaphylaxis may occur
with severe allergic reactions and patients
727
728
should be administered epinephrine. Sepsis
presents with hypotension, confusion, hyper-
ventilation, hyperglycemia, and shock in the
setting of a known or suspected infection.
Treatment involves a multifaceted approach
with volume resuscitation, antibiotics, and
source control at its core. Fluid resuscitation
can be guided by mean arterial pressure and
central venous pressure goals as well as uri-
nary output, lactate clearance, and venous
saturations.
D. Hypovolemic shock occurs as a result of large
fluid losses such as with trauma, burns, hem-
orrhage, vomiting, or diarrhea. In hemody-
namically unstable trauma patients, they are
considered to be bleeding unless proven oth-
erwise. A focused assessment with sonogra-
phy for trauma (FAST) exam or other imaging
may be necessary to identifying bleeding not
J. Engelbart and L. J. Garcia
obvious during the primary or secondary
­survey. Treatment includes volume resuscita-
tion, direct pressor, and emergent surgical
control of bleeding.
E. Obstructive shock often presents in the set-
ting of cardiac tamponade, pulmonary embo-
lism, or tension pneumothorax. All three of
these may require emergent intervention
including pericardiocentesis, thrombolysis,
or needle decompression and a chest tube,
respectively.
F. Cardiogenic shock may occur as a result of
massive myocardial infarction, ruptured
valve, unstable arrhythmia, or severe conges-
tive heart failure. Treatment includes coro-
nary revascularization, intra-aortic balloon
pump, surgical valve repair, or following
advanced cardiac life support (ACLS) proto-
cols in the case of unstable arrhythmias.
175  Management of Shock 729

A Focused clinical history and examination of patient with shock

Initial stabilization, secure the airway if necessary, establish

B IV access, and administer initial intravenous fluid bolus while
considering etiology of shock, draw laboratory studies

Anaphylaxis – Epinephrine

Adrenal crisis – IV dexamethasone

C Distributive shock
Neurogenic shock – Volume resuscitation,
then phenylephrine

Sepsis – IV antibiotics, volume resuscitation,

vasopressors, source control

D Hemorrhagic shock – Volume resuscitation,

Hypovolemic shock
direct pressure, emergent surgery

Cardiac tamponade – Pericardiocentesis or

pericardial window, volume resuscitation

E Obstructive shock Pulmonary embolism – Thrombolysis

Tension pneumothorax – Chest tube

Myocardial infarction – Inotrope, coronary

revascularization, intra-aortic balloon pump

F Cardiogenic shock Ruptured valve – Surgical valve repair

Arrhythmia – ACLS protocols

Algorithm 175.1

Van Diepen S, Katz JN, Albert NM, et al. Contemporary

Suggested Reading
Rhodes A, et al. Surviving sepsis campaign: international
guidelines for management of severe sepsis and sep-
tic shock: 2016. Crit Care Med. 2017;45:486–552.
management of cardiogenic shock: a scientific
statement from the American Heart Association.
Circulation. 2017;136(16):e232–68.
Vincent JL, De Backer D.  Circulatory shock. N Engl J
Med. 2013;369(18):1726–34.
 Blood Transfusion Indications
Jacklyn Engelbart and Luis J. Garcia
Algorithmic Approach
A. Numerous guidelines on blood transfusion
indications have been published with many
describing specific thresholds for transfusion
within specified clinical scenarios. Most also
stress that blood products should only be
given when clinically necessary as hemoglo-
bin levels do not guarantee adequate delivery
of oxygen to tissue. Indications for blood
transfusion may include trauma with massive
blood loss (hemorrhage – surgical, traumatic,
or nonsurgical), anemia, major surgical oper-
ation, cancer patients requiring therapy, mas-
sive blood loss or anemia in the setting of
pregnancy and childbirth, hereditary disor-
ders like hemophilia and thalassemia, critical
illness, and severe burn victims.
B. In the setting of acute hemorrhage with hypo-
volemia, hematocrit does not immediately
correlate with blood loss. In this setting,
transfusions are indicated regardless of the
hemoglobin or hematocrit given the acute
hemorrhage will result in significant ongoing
blood loss at the time of presentation [1].
C. Transfusions should be given in patients with
symptomatic or life-threatening anemia.
Signs of ischemia or symptomatic anemia
J. Engelbart · L. J. Garcia (*)
Department of Surgery, University of Iowa Hospitals
and Clinics, Iowa City, IA, USA
e-mail: luis-garcia@uiowa.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_176
176
include orthostatic hypotension or tachycar-
dia not responsive to fluid replacement, myo-
cardial ischemia, angina, or dyspnea, hypoxia,
and neurologic changes. Chronic anemia
typically presents with additional symptoms
such as fatigue. Chronic anemia may occur
with chronic blood loss (hepatic disorders,
bleeding disorders) or decreased erythropoi-
esis (malignancies, chemotherapy, other
drugs suppressing bone marrow, renal disor-
ders, nutritional deficiencies). No definite
triggers have been defined so the decision to
transfuse is considered on an individual basis
guided by symptoms or functional impair-
ment [1, 2].
D. In hospitalized, hemodynamically stable
patients with acute coronary syndrome (i.e.,
unstable angina, myocardial infarction), the
evidence is unclear in support of liberal or
restrictive transfusion thresholds. However,
most guidelines recommend transfusion for
hemoglobin <8 g/dL and considering transfu-
sions with hemoglobin 8–10 g/dL [3–5].
E. In hospitalized, hemodynamically stable
patients with preexisting cardiovascular dis-
ease, transfusions should be considered with
hemoglobin concentrations of 8 g/dL or less
if the patient has congestive heart failure or if
patients are symptomatic with chest pain,
orthostatic hypotension, or tachycardia unre-
sponsive to fluid resuscitation. If a patient is
undergoing cardiac or orthopedic surgery,
731
732
consider transfusion for hemoglobin <8 g/dL
based on clinical evaluation of patient and
expected blood loss during surgery [2,
5–10].
F. In intensive care unit patients (i.e., nonsurgi-
cal/nontraumatic hemorrhage, sepsis), hemo-
globin concentrations of 7 g/dL or less should
prompt consideration of transfusion in accor-
J. Engelbart and L. J. Garcia
dance with a restrictive transfusion strategy
[1, 2, 11, 12]. In hospitalized, hemodynami-
cally stable patients, hemoglobin concentra-
tion and symptoms should be considered in
transfusion decisions. In patients with hemo-
globin <7 g/dL, transfusion is generally indi-
cated; however decision should still be made
based on clinical signs and symptoms [1, 2].
176  Blood Transfusion Indications 733

A Anemia/acute blood loss/massive hemorrhage

Yes
Life-threatening acute blood loss such as massive
B hemorrhage or trauma?
Consider transfusion

No
No
C Hemoglobin < 10 g/dL or hematocrit < 30%? No transfusion

Signs of ischemia or symptomatic?

(myocardiali schemia, orthostatic hypotension or Yes
D Consider transfusion
tachycardia not responsive to fluid replacement,
angina/dyspnea, hypoxia, neurologic changes)

No

Hemoglobin 8-10 g/dL – diagnosis of acute Yes

coronary syndrome or severe thrombocytopenia Consider transfusion
in hematology oncology patient?

No

Hemoglobin 7-8 g/dL – does the patient have Yes

E stable cardiovascular disease or is the patient Consider transfusion
undergoing orthopedic or cardiac surgery?

No

Hemoglobin < 7 g/dL – symptomatic Yes

F hospitalized or ambulatory patients, intensive Consider transfusion
care unit patients

Algorithm 176.1
734 J. Engelbart and L. J. Garcia

References American College of Physicians. Ann Intern Med.

2013;159(11):770–9.
6. Ferraris VA, Brown JR, Despotis GJ, et  al. 2011
1. Napolitano LM, Kurek S, Luchette FA, et al. Clinical
update to the Society of Thoracic Surgeons and the
practice guideline: red blood cell transfusion in adult
Society of Cardiovascular Anesthesiologists blood
trauma and critical care. J Trauma Inj Infect Crit Care.
conservation clinical practice guidelines. Ann Thorac
2009;67(6):1439–42.
Surg. 2011;91(3):944–82.
2. Carson JL, Stanworth SJ, Roubinian N, et  al.
7. Murphy GJ, Pike K, Rogers CA, et  al. Liberal or
Transfusion thresholds and other strategies for
restrictive transfusion after cardiac surgery. N Engl J
guiding allogeneic red blood cell transfusion.
Med. 2015;372(11):997–1008.
Cochrane Database Syst Rev. 2016;(10). Article No:
8. Brunskill SJ, Millette SL, Shokoohi A, et al. Red
CD002042.
blood cell transfusion for people undergoing hip
3. Hamm CW, Bassand JP, Agewall S, et  al. ESC
fracture surgery. Cochrane Database Syst Rev.
guidelines for the management of acute coronary
2015.
syndromes in patients presenting without persistent
9. Carson JL, Terrin ML, Noveck H, et  al. Liberal or
ST-segment elevation: the task force for the manage-
restrictive transfusion in high-risk patients after hip
ment of acute coronary syndromes (ACS) in patients
surgery. N Engl J Med. 2011;365:2453–62.
presenting without persistent ST-segment elevation of
10. Carson JL, Brooks MM, Abbott JD, et al. Liberal ver-
the European Society of Cardiology (ESC). Eur Heart
sus restrictive transfusion thresholds for patients with
J. 2011;32(23):2999–3054.
symptomatic coronary artery disease. Am Heart J.
4. Hanna EB, Alexander KP, Chen AY, Roe MT, Funk
2013;165:964–71.
M, Saucedo JF.  Characteristics and in-hospital out-
11. Holst LB, Haase N, Wetterslev J, et al. Lower versus
comes of patients with non-ST-segment elevation
higher hemoglobin threshold for transfusion in septic
myocardial infarction undergoing an invasive strat-
shock. N Engl J Med. 2014;371(15):1381–91.
egy according to hemoglobin levels. Am J Cardiol.
12. Retter A, Wyncoll D, Pearse R, et  al. Guidelines on
2013;111(8):1099–103.
the management of anaemia and red cell transfu-
5. Qaseem A, Humphrey LL, Fitterman N, Starkey M,
sion in adult critically ill patients. Br J Haematol.
Shekelle P.  Treatment of anemia in patients with
2013;160(4):445–64.
heart disease: a clinical practice guideline from the
 Abdominal Compartment
Syndrome
Jacklyn Engelbart and Luis J. Garcia
Algorithmic Approach
A. Abdominal compartment syndrome results
from massive interstitial swelling in the abdo-
B. The gold standard for measuring intra-­
men or rapid development of mass within the
abdomen such as ascites or hematoma lead-
ing to increase in pressure within the abdo-
men. The first step in evaluation of a patient
with abdominal compartment syndrome
(ACS) is the history. Questions regarding the
C. Normal intra-abdominal pressure (IAP) in
risk factors should be targeted toward identi-
fying diminished abdominal wall compli-
ance, increased intra-luminal contents,
increased abdominal contents, capillary leak,
or massive fluid resuscitation. These risk fac-
tors include but are not limited to acute respi-
ratory failure with prone positioning, elevated
intrathoracic pressure, major trauma or burns,
abdominal surgery with fascial closure, obe-
sity, gastroparesis, ileus, pseudo-obstruction,
sepsis, oliguria, ascites, pancreatitis, liver
dysfunction, coagulopathy, hemoperitoneum,
pneumoperitoneum, acidosis, or hypotension.
Patients with ACS may present with acute
kidney injury, bowel wall ischemia and
edema, reduced lung compliance with ele-
vated airway pressures and decreased tidal
volumes, increased intracranial pressure, and
J. Engelbart · L. J. Garcia (*)
Department of Surgery, University of Iowa Hospitals
and Clinics, Iowa City, IA, USA
e-mail: luis-garcia@uiowa.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_177
177
elevated central venous pressure though
decreased venous return leading to decreased
cardiac output [1–3].
abdominal pressure (IAP) is via the bladder by
instilling a specified volume and, measuring
the pressure. Non-­specific findings on CT may
include collapse of the vena cava, bowel wall
thickening, or bilateral inguinal hernias [2].
critically ill adults is 5–7 mmHg and in chil-
dren is 4–10 mmHg. When IAP is sustained
or repeatedly ≥12  mmHg in adults
or  >10  mmHg in children, it is considered
intra-abdominal hypertension (IAH). IAH
can be classified as hyperacute (lasts only
seconds—laughing, coughing, sneezing, def-
ecation), acute (develops over hours—trauma
or hemorrhage), subacute (develops over
days), and chronic (develops over months—
pregnancy, morbid obesity) [4]. IAH can be
graded by intra-abdominal pressure: Grade
I  =  IAP 12–15  mmHg, Grade II  =  IAP
16–20 mmHg, Grade III = IAP 21–25 mmHg,
and Grade IV = IAP > 25 mmHg. Abdominal
compartment syndrome (ACS) in adults is
defined as sustained IAP > 20 mmHg with or
without an abdominal perfusion pressure
(APP = MAP – IAP) < 60 mmHg (children
with IAP > 10 mmHg) and is associated with
new or progressing organ dysfunction and
failure that can be attributed to elevated IAP
735
736
[2, 5, 6]. ACS is better defined without E. Abdominal decompression with delayed
s­pecified pressure thresholds as no specific
IAP threshold can consistently be used to
diagnose ACS [5].
D. Supportive management and temporizing
measures for ACS include drainage of intra-
luminal contents with nasogastric and rectal
decompression; removal of intra-abdominal
ascites or hematomas; reduction of intra-­
abdominal volume by avoiding positive fluid F. Temporary abdominal closure techniques
balance after initial resuscitation and diure-
sis; improving abdominal wall compliance
with analgesia, sedation, and paralysis;
decreasing head elevation; escharotomy in
burn victims; and removal of constrictive
binders or dressings. Vasopressors may be
used to maintain an abdominal perfusion
pressure  >  60  mmHg. IAP should be mea-
sured at least every 4 h while patient is criti-
cally ill or with elevated IAP [1, 2, 7].
J. Engelbart and L. J. Garcia
c­ losure may be attempted with IAP >20 mmHg
and organ dysfunction not responding to medi-
cal treatment. There is a risk of hypotension
leading to pulseless electrical activity (PEA)
arrest from reperfusion and sudden decrease in
systemic vascular resistance. Even with tem-
porary closure there remains risk of recurrent
abdominal compartment syndrome [1, 2, 8].
include negative pressure systems including
towel- and sponge-based techniques (vacuum-­
assisted closure), patch closure, silo closure, or
skin-only closure. If primary approximation is
not able to be achieved upon return to the oper-
ating room, other adjunctive techniques may
be used to facilitate primary closure or approx-
imate the fascia closer to midline. If no
improvement, functional closure or a planned
ventral hernia may need to be attempted.
177  Abdominal Compartment Syndrome 737

Patient has two or more risk factors or in the presence of

A organ failure with clinical suspicion for ACS

B Assess intraabdominal pressure by measuring the

bladder pressure

C IAP < 20 mmHg IAP > 20 mmHg

Supportive management
No
(sedation, analgesia, Organ
D paralysis, paracentesis, dysfunction
nasogastric decompression)

Yes
No response
Surgical management
E (abdominal decompression)
Close monitoring Recurrence

Temporary abdominal
F closure

Improvement Return to OR

No
Advance fascial edges Abdominal
towards midline closure

No improvement
Yes

Functional closure
Planned ventral hernia Primary fascial closure

Algorithm 177.1
738 J. Engelbart and L. J. Garcia

References 4. Van Mook WN, et  al. Abdominal compartment

­syndrome. Lancet. 2002;360:1502.
5. Malbrain ML, et  al. Results from the international
1. Rogers WK, Garcia L.  Intra-abdominal hyperten-
conference of experts on intra-abdominal hyper-
sion, abdominal compartment syndrome, and the
tension and abdominal compartment syndrome.
open abdomen. Chest. Forthcoming 2017. https://doi.
I. Definitions. Intensive Care Med. 2006;32:1722–32.
org/10.1016/j.chest.2017.07.023.
6. Sugrue M. Abdominal compartment syndrome. Curr
2. Kirkpatrick AW, et  al. Intra-abdominal hyperten-
Opin Crit Care. 2005;11:333–8.
sion and the abdominal compartment syndrome:
7. Bailey J, et  al. Abdominal compartment syndrome.
updated consensus definitions and clinical practice
Crit Care. 2000;4:23–9.
guidelines from the World Society of the Abdominal
8. Chang MC, et  al. Effects of abdominal decompres-
Compartment Syndrome. Intensive Care Med.
sion on cardiopulmonary function and visceral perfu-
2013;39:1190–206.
sion in patients with intra-abdominal hypertension. J
3. Vidal MG, et  al. Incidence and clinical effects of
Trauma. 1998;44:440–5.
intra-abdominal hypertension in critically ill patients.
Crit Care Med. 2008;36:1823–31.
 Acute Renal Failure
Kathleen A. Iles and Richard J. King
Algorithmic Approach
A. Evaluation of acute renal failure requires
careful review of clinical history and physical
examination. Recent studies have estimated
that 3–21% of all hospitalized patients and up
to 50% of ICU patients develop acute kidney
injury (AKI) [1]. Clinicians should be aware
that AKI etiology is often multifactorial and
that epidemiological evidence purports that
even mild, reversible renal injury can have
severe clinical consequences, including
increased mortality [2]. Baseline renal status
should be obtained along with vital signs,
chest X-ray, and pertinent laboratory studies,
including BUN/Cr, hemoglobin/hematocrit,
and electrolytes. The presence of anuria or
oliguria can be prognostic.
B. AKI is diagnosed when a patient meets any
one of the following criteria: (1) an increase
in serum creatinine by ≥0.3  mg/dl within
48 h, (2) an increase in serum creatinine ≥1.5
K. A. Iles
SUNY Upstate Medical University College of
Medicine, Syracuse, NY, USA
Department of Surgery, University of North Carolina
Hospitals, Chapel Hill, NC, USA
e-mail: kathleen.iles@unchealth.unc.edu
R. J. King (*)
Department of Surgery, SUNY Upstate Medical
University, Syracuse, NY, USA
e-mail: Kingri@upstate.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_178
178
times the patient’s baseline, or (3) a urine
volume ≤0.5 ml/kg/h for 6 h [1]. Etiology of
AKI is broad and includes hypovolemia due
to dehydration or hemorrhage, intrinsic renal
disease, exposure to nephrotoxic agents, as
well as obstructive pathology such as renal
stones and bladder outlet obstruction due to
neoplasm. A common cause of acute renal
failure is acute tubular necrosis secondary to
impaired blood flow and resultant hypoxic
injury to renal tubular cells [1]. Post-surgical
acute tubular necrosis (ATN) contributes to
20–25% of all cases of hospital-acquired
AKI [3].
Classification systems such as RIFLE can
assist in clinical evaluation. To help differen-
tiate etiology, a clinician should first rule out
common post-renal causes with renal ultra-
sound. Urinalysis in addition to urine electro-
lytes should be obtained if renal ultrasound is
found to be negative [2]. A clinician should
be mindful that certain pathologic states such
as compartment syndrome can lead to vascu-
lar compromise and decreased renal perfu-
sion with resultant kidney injury.
C. The fluid challenge is the gold standard used
to assess fluid responsiveness and to guide
fluid administration [4]. The most common
approach involves the administration of
500  cc crystalloid within a 30-min time
frame. Although there exists variability in
measurement and precision of technology
739
740
used, responsiveness is defined as an increase
of 10–15% in stroke volume following a fluid
challenge [4]. Fractional excretion of Na
(FeNa) can differentiate between pre-renal
and renal causes. A FeNa <1% is diagnostic
of pre-renal causes. FeNa = (urine Na/creati-
nine)/(plasma Na/creatinine).
D. Certain insults such as major burns and sepsis
often create a mixed etiology of hypovolemia
and acute tubular necrosis due to depressed
renal blood flow. Such a condition may
require renal replacement therapy (RRT) as a
temporizing measure until the kidneys
recover. A nephrology consult should be con-
sidered to help guide renal replacement ther-
apy management.
E. If the patient is responsive to fluid resuscita-
tion, this is diagnostic for AKI secondary to
pre-renal hypovolemia. Urine output guides
fluid resuscitation in addition to blood pressure,
heart rate, and both invasive and noninvasive
monitoring. Central venous pressure (CVP),
PA catheter monitoring, cardiovascular ultra-
sound, and hemodynamic monitors such as
Vigileo™ are often utilized for this purpose.
K. A. Iles and R. J. King
F. Mortality has been estimated to be up to 50%
when patients with AKI require renal replace-
ment therapy [3]. There are currently no pub-
lished guidelines indicating when renal
replacement therapy should be initiated.
Nevertheless, consensus agrees that early
renal replacement therapy results in better
clinical outcomes. Absolute indications for
renal replacement therapy include the fol-
lowing: (1) anuria for 6 h, (2) severe oliguria
(urine output <200 ml over 12 h), (3) hyper-
kalemia (>6.5 mmol/L), (4) severe metabolic
acidosis (pH <7.2 despite low-normal pCO2
level), (5) volume overload, (6) severe azote-
mia (urea concentration > 30 mmol/L or cre-
atinine concentration > 300 μmol/L), and (7)
uremic complications (encephalopathy, peri-
carditis, etc.) [1]. Hemodynamic stability
should be taken into consideration prior to
initiation of RRT. Patients that are stable and
more apt to tolerate larger fluid shifts may be
candidates for intermittent hemodialysis,
while unstable patients may benefit from
continuous veno-­ venous hemofiltration
(CVVH).
178  Acute Renal Failure 741

24 year-old with multiple gunshot wounds s/p exploratory

laparotomy. Post-operative day #1 urine output < 0.5 ml/kg/h over
past 6 h

A Obtain vital signs and blood work

T 37.6 C, HR 103, RR 19, BP 110/82 Life-threatening

Labs: elevated crt, electrolytes fluid or electrolyte
abnormalities?

Yes
AKI
B etiology? Urgent
dialysis

Renal ultrasound Post-renal

Check Foley catheter

Obtain UA & Renal

urine electrolytes

Compartment syndrome Patient reassessment Nephrology consult

C D

Yes Responsive No
Pre-renal to fluid Mixed etiology: pre-renal & renal
challenge?

F Renal replacement therapy

Consider adjunct
Fluid measures to assess
resuscitation volume status Stable?

Yes No

Hemodialysis CVVH

Algorithm 178.1
742 K. A. Iles and R. J. King

References 3. Lameire N, Biesen WV, Vanholder R.  Acute renal

failure. Lancet. 2005;365(9457):417–30.
4. Toscani L, Aya HD, Antonakaki D, Bastoni D, Watson
1. Koza Y.  Acute kidney injury: Current concepts and
X, Arulkumaran N, et  al. What is the impact of the
new insights. J Inj Violence Res. 2016;8(1):58–62.
fluid challenge technique on diagnosis of fluid respon-
2. Kellum JA, Lameire N.  Diagnosis, evaluation, and
siveness? A systematic review and meta-analysis. Crit
management of acute kidney injury: a KDIGO sum-
Care. 2017;21(1):207.
mary (Part 1). Crit Care. 2013;17(1):204–19.
 Postoperative Pulmonary Emboli
Kathleen A. Iles and Richard J. King
Algorithmic Approach
A. Surgical injury alters the balance between
coagulation and fibrinolysis, predisposing
patients to increased risk of deep venous and
pulmonary thromboembolism [1]. The first
step in evaluation of a patient with possible
pulmonary embolism is history and physical
examination. High index of clinical suspicion
based on patient history for genetic risk fac-
tors in addition to recent behavioral changes
and health risks should guide work-up and
evaluation. Presenting symptoms for pulmo-
nary emboli are often nonspecific and can
range from an asymptomatic presentation to
fever, dyspnea, hypotension, tachypnea, or
unexplained tachycardia. Chest pain may
develop acutely or worsen over several days.
Pleuritic chest pain and hemoptysis may also
be present; however this is likely to be sec-
ondary to pulmonary infarction [2]. Other eti-
K. A. Iles
SUNY Upstate Medical University College of
Medicine, Syracuse, NY, USA
Department of Surgery, University of North Carolina
Hospitals, Chapel Hill, NC, USA
e-mail: kathleen.iles@unchealth.unc.edu
R. J. King (*)
Department of Surgery, SUNY Upstate Medical
University, Syracuse, NY, USA
e-mail: Kingri@upstate.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_179
179
ologies for this compilation of symptoms
such as acute myocardial infarction should be
considered.
B. Immediate empiric treatment is determined
by patient stability and contraindications to
anticoagulation and/or thrombolysis.
Hemodynamically unstable patients require
immediate therapeutic anticoagulation and
consideration of thrombolysis or thrombec-
tomy. Stable patients can undergo further
diagnostic evaluation based on clinical suspi-
cion and availability of resources.
C. The Wells prediction scoring system is com-
monly employed to categorize patient risk for
thrombus formation. This scoring stratifica-
tion is often used to predict need for chemo-
prophylaxis but can also guide clinical
suspicion when pulmonary embolus is sus-
pected. Patients with moderate to high prob-
ability for PE can progress to imaging such as
CT angiography or ventilation-perfusion
radionuclide scanning. Patients who have low
probability and not subject to recent surgery,
trauma, or who are pregnant can be evaluated
with a D-dimer assay. Although a positive
D-dimer test is often nonspecific, it can be a
useful diagnostic tool in combination with
clinical probability. ELISA-based D-dimer
tests have been shown to demonstrate supe-
rior sensitivity [2].
D. Angiography is definitive imaging, although
now CT angiography has high sensitivity and
743
744
specificity for PE, especially in hemodynami-
cally significant PE.  Common radiologic
findings include filling defects in pulmonary
vasculature on CTA +/− evidence of pulmo-
nary infarction. V/Q scanning will often show
mismatched segment perfusion defects.
E. Treatment for pulmonary embolism is depen-
dent on anticoagulation contraindications and
patient stability. Treatment consists of thera-
peutic anticoagulation to prevent clot propa-
gation. If the patient is hemodynamically
unstable, catheter-directed thrombolysis may
be indicated and potentially thoracotomy
with thrombectomy. Patients unable to be
anticoagulated or undergo thrombolysis due
to recent surgery such as central nervous sys-
tem (CNS) interventions may need temporary
IVC filter placement.
Routine placement of IVC filters in sub-
massive PE and proximal deep vein thrombo-
sis (DVT) is not supported by evidence;
K. A. Iles and R. J. King
however, retrievable IVC filter insertion
should be ­performed if anticoagulation is con-
traindicated or temporary cessation of antico-
agulant is required in 1 month [3]. IVC filters
should be removed within the recommended
time scale in order to limit associated compli-
cations of IVC filter placement and retrieval.
The incidence of confirmed hospital-
acquired DVT is approximately 10–40%
among medical or general surgical patients
and up to 40–60% among orthopedic surgical
patients. The incidence of hospital deaths
attributed to pulmonary embolus is estimated
to be 10% [4]. These statistics highlight the
irrefutable need and awareness for thrombo-
prophylaxis, intermittent pneumatic compres-
sion devices, and early mobilization in the
hospitalized in order to decrease thrombus
formation and prevent PE, especially in the
surgical patient [1].
*signifies a level <500μg/L reliably excludes PE.
179  Postoperative Pulmonary Emboli 745

A Obtain vital signs, blood work, ECG and

73 year-old female with femur fracture s/p open
perform physical examination
reduction and internal fixation. Post-operative day
#6 with new onset dyspnea, tachycardia, and
chest pain
T 38.1 C, HR 108, RR 24, BP 100/78, WBC 16
Exam findings: mild distress, leg swelling, tachypnea
ECG: tachycardia, non-specific ST segment changes and T-wave abnormalities

B
No
C Assess PE probability Yes Hemodynamically
stable?
Resuscitate

Thrombolytics
embolectomy
Low Moderate High

D-dimer level*
D
Yes Anticoagulation
Elevated D-dimer & Obtain Imaging
high clinical suspicion
Stable?
E No
CTA: filling defects in pulmonary vasculature No
V/Q Scan: mismatched segment perfusion defects Thrombolytics
Contraindication
to anticoagulation
& thrombolytics?

Embolectomy
Yes thoracotomy
Yes
Stable?
No IVC filter

Algorithm 179.1

3. Condliffe R, Elliot CA, Hughes RJ, et al. Management

References dilemmas in acute pulmonary embolism. Thorax.
2014;69(2):174–80.
1. Kehlet H, Wilmore DW.  Multimodal strate- 4. Hirsh J, Guyatt G, Albers GW, Schünemann HJ. The
gies to improve surgical outcome. Am J Surg. seventh ACCP conference on antithrombotic and
2002;183(6):630–41. thrombolytic therapy. Chest. 2004;126(3):172S–3S.
2. Tapson VF.  Acute pulmonary embolism. N Engl J
Med. 2008;358(10):1037–52.
 Burns Management
Kathleen A. Iles and Richard J. King
Algorithmic Approach
A. Initial burns assessment can be performed in
the field or at the closest medical facility for
initial stabilization. Inhalation injuries may
require immediate securing of the airway.
Burns associated with structure or
transportation-­ related fires may require
trauma assessment and stabilization at the
nearest facility. Chemical burns may require
decontamination.
B. With the advent of regional burn centers and
advancements in burn care, a concurrent,
multimodal approach of fluid resuscitation,
wound care, nutritional support, and modula-
tion of the hypermetabolic state has led to
significant improvement in the care of the
critically ill burn patient [1]. Burns greater
than 20–30% TBSA and/or with inhalation
injury require triage preferably to an ABA-­
verified burn center for ICU-level care, fluid
C. Indeterminate and/or partial-thickness burns
K. A. Iles
SUNY Upstate Medical University College of
Medicine, Syracuse, NY, USA
Department of Surgery, University of North Carolina
Hospitals, Chapel Hill, NC, USA
e-mail: kathleen.iles@unchealth.unc.edu
R. J. King (*)
Department of Surgery, SUNY Upstate Medical
University, Syracuse, NY, USA
e-mail: Kingri@upstate.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_180
180
resuscitation, and appropriate wound treat-
ments. These may include escharotomy and
early excision and grafting of full-thickness
burns in addition to ancillary support of nutri-
tion, physical and occupational therapy, and
psychological support needs. Smaller burns
usually <20% TBSA can also require admis-
sion for burn wound and pain management as
well as for social services support. This
includes, but is not limited to, Child Protective
Services (CPS) consultations for possible
Non-accidental Trauma (NAT) and Red Cross
assistance for possible housing and/or homec-
are coordination. Most burns <10% TBSA
can be managed as an outpatient.
Regardless of inpatient versus outpatient
care, a physician or social worker should
address the patient’s functional capacity in
addition to their ability to provide adequate
wound care and infection monitoring prior to
discharge. Visiting nurses or transportation
may be needed to ensure patients receive suf-
ficient follow-up care [2].
are treated initially with dressings that
maintain a moist bacteriostatic or bacteri-
cidal wound environment to facilitate reepi-
thelialization. Dressings should also be
tailored to the needs of the patient to mini-
mize painful dressing changes, especially in
children. Dressings impregnated with silver
can be helpful in this regard as they can
747
748 K. A. Iles and R. J. King

remain in place for upward of 1–2  weeks. blood loss, infection, and length of hospital
Disruption of the innate immune barrier stay and provide increased graft take [3].
provided by the skin predisposes patients to Full-thickness burns are dressed with salves
bacterial infection. Infection in burn patients which penetrate eschar such as silver sulfadi-
is a­ ssociated with significant morbidity and azine (Silvadene) and mafenide acetate
mortality. Wound infection requires a rapid (Sulfamylon) to reduce risk of infection.
diagnosis followed by possible excision of Alternatively, large areas of partial and inde-
infected tissue and appropriate antibiotic terminate thickness mixed with areas of full-­
coverage. Inspection of wounds should be thickness burns may be dressed with
carried out by a qualified surgeon or wound petroleum-based salves such as bacitracin,
care expert [3]. Xeroform, and Vaseline while awaiting end
D. Fluid resuscitation with the modified Brooke points of initial resuscitation prior to excision
formula (2  ml/kg/%TBSA) can be titrated and grafting.
according to urine output, heart rate, and F. Various burn dressings exist and can be
blood pressure in addition to guidance by selected based on patient needs. Dressing of
invasive and noninvasive cardiac monitoring. the wound serves multiple purposes, includ-
Care should be taken to avoid over-­ ing a reduction in wound pain, protection,
resuscitation, which may result in acute lung and isolation from the environment and
injury or compartment syndrome. Use of absorption of wound drainage [2]. Most
nurse-driven protocols can be helpful in this silver-­impregnated dressings such as hydrofi-
regard. Nutritional support in the face of bers (Aquacel Ag) or silicone base (Mepitel
burn-induced catabolism should begin early, Ag) can be left in place for 2 weeks and are
and consideration should be given to the use useful for outpatient treatment, especially in
of the anabolic steroid oxandrolone and pro- children. Petroleum-based dressings, such as
pranolol. Use of high-dose vitamin C should bacitracin and Vaseline, Xeroform, and
be considered early in resuscitation to blunt Adaptic, are inexpensive and readily avail-
the deleterious inflammatory response. able but may require frequent reapplication.
E. Early excision and grafting is performed pref- Silver sulfadiazine (Silvadene), while com-
erably within 72  h of admission. This stan- monly known and widely available, may
dard of care has been shown to decrease impair wound healing and is less favored.
180  Burns Management 749

A
56 year-old female presenting Burns Assessment
with burn after house fire

>20–30% BSA
B
Fluid Resuscitation
Severe Pain Admission No
Outpatient Care
Wound Care Required?
Social Factors
NAT

D Yes

Fluid Resuscitation Social Services Nutrition Pain Control Hospital Admission

Modified Brooke Formula Initiate Tube Feeds Burn Depth

Nurse Driven C
Resuscitation
Protocol
Circumferential Full Deep Partial Indeterminate/Partial

Consider E Consider Reassess in 3 Weeks Infection?

Early Excision
Escharotomy
& Grafting

F Yes

Burn Dressings Consider Healing?

Grafting No
Antibiotics

Short Term Long Term

Algorithm 180.1

2. Herndon DN.  Total burn care. Saunders Elsevier:

References Edinburgh; 2012.
3. Rowan MP, Cancio LC, Elster EA, Burmeister DM,
1. Snell JA, Loh N-HW, Mahambrey T, Shokrollahi Rose LF, Natesan S, et  al. Burn wound healing and
K.  Clinical review: the critical care management of treatment: review and advancements. Crit Care.
the burn patient. Crit Care. 2013;17(5):241–51. 2015;19:243–55.
 Acid-Base Disorders
Kathleen A. Iles and Richard J. King
Algorithmic Approach
A. Diagnosis of acid-base disturbances can be
challenging and requires careful clinical eval-
uation. The initial approach to acid-base dis-
orders requires arterial blood gas analysis. pH
and determination of pCO2 indicate either
primary respiratory or metabolic disorder
with either metabolic or respiratory compen-
sation. Note that respiratory compensation
for primary metabolic disorders occurs rap-
idly. Conversely, metabolic compensation for
primary respiratory disturbances may require
3–5 days for renal adjustment [1].
B. Respiratory acidosis may require respiratory
support such as noninvasive positive pressure
ventilation or intubation with mechanical
ventilation. This state can occur from
hypoventilatory states, airway obstruction,
and CNS depression. Metabolic acidosis
requires determination of anion gap and a dif-
ferential diagnosis to guide treatment. Anion
K. A. Iles
SUNY Upstate Medical University College of
Medicine, Syracuse, NY, USA
Department of Surgery, University of North Carolina
C. Metabolic alkalosis as a primary disorder
Hospitals, Chapel Hill, NC, USA
e-mail: kathleen.iles@unchealth.unc.edu
R. J. King (*)
Department of Surgery, SUNY Upstate Medical
University, Syracuse, NY, USA
e-mail: Kingri@upstate.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_181
181
gap can be calculated from the following for-
mula: anion gap  =  Na  −  (Cl  +  HCO3).
Etiologies of non-anion gap metabolic acido-
sis are most often secondary to defective
acidification by renal tubules, gastrointestinal
bicarbonate losses, and iatrogenic excess
chloride administration [2]. If an anion gap is
present, consider the classically taught
“MUDPILES” differential diagnoses: metha-
nol, uremia, diabetic ketoacidosis, paralde-
hyde, iron/isoniazid, lactic acidosis, ethylene
glycol, and salicylates.
Surgical patients with a metabolic acidosis
may suggest reduced end-organ perfusion
and ischemia. Metabolic acidosis is impera-
tive to diagnose in this population as it predis-
poses the patient to arrhythmias, impaired
leukocyte function, decreased cardiac output,
insulin resistance, suppression of lymphocyte
function, and leads to an overall increase in
morbidity and mortality [3]. Lactic acidosis
accounts for 50% of all cases presenting with
a high anion gap metabolic acidosis. However,
anion gap is an insensitive measure of lactate
level and a lactate level should be obtained
for further evaluation [2].
reflects either a loss of acid through vomiting
and/or nasogastric suctioning or excessive
loss of bicarbonate-rich fluids through diar-
rhea or renal losses [4]. Respiratory alkalosis
often presents in mechanically ventilated
751
752
patients with increased minute ventilation
either due to improved lung compliance or
correction of an underlying metabolic
­acidosis. If the patient is intubated, ventilator
settings should be reevaluated and minute
ventilation reduced. In non-ventilated
patients, CNS lesions, anxiety/pain, and
chronic pulmonary disease should be
considered.
D. Correction of lactate acidosis requires ade-
E. Adequate fluid resuscitation and oxygen
quate volume and oxygen-carrying hemoglo-
bin, as well as maintenance of adequate
perfusion pressure. Blood transfusion and/or
vasopressors may be needed depending on
the underlying pathophysiology. In patients
with lactic acidosis and cardiovascular com-
K. A. Iles and R. J. King
promise, consider administration of bicar-
bonate if pH <7.1. These patients should be
carefully monitored with the goal of main-
taining a blood pH at approximately 7.2 [3].
Adequate monitoring of response to resusci-
tative efforts may require frequent laboratory
analysis as well as invasive and noninvasive
monitoring of volume status, blood pressure,
and cardiac function.
delivery can often be accomplished with
treatment of the underlying pathophysiology.
If sepsis is suspected by either clinical history
or pro-calcitonin levels, then appropriate
broad-spectrum antibiotic therapy should be
initiated.
 58 year-old male trauma victim s/p exploratory Assess Arterial pH, Partial Pressure of CO2,
A laparotomy. Mechanically ventilated, post- and Bicarbonate
operative day #1.
Gastrointestinal
Losses
Excessive
B pH <7.40 pH >7.40 Diuresis
Acidosis Alkalosis C NG Suction
Hypoventilation
181  Acid-Base Disorders

Airway
PCO2 >45
Obstruction Respiratory Acidosis Bicarbonate Level >30 mmol/L Metabolic Alkalosis
mmHg
CNS Depression
Drug Overdose
Metabolic Acidosis Bicarbonate Level <22 mmol/L PCO2 <35 mmHg Respiratory Alkalosis

Anion Gap Yes No

Present? Intubated?
No Yes
Dialysis
Hemofiltration
Non-Anion Gap Hyperventilation
Metabolic Acidosis “MUDPILES” Confirm Ventilator Settings Anxiety/Pain
Yes CNS Disease
Lung Disease
GI Bicarbonate Losses Decrease Minute Pregnancy
Lactate Level
Renal Tubular Acidoses Ventilation High Altitude
Excess Chloride Administration Overload or Renal
Impairment?
D
E
Hypotensive
Adequate Yes Despite Fluid
Resuscitation Assess Volume Status Hypovolemic? Resuscitate
Resuscitation (MAP
and Perfusion?
<65 mmHg)?

Sepsis? Yes
No Reversible Yes
Etiology & pH Bicarbonate
<7.1? Yes
Vasopressor
Antibiotics Support
753

Algorithm 181.1
754 K. A. Iles and R. J. King

References 3. Kraut JA, Madias NE.  Metabolic acidosis:

pathophysiology, diagnosis and management. Nat
­
Rev Nephrol. 2010;6(5):274–85.
1. Harber R.  A practical approach to acid-base disor-
4. Seifter JL, Chang H-Y. Disorders of acid-base balance:
ders. West J Med. 1991;155(2):146–51.
new perspectives. Kidney Dis. 2016;2(4):170–86.
2. Berend K, de Vries APJ, Gans ROB.  Physiological
approach to assessment of acid–base disturbances. N
Engl J Med. 2015;372(2):193–5.
 Part XXI
Electrolytes
 Hyponatremia
Kathryn W. Shaw and Andre A. S. Dick
Algorithmic Approach
A. Hyponatremia is one of the most common
electrolyte disorders seen in hospitalized
patients. It can be categorized as either hyper-
tonic, isotonic, or hypotonic hyponatremia,
where the tonicity is determined by the sol-
utes that cannot move freely across cell mem-
branes [1]. Hypertonic or isotonic
hyponatremia can occur when there are addi-
tional osmoles in the serum, such as glucose,
mannitol, or glycine (absorbed via irrigation
fluids used in urological or gynecological
procedures). These osmoles increase tonicity
and reduce the serum sodium concentration
by drawing water from the intracellular com-
partment [2]. The most common is hypotonic
hyponatremia, where there is an excess of
water relative to sodium stores and an overall
dilution of body solutes [1]. In the hypovole-
mic patient, possible etiologies include gas-
trointestinal sodium loss such as in vomiting,
K. W. Shaw (*)
Department of Surgery, Division of Transplant
Surgery, University of Washington Medical Center,
Seattle, WA, USA
e-mail: Kwshaw@uw.edu
A. A. S. Dick (*)
Department of Surgery, Section of Pediatric
Transplantation, Seattle Children’s Hospital and
University of Washington, Seattle, WA, USA
e-mail: Andre.dick@seattlechildrens.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_182
182
transdermal sodium loss from heavy sweat-
ing, diuretics (especially thiazides), primary
adrenal insufficiency, kidney dysfunction, or
third spacing from a process such as pancre-
atitis or sepsis [2]. Euvolemic hyponatremia
can be seen in cases of syndrome of inappro-
priate antidiuretic hormone secretion
(SIADH), secondary adrenal insufficiency,
hypothyroidism, and instances where the
patient has a high water and low solute intake
[2, 3]. In hypervolemic hyponatremia, the
patient may have renal disease, heart failure,
liver failure, or nephrotic syndrome [4].
Assessing volume status and measuring
urine electrolyte excretion can be used to help
determine the underlying etiology and decide
on further workup and therapy [4]. Unless the
kidney is the reason for the sodium loss, the
spot urine sodium should be <30 mmol/L in
hypovolemic hyponatremia [2]. A spot urine
should be > or = 20 to 30 mmol/L in cases of
euvolemic hyponatremia. In hypervolemic
hyponatremia, the spot urine sodium is typi-
cally low (<20–30 mmol/L) because of acti-
vation of the renin-angiotensin-aldosterone
system despite total-body volume overload
[4].
B. Nearly 8% of surgical patients have preopera-
tive hyponatremia, and it has been shown to
be a prognostic marker for perioperative
30-day morbidity and mortality [5].
Symptoms of hyponatremia can be mild to
757
758
severe, including nausea, confusion,
­headache, emesis, cardiorespiratory distress,
seizures, and coma [2]. Acute hyponatremia
is known to have a high mortality rate due to
osmotically induced brain edema. Chronic
hyponatremia is associated with more subtle
abnormalities, including gait disturbances
and concentration and cognitive deficits,
though the affected patient may appear
“asymptomatic” on initial exam [4].
C. In correcting severe, symptomatic hyponatre-
mia, there must be a balance between timely
therapy for this potentially fatal condition and
avoiding the severe neurological deficits and
death that can occur from osmotic demyelin-
ation when correction is done too rapidly. An
acceptable limit of correction of chronic
hyponatremia is 10–12  mmol/L/d or
18 mmol/L within 48 h [4, 6]. In acute symp-
tomatic hyponatremia, where the known
duration of hyponatremia is <24–48  h, the
rate of correction does not need to be
K. W. Shaw and A. A. S. Dick
restricted. Three percent NaCl can be used in
either repeated 100–150 ml IV boluses up to
3 times or as an infusion, depending on the
severity of symptoms, for an initial target of a
5–6  mmol/l increase [2, 3]. Serum sodium
levels should be checked 20  min after each
3% NaCl IV bolus and every 4 h for as long
as a 3% NaCl IV infusion is running [2].
D. In chronic hyponatremia patients who are
either asymptomatic or have mild symp-
toms, management should be cause-specific.
Hypervolemic and euvolemic patients are
generally treated with fluid intake restric-
tion, and the hypovolemic patient can be
treated with 0.9% NaCl IV infusion to
restore extracellular volume [2]. In cases
where there is concern for brain injury from
overcorrection, an electrolyte free water IV
infusion or IV desmopressin should be
administered under expert guidance to lower
the serum sodium level to the acceptable
correction range [2, 3].
182 Hyponatremia 759

Patient found to have hyponatremia on

inpatient laboratory results

History and Physical Exam:

Assess for severity of symptoms, whether it is acute or chronic in nature, volume status,
obtain blood and urine studies to help determine etiology
A

Hypertonic or
isotonic Yes
hyponatremia Treat hyperglycemia
from
hyperglycemia?

No

Consider immediate treatment with 3% hypertonic saline

Moderate to Yes
B severe
with frequent sodium level checks
May use repeated bolus dosing if severe symptoms vs
symptoms?
starting with infusion +/- initial bolus if moderate symptoms

No

If acute (<48hrs) → Do not need to restrict rate of correction

Treatment will be cause-specific
If chronic → Limit increase serum sodium concentration to
10-12 mmol/L/d and 18 mmol/L within first 48hrs

D Fluid restriction
Expanded Limit increase serum sodium concentration to 10-12 mmol/L/d and
18 mmol/L within first 48hrs for chronic hyponatremia
Expanded or reduced
cellular volume?
Reduced
Or euvolemic with
IV infusion of 0.9% saline solution at 0.5-1.0 ml/kg per hour
SIADH?
Limit increase serum sodium concentration to 10-12 mmol/L/d and
18 mmol/L within first 48hrs for chronic hyponatremia

SIADH

First line: restrict fluid intake for moderate or profound hyponatremia

Second line: increase solute intake with urea or use a combination of low-
dose loop diuretics and oral sodium chloride

Algorithm 182.1
760 K. W. Shaw and A. A. S. Dick

References 4. Verbalis JG, Goldsmith SR, Greenberg A,

Korzelius C, Schrier RW, Sterns RH, Thompson
CJ.  Diagnosis, evaluation, and treatment of hypona-
1. Adrogue HJ, Madias NE.  Hyponatremia. N Engl J
tremia: expert panel recommendations. Am J Med.
Med. 2000;342:1581–9.
2014;126(10):S1–S42.
2. Spasovski G, Vanholder R, Allolio B, Annane D, Ball
5. Leung AA, McAlister FA, Rogers SO Jr, Pazo V,
S, Bichet D, Decaux G, Fenske W, Hoorn EJ, Ichai
Wright A, Bates DW.  Preoperative hyponatremia
C, Joannidis M, Soupart A, Zietse R, Haller M, van
and perioperative complications. Arch Intern Med.
der Veer S, Van Biesen W, Nagler E.  Clinical prac-
2012;172(19):1474–81.
tice guideline on diagnosis and treatment of hypo-
6. Sterns RH, Cappuccio JD, Silver SM, Cohen
natraemia. Nephrol Dial Transplant. 2014;29(Suppl.
EP.  Neurologic sequelae after treatment of severe
2):i1–i39.
hyponatremia: a multicenter perspective. J Am Soc
3. Sterns RH, Nigwekar SU, Hix JK. The treatment of
Nephrol. 1994;4(8):1522–30.
hyponatremia. Semin Nephrol. 2009;29(3):282–99.
 Hypernatremia
Kathryn W. Shaw and Andre A. S. Dick
Algorithmic Approach
A. Hypernatremia is essentially a deficit of water
relative to the sodium stores of a patient. It is
a common electrolyte disorder, affecting up
to 3% of hospitalized patients and up to 9% of
patients admitted to the intensive care unit
(ICU), with associated mortality rates rang-
ing from 42% to 60% [1]. Hypernatremia
occurs when there is either a net water loss,
which is most often the case, or a hypertonic
sodium gain [2]. Net water loss can occur by
either renal mechanisms, such as diabetes
insipidus or osmotic diuresis, or by extra
renal mechanisms, such as gastrointestinal
losses, excessive sweating, or insensible loss
through the airway [3]. Sodium gain often
occurs in an ICU setting, where administer-
ing sodium-rich antibiotics, using hypertonic
solutions such as sodium bicarbonate, or
resuscitating with 0.9% saline in a patient
with multisystem organ failure can lead to
K. W. Shaw (*)
Department of Surgery, Division of Transplant
Surgery, University of Washington Medical Center,
Seattle, WA, USA
e-mail: Kwshaw@uw.edu
A. A. S. Dick (*)
Department of Surgery, Section of Pediatric
Transplantation, Seattle Children’s Hospital and
University of Washington, Seattle, WA, USA
e-mail: Andre.dick@seattlechildrens.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_183
183
sodium accumulation [4]. Less common is
pure sodium excess from instances of inges-
tion, such as taking sodium tabs, salt poison-
ing from near-drowning in sea water, or even
excessive soy sauce consumption in a suicide
attempt [3].
Sustained hypernatremia can only occur
when thirst or access to water is limited, so
the populations most at risk include patients
with altered mental status or intubation as
well as infants and elderly persons [2]. The
signs and symptoms of hypernatremia pri-
marily come from neurologic dysfunction;
hyperosmolality leads to a shift of free water
from the intracellular to the extracellular
space, causing brain cell shrinkage. The brain
cell shrinkage can progress to vascular rup-
ture and subsequent bleeding that results in
permanent neurological deficit or death [2].
The cerebral demyelination that can be seen
in the rapid correction of hyponatremia has
also been reported in hypernatremia as well
[4]. Hypernatremia can also cause impaired
glucose utilization and gluconeogenesis,
decreased left ventricular contractility, rest-
lessness or coma, seizures, cramping, and
even rhabdomyolysis with consequent acute
renal failure [4]. In chronic hypernatremia,
there has been time for the brain to adapt with
solute to restore cell water volume, so aggres-
sive correction of the hypernatremia with
hypotonic fluid does not address the
761
762
h­ yperosmolarity in the brain and can conse-
quently cause cerebral edema leading to
coma, convulsions, and death [2].
B. In treating hypernatremia, both the overall
state of hypertonicity and the underlying etiol-
ogy causing the disorder must be corrected.
Depending on the cause, this may entail con-
trolling pyrexia, hyperglycemia, and glucos-
uria, effectively managing gastrointestinal
secretions, withholding lactulose and diuret-
ics, or correcting the feeding of the patient [2].
C. Acute hypernatremia, which develops over
the course of hours, in the setting of severe
neurological symptoms or a sodium level
above 160  mmol/L, should be considered a
medical emergency. The patient should be
administered 5% dextrose in water intrave-
nously with the goal of normalizing the serum
sodium level within 24 h.
D. In cases of chronic hypernatremia, where
rapid correction may lead to brain edema and
K. W. Shaw and A. A. S. Dick
convulsions, the serum sodium concentration
should be reduced at a maximal rate of
0.5 mmol per liter per hour, with a target of
10 mmol per liter per day [2].
E. When the patient is hypovolemic, the patient
should be resuscitated with isotonic solutions
prior to attempting to correct the hypernatre-
mia. In cases where the patient is euvolemic
or hypervolemic, loop diuretics may also be
used in combination with 5% dextrose in
water to induce natriuresis [4]. The volume of
hypotonic saline that is needed to reduce the
serum sodium concentration to a given target
level may be calculated, but ongoing fluid
losses may be unpredictable and greatly influ-
ence the rate of correction. These losses as
well as the patient’s electrolytes and glucose
levels must be monitored and addressed
appropriately, with the serum sodium levels
being checked every 4-6 h [3].
183 Hypernatremia 763

Patient found to be hypernatremic on

inpatient laboratory results

A Review history and physical for signs and symptoms of

hypernatremia and to help identify underlying etiology

B Make changes to patient management to prevent further hypernatremia

Assess whether hypernatremia is acute or chronic in nature

C D

Patient with acute (<48h) hypernatremia with

severe neurological symptoms or a sodium level Patient with chronic (>48h) hypernatremia
above 160 mmol/L

Administer 5% dextrose in water IV

Administer 5% dextrose in water IV Reduce serum sodium concentration at a maximal
Goal of normalizing serum sodium within 24hrs rate of 0.5 mmol per liter per hour
Target reduction of 10 mmol per liter per day

Is the patient Consider the addition of loop diuretics for natriuresis,

hypovolemic? particularly if hypervolemic

Resuscitate with balanced crystalloid prior

to attempting to correct hypernatremia

Algorithm 183.1
764 K. W. Shaw and A. A. S. Dick

References 3. Rondon-Berrios H, Argyropoulos C, Ing TS,

Raj DS, Malhotra D, Agaba EI, Rohrscheib M,
Khitan ZJ, Murata GH, Shapiro JI, Tzamaloukas
1. Alshayeb HM, Showkat A, Babar F, Mangold T,
AH.  Hypertonicity: clinical entities, manifestations
Wall BM.  Severe hypernatremia correction rate and
and treatment. World J Nephrol. 2017;6(1):1–11.
mortality in hospitalized patients. Am J Med Sci.
4. Lindner G, Funk GC.  Hypernatremia in critically
2011;341(5):356–60.
ill patients. J Crit Care. 2013;28(2):216.e11. Epub
2. Adrogué HJ, Madias NE.  Hypernatremia. N Engl J
2012 Jul 2.
Med. 2000;342(20):1493–9.
 Hypokalemia
Kathryn W. Shaw and Andre A. S. Dick
Algorithmic Approach
A. Causes of hypokalemia are multifactorial.
They generally include redistribution of
potassium into the intracellular space, gastro-
intestinal losses, or excessive renal losses.
Shifting of potassium into the intracellular
space can be secondary to acute alkalosis,
administration of insulin and glucose (both
treatments for hyperkalemia), or response to
catecholamines [1]. Hypokalemia can also
result from increased gastrointestinal losses
in the setting of diarrhea, vomiting, or mucous
secreting colonic tumors such as villous ade-
nomas. Excessive renal losses of potassium
leading to hypokalemia are most commonly
seen with diuretic therapy [1].
B. Generally, patients do not become symptom-
atic until potassium levels fall below
3.0 mEq/L. Clinical manifestations of hypo-
kalemia include muscle weakness progress-
ing to paralysis and in extreme cases
K. W. Shaw (*)
Department of Surgery, Division of Transplant
Surgery, University of Washington Medical Center,
Seattle, WA, USA
e-mail: Kwshaw@uw.edu
A. A. S. Dick (*)
Department of Surgery, Section of Pediatric
Transplantation, Seattle Children’s Hospital and
University of Washington, Seattle, WA, USA
e-mail: Andre.dick@seattlechildrens.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_184
184
rhabdomyolosis [2, 3]. Dysrhythmias can
also be seen, and classic findings on electro-
cardiogram demonstrate ST segment depres-
sion, prolongation of QT interval, flattened T
waves, and prominent U waves.
C. The primary goal of treatment is to replete
potassium in order to prevent life-threatening
dysrhythmias and muscle weakness leading to
paralysis or rhabdomyolysis. Treatment is
based on the underlying causes of hypokale-
mia. Redistributive hypokalemia may be asso-
ciated with hypomagnesemia. In this scenario,
hypokalemia treatment with potassium
replacement alone may be refractory until
magnesium is appropriately replaced.
Redistributive hypokalemia associated with
increased catecholamine levels can be treated
with administration of nonselective beta-­
blocker. Patients undergoing diuretic therapy
may need to be supplemented with oral potas-
sium or use a potassium-sparing diuretic;
however, this treatment regimen should be
used with caution in patients with chronic kid-
ney disease. Patients who are symptomatic
with dysrhythmias, muscle weakness, or rhab-
domyolysis need urgent correction of hypoka-
lemia. This can be achieved orally in doses of
40 mEq three to four times per day or intrave-
nously 20 mEq every 2–3 h [4]. These patients
will require careful monitoring until symp-
toms have resolved. Care should be taken to
avoid rebound hyperkalemia.
765
766 K. W. Shaw and A. A. S. Dick

Patient found to be hypokalemic on

laboratory results

A Consider potential etiologies of hypokalemia, including acute

alkalosis, administration of insulin and glucose, response to
catecholamines, increased GI losses, or excessive renal loss

Evaluate for manifestations of hypokalemia, including muscle

B weakness, check for dysrhythmias with and EKG, and rule out
rhabdomyolysis if the case is severe

C Replete potassium, either PO or IV, depending on the clinical

condition of the patient, addressing the underlying etiology

Algorithm 184.1

3. Shintani S, Shiigai T, Tsukagoshi H.  Marked hypo-

References kalemic rhabdomyolysis with myoglobinuria due to
diuretic treatment. Eur Neurol. 1991;31:396.
1. Gennari FJ.  Hypokalemia. N Engl J Med. 4. Pullen H, Doig A, Lambie AT. Intensive intravenous
1998;339(7):451–8. potassium replacement therapy. Lancet. 1967;2:809.
2. Comi G, Testa D, Cornelio T, et al. Potassium deple-
tion myopathy: a clinical and morphological study of
six cases. Muscle Nerve. 1985;8:17.
 Hyperkalemia
Kathryn W. Shaw and Andre A. S. Dick
Algorithmic Approach
Causes  The major intracellular cation is potas-
sium, and it determines intracellular osmolality.
Alterations in the potassium concentration gradi-
ent have profound effects on transmembrane
potential and subsequently cellular function.
Hyperkalemia is a common clinical problem and
rarely develops from excessive potassium intake
in the absence of renal insufficiency. It most often
occurs as a result of impaired urinary excretion
due to acute kidney injury, chronic kidney dis-
ease, or redistribution of potassium [1]. Examples
of redistributive hyperkalemia include crush inju-
ries, massive transfusion, reperfusion of ischemic
limbs, and diabetic ketoacidosis.
A. Clinical manifestations of hyperkalemia
which require urgent treatment include car-
diac conduction abnormalities and neuromus-
cular abnormalities, such as weakness
K. W. Shaw (*)
Department of Surgery, Division of Transplant
Surgery, University of Washington Medical Center,
Seattle, WA, USA
e-mail: Kwshaw@uw.edu
A. A. S. Dick (*)
Department of Surgery, Section of Pediatric
Transplantation, Seattle Children’s Hospital and
University of Washington, Seattle, WA, USA
e-mail: Andre.dick@seattlechildrens.org
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_185
185
progressing to paralysis. Classic electrocar-
diogram changes associated with hyperkale-
mia include peaked T-waves and widened
QRS that progresses to a sine wave [2]. These
changes may lead to ventricular fibrillation
and arrest.
B. Multimodal therapies are needed for definitive
management to urgently correct severe hyper-
kalemia. The goal is to reduce the effect of
hyperkalemia on membrane potential, shifting
potassium intracellularly and increasing
potassium excretion. These patients should be
placed under continuous cardiac monitoring
with serial electrolyte evaluations. Therapy
should include rapid administration of intra-
venous calcium, which antagonizes the mem-
brane potential influence of hyperkalemia.
Calcium can be given in the form of calcium
gluconate or calcium chloride [3]. This effect
is transient and as a result should not be
administered as monotherapy. Shifting potas-
sium from the extracellular to the intracellular
space can be achieved with infusion of sodium
bicarbonate or insulin with glucose [4].
Sodium bicarbonate antagonizes the effects of
hyperkalemia on the membrane potential,
while the increase in extracellular pH redis-
tributes potassium into the intracellular space.
Hydrogen is exchanged for potassium to
maintain electroneutrality. Insulin achieves
the same redistribution of potassium from the
extracellular to the intracellular space.
767
768
Glucose has to be given concurrently to pre-
vent hypoglycemia. These effects are also
transient and may need to be repeated with
serial laboratory evaluations. Definitive man-
agement requires increasing potassium excre-
tion, and this can be achieved via loop
diuretics, administration of Na+-K+ resins
such as Kayexalate, and dialysis [5]. In
patients with normal renal function, loop
diuretics increases potassium excretion in the
urine. In patients with compromised renal
function, dialysis is indicated.
K. W. Shaw and A. A. S. Dick
In summary the urgency of hyperkalemic treat-
ment is based on the severity of the signs and
symptoms of hyperkalemia. In severe cases
antagonizing the membrane potential and redis-
tribution of potassium to the intracellular space
are temporary first-line management until defini-
tive management with exchange resins or dialy-
sis is available to excrete excess potassium from
the extracellular space.
185 Hyperkalemia 769

A Does the patient have clinical

manifestations of hyperkalemia?

B yes No

yes
Treat with rapid acting therapies: Potassium > 6.5 meq/L
· Intravenous Calcium
· Insulin & Glucose
· Sodium bicarbonate No
· Diuretics
If renal impairment:
· All of the above±diuretics Potassium > 5.5 meq/L and
· Dialysis renal impairment (ESRD or
oliguria)
· Cation exchange binders

Potassium should be lowered

with cation exchange binders
and dialysis

Patient should be monitored throughout

this process

Algorithm 185.1

3. Weisberg LS.  Management of severe hyperkalemia.

References Crit Care Med. 2008;36:3246–51.
4. Harel Z, Kamel KS.  Optimal dose and method of
1. Palaka E, Leonard S, Buchanan-Hughes A, Langford administration of intravenous insulin in the manage-
B, Grandy S. Evidence in support of hyperkalaemia ment of emergency hyperkalemia: a systemic review.
management strategies: a systematic literature review. PLoS One. 2016;11:e0154963.
Int J Clin Pract. 2018;72:e13052. 5. Sterns RH, Rojas M, Bernstein P, Chennupati S. Ion-­
2. Montague BT, Ouellette JR, Buller GK. Retrospective exchange resins for the treatment of hyperkalemia:
review of the frequency of ECG changes in hyperka- are they safe and effective? J Am Soc Nephrol.
lemia. Clin J Am Soc Nephrol. 2008;3:324–30. 2010;21:733–75.
 Management of Hypocalcemia
Robert S. Schoaps and Sprague W. Hazard III
Algorithmic Approach
A. The first step in evaluating a patient with
hypocalcemia is a thorough history and phys-
ical examination. Certain aspects of the his-
tory may indicate specific etiologies, such as
a history of chronic kidney disease, acute
pancreatitis, or hyper-catabolic states such as
rhabdomyolysis or tumor lysis syndrome. A
history of neck surgery or radiation may indi-
cate iatrogenic hypoparathyroidism, while
history of autoimmune disorders may indi-
cate autoimmune hypoparathyroidism. Many
medications can lower serum calcium levels
(e.g., calcium chelators [citrate, phosphate,
EDTA], bone resorption inhibitors [bisphos-
phonates, calcitonin], cinacalcet, foscarnet,
and phenytoin).
B. Serum calcium is largely bound to proteins,
primarily albumin; thus, free calcium concen-
trations will not be accurately reflected by
serum calcium measurements in patients with
derangements in serum albumin. This can be
corrected using the following formula:
Ca(corrected)  =  Ca(serum)  +  [0.8*(normal
albumin – Serum albumin)]. Ionized calcium
R. S. Schoaps · S. W. Hazard III (*)
Department of Anesthesiology and Perioperative
Medicine, Penn State Hershey Medical Center,
Hershey, PA, USA
e-mail: shazard@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_186
186
levels directly measure unbound calcium and
do not require correction.
C. Physical exam findings encountered in hypo-
calcemia include paresthesias, carpopedal
spasm, neuromuscular irritability, Chvostek’s
(contraction of facial muscles elicited by tap-
ping on the facial nerve) and Trousseau’s
(carpopedal spasm induced by BP cuff
inflated for 3  min) signs, and, if chronic or
severe, disorientation, seizures, cardiac dys-
rhythmia, impaired cardiac contractility, and
QT prolongation.
D. Serum intact parathyroid hormone (PTH)
should be measured in all patients with hypo-
calcemia [1]. Low or normal PTH indicates
hypoparathyroidism or hypomagnesemia.
Elevated PTH indicates renal losses, vitamin
D deficiency, or pseudohypoparathyroidism.
Hypomagnesemia can induce PTH resistance
or deficiency, while hypermagnesemia is con-
sistent with renal losses. Hypophosphatemia
indicates secondary hyperparathyroidism or
low dietary intake (rare in developed coun-
tries), while hyperphosphatemia can occur
with chronic kidney disease, hypercatabolic
states, hypoparathyroidism, or pseudohypo-
parathyroidism. Low 25-hydroxyvitamin D
levels indicate deficient absorption or dietary
intake of vitamin D, while low
1,25-­dihydroxyvitamin D levels indicate
hypoparathyroidism or renal insufficiency
(when coupled with hyperphosphatemia).
771
772
E. Hypomagnesemia should be corrected with
2.0  g magnesium sulfate prior to replacing
calcium to prevent ongoing PTH resistance.
Severe hyperphosphatemia, such as is seen in
tumor lysis syndrome, should be corrected
with fluids and phosphate restriction prior to
administration of IV calcium to prevent in situ
formation of calcium-phosphate precipitates
[2]. In the setting of renal failure, hemodialy-
sis may be indicated to correct hyperphospha-
R. S. Schoaps and S. W. Hazard III
temia prior to calcium repletion. Patients with
vitamin D deficiency should have concurrent
vitamin D supplementation.
F. Intravenous calcium replacement is indicated
in the setting of symptomatic hypocalcemia,
prolonged QTc interval, or inability to take
oral supplements, administered as 1–2 g over
10–20  min. Asymptomatic hypocalcemia
may be replaced with 1500–2000 mg elemen-
tal calcium divided daily.
186  Management of Hypocalcemia 773

A History & physical exam

Medications? CKD? Pancreatitis? Hypercatabolic state?

Confirm with repeated testing

B Serum calcium corrected for albumin vs. ionized calcium

Obtain blood work and perform a physical examination

C Paresthesias, Carpopedal spasm, Chvostek’s and
Trousseau’s signs

Serum intact Other

Serum Serum Vitamin D
D parathyroid
magnesium phosphorous metabolites
(creatinine, alkaline
hormone (PTH) phosphatase,
amylase/lipase,
urinary calcium)

E
Correct prior to replacing calcium

Symptomatic?

Yes No

F IV Calcium PO Calcium

Algorithm 186.1

2. Coiffier B, et  al. Guidelines for the management of

References pediatric and adult tumor lysis syndrome: an evidence-­
based review. J Clin Oncol. 2008;26(16):2767–78.

1. Goltzman D, Cole DEC. “Hypoparathyroidism.”
Primer on the metabolic bone diseases and disorders of
bone metabolism. 6th ed. Washington, DC: American
Society of Bone and Mineral Research; 2006. p. 216.
 Management of Hypercalcemia
Robert S. Schoaps and Sprague W. Hazard III
Algorithmic Approach
A. The first step in evaluating a patient with
hypercalcemia is a thorough history and
physical examination. Hyperparathyroidism
and malignancy account for >90% of cases of
hypercalcemia [1]. Certain aspects of the his-
tory, however, may indicate other specific eti-
ologies, such as prolonged immobilization, a
long-standing history of chronic kidney dis-
ease, granulomatous disease such as sarcoid-
osis or tuberculosis, and review of medications
and supplements (e.g., calcium supplements,
vitamin A and D supplements, lithium, thia-
zide diuretics, theophylline).
B. Signs and symptoms attributable to hypercal-
cemia vary based on acuity and severity. Mild
or chronic hypercalcemia may be asymptom-
atic or associated with relatively mild symp-
toms such as constipation, fatigue, or
depression. Acute or severe elevations in
serum calcium (>14  mg/dL) may be associ-
ated with more severe symptoms, such as
renal dysfunction (nephrolithiasis, renal tubu-
lar acidosis), nephrogenic diabetes insipidus
(polydipsia, polyuria, dehydration), gastroin-
testinal disturbances (severe constipation,
R. S. Schoaps · S. W. Hazard III (*)
Department of Anesthesiology and Perioperative
Medicine, Penn State Hershey Medical Center,
Hershey, PA, USA
e-mail: shazard@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_187
187
nausea, anorexia), or neuropsychiatric
­disturbances (cognitive dysfunction, lethargy,
coma).
C. Serum calcium is largely bound to proteins,
primarily albumin; thus, free calcium concen-
trations will not be accurately reflected by
serum calcium measurements in patients with
serum albumin derangements. This can be
corrected using the following formula:
Ca(corrected)  =  Ca(serum)  +  [0.8*(normal
albumin – serum albumin)]. Ionized calcium
levels directly measure unbound calcium and
do not require correction.
D. The first step in work-up after confirming
hypercalcemia is measuring serum intact
parathyroid hormone (PTH) [2]. Elevated
PTH indicates either primary hyperparathy-
roidism (the most common cause of hypercal-
cemia in the outpatient setting, typically
manifested by corrected serum calcium
<11  mg/dL and mild symptoms) or familial
hypocalciuric hypercalcemia (FHH, a rare
genetic condition). If PTH is low, the next
step in diagnosis is measuring parathyroid
hormone-related peptide (PTHrp, elevation
associated with various malignancies) and
vitamin D metabolites. Elevation of
25-hydroxyvitamin D is associated with
hypervitaminosis D, while elevation of
1,25-dihydroxyvitamin D is associated with
granulomatous disease and lymphoma.
775
776
E. If PTH, PTHrp, and vitamin D metabolites H. The first step in treatment is ensuring
are all low or normal, proceed with further
testing: thyroid stimulating hormone (TSH,
15–20% of patients with hyperthyroidism
exhibit thyroid-mediated increase in bone
resorption), serum vitamin A (hypervitamin-
osis A leads to increased bone resorption),
urinary calcium excretion (reduced in milk-­
alkali syndrome, thiazide diuretic use, and I. Initial medical therapy is aimed at inhibition
FHH; elevated in hyperparathyroidism), and
serum/urinary protein electrophoresis (multi-
ple myeloma results in increased bone resorp-
tion). Because malignancy is the most
common cause of hypercalcemia in the inpa-
tient setting, additional work-up for occult
neoplasms or granulomas may be indicated
(e.g., chest radiograph, bone survey, CT
scans, etc.).
F. Patients who are asymptomatic or exhibit only J. Etiology-specific therapy is aimed at pre-
mild symptoms (e.g., constipation) may often
be treated with avoidance of inciting factors
(e.g., dehydration, supplements, medications)
or by treatment of the causative condition.
Immediate treatment is indicated for patients
with severe symptoms, an acute increase in
corrected serum calcium levels to >12 mg/dL,
or corrected serum calcium >14 mg/dL.
G. Patients with severe elevations (>18 mg/dL),
neurologic symptoms (lethargy, coma), or
renal failure should undergo hemodialysis.
Hemodialysis may also be indicated in
patients with severe heart failure who cannot
tolerate IV hydration [3].
R. S. Schoaps and S. W. Hazard III
euvolemia with isotonic crystalloid intrave-
nous fluids to increase urinary calcium excre-
tion. Loop diuretics are generally not
recommended as additional metabolic
derangements should be avoided but may be
necessary in the setting of renal insufficiency
or heart failure.
of bone resorption with the use of calcitonin
(4  IU/kg q6h) and bisphosphonates.
Zoledronic acid and pamidronate are the
agents of choice in hypercalcemia of malig-
nancy. Denosumab is an emerging treatment
option for patients with severe renal failure
or other contraindications for bisphospho-
nates, although clinical data to support its
use is limited.
venting recurrence after normalization of
serum calcium levels. Dietary calcium
restriction is often useful, especially in the
setting of lymphoma, sarcoidosis, or other
granulomatous diseases. Glucocorticoids
(prednisone 20–40  mg daily) decrease
intestinal calcium absorption and may be
used in the setting of hypervitaminosis D or
chronic granulomatous disease [4]. In
patients with parathyroid carcinoma and
secondary hyperparathyroidism in the set-
ting of renal failure, cinacalcet is used to
agonize calcium-sensing receptors and
inhibit PTH secretion.
187  Management of Hypercalcemia 777

A History and physical exam

Medications/supplements? Malignancy? CKD? Granulomatous disease?
Signs/symptoms: constipation, fatigue, renal dysfunction, cognitive dysfunction
B

Confirm with repeated testing

C Serum calcium corrected for albumin vs. ionized calcium

Additional lab work, start with: intact parathyroid

D hormone (PTH), parathyroid hormone related peptide
(PTHrp), and vitamin D metabolites

Based on results in conjunction with clinical presentation,

E consider: TSH, serum vitamin A, serum & urinary protein
electrophoresis, urinary calcium excretion, imaging

F Symptomatic?

Yes

No
Neurologic
symptoms or
renal failure?
Avoid inciting No Yes G
factors, dietary
restriction,
etiology-specific
intervention H Crystalloid IVF Hemodialysis

Calcitonin +
I Bisphosphonate

J Etiology-specific
therapy

Algorithm 187.1
778 R. S. Schoaps and S. W. Hazard III

References 3. Koo WS, et  al. Calcium-free hemodialysis for

the ­management of hypercalcemia. Nephron.
1996;72(3):424.
1. Lafferty FW. Differential diagnosis of hypercalcemia.
4. Sandler LM, et al. Studies of the hypercalcemia of sar-
J Bone Miner Res. 1991;6(S2):S51–9.
coidosis: effect of steroids and exogenous vitamin D3
2. Ratcliffe WA, et  al. Role of assays for parathyroid-­
on the circulating concentrations of 1,25-­dihydroxy
hormone-­related protein in investigation of hypercal-
vitamin D3. Q J Med. 1984;53(210):165–80.
cemia. Lancet. 1992;339(8786):164–7.
 Paradoxical Aciduria
188
Robert S. Schoaps and Sprague W. Hazard III

Algorithmic Approach ference (SID = [Na+] + [K+] + [Ca+2] + [Mg+

A. The first step in evaluating a patient with
­paradoxical aciduria is a thorough history and
physical examination. Paradoxical aciduria
occurs most commonly as a result of exces- C. Urinary electrolytes vary as the kidney transi-
sive gastric losses via vomiting, suction of
gastric contents, or a proximal fistula. As
large volumes of gastric contents are lost,
there is depletion of hydrochloric acid (HCl)
and extracellular fluid, producing a hypochlo-
remic hypokalemic metabolic alkalosis with
an increased strong ion difference. Persistent
hypovolemia induces the renin-angiotensin-­
aldosterone axis, stimulating retention of D. Initial therapy should be aimed at volume
sodium (Na) and water via Na-H exchangers
in the proximal tubule and collecting duct
sodium channels. Hypokalemic alkalosis
stimulates potassium (K) retention via H-K-­
ATPase and maximal bicarbonate (HCO3)
reabsorption to maintain electroneutrality,
resulting in paradoxical acidification of urine.
The alkalemia produced in this setting can
only be corrected by replacement of the
depleted strong ions: Na, Cl, and K [1].
B. Confirm metabolic alkalosis with arterial
blood gas and calculate plasma strong ion dif- E. If indicated, reduce gastric HCl secretion
R. S. Schoaps · S. W. Hazard III (*)
Department of Anesthesiology and Perioperative
Medicine, Penn State Hershey Medical Center,
Hershey, PA, USA
e-mail: shazard@pennstatehealth.psu.edu
]  – [Cl−]  – [HCO3−]) [1]. In hypochloremic
hypokalemic metabolic alkalosis, due to
excessive gastric strong ion losses, the strong
ion difference will be >40.
tions from acutely alkalotic urine production
to paradoxical aciduria. In the acute alkalotic
phase (urine pH  >  6.5), urine Na, K, and
HCO3 are elevated, with depressed Cl. As the
kidneys attempt to correct the strong iron dif-
ference, urine becomes paradoxically acidic
(pH < 5.5) with low concentrations of Na, K,
Cl, and HCO3.
expansion and replacing depleted strong ions,
initially with normal sterile saline (NSS)
infusion and potassium chloride (KCl). Aim
to replace the volume deficit with NSS, fol-
lowed by an infusion rate adequate to replace
ongoing losses plus an additional 100 mL/h.
If profoundly hypovolemic, start with 20 mL/
kg bolus NSS and then infusion rate of 4 mL/
kg/h, and titrate to replace losses plus
100  mL/h. Add KCl replacement to goal
K > 3.5 mmol/L.
with H2 blockers or proton pump inhibitors.
Limit alkalotic solutions as much as possible
(e.g., solutions containing HCO3, citrate, and
lactate).

© Springer Nature Switzerland AG 2019 779

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_188
780 R. S. Schoaps and S. W. Hazard III

F. Trend labs to normal values for all plasma
strong ions and aim for normal volume status.
As renal fluid and chloride delivery increase,
Cl-HCO3 exchangers will promote HCO3
secretion in the collecting duct, and urine will
alkalinize (pH > 7) [2]. The plasma pH will
follow as the strong ion difference is
corrected.
G. Treat the underlying etiology for definitive
resolution.

History & physical exam

A Vomiting? Gastric outlet obstruction? Fistula?

Arterial blood gas, serum electrolytes

B Calculate strong ion difference

Urine pH & electrolytes

C pH < 5.5, UNa < 10, UK < 20, UCl < 10, UHCO3 < 15

Volume Expansion with NSS (losses + 100mL/h)

D KCl replacement to K > 3.5

Reduce gastric HCl secretion (H2-blocker,

E PPI) Limit administration of alkalotic solutions

Goal of intravascular euvolemia Trend labs

F to normal plasma values and follow urine pH

G Treat underlying etiology

Algorithm 188.1

2. Luke RG, Galla JH. It is chloride depletion a­ lkalosis,

References not contraction alkalosis. J Am Soc Nephrol.
2012;23(2):204–7.
1. Seifter JL.  Integration of acid-base and electrolyte
disorders. N Engl J Med. 2014;371(19):1821–31.
Part XXII
Hernia
 Inguinal Hernia
Q. Lina Hu and David C. Chen
Algorithmic Approach
A. The first step in the evaluation of a patient
with an inguinal hernia is a thorough history.
The most common symptom is a groin bulge
that is worse with straining (urination, defe-
cation, or lifting), exercise, or prolonged
periods of standing. The patient may or may
not complain of symptoms of pain or dis-
comfort. Associated pain, gastrointestinal or
urinary dysfunction should raise concern for
intermittent incarceration.
B. Clinical examination of the groin is the gold
standard of hernia diagnostics, with sensitiv-
ity and specificity of 74.5% and 96.3%,
respectively [1]. The groin area should be
observed for evidence of bulging or asymme-
try with coughing. Then, the tip of the exam-
iner’s index finger is invaginated into the
external ring to palpate for a bulge or mass
while the patient coughs or performs a
Valsalva maneuver.
Q. L. Hu
Department of Surgery, David Geffen School of
Medicine at University of California, Los Angeles,
Los Angeles, CA, USA
D. C. Chen (*)
Department of Surgery, Lichtenstein Amid Hernia
Clinic at University of California at Los Angeles,
Los Angeles, CA, USA
e-mail: Dcchen@mednet.ucla.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_189
189
C. Ultrasound may be helpful when no palpable
defect or bulge is detected on exam in a
symptomatic patient. While the reported
diagnostic sensitivity and specificity of ultra-
sound reach upwards of 97.6% and 99.8%,
respectively, it is highly operator dependent
[2]. When there is clinical uncertainty, com-
puted tomography (CT) or magnetic reso-
nance imaging (MRI) may provide a more
consistent and detailed view of the groin
anatomy. If an inguinal hernia is not detected
on cross-sectional imaging, other differential
diagnoses for groin bulge or discomfort
should be pursued.
D. Once the diagnosis of inguinal hernia is
established, either by physical exam, imag-
ing, or both, the next step is to assess how
symptomatic the patient is.
E. If the hernia is asymptomatic or minimally
symptomatic, watchful waiting is a safe and
reasonable alternative in male patients.
However, the natural history is progressive
enlargement and an intervention will likely
be needed eventually [3]. In women, repair is
advisable due to higher incidence of femoral
hernias and hernia adverse events [4].
F. For symptomatic inguinal hernias, the next
step is to establish the reducibility of the her-
nia. If the mass is incarcerated, it is important
to assess for signs of strangulation (fever,
tenderness, erythema, or overlying skin
changes). If strangulation is suspected, blood
783
784
work such as white blood cell count and lac-
tate can be informative.
G. If the hernia is reducible, elective repair in an
outpatient setting is recommended.
H. If the hernia is incarcerated, but not strangu-
lated, manual reduction may be attempted.
Sedation, Trendelenburg positioning, and ice
over the groin may be helpful. If the hernia is
reduced, the patient maybe scheduled for
elective or urgent repair given the risk for re-­
incarceration and strangulation. If the hernia
cannot be reduced manually, surgery is
indicated.
I. A strangulated inguinal hernia is a surgical
emergency. Preoperatively, the patient should
be optimized with IV hydration, electrolyte
correction, nasogastric tube decompression,
and IV antibiotics when possible.
J. There are many options for surgical inguinal
hernia repair and should be individualized to
the patient’s and the surgeon’s preference
and level of experience. The open anterior
tension-free mesh approach remains the gold
standard, but minimally invasive (laparo-
scopic and robotic) techniques have become
highly effective, standardized, and safe in
recent decades and have been found to be
associated with less postoperative pain and
numbness, reduced recovery time, and the
ability to treat bilateral hernias through the
same incision [5]. However, operative times
are longer, and there is a higher risk of rare
serious complications such as visceral and
vascular injuries [5]. Recurrence rates
between open mesh-based repairs and lapa-
roscopic repairs are similar [5]. Given the
learning curve associated with laparoscopic
repairs, use of these techniques depends on
the availability of surgical expertise. In
women, the operation of choice is laparo-
scopic or open pre-peritoneal repair given the
higher risk of concurrent femoral hernia.
K. The open anterior tension-free mesh tech-
nique (modified Lichtenstein repair) is the
most common technique for inguinal hernias.
In this technique, the apex of the prosthetic
mesh is fixed to the pubic tubercle and the
mesh is sutured to the conjoint tendon medi-
Q. L. Hu and D. C. Chen
ally and inguinal ligament laterally. The
mesh is split and wrapped around the sper-
matic cord and then the tails sutured together
to recreate the inguinal ring. The advantages
of this technique are that it can be performed
with local anesthesia in the outpatient setting
and is associated with low cost and low
recurrence rates.
L. Although primary tissue repairs have been
largely abandoned owing to the success of
mesh-based repairs, they may be useful in
small hernias, young patients, or circum-
stances where there is a contraindication for
mesh placement (strangulated hernia with
bowel ischemia and perforation or contami-
nated field or patient refusal). Options for tis-
sue repairs include Shouldice, Bassini, and
McVay repairs. The best available tissue-­
based technique is the Shouldice repair,
which is a four-layer imbricated repair of the
posterior wall of the inguinal canal with run-
ning sutures. In specialized centers, its effi-
cacy is similar to mesh-based repairs.
M. The open posterior approach uses a trans-
verse skin incision above the traditional ante-
rior incision. The preperitoneal space may be
entered using either a transinguinal preperi-
toneal (TIPP) or trans-rectus sheath extra-
peritoneal (TREPP) technique. The
preperitoneal space is then dissected and the
myopectineal orifice exposed. A prosthetic
mesh is used to cover the entire myopectineal
orifice. In bilateral hernias, a lower midline
or Pfannenstiel incision may be used to
address both sides (Stoppa repair).
N. In the totally extraperitoneal (TEP) tech-
nique, a specialized dissecting balloon is
passed along the posterior rectus sheath and
is used to dissect the preperitoneal space. The
hernia sac is dissected from the cord and
reduced. A prosthetic mesh is then used to
cover the entire myopectineal orifice. The
advantage of this technique is that it avoids
violation of the peritoneum.
O. In the transabdominal preperitoneal (TAPP)
approach, the peritoneal cavity is entered
first. Then, peritoneum is incised and a flap is
created to enter to preperitoneal space. Once
189  Inguinal Hernia
in the preperitoneal space, the technique is
similar to the TEP approach. At the end of the
procedure, the mesh is covered with the peri-
toneum. The advantage of this technique is
that is allows for easy visual inspection of the
contralateral side and intra-abdominal
organs. However, the disadvantage of enter-
ing the peritoneal cavity is that it exposes the
patient to potential intra-abdominal injury
and adhesion formation.
P. Emergent repair for strangulated hernia may
be performed through the standard anterior
inguinal incision. The hernia sac is dissected
and controlled at the base to prevent drop-
ping the contents into the abdominal cavity.
The sac should be opened under direct vision
and all contents inspected carefully. It is pos-
785
sible to perform bowel resection and anasto-
mosis through the inguinal incisions but
there should be a low threshold for convert-
ing to a midline incision. An open preperito-
neal (posterior) approach may also be used.
The advantage of this incision is ability to
convert to laparotomy without creating a sep-
arate incision. Finally, if surgical expertise is
available, a laparoscopic or hybrid laparo-
scopic approach may be used to address the
bowel. Due to concern for infection, mesh is
not recommended in the repair of strangu-
lated inguinal hernia. From an anterior
approach, a tissue-based repair, such as the
Shouldice repair, may be performed. In an
open posterior or laparoscopic approach, a
delayed mesh-based repair is recommended.
786 Q. L. Hu and D. C. Chen

Groin bulge
A Pain/vague discomfort

B Perform a physical examination

Palpable bulge No
or defect?
Imaging C

Yes
D

Asymptomatic inguinal No Yes Inguinal hernia

E hernia
Symptomatic?
on imaging?

Yes No

Watchful waiting Symptomatic inguinal hernia No inguinal hernia. Consider

other differential diagnoses.

F
Reducible?

G Reducible H Incarcerated Strangulated I

Yes Manually No
Elective/urgent repair
reducible?
Emergent repair P

Operative approach depends on surgeon expertise and

J surgeon/patient preference

Laparoscopic/robotic approach Open approach

N TEP O TAPP Anterior approach Posterior approach M

K Mesh-based repair Tissue-based repair L

Algorithm 189.1
189  Inguinal Hernia 787

References 3. Ramanan B, Maloley BJ, Fitzgibbons RJ Jr. Inguinal

hernia: follow or repair? Adv Surg. 2014;48:1–11.
4. Koch A, Edwards A, Haapaniemi S, Nordin P, Kald
1. van den Berg JC, de Valois JC, Go PM, Rosenbusch
A. Prospective evaluation of 6895 groin hernia repairs
G. Detection of groin hernia with physical examina-
in women. Br J Surg. 2005;92(12):1553–8.
tion, ultrasound, and MRI compared with laparo-
5. McCormack K, Scott NW, Go PM, Ross S, Grant
scopic findings. Investig Radiol. 1999;34(12):739–43.
AM. Laparoscopic techniques versus open techniques
2. Niebuhr H, Konig A, Pawlak M, Sailer M, Kockerling
for inguinal hernia repair. Cochrane Database Syst
F, Reinpold W.  Groin hernia diagnostics: dynamic
Rev. 2003;(1):CD001785.
inguinal ultrasound (DIUS). Langenbeck’s Arch
Surg. 2017;402(7):1039–45.
 Recurrent Inguinal Hernia
Q. Lina Hu and David C. Chen
Algorithmic Approach
A. Inguinal hernia recurrence rates are report-
edly between 1% and 40% depending on the
type of initial repair technique [1]. Similar to
a primary inguinal hernia, the first step in the
evaluation of a patient with a recurrent ingui-
nal hernia is a thorough history. The patient
may present with a groin bulge at the site of a
prior hernia repair. More commonly, the pre-
senting symptom of a recurrent inguinal her-
nia is pain or discomfort. It is important to
assess for risks of recurrence, including prior
repair technique, factors that contribute to
poor healing (immunosuppression, diabetes,
infection, smoking, and obesity), and genet-
ics (collagen synthesis disorders).
B. Physical exam remains the initial method in
the diagnosis of a recurrent inguinal hernia.
A bulge or mass can be palpated for by
invaginating the tip of the examiner’s index
finger into the external ring while the patient
coughs or performs a Valsalva maneuver.
Q. L. Hu
Department of Surgery, David Geffen School of
Medicine at University of California, Los Angeles,
Los Angeles, CA, USA
D. C. Chen (*)
Department of Surgery, Lichtenstein Amid Hernia
Clinic at University of California at Los Angeles,
Los Angeles, CA, USA
e-mail: Dcchen@mednet.ucla.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_190
190
However, in the recurrent inguinal hernia,
physical exam may not always be
diagnostic.
C. When the physical exam findings are equivo-
cal, imaging modalities may be helpful.
Ultrasound should still be used as the initial
modality as it is an inexpensive and effective
tool, but its sensitivity is lower in recurrent
compared to primary inguinal hernias. When
the ultrasound is non-diagnostic, cross-­
sectional imaging such as computed tomog-
raphy (CT) or magnetic resonance imaging
(MRI) may provide a more consistent and
detailed view of the groin anatomy. If an
inguinal hernia is not detected on cross-­
sectional imaging, other differential diagno-
ses should be pursued. It is especially
important to differentiate chronic groin pain
from recurrence.
D. Once the diagnosis of recurrent inguinal her-
nia is established, either by physical exam,
imaging, or both, the next step is to assess
how symptomatic the patient is.
E. Because redo hernia repairs are associated
with higher risk of complications and recur-
rence rates and the risk of strangulation is
low, watchful waiting is a reasonable treat-
ment approach in the asymptomatic or mini-
mally symptomatic patient [2].
F. For symptomatic inguinal hernias, the next
step is to establish the reducibility of the her-
nia. If the mass is incarcerated, it is important
789
790
to assess for signs of strangulation (fever,
tenderness, erythema, or overlying skin
changes). If strangulation is suspected, blood
work such as white blood cell count or lactate
can be informative.
G. If the hernia is incarcerated but not strangu-
lated, manual reduction may be attempted. If
the hernia cannot be reduced manually or
there is evidence of strangulation, then emer-
gent repair is indicated. The approach to
emergent repair is similar to that of the emer-
gent primary hernia repair and depends on
surgeon preference, experience, and
expertise.
H. If the hernia is reducible, elective repair in an
outpatient setting is recommended. The oper-
ative repair technique for a recurrent inguinal
hernia depends on the prior technique of
repair and surgeon expertise.
I. If the prior repair was a primary tissue repair,
the redo operation should be a mesh-based
repair if not otherwise contraindicated and
may be approached from either the open
anterior or posterior approach. For open
anterior repairs, the Lichtenstein tension-free
mesh repair, in which a prosthetic mesh is
used to reinforce the inguinal floor, is recom-
mended. For open posterior repairs, either
transinguinal preperitoneal (TIPP) or trans-­
rectus sheath extra-peritoneal (TREPP) tech-
nique may be used to enter the preperitoneal
space and a prosthetic mesh used to cover the
entire myopectineal orifice. If the recurrence
is bilateral or if the patient has a primary her-
nia on the contralateral side, a Stoppa repair
through a lower midline or Pfannenstiel inci-
sion is advisable to address both sides simul-
taneously. If surgical expertise is available, a
minimally invasive (laparoscopic or robotic)
Q. L. Hu and D. C. Chen
approach is appropriate as well [3]. Either
the totally extraperitoneal (TEP) or transab-
dominal preperitoneal (TAPP) technique
may be used [4]. In TEP, a specialized bal-
loon is passed along the posterior rectus
sheath and is used to dissect the preperitoneal
space. The hernia sac is reduced and a pros-
thetic mesh is used to cover the entire myo-
pectineal orifice. The TAPP technique is
performed in the same manner except that
the peritoneal cavity is first entered and then
the peritoneum is incised to enter the preperi-
toneal space.
J. If the prior repair was a mesh-based repair,
the redo operation technique depends on the
original approach.
K. If the original repair was performed using an
open anterior approach, a posterior approach
is advised for the redo operation given lower
complication rates and the ability to operate
in the non-scarred field. Depending on sur-
geon expertise, either an open posterior
(TIPP, TREPP, or Stoppa repair) or laparo-
scopic approach (TEP or TAPP) may be
used.
L. If the original repair was performed using a
posterior approach (either open posterior or
laparoscopic), an open anterior approach,
such as the Lichtenstein technique, is advis-
able for the redo operation.
M. If surgical expertise is available, it is rea-
sonable to attempt the redo operation lapa-
roscopically through a transabdominal
preperitoneal (TAPP) approach. The poten-
tial advantage of this technique is the abil-
ity to assess and fix the problem from the
prior repair and this may be performed in
conjunction with an open anterior
technique.
190  Recurrent Inguinal Hernia 791

Groin bulge/pain/discomfort at site of

A prior inguinal hernia repair

B Perform a physical examination

Palpable bulge No
or defect?
Imaging C

Yes
Yes
D
Asymptomatic No Inguinal hernia
recurrent inguinal Symptomatic?
on imaging?
hernia

Yes No

Symptomatic recurrent inguinal hernia No inguinal hernia. Consider

other differential diagnoses.

F
Reducible? Signs
E Watchful waiting
of strangulation? Incarcerated/strangulated

Reducible Manual reduction

Emergent repair
G

Elective repair H

Prior repair
technique?

Prior tissue repair Prior mesh-based repair J

Open anterior or Prior anterior approach Prior posterior/laparoscopic approach

I posterior approach
Laparoscopic approach
Open posterior or Open anterior
K laparoscopic approach approach L TAPP M

Algorithm 190.1

3. Pisanu A, Podda M, Saba A, Porceddu G, Uccheddu

References
1. Barrat C, Surlin V, Bordea A, Champault
G.  Management of recurrent inguinal hernias: a
prospective study of 163 cases. Hernia J Hernias
Abdominal Wall Surg. 2003;7(3):125–9.
2. Haapaniemi S, Gunnarsson U, Nordin P, Nilsson
E. Reoperation after recurrent groin hernia repair. Ann
Surg. 2001;234(1):122–6.
A. Meta-analysis and review of prospective random-
ized trials comparing laparoscopic and Lichtenstein
techniques in recurrent inguinal hernia repair. Hernia
J Hernias Abdominal Wall Surg. 2015;19(3):355–66.
4. Gass M, Scheiwiller A, Sykora M, Metzger J. TAPP
or TEP for recurrent inguinal hernia? Population-­
based analysis of prospective data on 1309 patients
undergoing endoscopic repair for recurrent inguinal
hernia. World J Surg. 2016;40(10):2348–52.
 Femoral Hernia
Q. Lina Hu and David C. Chen
Algorithmic Approach
A. The presentation of a femoral hernia is very
similar to that of an inguinal hernia. Patients
will complain of a groin bulge, pain, or dis-
comfort. Femoral hernias are relatively
uncommon and account for 3–4% of all her-
nias [1]. They occur more frequently in
women, with incidence traditionally reported
to vary between 2% in males and 7% in
females [2].
B. Femoral hernias are more difficult to detect
on physical exam compared to inguinal her-
nias. The femoral canal is bounded by the
iliopubic tract superiorly, Cooper’s ligament
inferiorly, lacunar ligament medially, and
femoral vein laterally. On exam, the femoral
hernia may be found medial to the femoral
artery pulsation below the inguinal ligament.
However, sometimes the hernia sac may pro-
trude through the femoral canal and then slide
up over the inguinal ligament, making it dif-
ficult to distinguish from an inguinal hernia.
Q. L. Hu (*)
Department of Surgery, David Geffen School of
Medicine at University of California, Los Angeles,
Los Angeles, CA, USA
D. C. Chen (*)
Department of Surgery, Lichtenstein Amid Hernia
Clinic at University of California at Los Angeles,
Los Angeles, CA, USA
e-mail: Dcchen@mednet.ucla.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_191
191
C. Imaging can be especially helpful in identify-
ing femoral hernias when there is diagnostic
uncertainty. Ultrasound is the initial modality
of choice and can help differentiate femoral
hernias from inguinal hernias or detect an
occult hernia. When the ultrasound finding is
equivocal, cross-sectional imaging such as
computed tomography (CT) or magnetic res-
onance imaging (MRI) may provide a more
consistent and detailed view of the groin
anatomy. If a hernia is not detected on cross-­
sectional imaging, other differential diagno-
ses should be pursued.
D. Femoral hernias are often diagnosed intraop-
eratively when patients are taken to the oper-
ating room for a small bowel obstruction or
concurrent inguinal hernia. If found intraop-
eratively, it is advisable to repair the hernia
concurrently.
E. All femoral hernias should be repaired due to
the high risk of incarceration and strangula-
tion [3]. There are many options for surgical
repair and should be individualized to the
patient and the surgeon’s preference and level
of experience.
F. Minimally invasive (laparoscopic and
robotic) techniques are preferable when
expertise is available as it provides direct
access to the femoral canal and allows for
easy assessment of the contralateral side for
an occult hernia.
793
794
G. Either a totally extraperitoneal (TEP) or
transabdominal preperitoneal (TAPP) tech-
nique may be used for the repair of a femoral
hernia. In TEP, a specialized balloon is passed
along the posterior rectus sheath and is used
to dissect the preperitoneal space. The hernia K . In an open posterior preperitoneal approach,
sac is reduced and a prosthetic mesh is used
to cover the entire myopectineal orifice. The
TAPP technique is performed in the same
manner except that the peritoneal cavity is
first entered and then the peritoneum is
incised to enter the preperitoneal space. This
approach is advantageous as it allows for
visual inspection of the bowel to assess for
viability. As in the open approach, if there is
suspicion for bowel compromise, the perito-
neal cavity should be entered (if using TEP
technique) to assess bowel viability and per-
form bowel resection if necessary.
H. If the bowel is necrotic and surgical expertise
is available, the bowel resection may be per-
formed laparoscopically. Due to concern for
infection, a synthetic mesh is not advisable in L. If bowel compromise is suspected, then an
the setting of strangulation, perforation, gross
contamination, or bowel resection. In this
scenario, a tissue repair or delayed mesh-­
based repair at a later date is advised.
I. There are many options for open femoral her-
nia repairs. If the diagnosis is made preopera-
tively and strangulation is not suspected, the
repair may be performed from either an ante-
rior or posterior approach.
J. From the anterior approach, a femoral modi-
fied Lichtenstein technique may be used. This
technique follows the traditional Lichtenstein
technique, except that an additional lateral
Q. L. Hu and D. C. Chen
triangular extension is included to ensure
proper coverage of the femoral canal and
secured to the inguinal ligament, ilioinguinal
tract, lacunar ligament, and Cooper’s
ligament.
a transinguinal preperitoneal (TIPP) or tran-
srectus preperitoneal repair (TREPP) may be
used to place a mesh prosthetic into the pre-
peritoneal space to cover the entire myopec-
tineal orifice including the femoral canal. For
large, complicated, or bilateral defects, a
Stoppa repair or giant prosthetic reinforce-
ment of visceral sac (GPRVS) may be per-
formed though a lower midline or Pfannenstiel
incision. A large synthetic mesh is placed in
the preperitoneal space to the cover the entire
myopectineal orifices bilaterally, including
both the femoral and inguinal areas. If there is
concern for bowel compromise on visual
inspection, the peritoneal cavity may be
entered for bowel resection.
open anterior or abdominal approach is
advised. In the setting of strangulation, per-
foration, gross contamination, or bowel
resection, a McVay (Cooper’s ligament)
repair is preferred as it obliterates the femo-
ral space without the need for mesh. In this
technique, a relaxing incision is made to
relieve tension in the suture line. Then, the
transversus abdominis aponeurosis is
approximated to Cooper’s ligament medial
to the femoral canal and iliopubic tract lat-
eral to the canal with interrupted nonabsorb-
able sutures.
191  Femoral Hernia 795

Groin bulge
A Pain/vague discomfort

B Perform a physical examination

C
Palpable bulge No
below inguinal Imaging
ligament?

Yes
Yes Femoral hernia
D Intraoperative diagnosis Femoral hernia
on imaging?

E Operative repair No
No femoral hernia.
Operative approach depends on surgeon expertise and Consider other
surgeon/patient preference differential diagnoses.

F Laparoscopic approach Open approach I

Bowel viable? Bowel viable?

Viable bowel Necrotic bowel Viable bowel Necrotic bowel

G TEP TAPP Laparoscopic

J Anterior
K Posterior Open anterior or
L
bowel approach approach abdominal approach
H resection and
delayed repair
Femoral Modified TIPP, TREPP, McVay
Lichtenstein Stoppa repair repair

Algorithm 191.1

Hernias Abdominal Wall Surg. 2015;19(3):513–6.

References
1. Powell BS, Lytle N, Stoikes N, Webb D, Voeller
G.  Primary prevascular and retropsoas hernias:
incidence of rare abdominal wall hernias. Hernia J
2. Bendavid R.  Femoral pseudo-hernias. Hernia J
Hernias Abdominal Wall Surg. 2002;6(3):141–3.
3. Dahlstrand U, Wollert S, Nordin P, Sandblom G,
Gunnarsson U.  Emergency femoral hernia repair:
a study based on a national register. Ann Surg.
2009;249(4):672–6.
 Obturator Hernia
Q. Lina Hu and David C. Chen
Algorithmic Approach
A. Obturator hernias occur when the abdominal
contents protrude through the obturator canal.
They are quite rare, accounting for less than
1% of abdominal wall hernias, and are more
common in thin elderly women, likely due to
loss of supporting connective tissue and
wider female pelvis [1]. In more than 90% of
cases, the presenting symptom is a small
bowel obstruction and the diagnosis is made
intraoperatively [2]. Other symptoms include
groin pain radiating medially to the knee
(obturator neuralgia), palpable proximal
thigh mass, or ecchymosis of the thigh in the
setting of bowel necrosis.
B. Obturator hernias are often not detectable on
physical exam as the hernia is concealed
beneath the adductor muscles. However,
sometimes a palpable mass in the groin can
be identified when the patient is supine with
the hip flexed and laterally rotated. Two exam
maneuvers that have been described are
Q. L. Hu
Department of Surgery, David Geffen School of
Medicine at University of California, Los Angeles,
Los Angeles, CA, USA
D. C. Chen (*)
Department of Surgery, Lichtenstein Amid Hernia
Clinic at University of California at Los Angeles,
Los Angeles, CA, USA
e-mail: Dcchen@mednet.ucla.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_192
192
Howship-­Romberg sign (medial thigh pain
on extension, adduction, or medial rotation of
the hip) and Hannington-Kiff sign (loss of
adductor reflex) and are suggestive of an
obturator hernia when positive [2].
C. Due to the diagnostic difficulty, if physical
exam findings are suggestive of obturator her-
nia or if clinical suspicion is high, computed
tomography (CT) is considered the gold stan-
dard for diagnosis. CT scan may also provide
information on bowel compromise or
perforation.
D. As previously described, the majority of
obturator hernias are diagnosed intra-­
operatively when patients are taken to the
operating room for a small bowel obstruction
or concurrent inguinal or femoral hernia.
E. Obturator hernias are associated with high
mortality of 13–40%, likely due to late diag-
nosis, and, thus, whenever an obturator hernia
is discovered, operative repair is strongly rec-
ommended [3].
F. If the diagnosis is made preoperatively and
strangulation is not suspected, a posterior
approach is advised.
G. For an open approach, a Stoppa repair or
giant prosthetic reinforcement of visceral sac
(GPRVS) may be performed though a lower
midline or Pfannenstiel incision. A large syn-
thetic mesh is placed in the preperitoneal
space to cover the obturator orifice as well as
the rest of the myopectineal orifice, including
797
798
both the femoral and inguinal areas. If there is
concern for bowel compromise on visual
inspection, the peritoneal cavity may be
entered for bowel resection.
H. If surgical expertise is available, a minimally
invasive (laparoscopic or robotic) approach is
preferred. Either the totally extraperitoneal
(TEP) or transabdominal preperitoneal
(TAPP) technique may be used. In TEP, a
specialized balloon is passed along the poste-
rior rectus sheath and is used to dissect the
preperitoneal space. The hernia contents are
reduced, and a prosthetic mesh is used to
cover the obturator orifice as well as the rest
of the myopectineal orifice. The TAPP tech-
nique is performed in the same manner except
that the peritoneal cavity is first entered and
then the peritoneum is incised to enter the
preperitoneal space. This approach is advan-
tageous as it allows for visual inspection of
the bowel to assess for viability. It is impor-
tant to note that in both techniques, the mesh
prosthesis should be larger than that used in
traditional inguinal hernia repairs as it must
cover both the inguinal and obturator spaces.
If the appropriate-size mesh is not available,
the mesh may be seated more inferiorly than
usual to ensure proper coverage of the obtura-
tor orifice. As in the open approach, if there is
suspicion for bowel compromise, the perito-
neal cavity should be entered (if using the
TEP technique) to assess bowel viability and
perform bowel resection if necessary.
I. If bowel compromise is suspected, a transab-
dominal approach is advised. This algorithm
Q. L. Hu and D. C. Chen
may also be used if the diagnosis is made
intraoperatively in an abdominal operation.
J. Depending on surgical expertise availability,
an open lower midline laparotomy incision or
laparoscopic approach may be used. The her-
nia sac should be reduced and the sac content
inspected for viability.
K. If the bowel is viable and an open approach
was used, then the preperitoneal space may
be entered by opening the parietal perito-
neum. Once in the preperitoneal cavity, a
Stoppa repair maybe performed by placing a
synthetic mesh over the obturator orifice as
well as the rest of the myopectineal orifice. If
a laparoscopic approach was used, then the
TAPP technique may be used to complete the
repair by incising the peritoneum and enter-
ing the preperitoneal space.
L. If the bowel is necrotic and an open approach
was used, then an open bowel resection
should be performed. Due to concern for
infection, a synthetic mesh is not advisable in
the setting of strangulation, perforation, gross
contamination, or bowel resection. The her-
nia defect may be suture repaired in two lay-
ers [4]. Alternatively, a biologic mesh may be
used or the defect may be reinforced with
adjacent tissues such as periosteal flaps, blad-
der wall, uterine fundus, or ligaments [2]. If a
laparoscopic approach was used, then a lapa-
roscopic bowel resection may be performed if
surgical expertise is available. The hernia
defect then may be repaired primarily.
Alternatively, a delayed mesh repair may be
performed at a later date.
192  Obturator Hernia 799

Proximal thigh mass

A Groin/medial thigh pain
Small bowel obstruction

B Perform a physical examination

C Imaging

No No obturator hernia.
Obturator hernia
Consider other differential
on imaging?
diagnoses.

Yes

D Intraoperative diagnosis Obturator hernia

E Operative repair

Preoperative
diagnosis?
Strangulation?

Preoperative diagnosis Intraoperative diagnosis

F AND OR I
Strangulation not suspected Strangulation suspected

G
Stoppa Laparoscopic
H Abdominal approach J
repair repair

K Viable bowel Necrotic bowel L

Open posterior Laparoscopic Open tissue Laparoscopic

repair repair repair repair

Algorithm 192.1
800 Q. L. Hu and D. C. Chen

References 2. Salameh JR.  Primary and unusual abdominal wall

hernias. Surg Clin North Am. 2008;88(1):45–60, viii.
3. Hodgins N, Cieplucha K, Conneally P, Ghareeb
1. Stamatiou D, Skandalakis LJ, Zoras O, Mirilas
E.  Obturator hernia: a case report and review of the
P.  Obturator hernia revisited: surgical anatomy,
literature. Int J Surg Case Rep. 2013;4(10):889–92.
embryology, diagnosis, and technique of repair. Am
4. Shipkov CD, Uchikov AP, Grigoriadis E. The obtura-
Surg. 2011;77(9):1147–57.
tor hernia: difficult to diagnose, easy to repair. Hernia
J Hernias Abdominal Wall Surgery. 2004;8(2):155–7.
 Ventral Hernia Repair
Justin A. Doble and Eric M. Pauli
Algorithmic Approach
A. Initial evaluation for any ventral hernia
requires complete medical history, physical
examination, and radiologic assessment
(ultrasound [US] or computed tomography
[CT] scan). Modification of patient-specific
risk factors (including smoking cessation, E. For patients with risk factors and 10–20 cm
reduction in immunosuppression, improved
glycemic control, and weight loss/obesity
surgery) has been shown to reduce complica-
tions and recurrence.
B. Multiple hernia staging systems exist, includ-
ing the Ventral Hernia Working Group clas-
sification, European Hernia Society
classification, and Hernia, Patient, Wound
(HPW) staging system. Here, we utilize the
HPW staging system as it provides a TNM-­
like (Tumor Node Metastasis) approach help- F. The presence of a contaminated wound
ful for patient management and operative
decision-making [1].
C. Fascial defect closure is preferred for most
patients as it may provide a more durable
repair and reduce the risks of both short- and
long-term complications. However, closure
of the hernia defect in a geriatric population
or patients with comorbid diseases may
exceed the risk-to-benefit ratio.
J. A. Doble · E. M. Pauli (*)
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: epauli@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_193
193
D. Operative approach to defect closure is based
upon surgeon expertise/preference but modi-
fied based on patient risk factors that will per-
mit (or preclude) a minimally invasive
approach, the presence (or absence) of old
mesh, and the potential need for a component
separation [2].
defects, a minimally invasive operation
reduces wound complications at the expense
of fascial closure difficulties (e.g., component
separation may be needed). An open opera-
tion facilitates defect closure but at a greater
risk of surgical site infections. We prefer a
robotic repair with transversus abdominus
release or an open retrorectus repair depend-
ing on patient candidacy for a minimally
invasive herniorrhaphy [3, 4].
(ostomy, fistula, concomitant organ resection,
or inadvertent enterotomy) is the predomi-
nant consideration for stage III hernia. Wound
contamination decreases the likelihood of a
safely performed definitive repair in a single
procedure. Thus, attempts to downstage her-
nia with a staged operative approach can be
considered.
G. In a contaminated field, options for tempo-
rary repair include suture repair (if possible
passed on defect size) or bridge repair using a
biologic or a bioabsorbable mesh. Although
bridged repairs have a high recurrence rate,
801
802 J. A. Doble and E. M. Pauli

controlling wound contamination first per-
mits definitive repair during a second opera-
tion. This controlled/planned failure approach
permits downstaging of wound class.
H. Mesh choice in the setting of potential bacte-
rial contamination remains a controversial
topic. Options include no mesh, biologic
mesh, bioabsorbable mesh, or permanent
synthetic mesh. The risks-to-benefit ratio
should be determined by the surgeon on a
case-by-case basis. Emerging data suggests
that the retromuscular placement of
intermediate-­weight polypropylene synthetic
mesh may have short-term benefits over bio-
logic mesh in select contaminated circum-
stances; however, the long-term results are
not known [5].
I. While attempting definitive repair for large
defects (>20 cm), complete fascial closure may
be impossible, resulting in a partial bridged
repair (usually in the mid-abdomen). The use
of lighter-weight mesh may reduce risk for
infection but carries increased risk for central
mesh fracture and recurrence. Conversely,
heavyweight mesh is less likely to fracture but
carries increased risk for mesh infection. Mesh
determination for each individual patient
should be based off intraoperative findings.

A H&P; abdominal imaging (CT/US)

1. Smoking cessation
Yes 2. Reduce immunosuppression
Risk reduction possible?
3. Lower HbA1c
No 4. Weight loss/obesity surgery

B Stage hernia

Stage I Stage II Stage III Stage IV

<10cm, low risk, clean <20cm, ± risk factors >20cm, ± risk factors

<10cm + risk factors

C
F
Close No Contamination
LVHR (Bridged) present?
defect?
No

Yes Definitive repair

D E
Yes
Minimally invasive vs <20cm, ± risk factors I
open VHR
See abdominal wall
reconstruction
Robotic vs open vs
hybrid VHR ± G
component separation Downstage
possible?

H Remove contamination,
temporary repair

Algorithm 193.1
193  Ventral Hernia Repair 803

References 3. Carbonell AM, Cobb WS, Chen SM. Posterior com-

ponents separation during retromuscular hernia repair.
Hernia. 2008;12(4):359–62.
1. Kanters AE, Krpata DM, Blatnik JA, Novitsky YM,
4. Martin-Del-Campo LA, Weltz AS, Belyansky I,
Rosen MJ.  Modified hernia grading scale to stratify
Novitsky YW. Comparative analysis of perioperative
surgical site occurrence after open ventral hernia
outcomes of robotic versus open transversus abdomi-
repairs. J Am Coll Surg. 2012;215(6):787–93.
nis release. Surg Endosc. 2018;32(2):840–5.
2. Orenstein SB, Dumeer JL, Monteagudo J, Poi MJ,
5. Majumder A, Winder JS, Wen Y, Pauli EM, Belyansky
Novitsky YW. Outcomes of laparoscopic ventral her-
I, Novitsky YW.  Comparative analysis of biologic
nia repair with routine defect closure using “shoelac-
versus synthetic mesh outcomes in contaminated her-
ing” technique. Surg Endosc. 2011;25(5):1452–7.
nia repairs. Surgery. 2016;160(4):828–38.
 Incarcerated and Strangulated
Hernia
Justin A. Doble and Eric M. Pauli
Algorithmic Approach
A. It is essential to determine the chronicity of
incarceration during initial patient history
and examination as this will establish the
need for an emergent surgery. Directed ques-
tioning should elicit any previous history of
incarceration (chronic vs. acute), history of
obstruction symptoms, and timing/duration
of an acute event. Examination must identify
any “hard” surgical signs such as peritonitis,
subcutaneous crepitus, discoloration of her-
nia sac, and necrotic skin changes. Chronically
incarcerated hernias without symptoms of
obstruction or strangulation can be managed
electively.
B. Indication for manual reduction (taxis) of an
incarcerated hernia is an area of debate in
surgical literature. Published literature sug-
gests bedside reduction not be attempted if
acute incarceration occurred 4–12 h prior to
attempt. Several laboratory findings (WBC
>20,000, lactic acid >2  mmol/L) can help
with determination of safety, but attempting
bedside reduction is ultimately a clinical
decision [1–3].
J. A. Doble · E. M. Pauli (*)
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: epauli@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_194
194
C. In a hemodynamically stable patient, abdomi-
nal imaging (CT) has some utility for pre-­
operative surgical planning (especially
ventral hernia). Abdominal imaging may also
identify the bowel that is at risk for necrosis
and/or perforation (wall thickening, abdomi-
nal free fluid, pneumatosis, and free air), but
obtaining imaging should not delay surgery
in a patient with surgical indications.
D. Operative approach to defect closure is based
upon surgeon expertise/preference but modi-
fied based on patient risk factors that will
permit (or preclude) a minimally invasive
approach (inability to close defect).
E. Laparoscopy may be necessary to inspect the
bowel even in an open inguinal repair. This
can be easily performed in an open procedure
via insertion of the laparoscope into the her-
nia sac [4].
F. The choice of a primary suture repair vs.
mesh-based repair of the hernia defect
depends on the following: Defect size, defect
location, surgeon expertise, patient risk fac-
tors (Diabetes Mellitus, tobacco use, immu-
nosuppressed), and presence of bowel injury/
contamination (bacterial translocation with
incarcerated bowel). The surgeon must deter-
mine if the risk of hernia recurrence with a
suture repair exceeds the potential risk of
mesh complication. We advocate for a tempo-
rary repair (suture repair or a simple bridged
mesh repair) rather than a component separa-
805
806 J. A. Doble and E. M. Pauli

tion for the majority of acute presentations. In
these patients, definitive repair proceeds elec-
tively with pre-operative risk reduction and
patient optimization [5].
G. Although rarely reported in the literature, the
successful manual reduction of necrotic
bowel can occur. A brief period of observa-
tion will identify any consequence from
failed identification/manual reduction of
necrotic bowel. Diagnostic laparoscopy may
be used selectively to assist in ruling out this
possibility. Patients with successfully reduced
hernias should be closely followed and sched-
uled for definitive repair electively [1].

Algorithm 194.1
History and physical
examination
A

B
Yes
Safe to reduce Reducible?

No No Yes

Acute repair indicated C Observe

Ventral hernia Inguinal hernia

D E
Open repair MIS repair Open repair MIS repair

Perform necessary concomitant Plan definitive

F procedures (e.g. organ resection) repair
Repair hernia defect
194  Incarcerated and Strangulated Hernia 807

References 4. Sajid MS, Ladwa N, Colucci G, Miles WF, Baig

MK, Sains P.  Diagnostic laparoscopy through
deep inguinal ring: a literature-based review on
1. Harissis HV, Douitsis E, Fatouros M.  Incarcerated
the forgotten approach to visualize the abdominal
hernia: to reduce or not to reduce? Hernia.
cavity during emergency and elective groin her-
2009;13(3):263–6.
nia repair. Surg Laparosc Endosc Percutan Tech.
2. Tanaka K, Hanyu N, Iida T, et  al. Lactate levels in
2013;23(3):251–4.
the detection of preoperative bowel strangulation. Am
5. Slater NJ, van Goor H, Bleichrodt RP.  Large and
Surg. 2012;78(1):86–8.
complex ventral hernia repair using “components
3. Kauffman HM Jr, O’Brien DP.  Selective reduc-
separation technique” without mesh results in a high
tion of incarcerated inguinal hernia. Am J Surg.
recurrence rate. Am J Surg. 2015;209(1):170–9.
1970;119(6):660–73.
 Management of Open Abdomen
Justin A. Doble and Eric M. Pauli
Algorithmic Approach
A. All abdominal closure therapies should pri-
marily focus on prevention of gastrointestinal
fistula formation with a secondary endpoint
of definitive abdominal closure.
B. Options for a bridged repair include Vicryl
and biologic mesh. Vicryl mesh will be reab-
sorbed quickly (6 weeks) leading to an early,
large hernia formation, and in the event of a
deep surgical site infection, the exposed mesh
will permit large hydraulic shift of fluid from
the bowel leading to desiccation and possible
fistula formation. Biologic mesh will fail over
a longer period of time (80% at 2 years [1])
but carries an increase in cost and risk of bio-
logic mesh complication (seroma/wound
infection). However, in the event of a deep
surgical site infection, the mesh will not per-
mit underlying bowel desiccation and permits
negative-pressure wound therapy (NPWT)
directly on the mesh.
C. Performing a component separation in an
acute or emergent procedure should be done
with extreme caution as it carries a higher set
of risks than in the elective setting. Moreover,
it eliminates viable options for definitive
repair of the hernia at a later date and gener-
J. A. Doble · E. M. Pauli (*)
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: epauli@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_195
195
ally makes the reoperation much more com-
plex. The division of anterior and posterior
components should not be performed during
a single operation, and operations that inten-
tionally divide the linea semilunaris should
be avoided altogether.
D. The success rate for primary fascial closure
decreases by approximately 1.1% for each
24-h delay after initial laparotomy [2]. Early
anticipation of delayed closure and the use of
a Wittman patch and transabdominal wall
traction (TAWT) systems have been shown to
increase abdominal closure rates. These
devices facilitate closure by facilitating
sequential isometric contraction of the
abdominal wall via Velcro sheets sewn to the
fascia (Wittman patch) or with transfascial
sutures secured over a plastic skin bolster
(TAWT). Additionally, chemical component
separation with botulinum toxin has been
described to increase the probability of pri-
mary fascial closure [3].
E. Negative-pressure wound therapy systems
are available as a preassembled commercial
product or can be created out of standard
operative supplies. NPWT devices can be
safely used for temporary abdominal closures
and may improve success rates of primary
fascial closure [4].
F. There are several options for temporary
abdominal closure when a large intraabdomi-
nal fluid (blood or ascites) volume is not
809
810 J. A. Doble and E. M. Pauli

expected. The Bogota bag technique is per-
formed by suturing a sterile, clear plastic
sheet, usually from an X-ray cassette sheet or
IV bag to the fascia. A silo closure wraps the
externalized bowel in plastic secured to the
fascial edges. The zipper closure method
attaches both fascial edges to a slide fastening
device, thus allowing for quick temporary
exposure/closure of the abdomen. The barker
bag technique is an intraoperatively con-
structed negative-pressure wound therapy
system.

Open abdomen

A
Re-exploration
indicated

No Yes

Fascial closure Delayed closure D

possible anticipated
Yes Consider: Wittman
patch, TAWT or
No
Yes No abdominal wall botox

Suture
closure NPWT Yes
available? E
NPWT

No

Anticipate
Mesh available fluid egress

No Yes
Yes No

B F
Bridged Bogota bag Barker bag
repair Zipper closure or
Silo closure NPWT

Delayed
incisional
hernia repair
Component
separation
possible?
C

Yes No

Component Skin closure w/

separation retention sutures

Algorithm 195.1
195  Management of Open Abdomen 811

References 3. Zielinski MD, Goussous N, Schiller HJ, Jenkins

D.  Chemical components separation with botuli-
num toxin a: a novel technique to improve primary
1. Blatnik J, Jin J, Rosen M.  Abdominal hernia repair
fascial closure rates of the open abdomen. Hernia.
with bridging acellular dermal matrix – an expensive
2013;17(1):101–7.
hernia sac. Am J Surg. 2008;196(1):47–50.
4. Cirocchi R, Birindelli A, Biffl WL, et al. What is the
2. Pommerening MJ, DuBose JJ, Zielinski MD, et  al.
effectiveness of the negative pressure wound ther-
Time to first take-back operation predicts successful
apy (NPWT) in patients treated with open abdomen
primary fascial closure in patients undergoing damage
technique? A systematic review and meta-analysis. J
control laparotomy. Surgery. 2014;156(2):431–8.
Trauma Acute Care Surg. 2016;81(3):575–84.
 Abdominal Wall Reconstruction
Justin A. Doble and Eric M. Pauli
Algorithmic Approach
A. The initial evaluation for any hernia requires
a complete medical history, physical exami-
nation, and radiologic assessment (ultrasound
[US] or computed tomography [CT] scan).
Modification of patient-specific risk factors
(including smoking cessation, reduction in
immunosuppression, improved glycemic
control, and weight loss/obesity surgery) has
been shown to reduce complications and
recurrence [1].
B. The phrase “Abdominal Wall Reconstruction”
describes a variety of surgical procedures
aimed at restoring abdominal wall anatomy
and function. In general, this is achieved
through closure of fascial defects and wide
reinforcement with mesh prosthesis. There
are a variety of indications that determine the
need for an abdominal wall reconstruction
procedure, including abdominal pain limiting
activities of daily life, risk for bowel strangu-
lation or incarceration, young age, and the
need for a functional abdominal wall. A large
hernia with loss of domain is not, by itself, an
indication for abdominal wall reconstruction
as in some patients the risk of surgery may
outweigh the benefit [1].
J. A. Doble · E. M. Pauli (*)
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: epauli@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_196
196
C. Operative planning prior to abdominal wall
reconstruction requires consideration of several
patient-specific risk factors. For the purpose of
this chapter, we will use hernia defect size to
simplify the treatment algorithm. Other factors
(patient risk factors, hernia stage, and wound sta-
tus) have been discussed in previous chapters.
All listed measurements are approximations and
should not be used in isolation to determine the
operative technique or type of component sepa-
ration. Patient body habitus, abdominal anat-
omy, and laxity of the abdominal wall must also
be considered pre-operatively.
D. A minimally invasive operative (robotic, lapa-
roscopic, or enhanced-view totally extraperito-
neal [eTEP]) approach is ultimately determined
by surgeon experience and preference; how-
ever, the presence of adhesive disease, previous
mesh, or wound contamination may require an
open procedure [2].
E. Rectus muscle size is an important consider-
ation during an open retrorectus repair as
midline fascial closure with prosthetic mesh
overlap is required. Technical limitations of
the minimally invasive approach may require
additional component separation (transversus
abdominis release [TAR]), whereas an open
approach may not require any additional
component release. The surgeon must deter-
mine if the decreased wound morbidity and
enhanced recovery benefits outweigh the risk
of an extended tissue dissection.
813
814
F. The vast majority of medium-sized defects
are managed by either a transversus abdomi-
nis release (TAR) or external oblique release
(EO). The TAR allows for greater medializa-
tion of the tissues and wider mesh overlap for
midline and non-midline defects. It is rapidly
becoming the more commonly used proce-
dure as data indicates that TAR has a lower
recurrence and complication rate than an EO
release. However, the EO remains viable as
the dissection is entirely extraperitoneal. It
can be used when the abdominal cavity is
deemed unapproachable/hostile (adhesive
disease, previous radiation, and previous pos-
terior component resection).
G. External oblique release can be completed by
creating subcutaneous flaps that preserve
periumbilical perforator vessels from a mid-
line incision or with laparoscopic tools from a
lateral incision. EO repairs allow for the mesh
to be placed directly on the muscle with fas-
cia closed underneath (onlay). If additional
mesh coverage is required, a retrorectus dis-
J. A. Doble and E. M. Pauli
section will enable sublay mesh placement or
“sandwich” repair with two pieces of mesh
(sublay and onlay mesh placement) [3, 4].
H. As mentioned earlier, TAR is preferably given
a lower rate of wound complication and hernia
recurrence. When approaching large defects,
you must acknowledge the possibility that
midline fascial closure may not be possible. In
such a case, accept the necessity of a bridged
repair. It is generally felt that a simultaneous
external oblique (EO) and transversus abdom-
inis release (TAR) should not be performed. If
you suspect you may be unable to re-approxi-
mate fascia, you may consider preoperative
pneumoperitoneum or botulism toxin injec-
tions to the lateral musculature to provide
additional fascial mobility [3].
I. All patients, regardless of technique, should
be closely monitored for signs of abdominal
hypertension and abdominal compartment
syndrome (high peak airway pressure,
decreased urine output, and elevated bladder
pressure).
196  Abdominal Wall Reconstruction 815

H&P; abdominal CT imaging

Surgical risk reduction:

1. Smoking cessation
A 2. Reduce immunosuppression
3. Lower HbA1c
4. Weight loss/obesity surgery

See previous Yes

Contaminated
chapter

No
B Meets criteria for abdominal
wall reconstruction?

C
Small defect Large defect
8–10 cm >20 cm

Contamination Fascia
or adhesions? closable?

Yes No
D No Yes
E H
Open Medium weight Bridged repair
MIS repair mesh w/ heavy mesh
retrorectus

I
ICU evaluation and
monitoring if
Medium defect needed
10–20 cm

TAR F EO

G
MIS w/ Open repair w/ MIS or open EO
sublay mesh sublay mesh ± retrorectus
mesh: onlay, sublay,
or ‘sandwich’

Algorithm 196.1

retromuscular hernia repair. Surg Endosc.

References
1. Majumder A, Novitsky Y. Retrorectus hernia and
transversus abdominis release. In: Hope WW, Cobb
WS, Adrales GL, editors. Textbook of hernia. New
York: Springer; 2017. p. 225–32.
2. Belyansky I, Daes J, Radu VG, et  al. A novel
approach using the enhanced-view totally extra-
peritoneal (eTEP) technique for laparoscopic
2018;32(3):1525–32.
3. Novitsky YW, Fayezizadeh M, Majumder A, Neupane
R, Elliott HL, Orenstein SB.  Outcomes of posterior
component separation with transversus abdominis
muscle release and synthetic mesh sublay reinforce-
ment. Ann Surg. 2016;264(2):226–32.
4. Pauli EM, Rosen MJ.  Open ventral hernia repair
with component separation. Surg Clin North Am.
2013;93(5):1111–33.
 Part XXIII
Bariatric Surgery
 Indications for Bariatric Surgery
Jin Sun Kim and Ann M. Rogers
Algorithmic Approach
A. Bariatric surgery is the only effective and
durable treatment for most patients with
severe obesity and its associated medical
comorbidities [1]. Guidelines and recommen-
dations for application of bariatric surgery
differ by country [2].
B. In the United States, patients with Class 3
obesity, defined as having a body mass index
(BMI) >40 kg/m2, or Class 2 obesity with a
BMI between 35 and 39.9 kg/m2 along with
at least one severe associated weight-related
condition are potential candidates for weight
loss surgery [3].
C. Obesity-related comorbidities include type 2
diabetes, obstructive sleep apnea, hyperten-
sion, hyperlipidemia, obesity-hypoventilation
syndrome, nonalcoholic fatty liver disease,
pseudotumor cerebri, gastroesophageal reflux
disease, asthma, venous stasis disease, stress
urinary incontinence, debilitating arthritis,
J. S. Kim
Pennsylvania State University College of Medicine,
Hershey, PA, USA
A. M. Rogers (*)
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: arogers@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_197
197
impaired quality of life, and disqualification
from other surgeries resulting from obesity
(e.g., joint replacement, organ transplanta-
tion, and ventral hernia repair) [4].
D. Patients generally excluded from bariatric
surgery include those with reversible disor-
ders that cause obesity, active drug or alcohol
abuse, poorly controlled psychiatric condi-
tions, current pregnancy, history of active sui-
cide attempt, cancer not in remission, and
severe heart or lung disease making the
patient a poor surgical candidate [3]. Patients
under the age of 18 are best treated at a mul-
tidisciplinary adolescent weight loss surgery
program with appropriate pediatric special-
ties available [5].
E. Currently approved surgical weight loss
options in the United States include vertical
sleeve gastrectomy, roux-en-Y gastric bypass,
adjustable gastric band, and biliopancreatic
diversion with duodenal switch [6].
819
820 J. S. Kim and A. M. Rogers

Algorithm 197.1
Patient has obesity

Does the
A patient live
in the US?

No
Yes

See local guidelines B

Does the
patient have
a BMI > 35?
No

Yes
Seek medical weight
management

BMI 35–39.9 BMI > 40

Yes
Any contraindications? D
Yes No E
Does the
patient have
No Recommend
significant
weight-related bariatric surgery
problems?

4. Mechanick JI, Youdim A, Jones DB, et  al. Clinical

References
1. Burguera B, Agusti A, Arner P, et al. Critical assess-
ment of the current guidelines for the management and
treatment of morbidly obese patients. J Endocrinol
Investig. 2007;30:844.
2. Borisenko O, Colpan Z, Dillemans B, et al. Clinical
indications, utilization, and funding of bariatric sur-
gery in Europe. Obes Surg. 2015;25:1408–16.
3. NIH conference. Gastrointestinal surgery for severe
obesity. Consensus Development Conference Panel.
Ann Int Med. 1991;115:956–61.
practice guidelines for the perioperative nutritional,
metabolic, and nonsurgical support of the bariat-
ric surgery patient—2013 update: cosponsored by
American Association of Clinical Endocrinologists,
The Obesity Society, and American Society for
Metabolic & Bariatric Surgery. Obesity (Silver Spring,
Md). 2013;21(1):S1–27. https://doi.org/10.1002/
oby.20461.
5. Michalsky M, Reichard K, Inge T. ASMBS pediatric
committee best practice guidelines. Surg Obes Relat
Dis. 2012;8:1–7.
6. Lee WJ, Almalki O.  Recent advancements in bar-
iatric/metabolic surgery. Ann Gastroenterol Surg.
2017;1:171–9.
 Work-Up of Abdominal Pain
in the Bariatric Patient
Sarayna S. McGuire and Ann M. Rogers
Algorithmic Approach
A. Bariatric patients presenting with abdominal
pain should undergo a complete history and
physical examination to determine the qual-
ity, location, and timing of the pain and asso-
ciated symptoms. The operative date,
procedure type, and postoperative course will
help guide the work-up and diagnosis. Vital
signs and laboratory work can provide crucial
information on acuity and potential causes of
the pain.
B. In the early postoperative setting, complica-
tions may arise specific to the patient’s proce-
dure type—the anastomoses in the roux-en-Y
gastric bypass (RYGB) (e.g., strictures, leaks,
ulcers), band malfunction or malposition
after adjustable gastric band (AGB), and
leaks after biliopancreatic diversion with
duodenal switch (BPD/DS). Missed bowel
perforation due to mobilization difficulty
(e.g., strictures, adhesions, and internal her-
nia) may also occur after any of these [1].
C. For any AGB patient with abdominal pain,
nausea, or vomiting, the band should be com-
pletely deflated prior to pursuing a diagnostic
work-up because of the risk of gastric isch-
emia or the possibility of aspiration of gastric
S. S. McGuire · A. M. Rogers (*)
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: arogers@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_198
198
contents. An upper gastrointestinal (UGI)
swallow study is the test of choice for band-­
related symptoms, but its performance is not
always feasible outside of normal work hours.
D. An abdominal and pelvic computed tomogra-
phy (CT) scan should be performed to exclude
the potentially life-threatening complications
of a closed-loop bowel obstruction, bowel
perforation, or gastric prolapse when UGI is
not available [2]. Use of oral contrast is gen-
erally helpful in the examination of post-­
bariatric anatomy; use of intravenous contrast
is optional, depending on suspected diagno-
ses related to inflammation or blood supply.
E. Exploratory laparotomy or laparoscopy
(depending on surgeon preference or patient
factors) is indicated when internal hernia is
suspected as this can be missed with plain
films, upper gastrointestinal contrast studies,
and CT scans [1]. It is also appropriate for
perforated marginal ulcer, intussusception,
adhesive bowel obstruction, or symptomatic
gastric prolapse through a band.
F. In the later postoperative setting (>30 days),
patients may present with intestinal obstruc-
tion after any bariatric procedure, marginal
ulcers with or without associated strictures
after RYGB, dumping syndrome after RYGB,
gallstone disease, nutritional deficiencies, and
gastrointestinal problems unrelated to bariat-
ric surgery (e.g., gastroesophageal motility
821
822 S. S. McGuire and A. M. Rogers

disorders, celiac disease, or irritable bowel
syndrome).
G. Depending on the history, symptoms, and
physical examination, work-up of the patient
in this later setting can include abdominal
ultrasound and/or nuclear scan (gallstone dis-
ease), abdominal CT scan (intestinal obstruc-
tion), stool specimen (C. difficile colitis and
hematochezia), upper or lower endoscopy, or
contrast studies (reflux/regurgitation).

Abdominal pain in bariatric patient

· History and physical exam
A · Establish operative date, procedure type, and postoperative course
· Obtain vital signs and blood work. If febrile, work up for infection.

B Early postoperative setting:

Consider complications specific to procedure: Later postoperative setting

· RYGB: strictures, leaks, and ulcers (>30 days)
· AGB: band malfunction/malposition
F
· BPD/DS: leaks
Rule-out missed bowel perforation.
Patients may present with intestinal
obstruction after any procedure,
marginal ulcers with or without
associated strictures after RYGB,
C dumping syndrome after RYGB,
gallstone disease, nutritional
For AGB patients, Obtain abdominal and deficiencies, and gastrointestinal
deflate the band pelvic CTscan to problems unrelated to bariatric
prior to work-up. D exclude closed loop surgery.
UGI swallow study bowel obstruction,
is the test of choice. bowel perforation, or
gastric prolapse when
UGI is not available.
Use of oral contrast is
preferred.
Depending on history, symptoms,
G and physical exam, work-up can
Exploratory laparotomy or include abdominal ultrasound
E and/or nuclear scan, abdominal
laparoscopy is indicated when
internal hernia, perforated CT scan, stool specimen, upper
marginal ulcer, intussusception, or lower endoscopy, or contrast
adhesive bowel obstruction, or studies.
symptomatic gastric prolapse
through a band are suspected.

Follow-up care

Algorithm 198.1
198  Work-Up of Abdominal Pain in the Bariatric Patient 823

References metabolic, and nonsurgical support of the bariat-

ric surgery patient—2013 update: cosponsored by
American Association of Clinical Endocrinologists,
1. Lee CW, Kelly JJ, Wassef WY.  Complications of
The Obesity Society, and American Society for
bariatric surgery. Curr Opin Gastroenterol. 2007;
Metabolic & Bariatric Surgery. Surg Obes Relat Dis.
23(6):636–43.
2013;9:159–91.
2. Mechanick JI, Youdim A, Jones DB, et  al. Clinical
practice guidelines for the perioperative nutritional,
 Internal Hernia: Diagnosis
and Treatment
Brandon LaBarge and Ann M. Rogers
Algorithmic Approach
A. Internal hernias have an incidence of less than
1% after abdominal operations but constitute
up to 5.8% of all small bowel obstructions
and if untreated have a reported mortality rate
exceeding 50% in some series when associ-
ated with strangulation [1]. Patients who have
undergone gastric bypass or the duodenal
switch procedure are at risk for internal her-
nia bowel obstructions because of new mes-
enteric defects created during such operations.
Patients with acute intestinal obstruction
related to an internal hernia may present with
vomiting, abdominal distension, and colicky
abdominal pain, as well as physical signs of
rebound tenderness and involuntary guard-
ing. If the hernia is spontaneously reducible,
symptoms may be vague and can include
recurrent central abdominal pain and nausea.
B. LaBarge
Department of Surgery, Penn State College of
Medicine, Penn State Milton S. Hershey Medical
Center, Hershey, PA, USA
A. M. Rogers (*)
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: arogers@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_199
199
B. Because of altered anatomy, internal hernia
bowel obstructions in post-bariatric patients
cannot be definitively diagnosed with plain
abdominal radiographs [2]. Contrast com-
puted tomography (CT) is most commonly
used to make a diagnosis, with characteristics
including bowel configuration consisting of a
saclike mass of dilated bowel loops in the
presence of small bowel obstruction, or a
mesenteric “swirl,” related to a mesenteric
vascular pedicle that is engorged, stretched,
displaced, or twisted, along with converging
vessels at the hernia orifice [3].
C. Definitive diagnosis and treatment is via
diagnostic laparoscopy or laparotomy in
cases where bowel dilation precludes safe
port placement, when laparoscopic correc-
tion is unsuccessful or when such skills are
unavailable [4].
825
826 B. LaBarge and A. M. Rogers

Post-bariatric patient with acute

A or recurrent central abdominal
pain, +/– nausea and vomiting

CT scan with oral, +/–

B i.v. contrast

Normal/Non-
Internal hernia Other findings
diagnostic

Symptoms persist Symptoms improve

C Exploration Observe Treat as appropriate

Algorithm 199.1  Reprinted by permission from Springer Nature: Obes Surg. Diagnosis and management of internal
hernias after laparoscopic gastric bypass. Parakh S, Soto E, Merola S. Copyright 2007

2. Martin L, Merkle E, Thompson W. Review of inter-

References
1. Salar O, El-Sharkawy AM, Singh R, et  al. Internal
hernias: a brief review. Hernia. 2013;17(3):373–7.
nal hernias: radiographic and clinical findings. Am J
Roentgenol. 2006;186(3):703–17.
3. Takeyama N, Gokan T, Ohgiya Y, et al. CT of internal
hernias. Radiographics. 2005;25(4):997–1015.
4. Parakh S, Soto E, Merola S. Diagnosis and manage-
ment of internal hernias after laparoscopic gastric
bypass. Obes Surg. 2007;17(11):1498–502.
 Marginal Ulcer: Diagnosis
and Treatment 200
Ye Tian and Ann M. Rogers

Algorithmic Approach ment of these conditions is beyond the scope

A. Marginal ulcer (MU), which occurs at or near B. If upper GI symptoms are present in post-­
the intestinal side of a gastrojejunal anasto-
mosis, is a common complication of Roux-­
en-­Y gastric bypass (RYGB) surgery, seen in
up to 16% of patients. Most MUs are seen
within 1  year after RYGB [1]. Early MU is
likely due to technical issues such as anasto-
motic tension, ischemia, or type of staples or
sutures used but may be related to patient fac-
tors such as diabetes or hypertension. Later
presentations of MUs may be associated with C. Management of uncomplicated MUs includes
smoking, alcohol use, steroid or nonsteroidal
anti-inflammatory drug (NSAID) use, or
larger pouch size [2]. Patients with MUs
commonly present with upper gastrointesti-
nal (GI) symptoms including abdominal pain,
nausea, vomiting, dysphagia, and hemateme-
sis. Fever may also be present [3]. History
and physical exam are the first steps in the
diagnosis of MU. It is important to note that
28–61% of patients report no prior symptoms
and may present with massive bleeding or
perforation of the MU [2]. Emergent treat-
Y. Tian
Penn State Health Milton S. Hershey Medical Center,
Hershey, PA, USA
A. M. Rogers (*)
Department of Surgery, Penn State Milton S. Hershey
Medical Center, Hershey, PA, USA
e-mail: arogers@pennstatehealth.psu.edu
of this algorithm.
RYGB patients, an upper endoscopy should
be the first diagnostic step [3]. Endoscopic
findings may include normal anatomy, MU
alone, MU with associated anastomotic stric-
ture, MU with exposed staples or sutures, or
MU with gastro-gastric fistula [4]. If MU is
present with or without associated findings,
biopsy for Helicobacter pylori (H. pylori)
testing should be performed [5].
3 months of proton pump inhibitor (PPI) +/−
sucralfate. Cessation of smoking and steroid
or chronic NSAID use should be imple-
mented if applicable [2]. If H. pylori testing is
positive, the patient should be treated with
appropriate antibiotic therapy in addition [5].
If anastomotic stricture is identified, then
endoscopic balloon or Bougie dilation of the
stricture should be performed [5]. If exposed
staples or sutures are identified, they should
be removed and associated ulceration should
be treated as above [3]. If gastro-gastric fis-
tula is identified in addition to MU, then elec-
tive interventions to close the fistula are
appropriate.
D. If MU symptoms persist or worsen after
3  months of treatment, or in the setting of
bleeding or perforation, then surgical inter-
vention may be necessary.

© Springer Nature Switzerland AG 2019 827

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_200
828 Y. Tian and A. M. Rogers

History and Physical Exam:

Epigastric abdominal pain, nausea, vomiting, dysphagia, hematemesis +/-fever
A after RYGB surgery

Obtain upper endoscopy

Further work-up

Normal post-
RYGB anatomy What does the MU with
upper endoscopy
B show?
Stricture

Gastro-gastric
fistula with
marginal ulcer

Marginal ulcer

C Cessation of smoking and

Treat MU and NSAID use if applicable Endoscopic balloon
consider closure dilation; initiate 3
of fistula mo therapy with
PPI, +/- sucralfate
Check H. pylori
biopsy result

Initiate 3 mo medical
H. pylori Yes therapy with PPI, +/-
positive? Sucralfate, and eradicate
H pylori

No

Initiate 3 months of medical

therapy with PPI +/-
Sucralfate

Are symptoms
persisting or
worsening?

Algorithm 200.1
200  Marginal Ulcer: Diagnosis and Treatment 829

Yes No
D

Repeat endoscopy Continue medical

therapy for
another 3 months
and discontinue if
asymptomatic

No
MU
present?

Yes

Consider surgical intervention to resect

and reconstruct GJ anastomosis

Follow-up Care

Algorithm 200.1 (continued)

3. Racu C, Mehran A. Marginal ulcers after roux-en-Y

References gastric bypass: pain for the patient…pain for the sur-
geon. Bariatric Times. 2010;7(1):23–5.
1. Steinemann DC, Bueter M, Schiesser M, et  al. 4. Nguyen NT, Hinojosa MW, Gray J, Fayad
Management of anastomotic ulcers after roux-en-Y C. Reoperation for marginal ulceration. Surg Endosc.
gastric bypass: results of an international surgery. 2007;21:1919–21.
Obes Surg. 2014;24:741–6. 5. Chaves LCL, Borges IKLC, de Souza MDG, et  al.
2. Coblijn UK, Lagarde SM, de Castro Inflammatory disorders associated with helicobacter
SMM.  Symptomatic marginal ulcer disease after pylori in the roux-en-Y gastric pouch. Arq Bras Cir
roux-en-Y gastric bypass: incidence, risk factors and Dig. 2016;29(Suppl 1):31–4.
management. Obes Surg. 2015;25:805–11.
 Ventral Hernia Repair in Bariatric
Patients
Anish Shah and Salvatore Docimo Jr.
Algorithmic Approach
A. The risk of ventral hernia development
increases from 13% to 39% for patients
with body mass index (BMI)  >  25  kg/m2.
An increased incidence of ventral hernias
in these patients is secondary to elevated
intra-­abdominal pressure as well as systemic
hypertension often seen with morbid obesity.
In patients undergoing open gastric bypass
surgery, the incidence of incisional hernias
has been reported to be as high as 20%. With
laparoscopic bariatric surgery, this rate has
decreased to less than 1%. The first step in
managing ventral hernias in bariatric patients
is determining the presence and severity of an
obstruction based on a complete history and
physical exam. Because physical exam can be
limited in bariatric patients, further imaging
can help in the evaluation of hernias in this
patient population. Particularly, computed
tomography (CT) can be useful in monitoring
hernias over time and determining the extent
of any underlying obstruction.
A. Shah
Department of Surgery, Stony Brook University
Hospital, Stony Brook, NY, USA
S. Docimo Jr. (*)
Division of Bariatric, Foregut, and Advanced
Gastrointestinal Surgery, Stony Brook Medicine,
Stony Brook, NY, USA
e-mail: salvatore.docimo@stonybrookmedicine.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_201
201
B. Once the need for acute surgical intervention
for hernia repair in bariatric patients is ruled
out, careful consideration must be given to the
timing and feasibility of hernia surgery. Hernia
repair in the obese patient has been associated
with complications such as surgical site infec-
tion and recurrence [1, 2]. As a result, it is
important to determine whether hernia repair
can be delayed, what the safest and most effec-
tive surgical approach would be, and whether
the patient qualifies for weight loss surgery.
C. If a ventral hernia is known prior to bariat-
ric surgery, the surgeon has three options:
(1) perform planned bariatric surgery and
defer hernia repair to a later time; (2) per-
form the bariatric surgery and hernia repair
simultaneously; (3) repair the hernia first
and then perform bariatric surgery at a later
time. However, the third option is only viable
if the hernia becomes clinically significant
(obstructed, incarcerated, and strangulated)
prior to bariatric surgery.
D. Significant weight loss is the benefit of per-
forming bariatric surgery prior to ventral her-
nia repair. In setting of open ventral hernia in
the obese patient, the incidence of compli-
cations (surgical site infection (SSI), recur-
rence, cardiovascular, pulmonary) has been
directly correlated to the rise in BMI [1, 3].
An evaluation of BMI and ventral hernia dem-
onstrated that patients with a BMI  >  40  kg/
m2 had a 2.89 times greater chance of h­ aving
 A. Shah and S. Docimo Jr.

a ­
complication compared to a group with
BMI < 25 kg/m2 [4].
E. In bariatric patients with a hernia causing
worsening symptoms, it is reasonable to per-
form the hernia repair first and defer bariat-
ric surgery until recovery. However, it is key
that this time is short so that recurrence is
unlikely.

Patient undergoing bariatric surgery with a

concomitant hernia
A

History, physical exam, radiography to

evaluate hernia characteristics

Symptomatic hernia: obstruction,

incarceration, strangulation Asymptomatic hernia

Obstructed or BMI > 40 kg/m2 BMI < 40 kg/m2 C

Strangulated or
incarcerated
contaminated case
hernia

Weight loss prior to Concomitant

ventral hernia repair: hernia and D
surgical or medicinal bariatric surgery
Open or LVHR: Open or LVHR:
fascial closure Fascial closure
with mesh with no mesh
Ventral hernia Concomitant
repair after adequate hernia and
weight loss bariatric surgery: E
Bariatric surgery Bariatric surgery
fascial closure
with mesh

Algorithm 201.1
201  Ventral Hernia Repair in Bariatric Patients

References elective abdominal surgery based on 12,373 cases.

The case for targeted prophylactic intervention. Ann
Surg. 2016;263:1010–7.
1. Veljkovic R, Protic M, Gluhovic A, et al. Prospective
3. Flancbaum L, Choban PS.  Surgical implications of
clinical trial of factors predicting the early develop-
obesity. Annu Rev Med. 1998;49:215–34.
ment of incisional hernia after midline laparotomy. J
4. Pernar LIM, Pernar CH, Dieffenbach BV, Brooks
Am Coll Surg. 2010;210:210–9.
DC, Smink DS, Tavakkoli A. What is the BMI thresh-
2. Fischer JP, Basta MN, Mirzabeigi MN, et al. A risk
old for open ventral hernia repair? Surg Endosc.
model and cost analysis of incisional hernia after
2017;31(3):1311–7.
 Acute Leak Following Bariatric
Surgery: Endoscopic Stent
Management
Salvatore Docimo Jr.
Algorithmic Approach
A. The occurrence of anastomotic and staple line
leak is 1.6–4.8% after laparoscopic roux-en-y
gastric bypass (LRYGB) and 1.7–2.4% after
laparoscopic sleeve gastrectomy (LSG),
respectively [1–3]. Patients often present with
complaints of abdominal pain, fever, chills,
and possible nausea and vomiting. Vitals
typically demonstrate tachycardia, fever,
­ treatment paradigm to follow. If a patient
tachypnea, and possibly hypotension. A leuko-
cytosis is often noted. Typical surgical options
for leak management include anastomotic
revision, primary repair, and bowel, gastric, or
omental patching [4]. Flexible endoscopy has
recently emerged as both diagnostic and thera-
peutic options in the setting of acute leaks. A
covered (full or partial) self-expanding metal
stent is the ideal type to be utilized.
B. Sleeve Gastrectomy Leaks: Most sleeve gas-
trectomy leaks occur in the proximal third of
the stomach (75–89%) [5], carry a mortality
rate of 0.11–9.0%, and occur at a mean of
7 days [6]. Risk factors for a leak include isch-
emia at the proximal portion of the staple line,
previous gastric surgery, and an area of steno-
S. Docimo Jr. (*)
Division of Bariatric, Foregut, and Advanced
Gastrointestinal Surgery, Stony Brook Medicine,
Stony Brook, NY, USA
e-mail: salvatore.docimo@stonybrookmedicine.edu
© Springer Nature Switzerland AG 2019
S. Docimo, E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_202
202
sis within the gastric sleeve causing an increase
of proximal intraluminal pressure [7]. The
optimal diagnostic modality is a contrast com-
puted tomography (CT) as it offers improved
sensitivity and additional information such as
possible fluid collections in the left upper
quadrant or free intraperitoneal air [8].
C. Once a leak is confirmed, peritonitis or septic
shock will play a large role in deciding which
demonstrates septic shock or peritonitis, intra-
operative management with surgical explora-
tion should be the first line of treatment. If the
patient is stable, leaks in the proximal or mid-
portion of the sleeve are most amenable to
treatment with a stent [9, 10]. Any abscess that
is associated with a sleeve gastrectomy leak
will require radiographic drainage if a stent is
being utilized as treatment. In a study of 21
SG leak cases, 71% of patients treated with a
stent noted leak closure in 55  days. Of the
remaining six patients, five noted leak resolu-
tion at 128 days [11].
D. Roux-en-Y Leaks: Leaks most commonly
occur at the gastrojejunal anastomosis (70–
80%), at the gastric pouch (10–15%), at the
jejuno-jejunal anastomosis (5%), and at the
gastric remnant (3–5%) [12]. Factors such as
excess tension, staple-line malformation, and
ischemia all play a role in leak occurrence.
Evaluation of a suspected leak following a
Roux-en-Y gastric bypass includes an
835
836
upper gastrointestinal (GI) contrast study
or a contrast computed tomography (CT)
scan. An upper GI study has demonstrated a
sensitivity and specificity of 79.4% and 95%,
whereas a contrast CT scan has demonstrated
a sensitivity and specificity of 95% and 100%
[13]. Leaks noted at the gastrojejunal anasto-
mosis are amenable to treatment with stent
deployment. Jejuno-jejunal anastomosis
leaks are often not amenable to treatment
with a stent due to the difficulty to access the
site and also stent migration. A retrospective
review of 35 Roux-en-Y patients who under-
went stent placement for gastrojejunal leaks
notes complete closure in 30 cases on con-
trast studies [14].
S. Docimo Jr.
E. Postoperative Care: An upper GI is obtained
following placement of an endoscopic stent.
If no leak is noted, the patient is started on a
clear liquid diet. Stents are typically left in
position for at least 2 weeks. Stent migration
is noted in 5–62% of cases [15–18] requiring
endoscopic repositioning. A well-embedded
stent due to hyperplastic mucosal growth may
be treated with argon plasma coagulation of
the hyperplastic tissue. A second option
includes the “stent-in-stent” method whereby
a new stent of the same diameter and length is
placed within the first stent. Radial tension on
the hyperplastic mucosa causes ischemia and
necrosis. Both stents are then removed
1–2 weeks later [19].
202  Acute Leak Following Bariatric Surgery: Endoscopic Stent Management 837

Recent history of a Roux-en-Y gastric bypass or sleeve

gastrectomy. Patient presents with complaints of abdominal pain.

A
· Vital signs: possible tachycardia, hypotension, fever, and tachypnea
· Laboratory analysis: leukocytosis
· Physical exam: likely will demonstrate abdominal pain

No

Patient Stable? · Resuscitation and operative intervention

B Yes

· Demonstration of a Leak within

· CT Scan with PO/IV Contrast
· Localize Leak if possible
the sleeve or gastro-jejunal D
C anastomosis
· Evaluate for an abscess

Yes
· CT guided drainage · Abscess?

No

· Endoscopic placement of a self-

· UGI to evaluate for leak occlusion
expanding covered metal stent

· Continued Leak
· Leak is occluded
E
· Endoscopic re-positioning or
placement of a second stent
· Any change in clinical status
warrants evaluation of stent
position with an UGI or X-ray

· Difficult removal due to mucosal

· Remove in 2 weeks.
hyperplasia during initial removal

· Argon plasma coagulation of hyperplastic mucosa and

immediate removal of stent
· Stent-in-stent with removalin 2 weeks of both stents

Algorithm 202.1
838 S. Docimo Jr.

References 10. Martin-Malagon A, Rodriguez-Ballester L, Arteaga-­

Gonzalez I.  Total gastrectomy for failed treatment
with endotherapy of chronic gastrocutaneous fis-
1. Whitlock KA, Gill RS, Ali T, et al. Early outcomes of
tula after sleeve gastrectomy. Surg Obes Relat Dis.
roux-en-Y gastric bypass in a publically funded obe-
2011;7:240–2.
sity program. ISRN Obes. 2013;2013:296597.
11. El Mourad H, Himpens J, Verhofstadt J. Stent treat-
2. van Rutte PW, Smulders JF, de Zoete JP, et  al.
ment for fistula after obesity surgery: results in 47
Outcome of sleeve gastrectomy as a primary bariatric
consecutive patients. Surg Endosc. 2013;27:808–16.
procedure. Br J Surg. 2014;101(6):661–8.
12. Lo Menzo E, Szomstein S, Rosenthal RJ. Laparoscopic
3. Weiner RA, El-Sayes IA, Theodoridou S, et  al.
gastric bypass: management of complications. In:
Early post operative complications: incidence, man-
Brethauer SA, Schauer PR, Schirmer BD, edi-
agement, and impact on length of hospital stay.
tors. Minimally invasive bariatric surgery. 2nd ed.
A retrospective comparison between laparoscopic
New York: Springer; 2015. p. 261–9.
gastric bypass and sleeve gastrectomy. Obes Surg.
13. Bingham J, Shawhan R, Parker R, Wigboldy J, Sohn
2013;23(12):2004–12.
V. Computed tomography scan versus upper gastroin-
4. Andrade JE, Martinez JM. Management of postsurgi-
testinal fluoroscopy for diagnosis of staple line leak fol-
cal leaks and fistulae. In: Thompson C, Ryan MB, edi-
lowing bariatric surgery. Am J Surg. 2015;209(5):810–4.
tors. Bariatric endoscopy. New York: Springer; 2013.
14. Salinas A, Baptista A, Santiago E, Antor M, Salinas
p. 91–101.
H. Self-expandable metal stents to treat gastric leaks.
5. Aurora AR, Khaitan L, Saber AA. Sleeve gastrectomy
Surg Obes Relat Dis. 2006;2:570–2.
and the risk of leak: a systematic analysis of 4,888
15. Puli SR, Spofford IS, Thompson CC.  Use of self-­
patients. Surg Endosc. 2012;26(6):1509–15.
expandable stents in the treatment of bariatric sur-
6. Sakran N, Goitein D, Raziel A, Keidar A, Beglaibter
gery leaks: a systematic review and meta-analysis.
N, Grinbaum R, et  al. Gastric leaks after sleeve
Gastrointest Endosc. 2012;75(2):287–93.
gastrectomy: a multicenter experience with 2,834
16. Ross AS, Kozarek RA. Esophageal stents: indications
patients. Surg Endosc. 2013;27(1):240–5.
and placement techniques. Self-expandable stents in
7. Kim J, Azagury D, Eisenberg D, DeMaria E, Campos
GI tract. In: Kozarek R, Baron T, Song H, editors.
GM. ASMBS position statement on prevention, detec-
Self-expandable stents in the gastrointestinal tract.
tion, and treatment of gastrointestinal leak after gastric
New York: Springer; 2013. p. 129–40.
bypass and sleeve gastrectomy, including the roles of
17. Eisendrath P, Cremer M, Himpens J, et al. Endotherapy
imaging, surgical exploration, and nonoperative man-
including temporary stenting of fistulas of the upper
agement. Surg Obes Relat Dis. 2015;11(4):739–48.
gastrointestinal tract after laparoscopic bariatric sur-
8. Prathanvanich P, Chand B.  Laparoscopic sleeve
gery. Endoscopy. 2007;39:625–30.
gastrectomy: management of complications. In:
18. Efthimiou E, Stein L, Szego P, et al. Stent migration
Brethauer SA, Schauer PR, Schirmer BD, edi-
causing alimentary limb obstruction necessitating
tors. Minimally invasive bariatric surgery. 2nd ed.
laparotomy and surgical stent extraction. Surg Obes
New York: Springer; 2015. p. 151–71.
Relat Dis. 2009;5:375–7.
9. de Aretxabala X, Leon J, Wiedmaier G, Turu I,
19. Aiolfi A, Bona D, Ceriani C, Porro M, Bonavina

Ovalle C, Maluenda F, Gonzalez C, Humphrey J,
L.  Stent-in-stent, a safe and effective technique to
Hurtado M, Benavides C.  Gastric leak after sleeve
remove fully embedded esophageal metal stents:
gastrectomy: analysis of its management. Obes Surg.
case series and literature review. Endosc Int Open.
2011;21:1232–7.
2015;3(4):E296–9.
 Vitamin and Micronutrient
Deficiencies After Bariatric
Surgery
Salvatore Docimo Jr.
Algorithmic Approach
A preoperative assessment of micronutrients
prior to bariatric surgery demonstrated deficien-
cies of zinc (24.6%), vitamin B12 (18.1%), mag-
nesium (6.9%), phosphorous (4.7%), folic acid
(3.4%), and vitamin D (25.4%) [1]. These miner-
als are cofactors vital to functions of appetite,
metabolism, nutrient absorption, glucose homeo-
stasis, and neural activities [2]. Procedures such
as Roux-en-Y gastric bypass and biliopancreatic
diversion with or without duodenal switch are
inherently at risk for deficiencies such as vitamin
B12, calcium, iron, as well as vitamins A, D, E,
and K [2, 3]. However, sleeve gastrectomy
patients are not without nutrient deficiency [4].
A. The initial work-up of any patient under con-
sideration for bariatric surgery should include
a full laboratory assessment of micronutrients.
Postoperatively, evaluation of micronutrients
should take place at 3 months. A patient with
a history of bariatric surgery who is newly
enrolled into our program will undergo labo-
ratory evaluation for micronutrient derange-
ments. A history and physical examination
S. Docimo Jr. (*)
Division of Bariatric, Foregut, and Advanced
Gastrointestinal Surgery, Stony Brook Medicine,
Stony Brook, NY, USA
e-mail: salvatore.docimo@stonybrookmedicine.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_203
203
should be completed in order to narrow one’s
differential diagnoses.
B. Thiamin: Absorbed in the proximal small
intestine, it plays a role in the metabolism of
carbohydrates and can quickly be depleted in
the setting of intractable vomiting. Prolonged
deficiency can lead to Wernicke’s encepha-
lopathy with concern for visual disturbances,
ataxia, peripheral neuropathy, memory loss,
and confusion. Thiamin supplementation,
including IV infusion, is required [2].
C. Vitamin B12: Roux-en-Y gastric bypass
patients are at a high risk for vitamin B12
deficiency due to incomplete digestion and
release of B12 from proteinaceous food [2,
3]. Vitamin B12 deficiency measured at 1 and
3 years postoperatively in sleeve gastrectomy
patients demonstrated a 10–26% prevalence
[5]. Patients may experience parenthesis of
the limbs and macrocytic anemia. Treatment
involves 700–2000 mcg of vitamin B12
weekly [6].
D. Folic Acid: Folic acid is absorbed in the
proximal small bowel. Poor oral intake, lack
of adherence to vitamin regimen, malabsorp-
tion, and medications such as anticonvulsants
and oral contraceptives can lead to deficiency
[7]. Symptoms of deficiency lead to fatigue,
headaches, diarrhea, and palpitations [2].
Treatment involves 1 mg/day of folic acid [8].
E. Iron: Obesity itself increases the risk of iron
deficiency due to low-grade inflammation
839
840
and induction of hepcidin, which blocks iron
absorption proteins [9], making iron defi-
ciency prevalent prior to surgery. Iron defi-
ciency has been noted in 10% of sleeve
gastrectomy patients [5]. Symptoms of defi-
ciency include cravings for ice, pallor, leth-
argy, koilonychias, and anemia [8]. Total
iron-binding capacity or serum transferrin
receptors are better measures of iron defi-
ciency compared with serum iron or ferritin
[10]. Supplementation of two daily vitamins
(for a total of 36  mg of iron) is sufficient.
Anemia may require additional supplemen-
tation [2].
F. Calcium and Vitamin D: Calcium functions in
cell signaling and the mineralization of bone
and teeth and vitamin D functions in the
homeostasis of calcium via absorption of cal-
cium in the small intestines [11, 12]. Calcium
deficiency can lead to low bone density, osteo-
porosis, muscle contractions, spasms, and
parenthesis. Recommendations are for daily
supplementation of 1200–1500  mg calcium
and 3000 international units of vitamin D [13].
G. Copper: Copper is an essential cofactor in
many enzymes that function in electron trans-
fers. These enzymes include cytochrome c
S. Docimo Jr.
oxidase (electron transport chain), superox-
ide dismutase (antioxidant), amine oxidases
(synthesis of neurotransmitter norepineph-
rine), and lysyl oxidase (involved in collagen
crosslinking) [cousin RJ, allied health].
Severe deficiency of copper may present as
unsteady gait, extremity numbness, parenthe-
sis, or paralysis [cousins RJ]. In some cases,
copper deficiency can be misdiagnosed as an
iron or vitamin B12 deficiency, delaying
proper copper replacement.
H. Zinc: Zinc is a cofactor for enzymes utilized
in protein synthesis, digestion, immunity,
and gene transcription [14]. Zinc absorption
requires an acidic environment and is absorbed
in the proximal intestines. Deficiency presents
as hair loss, poor wound healing, and changes
of taste perception [10]. Excess zinc can cause
sequestration of copper in the gut enterocytes,
preventing the uptake of copper [14]. Zinc
supplementation requires 1 mg of copper for
every 8–15 mg of zinc [13].
I. All micronutrient derangements should be
managed to improve any acute symptoms.
Long-term micronutrient replacement with
daily vitamins is of critical importance and
should be stressed for the patient.
203  Vitamin and Micronutrient Deficiencies After Bariatric Surgery 841

A patient undergoing bariatric surgery or presenting with acute

symptomatology not explained by an anatomical abnormality

· Any preoperative micronutrient and vitamin deficiencies should be replaced

· A history and physical examination is utilized to narrow the possible micronutrient deficiency

· Visual disturbance,
ataxia, peripheral Thiamin
B deficiency
neuropathy, memory
loss, confusion

· Parathesias of limbs,
C macrocytic anemia Vitamin B12
deficiency

D · Fatigue, headache,
diarrhea, palpatations Folic Acid
deficiency

· Pallor, lethargy,
Draw blood Iron
E koilonychias, anemia,
samples deficiency
craving for ice

· Low bone density, Calcium &

F osteoporosis, muscle vitamin D
contractions, spasms deficiency

· Unsteady gait, extremity

G numbness, parathesiasis, Copper
paralysis deficiency

· Hair loss, poor wound

H healing, change in taste Zinc
perception deficiency

· Treat all acute deficiencies

with replacement
I · Maintenancewith daily
vitamin use

Algorithm 203.1
842 S. Docimo Jr.

References 9. Cepeda-Lopez AC, Aeberli I, Zimmermann MB. Does

obesity increase the risk for iron deficiency? A review
of the literature and the potential mechanisms. Int J
1. Ernst B, Thurnheer M, Schmid SM, Schultes
Vitam Nutr Res. 2010;80:263–70.
B. Evidence for the necessity to systematically assess
10. Zimmermann MB, Hurrell RF. Nutritional iron defi-
micronutrient status prior to bariatric surgery. Obes
ciency. Lancet. 2007;370:511–24. Hoffman HNI,
Surg. 2009;19(1):66–73.
Phyliky RL, Fleming CR. Zinc-induced copper defi-
2. Allied Health Sciences Section Ad Hoc Nutrition
ciency. Gastroenterology. 1988;94:508–12.
Committee, Aills L, Blankenship J, Buffington C,
11. Wood RJ.  Calcium and phosphorus. In: Stipanuk

Furtado M, Parrott J. ASMBS allied health nutritional
MH, editor. Bio- chemical and physiological aspects
guidelines for the surgical weight loss patient. Surg
of human nutrition. Philadelphia: Elsevier; 2000.
Obes Relat Dis. 2008;4(5 Suppl):S73–108.
p. 643–70.
3. Bloomberg RD, Fleishman A, Nalle JE, Herron
12. Weaver CM, Fleet JC. Vitamin D requirements: cur-
DM, Kini S.  Nutritional deficiencies following bar-
rent and future. Am J Clin Nutr. 2004;80:S1735–9.
iatric surgery: what have we learned? Obes Surg.
13. Mechanick JI, Youdim A, Jones DB, Garvey WT,

2005;15(2):145–54. Review.
Hurley DL, McMahon MM, Heinberg LJ, Kushner
4. Schweiger C, Weiss R, Keidar A. Effect of different
R, Adams TD, Shikora S, et  al. Clinical practice
bariatric operations on food intolerance and quality of
guidelines for the perioperative nutritional, meta-
eating. Obes Surg. 2010;20:1393–9.
bolic, and nonsurgical support of the bariatric sur-
5. Himpens J, Dapri G, Cadière GB. A prospective, ran-
gery patient-2013 update: cosponsored by American
domized study between laparoscopic gastric banding
Association of Clinical Endocrinologists, The
and laparoscopic isolated sleeve gastrectomy: results
Obesity Society, and American Society for Metabolic
after 1 and 3 years. Obes Surg. 2006;16(11):1450–6.
and Bariatric Surgery. Obesity (Silver Spring).
6. Kaplan LM.  Pharmacological therapies for obesity.
2013;21(Suppl 1):S1–27.
Gastroenterol Clin N Am. 2005;34:91–104.
14. Cousins RJ, Blanchard RK, Moore JB, Cui L,

7. Charney P, Malone A, editors. ADA pocket guide to
Green CL, Liuzzi JP, Cao J, Bobo JA.  Regulation
nutrition assessment. Chicago: American Dietetic
of zinc metabolism and genomic outcomes. J Nutr.
Association; 2004.
2003;133:S1521–6.
8. Malinowski SS.  Nutritional and metabolic com-
plications of bariatric surgery. Am J Med Sci.
2006;331:219–25.
 Part XXIV
Pregnancy and General Surgery
 Pregnancy and Cholelithiasis
Jaimey M. Pauli
Algorithmic Approach
A. Gallstones are present in 1–3% of pregnant
women, although approximately 50% of
them are asymptomatic [1]. Pregnant and
postpartum women are predisposed to gall-
stone formation due to the hormonal effects
of estrogen and progesterone that increase
cholesterol secretion and decrease soluble
bile acid secretion. Additionally, progester-
one also decreases smooth muscle contractil-
ity and slows gallbladder emptying. Up to
30% of pregnant women have biliary sludge,
which develops into gallstones, on ultra-
sound. Risk factors for cholelithiasis include
obesity, multiparity, and increasing gesta-
tional age [2]. Complications of gallbladder
disease are the second most common reason
for non-obstetric surgery in the pregnant
patient and the most common non-obstetric
cause of hospitalization in the first postpar-
tum year [2, 3].
B. Gallstones cause biliary colic, acute chole-
cystitis, gallstone pancreatitis, choledocho-
lithiasis, gallstone ileus, and cholangitis.
Signs and symptoms include intermittent
right upper quadrant pain, nausea, vomiting,
J. M. Pauli (*)
Maternal-Fetal Medicine, Department of Obstetrics
and Gynecology, Penn State Health Milton S.
Hershey Medical Center, Hershey, PA, USA
e-mail: jpauli@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_204
204
epigastric pain, anorexia, intolerance of fatty
foods, fever, elevated white blood cell count,
elevated amylase and lipase, elevated AST
and ALT, jaundice, and positive Murphy’s
sign (pain with deep inspiration on palpation
or ultrasound examination of the right upper
quadrant in the area of the gallbladder fossa).
It is imperative that other potentially life-­
threatening pregnancy-related diagnoses are
considered on the differential of right upper
quadrant pain, including preeclampsia;
hemolysis, elevated liver enzymes, and low
platelet count (HELLP) syndrome; placental
abruption; uterine rupture; acute fatty liver
of pregnancy; and myocardial infarction [4].
Fetal monitoring should occur during evalu-
ation as appropriate for gestational age per
obstetrics.
C. Ultrasound has 95–98% accuracy in diagnos-
ing cholelithiasis [2, 5]. Findings of cholecys-
titis are thickened gallbladder wall (>3–5 mm)
or edema, presence of gallstones, perichole-
cystic fluid, and a sonographic Murphy’s sign
[1, 5]. Other imaging that may be useful for
the diagnosis and treatment of small or extra-
hepatic stones includes endoscopic retro-
grade cholangiopancreatography (ERCP),
which has minimal radiation exposure (300
mrad) in an acceptable range for pregnancy
after the first trimester [1]. Non-contrast
845
846
magnetic resonance cholangiopancreatogra-
phy (MRCP) may also be considered in com-
plex cases.
D. Surgical intervention via laparoscopic or
open cholecystectomy (see algorithm for
“Cholecystectomy of the Pregnant Patient”)
is clearly indicated for obstructive jaundice,
acute cholecystitis failing medical manage-
ment (approximately one-fourth of patients
with cholecystitis), gallstone pancreatitis,
or suspected peritonitis [3, 6]. The appropri-
ate management of symptomatic cholelithi-
asis and biliary colic is less clear, particularly
since there is a hesitancy to operate on preg-
nant patients [2, 6]. Conservative manage-
ment includes intravenous hydration, bowel
rest, and pain management, with broad-­
J. M. Pauli
spectrum antibiotics for patients with sys-
temic signs [1, 4–6].
E. Lu et  al. demonstrated that if conservative
management is chosen for gallstone disease
in pregnancy, there is a 38% chance of sub-
optimal outcome, with a 34% risk of relapse
and increased severity of disease at relapse
[6]. Although there is a higher risk for pre-
term contractions with operative manage-
ment, there is a higher rate of preterm
delivery, induction of labor for symptoms,
and cesarean delivery with non-operative
management. Consideration for definitive
surgical management of gallstone disease
during pregnancy, especially in the first and
second trimesters, has further been supported
by other authors [1].
204  Pregnancy and Cholelithiasis 847

History:
A Pregnant
Right upper quadrant pain +/– nausea/vomiting/fever

Obtain vital signs, blood work, and perform a physical examination

B Consider fetal monitoring depending on gestational age

+ Fever, leukocytosis, abnormal labs

+ Murphy’s sign
No evidence of pregnancy related diseases(HELLP,
preeclampsia, etc.)

Ultrasound
C

Thickened gallbladder wall or edema No gross abnormalities:

Gallstones consider ERCP or MRCP to
Pericholecystic fluid evaluate/treat small stones or
Sonographic Murphy’s sign extrahepatic stones
D

Obstructive jaundice Biliary colic

Gallstone pancreatitis Acute cholecystitis
Peritonitis

Immediate Conservative management:

cholecystectomy IVF, bowel rest, narcotics
(open or laparoscopic) +/– antibiotics

E Symptoms worsen or recur

Symptoms improve:
plan postpartum followup

Algorithm 204.1
848 J. M. Pauli

References 4. Sharp HT. The acute abdomen during pregnancy. Clin

Obstet Gynecol. 2002;45(2):405–13.
5. Diegelmann L. Nonobstetric abdominal pain and sur-
1. Gilo NB, Amini D, Landy HJ.  Appendicitis and
gical emergencies in pregnancy. Emerg Med Clin N
cholecystitis in pregnancy. Clin Obstet Gynecol.
Am. 2012;30:885–901.
2009;52(4):586–96.
6. Lu EK, Curet MJ, El-Sayed YY, Kirkwood KS. Medical
2. Williamson C, Mackillop L, Heneghan MA. Diseases
versus surgical management of biliary tract disease in
of the liver, biliary system, and pancreas. In: Creasy
pregnancy. Am J Surg. 2004;188:755–9.
and Resnik’s maternal fetal medicine: principles and
practice. 7th ed. Philadelphia: Elsiever; 2014.
3. Date RS, Kaushal M, Ramesh A.  A review of the
management of gallstone disease and its complica-
tions in pregnancy. Am J Surg. 2008;196(4):599–608.
 Pregnancy and Appendicitis
Emily Smith and Jaimey M. Pauli
Algorithmic Approach
A. Evaluation of possible appendicitis in preg-
nancy begins with a thorough history and
physical examination. Right lower quadrant
pain, even in pregnancy, is still the most com-
mon presenting symptom (regardless of ges-
tational age) [1, 2]. However, the differential
diagnosis should also include cholecystitis,
pancreatitis, gastroenteritis, right lower lobe
pneumonia, ovarian torsion, uterine myoma
degeneration, pyelonephritis, urinary tract
infection (UTI), and round ligament pain [3].
B. Vital signs, blood work, and physical exami-
nation are the foundation of diagnosis; how-
ever, in pregnancy, some abnormalities, such
as mild tachycardia and leukocytosis, can be
normal physiologic changes [1]. Additionally,
the Rovsing and Psoas signs are not clinically
significant [4]. Urine analysis should be con-
sidered in order to eliminate urinary tract
infection as the source of symptoms. Chest
X-ray should also be considered to rule out
E. Smith
Maternal-Fetal Medicine, Department of Obstetrics
and Gynecology, Medical College of Wisconsin,
Milwaukee, WI, USA
J. M. Pauli (*)
Maternal-Fetal Medicine, Department of Obstetrics
and Gynecology, Penn State Health Milton S.
Hershey Medical Center, Hershey, PA, USA
e-mail: jpauli@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_205
205
right lower lobe pneumonia [4]. Consider an
obstetrical consult for fetal evaluation and
evaluation for obstetrical or gynecologic
etiologies.
C. Further imaging in pregnancy to demonstrate
an inflamed appendix is complicated by the
need to minimize radiation exposure to the
fetus [5]. Ultrasound is the first-choice imag-
ing modality. Unfortunately, ultrasound accu-
racy may be operator dependent, and as
gestational age increases, the appendix is fre-
quently not visualized [5]. MRI without gad-
olinium has no known adverse fetal effects
[6]. It also has a high negative predictive
value [7].
D. Treatment for appendicitis in pregnancy is
appendectomy [8]. Early intervention (opera-
tion within 24 h of presentation) is associated
with better outcomes [9]. Unlike non-­
pregnant appendicitis, conservative manage-
ment with antibiotics is not currently
considered appropriate [8]. More extensive
studies in support of conservative manage-
ment are currently ongoing [8].
E. The surgical approach may be either open or
laparoscopic depending on both surgeon
preference and the size of the gravid uterus,
which limits the placement of laparoscopic
ports [10]. If there is a concern for uterine
injury when placing Veres needle for insuffla-
tion, a Hassan/open entry should be consid-
ered [11]. Other considerations are to use a
849
850
midline incision if peritonitis is suspected
and to keep intraabdominal pressures
<12  mmHg during laparoscopy. All patients
for appendectomy should receive ­preoperative
antibiotics (second-generation cephalospo-
rin, extended-spectrum penicillin, or triple-
agent therapy) [8]. Continuous fetal
monitoring during surgery and corticosteroid
administration for fetal lung maturity after
fetal viability (generally defined as
23–24 weeks) should be considered if feasi-
ble. Preparations for emergent cesarean deliv-
ery if indicated should be made by the
obstetrical service.
F. Women diagnosed with appendicitis in
pregnancy should be counseled about the
E. Smith and J. M. Pauli
increased risk of preterm delivery or fetal
loss [8]. Appendiceal perforation, which is
most likely to occur in the third trimester,
determines the risk of fetal loss (1.5%
without perforation versus up to 36% with
perforation) [9]. Although the rate of pre-
term contractions after appendectomy is as
high as 83%, the rate of preterm labor and
delivery is much lower at 5–14% [9].
Tocolytic therapy, although not proven to
be effective, may be considered by the
obstetrical consultants. Monitoring for
fetal well-being and labor symptoms
should occur in the postoperative period,
with frequency and intensity determined
by gestational age.
205  Pregnancy and Appendicitis 851

History and physical exam:

A Right lower quadrant pain in pregnancy

Obtain vital signs, blood work and perform a physical

examination
B Consider chest x-ray and urinalysis
Obstetrical consult
Fetal monitoring

Unable to suggest etiology other than appendicitis. Obtain imaging.

C Ultrasound

Normal ultrasound Unable to visualize appendix

(appendix visualized) and no other pelvic pathology

Continue to monitor
Consider other MRI
etiologies

Abnormal appendix Normal appendix

Continue to monitor
D Pre-operative antibiotics
Consider other
Corticosteroids
Appendectomy (open or laparoscopic) etiologies
Fetal monitoring
E

Postoperative care:
Counseling about risk of fetal loss or preterm labor
F Fetal monitoring
Tocolytic therapy if indicated

Algorithm 205.1
852 E. Smith and J. M. Pauli

References 2004 update and revisions. AJR Am J Roentgenol.

2004;182:1111–4.
7. Long SS, Long C, Lai H, et al. Imaging strategies for
1. Mourad J, Elliott JP, Erickson L, et  al. Appendicitis
right lower quadrant pain in pregnancy. AJR Am J
in pregnancy: new information that contradicts
Roentgenol. 2011;196:4–12.
long-held clinical beliefs. Am J Obstet Gynecol.
8. De Franca NA, Ramos do Amorim M, Nobrega
2000;182:1027–9.
SV.  Acute appendicitis in pregnancy: literature
2. Tracey M, Fletcher HS.  Appendicitis in pregnancy.
review. Rev Assoc Med Bras. 2015;61(2):170–7.
Am Surg. 2000;66:555–9.
9. Sharp HT. The acute abdomen during pregnancy. Clin
3. Weingold AB. Appendicitis in pregnancy. Clin Obstet
Obstet Gynecol. 2002;45(2):405–13.
Gynecol. 1983;26:801–9.
10. Affleck DG, Handrahan DL, Egger MJ, et al. The lap-
4. Al-Mulhim AA.  Acute appendicitis in pregnancy: a
aroscopic management of appendicitis and cholelithi-
review of 52 cases. Int Surg. 1996;81:295–7.
asis during pregnancy. Am J Surg. 1999;178:523–9.
5. Williams R, Shaw J. Ultrasound scanning in the diag-
11. Friedman JD, Ramsey PS, Ramin KD, et  al.

nosis of acute appendicitis in pregnancy. Emerg Med
Pneumoamnion and pregnancy loss after second-­
J. 2007;24:359–60.
trimester laparoscopic surgery. Obstet Gynecol. 2002;
6. Kanal E, Borgstede JP, Barkovich AJ, et al. American
99:512–3.
College of Radiology White Paper on MR safety:
 Pregnancy and Breast Cancer
James M. O’Brien and Jaimey M. Pauli
Algorithmic Approach
A. The definition of pregnancy-associated breast
cancer is cancer diagnosed during pregnancy
itself, within the first postpartum year, or any
time during lactation, and has an incidence of
15–35/100,000 deliveries [1, 2]. Breast can-
cer remains one of the most common cancers
in the pregnant population, with up to 20% of
breast cancer in women less than 30  years
being associated with pregnancy [3]. The
majority of breast cancer associated with
pregnancy is infiltrating ductal adenocarci-
noma and is predominately poorly differenti-
ated and advanced at the time of diagnosis.
There is additionally a lower incidence of
hormone receptor positivity seen in
pregnancy-­associated breast cancer [4, 5].
B. Diagnosis is often challenging due to normal
physiological changes which occur in breast
tissue during pregnancy such as engorgement
and hypertrophy. Rarely an early diagnosis is
suspected and aided by a phenomenon called
the milk rejection sign, in which a nursing
infant refuses breast milk with occult carci-
noma [6].
J. M. O’Brien · J. M. Pauli (*)
Maternal-Fetal Medicine, Department of Obstetrics
and Gynecology, Penn State Health Milton S.
Hershey Medical Center, Hershey, PA, USA
e-mail: jpauli@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_206
206
Mammography is not contraindicated in
pregnancy as long as there is abdominal
shielding, although breast ultrasound is often
the first image modality ordered in pregnancy
[2]. MRI itself is not contraindicated,
although gadolinium should be avoided in
pregnancy due to its association with adverse
fetal and neonatal events. Other diagnostic
methods such as chest X-ray with abdominal
shielding and breast biopsy remain appropri-
ate, while computed tomography (CT) scans
are generally avoided due to their high level
of radiation exposure. Breast and axillary
lymph node dissection during any trimester
of pregnancy is associated with minimal fetal
risk [7]. However, sentinel lymph node biop-
sies during pregnancy remain controversial
and are not currently recommended [8].
C. Treatment should not be delayed secondary to
pregnancy; therefore, a treatment plan should
be made by a multidisciplinary team of mater-
nal fetal medicine, breast surgery, and oncol-
ogy. Although a difficult conversation,
termination should be discussed and offered as
an option prior to initiating treatment, although
elective termination of pregnancy has not been
shown to improve maternal outcomes [9].
Treatment should be approached similarly
to non-pregnant women, with certain modifi-
cations and considerations. Mastectomy is an
appropriate treatment option, while radiation
therapy is contraindicated due to associated
853
854
fetal risks of miscarriage, congenital malfor-
mations, development and growth alterations,
and carcinogenic effects [10]. Chemotherapy
in the second and third trimester of pregnancy
has been associated with intrauterine growth
restriction, prematurity, and low birth weight
in approximately 50% of exposed fetuses
[11]. However, there appears to be a low level
of neonatal complications with in utero expo-
sure to chemotherapy [12].
D. Long-term prognosis for both the mother
and fetus appears to be reassuring if breast
J. M. O’Brien and J. M. Pauli
cancer is diagnosed early and appropriately
treated. The risk of vertical transmission to
the fetus remains unknown, but metastasis to
the placenta is rarely encountered [13].
Studies have demonstrated that survival is
not negatively affected with breast cancer
being diagnosed during the pregnant state,
that women who become pregnant after
undergoing treatment for breast cancer do
not worsen their prognosis, and that preg-
nancy after breast cancer may in fact have a
protective effect [14–16].
206  Pregnancy and Breast Cancer 855

Non physiologic breast changes during pregnancy, first year post-

A partum, or during lactation

B Imaging

Chest X ray Mammography Breast MRI (without

with abdominal with abdominal ultrasound gadolinium if
shielding shielding pregnant)

Continued suspicion of pregnancy associated breast cancer

Breast and axillary lymph node biopsy

Diagnosis of pregnancy associated breast cancer

Is treatment Is termination
No during of pregnancy
Yes
pregnancy desired?
desired?

Treatment after
delivery
Treatment No Yes

Chemotherapy Treatment after

D after appropriate Mastectomy termination
counseling

Algorithm 206.1
856 J. M. O’Brien and J. M. Pauli

References sus conference of the role of sentinel lymph node

biopsy in carcinoma of the breast, April 19-22, 2001,
Philadelphia, Pennsylvania. Cancer. 2002;94:2542.
1. Wallack MK, Wolf JA Jr, Bedwinek J, et al. Gestational
9. Nugent P, O’Connell TX.  Breast cancer and preg-
carcinoma of the female breast. Curr Probl Cancer.
nancy. Arch Surg. 1985;120:1221.
1983;7:1.
10. Kal HB, Struikmans H.  Radiotherapy during preg-
2. Liberman L, Giess CS, Dershaw DD, et al. Imaging
nancy: fact and fiction. Lancet Oncol. 2005;6:328.
of pregnancy associated breast cancer. Radiology.
11. Cardonick E, Iacobucci A. Use of chemotherapy dur-
1994;191:245.
ing human pregnancy. Lancet Oncol. 2004;5:283.
3. Antonelli NM, Dotters DJ, Katz VL, Kuller JA. Cancer
12. Giacalone PL, Laffargue F, Benos P.  Chemotherapy
in pregnancy: a review of the literature. Part I. Obstet
for breast carcinoma during pregnancy: a French
Gynecol Surv. 1996;51:125.
national survey. Cancer. 1999;86:2266.
4. Anderson BO, Petrek JA, Byrd DR, et al. Pregnancy
13. Dessolle L, Dalmon C, Roche B, Darai E. Placental
influences breast cancer stage at diagnosis in women
metastases from maternal malignancies: review of
30 years of age and younger. Ann Surg Oncol.
the literature. J Gynecol Obstet Bio Reprod (Paris).
1996;3:204.
2007;36:344.
5. Stensheim H, Moller B, van Dijk T, Fossa SD. Cause
14. Amant F, von Minckwitz G, Han SN, et al. Prognosis
specific survival for women diagnosed with can-
of women with primary breast cancer diagnosed dur-
cer during pregnancy and lactation: a registry based
ing pregnancy: results from an international collab-
cohort study. J Clin Oncol. 2009;27:45.
orative study. J Clin Oncol. 2013;31:2532.
6. Saber A, Dardik H, Ibrahim IM, Wolodiger F.  The
15. Mueller BA, Simon MS, Deapen D, et al. Childbearing
milk rejection sign: a natural tumor marker. Am Surg.
and survival after breast carcinoma in young women.
1996;62:998.
Cancer. 2003;98:1131.
7. Woo JC, Yu T, Hurd TC. Breast cancer in pregnancy:
16. Azim HA Jr, Santoro L, Pavlidis N, et  al. Safety of
a literature review. Arch Surg. 2003;138:91.
pregnancy following breast cancer diagnosis. A meta-­
8. Schwartz GF, Giuliano AE, Veronesi U, Consensus
analysis of 14 studies. Eur J Cancer. 2011;47:74.
Conference Committee. Proceedings of the consen-
 Pregnancy and Hernia
Jaimey M. Pauli
Algorithmic Approach
A. Abdominal wall hernias (umbilical, inguinal,
femoral, incisional, ventral, parastomal, etc.)
are defects in the fascia that can develop as a
result of increased intraabdominal pressure
and tension on the abdominal wall, both of
which are increased during pregnancy [1].
This may lead to discomfort during a preg-
nancy in a previously undiagnosed or asymp-
tomatic hernia [2]. Symptoms of pain and
obstruction occur when intraabdominal con-
tents, such as peritoneum, omentum, bowel,
or other visceral organs, protrude through the
hernia; however, the growing uterus may
block these from protruding. A very rare
complication occurs when the gravid uterus
itself prolapses through the hernia (usually
incisional or umbilical), which can cause
uterine strangulation, fetal demise, uterine
rupture, preterm labor, hemorrhage, and skin
necrosis [3].
B. Hernia repair is one of the most common sur-
geries in the nonpregnant population but tra-
ditionally has been postponed until the
postpartum period and preferably until child-
bearing is complete. The potential risks to the
J. M. Pauli (*)
Maternal-Fetal Medicine, Department of Obstetrics
and Gynecology, Penn State Health Milton S.
Hershey Medical Center, Hershey, PA, USA
e-mail: jpauli@pennstatehealth.psu.edu
© Springer Nature Switzerland AG 2019
S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1_207
207
fetus during surgery, the risk of recurrence as
the abdominal wall expands during preg-
nancy, and concern for limited abdominal
wall stretching in a subsequent pregnancy
have all been cited as reasons for the delay.
C. Evaluation of the patient with a suspected
hernia should include a history and physical
exam, with attention to history of prior sur-
geries (for incisional hernias) and bowel
symptoms such as vomiting, distention, or
absence of flatus or stool passage. Generally,
there is a lump or palpable defect with con-
tents that may or may not be reducible. The
presence of skin erythema or tenderness indi-
cates possible bowel perforation [4].
Ultrasound is not often required but may be
used to confirm the diagnosis and rule out
other conditions such as round ligament vari-
cosities, which mimic a groin hernia on exam
but have a characteristic appearance of a “bag
of worms” on color Doppler that become
more prominent with Valsalva [4, 5].
D. Pregnant patients should undergo emergent
hernia repair for the same indications as non-
pregnant patients—bowel incarceration,
strangulation, or suspected perforation [2, 4].
Due to the risk of worsening symptoms or
incarceration that may increase the risk of
perinatal complications, symptomatic irreduc-
ible umbilical hernias should be urgently
repaired and asymptomatic irreducible umbil-
ical hernias should be semi-urgently repaired
857
858
during pregnancy [4]. Monitoring for fetal
well-being and signs and symptoms of labor
should occur as appropriate for gestational age
in the perioperative period per obstetrical
recommendations.
E. Although the data are limited, more recent
reviews indicate that elective hernia repair
during pregnancy should be considered to
avoid worsening symptoms or incarceration
during the pregnancy that could lead to emer-
gent surgery with higher perinatal complica-
tions [2]. The decision to proceed with a
non-urgent hernia repair during pregnancy
should take into account several consider-
ations: gestational age (with the second tri-
mester being the ideal time to operate), the
likelihood of hernia recurrence causing
symptoms during pregnancy, the risk of her-
nia recurrence requiring reoperation, the risk
of pregnancy complications related to the sur-
gery, and the risk of complications in a future
pregnancy as a result of the hernia repair [6].
F. Both open and laparoscopic hernia repairs,
with and without mesh, have been performed
during pregnancy, with little consensus on
J. M. Pauli
the ultimately preferred method. A review of
the literature suggests that laparoscopic
repair may be used safely in pregnancy (as it
is with appendectomy and cholecystectomy)
and has the advantages of smaller incisions,
shorter hospital stay, earlier mobilization,
etc. [2, 4, 7]. The use of mesh is associated
with a lower hernia recurrence rate [2, 4, 6,
8]. The risk of obstetrical complications
does not appear higher in pregnancies after
hernia repair, but increased abdominal wall
pain has been noted in the third trimester,
purportedly due to decreased elasticity of
the repair abdominal wall. Combined repair
of small inguinal and umbilical hernias at
the time of cesarean has also been reviewed
in small case series with the advantage of
convenience and saved time and cost, with
no difference in outcomes beyond longer
operating times [9]. Until larger, random-
ized prospective trials are performed to
determine the best way to approach these
patients, the repair will be determined by the
clinical judgment and experience of the sur-
geon performing it.
207  Pregnancy and Hernia 859

A
History:
Abdominal “lump”or discomfort Known hernia
Nausea/vomiting/distention/absence of flatus or stool
B Prior surgery

C Obtain vital signsandperform a physical examination

Palpable Yes No Perforation

Irreducible
lump or or
(umbilical)?
defect? obstruction?

Yes
D OR Yes
No

Skin Yes
erythema or Urgent
tenderness? Hernia repair

No

Consider ultrasound for further

evaluation

Hernia Yes Evaluate for elective hernia

present? repair

E
No

Evaluate for other conditions

Start antibiotics, NPO, IVF, CT-guided drainage

Pain for over 24 hours, a wbc greater than 15, and temperature exceeding 39.4 C are
concerns for a perforated appendix. Obtain a CT Scan.

· Discharge home on antibiotics.

· Colonoscopy followed by interval
appendectomy is recommended

Algorithm 207.1
860 J. M. Pauli

References 5. Uzun M, Akkan K, Coskun B. Round ligament vari-

cosities mimicking inguinal hernias in pregnancy:
importance of color Doppler sonography. Diagn
1. Wai PY, Ruby JA, Davis KA, Roberts AC, Roberts
Interv Radiol. 2010;16:150–2.
KE.  Laparoscopic ventral hernia repair during preg-
6. Schoenmaeckers E, Stirler V, Raymakers J, Rakic
nancy. Hernia. 2009;13:559–63.
S.  Pregnancy following laparoscopic mesh repair of
2. Jensen KK, Henriksen NA, Jorgensen LN. Abdominal
ventral abdominal wall hernia. JSLS. 2012;16:85–8.
wall hernia and pregnancy: a systematic review.
7. Bisharah M, Tulandi T. Laparoscopic surgery in preg-
Hernia. 2015;19:689–96.
nancy. Clin Obstet Gynecol. 2003;46(1):92–7.
3. Banerjee N, Deepika D, Sinha A, Prasad R.  Gravid
8. Buch KE, Tabrizian P, Divino CM.  Management
uterus in an incisional hernia. J Obstet Gynaecol Res.
of hernias in pregnancy. J Am Coll Surg.
2001;27(2):77–9.
2008;207(4):539–42.
4. Augustin G, Matosevic P, Kekez T, Majerovic M,
9. Ochsenbein-Kölble N, Demartines N, Ochsenbein-­
Delmis J. Abdominal hernias in pregnancy. J Obstet
Imhof N, Zimmermann R. Cesarean section and simul-
Gynaecol Res. 2009;35(2):203–11.
taneous hernia repair. Arch Surg. 2004;139:893–5.
Index

A Adrenal vein sampling (AVS), 466

Abdominal aortic aneurysms (AAA), 551, 552 Adrenalectomy, 449, 454
Abdominal bruising, 669 Adrenocorticotropic hormone (ACTH), 449
Abdominal compartment syndrome (ACS), 735, 736 Adson test, 589
Abdominal evaluation, 615 Advanced cardiac life support (ACLS), 632, 634, 637
Abdominal injuries, concurrent, 661 Advanced trauma life support (ATLS)
Abdominal pain, 195, 225, 237, 391, 821 bladder injury, 683
Abdominal perfusion pressure (APP), 735, 736 blunt aortic injury, 641
Abdominal plain X-ray, 501 blunt cardiac injury, 637
Abdominal roentgenograms, 645 blunt chest wall trauma, 633
Abdominal trauma, 665 diaphragmatic injury, 653
Abdominal wall hernia, 857, 858 ED thoracotomy, 632
Abdominal wall reconstruction, 191, 192, 813, 814 pelvic fracture, 679
ABI, see Ankle brachial index (ABI) penetrating abdominal trauma, 645
Abscess drainage, 325 penetrating chest trauma, 627
Absent esophageal contractility, 120 penetrating neck trauma, 623
Acarbose, 157 splenic injury, 665
Accelerated partial breast irradiation (APBI), 91 traumatic brain injury, 619
Achalasia, 123 Aganglionosis, 513, 514
Acholic stools, 541 Airway compromise, 17, 18, 431
Acid-base disorder, 751, 752 Airway management, 43, 707, 708
ACS, see Abdominal compartment syndrome (ACS) Airway, breathing, circulation, disability and exposure
Acute abdomen, 225 (ABCDE), 633
Acute acalculous cholecystitis (AAC), 349 AKI, see Acute kidney injury (AKI)
Acute appendicitis, 225, 226 Alcohol, 17
Acute calculous cholecystitis (ACC), 345, 346 abuse, 609
Acute cholangitis, 355, 359 Aldosterone, 453
Acute deep vein thrombosis (DVT), 577 Aldosterone to renin ratio (ARR), 453
Acute kidney injury (AKI), 669, 670 Aldosteronoma, 465, 466
diagnosis, 739 ALI, see Acute limb ischemia (ALI)
etiology, 739 Allergies, Medications, Past Medical History,
Acute leak, 835, 836 Last Meal, and Events or Mechanism of
Acute limb ischemia (ALI), 565 injury (AMPLE), 657
Acute mesenteric ischemia, 581 Alpha-blockade, 462
Acute pancreatitis (AP), 379, 380, 403 American Association for the Study of Liver Diseases
Acute renal failure, 739, 740 (AASLD), 308
Acute respiratory distress syndrome (ARDS), 719 American Association for the Surgery of Trauma
sepsis, 724 (AAST), 657
Adenocarcinoma, 181 American Urological Association, 601
Adenomatous colon polyp, 251 Amoebic liver abscess, 324–325
Adjuvant therapy, male breast cancer, 114 Anal cancer, 301
Adrenal crisis, 727 Anal fissure, 293, 294
Adrenal insufficiency, 727 Anal margin, 301
Adrenal masses, 465 Anaphylaxis, 727

© Springer Nature Switzerland AG 2019 861

S. Docimo Jr., E. M. Pauli (eds.), Clinical Algorithms in General Surgery,
https://doi.org/10.1007/978-3-319-98497-1
862 Index

Androgen deprivation therapy, 602 Biliary atresia, 541, 542

Angioembolization, 657, 658, 666 Biliary colic, 346
Angiography Biliary cysts, see Choledochal cyst (CC)
pulmonary emboli, 743 Biliary disease, 199
with/without embolization, 665 Biliary drainage procedure, 396
Angiomyolipoma (AML), 597 Biliary ducts, 335
Anion gap, 751 Biliary leak, 351
Ankle brachial index (ABI), 569, 573 Biliary reflux, 159
Anoplasty, 510 Biliary tract, 362, 365, 366, 373
Anorectal malformations (ARMs), 509, 510 Bilious emesis, 505
Anorectal physiology, 303 Biloma, 352
Anterior injuries, 627, 675 Biofeedback therapy, 303
Anterolateral thoracotomy, 627 Biologic mesh, 798, 809
Antibiotics, 325, 609 Biomarker analysis, male breast cancer, 114
Anticoagulation, 702, 743, 744 Bladder injury, 683, 684
acute DVT, 577 Bleb, 59
thoracic outlet syndrome, 589 Blood glucose, 473
Anti-diarrheals, 303 Blood pressure, intracranial hematoma, 702
Anti-HER-2 treatment, 106 Blood transfusions, 731, 732
Anti-HER-2/neu therapy, 101, 102 Bloody diarrhea, 229, 237
Antimicrobial therapy, 723 Blunt abdominal trauma, 649, 650
Antireflux surgery, 127 Blunt aortic injury, 633, 641, 642
Anti-TNF agents, 230 Blunt cardiac injury (BCI), 634, 637
Antral G-cell hyperplasia, 162 Blunt chest wall trauma, 633, 634
Aortic dissection, 559, 560 Blunt injury, 631, 687
Aortogram, 585 Blunt scrotal trauma, 605
Aperistalsis, 123 Blunt traumatic cardiac arrest, 631
Appendicitis, 225, 226, 849, 850 Blunt traumatic injury, 615, 616
ARDS, see Acute respiratory distress syndrome (ARDS) Bochdalek hernia, 495
Arrhythmias, 637 Bogota bag technique, 810
Arterial blood gas analysis, 751 Bosniak classification system, 597
Arterial embolization, 316 Botulinum toxin injection, 119, 120, 293–294
Arterial occlusive disease, 585 Bowel obstruction, 525, 825
Arterial TOS, 589 Brachytherapy, 44
Arterial venous (AV) shunt, 593 Brain cell shrinkage, 761
Atraumatic indications, for splenectomy, 413, 414 BRCA2 mutation, 113, 114
Atypical fissure, 293 Breast cancer
Autologous islet cell transplantation, 384 inflammatory, 105, 106
Autologous tissue reconstruction, 110 locoregional recurrence of, 97, 98
Autosomal dominant polycystic kidney disease metastatic, 87, 101, 102
(ADPKD), 313 pregnancy, 853, 854
Axillary lymph node, enlarged, 85 recurrent, 91, 92
Breast conservation surgery (BCT), 95, 97
Breast Imaging Reporting and Data System (BIRADS),
B 73, 74
Balloon expandable stent, 586 Breast mass evaluation, 73, 74
Bariatric surgery, 819, 821 Breast reconstruction, 109–111
acute leak, 835, 836 Broad spectrum antibiotics, 11
vitamin/micronutrient deficiencies, 839, 840 Bronchoscopy for bleeding, 35
work-up of abdominal pain, 821, 822 Brooke formula, 748
Barium esophagram, 119, 123 Bullectomy, 59
Barker bag technique, 810 Burns, 747, 748
Barrett’s esophagus, 127
Basal cell carcinoma, 5
Baseline severity score, 701 C
Bell’s Staging Criteria, 534 CA19-9, 399
Benign cystic masses, 605 Calcium, 771, 772
Benign liver masses, 319, 320 arteriography, 473
Beta blocker, 641 channel blocker, 641
Bethesda system, 435 deficiency, 840
Bilateral chest, 615 testing, 443, 444
Index 863

Cancer staging, 256 Cholelithiasis, 477

Cancer treatment, 255–257 pregnancy and, 845, 846
Cannot intubate, cannot oxygenate (CICO), 708 Chromogranin A level (CgA), 185
Capnography, 707 Chronic anemia, 731
Carcinoembryonic antigen (CEA), 399 Chronic hyponatremia, 758
Carcinoid syndrome, 182, 185, 186 Chronic limb ischemia, 569
Carcinoid tumors, 181 Chronic mesenteric ischemia (CMI), 585, 586
Cardiac arrest, 711, 712 Chronic pancreatitis, 383, 384
blunt traumatic, 631 Cirrhosis, 339
Cardiac tamponade, 627 Claudication, 573
Cardiac ultrasound, 631 Clavicle fractures, 634
Cardinal sign, for traumatic injury, 683 Cloaca, 509, 510
Cardiogenic shock, 727, 728 Clostridium difficile, 229
Cardiopulmonary arrest, 627 colitis, 241, 242
Cardiopulmonary resuscitation (CPR), 631 toxin, 241
Caroli disease Closure of wounds, see Wound closure
etiology, 313 Clots in Legs Or sTockings after Stroke 3 (CLOTS 3)
imaging, 314 trial, 702
management, 316 CMI, see Chronic mesenteric ischemia (CMI)
Carotid artery stenosis, 547, 548 Coagulation necrosis, 143
Carotid artery stenting (CAS), 547 Coagulopathy, 702
Carotid duplex, 548 Colon cancer, 251, 255–257
Carotid endarterectomy (CEA), 547 Colon polyps, 251
Catecholamines, 461 Colonic ischemia, 237, 238
Catheter Directed Thrombolysis (CDT), 565 Colonic pseudo-obstruction (CPO), 217, 218
Caustic injuries, 143, 144 Colonic volvulus, 221, 222
Cavo-atrial shunting, 658 Colonoscopy, 205, 230, 245, 256, 257
Cecal volvulus, 221, 222 Combined resection, 327
Central injuries, 627 Common bile duct, 357
Central lumpectomy, 95 Common bile duct exploration, 357
Central neck dissection (CND), 439 Common bile duct stones (CBDS), 345
Cerebral demyelination, 761 Compartment syndrome, 739
Cerebral perfusion pressure (CPP), 702 Complete skin exam, 5
Cervical lymph node, enlarged, 25, 26 Complex injury, 684
Cervical lymphadenopathy, 26 Compressive symptom, 435, 436
Charcot’s triad, 359 Computed tomography (CT), 17
Chemoradiation, 136 bladder injury, 683
Chemotherapy, pregnancy, 854 blunt abdominal trauma, 649, 650
Chest imaging, renal cell carcinoma, 597 blunt aortic injury, 641
Chest pain, 743 cystadenoma, 315
Chest trauma, penetrating, 627, 628 diaphragmatic injury, 653
Chest tube, 59, 60 Fournier’s gangrene, 609
Chest X-ray (CXR), 679 hepatic abscess, 324
appendicitis, 849 hydatid cysts, 314
blunt aortic injury, 641 hypotension, 615
blunt chest wall trauma, 634 inguinal hernia, 783
intubation, 712 intracranial hemorrhage, 701
penetrating chest trauma, 627 neck mass, 21
thoracic outlet syndrome, 589 obturator hernia, 797
Child Protective Services (CPS), 747 pancreatic injury, 661
Child-Pugh Classification, 331, 332 PCLD, 315
Cholangiocarcinoma, 361, 362 pelvic fracture, 680
Cholangioscopy, 335 rectal injury, 687
Cholangitis, 373 recurrent inguinal hernia, 789
Cholecystectomy, 346, 357, 373, 374, 380 renal mass, 597
Cholecystectomy, post, 351, 352 simple cysts, 314
Cholecystitis, 373 traumatic brain injury, 619, 620
Cholecystocholangiography, 662 traumatic liver injury, 657, 658
Choledochal cyst (CC), 369–370 ureter injury, 671
Choledocholithiasis, 357 ventral hernia repair, 831
Choledochotomy, 359 von Meyenburg complexes, 315
864 Index

Computed tomography angiography (CTA) Deep vein thrombosis (DVT), 577, 744
abdomen and pelvis, 581, 585 Definitive repair, 658
arterial occlusion, 581 Delayed mesh-based repair, 785
penetrating neck trauma, 624 Delayed primary closure, 695
pulmonary emboli, 743, 744 Denosumab, 776
Concurrent abdominal injuries, 661 Dermal lymphatics, 105
Congenital anomaly, 21, 537 Dermoid cyst, 26
Congenital diaphragmatic hernia (CDH), 487, 488, Devitalized tissue, 675
495, 496 Diabetes mellitus, 609
Conn’s syndrome, 453, 454 Diagnostic peritoneal aspiration (DPA), 615, 616,
Contrast enema, 501, 506 646, 650
Cooper’s ligament, 793, 794 Diagnostic peritoneal lavage (DPL), 615, 616, 646, 650
Copper deficiency, 840 Dialysis access, 593
Core needle biopsy (CNB) Diaphragmatic injury, 628, 653, 654
neck mass, 21 Diarrhea, 159, 241, 481
salivary gland tumors, 29 Dietary calcium restriction, 776
Corkscrew appearance, 123 Diffuse esophageal spasm, 119
Cortisol, 449 Digital rectal exam (DRE), 276, 687
Cough peak flow (CPF), 715 prostate cancer, 601
C-peptide, 473 Diligence, 715
Crawford classification, 63 Diltiazem, 641
Creatinine, 669 Diphenoxylate-atropine, 303
Cricothyroidotomy, 623, 708 Direct oral anticoagulants (DOACs), acute DVT, 577
Crohn’s disease, 195, 233, 234 Disseminated disease, 602
Cryptorchidism, 605 treatment, 606
CT angiography (CTA), 205 Distal esophageal spasm, 119
Cuff-leak test, 715 Distal intestinal obstruction syndrome (DIOS), 522
Cullen’s sign, 379 Distributive shock, 727
Cushing’s syndrome, 449 Diverticular abscess, 209
Cutaneous anesthesia, 11 Diverticular fistula, 209
Cutaneous lesion, 7 Diverticulitis, 209, 210
Cutaneous melanoma, 3 Doppler waveforms, 573
Cyst aspiration, 314 Dorsalis pedis (DP), 573
Cystadenocarcinoma Dressings, burns, 747, 748
etiology, 313 Driving pressure, 719
imaging, 315 Ductal carcinoma in situ (DCIS), 77, 78
management, 316–318 Ductal injury, 661, 662
Cystadenoma Ductography, 70
etiology, 313 Ductoscopy, 70
imaging, 315 Dumping syndrome, 157
management, 316 Duodenal adenocarcinoma, 395
Cystduodenostomy, 391 Duodenal atresia, 499
Cystectomy, hydatid cyst, 315 Duodenal obstruction, 499
Cystgastrostomy, 391, 392 Duodenal-jejunal junction (DJJ), 506
Cystic fibrosis, 522 Dysphagia, 17
Cystogram, 683, 684 Dysrhythmia, 765
Cystoscopy, bladder injury, 683, 684
Cysts of the liver, 313–316
Cytology, 435, 436 E
Cytomegalovirus (CMV), 229 Early satiety, 169
Echocardiogram, 637
Electrocardiogram (EKG), 637
D Elevated Arm Stress Test, 589
Damage control surgery, 658 Elvey test, 589
DCIS, see Ductal carcinoma in situ (DCIS) Embolization, 665, 666
D-dimer test, 743 Emergency department (ED), thoracotomy, 631, 632
De Quervian’s thyroiditis, 427 Empyema, management of, 55, 56
Debridement, 11 Endoanal ultrasound testing, 303
De-clot, 593 Endobronchial ultrasound (EBUS), 52
Decompressive craniectomy, 620, 703 Endocrine therapy, 102
Index 865

Endorectal advancement flap, 285 Fasciotomy, extremity compartment syndrome, 694, 695
Endo-rectal pull-through, 514 Fecal contamination, 688
Endoscopic eradication therapy, 127 Fecal diversion, 609
Endoscopic mucosal resection (EMR), 127 Fecal incontinence, 285, 303
Endoscopic retrograde cholangiopancreatography Fecal microbiota transplant, 242
(ERCP), 335, 336, 351, 352, 355, 357, 359, Feeding intolerance, 533
380, 387, 403, 845 Femoral hernia, 793, 794
Endoscopic ultrasound (EUS), 383, 387, 399 Fenestration
Endotracheal tube, 712 PCLD, 316
Endovascular abdominal aortic aneurysm simple cyst, 315
(EVAR), 555, 556 Fever management, intracranial hemorrhage, 702
Endovascular aortic repair (EVAR), 551, 552 Fiber supplementation, 293
Endovascular blunt aortic injury, 641 Fiberoptic bronchoscope, 708
Endovascular techniques, revascularization, 586 Fiberoptic endoscopy, 17, 143
Enema reduction, 526 Fibrinolytic, 55, 56
Enlarged axillary lymph node, 85 Fine needle aspiration (FNA), 427, 435
Enlarged cervical lymph node, 25, 26 neck mass, 21
Enterocutaneous (EC) fistula, 191, 192 Fine Needle Aspiration Biopsy (FNAB), 309
Enterolithotomy, 199 Fine Needle Aspiration cytology (FNAC), 29
Epididymis, 605 First rib resection, 589
Epididymo-orchitis, 605 Fistula, 199
Epidural hematoma, 619, 620 Fistulagram, 593
Eplerenone, 466 Fistulogram, 192
Escharotomy, 747 Fistulotomy, 298
Esmolol, 641 5-Hydroxyindole acetic acid (5-HIAA), 185
Esophageal adenocarcinoma, 135 Flat perineum, 509
Esophageal atresia (EA), 491 Flexible endoscopy, acute leaks, 835
Esophageal cancer, 135, 136 Fluid resuscitation, 747, 748
Esophageal injury, 624 and oxygen delivery, 752
Esophageal motility disorders, management of, 119, 120 Fluoroquinolone antibiotic prophylaxis, 601
Esophageal mucosa, 144 Fluoroscopic cholecystocholangiography, 662
Esophageal perforation, 139, 140, 144 Flushing rash, 481
Esophageal stenting, 139 Focal nodular hyperplasia (FNH), 308, 320
Esophagectomy, 135 Focused assessment with sonography in trauma
Esophagogastroduodenoscopy (EGD), 123, 161 (FAST), 616
Etiology-specific therapy, 776 blunt abdominal trauma, 649
Euvolemic hyponatremia, 757, 758 diaphragmatic injury, 653
Ewing’s sarcoma, 9 pelvic fracture, 680
Excisional biopsy penetrating chest trauma, 627
breast mass, 74 splenic injury, 665
lobular carcinoma in situ, 81 Foley, 683, 684
Exercise program, supervised, 573 Foley balloon catheterization, 623
Extended cholecystectomy, 366 Folic acid, 839
External hemorrhoid, 289, 290 Fournier’s gangrene, 609, 610
External oblique release (EO), 814 Fractionated metanephrines, 461
Extracorporeal membrane oxygenation Free fluid without obvious solid organ injury
(ECMO), 487, 488 (FFWOSOI), 650
Extrahepatic cholangiocarcinoma, 362 Fulminant Colitis, 234
Extrahepatic hilar tumor, 361 Functional liver remnant, 327
Extrahepatic metastasis, 331 Fundoplication, 134
Extraperitoneal injury, 683, 684
Extravasation, 671
Extremity compartment syndrome, 693–695 G
Extubation, 715 Ga-DOTANOC scan, 481
Galactorrhea, 69
Gallbladder cancer (GC), 365, 366
F Gallbladder disease (GD), 373
Familial hypocalciuric hypercalcemia (FHH), 443 Gallium-labeled radioligands, 481
Fascial defect closure, 801 Gallstone disease, 845, 846
Fascial violation, 646 Gallstone ileus, 199
866 Index

Gallstone pancreatitis, 373, 380 epidemiology, 323

Gallstones, 345 etiology, 323–324
Gastrectomy, 162 malignant, 324
Gastric cancer, 165–166 management, 324–326
Gastric outlet obstruction, 391 primary source control, 325
Gastric stasis, 159 pyogenic, 323
Gastrinoma, 469, 470 serologic diagnosis, 324
Gastrinoma triangle, 469 stool, 324
Gastroenterologist, 585 Hepatic adenoma, 308, 319–320
Gastroesophageal reflux disease (GERD), 119, 129, 130 Hepatic hemangioma, 309, 319
Gastrografin ®, 521 Hepatic injury, 657, 658
Gastrointestinal stromal tumors (GISTs), 169, 181 Hepatic resection, 362
Gastro-jejunal anastomosis, 827 Hepatocellular carcinoma (HCC), 307, 331, 332
Gastro-jejunal anastomosis leaks, 836 Hereditary colon cancer syndromes, 243–245
Gastroschisis, 537, 538 Hereditary nonpolyposis colorectal cancer (HNPCC),
Genital cellulitis, 609 243–245
Genitourinary injury, 671 Hernia
Giant hiatal hernia, 495, 496 bedside reduction, 805
Giant omphalocele, 538 pregnancy and, 857, 858
Giant prosthetic reinforcement of visceral sac small bowel obstruction, 177
(GPRVS), 797 See also specific hernia
Glasgow Coma Score (GCS), 619 Hernia, Patient, Wound (HPW) staging system, 801
Gleason score, 601 Hiatal hernia, 133, 134
Globular filtration rate, 669 HIDA, 349
Glucagon-like peptide (GLP-1), 473 High-grade dysplasia, 399
Glucagonoma, 457 Highly selective vagotomy (HSV), 157
Glucocorticoids, 776 Hirschsprung disease (HD), 513, 514
Goiter, 431 Histamine-2 (H2) Blockers, 161
Graves’ disease, 423 Histology, sarcoma, 9
Grey Turner sign, 379 Howship-Romberg sign, 797
Gross hematuria, 683 Human-papilloma virus (HPV), 17
Hydatid cysts
etiology, 313
H imaging, 314
Hannington-Kiff sign, 797 management, 315
Hard signs, vascular/tracheoesophageal injury, 623–625 Hydrocolpos, 509, 510
Hashimoto’s thyroiditis, 419, 427 Hyperbaric oxygen therapy, Fournier’s gangrene, 610
Heartburn, 129, 130, 133 Hypercalcemia, 443, 775, 776
Hedgehog pathway inhibitor, 5 Hypercortisolism, 449
Hematemesis, 171 Hypergastrinemia, 469
Hematochezia, 171 Hyperglycemia, 477
Hematoma, 624 Hyperkalemia, 767, 768
Hematuria, 669 Hypernatremia, 761, 762
Hemodialysis, 593 Hyperosmolality, 761
Hemodynamic instability, 627, 645 Hyperparathyroidism, 443, 444, 775, 776
Hemodynamic stability, 657 Hyperphosphatemia, 772
Hemodynamically unstable, 615, 637 Hyperthyroidism, 423, 424, 435
Hemoptysis, massive, 35, 36 Hypertonic hyponatremia, 757
Hemorrhagic shock, 727 Hypertonicity, 762
Hemorrhoid thrombosis, 290 Hyperventilation, 620
Hemorrhoidectomy, 290 Hypervolemic hyponatremia, 757, 758
Hemorrhoids, 289, 290 Hypocalcemia, 771, 772
Hemothorax, 627, 628, 633 Hypoglycemia, 473, 474
Heparin-Induced Thrombocytopenia, 565 Hypokalemia, 765
Hepatic abscess Hypokalemic alkalosis, 779
amoebic, 323 Hypokalemic hypochloremic metabolic alkalosis, 529
clinical presentation and diagnosis, 323 Hypomagnesemia, 765, 771, 772
culture, 324 Hyponatremia, 757, 758
diagnosis, 324 Hypoperfusion, 237
drainage, 325 Hypophosphatemia, 771
Index 867

Hypotension, 615, 616, 657 Intraperitoneal injury, 684

Hypothyroidism, 419, 420 Intravenous (IV) fluid replacement, 404
Hypotonic hyponatremia, 757 Intubation, 707, 711, 712
Hypotonic saline, 762 Intussusception, 525, 526
Hypovolemic shock, 728 Iron deficiency, 840
Ischemia, 731
Ischemic bowel, 538
I Ischemic colitis, 213, 237, 238
Iatrogenic injuries, 654 Ischiorectal abscesses, 297
ICH, see Intracranial hemorrhage (ICH) Ischiorectal fossa, 297
Idiopathic adrenal hyperplasia (IAH), 465 Isotonic hyponatremia, 757
Idiopathic pancreatitis, 387 IVC filter, 744
Ileal pouch anal anastomosis (IPAA), 229
Imatinib, 169
Immediate empiric treatment, 743 J
Immediate life-threatening injuries, 633 Jackhammer esophagus, 119
Imperforate anus, see Anorectal malformations (ARMs) Jejuno-jejunal anastomosis leaks, 836
Implant reconstruction, 110
Incarcerated hernia, 805, 806
Incarceration, 517 K
Incentive spirometry, 634 Kaopectate, 303
Incidental lung nodule, 47 Kasai procedure, 542
Incomplete pancreas divisum, 387 Ki-67 index, 186
Indeterminate/partial thickness burns, 747 Kidney grades, 669
Inflammatory bowel disease (IBD), 195, 233 KIT, 169
Inflammatory breast cancer, 105, 106 Klatskin tumor, 361
Inguinal hernia, 517, 518, 783–785
recurrence, 789, 790
Inspissated meconium, 521–522 L
Insulin, 473 Laboratory Risk Indicatory for Necrotizing
Insulinoma, 473, 474 Fasciitis (LRINEC), 11
Intensive Blood Pressure Reduction in Acute Cerebral Laceration, 684
Hemorrhage 2 (INTERACT-2) trial, 702 Lactate acidosis, 752
Intensive care unit (ICU) Lactic acidosis, 752
blood transfusion, 732 Ladd’s procedure, 505, 506
sepsis, 724 Laparoscopic adrenalectomy, 466
Intermittent hemodialysis, 740 Laparoscopic appendectomy, 225, 226
Intermittent sedation, sepsis, 724 Laparoscopic cholecystectomy (LC), 346, 373
Internal hemorrhoid, 289 Laparoscopic hernia repair, 858
Internal hernia, 825 Laparoscopic partial cholecystectomy (LPC), 346
Internal rectal intussusception, 270 Laparoscopy
Intersphincteric abscesses, 297 obturator hernia, 798
Intersphincteric fistula tract (LIFT), 298 open inguinal repair, 805, 806
Interventional bronchoscopy, 35 penetrating chest trauma, 628
Intestinal transplantation, 201 Laparotomy, 615
Intimal tear, 641 acute kidney injury, 669
Intraabdominal hypertension (IAH), 735 blunt abdominal trauma, 650
Intra-abdominal injury, 649 diaphragmatic injury, 653
Intraabdominal pressure (IAP), 735, 736 splenic injury, 665
Intracranial hemorrhage (ICH), 701–703 Large bowel obstruction (LBO), 213, 214
Intracranial pressure (ICP), 701, 702 Laryngoscopy, 707, 708
monitoring, 702 Lateral neck dissection (LND), 439
traumatic brain injury, 620 LCIS, see Lobular carcinoma in situ (LCIS)
Intraductal papillary mucinous neoplasms Left-sided portal hypertension, 339
(IPMN), 399 Lethal triad, 658
Intrahepatic cholangiocarcinoma, 361, 362 Levothyroxine, 419, 420
Intramural hematoma, 642 Life-threatening complications, intubation, 711
Intraoperative parathyroid hormone monitoring Life-threatening injury, 634, 665
(IOPM), 444 Limb preservation, 9
Intraoperative technique, diaphragmatic injury, 654 Linezolid, Fournier’s gangrene, 609
868 Index

Lipase, 379 Mammalian target of rapamycin inhibitors, 316

Liquefactive necrosis, 143 Mammography, 853
Liver cyst, 313 axillary lymph node, 85
Liver directed therapies, 328 breast mass, 73
Liver nodule, 307–309 Marginal ulcer (MU), 827
Liver resection, 331 Marsupialization, simple cyst, 316
Liver transplantation, 331 Martius flap, 285, 286
PCLD, 316 Massive hemoptysis, 35, 36
Lobectomy, 51 Massive hemorrhage, 727
Lobular carcinoma in situ (LCIS), 81, 82 Mastectomy, 91, 853
Local recurrence, 92 breast reconstruction after, 109, 110
Locoregional recurrence, of breast cancer, 97, 98 male breast cancer, 114
Longitudinal intestinal lengthening and tailoring Paget’s disease, 95
(LILT), 201 McVay repair, 794
Loperamide, 303 Mechanical ventilation, 724
Low birth weight infants, 533 Mechanism of injury (MOI), 661
Lower gastrointestinal bleeding (LGIB), 205, 206 Meconium ileus, 521, 522
Lumen-apposing metal stent, 391 Meconium peritonitis, 521, 522
Lung cancer, 47 Meconium pseudocyst, 521, 522
management of, 51, 52 Median sternotomy, 627
Lung lesion, 47 Mediastinal cyst, 39
Lung nodule, 47, 51 Mediastinal mass, 39, 40
Lung resection, 51 Mediastinoscopy, 52
Lymph node Mediastinum, 39, 40
axillary, 85 Medical management, hydatid cyst, 315
cervical, 25, 26 Medical therapy, acute limb ischemia, 565
Lymphadenectomy, 3 Melanoma, 3
Lymphadenopathy, 29 Melena, 171
Lymphocytic thyroiditis, 427 Mesenteric angiography, 206
Lymphoma, 182 Mesenteric arteries, stenosis of, 585
Lynch syndrome, 243, 244 Mesenteric ischemia, 581
acute, 581
chronic, 585, 586
M Mesocaval shunting, 339
MACOCHA scoring system, 711 Metabolic acidosis, 751
Mafenide acetate, 748 Metabolic alkalosis, 751, 779
Magnetic resonance cholangiopancreatography (MRCP), Metastatic breast cancer, 85, 87, 101, 102
335, 336, 357, 383, 846 Metastatic disease, 308
Magnetic resonance imaging (MRI), 17 Metastatic liver disease, 327, 328
axillary lymph node, 85 Metronidazole, 284, 324
cystadenocarcinoma, 315 Micronutrient deficiency, 839, 840
cystadenoma, 315 Midgut, 185
hepatic abscess, 324 Midgut volvulus, 505
hydatid cysts, 314 Milk rejection sign, 853
inguinal hernia, 783 Minimally invasive technique
neck mass, 21 diaphragmatic injury, 653
Paget’s disease, 95 femoral hernia, 793
PCLD, 314 ventral hernia repair, 801
recurrent inguinal hernia, 789 Modified Wells score, acute DVT, 577
renal cell carcinoma, 597 Mohs micrographic surgery, 5, 7
salivary gland tumors, 29 Morgagni hernia, 495, 496
simple cysts, 314 Motor vehicle collisions (MVCs), 665
von Meyenburg complexes, 315 MUDPILES differential diagnoses, 751
Magnetic sphincter augmentation, 130 Multidisciplinary rehabilitation, 703
Major salivary gland, 29 Multiple Endocrine Neoplasia 1 (MEN1)
Malabsorption, 201 syndrome, 457, 469, 470, 473, 481
Male breast cancer, 113, 114 Multisystem organ failure, 761
Mallory-Weiss tear, 139, 171 Murphy’s sign, 845
Malperfusion, 559 Mycobacterial infection, 26
Malrotation, 505, 506 Myocardial infarction, 637
Index 869

N Organ dysfunction, 723

N-acetylcysteine, 521 Oropharyngeal squamous cell carcinoma
Nasogastric tubes, 18 (OPSCC), 17, 18
Neck mass, 21, 22, 25 Orotracheal intubation, 623
Neck trauma, penetrating, 623, 624 Orthopedic surgery, 680
Neck ultrasonography (US), 435, 439 Orthotopic liver transplantation (OLTx), 332, 336
Necrosectomy, 403, 404 Osteoporosis, 443
Necrotizing Enterocolitis (NEC), 533, 534 Ovarian stromal (OS), 314
Necrotizing soft tissue infection (NSTI), 11 Oxandralone, 748
Negative pressure wound therapy (NPWT), 809
Neoadjuvant chemotherapy, 91, 106
Neoadjuvant therapy, 276, 278, 279, 396 P
Neonatal jaundice, 541 PAC, see Periampullary adenocarcinoma (PAC)
Neostigmine, 217 Paget’s disease, 95
Nephrectomy, 598 Paget-von Schrotter syndrome, 589
Neurocritical Care Society, 701 Pain out of proportion to exam, 11
Neurocritical care unit, 701, 702 Painless mass, 9
Neurogenic shock, 727 Painless thyroiditis, 427
Neurogenic TOS, 589 Palliative care, 101, 102
Neurologic injury, 619 Palliative mastectomy, 87
Neuromuscular blockade, 724 Palpable lymph nodes, 7
Neuromuscular blockade agent, 719 Pamidronate, 776
Nicardipine, 641 Pancreas, 399
Nipple discharge, 69, 70 Pancreas divisum, 387, 388
Nipple-areolar complex (NAC), 95 Pancreatectomy, 662
Nissen fundoplication, 130, 134 Pancreatic ascites, 391
Nitroglycerin, 641 Pancreatic calcification, 383
Nitroprusside, 641 Pancreatic cancer, 383
Non-anion gap metabolic acidosis, 751 Pancreatic duct stent, 384
Non-cirrhotic etiologies, 339 Pancreatic ductal adenocarcinoma (PDAC), 395
Non-epithelial GI tumor, 169 Pancreatic injury, 661, 662
Non-occlusive mesenteric ischemia, 581 Pancreatic insufficiency, 383, 384
Non-steroidal anti- inflammatory drugs (NSAIDs), 161 Pancreatic necrosis, 403, 404
Non-toxic goiter, 431 Pancreatic trauma, 391
Normal sterile saline (NSS) infusion, 779 Pancreaticoduodenectomy (PD), 362, 396, 398, 470
North American Symptomatic Carotid Endarterectomy Pancreatitis, 391
Trial (NASCET), 547 Papillary thyroid cancer (PTC), 355, 359, 439
Nuclear scintigraphy, 205 Papillotomy, 388
Paradoxical aciduria, 779, 780
Paraesophageal hernia, 133, 134
O Parapneumonic effusion, 55
Obstetrical trauma, 283, 285 Paratesticular sarcomas, 606
Obstructive shock, 727, 728 Parathyroid hormone (PTH), 443, 444, 771, 775
Obturator hernia, 797, 798 Partial hepatectomy, 316
Occluded dialysis access, 593 Past medical history (PMH), 637
Occult breast cancer, 85 Patent processus vaginalis (PPV), 517, 518
Octreotide, 157, 470 Patient-controlled analgesia (PCA) pumps, 380
Olive, 529 PCT, see Penetrating chest trauma (PCT)
Omphaloceles, 537, 538 Pediatric inguinal hernia, 517, 518
Oncoplastic techniques, 109 Pediatric intussusception, 525, 526
Oopiods, 303 Pelvic fracture, 679, 680, 687
Open anterior tension-free mesh technique, 784 Pelvic fracture urethral injury (PFUI), 675, 676
Open cholecystectomy (OC), 346 Pelvic ring injuries, 679
Open surgical repair (OSR), 551 Pelvic roentgenograms, 645
Operating room (OR), 687 Penetrating abdominal trauma, 645, 646
Operative approach, diaphragmatic injury, 653 Penetrating chest trauma (PCT), 627, 628
Operative management, penetrating neck trauma, 624 Penetrating neck trauma (PNT), 623, 624
Oral calcium supplementation, 444 Penetrating trauma, 631, 675, 687
Oral contraceptives (OCPs), 308 abdomen, 631
Orchiectomy, 605, 606 chest, 631
870 Index

Peptic ulcer disease (PUD), 157–159, 161 cholecystectomy, 373–374

Peptic ulcers, 171 and cholelithiasis, 845, 846
Percutaneous catheter drainage(PCD), 325 hernia, 857, 858
Percutaneous cholecystostomy, 349 termination of, 853
Percutaneous drain, 534 Pre-renal, 740
Percutaneous needle aspiration (PNA), 325 Pre-sacral drainage, 688
Perforation, 144, 533, 538 Primary hyperaldosteronism, see Conn’s syndrome
Periampullary adenocarcinoma (PAC), 395, 396, 398 Primary hyperparathyroidism (pHPT), 443, 444
Pericardial effusion, 633 Primary realignment, urethral injury, 675, 676
Pericatheter retrograde urethrography, 676 Primary sclerosing cholangitis (PSC), 335, 336
Perineal fistula, 509, 510 Proctoscopy, 289
Perineal proctosigmoidectomy, 265 Proinsulin, 473
Perineural invasion, 7 Propranolol, 748
Peripheral arterial disease (PAD), 573 Prostate cancer, 601, 602
Peripheral lymphadenopathy, 25 Prostate specific antigen (PSA), 601
Perirectal abscess and fistulae, 297, 298 Prostatectomy, 602
Peritoneal seeding, 165 Prosthetic mesh, 784
Persistent hypovolemia, 779 Proton pump inhibitors (PPI), 127, 161
Pertinent medical history, 707 Provoked DVT, 577
PET-CT, 17 Proximal DVT, 577
Petroleum-based dressings, 748 PSC, see Primary sclerosing cholangitis (PSC)
Peyer’s patches, 525 Pseudoaneurysm, 642
Pharmaco-mechanical thrombolysis, 589 Pseudocysts (PC), 391
Phenylephrine, 727 Pseudo-Zollinger Ellison syndrome, 162
Pheochromocytomas, 461, 462 Psoas signs, 849
Phlegmasia cerulea dolens, 577 Pulmonary artery catheter (PAC), 637
Plasma aldosterone concentration (PAC), 465 Pulmonary emboli
Plasma renin activity (PRA), 465 post-operative, 743, 744
Platelet-derived growth factor receptor alpha symptoms, 743
(PDGFRA), 169 Pulselessness, 694
Platinum-based multi-drug chemotherapy, 606 Puncture, Aspiration of cyst, Injection of protoscolicidal
Pleomorphic LCIS (PLCIS), 82 solution, reaspiration of fluid (PAIR), 315
Pleurodesis, 59, 60 Pyloric stenosis, 529, 530
Pneumatic dilation, 123, 124 Pyloromyotomy, 530
Pneumatosis intestinalis, 533 Pyogenic liver abscess, 325–327
Pneumonectomy, 51
Pneumothorax, 59, 60, 627, 633
Polycystic liver disease (PCLD), 314 Q
etiology, 313 Quality of life, 102
imaging, 314
management, 316
Polypectomy, 251, 252 R
Portal hypertension, 339, 340 Radiation therapy
Portal venous gas, 533, 534 breast, 97, 98
Positive end expiratory pressure (PEEP), 719 pregnancy, 853
Post cholecystectomy, 351, 352 sarcoma, 9
Post-cholecystectomy cholangitis, 355 Radiation treatment (RT), 98
Posterior mesh rectopexy, 266 Radical surgery, hydatid cyst, 315
Posterior Sagittal Anorectoplasty, 510 Radioactive iodine, 423, 431, 440
Posterior Sagittal Anorectovaginourethroplasty, 510 Radiofrequency Ablation (RFA), 331
Posterior tibial (PT), 573 Radiographs, Fournier’s gangrene, 609
Posterolateral thoracotomy, 627 Radiotherapy, squamous cell carcinoma, 17, 18
Post-mastectomy radiation therapy (PMRT), 110 Randomised Evaluation of Surgery with Craniectomy for
Postoperative ileus, 197 Uncontrollable Elevation of Intracranial
Postpartum thyroiditis, 427 Pressure (RESCUEicp) trial, 702–703
Post-renal, 739 Rapid shallow breathing index (RSBI), 715
Pregnancy Reconstruction, Fournier’s gangrene, 610
appendicitis in, 849, 850 Recruitment maneuver, 719
breast cancer, 853, 854 Rectal adenocarcinoma, 278
btermination of, 853 Rectal bleeding, 270
Index 871

Rectal cancer, 275–279 simple cyst, 315

Rectal gas, 510 Scrotal abscess, 609
Rectal injury, 687, 688 Scrotal mass, 605, 606
Rectal prolapse, 263–266, 270, 271 Scrotal ultrasound, 605
Recto-urethral fistula, 509, 510 Seatbelt sign, 683
Rectovaginal fistula, 283–286 Secretin stimulation test, 469
Recurrent breast cancer, 91, 92 Secretin test, 161
Recurrent inguinal hernia, 789, 790 Secretin-enhanced MRCP, 387
Recurrent laryngeal nerve (RLN), 439 Secretory diarrhea, 481
Recurrent peptic ulcer disease, 161–162 Segmental blood pressures, 573
Redistributive hypokalemia, 765 Self-examination, 7
Regional recurrence, 92 Sellar mass, 420
Regorafenib, 332 Seminoma, 606
Regurgitation, 133 Sentinel lymph node biopsy, 78
Reintubation, 715 Sentinel node biopsy, 3
Renal cell carcinoma (RCC), 597, 598 Sepsis, 723, 724
Renal cysts, 597 Sepsis-induced ARDS, 724
Renal insufficiency, 767 Sepsis-induced hypoperfusion, 723
Renal replacement therapy (RRT), 740 Septic shock, 723
Renal ultrasound, 739 Serial endoscopy, 144
Renin-angiotensin-aldosterone system, 757 Serial transverse enteroplasty procedure (STEP), 201
Repair options, thoracoabdominal aortic aneurysm, 64 Serotonin, 185, 186
Resection rectopexy, 265, 266 Serum cortisol, 449
Respiratory acidosis, 751 Serum gastrin levels, 469
Respiratory alkalosis, 751 Sestamibi scan, 444
Resuscitation, 631 Seton, 298
Resuscitative endovascular balloon occlusion of the aorta Shock, 727, 728
(REBOA), 631, 632, 679 Short bowel syndrome, 201
Resuscitative thoracotomy, 627 Sigmoid colectomy, 210
Retained antrum, 161 Sigmoid volvulus, 221
Retrograde pyelography, 671 Silo, 538
Retrograde urethrogram, 676 Silver impregnated dressings, 747, 748
Retrohepatic caval injury, 658 Silver sulfadiazine, 748
Revascularization, 565 Simple cysts
CDT, 565 etiology, 313
chronic limb ischemia, 569 imaging, 314
Rhabdomyosarcoma, 9 management, 315–316
Rib fractures, 633 Single perineal orifice, 510
Rib plating, 633 “6 Ps” of arterial ischemia, 693
Riedel’s thyroiditis, 428 Skin rashes, 669
Right lower quadrant (RLQ), 225 Sleeve gastrectomy (SG), leaks, 835
Right Upper Quadrant US, hepatic abscess, 324 Small bowel mass, 181, 182
Rigler’s triad, 199 Small bowel neuroendocrine tumors, 185, 186
Roux-en-Y gastric bypass (RYGB), 130, 827 Small bowel obstruction
Roux-en-Y hepatic portoenterostomy, 542 concerning findings, 176
Roux-en-Y leaks, 835, 836 hernia, 177
Roux-en-Y reconstruction, 158, 176 imaging, 176
Rovsing signs, 849 impaired patient, 177
RRT, see Renal replacement therapy (RRT) laboratory, 176
Rupture, 642 Roux-en-Y reconstruction, 176
Ruptured abdominal aortic aneurysm (AAA), 555, 556 symptoms, 175
treatment, 177
virgin abdomen, 176
S work-up, 175
Sacral neuromodulation, 303 Small bowel tumors, 181, 182
Salivary gland tumors, 29 Small intestine atresia, 501
Sarcoma, 9, 181 Soft tissue sarcoma, 9
SBRT, 51, 52 Solitary rectal ulcer syndrome (SRUS), 269–272
Sclerotherapy, 289 Somatostatin, 185, 186, 477
PCLD, 316 Somatostatin analogs, PCLD, 316
872 Index

Somatostatin inhibitors, 481 Testicular ultrasound, 606

Somatostatinoma, 477 TEVAR, 560
Somatostatin-receptor-scintigraphy, 470 Thiamin, 839
Spermatic cord, 605 Thoracentesis, 55
Sphincterotomy, 293, 294, 380 Thoracic outlet syndrome (TOS), 589
Spine immobilization, 623 Thoracic spine fractures, 634
Spironolactone, 466 Thoracic surgery, 641
Spleen, 665, 666 Thoracoabdominal aortic aneurysm (TAAA), 63, 64
Splenectomy, 409 Thoracotomy, 56, 744
atraumatic indications for, 413, 414 emergency department, 631, 632
Splenic abscess, 409 3-phase abdominal CT scan, renal mass, 597
Splenic injury, 665, 666 Thrombolysis, thoracic outlet syndrome, 589
Spontaneous pneumothorax, management of, 59, 60 Thymoma, 39, 40
Squamous cell carcinoma, 7, 135 Thyroglossal duct cyst, 26
of oropharynx, 17, 18 Thyroid cancer, 439, 440
Staged resection, 327 Thyroid function, 435
Standard meal test, 162 Thyroid hormone, 431
Steatorrhea, 477 Thyroid masses, 21
Step-up approach, 403 Thyroid nodule, 435, 436
Stoppa repair, 790, 797, 798 Thyroid peroxidase, 419
Straddle injury, 676 Thyroid stimulating hormone (TSH) level, 423
Strangulated hernia, 805, 806 Thyroid storm, 423
Strangulation, 517, 518 Thyroidectomy, 427
Stricturoplasty, 195 Thyroiditis, 427, 428
Stroke, 547, 548 Tissue expander, 110
Stryker needle, 694 TNM-staging, 135, 136, 277
Subclavian-axillary vein thrombosis, 589 Tobacco, 17
Subdural hematoma, 620 Tocolytic therapy, 850
Sub-epithelial fistula, 510 TOS, see Thoracic outlet syndrome (TOS)
Subphenotypes of ARDS, 719 Total abdominal colectomy, 229, 234
Substernal extension, 431 Total proctocolectomy, 234
Succinylcholine, 711 Total thyroidectomy, 435, 436, 439
Sun exposure, 7 Totally extraperitoneal (TEP) technique, 784
Superior mesenteric artery (SMA), 581 femoral hernia, 794
Supervised exercise program, 573 obturator hernia, 798
Supraglottic airway (SGA), 707, 708 recurrent inguinal hernia, 790
Supralevator abscess, 297 Toupet fundoplication, 130
Surgical airway, intervention, 708 Toxic megacolon, 195, 234
Sustained hypernatremia, 761 Toxic multinodular goiter, 423, 431
Suture rectopexy, 265, 266 Tracheal dilation, 44
Symptomatic anemia, 731 Tracheal laser ablation, 44
Symptomatic gallbladder disease, 346 Tracheal resection, 43
Symptomatic hyponatremia, 758 Tracheal stenosis, 43
Syndrome of inappropriate antidiuretic hormone Tracheal stenting, 43
secretion (SIADH), 757 Tracheoesophageal fistula (TEF), 491, 492
Synthetic mesh, 654 Tracheoesophageal injury, hard signs of, 623
Systemic therapy, 98, 101, 102 Tracheotomy, 18
Trans abdominal wall traction (TAWT) system, 809
Transabdominal preperitoneal (TAPP) technique, 784
T femoral hernia, 794
Tachycardia, 657 obturator hernia, 798
Target sign, 525 recurrent inguinal hernia, 790
TBI, see Traumatic brain injury (TBI) Transient ischemic attacks (TIA), 547
Telemetry, 637 Transinguinal preperitoneal (TIPP) technique, 784, 790
Temporary abdominal closure, 736, 809 Transmediastinal injury, 627
Tension pneumothorax, 728 Trans-pulmonary pressure, 719
Teratoma, 39 Trans-rectus sheath extra-peritoneal (TREPP)
Termination of pregnancy, 853 technique, 784
Testicular mass, 605, 606 recurrent inguinal hernia, 790
Testicular torsion, 605 Transversus abdominis release (TAR), 814
Index 873

Traumatic brain injury (TBI), 619, 620 Vascular malformation, 26

Traumatic cardiac arrest, 631 Vascular surgery, 641
Traumatic injury, cardinal sign for, 683 Vasoactive intestinal peptide (VIP), 481, 482
Traumatic liver injury, 657, 658 Vasopressors, sepsis, 723
Troponin, 637 Vedolizumab, 230
T-tube, 355 Venous TOS, 589
Tube thoracostomy, 59 Ventilation-perfusion radionuclide scanning, 743
Tumors of the mediastinum, 39, 40 Ventral hernia repair, 801, 802, 831, 832
Typical fissure, 293 Ventral mesh rectopexy, 266
Vestibular fistula, 510
Vicryl mesh, 809
U Video-assisted retroperitoneal debridement (VARD),
U.S. Preventative Services Task Force (USPSTF), 601 403, 404
Ulceration, 3 Video-assisted thoracoscopic surgery
Ulcerative colitis (UC), 229, 230 (VATS), 55, 56
Ultrasound (US) Video-assisted thoracoscopy, penetrating chest
axillary lymph node, 85 trauma, 628
breast mass, 73 Virgin abdomen, 176
cholelithiasis, 845 Vitamin B12 deficiency, 839
cystadenocarcinoma, 315 Vitamin C, 748
cystadenoma, 315 Vitamin D, 443, 444, 775, 776
femoral hernia, 793 Vitamin D deficiency, 772
Fournier’s gangrene, 609 Vitamin deficiency, 839, 840
hydatid cysts, 314 Vocal cord paralysis, 439
inguinal hernia, 783 von Meyenburg complexes
male breast cancer, 114 etiology, 313
PCLD, 314 imaging, 315
scrotal, 605 management, 316
simple cysts, 314
splenic abscess, 409
testicular, 606 W
von Meyenburg complexes, 315 Walled-off pancreatic fluid collection, 391, 392
Umbilical hernia, 857, 858 Walled-off pancreatic necrosis (WOPN), 391, 392
Unprovoked DVT, 577 Waveform capnography, 711–712
Upper extremity swelling, 589 WDHA syndrome, 481
Upper gastrointestinal symptoms, 827 Weight loss, 585
Upper gastrointestinal swallow, 821 Wells prediction scoring system, 743
Upper gastrointestinal endoscopy, 165 Whipple’s triad, 473
Upper gastrointestinal hemorrhage, 171 Whole breast radiation (WBI), 91
Ureter injury, 671 Wittman patch, 809
Urethral catheterization, 610 Wound closure, 610, 695
Urethral injury, 675, 676
Urinalysis, 739
Urinary electrolytes, 779 Y
Urinoma, 671 Yttrium-90, 328, 332

V Z
Valsalva maneuver, 789 Zinc deficiency, 840
Van Nuys Prediction Index, 78 Zipper closure method, 810
Vancomycin, 241 Zoledronic acid, 776
Fournier’s gangrene, 609 Zollinger-Ellison syndrome (ZES), 161, 469
Varicoceles, 605, 606 Zone I injury, 624
Vascular injury, 693 Zone II injury, 624
hard signs of, 623–625 Zone III injury, 624