Clinical Algorithms in General Surgery. A Practical Guide 9783319984964, 9783319984971, 2019930648

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

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Salvatore Docimo Jr.  •  Eric M. Pauli Editors

Clinical Algorithms in General Surgery A Practical Guide

Editors Salvatore Docimo Jr. Department of Surgery Stony Brook Medicine Stony Brook, NY USA

Eric M. Pauli Department of Surgery Penn State Milton S. Hershey Medical Center 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 challenging 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 knowledge base as they prepare for the American Board of Surgery certifying examination. Stony Brook, NY, USA Hershey, PA, USA

Salvatore Docimo Jr. Eric M. Pauli

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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.

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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

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xxiv

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

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

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

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

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

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

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

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

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

Contributors

Part I Skin and Soft Tissue

1

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 intraoperative use of gamma probe with or without vital blue dye injection, followed by meticulous 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: [email protected]

and pelvis with IV contrast or full body PET/ CT, and consider brain MRI.  If there is evidence 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 metastatic 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 complete 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.

© 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

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4

• • •

A

History and Physical Exam: pigmented cutaneous lesion Complete skin exam and nodal exam Biopsy

Primary melanoma

Melanoma with suspicion of mets, palpable LN

B

• •

High or low risk?

Low

WLE with 1 cm margin

C

WLE with 1-2 cm margin and sentinel lymph node biopsy

Sentinel node negative for malignancy

Staging imaging FNA/core biopsy of suspicious nodes or metastatic lesions

Metastatic disease

High

Systemic chemotherapy or clinical trial

Sentinel node positive for malignancy

E

D

Regional disease WLE and lymph node dissection

Consider systemic chemotherapy or clinical trial

Staging imaging

Regional disease Completion lymphadenectomy

Metastatic disease Consider systemic chemotherapy or clinical trial

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

Algorithm 1.1

Suggested Reading National Comprehensive Cancer Network. NCCN clinical practice guidelines in oncology: melanoma (version 1.2017). https://www.nccn.org/professionals/physician_gls/pdf/melanoma.pdf. Accessed 17 July 2017.

F

2

Basal Cell Carcinoma Julie A. DiSano and Colette R. Pameijer

Algorithmic Approach

D. The lesion should be risk stratified to determine if there is a high risk or low risk for recur A. The first step in the evaluation of a patient rence. High-risk lesions have any of the with a suspicious skin lesion is the history following features: Location on mask areas of and physical examination. The typical appearthe face, genitalia, hands, or feet; lesion greater ance of basal cell carcinoma is a pearly, flesh-­ than 20 mm on the trunk or extremities; lesion colored bump on sun-exposed skin. A greater than 10 mm on the cheeks, forehead, complete skin exam should be performed as scalp, neck, and feet; poorly defined borders; well as a nodal exam. The lesion should be recurrent disease; patient on immunosuppresbiopsied; lymph nodes should only be biopsion; lesion at the site of prior radiation thersied if palpable on exam. apy; perineural involvement; and pathology B. Once diagnosis of basal cell carcinoma is showing aggressive growth pattern. established, surgical excision is the treatment E. Patients with high-risk lesions should be conof choice. The choice of Mohs micrographic sidered for further treatment with radiation surgery or surgical excision is based on size, therapy. Addition of a hedgehog pathway location, cosmesis, and patient comorbidities. inhibitor (vismodegib or sonidegib) should Excision should achieve at least a 4  mm also be considered. margin. F. Follow-up care: Patient should have a com C. If the lesion is not able to be excised, the plete skin exam every 6–12  months for the patient should undergo radiation therapy. first 5  years and at least annually for life. Treatment with a hedgehog pathway inhibitor Patient should be educated about sun protec(vismodegib or sonidegib) can be considered. tion and self-examination.

J. A. DiSano · C. R. Pameijer (*) Department of General Surgery, Penn State Milton S. Hershey Medical Center, Hershey, PA, USA e-mail: [email protected] © 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

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J. A. DiSano and C. R. Pameijer

6

History and Physical Exam: Suspicious skin lesion

A • •

Complete skin exam and nodal exam Biopsy Basal Cell Carcinoma

C Candidate for surgical excision?

B

No Consider radiation therapy or hedgehog pathway inhibitor

Yes Surgical excision +/- Mohs

D

High or low risk?

High risk

E Low risk

F

Consider radiation therapy or hedgehog pathway inhibitor

Follow-up care: Regular complete skin exam 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.

3

Squamous Cell Carcinoma Julie A. DiSano and Colette R. Pameijer

Algorithmic Approach A. The typical appearance of squamous cell carcinoma 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, abdomen, and pelvis should be done. If disease is limited to the regional lymph nodes, the patient should have wide excision of the primary site and lymphadenectomy. C. If there are no palpable nodes or the node biopsy shows no evidence of malignancy, surgical 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 positive, patient should undergo Mohs micrographic surgery to achieve negative margins.

If excision is not possible, the patient should undergo radiation therapy with or without systemic chemotherapy. D. The lesion should be risk stratified to determine 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 considered for further treatment with radiation therapy. F. Follow-up care: Patients should have a complete 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.

J. A. DiSano · C. R. Pameijer (*) Department of General Surgery, Penn State Milton S. Hershey Medical Center, Hershey, PA, USA e-mail: [email protected] © 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

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J. A. DiSano and C. R. Pameijer

8

History and Physical Exam: Skin lesion that is ulcerated.

A · ·

Complete skin exam and nodal exam Biopsy

Squamous cell carcinoma

B Palpable nodes?

Yes

FNA or core needle biopsy of node

No

Consider radiation therapy

Malignant

Benign

C No

Candidate for surgical excision?

Staging CT Excision of primary and lymph node dissection if limited to regional disease.

Yes

High or low risk?

D

High risk

E

Consider radiation therapy Low risk

F

Follow-up care: Regular complete skin exam 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/professionals/physician_gls/pdf/squamous.pdf. Accessed 17 July 2017.

4

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 history of radiation to the area. Patients often report a history of trauma, which is not causative 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 established, 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 sarcoma should be referred for chemotherapy and/or radiation. Following treatment, they

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, consider further therapy with radiation or chemotherapy, 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.

J. A. DiSano · C. R. Pameijer (*) Department of General Surgery, Penn State Milton S. Hershey Medical Center, Hershey, PA, USA e-mail: [email protected] © 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

9

J. A. DiSano and C. R. Pameijer

10

History and Physical Exam: Painless mass, increasing in size.

A

· Imaging with MRI or CT · Image guided biopsy

B

C

Sarcoma

D

Rhabdomyosarcoma

E · ·

Low grade Resectable

· ·

High grade Borderline resectable

Margin negative resection

Neoadjuvant therapy

Consider radiation therapy

Reassess with imaging (MRI/CT)

Margin negative resection

F

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

Algorithm 4.1

Suggested Reading National Comprehensive Cancer Network. NCCN clinical practice guidelines in oncology: sarcoma (version 1.2017). https://www.nccn.org/professionals/physician_gls/pdf/sarcoma.pdf. Accessed 17 July 2017.

· · ·

Unresectable Desmoid Ewings

Systemic chemotherapy and radiation

Consider resection based on response to treatment

Refer to specialty center

5

Necrotizing Soft Tissue Infection Julie A. DiSano and Colette R. Pameijer

Algorithmic Approach A. Patients with necrotizing soft tissue infections (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 systemic toxicity. NSTIs most commonly involve the extremities, perineum, and genitalia [1, 2]. B. Laboratory analysis should include a CBC, complete metabolic panel, and CRP.  The LRINEC (laboratory risk indicatory for necrotizing 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 1.6). If the LRINEC score is ≥6, there is a high likelihood of NSTI [3]. C. The patient should be appropriately resuscitated. 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: [email protected]

patient should be started on broad-spectrum antibiotics, including coverage for gram-­ positive cocci, gram-negative rods, and anaerobes, including clostridial species (penicillin G, vancomycin, gentamicin, clindamycin). NSTI is a surgical emergency, and nonoperative 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 resuscitation, broad-spectrum antibiotics, and management of comorbidities. They should return to the operating room within 24 h for further evaluation, and debridement if necessary. Patients with necrotizing soft tissue infections 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 surgeon 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 surgical debridement. F. Follow-up care: Patients will require a multidisciplinary team to aid in recovery. They will require rehabilitation, wound management, and possible flap coverage.

© 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

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12

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

A

Obtain vital signs, blood work, and perform physical exam

B

C

Calculate LRINEC score

Yes

OR for debridement

High suspicion for NSTI?

D Yes

No

E

Broad, spectrum antibiotics, resuscitation, serial debridement

Bedside I&D reveals NSTI?

No

Broad, spectrum antibiotics, IVF resuscitation, close observation

F Algorithm 5.1

Follow-up Care: Wound management, flap coverage, and rehabilitation

5  Necrotizing Soft Tissue Infection

References 1. Bonne SL, Kadri SS. Evaluation and management of necrotizing soft tissue infections. Infect Dis Clin N Am. 2017;31(3):497–511. https://doi.org/10.1016/j. idc.2017.05.011. 2. Hakkarainen TW, Kopari NM, Pham TN, Evans HL.  Necrotizing soft tissue infections: review and current concepts in treatment, systems of care, and outcomes. Curr Probl Surg. 2014;51(8):344–62. https://doi.org/10.1067/j.cpsurg.2014.06.001.

13 PubMed PMID: 25069713; PubMed Central PMCID: PMCPMC4199388. 3. Wong CH, Khin LW, Heng KS, Tan KC, Low CO.  The LRINEC (laboratory risk indicator for necrotizing fasciitis) score: a tool for distinguishing necrotizing ­fasciitis from other soft tissue infections. Crit Care Med. 2004;32(7):1535–41. PubMed PMID: 15241098. 4. Anaya DA, Dellinger EP.  Necrotizing soft-tissue infection:diagnosis and management. Clin Infect Dis. 2007;44(5):705. Pubmed PMID: 17278065.

Part II Head and Neck

6

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 carcinoma (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 sexual 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 Surgery, University of Miami Miller School of Medicine, Miami, FL, USA e-mail: [email protected] 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: [email protected]

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 synchronous lesions. Cranial nerve IX-XII function 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 contrastenhanced CT or MRI of the head and neck for precise evaluation, staging, and treatment planning [2]. Patients with lymph node irregularities and an unknown primary lesion should first undergo an ultrasoundguided fine needle aspiration of the node, followed by imaging if the results are positive for malignancy [3]. D. Definitive diagnosis requires histopathological 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 performed to evaluate for metastatic disease [5] and stage-dependent treatment discussed with a head and neck surgeon, including s­urgical resection with possible reconstruction, radiotherapy, and/or chemotherapy [1, 6].

© 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

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F. Postoperative maintenance of the three major 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

A

initiated. A temporary tracheotomy may rarely be required to maintain a patent airway. All patients should maintain adequate oral hygiene with regular suctioning and use of antiseptic mouthwashes. Patients should regularly be monitored for detection of possible recurrence and subsequent early intervention [1].

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

B 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 +/- lymphadenopathy

Irregular lymph node with 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-local invasion)

Unresectable (T4b +)

or

or

or

1º resection, selective ND RT +/- chemo if high risk

Radiotherapy +/- chemo

Chemoradiation

Salvage surgery

1º resection, bilateral ND

Chemoradiation

Palliation

RT +/- chemo if high risk

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

Algorithm 6.1

F

6  Management of Squamous Cell Carcinoma of the Oropharynx

References 1. Flint PW, Cummings WC.  Malignant neoplasms of the oropharynx. In: Cummings otolaryngology: head and neck surgery. Philadelphia: Elsevier, Saunders; 2015. 2. Wippold FJ. Head and neck imaging: the role of CT and MRI. J Magn Reson Imaging. 2007;25:453. 3. Righi PD, Kopecky KK, Caldemeyer KS, et  al. Comparison of the ultrasound- fine needle aspiration and computed tomography in patients undergoing elective neck dissection. Head Neck. 1997;19(7):604–10.

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4. Lewis JS, Thorstad WL, Chernock RD, et  al. p16 positive oropharyngeal squamous cell carcinoma: an entity with a favorable prognosis regardless of tumor HPV status. Am J Surg Pathol. 2010;34(8):1088–96. 5. Quon A, Fischbein NJ, McDougall IR, et al. Clinical role of F-FDG PET/CT in the management of squamous cell carcinoma of the head and neck and thyroid carcinoma. J Nucl Med. 2007;48(Suppl 1):58S–67S. 6. Yousem DM, Gad K, Tufano RP. Resectability issues with head and neck cancer. Am J Neuroradiol. 2006;27(10):2024–36.

7

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, hemoptysis, 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: [email protected] 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: [email protected]

symptoms of infection including symptoms of fever, chills, fluctuance, erythema, tenderness, or warmth should prompt treatment with antibiotics and re-evaluation. B. A detailed head and neck examination is critical. 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 commonly utilized imaging modality. To avoid ionizing radiation, ultrasonography may be initially useful in the pediatric population as they have a higher likelihood of an inflammatory, infectious, or congenital process [5]. Ultrasonography should also be considered for thyroid masses, as use of CT with iodine contrast can delay potential radioiodine treatment. 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.

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E. If the lesion is found to be infectious, conservative therapy with antibiotic treatment and possible steroids may be administered while congenital lesions should undergo observation with reassessment for surgical excision. Neoplastic lesions should be referred to a

A-B

head and neck oncologic surgeon for further workup for staging and appropriate management.

History and physical

Yes

Signs of infection

Antibiotics with reevaluation

No Diagnostic Imaging CT: Standard CTA/MRA: Vascular lesion MRI: Soft tissue concern Ultrasound: Pediatric/thyroid

C

D

E Concern for malignancy?

No Congenital or inflammatory

Yes Biopsy and referral to head and neck oncologic surgeon

Algorithm 7.1

Trial of antibiotics ± steroids. Refer to otolaryngologist.

7  Evaluation of Neck Mass

References 1. Goff CJ, Allred C, Glade RS.  Current management of congenital branchial cleft cysts, sinuses and fistulae. Curr Opin Otolaryngol Head Neck Surg. 2012;20:533–9. 2. Tracy TF, Muratore CS. Management of common head and neck masses. Semin Pediatr Surg. 2007;16:3–13. 3. Chen AY, Otto KJ.  Differential diagnosis of neck masses. In: Flint PW, Haughey BH, Lund VJ, editors.

23 Cummings otolaryngology: head and neck surgery. 5th ed. Philadelphia: Elsevier; 2010. 4. Kadom N, Lee EY.  Neck masses in children: current imaging guidelines and imaging findings. Semin Roentgenol. 2012;47:7–20. 5. Layfield L.  Fine-needle aspiration in the diagnosis of head and neck lesions: a review and discussion of problems in differential diagnosis. Diagn Cytopathol. 2007;35:798–805.

8

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 malignancy. 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 physical 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: [email protected] 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: [email protected]

mass as well as its rate of growth are important, 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 infections; hard nodes fixed to the skin or deeper structures can suggest malignancy; and fluctuant 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 lymphadenopathy, 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 infectious 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

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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, oncologist, 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 dermoid 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?

B

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

C

Signs of infection: tenderness and erythema of node, chills, fatigue?

YES

NO

D

Trial of oral antibiotics

Developmental mass suspected? YES

Improvement in 2-3 days?

YES

CBC, blood smear, FNA/ excisional biopsy Referral to ENT

E NO

Developmental mass suspected?

NO YES •

Complete 10 daycourse

• •

YES

Treat and follow up with ENT and/or infectious disease as appropriate

Algorithm 8.1

Ultrasound with reflex CT for abscess vs. cyst CBC, CRP, LDH, CXR for inflammatory process HIV, EBV, CMV, toxo serology

Positive results?

NO

Referral to ENT

Consider LAD secondary to drug reaction or benign etiology

Observe for 4-6 weeks

NO

Evaluate for possible malignancy (see D)

Refer to ENT if node increases in size or remains >2 cm

8  Evaluation of an Enlarged Cervical Lymph Node

References 1. Connolly AA, MacKenzie K.  Paediatric neck masses—a diagnostic dilemma. J Laryngol Otol. 1997;111(6):541–5. 2. Bauer PW, Lusk RP.  Neck masses. In: Bluestone CD, Stool SE, Alper CM, et al., editors. Pediatric otolaryngology. 4th ed. Philadelphia: Saunders; 2003. p. 1629–47. 3. Torsiglieri AJ Jr, Tom LW, Ross AJ III, Wetmore RF, Handler SD, Potsic WP. Pediatric neck masses: guidelines for evaluation. Int J Pediatr Otorhinolaryngol. 1988;16(3):199–210.

27 4. Acierno SP, Waldhausen JH.  Congenital cervical cysts, sinuses and fistulae. Otolaryngol Clin N Am. 2007;40(1):161–76. vii–viii. 5. Leung AK, Robson WL.  Childhood cervical lymphadenopathy. J Pediatr Health Care. 2004;18(1):3–7. 6. Anne S, Teot LA, Mandell DL.  Fine needle aspiration biopsy: role in diagnosis of pediatric head and neck masses. Int J Pediatr Otorhinolaryngol. 2008;72(10):1547–53. 7. Dickson PV, Davidoff AM.  Malignant neoplasms of the head and neck. Semin Pediatr Surg. 2006;15(2):92–8.

9

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 commonly reported in malignant lesions and may suggest perineural invasion (PNI) [1]. B. Physical findings that increase the index of suspicion for malignancy include facial paresis, cervical lymphadenopathy, and fixation of mass to overlying skin or deep structures [2]. Lymphadenopathy is seen on presentation 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: [email protected] 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: [email protected]

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 recommended 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 symptoms 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 histology should undergo neck dissection (ND). H. Adjuvant radiotherapy should be considered in cases of high grade, T3/T4, close (8]) to allow for an interventional bronchoscopy. Flexible bronchoscopy is key to evacuate clots, identify the source, and control the bleeding. Cold saline, epinephrine wash, and direct pressure (with the scope or balloon) are commonly used effective modalities. Other possible modalities 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, iatrogenic injuries, and fistulae. D2. If bronchoscopy was unsuccessful, further actions should be taken to protect and ventilate 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-

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sidered as a last resort since it does not help tamponade the bleed [3]. E. Subsequently, the definitive treatment of airway (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 overinflation, 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

Secure the airway to maintain gas exchange - Position patient in lateral decubitus (bleeding side down) - Intubate with large ET tube

C -

-

Support hemodynamics Correct coagulopathy Transfuse as needed Complete Hx and physical exam (while bronchoscopy is being set up)

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

Is the bleeding controlled?

D

Yes

No

Address underlying etiology

-

E Airways

Angiography with embolization

Algorithm 10.1

Parenchyma

Lung resection

Protect and ventilate unaffected lung Endobronchial blocker in bleeding side Switch to a double lumen ET tube Advance ET tube to unaffected side

What is the source of bleeding?

Tracheoesophageal

TE fistulae repair

10  Massive Hemoptysis

References

37

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 managehospital mortality of patients with hemoptysis: an ment of hemoptysis: a comprehensive review of diagapproach 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 managetracheoarterial fistula in patients with chronic trachement. 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

11

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 cavities 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, teratomas [and other germ cell tumors], thyroid tumors, and lymphomas [3]. A mass in the middle mediastinal compartment, which houses the visceral organ and structures, is usually a cyst [cardiac, bronchogenic, 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: [email protected] M. B. Yammine Department of Cardiovascular Surgery, Icahn School of Medicine at Mount Sinai, New York, NY, USA

thenia gravis, Horner syndrome, paraneoplastic 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 invasion 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 resection 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 systemic disease [9]. (b) Technetium scan to locate ectopic thyroid 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 suspected [percutaneous vs. endobronchial vs. surgical].

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Germ cell tumors are treated by chemotherapy, lymphomas with ChemoRad, and thyroid and thymic tumors with resection.

Thymomas: Most common neoplasm of the anterior mediastinum [12, 13]. The decision to operate 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

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

E Yes

Treatment of germ cell tumors [chemotherapy]

Anterior

Middle

AFP/BHCG +ve?

D

Surgical resection recommended if symptomatic

Posterior

Tissue Bx may be helpful

No

Needle Bx followed by ChemoRad if confirmed

Yes

Surgical resection recommended in conjunction with neurosurgery

Lymphoma suspected?

No Tissue biopsy needed prior Yes to definitive ChemoRad

Vital organs invaded (arch vessel, SVC, pulmonary hilum) No

Tumor resection with curative intent for thymic tumor [thoracoscopic vs. median sternotomy]

Algorithm 11.1

C

11  Mediastinal Masses

References 1. Carter BW, Tomiyama N, Bhora FY, Rosado de Christenson ML, Nakajima J, Boiselle PM, et  al. A modern definition of mediastinal compartments. J Thorac Oncol. 2014;9(9 Suppl 2):S97–101. 2. Duwe BV, Sterman DH, Musani AI.  Tumors of the mediastinum. Chest. 2005;128(4):2893–909. 3. Carter BW, Marom EM, Detterbeck FC. Approaching the patient with an anterior mediastinal mass: a guide for clinicians. J Thorac Oncol. 2014;9(9 Suppl 2):S102–9. 4. Reeder LB.  Neurogenic tumors of the mediastinum. Semin Thorac Cardiovasc Surg. 2000;12(4):261–7. 5. Mazel C, Grunenwald D, Laudrin P, Marmorat JL.  Radical excision in the management of thoracic and cervicothoracic tumors involving the spine: results in a series of 36 cases. Spine (Phila Pa 1976). 2003;28(8):782–92. discussion 92. 6. Forsythe A, Volpe J, Muller R. Posterior mediastinal ganglioneuroma. Radiographics. 2004;24(2):594–7.

41 7. Takeda S, Miyoshi S, Minami M, Ohta M, Masaoka A, Matsuda H. Clinical spectrum of mediastinal cysts. Chest. 2003;124(1):125–32. 8. Esme H, Eren S, Sezer M, Solak O. Primary mediastinal cysts: clinical evaluation and surgical results of 32 cases. Tex Heart Inst J. 2011;38(4):371–4. 9. Schiepers C, Filmont JE, Czernin J.  PET for staging of Hodgkin’s disease and non-Hodgkin’s lymphoma. Eur J Nucl Med Mol Imaging. 2003;30(Suppl 1):S82–8. 10. Javadpour N.  Significance of elevated serum alphafetoprotein (AFP) in seminoma. Cancer. 1980;45(8):2166–8. 11. Hori K, Uematsu K, Yasoshima H, Yamada A, Sakurai K, Ohya M.  Testicular seminoma with human chorionic gonadotropin production. Pathol Int. 1997;47(9):592–9. 12. Mullen B, Richardson JD. Primary anterior mediastinal tumors in children and adults. Ann Thorac Surg. 1986;42(3):338–45. 13. Gerein AN, Srivastava SP, Burgess J. Thymoma: a ten year review. Am J Surg. 1978;136(1):49–53.

Tracheal Stenosis

12

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 respiratory distress and include a complete history and physical exam. Suspicious symptoms include SOB nonresponsive to bronchodilators 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 emergent 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: [email protected] M. B. Yammine Department of Cardiovascular Surgery, Icahn School of Medicine at Mount Sinai, New York, NY, USA

v­entilation and therapeutic coring or dilation. 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 specificity, a CT is more useful in diagnosing and assessing severity [3]. D. Following airway establishment and for non-­life-­threatening stenosis, further management should take into consideration the following factors: Etiology of the lesion, prognosis, life expectancy, and ability to tolerate planned procedures. E1. For extrinsic compression of the trachea or systemic diseases causing stenosis, a disease-­ specific plan should be implemented. For example, ChemoRad for lymphoma, vascular intervention for aneurysms and rings, and resection for substernal thyroid tumors and thymomas [3]. E2. For intrinsic pathologies, the following treatment options are available [7–9]: (a) Tracheal resection of the affected segmented 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].

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(c) Tracheal dilation provides temporary relief and is achieved with dilators or balloons [9].

(d) Tracheal laser ablation and brachytherapy are used to excise scar tissue and 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

B Is the patient in respiratory distress? Yes

C

No

- O2 therapy - Bronchoscopy-guided intubation or surgical airway - Bronchoscopic assessment of severity, extent, and location of stenosis

D

-

Once stable

- CXR: r/o foreign body and tracheal deviation and mediastinal shift - CT Chest: Superior in diagnosis and assessing severity, extent, and location of stenosis

Etiology Prognosis/life expectancy Ability to tolerate therapeutic intervention

E

Extrinsic compression: Implement a disease-specific plan, for example, ChemoRad for lymphoma

Algorithm 12.1

-

Intrinsic compression: Tracheal resection Tracheal stenting/dilation Tracheal laser ablation

12  Tracheal Stenosis

References 1. Zias N, Chroneou A, Tabba MK, Gonzalez AV, Gray AW, Lamb CR, et al. Post tracheostomy and post intubation tracheal stenosis: report of 31 cases and review of the literature. BMC Pulm Med. 2008;8:18. 2. Koshkareva Y, Gaughan JP, Soliman AM. Risk factors for adult laryngotracheal stenosis: a review of 74 cases. Ann Otol Rhinol Laryngol. 2007;116(3):206–10. 3. Bacon JL, Patterson CM, Madden BP. Indications and interventional options for non-resectable tracheal stenosis. J Thorac Dis. 2014;6:258–70. 4. Majid A, Guerrero J, Gangadharan S, Feller-Kopman D, Boiselle P, DeCamp M, et al. Tracheobronchoplasty for severe tracheobronchomalacia: a prospective outcome analysis. Chest. 2008;134(4):801–7. 5. Papla B, Dyduch G, Frasik W, Olechnowicz H. Post-­ intubation tracheal stenosis  – morphological-clinical investigations. Pol J Pathol. 2003;54(4):261–6. 6. Allen AM, Abdelrahman N, Silvern D, Fenig E, Fruchter O, Kramer MR.  Endobronchial brachytherapy provides excellent long-term control of recurrent granulation tissue after tracheal stenosis. Brachytherapy. 2012;11(4):322–6.

45 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 bronchoscopic guidance. Zhonghua Yi Xue Za Zhi. 2011;91(42):2995–8. 8. Ciccone AM, De Giacomo T, Venuta F, Ibrahim M, Diso D, Coloni GF, et al. Operative and non-operative treatment of benign subglottic laryngotracheal stenosis. Eur J Cardiothorac Surg. 2004;26(4):818–22. 9. Dalar L, Karasulu L, Abul Y, Ozdemir C, Sokucu SN, Tarhan M, et al. Bronchoscopic treatment in the management of benign tracheal stenosis: choices for simple and complex tracheal stenosis. Ann Thorac Surg. 2016;101(4):1310–7. 10. Yamamoto K, Kojima F, Tomiyama K, Nakamura T, Hayashino Y. Meta-analysis of therapeutic procedures for acquired subglottic stenosis in adults. Ann Thorac Surg. 2011;91(6):1747–53. 11. Chin CS, Litle V, Yun J, Weiser T, Swanson SJ. Airway stents. Ann Thorac Surg. 2008;85(2):S792–6. 12. Leventhal DD, Krebs E, Rosen MR.  Flexible laser bronchoscopy for subglottic stenosis in the awake patient. Arch Otolaryngol Head Neck Surg. 2009;135(5):467–71.

Incidental Lung Nodule

13

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 discussion, 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 malignancy. The differential diagnosis includes infectious and inflammatory processes as well as benign and malignant tumors [3]. B. For patients with no previous history of cancer 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: [email protected] M. B. Yammine Department of Cardiovascular Surgery, Icahn School of Medicine at Mount Sinai, New York, NY, USA

C. If the nodule is >8 mm, a PET/CT is indicated to help categorize it. A hypometabolic nodule can undergo a repeat CT scan at 6  months, whereas a hypermetabolic one should undergo tissue biopsy (CT guided, endobronchial, or excisional) [4, 6, 7]. D1. If primary lung cancer is confirmed, staging 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 therapy. For stage 3 or 4, chemoradiation is the most common treatment. For patients who are poor candidates for surgery, alternative local therapies include cryoablation, stereotactic radiation, and radiofrequency ablation [8]. D2. For a metastatic lung nodule, a complete metastatectomy is reserved for controlled primary malignancies with favorable prognosis 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 imaging 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.

© 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

47

H. Tannous et al.

48

History and Physical exam: Smoking history, exposure to carcinogens (asbestos, silica, etc.), recent travel, previous malignancy, or family Hx of malignancy

A

B

Follow up CT in 6 months only if there is low index of suspicion: - No previous Hx of cancer - Prior imaging comparison

No

Is the nodule > 8 mm?

Yes PET/CT

C No Is the lesion hypermetabolic?

Active imaging surveillance (documenting interval growth warrants repeat PET/CT)

Yes Tissue biopsy (CT guided, endobronchial, or excisional)

Yes

D

1- Primary lung CA: Staging workup, preoperative evaluation, definitive resection 2- Metastatic nodule: Consider metastasectomy

Is the lesion malignant?

E

Algorithm 13.1

No

Address underlying etiology (autoimmune, infectious, etc.)

13  Incidental Lung Nodule

References 1. Ost D, Fein AM, Feinsilver SH.  Clinical practice. The solitary pulmonary nodule. N Engl J Med. 2003;348(25):2535–42. 2. Gould MK, Donington J, Lynch WR, Mazzone PJ, Midthun DE, Naidich DP, et  al. Evaluation of individuals with pulmonary nodules: when is it lung cancer? Diagnosis and management of lung cancer, 3rd ed: American College of Chest Physicians evidence-­ based clinical practice guidelines. Chest. 2013;143(5 Suppl):e93S–e120S. 3. McWilliams A, Tammemagi MC, Mayo JR, Roberts H, Liu G, Soghrati K, et al. Probability of cancer in pulmonary nodules detected on first screening CT. N Engl J Med. 2013;369(10):910–9. 4. Wood DE. National Comprehensive Cancer Network (NCCN) clinical practice guidelines for lung cancer screening. Thorac Surg Clin. 2015;25(2):185–97. 5. MacMahon H, Naidich DP, Goo JM, Lee KS, Leung ANC, Mayo JR, et  al. Guidelines for management of incidental pulmonary nodules detected on CT

49 images: from the Fleischner Society 2017. Radiology. 2017;284(1):228–43. 6. Jaklitsch MT, Jacobson FL, Austin JH, Field JK, Jett JR, Keshavjee S, et al. The American Association for Thoracic Surgery guidelines for lung cancer screening using low-dose computed tomography scans for lung cancer survivors and other high-risk groups. J Thorac Cardiovasc Surg. 2012;144(1):33–8. 7. Berghmans T, Dusart M, Paesmans M, Hossein-­ Foucher C, Buvat I, Castaigne C, et al. Primary tumor standardized uptake value (SUVmax) measured on fluorodeoxyglucose positron emission tomography (FDG-PET) is of prognostic value for survival in non-­ small cell lung cancer (NSCLC): a systematic review and meta-analysis (MA) by the European Lung Cancer Working Party for the IASLC Lung Cancer Staging Project. J Thorac Oncol. 2008;3(1):6–12. 8. Rivera MP, Mehta AC, Wahidi MM. Establishing the diagnosis of lung cancer: diagnosis and management of lung cancer, 3rd ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2013;143(5 Suppl):e142S–e65S.

Management of Lung Cancer

14

Scott C. Tiedebohl and Matthew D. Taylor

Algorithmic Approach A. Lung cancer should be included in the differential diagnosis of any pulmonary nodule discovered 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 spiculated 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: [email protected]

D. If the nodule is suspicious for malignancy, a PET/CT is used to evaluate for nodal involvement and metastatic disease [2]. E. If there is no evidence of lymph node involvement 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 cardiopulmonary exercise testing. If the values are   1.4 required for single lung ventilation during open repair) E. All repair options carry considerable risk for complications. The most significant complications are the following: Paralysis, renal failure, visceral ischemia, and myocardial infarction [3]. Given the high risk of operation, the repair of a TAAA should only be

A. G. Pavalonis and A. Hingorani

considered when the risk of rupture overshadows potential complications. F. Repair options involve open repair, endovascular repair, and hybrid repair. Open repair is the original 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 custom-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 subsequent 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)

B

Classification of TAAA based on the Crawford system 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

C

Identify risk of rupture > 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

F Algorithm 17.1

Discussion of Risks and Complications Related to Therapeutic Intervention

Referral to High-Volume Center for Repair

66

Suggested Reading Black SA, Wolfe JH, Clark M, et  al. Complex thoracoabdominal aortic aneurysms: endovascular exclusion with visceral revascularization. J Vasc Surg. 2006;43:1081–9. Davies RR, Goldstein LJ, Coady MA, et  al. Yearly rupture or dissection rates for thoracic aortic aneurysms: simple prediction based on size. Ann Thorac Surg. 2006;81:169–77. Escobar GA, Upchurch GR Jr. Management of thoracoabdominal aortic aneurysms. Curr Probl Surg. 2011;48:70–133.

A. G. Pavalonis and A. Hingorani 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 repair of aortic aneurysms involving the visceral and renal vessels. Ann Vasc Surg. 2010;24:219–24. Stein LH, Berger J, Tranquilli M, et  al. Effect of statin drugs in thoracic aortic aneurysms. Am J Cardiol. 2010;55:841–57. Zinganshin BA, Elefteriades JA.  Surgical management of thoracoabdominal aneurysms. Heart. 2014;100:1577–82.

Part IV Breast

Nipple Discharge

18

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 differentiate pathologic from physiologic discharge. Questions regarding the timing (spontaneous vs. expressed), side, color/character, single vs. multiple ducts, history of pregnancy and nursing, 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 physiologic discharge may be serous, milky (galactorrhea), green, or brown [1, 2]. C. Pathologic nipple discharge is generally unilateral, 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, especially 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: [email protected]

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 discharge should be made, within reason. Regional lymphadenopathy should also be assessed [1, 2]. E. In the case of physiologic discharge, appropriate work-up may include mammogram, ultrasound, and hormone levels to include prolactin and TSH. Galactorrhea can be caused by elevated prolactin levels, which in turn can be caused by many medications which increase prolactin levels, including psychotropics, antihypertensives, gastrointestinal drugs, anesthetics, 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 associated with periductal mastitis and generally resolves on its own, as long as no active infection is present [2]. G. In the case of pathologic nipple discharge, diagnostic mammogram and subareolar ultrasound are the imaging modalities of choice. Although historically the sensitivity and specificity of mammogram and US was ­considered low for diagnosis of malignancy

© 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

69

70

[3, 5], newer data suggests otherwise [6, 7]. If no abnormalities (defined as a mass, indeterminate/suspicious calcifications, or architectural 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 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 jejunum away from pacemaker cells in the duodenum. 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 postoperatively. It is thought to be caused by dysmotility 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 (loperamide, opioids, etc.). If medical treatment fails, the surgical treatment 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 symptoms of nausea/vomiting, epigastric pain, bloating, and/or weight loss. They can both result from disordered motility of the remaining stomach, 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 gastric stasis, aggressive management of the PUD (maximal PPI therapy, smoking cessation, and eradication of Helicobacter pylori), concurrently with serial dilations, is of paramount importance. B. If there is no evidence of stricture, the next diagnostic 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 modifications and promotility agents). D. If treatment is refractory, then surgery (subtotal 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 biliary reflux and can often be diagnosed, and even managed, endoscopically. D. Patients with biliary reflux and failure of medical therapy are best managed with conversion to Roux-en-Y gastrojejunostomy, with or without subtotal gastrectomy. If biliary reflux occurs in patients with Roux-en-Y configuration, elongation of the Roux limb will often alleviate the pathology.

C. J. Dickler and K. Spaniolas

160 Prior surgery for peptic ulcer disease

Gastric stasis

Biliary reflux

A

A

EGD

Roux Syndrome

EGD

Roux Syndrome

Bile

UGI or Gastric Emptying Scan

No

B

Anastomotic stricture

HIDA

Dilate

Yes

C Persists

Yes

No

Cholestyramine + Sucralfate

Reflux

Persists

B Nuclear gastric emptying study Delayed

Revise anastomosis

D

Subtotal gastrectomy

Promotility Agents Revise Gastric Remnant or Subtotal/Total Gastrectomy

Normal variant

No delay

Promotility agents

C

Persists Subtotal gastrectomy

D

Algorithm 41.2

Suggested Reading Bolton JS, Charles Conway W.  Postgastrectomy syndromes. 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.

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

42

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 managed 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 counseling patients to adhere to lifestyle modificaC. 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

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 esophagogastroduodenoscopy (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 suspicion 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 esophagogastroduodenoscopy (EGD). C. Having a thorough knowledge of a patient’s prior surgical procedures can help rule out postsurgical causes of recurrent disease. In the literature, 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 curvature). 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).

© 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

161

C. J. Dickler and K. Spaniolas

162

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 pseudoZollinger–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 partial gastrectomy with or without vagotomy.

Recurrent peptic ulcer disease

Endoscopy with biopsy (Cancer vs. H. pylori Medical Management (PPI BID, Smoking cessation, Treat H. pylori

A

B Rule out cancer (Repeat endoscopy with Biopsy or screen with CT Scan)

Re-evaluation of symptoms

Equivalent

C

Negative Prior surgical history? Surgical resection

Yes

Positive

No

D Octreotide scan

Zollinger–Ellis Syndrome

Tc-99 scan (Retained antrum)

Completion antrectomy with redo anastomosis or conversion to Roux En Y

Gastrin levels (Secretin test) Elevated Normal

E Standard meal test

Pseudo-Zollinger– Ellison Syndrome Elevated

Normal

Nonhypergastrinemia related ulcer

F Medical management Fails

Algorithm 42.1

Revision gastrectomy +/- vagotomy

42  Management of Recurrent Peptic Ulcer Disease

Suggested Reading Cameron JL, Cameron AM. Stomach. In: Current surgical therapy. 11th ed. Philadelphia, PA: Saunders; 2014. p. 69–107. Dacha S, et  al. Hypergastrinemia. Gastroenterol Rep. 2015;3(3):201–8. https://doi.org/10.1093/gastro/ gov004. Fisher WE, et  al. Pancreas. In: Schwartz’s principles of surgery. New York City, NY: McGraw-Hill Education\ Medical; 2015. p. 1392–3. Gray GR, et al. Extragastric gastrinoma or G-cell hyperplasia of the antrum? The preoperative diagnosis in a case of hypergastrinaemia. Br J Surg. 1976;63(8):596– 8. https://doi.org/10.1002/bjs.1800630809.

163 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/ pubmed/7362294. Kitagawa Y, Dempsey DT. Stomach. In: Schwartz’s principles of surgery. New York City, NY: McGraw-Hill Education\Medical; 2015. p. 1035–95. Teitelbaum EN, et  al. Stomach. In: Sabiston textbook of surgery: the biological basis of modern surgical practice. 12th ed. Philadephia, PA: Elsevier; 2017. p. 1188–236. Vakil N. Approach to refractory or recurrent peptic ulcer disease. Approach to refractory or recurrent peptic ulcer disease. UpToDate5, 5 July 2017, www.uptodate.com/contents/approach-to-refractory-or-recurrent-peptic-ulcer-disease.

Management of Gastric Cancer

43

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, nausea, pain, obstruction, GI bleed, weight loss, and anemia) as the presence of such symptoms 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 obstruction, malnutrition and weight loss from dysphagia, 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: [email protected]

C. Upper gastrointestinal endoscopy and biopsy is important for confirmation of the diagnosis. Endoscopic ultrasound can give additional 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, considering 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, chemotherapy, chemoradiation, and/or palliative procedures (stenting, resection for obstruction or uncontrollable bleeding, and gastrostomy tube placement for decompression) are the preferred modes of treatment. Once the treatment is concluded, restaging may be ­performed to re-evaluate the mass for possible resection.

© 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

165

C. L. Wolchok and G. V. Georgakis

166

G. When resectable, an initial diagnostic laparoscopy with washings and cytology is strongly recommended [3, 4]. H. If cytology is positive, then the patient should receive chemotherapy according to the multidisciplinary approach. Once the treatment is

concluded, restaging may be performed to reevaluate the mass for resection [4]. I. If cytology is negative, surgery with perioperative chemotherapy or chemoradiation is warranted [5, 6].

A

Vague abdominal pain or more specific symptoms Sings of obstruction, GI bleed, weight loss, anemia

B

In the event of a patient presenting in extremis (obstruction, dehydration, severe malnutrition), immediate measures to restore homeostasis (e.g., NG decompression, IV hydration, and TPN initiation) are warranted.

· · · · ·

C

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

D

Staging

E

Absence of metastatic disease Surgically resectable Surgical candidate

Presence of metastatic disease Surgically unresectable Nonsurgical candidate

G

Consider diagnostic laparoscopy with cytology

Chemotherapy or Chemoradiation Palliative procedures for obstruction, uncontrollable bleeding, etc.

I

Cytology negative

Cytology positive

Surgery Perioperative chemotherapy Perioperative chemoradiation

Chemotherapy

Algorithm 43.1  Treatment algorithm for gastric cancer

H

F

43  Management of Gastric Cancer

References 1. Park SR, Lee JS, Kim CG, Kim HK, Kook MC, Kim YW, et  al. Endoscopic ultrasound and computed tomography in restaging and predicting prognosis after neoadjuvant chemotherapy in patients with locally advanced gastric cancer. Cancer. 2008;112(11):2368–76. 2. Amin MB, Edge S, Greene F, Byrd DR, Brookland RK, Washington MK, Gershenwald JE, Compton CC, Hess KR, Sullivan DC, Jessup JM, Brierley JD, Gaspar LE, Schilsky RL, Balch CM, Winchester DP, Asare EA, Madera M, Gress DM, Meyer LR, editors. AJCC Cancer staging manual. 8th ed. Chicago: Springer; 2017. p. 1032. 3. Sarela AI, Lefkowitz R, Brennan MF, Karpeh MS.  Selection of patients with gastric adeno-

167 carcinoma for laparoscopic staging. Am J Surg. 2006;191(1):134–8. 4. Mezhir JJ, Shah MA, Jacks LM, Brennan MF, Coit DG, Strong VE.  Positive peritoneal cytology in patients with gastric cancer: natural history and outcome of 291 patients. Ann Surg Oncol. 2010;17(12):3173–80. 5. Cunningham D, Allum WH, Stenning SP, Thompson JN, Van de Velde CJ, Nicolson M, et al. Perioperative chemotherapy versus surgery alone for resectable gastroesophageal cancer. N Engl J Med. 2006;355(1):11–20. 6. Smalley SR, Benedetti JK, Haller DG, Hundahl SA, Estes NC, Ajani JA, et  al. Updated analysis of SWOG-directed intergroup study 0116: a phase III trial of adjuvant radiochemotherapy versus observation after curative gastric cancer resection. J Clin Oncol. 2012;30(19):2327–33.

Management of Gastrointestinal Stromal Tumors

44

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 factor 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 familial/genetic pattern; most are sporadic. They are found in the wall of the gastrointestinal tract and can have various types of presentation. Symptomatology includes early satiety, abdominal discomfort, and bleeding. Other times, they are asymptomatic and are incidentally found on imaging and endoscopy. B. Initial examination of patients begins with a history and physical characterizing symptoms 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 contrast. CT scans can also identify any potential sites of metastasis (majority of metastasis

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 normal mucosa. If there are any diagnostic discrepancies, 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 ultrasoundguided biopsy may assist in establishing a diagnosis in metastatic disease or if any clinical 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/unresectable 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.

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

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I. G. Elyash

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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 EUS guided biopsy for confirmation.

Surgical resection with negative margins.

High risk of reoccurrence?

Yes

No

D

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 stromal tumors. Surg Clin North Am. 2017;97(2):437–52.

Imatinib treatment

Surgical resection if resectable tumor

Management of Upper Gastrointestinal Hemorrhage

45

Igor G. Elyash

Algorithmic Approach A. Upper gastrointestinal hemorrhage can present as hematemesis, melena, and also hematochezia 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 intravenous (IV) fluids and blood products as needed. Patients should be in a monitored setting with strict monitoring of outputs and hemodynamics. The source of bleeding is further investigated 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.

B. Baseline hemoglobin levels, coagulation profiles, 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 surgical intervention. Bleeding may be controlled with oversewing and may occasionally require resection. Recurrent bleeding often requires surgical intervention 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_45

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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.

C Source of bleeding is identified? Yes

No Slow Bleeding or Massive

Endoscopic control of bleeding followed by observation Slow

D If re-bleed, repeat endoscopy. Additional bleeding requires surgery.

Consider RBC scan. If negative, observe or consider other source.

Algorithm 45.1

Suggested Reading Barkun AN, et  al. International Consensus recommendations on the management of patients with nonvariceal 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.

Massive Angiography/surgical intervention

Part VII Small Bowel

Small Bowel Obstruction

46

Ryan M. Juza and Vamsi V. Alli

Algorithmic Approach A. Symptoms: Symptoms of small bowel obstruction include progressive abdominal pain and distention with accompanying nausea and vomiting. Symptom development, however, can be variable depending on the degree of obstruction. Partial bowel obstruction 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 adhesive 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: [email protected]

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 progression. 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 rectal mass. The first diagnostic test typically obtained is a plain abdominal X-ray, followed shortly after with a computed tomography (CT) of the abdomen, preferably with oral contrast. Typical findings include continuously 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, physical 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-

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ized ratio are required. Depending on the duration and severity of symptoms, significant electrolyte a­bnormalities and acute kidney injury are possible and require aggressive fluid resuscitation with intravenous crystalloid solution and electrolyte replacement. In a patient without preexisting kidney disease, endpoints of resuscitation include achieving adequate urine output [1]. (a) Concerning findings: Abdominal complaints should be limited to mild generalized 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, hematologic, or electrolyte abnormalities. The presence of these findings should prompt closer evaluation. Depending on the duration of symptoms, patients may demonstrate tachycardia associated with hypovolemia, which should respond to intravenous fluid resuscitation. Additionally, hypotension that is unresponsive 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 acidosis should prompt earlier surgical inter-

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 obstruction [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 command a lower threshold for operation. (b) Altered gastrointestinal (GI) tract anatomy, 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 rouxen-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 intervening segments of decompressed bowel. Some surgeons advocate diagnostic laparoscopy 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 strangulation 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 alleviates the obstruction. If the patient has exam findings suggestive of strangulation, 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 underlying ischemic bowel. (d) Impaired patient: Nonoperative management of patients with small bowel obstruction 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 manifest 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 nasogasD 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 hyperosmotic water-soluble contrast dye, which may decrease the time to return of bowel function [4]. Patients who fail to resolve their symptoms after a 24–48-h trial of nonoperative management require surgical exploration.

R. M. Juza and V. V. Alli

178

A

Patient with obstructive symptoms

Nasogastric tube decompression, IV fluid resuscitation

Thorough and focused history and physical examination

B Plan films – supine/upright Abdominal X-ray CT abdomen/pelvis with oral and intravenous contrast Laboratory studies

Workup consistent with small bowel obstruction

High-risk group

Yes

OR

C No

High-risk features

No

24–48 hour trial nonoperative management

Algorithm 46.1

Yes

OR

46  Small Bowel Obstruction

179

D Return of bowel function

Partial

Consider small bowel followthough study No

Yes

Contrast reaches colon

No Yes

Remove NG and slow diet advancement

OR

Algorithm 46.1 (continued)

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-

tion in the virgin abdomen: the need for a mandatory 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 operation 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, randomized, controlled, clinical trial. World J Surg. 2008;32(10):2293–304.

Small Bowel Tumors

47

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 incidental finding or as an unexpected source of nonspecific 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: [email protected]

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].

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182

Review of symptoms relevant to metastatic disease should cover chest pain, shortness of breath, cough, wheezing, hemoptysis, jaundice, acholic stool, neurologic symptoms, dermatitis, diarrhea, and mental status changes. A focused abdominal exam should evaluate 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 anemia 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-hydroxyindoleacetic 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 resonance imaging (MRI) (both have >80% sensitivity). Endoscopic evaluation: Upper/lower endoscopy for direct endoscopic identification and potential biopsy. Twenty-five percent of small bowel masses occur in the duodenum. . Additional Diagnostic Modalities D Additional contrast-enhanced imaging of the small bowel may be required if initial studies fail to localize the tumor. These options include CT enterography (85% sensitivity) and MR enterography (91–97% sensitivity).

Additional endoscopic evaluation may identify the tumor. This includes capsule endoscopy (passive study with purely diagnostic 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 500 ml). B. EC fistulas carry high morbidity and mortality and therefore require a multidisciplinary approach. Principal management involves fluid resuscitation with electrolyte correction and replacement of fluid losses, characterization 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

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 sepsis should mandate early administration of broad spectrum antibiotics. In addition, crosssectional 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 times baseline Cr) is treated with 125 mg vancomycin PO qid for 10–14 days. (c) Severe-complicated disease is characterized by additional complicating factors, including ileus, shock requiring vasopressors, 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,

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K. T. Crowell and E. Messaris

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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-

A

apy should be evaluated for surgical intervention. Patients with refractory or recurrent disease should be considered for fecal microbiota transplant prior to surgical intervention [6].

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

Positive Clostridium difficile toxin assay?

B

C

Physical exam, vital signs, laboratories

D

Fulminant C. difficile colitis or colonic perforation? Yes

E

No

Continue to reassess

Initiate antibiotic therapy

F

Immediate surgical intervention

G

Mild: metronidazole

Severe: vancomycin PO

Severecomplicated: PO vanco + IV metro, ± vanco enema

Algorithm 63.1

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 fulminant Clostridium difficile colitis. Am J Surg. 2010;200(1):131–5.

4. Kaiser AM, Hogen R, Bordeianou L, Alavi K, Wise 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 microbiota transplantation and clinical resolution of diarrhea in patients with recurrent Clostridium difficile infection: a randomized clinical trial. JAMA. 2016;315(2):142–9.

Hereditary Colorectal Cancer Syndromes

64

Emily Huang and Michael F. McGee

Algorithmic Approach Approximately 30% of colorectal cancer cases are associated with a family history of colorectal polyps or cancer, but only 3–5% of cases are associated with a specifically identifiable inheritable colorectal cancer syndrome. The most commonly identifiable cause of inheritable colorectal cancer is Lynch syndrome, characterized by a specific mutation in one of the DNA mismatch repair (MMR) or EPCAM genes. Although the terms Lynch syndrome and hereditary nonpolyposis colorectal cancer (HNPCC) are often used interchangeably, the term Lynch syndrome refers to patients with a specifically 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 plethora of polyps throughout the gastrointestinal tract that predispose the patient to cancer. It is important to distinguish Lynch syndrome from polyposis 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: [email protected]

The surgeon typically encounters two clinical situations which are outlined in this chapter’s flow charts: [1] management of a patient or kindred with recently diagnosed colorectal cancer with suspicion of Lynch syndrome and [2] management of a patient with personal or family history 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 abnormal 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 cancers). 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

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E. Huang and M. F. McGee

244 Table 64.1  Amsterdam II criteria for hereditary nonpolyposis colorectal cancer [1] 1 2 3 4

At least three family members affected, one of whom is a first-degree relative of the other two, with HNPCCrelated cancers (colorectal, endometrial, small bowel, ureter, renal pelvis) Two successively related generations At least one of the HNPCC-related cancers diagnosed before age 50 Familial adenomatous polyposis excluded

Table 64.2  Bethesda guidelines to guide tumor testing for MMR gene defects [2] 1 2 3 4 5

Colorectal cancer diagnosed in patient under 50 years of age Synchronous or metachronous colorectal cancer or other HNPCC-associated tumors, regardless of age Colorectal cancer with high levels of microsatellite instability (MSI-H) histology in a patient younger than 60 years old 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 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 common cause of abnormal MLH1 testing is somatic promoter methylation caused by a BRAF gene defect, a condition which is typically 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 sporadic (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 attributed to a BRAF mutation are likely to have Lynch or Lynch-like syndrome and merit confirmation through germline (blood) testing 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 management and surveillance of Lynch-like patients; however, many advocate total colectomy in lieu of segmental colectomy in appropriate patients. For this reason, germline testing typically should not delay surgical 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 colectomy 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 establishing a new diagnosis, performing surgery for cancer or prophylaxis, or counseling members from a polyposis kindred, the surgeon must be aware of polyposis 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 syndromes will be (1) the patient with a new colonoscopic 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 organized fashion and include any relatives (focusing on first- or second-degree relatives) with cancer, the type and location of the cancer (colorectal vs. extraintestinal), and age at diagnosis. Using a pedigree to organize this information can be helpful. Furthermore, because phenotypes for the various polyposis and nonpolyposis 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 clinical suspicion of a hereditary polyposis syndrome (e.g., the young patient with newly diagnosed colon cancer with a duodenal adenoma) should be referred for genetic counseling 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 subsequent 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 prevention that arise from a new genetic diagnosis and can adjust misperceptions [4].

245

I. Depending on the specific syndrome, surveillance of the colon, the entire GI tract, or the GI tract and other organs may be warranted. Recommendations for modalities and intervals are outlined in Table  64.3 by syndrome [5–16]. For familial adenomatous polyposis (FAP), recommendations are generally concurrent 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 enteroscopy, 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 PeutzJeghers 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 syndrome. In classic FAP, where the colorectal cancer risk reaches a lifetime risk of 100% by around age 40, recommendations for proctocolectomy are very strong, although procedures can be staged to be tailored to patients’ individual needs, such as fecundity preservation or rectal polyp burden. In Peutz-Jeghers syndrome, recommendations are targeted toward symptomatic and nonmalignant complications of the hamartomatous polyps, including intussusception and bleeding. The exact mechanism of carcinogenesis in Peutz-­ Jeghers syndrome is yet unknown, so surveillance 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.

Polyp type Adenoma

Inheritance Autosomal dominant

Autosomal recessive

Genes APC

MYH

Syndrome Familial adenomatous polyposis (FAP)

MUTYHassociated polyposis (MAP)

Clinical findings  Profuse: over 1000 polyps  Classic: hundreds of polyps  Attenuated: fewer than 100 polyps Duodenal adenomas and carcinomas, gastric fundic gland polyps; desmoid tumors, epidermoid cysts, supernumerary teeth, osteomas 0–1000 adenomas, CRC 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 resection 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.

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Large postpolypectomy defects may benefit from prophylactic clip closure to decrease the risk of postpolypectomy hemorrhage. E. Malignant appearing lesions should be biopsied and tattooed, and not removed, since malignancy merits oncologic surgical resection. 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 submucosal scarring and prohibit later EMR attempts by an expert. Special situations may mandate surgical resection regardless of polyp histology. For example, polyps growing into the appendiceal orifice or ileocecal valve are frequently not amenable to endoscopic 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 consideration of surgical resection. F. If polyp pathology demonstrates no evidence of cancer, surveillance colonoscopy should continue based on the number, size, histology, completeness of polypectomy, bowel preparation quality, and patient and family history. Periodically updated guidelines dictate the frequency of postpolypectomy surveillance for commonly resected polyps in average-risk individuals [7]. G. “Carcinoma in situ” or “intramucosal carcinoma” 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 margin from the cut polyp edge [8]. The analogous Kikuchi classification for sessile polyps has shown polypectomy to be sufficient for favorable-histology tumor penetration limited to the upper third (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 situations, 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 determine the course of subsequent care.

65  Colorectal Polyps

A

253

Polyp identified

Evaluate polyp features: size, morphology, firmness, villous pattern, ulceration,central depression

B Malignant features?

Yes

Stop: Tattoo polyp site and biopsy extensively

No

C

Consider tattooing all polyps > 1–2 cm

E D

Sessile polyp < 10 mm: cold snare

Any pedunculated polyp: hot snare, consider clipping base

Pathology: no malignancy, no neoplasia at margins

F

Endoscopic surveillance

Algorithm 65.1

Sessile polyp >10 mm: hot snare or EMR, consider clipping base

OR

Carcinoma in situ, negative margins, no high risk features

Await pathology and consider referral to advanced endoscopist or oncologic surgical resection

Technically infeasible

Multi-disciplinary review: consider oncologic surgical resection, EMR, endoscopic surveillance

Pathology: malignancy

Pedunculated T1 cancer, >2 mm margins, no high risk features

H G 1 mm SM depth, high risk features

Uncertain margins or uncertain histologic features

Oncologic surgical resection

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References

E. Huang and M. F. McGee

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 prediminutive 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 classicancer. 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 aris2002. 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 invareview, 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,

66

Colon Cancer Emily Huang and Michael F. McGee

Algorithmic Approach 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 elective 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 diagnosis; however, the remainder of patients will experience symptoms. The most common symptoms of colon cancer are “alarm” symptoms such as changes in bowel habits or bloody bowel movements. Abdominal pain, which is infrequently associated with cancer, is a worrisome sign associated with obstruction, 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: [email protected]

B. For patients with suspected colon cancer, 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 jaundice or anicteric stools may suggest pulmonary 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 metastatic disease to the inguinal, supraclavicular, or cervical lymph node chains. A digital rectal 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.

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C. The first diagnostic procedure, if not already colorectal), medical oncologists, patholoperformed, is colonoscopy with tumor localgists, radiologists, and radiation oncologists ization, diagnostic biopsy, and location tatand considered for neoadjuvant chemothertooing. As noted in the chapter on colon apy versus primary surgery. polyps, endoscopic evaluation of the lesion is F. Stage IV colon cancer patients presenting very important, as certain features are sugwith significantly obstructing, bleeding, or gestive of malignancy. Tattooing lesions is perforated tumors may be candidates for palessential and guides surgical resection, liative interventions in conjunction with input whereas complete and thorough evaluation of from a multidisciplinary management team the remaining colon excludes synchronous and the patient. Obstructing lesions may be cancers or polyps and other conditions which evaluated for self-expanding metal stents, may impact surgical decision-making. Rarely, proximal diverting loop stoma, or palliative occult adenocarcinoma may be discovered in resection. Similarly, tumor-related hemoran initially benign-appearing adenomatous rhage may prompt palliative surgical resecpolyp. Management of such malignant polyps tion or targeted palliative radiotherapy in is discussed in the colon polyps section of select patients. Perforated lesions should be this text. managed on clinical context and acuity, bal D. Following confirmation of colon cancer, staganced carefully on the desires of the patient, ing computed tomography (CT) of the chest, surgical risks, and likelihood of meaningful abdomen, and pelvis is performed. survival. Treatment of perforated cancers Complementary ultrasound, magnetic resoranges from nonoperative management with nance imaging (MRI), or positron emission antibiotics, bowel rest, and percutaneous tomography (PET) imaging and imagedrain placement to emergent proximal divertguided biopsy may help characterize equivoing stoma or colectomy. The surgeon must be cal findings found on initial staging studies. A particularly conscientious when considering complete blood count (CBC), serum chemispalliative surgery and predicate all decision-­ try, liver function tests, and carcinoembrymaking to be commensurate with patient’s onic antigen (CEA) should be drawn at this long-term wishes since comorbidities and initial encounter. Unexplained anemia may advanced disease may subject patients to suggest a chronically bleeding lesion, abnorunacceptably high surgical risks. mal LFTs may raise suspicion for metastatic G. In the absence of metastatic disease, the surdisease and provide a nutritional evaluation, geon should assess appropriateness of curaand a baseline CEA level serves as a refertive attempt surgery. Imaging typically guides ence to guide postoperative survivorship [4]. the surgeon to determine resectability of the E. Approximately one quarter of newly diagcancer while ensuring adequate margins and nosed colon cancer patients will present with lymphadenectomy without collateral damage metastatic disease. Patients with metastatic of adjacent structures. Moreover, the patient disease absent significant symptoms benefit should prove to be a good candidate for the from multidisciplinary evaluation in conjuncproposed intervention. Principles of oncotion with a medical oncologist. Curative-­ logic colectomy include 5 cm margins proxiattempt multivisceral resection may confer mally and distally along the colon wall, survival benefits in select situations with or grossly negative circumferential margins for without neoadjuvant chemotherapy in T4b cancers (where tumor directly invades patients with isolated liver and/or lung metasother structures), high ligation of the arterial tases [5, 6]. Patients with potentially resectsupply to the affected colon segment, and able metastatic disease should be discussed complete en bloc lymphadenectomy to assure with a multidisciplinary team consisting of a minimum of 12 lymph nodes for pathology surgeons (thoracic, hepatobiliary, and review. Patients with completely resected

66  Colon Cancer

tumors who are found to have nodal metastases (stage III) should be referred to a medical oncologist for adjuvant chemotherapy. Stage II (T3 or T4  N0) cancer patients should be referred to a medical oncologist to discuss the role of adjuvant chemotherapy; however, survival advantages conferred by adjuvant chemotherapy for stage II colorectal cancers are modest and merit balance of chemotherapy risks and side effects with expected survival benefits. Regardless of the prescribed adjuvant treatments, all curative intent colectomy patients follow surveillance protocols with

257

imaging, physical exams, CEA, and colonoscopy determined by periodically updated guidelines. H. Occasionally, local resectability may be in 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.

E. Huang and M. F. McGee

258

A

Patient with “alarm” symptoms worrisome for colorectal cancer, or abnormal imaging

B

Thorough and appropriate history and physical Symptoms; no colonoscopy yet Colonoscopy already completed (for symptoms or screening)

Colonoscopy, biopsy, tattoo

C

Endoscopic confirmation of adenocarcinoma

Metastatic workup: CT chest, abdomen, and pelvis; CBC, chemistry, LFTs, CEA

D

Metastatic disease?

H

Locally resectable disease in medically operable patient?

No

No

Yes Yes Significantly obstructing, bleeding, or perforated tumor?

G

Surgical resection

Adjuvant chemotherapy, surveillance

Yes No

E

Algorithm 66.1

Multidisciplinary discussion Special cases: isolated liver and/or lung metastases

Multidisciplinary discussion Special discussion of neoadjuvant chemotherapy, intraoperative radiation therapy

Consider palliative resection, diversion, stenting, or radiotherapy

F

66  Colon Cancer

References 1. National Comprehensive Cancer Network (NCCN). NCCN clinical practice guidelines in oncology: colon cancer. Version 2.2017. Accessed at www.nccn.org/ professionals/physician_gls/PDF/colon.pdf on 7 Aug 2017. 2. Vasen HF, Watson P, Mecklin JP, Lynch HT.  New clinical criteria for hereditary nonpolyposis colorectal cancer (HNPCC, Lynch syndrome) proposed by the International Collaborative group on HNPCC. Gastroenterology. 1999;116(6):1453–6. 3. Umar A, Boland CR, Terdiman JP, Syngal S, Chapelle AD, Rüschoff J, Fishel R, Lindor NM, Burgart LJ, Hamelin R, Hamilton SR.  Revised Bethesda guide-

259 lines for hereditary nonpolyposis colorectal cancer (Lynch syndrome) and microsatellite instability. J Natl Cancer Inst. 2004;96(4):261–8. 4. Slentz K, Senagore A, Hibbert J, Mazier WP, Talbott TM.  Can preoperative and postoperative CEA predict survival after colon cancer resection? Am Surg. 1994;60(7):528–31. 5. Rosen SA, Buell JF, Yoshida A, Kazsuba S, Hurst R, Michelassi F, Millis JM, Posner MC. Initial presentation with stage IV colorectal cancer: how aggressive should we be? Arch Surg. 2000;135(5):530–4. 6. Pfannschmidt J, Dienemann H, Hoffmann H. Surgical resection of pulmonary metastases from colorectal cancer: a systematic review of published series. Ann Thorac Surg. 2007;84(1):324–38.

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 practimes, these abnormalities are of congenital deri- tice patterns and some degree of confusion, parvation; 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 proprior 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 prolapse itself results in a self-perpetuating cycle of A. Patients with prolapse usually describe a rubworsening 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 (constiQ. M. Hatch pation, diarrhea, incomplete evacuation) [11– Department of Surgery, Madigan Army Medical 15]. On physical exam, full-thickness rectal Center, Tacoma, WA, USA prolapse must be differentiated from internal E. K. Johnson (*) hemorrhoids, which may also prolapse to an Cleveland Clinic Foundation, Cleveland, impressive degree. Prolapse will display either OH, USA concentric folds or will be completely smooth Department of Surgery, Division of Colorectal circumferentially. Hemorrhoids, in contrast, Surgery, Hillcrest Hospital, Mayfield Heights, OH, USA will always appear as radially oriented col© 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_67

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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 demonstrate rectal prolapse in the lateral decubitus position, the most consistent way of evaluating 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 estimate 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 clinicians. 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 incarceration. Nevertheless, incarceration and strangulation may occur, and delay in surgical intervention will result in grave consequences for the patient [8]. If acutely incarcerated or strangulated rectum is encountered, the appropriate surgical intervention is a perineal proctectomy or Altemeier procedure. 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 apparent incarceration, application of sugar to the prolapse 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 counseling. Patients should be reassured that prolapse 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 procidentia 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 candidates should undergo further evaluation to guide operative decision-making. The rationale behind this is that rectal prolapse is rarely an isolated disorder but rather a manifestation of global pelvic floor herniation. Cystoceles, enteroceles, rectoceles, sigmoidoceles, or vaginal vault prolapses are frequent cooccurrences and may necessitate complex pelvic floor reconstruction in combination with urogynecology. Dynamic pelvic 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 promotes complete evacuation of stool. These

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265

studies will affect the management strategy in up to 40% of cases [19].

the sacrum and/or resection or plication of redundant bowel [2, 5, 7, 11].

Prior to pursuing an operative procedure to correct a prolapse in a patient with chronic constipation, it is also important to rule out functional 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, nonoperative optimization of these abnormalities likely will not correct the prolapse itself. In fact, the prolapse will only serve to exacerbate the difficulty 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 clinically 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 fourfold increase in relative risk of colorectal malignancy [20]. It is therefore wise practice to evaluate for luminal lesions prior to planning any colorectal operation in a patient who has not been recently screened. It is unlikely that there is a causal relationship 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.

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 superiority, 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 rectopexy, resection rectopexy, Delorme, or Altemeier, suggested a 10-year recurrence rate of approximately 40%, with no difference between procedures [22].

E. As a general rule in treating difficult disorders, 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 procedures rely on the fundamental principles of prolapse repair, which are rectal fixation to

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 therefore become the procedure of choice for frail, elderly patients suffering from rectal prolapse. This procedure involves a circumferential, full-thickness incision just above the dentate line, pulling through of redundant rectum and sigmoid colon, resection of the redundant segment, and a coloanal anastomosis. Unfortunately, some of what is saved by sparing abdominal surgery is lost in functional morbidity, as proctectomy often results in high rates of incontinence, soilage, and urgency due to loss of the normal rectal resorvior [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 prolapse in the modern era. G. Abdominal procedures are more often selected in young, fit patients who are better able to tolerate an abdominal operation. While this approach has not produced a definitive benefit in terms of recurrence or functional outcomes in randomized controlled trials, the prevailing sentiment is that the abdominal approach is superior in both regards.

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Abdominal approaches to rectal prolapse repair include suture rectopexy, resection rectopexy, 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 perhaps in ventral mesh rectopexy, where the mechanism 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 rectopexy 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 difference in outcomes between minimally invasive and open approaches, although avoidance of an abdominal incision results in faster overall recovery 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 psyllium 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 or strangulated

Reducible

C

B

Functional evaluation: Perineal proctectomy (Altmeier)

Table sugar

–Defecography –Consider Sitz markers –Consider manometry –Consider EMG

Low-risk patient

High-risk patient

F

Observation with PRN manual reduction

Algorithm 67.1

Prosthetic anal encirclement (Thiersch)

G

Perineal prolapse repair: –Altemeier –Delorme

Abdominal prolapse repair: –Suture rectopexy –Resection rectopexy –Posterior mesh rectopexy –Ventral mesh rectopexy

D

268

References 1. Jacobs L, Lin Y, Orkin B. The best operation for rectal prolapse. Surg Clin North Am. 1997;77:49–70. 2. Madiba T, Baig M, Wexner S. Surgical management of rectal prolapse. Arch Surg. 2005;140:63–73. 3. Broden B, Snellman B.  Procidentia of the rectum studied with cineradiography: a contribution to the discussion of causative mechanism. Dis Colon Rectum. 1968;11:330–47. 4. Roig J, Buch E, Alo´s R, et al. Anorectal function in patients with complete rectal prolapse: differences between continent and incontinent individuals. Rev Esp Enferm Dig. 1998;90:794–805. 5. Kuijpers H. Treatment of complete rectal prolapse: to narrow, to wrap, to suspend, to fix, to encircle, to plicate or to resect? World J Surg. 1992;16:826–30. 6. Nicholls R. Rectal prolapse and the solitary ulcer syndrome. Ann Ital Chir. 1994;65:157–62. 7. Yakut M, Kaymakciioglu N, Simsek A, et al. Surgical treatment of rectal prolapse: a retrospective analysis of 94 cases. Int Surg. 1998;83:53–5. 8. Stein E, Stein DE.  Rectal procidentia: diagnosis and management. Gastrointest Endosc Clin N Am. 2006;16:189–201. 9. Marceau C, Parc Y, Debroux E, et al. Complete rectal prolapse in young patients: psychiatric disease a risk factor of poor outcome. Color Dis. 2005;7:360. 10. Mellgren A, Bremmer S, Johansson C, et  al. Defecography. Results of investigations in 2,816 patients. Dis Colon Rectum. 1994;37:1133. 11. Hatch Q, Steele S.  Rectal prolapse and intussusception. Gastroenterol Clin N Am. 2013;42:837–61. 12. Hiltunen K, Matikainen M, Auvinen O, et al. Clinical and manometric evaluation of anal sphincter function in patients with rectal prolapse. Am J Surg. 1986;151:489. 13. Keighley M, Fielding J, Alexander-Williams J.  Results of Marlex mesh abdominal rectopexy for rectal prolapse in 100 consecutive patients. Br J Surg. 1983;70:229. 14. Madoff R, Mellgren A.  One hundred years of rectal prolapse surgery. Dis Colon Rectum. 1999;42:441.

Q. M. Hatch and E. K. Johnson 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. 16. Ternent C, Bastawrous A, Morin N, et  al. Practice parameters for the evaluation and management of constipation. Dis Colon Rectum. 2007;50:2013. 17. Jorge J, Habr-Gama A, Wexner SD.  Biofeedback therapy in the colon and rectal practice. Appl Psychophysiol Biofeedback. 2003;28:47–61. 18. Khaikin M, Wexner S.  Treatment strategies in obstructed defecation and fecal incontinence. World J Gastroenterol. 2006;12(20):3168–73. 19. Harvey C, Halligan S, Bartram C, et  al. Evacuation proctography: a prospective study of diagnostic and therapeutic effects. Radiology. 1999;211:223–37. 20. Rashid Z, Basson M.  Association of rectal pro lapse with colorectal cancer surgery. Surgery. 1996;119:51–5. 21. Deen K, Grant E, Billingham C, et  al. Abdominal resection rectopexy with pelvic floor repair versus perineal rectosigmoidectomy and pelvic floor repair for full thickness rectal prolapse. Br J Surg. 1994;81(2):302–4. 22. Senapati A, Gray RG, Middleton LJ, et al. PROSPER: a randomised comparison of surgical treatments for rectal prolapse. Color Dis. 2013;15(7):858–68. 23. Johansen O, Wexner S, Daniel L, et al. Perineal rectosigmoidectomy in the elderly. Dis Colon Rectum. 1993;36:767–72. 24. Yoshioka K, Ogunbiyi O, Keighley M.  Pouch perineal rectosigmoidectomy gives better functional results than conventional rectosigmoidectomy in elderly patients with rectal prolapse. Br J Surg. 1998;85:1525–6. 25. Consten EC, van Iersel JJ, Verheijen PM, et al. Long-­ term outcome after laparoscopic ventral mesh rectopexy: an observational study of 919 consecutive patients. Ann Surg. 2015;262(5):742–7. 26. Kellokumpu I, Virozen J, Scheinin T.  Laparoscopic repair of rectal prolapse: a prospective study evaluating surgical outcome and changes in symptoms and bowel function. Surg Endosc. 2000;14:634–40.

Solitary Rectal Ulcer Syndrome

68

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/proctitis 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 individuals per year will suffer from SRUS with similar incidences in both female and male populations 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

rectal pressures resulting in a relative ischemia of the mucosa while creating shearing of the rectum against the pelvic floor muscles, namely the puborectalis muscle. This phenomenon ultimately 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 conservatively manage these patients. Unfortunately, conservative management fails in approximately one third of patients who require surgical intervention 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 various approaches in hopes of providing a helpful reference for surgeons who are called on to manage SRUS. A. A complete history and physical exam in the office is perhaps the single most important step in determining if a patient has SRUS.  Rectal ulcers can be due to various etiologies (see B). The clinician should attempt to elicit any and all underlying etiologies 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.

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The most common complaint is rectal bleeding 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 mucosal 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 rectal 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 immunosuppressive disorders such as HIV/AIDS as opportunistic viral infections may cause rectal ulceration. These causes should be managed 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 synonymous 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 disease 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 rectal 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 chapters 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 histological analysis can confirm the diagnosis. Solitary rectal ulcer syndrome may be discovered to be a misleading name on endoscopic analysis, as there is a high variability in the appearance of SRUS ranging from simple mucosal erythema to a chronicappearing 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 without evidence of full-thickness rectal prolapse. These studies can aid both in supporting the diagnosis 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, conservative management should be the first line of treatment. On rare occasions, symptoms may be so severe that early operative intervention may be warranted; however, every attempt at conservative management should be made. The mainstay of conservative management includes patient education focusing on behavioral modification. Patients should understand the benefits of healthy stooling habits including high-fiber diets, regular toileting, 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 administered 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 symptoms 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 defecation. 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 associated symptoms [3, 17, 18]. If conservative management fails, surgical intervention remains an option. In fact, up to one third of patients will require surgical intervention. [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 continuity. 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 strategies 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 symptomatic 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 recommended. If there is evidence of a hypertonic or thickened sphincter muscle, injection of botulinum toxin may relax the sphincter complex and allow healing of the ulcer [21]. Although it has been described, division of the puborectalis muscle is a particularly morbid operation resulting in high rates of incontinence 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 effective and possible in either scenario and is supported 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 intussusception), 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 transanal excision if possible [26]. In some severe, persistent, or recurrent cases, a low anterior resection with coloanal anastomosis/reconstruction 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, conserH 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 willing 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 consideration of a restorative procedure. It is important to consider the most likely etiology for the disorder and to employ a strategy to correct it as a cornerstone in the patient’s treatment plan. As mentioned earlier, any plan that addresses the ulcer without attention to the underlying cause will typically result in recurrence and frustration for both the patient and surgeon.

68  Solitary Rectal Ulcer Syndrome

273

A

-Colonoscopy with biopsies Barium enema -Defecography Manometry/Electromyograph y -Rectal ultrasound

C

B

History and Physical Bleeding/Mucous Discharge Constipation Tenesmus/Straining Digital rectal exam Anoscopy Proctosigmoidoscopy

-Cancer -Prolapse Infectious Ulcerative colitis -Ischemic colitis Retained foreign body

Separate Algorithms

Benign solitary Rectal ulcer

Conservative management

D Severe symptoms

E

-Patient education Behavior modification -High fiber, bulking Sulcralfate enema Topical steroids Sulfasalazine

Failure

Bio feedback

Failure No intussusception

Intussusception

G

F

Surgical repair of prolapse

Local repair

Failure

Sclerotherapy

Botulinum toxin

Local excision Fecal diversion TAMIS

Transanal End colostomy

Algorithm 68.1

H

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References 1. Zhu QC, et al. Solitary rectal ulcer syndrome: clinical features, pathophysiology, diagnosis and treatment strategies. World J Gastroenterol. 2014;20(3):738–44. 2. Morio O, et al. Anorectal physiology in solitary ulcer syndrome: a case-matched series. Dis Colon Rectum. 2005;48(10):1917–22. 3. Rao SS, et  al. Pathophysiology and role of biofeedback therapy in solitary rectal ulcer syndrome. Am J Gastroenterol. 2006;101(3):613–8. 4. Bulut T, et  al. Solitary rectal ulcer syndrome: exploring possible management options. Int Surg. 2011;96(1):45–50. 5. Niv Y, Bat L.  Solitary rectal ulcer syndrome--clinical, endoscopic, and histological spectrum. Am J Gastroenterol. 1986;81(6):486–91. 6. Vaizey CJ, et al. Solitary rectal ulcer syndrome. Br J Surg. 1998;85(12):1617–23. 7. Tjandra JJ, et al. Clinical and pathologic factors associated with delayed diagnosis in solitary rectal ulcer syndrome. Dis Colon Rectum. 1993;36(2):146–53. 8. Tjandra JJ, et al. Clinical conundrum of solitary rectal ulcer. Dis Colon Rectum. 1992;35(3):227–34. 9. Mackle EJ, Parks TG.  The pathogenesis and pathophysiology of rectal prolapse and solitary rectal ulcer syndrome. Clin Gastroenterol. 1986;15(4):985–1002. 10. Chiang JM, Changchien CR, Chen JR.  Solitary rectal ulcer syndrome: an endoscopic and histological presentation and literature review. Int J Color Dis. 2006;21(4):348–56. 11. Madigan MR, Morson BC. Solitary ulcer of the rectum. Gut. 1969;10(11):871–81. 12. Mahieu PH. Barium enema and defaecography in the diagnosis and evaluation of the solitary rectal ulcer syndrome. Int J Color Dis. 1986;1(2):85–90. 13. Goei R, Baeten C, Arends JW.  Solitary rectal ulcer syndrome: findings at barium enema study and defecography. Radiology. 1988;168(2):303–6. 14. Marshall M, et  al. Predictive value of internal anal sphincter thickness for diagnosis of rectal intussusception in patients with solitary rectal ulcer syndrome. Br J Surg. 2002;89(10):1281–5.

J. Kuckelman and E. K. Johnson 15. Zargar SA, Khuroo MS, Mahajan R.  Sucralfate retention enemas in solitary rectal ulcer. Dis Colon Rectum. 1991;34(6):455–7. 16. Aad G, et  al. Combined measurement of the Higgs boson mass in pp collisions at sqrt[s]=7 and 8 TeV with the ATLAS and CMS experiments. Phys Rev Lett. 2015;114(19):191803. 17. Rao SS, et  al. ANMS-ESNM position paper and consensus guidelines on biofeedback therapy for anorectal disorders. Neurogastroenterol Motil. 2015;27(5):594–609. 18. Vaizey CJ, Roy AJ, Kamm MA. Prospective evaluation of the treatment of solitary rectal ulcer syndrome with biofeedback. Gut. 1997;41(6):817–20. 19. Walega P, Kenig J, Richter P.  Transanal endoscopic microsurgery combined with endoscopic posterior mesorectum resection in the treatment of patients with T1 rectal cancer - 3-year results. Wideochir Inne Tech Maloinwazyjne. 2014;9(1):40–5. 20. Somani SK, et  al. Healing of a bleeding solitary rectal ulcer with multiple sessions of argon plasma. Gastrointest Endosc. 2010;71(3):578–82. 21. Keshtgar AS, et al. Botulinum toxin, a new treatment modality for chronic idiopathic constipation in children: long-term follow-up of a double-blind randomized trial. J Pediatr Surg. 2007;42(4):672–80. 22. Sitzler PJ, et  al. Long-term clinical outcome of surgery for solitary rectal ulcer syndrome. Br J Surg. 1998;85(9):1246–50. 23. Choi HJ, et al. Clinical presentation and surgical outcome in patients with solitary rectal ulcer syndrome. Surg Innov. 2005;12(4):307–13. 24. Ihnat P, et  al. Novel combined approach in the management of non-healing solitary rectal ulcer syndrome  - laparoscopic resection rectopexy and transanal endoscopic microsurgery. Wideochir Inne Tech Maloinwazyjne. 2015;10(2):295–8. 25. Tweedie DJ, Varma JS. Long-term outcome of laparoscopic mesh rectopexy for solitary rectal ulcer syndrome. Color Dis. 2005;7(2):151–5. 26. Laubert T, et al. Obstructive defecation syndrome: 19 years of experience with laparoscopic resection rectopexy. Tech Coloproctol. 2013;17(3):307–14.

69

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 process but to the treatment as well. An abdominoperineal 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 administration of radiotherapy may result in sexual dysfunction, urinary dysfunction, or chronic pelvic pain [4]. Fortunately, these risks are at least in part counterbalanced by vastly improved oncologic outcomes over the past century [1, 5–8]. Key breakthroughs allowing for these improvements include surgical innovation (abdominoperineal 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

ment of rectal cancer has become a complex multidisciplinary 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 complaints, 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

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secondary to a rectal cancer is a surgical emergency 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 anorectal ring [11]. In rare instances, the colon proximal to the tumor may be compromised or perforated, in which case a subtotal colectomy with end ileostomy 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 adjacent 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 perform 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 diagnostic decision-making. Small sessile polyps or pedunculated polyps may undergo polypectomy 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 polyps), it is best to proceed with staging prior to tissue biopsy. Unfortunately, it is all too common 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 determines which patients will derive benefit from neoadjuvant therapy. Regardless of the specific 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 invasive 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 superiority, 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 circumferential resection margin) [17]. Computed tomography of the chest, abdomen, and pelvis 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) scanning may be helpful. E. The staging of rectal cancer can be seen in Tables 69.1 and 69.2 [18]. Stage 1 disease encompasses T1 and T2 lesions without nodal involvement. For small (18 years old

2 loculations or septations

Anatomically amenable to percutaneous access

Deep or hilar abscess

C

Percutaneous drainage

Splenectomy

3cm

Leave drain

D

Aspirate

Post-splenectomy vaccines Post-procedure ultrasound

Remove drain once 1mg/dL above reference range 24-hr UCa > 400 mg/dL Renal insufficiency Osteoporosis (t-score < –2.5) Patient prefers surgery

Yes

No

Non-operative management

D

Nephrolithiasis Fragility fractures Neurocognitive symptoms (shortterm memory loss, difficulty concentrating), irritability, anxiety Fatigue, myalgias, arthralgias Constipation, polyuria, polydipsia

Surgical candidate

Pre-operative localization Ultrasound Sestamibi (parathyroid scan) 4D-CT (neck/upper chest)

Non-localized

Localized

Bilateral neck exploration IOPM

Focused parathyroidectomy vs. bilateral neck exploration

C

E

IOPM PTH ¯50% and into normal range

F

Algorithm 109.1

End surgery/Follow-up

Abbreviations: 4D-CT, four dimensional computed tomography; Ca, calcium; FHH, familial hypocalciuric hypocalcemia; IOPM, intraoperative parathyroid hormone monitoring; PTH, parathyroid hormone; UCa, urine calcium

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References 1. Wilhelm SM, Wang TS, Ruan DT, et  al. The American Association of Endocrine Surgeons guidelines for definitive management of

M. Boltz p­ rimary h­ yperparathyroidism. JAMA Surg. 2016;151(10):959–68. 2. Sneider MS, Solorzano CC, Lew JI.  Primary hyperparathyroidism. In: Morita SY, APB D, Zeiger MA, editors. McGraw-Hill manual endocrine surgery. 1st ed. New York: McGraw-Hill; 2009.

Part XV Endocrine

Cushing’s Syndrome and Disease

110

Edwina Moore and Vikram D. Krishnamurthy

Algorithmic Approach A. The signs and symptoms associated with Cushing’s syndrome and disease include central 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 cortisol and creatinine. Late-night salivary cortisol levels on two to three separate evenings, if elevated, demonstrate the loss of normal diurnal variation [2]. C. The second step involves distinguishing between Cushing’s syndrome and Cushing’s disease or ectopic ACTH secretion by obtaining a serum ACTH measurement. If the ACTH level is normal or suppressed, then autonomous secretion of cortisol from the adrenal should be suspected. If the ACTH level is elevated, then either a pituitary adenoma or ectopic secretion from a neuroendocrine tumor should be suspected. A high-dose dexamethasone suppression test will differentiate E. Moore · V. D. Krishnamurthy (*) Department of Endocrine Surgery, The Cleveland Clinic, Cleveland, OH, USA e-mail: [email protected]

between pituitary and ectopic etiology. Serum cortisol levels will not suppress after highdose 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 abdomen, especially “adrenal protocol” when available. Cushing’s disease from a pituitary adenoma is identified by magnetic resonance imaging of the pituitary and/or inferior petrosal sinus sampling. Neuroendocrine tumors secreting ectopic ACTH can be found throughout the body and identification should be directed at the lung, mediastinum, gastrointestinal tract, retroperitoneum, pancreas, and neck. E. Surgery is the first-line treatment option for most causes of Cushing’s syndrome, such as unilateral adrenalectomy for adrenal adenomas and carcinomas, transsphenoidal selective 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-

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ers. Lifelong follow-up and treatment of ­comorbidities such as hypertension, glucose intolerance, and bone loss may be

A

necessary. Depending on the etiology, patients also may need to be followed up for recurrence [4, 6].

Suspicion for hypercortisolism based on phenotype, hypertension, glucose intolerance, weight gain, fluid retention, easy bruising, abdominal striae

B

Obtain a 24-h urine collection for cortisol and creatinine and repeated latenight salivary cortisol measurements

C

Obtain a serum ACTH level, and if elevated, perform a high-dose dexamethasone 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

E

Treatment is unilateral adrenalectomy for adrenal adenomas and carcinomas, trans-sphenoidal selective adenectomy for pituitary adenomas, and resection of tumor secreting ectopic ACTH

F

Postoperatively, screen for adrenal insufficiency, treat comorbidities, and monitor for recurrence

Algorithm 110.1

110  Cushing’s Syndrome and Disease

References 1. Dekkers OM, Horvath-Puho E, Jorgensen JO, Cannegieter SC, Ehrenstein V, Vandenbroucke JP, et  al. Multisystem morbidity and mortality in Cushing’s syndrome: a cohort study. J Clin Endocrinol Metab. 2013;98(6):2277–84. 2. Nieman LK, Biller BM, Findling JW, Newell-Price J, Savage MO, Stewart PM, et  al. The diagnosis of Cushing’s syndrome: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2008;93(5):1526–40. 3. Biller BM, Grossman AB, Stewart PM, Melmed S, Bertagna X, Buchfelder M, et  al. Treatment of adrenocorticotropin-dependent Cushing’s syndrome:

451 a consensus statement. J Clin Endocrinol Metab. 2008;93(7):2454–62. 4. Nieman LK, Biller BM, Findling JW, Murad MH, Newell-Price J, Savage MO, et  al. Treatment of Cushing’s syndrome: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2015;100(8):2807–31. 5. Findling JW, Raff H.  Cushing’s syndrome: important issues in diagnosis and management. J Clin Endocrinol Metab. 2006;91(10):3746–53. 6. Mitchell J, Barbosa G, Tsinberg M, Milas M, Siperstein A, Berber E. Unrecognized adrenal insufficiency in patients undergoing laparoscopic adrenalectomy. Surg Endosc. 2009;23(2):248–54.

Primary Hyperaldosteronism (Conn’s Syndrome)

111

Iuliana Bobanga, Cassandre Bénay, and Vikram D. Krishnamurthy

Algorithmic Approach

ing may be performed (e.g., oral sodium loading, saline infusion, or captopril chal A. Primary hyperaldosteronism is the most comlenge testing) [1, 2]. mon cause of secondary hypertension and C. After establishing the diagnosis of hyperaldoshould be suspected in patients with hypersteronism by biochemical studies, the next step tension that is diagnosed earlier than age 35, is localizing the production to either a unilateral severe (BP 3 adenoma or bilateral hyperplasia. The imaging medications, and present along with hypokamodality of choice is an “adrenal protocol” thinlemia and/or an adrenal incidentaloma [1]. cut computed tomography (CT) scan, which B. The first diagnostic assessment in patients can demonstrate normal adrenal glands, thickwith Conn’s syndrome requires demonstraened glands, or a unilateral adrenal mass [3]. An tion of aldosterone excess along with supaldosterone-­producing adenoma should be suspressed plasma renin activity. Before pected in younger patients with hypertension measuring serum aldosterone levels and whose CT scan reveals a unilateral adrenal mass plasma renin activity, medications that can and a contralateral normal adrenal gland. affect these measurements (e.g., angiotensin-­ D. The laterality of aldosterone hypersecretion is converting enzyme inhibitors, angiotensin then confirmed by bilateral adrenal venous receptor blockers, aldosterone receptor antagsampling (AVS), which is the gold standard for onists, and beta-blockers) are replaced with distinguishing between unilateral and bilateral others (e.g., calcium channel blockers or disease. The acquisition of AVS in every alpha-adrenergic blockers) for several weeks. patient with primary hyperaldosteronism is The aldosterone-to-renin ratio (ARR) is then controversial; however, many centers perform calculated, with a ratio >20–40:1 along with this routinely. Reliance on CT findings alone is an aldosterone level >15 ng/dL being suggesquestionable for two reasons: (1) aldosteronotive of primary hyperaldosteronism (furthermas are typically small and may be missed more, an ARR  >35 is 100% sensitive and (false negatives) and (2) non-­ aldosterone-­ 92% specific). If the ARR is equivocal but the secreting/nonfunctional adrenal adenomas diagnosis is still suspected, confirmatory testincrease with age (false positives). During AVS, aldosterone levels are obtained from the SVC, IVC, and adrenal veins. Cortisol levels I. Bobanga · C. Bénay · V. D. Krishnamurthy (*) Department of Endocrine Surgery, The Cleveland are also obtained, with an adrenal vein to IVC Clinic, Cleveland, OH, USA cortisol ratio  >2:1 confirming successful e-mail: [email protected]

© 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

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I. Bobanga et al.

454

c­ annulation of the adrenal veins. The aldosterone-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

A

B

the vascular damage caused by the prior long-­ standing, severe hypertension. Factors predictive of the resolution of hypertension include female sex, body mass index (BMI)  ≤25, hypertension lasting ≤6  years, prescription of ≤2 antihypertensive medications, and decline in plasma aldosterone by 10 ng/dL on postoperative day 1 [6, 7].

Suspect primary hyperaldosteronism in patients when: Age 160/100) >3 antihypertensive medications required Hypokalemia Adrenal incidentaloma

Obtain Plasma Aldosterone Concentration (PAC) and Plasma Renin Activity (PRA)

PAC/PRA >20?

No

Unlikely primary hyperaldosteronism

Y es

C

Obtain adrenal CT scan

D

Obtain adrenal venous sampling

Lateralization? No

Yes

E Medical management

Algorithm 111.1

Unilateral adrenalectomy

111  Primary Hyperaldosteronism (Conn’s Syndrome)

References 1. Harvey AM.  Hyperaldosteronism: diagnosis, lateralization, and treatment. Surg Clinic N Am. 2014;94(3):643–56. 2. Yin G, Zhang S, Yan L, et  al. One-hour upright posture is an ideal position for serum aldosterone concentration and plasma renin activity ­measuring on primary aldosteronism screening. Exp Clin Endocrinol Diabetes. 2012;120(7):388–94. 3. Bobanga ID, McHenry CR.  Chapter 6. Imaging modalities for adrenal cortical tumors. In: Kebebew E, editor. Management of adrenal masses in children and adults. 1st ed. Switzerland: Springer; 2017. 4. Zeiger MA, Thompson GB, Duh Q-Y, Hamrahian AH, Angelos P, Elaraj D, et  al. American Association of Clinical Endocrinologists and American Association

455 of Endocrine Surgeons medical guidelines for the management of adrenal incidentalomas. Endocr Pract. 2009;15(Suppl 1):1–20. 5. Chao CT, Wu VC, Kuo CC, Lin YH, Chang CC, Chueh SJ, et  al. Diagnosis and management of primary aldosteronism: an updated review. Ann Med. 2013;45(4):375–83. 6. Aranova A, Gordon BL, Finnerty BM, Zarnegar R, Fahey TJ.  Aldosterone resolution score predicts long-term resolution of hypertension. Surgery. 2014;156(6):1387–92. 7. Swearingen AJ, Kahramangil B, Monteiro R, Krishnamurthy VD, Jin J, Shin JJ, et  al. Analysis of postoperative biochemical values and clinical outcomes after adrenalectomy for primary aldosteronism. Surgery. 2017. https://doi.org/10.1016/j. surg.2017.10.045.

Glucagonoma

112

Talia Burneikis and Vikram D. Krishnamurthy

Algorithmic Approach

C. Initial treatment is supportive and involves glycemic control and improving nutritional A. When suspected, the diagnosis is established status. When disease burden is amenable, by an elevated fasting glucagon level >500 pg/ resection of the primary tumor and debulking mL (normal reference range  3 cm [2]. If CT does not Systemic therapies include streptozocin, temodemonstrate an obvious pancreatic lesion, zolomide, everolimus, and sunitinib [7]. endoscopic ultrasound (EUS) can detect E. Subsequent follow-up is dependent on stage at tumors as small as 2–3  mm [3]. Extra-­ presentation, as well as multiple endocrine neopancreatic disease can be detected with plasia syndrome type 1 (MEN1) status. Generally, somatostatin-­ receptor scintigraphy (octreoguidelines recommend evaluation every tide scan) or gallium Ga-68 DOTATATE3–12  months with history and physical exam, PET scan [4]. serum glucagon measurement, and imaging [7].

T. Burneikis · V. D. Krishnamurthy (*) Department of Endocrine Surgery, The Cleveland Clinic, Cleveland, OH, USA e-mail: [email protected]

© 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_112

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458

Suspect glucagonoma with weight loss, rash, glucose intolerance, diabetes, diarrhea, venous thrombosis and serum glucagon measurement >500 pg/mL.

A

Imaging and staging with triple-phase contrast CT (or MRI). EUS, octreotide scan, and dotatate-PET may further characterize tumor burden.

B

C

Provide nutritional support, optimize glycemic control, and determine resectability.

Localized or metastatic disease with >90% resectable and acceptable operative risk.

D

E

Algorithm 112.1

Unresectable disease or unacceptable operative risk.

Pancreatic resection with or without resection/ablation of liver metastases

Palliative procedures: cytoreductive surgery, radiofrequency ablation, cryoablation, hepatic artery embolization (+/– chemotherapy) and/or liver transplantation and/or systemic therapies: somatostatin analogues, molecular-targeted (everolimus, sunitinib), and/or chemotherapy (temozolomide, stretozocin).

Surveillance and follow-up: H&P, glucagon levels, axial imaging (CT or MRI)

112 Glucagonoma

References 1. Wermers RA, Fatourechi V, Wynne AG, Kvols LK, Lloyd RV.  The glucagonoma syndrome. Clinical and pathologic features in 21 patients. Medicine (Baltimore). 1996;75(2):53. 2. Dromain C, de Baere T, Baudin E, Galline J, Ducreux M, Boige V, Duvillard P, Laplanche A, Caillet H, Lasser P, Schlumberger M, Sigal R. MR imaging of hepatic metastases caused by neuroendocrine tumors: comparing four techniques. AJR Am J Roentgenol. 2003;180(1):121. 3. Khashab MA, Yong E, Lennon AM, Shin EJ, Amateau S, Hruban RH, Olino K, Giday S, Fishman EK, Wolfgang CL, Edil BH, Makary M, Canto MI. EUS is still superior to multidetector computerized tomography for detection of pancreatic neuroendocrine tumors. Gastrointest Endosc. 2011;73(4):691.

459 4. Nauck C, Ivancevic V, Emrich D, Creutzfeldt W. 111In-pentetreotide (somatostatin analogue) scintigraphy as an imaging procedure for endocrine gastro-entero-pancreatic tumors. Z Gastroenterol. 1994;32(6):323–7. 5. Fraker DL, Norton JA.  The role of surgery in the management of islet cell tumors. Gastroenterol Clin N Am. 1989;18(4):805. 6. Karabulut K, Akyildiz HY, Lance C, Aucejo F, McLennan G, Agcaoglu O, Siperstein A, Berber E.  Multimodality treatment of neuroendocrine liver metastasis. Surgery. 2011;150(2):316–25. 7. National Comprehensive Cancer Network (NCCN). NCCN Clinical practice guidelines in oncology. http://www.nccn.org/professionals/physician_gls/f_ guidelines.asp. Accessed on 27 Feb 2016.

Management of Pheochromocytoma

113

Hadley E. Ritter and Benjamin C. James

Algorithmic Approach

bers or co-exist with other endocrine syndromes [2]. Presenting symptoms are related A. Pheochromocytomas are rare catecholamine-­ to the catecholamine excess and tend to be secreting tumors of the medullary adrenal paroxysmal, although hypertension can be chromaffin cells. They represent roughly 0.1– sustained or exhibit severe lability with ortho0.6% of patients with hypertension (HTN) static hypotension. Symptoms of tremors, paland occur in 3–7% of patients with an incipitations, diaphoresis, dyspnea, headache, dentally found adrenal mass. panic episodes, chest pain, and a sense of Pheochromocytomas generally occur in the impending death are typical of e­ pisodic spells third to fifth decade, and about 10% are maligand may be spontaneous or exacerbated by nant. Genetic syndromes associated with postural change, increased abdominal prespheochromocytomas include von Hippelsure, exercise, and ­medications. Chronic overLindau disease, neurofibromatosis type 1, and production of catecholamines can lead to multiple endocrine neoplasia type 2. In addiweight loss, cardiomyopathy, fatigue, constition, mutations in any of the succinate dehypation, chronic headaches, and sequelae of drogenase complex subunit genes, including chronic uncontrolled hypertension. Screening SDHA, SDHB, SDHC, and SDHD, may lead for a pheochromocytoma should be done in to pheochromocytomas with variable penepatients with recalcitrant hypertension, hypertrance [1]. Genetic testing may be considered tension diagnosed 6 cm, evidence of concerning features of malignancy

Laparoscopic adrenalectomy

Consideration for open adrenalectomy

D, E

H. E. Ritter and B. C. James

464

References 1. Assadiour Y, Sadowski SM, Alimchandani M, Quezado M, Steinberg SM, Nilubol N, Patel D, Prodanov T, Pacak K, Kebebew E.  SDHB mutation status and tumor size but not grade are important predictors of clinical outcome in pheochromocytoma and abdominal paraganglioma. Surgery. 2017;161:230–9. 2. Melmed S, Polonsky KS, Larsen PR, Kronenberg HM. Chapter 16 endocrine hypertension. In: Williams textbook of endocrinology. 13th ed. Philadelphia: Elsevier; 2016. p. 566–88. 3. Van Berkel A, Rao JU, Kusters B, et al. Correlation between in  vivo 18F-FDG PET and immunohistochemical markers of glucose uptake and metabolism

in pheochromocytoma and paraganglioma. J Nucl Med. 2014;55:1253–9. 4. Lenders JWM, Duh Q-Y, Eisenhofer G, Giminez-­ Roqueplo A-P, Grebe SKG, Murad MH, Naruse M, Pacak K, Young WF Jr. Pheochromocytoma and paraganglioma: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2014;99(6):1915–42.

Suggested Reading Clark OH, Duh Q-Y, Gosnell JE, Shen W.  Textbook of endocrine surgery. 3rd ed. New Delhi: Jaypee Brothers Medical Publishers; 2014.

Management of Aldosteronoma

114

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 polyuria 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: [email protected]

B. Biochemical evaluation should include a plasma aldosterone concentration (PAC), plasma renin activity (PRA), and a metabolic panel. Patients may occasionally have hypokalemia and hypernatremia but are more commonly within the normal range. A PAC >15  ng/dl, PRA 20 are suggestive of a primary hyperaldosteronism [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 idiopathic adrenal hyperplasia (IAH) is higher in this population [3]. Biochemical evaluation should be performed after cessation of mineralocorticoid receptor antagonists for at least 2  weeks. If possible, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers should be discontinued prior to evaluation as these medications may falsely elevate the PRA [4]. C. Adrenal masses are often identified incidentally. 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 adenoma. If multiple or bilateral small nodules are identified or if the adrenal glands have a

© 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

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466

thickened or micronodular appearance, a 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 hypersecretion. AVS should also be considered in patients >40 to exclude IAH. The presence of adrenocortical carcinoma in the setting of primary hyperaldosteronism is rare [4]. D. Medical management is the preferred treatment in patients with bilateral aldosterone

A

B

oversecretion and may include mineralocorticoid receptor antagonists such as spironolactone 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, surgical resection with laparoscopic adrenalectomy is recommended and may result in a reduction in the number of required antihypertensives [1, 2, 4].

History and physical exam: -Hypertension: early onset, severe or medically recalcitrant -Occasional muscle weakness, cramping, headaches, polydipsia, polyuria

Laboratory evaluation: -May have hypokalemia and slight hypernatremia -Elevated PAC >15ng/ml and decreased PRA 20 If needed confirmatory aldosterone suppression test

C Tumor localization, staging, and tissue diagnosis -Non-contrast CT If needed: adrenal vein sampling

D

Algorithm 114.1

Idiopathic adrenal hyperplasia

Adenoma

-Mineralocorticoid suppression

-Unilateral adrenalectomy -Mineralocorticoid suppression if poor operative candidate

D, E

114  Management of Aldosteronoma

References 1. Melmed S, Polonsky KS, Larsen PR, Kronenberg HM.  Chapter 16: Endocrine hypertension. In: Williams textbook of endocrinology. 13th ed. Philadelphia: Elsevier; 2016. p. 566–88. 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 clinical practice guideline. J Clin Endocrinol Metab. 2008;93(9):3266–81. 3. Arlt W. A detour guide to the Endocrine Society clinical practice guideline on case detection, diagnosis and

467 treatment of patients with primary aldosteronism. Eur J Endocrinol. 2010;162:435–8. 4. Montori VM, WF Y.  Use of plasma aldosterone concentration-­ to-plasma renin activity ratio as a screening test for primary aldosteronism. A systematic review of the literature. Endocrinol Metab Clin N Am. 2002;31:619–32.

Suggested Reading Clark OH, Duh Q-Y, Gosnell JE, Shen W.  Textbook of endocrine surgery. 3rd ed. New Delhi: Jaypee Brothers Medical Publishers; 2014.

Management of Gastrinoma

115

Rachel E. Simpson and Benjamin C. James

Algorithmic Approach A. Gastrinoma is the second most common functional pancreatic neuroendocrine tumor [1]. The first step in diagnosis is a full history and physical exam. The most common clinical presentation includes symptoms of abdominal pain, diarrhea, and reflux [2]. These symptoms are vague with a broad differential. Zollinger-Ellison syndrome (ZES) is characterized by gastrin-producing tumors stimulating marked gastric acid production, with resultant refractory peptic ulcer disease [3]. Around 75% of gastrinomas are sporadic, while 25% are associated with multiple endocrine 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: [email protected]

C. Once hypergastrinemia has been established, other causes of hypergastrinemic state (gastric outlet obstruction, prior vagotomy, renal failure, and atrophic gastritis, among others) should be ruled out [1]. A fasting gastric pH  160 pg/mL

C

Tumor localization, staging, and tissue diagnosis -Cross sectional imaging, endoscopic ultrasound with FNA biopsy

Metastatic disease?

D, E

-Surgical resection -Somatostatin analogues

Algorithm 117.1

-Somatostatin analogues -Systemic chemotherapy -Surgical debulking/hepatic artery embolization

D, F

117  Management of Somatostatinoma

References 1. Townsend CM Jr, Beauchamp RD, Evers BM, Mattox KL.  Chapter 38: Endocrine pancreas. In: Sabiston textbook of surgery. 20th ed. Philadelphia: Elsevier; 2017. p. 941–62. 2. Jameson JL, De Groot LJ, de Kretser DM, Giudice LC, Grossman AB, Melmed S, Potts JT, Weir GC.  Chapter 42: Hyperglycemia secondary to nondiabetic conditions and therapies. In: Endocrinology: adult and pediatric. 7th ed. Philadelphia: Elsevier; 2016. p. 737–51. 3. Feldman M, Friedman LS, Brandt LJ.  Chapter 33: Neuroendocrine tumors. In: Sleisenger and Fordtran’s gastrointestinal and liver disease. 10th ed. Philadelphia: Elsevier; 2016. p. 501–41.

479 4. Melmed S, Polonsky KS, Larsen PR, Kronenberg HM.  Chapter 38: Gastrointestinal hormones and gut endocrine tumors. In: Williams textbook of endocrinology. 13th ed. Philadelphia: Elsevier; 2016. p. 1701–22. 5. Goldman L, Schafer AI. Chapter 195: Pancreatic neuroendocrine tumors. In: Goldman-cecil medicine. 25th ed. Philadelphia: Elsevier; 2016. p. 1334–9. 6. Anderson CW, Bennett JJ.  Clinical presentation and diagnosis of pancreatic neuroendocrine tumors. Surg Oncol Clin N Am. 2016;25(2):363–74. 7. Yeo CJ.  Chapter 94: Neuroendocrine tumors of the pancreas. In: Shackelford’s surgery of the alimentary tract. 7th ed. Philadelphia: Elsevier; 2013. p. 1206–16. 8. Azimuddin K, Chamberlain RS.  The surgical management of pancreatic neuroendocrine tumors. Surg Clin N Am. 2001;81(3):511–25.

Management of VIPoma

118

Rachel E. Simpson and Benjamin C. James

Algorithmic Approach A. Tumors that secrete vasoactive intestinal peptide (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 endocrine neoplasia 1 (MEN1) [4]. B. The classic biochemical finding is hypochloremic, 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: [email protected]

levels >200  pg/mL are considered diagnostic, though individuals with VIPoma tend to have levels >1000 pg/mL [5]. In the acute setting, fluids 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 identify 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 1,4,7,10tetraazacyclododecane-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 levels of VIP and also directly decrease diarrhea [5]. Somatostatin inhibits motilin and slows intestinal motility [7]. Through these various mechanisms, long-acting somatostatin ana-

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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-

A

sis [2]. In these cases, somatostatin analogs or systemic chemotherapy is the mainstay of treatment. Surgical resection is rarely curative 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 debulking surgery [4].

History and physical -Watery diarrhea, flushing, dehydration

B

Laboratory evaluation: -Hypokalemia, hypochloremia, metabolic acidosis. -VIP level >200 pg/mL

C

Tumor localization: -Cross-sectional imaging (CT/MRI), octreotide scan, endoscopic ultrasound

Metastatic disease?

No

D,E

Algorithm 118.1

-Somatostatin analogues -Surgical resection

Yes

-Somatostatin analogues -Systemic chemotherapy -Consideration for cytoreductive therapy

D,F

118  Management of VIPoma

References 1. James BC, Aschebrook-Kilfoy B, Cipriani N, Kaplan EL, Angelos P, Grogan RH.  The incidence and survival of rare cancers of the thyroid, parathyroid, adrenal, and pancreas. Ann Surg Oncol. 2016;23(2):424–33. 2. Melmed S, Polonsky KS, Larsen PR, Kronenberg HM.  Chapter 38: Gastrointestinal hormones and gut endocrine tumors. In: Williams textbook of endocrinology. 13th ed. Philadelphia: Elsevier; 2016. p. 1701–22. 3. Feldman M, Friedman LS, Brandt LJ.  Chapter 33: Neuroendocrine tumors. In: Sleisenger and Fordtran’s gastrointestinal and liver disease. Philadelphia: Elsevier; 2016. p. 501–41. 4. Townsend CM Jr, Beauchamp RD, Evers BM, Mattox KL.  Chapter 38: Endocrine pancreas. In: Sabiston textbook of surgery. 20th ed. Philadelphia: Elsevier; 2017. p. 941–62.

483 5. Jameson JL, De Groot LJ, de Kretser DM, Guidice LC, Grossman AB, Melmed S, Potts JT, Weir GC.  Chapter 150: Neuroendocrine tumor syndromes. In: Endocrinology: adult and pediatric. 7th ed. Philadelphia: Elsevier Saunders; 2016. p. 2606–14. 6. Maxwell JE, O’Dorisio TM, Howe JR. Biochemical diagnosis and preoperative imaging of gastroenteropancreatic neuroendocrine tumors. Surg Oncol Clin N Am. 2016;25(1):171–94. 7. O’Dorisio TM, Gaginella TS, Mekhjian HS, Rao B, O’Dorisio MS.  Somatostatin and analogues in the treatment of VIPoma. Ann N Y Acad Sci. 1988;527:528–35. 8. Niederhuber JE, Armitage JO, Doroshow JH, Kastan MB, Tepper JE.  Chapter 71: Cancer of the endocrine system. In: Abeloff’s clinical oncology. 5th ed. Philadelphia: Elsevier; 2014. p. 1112–42.

Part XVI Pediatric

Congenital Diaphragmatic Hernia

119

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 extracorporeal 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 (especially around feedings) and feeding difficulties including intestinal obstruction. The abdomen may appear scaphoid. Respiratory distress, cyanosis, sternal retractions, displaced 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: [email protected]

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 ventilation is avoided due to risk of gastric distension) (ii) Nasogastric (NG) tube insertion for gastric decompression (iii) Arterial and venous cannulation, typically via the umbilicus (iv) Monitoring of pre-ductal (right radial) and post-ductal (lower extremity) oxygen saturations, temperature, glucose level, volume status/urine output (v) Pharmacologic support of cardiac function 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 pathognomonic. Subsequently, echocardiography, cranial ultrasounds, and renal ultrasounds should be performed to assess for concurrent developmental abnormalities and to characterize the extent of disease. Echocardiography

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should further characterize right ventricular [6]. During ECMO, treatment is focused on function and pulmonary artery pressures. improving pulmonary hypertension and E. Following these diagnostic steps, ongoing avoiding further lung injury. physiologic optimization should occur. Goals G. A recent meta-analysis shows all infants with of ventilatory support should be to avoid lung CDH benefit from definitive surgical repair injury while maintaining a pre-ductal [7]. For infants not requiring ECMO, the diaPO2  >60  mm Hg (with corresponding pre-­ phragm defect should be repaired after stabiductal SaO2 90–95%) and tolerating relative lization and reversal of pulmonary hypercapnia. High-frequency oscillatory venhypertension. For infants requiring ECMO, tilation and nitric oxide may be useful. surgical repair after decannulation decreases Pulmonary hypoplasia and pulmonary hyperthe risk of hemorrhagic complications. tension ultimately determine the severity of Laparoscopic, thoracoscopic, or open respiratory failure and outcome [5]. approach can be used with equal effective F. Respiratory failure may progress and become ness of repair, though open repair is recoglife-threatening as a result of uncorrectable nized as most effective for prevention of pulmonary hypertension. ECMO is an approrecurrence [8]. Biologic and synthetic patches priate treatment unless pulmonary hypoplasia may be used if native tissues are inadequate. incompatible with life is present. Predictive Recurrence is more likely with prosthetic indices assist with these difficult decisions patches [9].

119  Congenital Diaphragmatic Hernia

489

A

B

Prenatal detection of CDH: -Delivery near term, experienced CDH center

Symptoms of CDH at birth: Respiratory distress, scaphoid abdomen

C

Delivery and initial management: Intubation, NG tube, pre and post-ductal sat monitoring, umbilical cannulation

D

Confirm CDH: CXR, ECHO, U/S Determine extent of disease or concurrent abnormalities

Monitoring and goals Pre-ductal PaO2 >60, non-injurious ventilation

E

ECMO required?

Yes

F

Monitor pulmonary hypertension, optimize cardiac function, decannulate prior to repair

G Algorithm 119.1

No

Ongoing resuscitation and pre-operative optimization

Operative repair: native tissue superior to prosthetic patch

Alternative diagnoses

490

References 1. Zani A, Zani-Ruttenstock E, Pierro A.  Advances in the surgical approach to congenital diaphragmatic hernia. Semin Fetal Neonatal Med. 2014;19(6):364–9. 2. Nasr A, Langer JC. Influence of location of delivery on outcome in neonates with congenital diaphragmatic hernia. J Pediatr Surg. 2011;46(5):814–6. 3. Odibo AO, Najaf T, Vachharajani A, Warner B, Mathur A, Warner BW.  Predictors of the need for extracorporeal membrane oxygenation and survival in congenital diaphragmatic hernia: a center’s 10-year experience. Prenat Diagn. 2010;30(6):518–21. 4. Kitano Y, Lally KP, Lally PA.  Late-presenting congenital diaphragmatic hernia. J Pediatr Surg. 2005;40(12):1839–43. 5. Dillon PW, Cilley RE, Mauger D, Zachary C, Meier A. The relationship of pulmonary artery pressure and survival in congenital diaphragmatic hernia. J Pediatr Surg. 2004;39(3):307–12.

C. J. McLaughlin et al. 6. Le LD, Keswani SG, Biesiada J, Lim FY, Kingma PS, Haberman BE, Frischer J, Habli M, Crombleholme TM.  The congenital diaphragmatic hernia composite prognostic index correlates with survival in left-­ sided congenital diaphragmatic hernia. J Pediatr Surg. 2012;47(1):57–62. 7. Harting MT, Hollinger L, Tsao K, Putnam LR, Wilson JM, Hirschl RB, Skarsgard ED, Tibboel D, Brindle ME, Lally PA, Miller CC. Aggressive surgical management of congenital diaphragmatic hernia: worth the effort? A multicenter, prospective, cohort study. Ann Surg. 2018;267(5):977–82. 8. Putnam LR, Tsao K, Lally KP, Blakely ML, Jancelewicz T, Lally PA, Harting MT, Group CD. Minimally invasive vs open congenital diaphragmatic hernia repair: is there a superior approach? J Am Coll Surg. 2017;224(4):416–22. 9. Moss RL, Chen CM, Harrison MR.  Prosthetic patch durability in congenital diaphragmatic hernia: a long-term follow-up study. J Pediatr Surg. 2001;36(1):152–4.

Tracheoesophageal Fistula

120

Rachel E. Hanke, Morgan K. Moroi, and Robert E. Cilley

Algorithmic Approach A. Tracheoesophageal fistula (TEF) and esophageal 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 ultrasound evidence of polyhydramnios and a small or absent stomach bubble [2]. All except type E present shortly after birth with some combination of excessive drooling, choking, regurgitation, and/or respiratory 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: [email protected]

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 present with choking when eating or unexplained cyanotic episodes [3]. B. If there is suspicion for EA/TEF in a newborn, 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 eventual surgical repair [1]. C. Initially, management should be focused on decreasing risk of aspiration and respiratory issues by maintaining the esophageal drainage catheter on suction. Perioperative antibiotics 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 associated anomalies. Echocardiography evaluates structural heart disease, which occurs in about 35% of patients. The position of the

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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 ligation of the TEF may be life-saving. Patients with progressive gastric distention may require emergent trans-abdominal needle decompression followed by urgent gastrostomy. 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 gastrostomy may be performed. Although not performed 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 lengthening and staged repairs are performed [3, 5]. Many pediatric surgeons have abandoned esophageal replacement. Colon interposition, gastric “pull-up,” or reversed gastric tubes are

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 discontinued [4]. Parenteral nutrition, gastrostomy feeds, or trans-anastomotic feeding tubes are used to support nutrition [3]. An esophagram is performed post-operatively to evaluate 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 stricture 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 surgery” or fibrin glue plugging). Airway instability/tracheomalacia usually responds to supportive care [3].

120  Tracheoesophageal Fistula

493

Newborn noted to have excessive salivation and regurgitation/choking after feeding

A

Perform thorough physical exam, place esophageal tube, obtain PA/lateral CXR

B

CXR shows coiling of tube in chest

C

Air in stomach?

Yes

No

Esophageal atresia with TEF

D

Pure esophageal atresia

Work up per EA/TEF. Plan staged/delayed repair using lengthening techniques *

Obtain echocardiogram

E

Severe respiratory distress with gastric distension (consider gastric decompression/ gastrostomy first)

No

Further evaluation: renal ultrasound and genetic testing

Thoracoscopy vs thoracotomy to divide/repair of TEF

Yes Urgent thoracotomy and ligation/clipping of TEF Repair after clinical improvement

Yes

Long gap EA?

* Esophageal lengthening and/or staged repair of EA

F Algorithm 120.1

Post-operative esophagram and surveillance

No Primary repair of EA

494

References 1. Lal DR, Gadepalli SK, Downard CD, Ostlie DJ, Minneci PC, Swedler RM, Chelius T, Cassidy L, Rapp CT, Deans KJ, Fallat ME, Finnell ME, Helmrath MA, Hirschl RB, Kabre RS, Leys CM, Mak G, Raque J, Rescorla FJ, Saito JM, St. Peter SD, von Allmen D, Warner BW, Sato TT. Perioperative management and outcomes of esophageal atresia and tracheoesophageal fistula. J Pediatr Surg. 2017;52(8):1245–51. 2. Slater BJ, Rothenberg SS. Tracheoesophageal fistula. Semin Pediatr Surg. 2016;25(3):176–8. 3. Harmon C, Coran A. Pediatric surgery. In: Coran AG, Adzick NS, Krummel TM, Laberge JM, Shamberger RC, Caldamone AA, editors. Congenital anomalies of the esophagus. 7th ed. Philadelphia: Saunders; 2012.

R. E. Hanke et al. 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 KJ, Fallat ME, Fraser JD, Grabowski J, Hebel F, Helmrath MA, Hirschl RB, Kabre R, Kohler J, Landman MP, Leys CM, Mak GZ, Raque J, Rymeski B, Saito JM, St. Peter SD, von Allmen D, Warner BW, Sato TT.  Challenging surgical dogma in the management of proximal esophageal atresia with distal Tracheoesophageal fistula: outcomes from the Midwest Pediatric Surgery Consortium. J Pediatr Surg. 2018;53(7):1267–72. 5. Foker JE, Krosch TCK, Catton K, Munro F, Khan KM. Long-gap esophageal atresia treated by growth induction: the biological potential and early follow-up results. Semin Pediatr Surg. 2009;18:23–9.

Other Diaphragmatic Hernias: Late-Presenting Bochdalek Hernia, Morgagni Hernia, and Giant Hiatal Hernia of Infancy

121

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 centrally 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 herniated through a large opening in the esophageal hiatus. Regardless of location, late-presenting patients do not have pulmonary 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: [email protected]

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 diagnosis. Diaphragm hernia should be considered in the differential diagnosis of a child with dysphagia, decreased appetite, vomiting, constipation, abdominal pain, recurrent respiratory 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 radiograph. 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 congenital abnormalities may be present and should be evaluated [1–3]. Echocardiography should be considered to evaluate for structural heart disease. D. Intestinal obstruction, caused by incarcerated intestine or gastric volvulus, may require emergency operation. For all of these diaphragmatic defects, correction is performed

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promptly. Late-presenting CDH may be repaired traditionally via laparotomy or thoracotomy. Thoracoscopic repair is gaining popularity [1, 2]. For Morgagni hernias, laparoscopic 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 procedure 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 encountered. Resection of the hernia sac likely reduces recurrence, although this customary

practice is not well supported by outcome studies [3, 4]. E. Post-operative imaging requirements are limited 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 neonates [1, 2]. Postoperative complications are extremely rare after Morgagni hernia repair [3]. Giant hiatal hernia patients do well, although they may experience typical problems 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. Obtain a chest radiograph.

C

Yes

Diaphragmatic hernia identified?

No

Continue workup for alternative diagnoses

Intestinal incarceration or gastric volvulus? No

Yes

Imaging for preoperative planning (GI contrast, possibly CT) and evaluation of other congenital abnormalities (consider echocardiography)

Emergent operative repair

D

Prompt surgical repair

E Repair via thoracic or abdominal approach, open or video-endoscopic procedure

Algorithm 121.1

Post-operative imaging and surveillance

498

References 1. Stolar C, Dillon P.  Pediatric surgery. In: Coran AG, Adzick NS, Krummel TM, Laberge JM, Shamberger RC, Caldamone AA, editors. Congenital diaphragmatic hernia and eventration. 7th ed. Philadelphia: Saunders; 2012. 2. Kitano Y, Lally KP, Lally PA.  Late-presenting congenital diaphragmatic hernia. J Pediatr Surg. 2005;40(12):1839–43.

M. K. Moroi et al. 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. 4. Kohn GP, Price RR, Demeester SR, Zehetner J, Muensterer OJ, Awad Z, Mittal SK, Richardson WS, Stefanidis D, Fanelli RD.  Guidelines for the management of hiatal hernia. Surg Endosc. 2013;27(12):4409–28.

Duodenal Obstruction in Newborns

122

Abdulraouf Y. Lamoshi, Sophia Abdulhai, and Todd A. Ponsky

Algorithmic Approach A. Prenatal diagnosis of duodenal atresia is usually 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 abdominal distension and failure to pass meconium are the main presenting symptoms [3]. Preampullary 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 abdominal X-ray, by placing a nasogastric (NG) tube and injecting about 50 ml of air into the stomach which can work as a contrast medium and makes the double-bubble sign clearer [3]. C. Initial resuscitation includes starting intravenous (IV) fluids, keeping the patient NPO, and inserting an NG tube to correct the electrolyte abnormalities and fluid balance and to stop vomiting. Workup for associated anomalies, such as cardiac defects, is of utmost importance during the preoperative time [2]. D. Abdominal plain X-ray should first be performed, 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

diagnose a duodenal atresia and mandates surgical 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 ultrasounds, should also be performed during the hospitalization to diagnose potential associated renal or spinal abnormalities [3]. E. Treatment: Laparoscopic or open duodenoduodenostomy 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, duodenogastric reflux, gastritis, delayed gastric emptying, and blind-­loop syndrome [3].

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500

Antenatal Diagnosis made?

A

Yes No Will present with early bilious vomiting

B

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

E

Duodeno-duodenostomy

F

Surgery (Duodeno-duodenostomy) or web-excision)

if no then likely duodenal web

Follow-up care

Algorithm 122.1

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”.

ECR 2016 / C-0486 / Final Year Radiography Students’ 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

123

Abdulraouf Y. Lamoshi, Sophia Abdulhai, and Todd A. Ponsky

Algorithmic Approach A. Antenatal diagnosis can be established in 41% of the patients [1], where polyhydramnios and dilated bowels together are highly suggestive of the diagnosis [2]. Postnatally, bilious vomiting, upper abdominal distension, 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 hypovolemia, electrolyte abnormalities, and minimize vomiting. Antibiotics are needed when there is suspicion for intestinal perforation. C. Diagnosis: Abdominal plain X-ray is the initial 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 contrast enema, which can diagnose other potential causes such as Hirschsprung disease,

meconium ileus, meconium plug syndrome, or colonic atresia [3]. A meconium pseudocyst may occur in the case of intrauterine intestinal perforation, and intraluminal calcifications of meconium have also been documented 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 evaluated [3]. Temporary gastrointestinal dysfunction is a common observation in these newborns [3].

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

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502

A

Antenatal Diagnosis made?

Yes

No Will present with early bilious vomiting

Resection and anastomosis

Obtain V/S and physical exam Peritonitis: No

Peritonitis: Yes

Urgent Surgery

B

C

NPO, NGT, and IVF

KUB (AXR)

Double-bubble (consider other pathologies)

Dilated bowels

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 Distal small bowel atresia/other surgical pathologies

D

E Algorithm 123.1

Yes

Micro-colon with no meconium

Surgery No

Follow-up care

Consider other pathologies

123  Small Intestinal Atresia

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.

503 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 pediatric surgery e-book. Philadelphia: Elsevier Health Sciences; 2014.

Management of Malrotation

124

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 distention (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 hemodynamic instability, then intestinal ischemia from malrotation with midgut volvulus should be considered and NG tube placement, fluid resuscitation, broad-spectrum antibiotics, and immediate operative exploration 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

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 midgut 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 enterocolitis should also be considered with these X-ray findings. (b) Proximal obstruction: Although duodenal 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 emergently. Additionally, duodenal atresia and web are the most common congenital anomaly associated with malrotation, occurring in up to 11% of patients [2].

© 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

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 pathology, 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 normal 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 presence 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

A

507

History and Physical Infant with bilious emesis.

Obtain vital signs and perform physical examinations

B

Peritonitis, hemodynamic instability?

YES

OR

NO Abdominal X-ray

C

Distal Obstruction

Free Air/Pneumatosis or Proximal Obstruction Unremarkable OR

Contrast Enema with Distal Pathology?

NO

D

Equivocal

E Repeat UGI in 1 month or Laparoscopy if still symptomatic

Upper GI Contrast Study

Abnormal DJJ position

Malrotation Consider other pathology Ladd’s Procedure

F Algorithm 124.1

Normal DJJ position

Follow-up Care

YES

508

References 1. El-Gohary Y, Alagtal M, Gillick J.  Long-term complications following operative intervention for intestinal malrotation: a 10-year review. Pediatr Surg Int. 2010;26(2):203–6. https://doi.org/10.1007/ s00383-009-2483-y.

S. Abdulhai et al. 2. Ford EG, Senac MO, Srikanth MS, Weitzman JJ. Malrotation of the intestine in children. Ann Surg. 1992;215(2):172–8. 3. Langer JC. Intestinal rotation abnormalities and midgut volvulus. Surg Clin North Am. 2017;97(1):147– 59. https://doi.org/10.1016/j.suc.2016.08.011.

Management of Imperforate Anus

125

Sophia Abdulhai and Aaron Garrison

Algorithmic Approach A. Anorectal malformations (ARMs), or imperforate 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 work­up 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 echocardiogram should be performed prior to any surgical intervention. (b) Urologic defects: About 50% of all ARM patients also have some type of urological defect, and incidence of urologic abnormalities is highest with cloaca. Renal ultrasound (US) should be performed 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 nasogastric tube and abdominal X-ray.

S. Abdulhai · A. Garrison (*) Division of Pediatric Surgery, Akron Children’s Hospital, Akron, OH, USA e-mail: [email protected]

(d) Musculoskeletal: Tethered cord, which occurs in about 25% of anorectal malformations 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 lateral films of the sacrum should also be performed to evaluate for other sacral anomalies, such as hemisacrum and hemivertebrae. 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 orifice 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 anatomy 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 performed after the colostomy.

© 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

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 posterior 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 complexity based on common channel length. This evaluation requires cystoscopy, vaginoscopy, 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 anorectoplasty (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 anorectoplasty or posterior sagittal anorectovaginourethroplasty should be performed about 1–2  months later after work-up for additional anomalies has been completed and the patient is exhibiting normal 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 performed 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 performed, and definitive repair deferred to a later date.

125  Management of Imperforate Anus

511

A

History and Physical 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.

B

In first 24 hours, work up for other congenital anomalies. 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.

D

Male

C

Female

Flat Perineum

Perineal fistula

No Fistula

Perineal or vestibular fistula

Single Perineal Opening (Cloaca)

Anoplasty (or fistula dilation)

Colostomy and drainage of Hydrocolpos (if present)

Meconium in Urine No

Anoplasty (or fistula dilation)

Yes

E

Undefined/ No fistula

Colostomy

Fistulogram

Cross Table Lateral Film

Fistulogram

Rectal Gas ABOVE coccyx

Rectal Gas BELOW coccyx

Colostomy

Anoplasty (with or without Colostomy)

PSARP PSARP

< 3 cm common channel

> 3 cm common channel

PSARVUP

Transfer to colorectal center for PSARVUP

Algorithm 125.1

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.

2. Peña A, Hong AR.  In: Mattei P, editor. Anorectal 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 malformations 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 transiContrast enema reveals proximal distended tion point within the rectosigmoid region, bowel that tapers through the transition zone while 15% have long-segment colonic disto a decompressed distal rectum. Anorectal ease, 5–10% have total colonic disease, manometry may be helpful in documenting and  30, Cl < 100, K < 3 · Typical lab values: CO2 > 25

· Bolus with NS @ 20cc/kg · 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

C

·

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 · Once labs normalize

E

Algorithm 130.1

Proceed with Pyloromyotomy

Post-pyloromyotomy Feeding Schedule: · Regimented feeding schedule · Ad lib feeding

532

References 1. 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.

D. W. Parrish et al. 2. Schwartz M. Hypertrophic pyloric stenosis. In: Coran A, et  al., editors. Pediatric surgery. 7th ed. London: Elsevier Inc; 2012. 3. Benson C, Alpern E.  Preoperative and postoperative care of congenital pyloric stenosis. AMA Arch Surg. 1957;75(6):877–9.

Necrotizing Enterocolitis

131

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 associated with hypoxia, infections, cyanotic heart defects, and initiation of enteral nutrition [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: [email protected]

remains largely unknown but is believed to be due to the immature epithelial gastrointestinal lining of neonates, leading to translocation of bacteria resulting in an inflammatory response that may eventually cause perforation [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 distended abdomen with more advanced disease demonstrating systemic symptoms such as hemodynamic instability (hypotension, shock), respiratory distress (apnea, respiratory acidosis), or decreased peripheral perfusion (metabolic acidosis) [1, 3]. B. Evaluation continues with laboratory assessments 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 bacteremia. Abdominal radiographs can be used to look for radiographic signs such as pneumatosis 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,

© 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

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small bowel obstruction, and bacterial or viral enteritis. C. The Modified Bell’s Staging Criteria is often used to clinically and radiographically diagnose and stage NEC [1, 4]. Management of suspected or confirmed NEC begins with gastric decompression with nasogastric or orogastric tube (NGT, OGT) placement, stopping enteral nutrition, broad IV antibiotics, and correction of respiratory and metabolic derangements as needed (IV fluid resuscitation, ventilation, or vasopressors). Fifty percent of infants with NEC require surgical intervention [1]. D. The only absolute surgical indication for NEC is pneumoperitoneum. However, relative indications include hemodynamic instability 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 development of the above indications. E. If a patient meets criteria for surgical intervention and is >1500  g, then may proceed with laparotomy. If 1500g HD Stable

Laparotomy

536

References 1. Castle SL, Speer AL, Grikscheit TC, Ford H. Necrotizing enterocolitis. In: Ziegler MM, Azizkhan RG, Dv A, Weber TR, editors. Operative pediatric surgery. New York: McGraw-Hill Education; 2014. 2. Tanner SM, Berryhill TF, Ellenburg JL, Jilling T, Cleveland DS, Lorenz RG, et al. Pathogenesis of nec-

J. H. DeAntonio et al. rotizing enterocolitis: modeling the innate immune response. Am J Pathol. 2015;185(1):4–16. 3. Neu J.  Necrotizing enterocolitis. World Rev Nutr Diet. 2014;110:253–63. 4. Walsh MC, Kliegman RM. Necrotizing enterocolitis: treatment based on staging criteria. Pediatr Clin N Am. 1986;33(1):179–201.

Omphalocele and Gastroschisis

132

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 eviscerated abdominal contents that are not surrounded by a membranous sac. The bowel is usually thickened and edematous. Believed to be caused by embryological failure, the lateral 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: [email protected]

factors including environmental exposures (tobacco), lower maternal age or socioeconomic 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 incidence 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 embryologically after gastroschisis and is not suspected to be associated with teratogen exposure [1]. Omphaloceles are classically associated with numerous congenital anomalies 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, currently 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

© 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

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538

J. H. DeAntonio et al.

be evaluated with diagnostic pre-natal ultratransparent 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 prenafor surgical closure in the perinatal period but tally, then chromosome evaluation by amniomay 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 susthe 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 covereventual 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 fashwith petroleum or saline-moistened gauze. ion (6 months to 1 year). Ruptured omphaloU/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 nutrisilo and slowly reducing them back into the tion (proper intestinal motility delayed by sevabdomen 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 conthere is ischemic bowel, perforation, or cerned with evaluation and management of other hemodynamic (HD) instability, immediate congenital defects. Abdominal compartment synexploration in the NICU or operating room drome (ACS) should be a concern, like gastrosfor 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

A

B

Gastroschisis · Abdominal wall defect-Right of umbilical cord · No sac covering eviscerated contents

· Evaluate bowel for dilatation, atresia, or necrosis · Cover contents with saline soaked gauze and place plastic covering to above defect.

Omphalocele · Midline abdominal wall defect · Sac covering eviscerated contents · Associated with cardiac, renal, genetic defects

· If intact sac over contents, cover with petroleum or saline soaked gauze · U/S evaluation for associated anomalies and karyotype sent if not done prenatally

C Evidence of perforation, malrotation, necrosis and HD instability?

ImmediatePrimary closure

D

YES

Exploration, Source Control, & Staged Closure

NO

Fails/Unable

Size and Other Congenital Abnormalities

Silo with daily reduction & delayed fascial closure

ImmediatePrimary Closure

Staged Closure

Delayed Closure

Postoperative Management · 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

References 1. Islam S.  Abdominal wall defects: omphalocele and gastroschisis. In: Ziegler MM, Azizkhan RG, Dv A, Weber TR, editors. Operative pediatric surgery.

J. H. DeAntonio et al. New York: McGraw-Hill Education; 2014. 2. Allman R, Sousa J, Walker MW, Laughon MM, Spitzer AR, Clark RH. The epidemiology, prevalence and hospital outcomes of infants with gastroschisis. J Perinatol. 2016;36(10):901–5.

133

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 colored stools for the first few days of life. Typical symptoms of biliary atresia are persistently elevated conjugated bilirubin, jaundice, 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: [email protected]

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 infection) 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 intraoperative cholangiogram can demonstrate the biliary anatomy and can rule out biliary atresia if contrast is seen in the intestines. A liver biopsy should be performed to evaluate the presence of bile ducts and ductular proliferation [2, 3]. C. Once the diagnosis of biliary atresia is made, operative timing is key. More favorable outcomes are seen when the definitive procedure is performed within 60 days of age, as cirrhosis begins to develop by 3–4 months of age. Preoperative steps to take are to maintain good hydration with intravenous fluid resuscitation, broad-spectrum antibiotic coverage,

© 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

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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 hepaticojejunostomy is performed. E. There is a large discrepancy in the morbidity and mortality rates that are presented in the literature, but successful postoperative outcomes 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 transplantation [3]. Cholangitis is the most common postoperative complication following a Kasai procedure. F. Controversy exists regarding the use of corticosteroids 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 portoenterostomy 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

B

· Ultrasound: evaluate liver contour and presence of gallbladder, bile ducts, or choledochal cysts · 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

Proceed with Roux-en-Y hepatic portoenterostomy

D

E

F

1/3 of patients will have successful long term biliary drainage

1/3 of patients will have temporary biliary drainage but will ultimately require a transplant

1/3 of patients will have no relief from the operation and will progress to liver failure

Complications: Cholangitis, Decreased bile flow, Portal Hypertension, Essential Fatty Acid deficiency, Intrahepatic cysts

544

References 1. Practice parameter: management of hyperbilirubinemia in the healthy term newborn. American Academy of Pediatrics. Provisional Committee for Quality Improvement and Subcommittee on Hyperbilirubinemia. Pediatrics. 1994;94(4 Pt 1):558–65.

D. W. Parrish et al. 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. 3. Schwartz M. Hypertrophic pyloric stenosis. In: Coran A, et al. Pediatric surgery. 7th. London. Elsevier Inc; 2012. 4. Nio M, Ohi R.  Biliary atresia. Semin Pediatr Surg. 2000;9:177–86.

Part XVII Vascular

Carotid Artery Stenosis

134

Ian Bailey and Faisal Aziz

Algorithmic Approach A. Introduction: Stroke is among the most common 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 prevention. 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: [email protected]

carotid endarterectomy (CEA) reduced the incidence of stroke from 26% to 9% [2]. B. Evaluation/ Physical Examination: Key elements of the physical examination include a neurologic exam, cardiac exam, neck auscultation, as well as an ocular exam. The neurologic 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 murmur 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 hemodynamically 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 suitable patients include carotid endarterectomy (CEA) and carotid artery stenting (CAS). CREST trial [3] showed that CEA was associated with 4.7% risk of stroke and death

© 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

547

I. Bailey and F. Aziz

548

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 differences 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 subsequently 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

B

Thorough physical examination: assessment of systemic vascular disease, neurologic examination, ocular examination

C

Duplex ultrasound: Degree of carotid stenosis

D

Symptomatic Carotid Stenosis >50%

Asymptomatic Carotid Stenosis >80%

CEA (Carotid Shunting, if indicated)

E

Contra indications to CEA (previous neck radiation, previous carotid surgery, unfit for general anesthesia) CAS

F Algorithm 134.1

Postoperative Care

134  Carotid Artery Stenosis

References 1. Grysiewicz RA, Thomas K, Pandey DK. Epidemiology of ischemic and hemorrhagic stroke: incidence, prevalence, mortality, and risk factors. Neurol Clin. 2008;26(4):871–95. 2. North American Symptomatic Carotid Endarterectomy Trial Collaborators, HJM B, Taylor DW, Haynes RB, Sackett DL, Peerless SJ, Ferguson GG, Fox AJ, Rankin RN, Hachinski VC, Wiebers DO, Eliasziw M.  Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med. 1991;325(7):445–53.

549 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, Voeks JH, Hopkins LN, Cutlip DE, Cohen DJ, Popma JJ, Ferguson RD, Cohen SN, Blackshear JL, Silver FL, Mohr JP, Lal BK, Meschia JF, Investigators CREST.  Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med. 2010;363(1):11–23.

Abdominal Aortic Aneurysm

135

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 recommends 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: [email protected]

nal mass, which is widely believed to represent an impending aneurysmal rupture [2]. C. Evaluation/physical examination: Risk factors 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, computed tomographic angiography (CTA) provides greater accuracy and more reliable 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

© 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

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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. Graftrelated complications following EVAR include endoleaks. Ischemic colitis can present with bloody diarrhea, abdominal pain, distension, fever, leukocytosis, or metabolic acidosis. G. Long-term follow-up: Following EVAR, contrast-enhanced CT scanning should be undertaken at 1 and 12  months; alternatively,

E. K. Greenleaf and F. Aziz

duplex ultrasound combined with non-contrast CT serves as a viable option in patients with renal insufficiency. An endoleak, a complication unique to EVAR, occurs due to persistent blood flow into the aneurysmal sac and if seen at 1  month would necessitate a CTA at 6  months to determine need for reintervention. There are five types of endoleaks: 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 following EVAR should be continued at least on an annual basis. Following open repair, imaging should be obtained at least every 5 years.

135  Abdominal Aortic Aneurysm

A

B

C

553

Presence of risk factors for development of aortic aneurysm (AAA)

Physical examination reveals pulsatile aortic mass

Duplex ultrasound: AAA diagnosis. Infrarenal 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 access vessels: Feasible for EVAR

D Yes

E

No

EVAR

Open AAA Repair

Post-operative Evaluation: Endoleaks

Post-operative Evaluation: ischemica of the colon, lower extremities, or spinal cord, cardiac ischemia, and renal failure

Algorithm 135.1

References 1. US Preventive Services Task Force: Abdominal Aortic Aneurysm. Web address: https://www. uspreventiveservicestaskforce.org/Page/Document/ UpdateSummaryFinal/abdominal-aortic-aneurysmscreening. Accessed 25 Aug 2017. 2. Sullivan CA, Rohrer MJ, Cutler BS. Clinical management of symptomatic but unruptured abdominal aortic aneurysm. J Vasc Surg. 1990;11(6):799–803.

3. Beede SD, Ballard DJ, James EM, Ilstrup DM, Hallet JW Jr. Positive predictive value of clinical suspicion of abdominal aortic aneurysm. Implications for effective 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 medicare population. N Engl J Med. 2015;373:328–38.

Ruptured Abdominal Aortic Aneurysm

136

Faisal Aziz

Algorithmic Approach A. Definitions: Rupture is the most feared complication 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 ruptured 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 tachycardia. 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: [email protected]

D. Imaging: Computed tomography ­angiography (CTA) is the standard imaging technology to diagnose rAAA and to determine the feasibility 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 landing zones required for EVAR placement. E. Management: Ruptured AAA can be repaired with either open surgical operation or endovascular repair (EVAR). For patients who present with relatively stable hemodynamics, CTA is used to determine the choice of operation. For patients who are unstable, a percutaneous 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 difference in patients presenting with ruptured AAA is the importance of obtaining quick inflow control to stop active hemorrhage. In patients undergoing EVAR, an occlusion balloon inserted via femoral access can be used for inflation in aorta and in patients undergoing open surgical repair, a supraceliac clamp can be used to stop active hemorrhage.

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F. Aziz

556

F. Postoperative complications: Overall mortality for patients with rAAA remains high, with majority of patients dying even before reaching 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 postoperative acute renal failure after rAAA surgery is the biggest predictor of mortality, and incidence of acute renal failure in patients treated

Triad of Abdominal Pain, Abdominal Distension and Hypotension

A

High Suspicion for rAAA. Determine feasibility of getting CTA

B

C D

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.

Unstable hemodynamics: Directly to OR, on table angiography to determine if candidacy for EVAR (Landing zone length of at least 15mm, neck angulation of 0.15 is clinically significant. Duplex ultrasound for routine surveillance of infrainguinal, autogenous vein bypass grafts or after endovascular revascularization is recommended.

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

565

A. Aurshina and A. Hingorani

566

A

Definition: Acute (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 for signs of PAD, non-healing wound/ulcer or gangrene.

A

Initial Test: Ankle Brachial Index (ABI) (Class I)3

Abnormal ABI: 65 years Age 50–64 years with Risk Factors for atherosclerosis (DM, HTN, smoking, hyperlipidemia, family Hx of PAD) Age 3 days. Minor risk factors include minor surgical procedures, pregnancy, or estrogen therapy. Persistent risk factors include reversible risk factors (malignancy or inflammatory bowel disease) and irreversible risk factors (inherited thrombophilia, CHF, and metastatic cancer) [2]. C. Proximal DVT has higher risk of complication 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 objective 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

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 (iliofemoral 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 Bedridden recently >3 days or major surgery within 4 weeks Calf swelling >3 cm compared to the other leg Measured 10 cm below tibial tuberosity Collateral (nonvaricose) superficial veins present Entire leg swollen Localized tenderness along the deep venous system Pitting edema, confined to symptomatic leg Paralysis, paresis, or immobilization of the lower extremity Previously documented DVT Alternative diagnosis to DVT as likely or more likely

1 1 1 1 1 1 1 1 1 1 −2

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

© 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

577

A. Aurshina and A. Hingorani

578

Patient presents with signs and symptoms of acute DVT: pain, swelling, tenderness, inflammatory signs of warmth and redness Excluding other causes based on H&P

A

Clinical suspicion of DVT

Determine Pretest probability using Modified Wells Score1 Assess for known risk factors of DVT

B

Low Perform D-Dimer assay

Negative DVT excluded

Intermediate or High Perform compression ultrasonography

Negative DVT excluded

Positive Perform compression ultrasonography

C

Contraindication to anticoagulation?

Yes

IVC filter Retrievable or Permanent filter; follow for 3-6 months with anticoagulation when contraindication resolves

Consider thrombolytics or thrombectomy

Distal DVT

Proximal DVT

No contraindication

Phlegmasia cerulea dolens

Positive DVT confirmed

High risk

D

No phlegmasia cerulean dolens

Low risk / contraindicated anticoagulation

No contraindication to anticoagulation

Initial Anticoagulation Heparin/Warfarin or LMWH for 3–6 months Alternative: DOAC3

OBSERVE, repeat proximal compressive ultrasound in 1–2 weeks

E Consider long-term indefinite anticoagulation Follow-up with riskbenefit assessment

Algorithm 141.1

Unprovoked proximal DVT/ Recurrent DVT/ Persistent DVT

Provoked DVT with identified risk factors: STOP anticoagulation after 3–6 months

DVT extension into or towards the proximal veins, patient at risk of extension

Stable, no extension, continue surveillance

141  Acute Deep Venous Thrombosis

References 1. Wells PS, Anderson DR, Rodger M, Forgie M, Kearon C, Dreyer J, et al. Evaluation of D-dimer in the diagnosis of suspected deep-vein thrombosis. N Engl J Med. 2003;349(13):1227–35. 2. Kearon C, Ageno W, Cannegieter SC, Cosmi B, Geersing GJ, Kyrle PA. Categorization of patients as having provoked or unprovoked venous thromboembolism: guidance from the SSC of ISTH.  J Thromb Haemost. 2016;14(7):1480–3.

579 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 report. Chest. 2016;149(2):315–52. 4. Meissner MH, Gloviczki P, Comerota AJ, Dalsing MC, Eklof BG, Gillespie DL, et  al. Early thrombus removal strategies for acute deep venous thrombosis: clinical practice guidelines of the Society for Vascular Surgery and the American Venous Forum. J Vasc Surg. 2012;55(5):1449–62.

Management of Acute Mesenteric Ischemia

142

Josh Radtka

Algorithmic Approach A. The first step in the management of a patient with acute mesenteric ischemia is the history 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 condition is important as there is only a 30% survival 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 ischemia, 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: [email protected]

occlusion. NOMI occurs in 20% of cases and is typically due to a low flow start due to shock or vascocontstrictors [3]. D. An emergent operative intervention will be required if the CTA demonstrates an arterial occlusion. The patient should receive intravenous 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 performed 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 abdomen 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 mesenteric ischemia.

© 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

581

J. Radtka

582

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

CTA of Abdomen and Pelvis

B

Arterial occlusion Start heparin drip, ABX, IVF, Exploratory Laparotomy SMA embolectomy/thrombectomy

D

Arterial Flow Restored? No Bypass or Retrograde stenting

E

F

Yes

Bowel Resection and Second look Laparotomy

Follow-up Care: Echo with agitated saline; and CTA of the chest

Algorithm 142.1

No arterial occlusion, possible NOMI, or another diagnosis

C

142  Management of Acute Mesenteric Ischemia

References 1. Jimenez, Quinones-Baldrich. Mesenteric vascular disease: general considerations. In: Cronenwett J, editor. Rutherford’s vascular surgery. Philadelphia: Elsevier; 2010. p. 2260–1. 2. Wyers. Mesenteric vascular disease: acute ischemia. In: Cronenwett J, editor. Rutherford’s vascular surgery. Philadelphia: Elsevier; 2010. p. 2292–4.

583 3. Cheng CC, Choi L, Cheema Z, Silva MB Jr. Acute mesenteric ischemia. Current surgical therapy. In: Cameron JL, Cameron AM, editors. Current surgical therapy. 11th ed. Philadelphia: Elsevier; 2014. p. 939–46.

Management of Chronic Mesenteric Ischemia

143

Josh Radtka

Algorithmic Approach A. The first step in the management of a patient with chronic mesenteric ischemia is the history and physical exam. The classic description 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 abdominal 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: [email protected]

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 mesenteric ischemia. The diagnosis of CMI requires that two of the three mesenteric vessels have severe stenosis or occlusion and one of these vessels needs to be the superior mesenteric artery. The work-up begins with a duplex of the mesenteric arteries. This modality has minimal patient risk and provides dynamic information about the degree of stenosis within the mesenteric vessels. Bowel gas and patient body habitus may obscure the visualization of the vessels. A computed tomography angiogram (CTA) of the abdomen and pelvis provides anatomic information 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 immediate therapeutic intervention. D. After the diagnosis of chronic mesenteric ischemia has been made, the treatment options are either an endovascular intervention or an open bypass. Medical management is not successful as it does not treat the underlying 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

© 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

585

J. Radtka

586

s­uperior mesenteric arteries as a possible treatment option. A balloon expandable stent is often utilized during endovascular treatments. Currently, endovascular techniques for revascularization are the first-line therapy

A

in many institutions. Open bypass options include an antegrade aorto-mesenteric, a retrograde aorto-mesenteric, or an ileo-mesenteric artery bypass [2].

History: 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

B

Standard GI Workup

Positive

Treat Other Pathology

Negative

C

Evaluate for Mesenteric Stenosis

Positive

D Algorithm 143.1

Revascularization Procedure: Endovascular or Open

Negative

Continue to evaluate for other etiologies

143  Management of Chronic Mesenteric Ischemia

References 1. Huber, Lee. Mesenteric vascular disease: chronic ischemia. In: Cronenwett J, editor. Rutherford’s vascular surgery. Philadelphia: Elsevier; 2010. p. 2274–5.

587 2. Schwartz, et al. Diagnosis and surgical management of the visceral ischemic syndromes. In: Moore W, editor. Vascular and endovascular surgery. Philadelphia: Elsevier; 2013. p. 423–35.

Thoracic Outlet Syndrome

144

Tarik Z. Ali and Josh Radtka

Algorithmic Approach A. Thoracic outlet syndrome (TOS) is a constellation of upper extremity symptoms resulting from compression of the brachial plexus, subclavian 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 different types of thoracic outlet syndromes. Neurogenic is the most common type and is usually a diagnosis of exclusion. Common symptoms are pain, paresthesia, and weakness in the affected extremity without localization 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 subclavian 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: [email protected]

B. In order to determine if the extremity swelling 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 associated 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 controversial 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 endovascular methods.

© 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

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T. Z. Ali and J. Radtka

590

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 compromise

B

C

D

Embolic/Ischemic Event

Arm Swelling

Arterial Duplex, CT Angiogram

Venous Duplex of RUE

Physical Therapy

Revascularization

Thrombolysis of Axillary and Subclavian Veins

First Rib Resection

First Rib Resection Possible Arterial Reconstruction

First Rib Resection Possible Venous Reconstruction

CXR Arterial and Venous Duplex MRI

Follow-up Care

Algorithm 144.1

144  Thoracic Outlet Syndrome

References 1. Sanders. Thoracic outlet syndrome: general considerations. In: Cronenwett J, editor. Rutherford’s vascular surgery. Philadelphia: Elsevier; 2010. p. 1865–77.

591 2. Thompson, Driskill. Thoracic outlet syndrome: neurogenic. In: Cronenwett J, editor. Rutherford’s vascular surgery. Philadelphia: Elsevier; 2010. p. 1878–98. 3. Schanzer, Messina. Thoracic outlet syndrome: general considerations. In: Cronenwett J, editor. Rutherford’s vascular surgery. Philadelphia: Elsevier; 2010. p. 1907–17.

AV Shunt Complications

145

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 information includes the following: is the access a fistula or graft, when it was created, when was the last dialysis session, and if any problems were occurring with the access (i.e., paresthesia 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 uremia, fluid overload, acidosis, and hyperkalemia. C. If the patient requires hemodialysis and the access is occluded, then a temporary hemodi-

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 surgical 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 diagnostic and therapeutic. It will allow for treatment of common causes of dialysis access occlusion such as arterial anastomotic stenosis, venous anastomotic stenosis, and central vein stenosis. After the cause of failure is discovered 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 preferentially in the right internal jugular vein. The patient will then require a work-up for placement of a new hemodialysis access. This may require ultrasound-guided vein mapping or moving the site of access creation to another extremity.

J. Radtka () Division of Vascular Surgery, Penn State Milton S. Hershey Medical Center, Hershey, PA, USA e-mail: [email protected] © 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

593

J. Radtka

594

A

History: 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 hemodialysis required?

B Yes

C

Place Temporary Dialysis Catheter

No

Surgical intervention to restore blood flow to access successful?

D

Yes

E

Evaluate for cause of failure Use for Hemodialysis

No

Place a permanent catheter Evaluate for other permanent dialysis options

F

Algorithm 145.1

References 1. Macasta, Sidawy. Hemodialysis access: general considerations. In: Cronenwett J, editor. Rutherford’s vascular surgery. Philadelphia: Elsevier; 2010. p. 1105–6.

2. Meier G.  Hemodialysis access: failing and thrombosed. In: Cronenwett J, editor. Rutherford’s vascular surgery. Philadelphia: Elsevier; 2010. p. 1132–6.

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 calcifications. Bosniak I and II cysts are benign A. A history and physical examination is the iniand do not require follow-up. Increasingly tial step in renal mass evaluation. Patients complex features are useful in predicting risk may exhibit nonspecific symptoms including of malignancy. Management strategies for gross or microscopic hematuria, flank pain, more complex cysts are based on AUA guideweight loss, fever, or diaphoresis. Physical lines which recommend routine surveillance signs are uncommon but may include hyper(Bosniak IIF) versus surgical resection tension, palpable flank mass, and/or ipsilat(Bosniak III and IV) [3]. eral varicocele. The majority of renal masses D. The differential diagnosis for a solid renal (up to 70%) are incidental findings and othermass includes malignant and non-malignant wise asymptomatic [1]. entities. Macroscopic fat (HU –20 to −80) is B. Dedicated imaging is necessary to further virtually diagnostic for angiomyolipoma characterize the renal mass as cystic or solid. (AML). Asymptomatic patients with small A three-phase abdominal computed tomogra(4 cm. Significant the gold standard cross-sectional study. active bleeding necessitates embolization or Abdominal magnetic resonance imaging open surgical control for life-threatening (MRI) with gadolinium and ultrasonography hemorrhage [4]. Renal mass biopsy should be are additional imaging modalities for renal considered when a mass is suspected to be mass characterization [2]. metastatic [5]. Enhancing solid renal masses C. The Bosniak classification system defines are usually malignant and most commonly cystic renal masses based on their contrast-­ renal cell carcinoma (RCC). enhanced CT imaging characteristics. Simple E. If RCC is suspected after imaging, obtain renal cysts (Bosniak I) do not enhance or conCBC, CMP, and UA. Chest imaging (CXR or CT) is performed to rule out pulmonary metastases. Additional studies include a J. Chris Riney and Neil J. Kocher contributed equally to this work. nuclear medicine bone scan and/or brain MRI if patients present with bone pain or neuroJ. C. Riney · N. J. Kocher · M. Kaag (*) Division of Urology, Penn State Milton S. Hershey logic symptoms, respectively [6]. Medical Center, Hershey, PA, USA e-mail: [email protected]

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F. Treatment of suspected RCC is based on 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

nephrectomy. Select medium-sized masses (T1b 4–7  cm) amenable to nephron-sparing surgery are managed with partial nephrectomy. Large tumors are managed with radical nephrectomy [5]. Locally advanced tumors may invade the vena cava and require cavotomy and reconstruction.

A

Perform focused history and physical exam · Nonspecific symptoms · Physical signs uncommon

B

Obtain 3-phase abdominal CT scan with/without IV contrast (“renal mass protocol”)

C

D

Cystic

Bosniak I or II

Bosniak IIF

Bosniak III or IV

No follow-up necessary

Surveillance imaging

Surgical removal

Solid

Enhancing >15HU

Concern for metastasis or lymphoma

Fat present

AML Consider biopsy

E 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

F

Small renal mass 4 cm(T1a)

Active Surveillance

Algorithm 146.1

Ablation

Select T1b (4-7cm)

Partial Nephrectomy

Large mass or not amendable to nephron sparing

Radical Nephrectomy

146  Management of the Renal Mass

References 1. Chen DY, Uzzo RG. Evaluation and management of the renal mass. Med Clin North Am. 2011;95(1):179–89. 2. Kang SK, Chandarana H. Contemporary imaging of the renal mass. Urol Clin North Am. 2012;39:161–70. 3. Israel GM, Bosniak MA.  An update of the Bosniak renal cyst classification system. Urology. 2005;66(3):484.

599 4. Nelson CP, Sanda M.  Contemporary diagnosis and management of renal angiomyolipoma. J Urol. 2002;168:1315. 5. National Comprehensive Cancer Network (NCCN) clinical practice guidelines in oncology: kidney cancer. V.1.2018, 2018. www.nccn.org. 6. Campbell S, Uzzo RG, Allaf ME, et  al. Renal mass and localized renal cancer: AUA guideline. J Urol. 2017 Sep;198(3):520–9.

Prostate Cancer

147

Rosa Park and Matthew Kaag

Algorithmic Approach A. Prostate cancer is the most common malignancy in US males after skin cancer, but the mortality rate in this usually unaggressive cancer is low [1]. Most patients present without symptoms, and the question of appropriate 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 prevalent in the United States until 2012 and consists 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 supporting prostate cancer screening, driven by the historic over-treatment of men with low-risk disease who were unlikely to die of their cancer 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: [email protected]

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 elevated 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 fluoroquinolone antibiotic prophylaxis is recommended at least 1  h prior to biopsy. Rectal cultures can be obtained prior to biopsy in patients with increased risk of resistant bacteria. Expected sequelae include gross hematuria, 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

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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 managed via a therapeutic algorithm that is structured around depriving tumor cells of their androgen source but also may include immunotherapy and conventional chemotherapy [7].

147  Prostate Cancer

603

History and physical exam: · Most are asymptomatic · Family History · Perform DRE

A

Normal DRE

Abnormal DRE

B Does the patient meet PSA based screening criteria?

D

C

No

Check PSA

Yes

E

Prostate needle biopsy

No further work-up Repeat DRE and PSA as appropriate

F

G

Active surveillance

Algorithm 147.1

Elevated PSA May repeat PSA

Normal PSA

No further work-up Follow up as indicated

Normal biopsy

Prostate cancer

Imaging by risk category: MRI pelvis, CT, or bone scan

Clinically localized disease

Radical prostatectomy ± pelvic lymph node dissection

Radiation

Regional disease

Androgen deprivation

Metastatic disease

Refer to oncology

604

References 1. Siegel RL, Miller KD, Jemal A.  Cancer statistics, 2015. CA Cancer J Clin. 2015;65(1):5–29. 2. Loeb S, Eastham JA. Chapter 111, Diagnosis and staging of prostate cancer. In: Campbell-Walsh urology. 11th ed. Philadelphia: Elsevier; 2016. p. 2601–8. 3. Moyer VA, U.S.  Preventive Services Task Force. Screening for prostate cancer: U.S. preventive services task force recommendation statement. Ann Intern Med. 2012;157(2):120–34. 4. Carter HB, Albertsen PC, Barry MJ, Etzioni R, Freedland SJ, Greene KL, Holmberg L, Kantoff P, Konety BR, Murad MH, Penson DF, Zietman AL.  Early detection of prostate cancer: AUA guideline. J Urol. 2013;190(2):419–26.

R. Park and M. Kaag 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 prostate-specific antigen levels: an evaluation of year-­ to-­year fluctuations. JAMA. 2003;289(20):2695–700. 6. Liss MA, Ehdaie B, Loeb S, Meng MV, Raman JD, Spears V, Stroup SP.  An update of the American Urological Association White Paper on the prevention and treatment of the more common complications related to prostate biopsy. J Urol. 2017 Aug;198(2):329–34. 7. National Comprehensive Cancer Network, Inc. NCCN clinic practice guidelines in oncology: prostate cancer. Version 1.2018. [Internet]. 2018. [cited 2018 Feb 14]. Available from: https://www.nccn.org/ professionals/physician_gls/pdf/prostate.pdf.

Management of Scrotal/Testicular Mass

148

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 neurological exams. The examiner should attempt to distinguish intratesticular from paratesticular lesions. The causes of scrotal masses may be classified as follows: benign/malignant, infectious/noninfectious, and emergent/nonemergent. 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 comB. M. Blair · M. Kaag (*) Division of Urology, Penn State Milton S. Hershey Medical Center, Hershey, PA, USA e-mail: [email protected]

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 irregularity. A scrotal mass may be noted, secondary to hematoma. Penetrating injury of the scrotum requires surgical exploration and repair. Blunt scrotal trauma may result in rupture of the tunica albuginea, requiring prompt surgical 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/inflammatory 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) antibiotics ± surgical drainage/orchiectomy if abscess develops. F. Benign cystic masses of the epididymis or spermatic cord include spermatocele, epididymal head cyst, and varicocele. These entities are classified as paratesticular and are generally benign. Observation is usually appropriate unless symptomatic. Varicoceles may be

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associated with infertility, prompting repair. While left-sided varicoceles are fairly common, 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 ultrasound 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 banking 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 pulmonary 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 ligation of the spermatic cord is required and assists in future surgery if a retroperitoneal 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, chemotherapy, or RPLND.  Patients with seminoma who have low-volume metastasis are eligible 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 disease is platinum-­based multi-drug chemotherapy [1, 5].

148  Management of Scrotal/Testicular Mass

History of Present Illness and Vitals/Physical Exam (genitals, abdomen, lymph nodes, breasts, neuro)

A

Painful and suspect testicular torsion?

B

C

607

Scrotal Ultrasound STAT

No blood flow?

Immediate exploration and orchiopexy

Scrotal Ultrasound STAT

Scrotal Ultrasound

E Epididymoorchitis

Abscess

IV antibiotics, surgical drainage or orchiectomy

F

Scrotal or testicular trauma?

Painless/painful mass and torsion not suspected?

Hydrocele

No Abscess

Antibiotics and/or NSAIDS

Evidence of testicular rupture?

Observe or elective repair

Scrotal exploration and repair

Epididymal/Spermatic Cord Mass

Solid Testicular Mass

Varicocele

Spermatocele, 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

G Algorithm 148.1

Radical inguinal orchiectomy with high spermatic cord ligation

D

608

References 1. Wein A, Kavoussi L, Partin A, Peters C.  Campbell-­ Walsh urology. 11th ed. Philadelphia: Elsevier; 2016. 2. Montgomery J, Bloom D.  The diagnosis and management of scrotal masses. Med Clin North Am. 2011;95(1):235–44. 3. Rabinowitz R, Hulbert W.  Acute scrotal swelling. Urol Clin North Am. 1995;22(1):101–5.

B. M. Blair and M. Kaag 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  – Testicular Cancer  – Version 2.2017 [Internet]. www. nccn.org. 2017 [cited 8 Oct 2017]. Available from: https://www.nccn.org/professionals/physician_gls/ pdf/testicular.pdf.

Diagnosis and Management of Fournier’s Gangrene

149

Augustyna Gogoj and Matthew Kaag

Algorithmic Approach

Radiographs may show swelling or subcutaneous emphysema. Ultrasound can demon A. Fournier’s gangrene is a necrotizing infection strate a thickened, edematous scrotal wall involving the genitals. Patients often present containing hyperechoic foci or paratesticular with, or rapidly develop signs of, sepsis, and fluid. Computed tomography can be used to this condition may be progressive and life-­ guide surgical management and visualize threatening. Treatment hinges on the rapid asymmetric fascial thickening, fluid collecinitiation of broad-spectrum antibiotics and tions, abscess formation, fat stranding, and aggressive local debridement with/without subcutaneous emphysema. Computed tomogurinary and fecal diversion. raphy has greatest specificity [4]. B. Diagnosis of Fournier’s gangrene starts with D. Broad-spectrum parenteral antibiotic therapy clinical findings on physical exam including is to be started immediately upon diagnosis. fluctuance, localized tenderness, and wounds Antibiotics must cover staphylococcal, strepof the genitalia and perineum [1]. Crepitus or tococcal, and gram-negative bacteria, colievidence of tissue necrosis differentiates forms, Pseudomonas, Bacteroides, and Fournier’s gangrene from genital cellulitis Clostridium. Adequate coverage typically and scrotal abscess. Vital signs and blood includes a broad-spectrum penicillin with work may be used as predictors for mortality. third-generation cephalosporin or aminoglyPatients older than 50 with diabetes mellitus coside and metronidazole or clindamycin. (in 20–70% of patients) or an alcohol abuse Expansion to include vancomycin or linehistory (in 20–50% of patients) are at greatest zolid may be necessary based on the clinical risk and should be thoroughly examined. situation. Culture results can guide eventual Other predisposing factors include poor narrowing of antibiotic coverage [3]. hygiene, malnutrition, malignancy, steroid E. Aggressive and timely surgical debridement use, or an immunocompromised state [2, 3]. is imperative for decreased mortality. All C. Imaging is not necessary unless disease devitalized tissues must be resected. Serial extent or diagnosis is not clear and should debridement is often necessary [5]. never prolong time to surgical management. F. Fecal diversion is indicated with anal sphincter involvement, fecal incontinence, or continued fecal contamination of the wound’s A. Gogoj · M. Kaag (*) Division of Urology, Penn State Milton S. Hershey margins [6]. In the event of extensive penile Medical Center, Hershey, PA, USA e-mail: [email protected]

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or urethral involvement, suprapubic urinary diversion may be necessary; however, urethral 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 preservation of genital function. Primary closure of wounds shows the best functional and cosmetic results. Closure of wounds through secondary 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

B

Disease extent or diagnosis unclear?

Yes

Obtain imaging CT is most specific: fascial thickening, fluid collections, paratesticular fluid

No

C

Start broad-spectrum IV antibiotics

D

Aggressive surgical debridement

E

Need for fecal/urinary diversion?

Yes

Fecal diversion through colostomy or Flexi-seal fecal management system urinary diversion through cystostomy, 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

References 1. Chennamsetty A, Khourdaji I, Burks F, Killinger K.  Contemporary diagnosis and management of Fournier’s gangrene. Ther Adv Urol. 2015;7(4):203–15. 2. Clayton M, Fowler J, Sharifi R, Pearl R. Causes, presentation and survival of fifty-seven patients with necrotizing fasciitis of the male genitalia. Surg Gynecol Obstet. 1990;170:49–55. 3. Mallikarjuna M, Vijayakuma A, Patil V, Shivswamy B. Fournier’s gangrene: current practices. ISRN Surg. 2012;942437. 4. Levenson R, Singh A, Novelline R. Fournier gangrene: role of imaging. Radiographics. 2008;28:519–28. 5. Sorenson M, Krieger J, Rivara F, Klein M, Wessells H.  Fournier’s gangrene: management and mortality predictors in a population based study. J Urol. 2009;182:2742–7.

A. Gogoj and M. Kaag 6. Ozturk E, Sonmez Y, Yilmazlar T. What are the indications for a stoma in Fournier’s gangrene? Color Dis. 2011;13:1044–7. 7. Ozkan O, Koksal N, Altinli E, Celik A, Uzun M, Cikman O, Akbas A, Ergun E, Kiraz HA, Karaayvaz M.  Fournier’s gangrene current approaches. Int Wound J. 2011;15(5):713–6. 8. Jallali N, Withey S, Butler P.  Hyperbaric oxygen as adjuvant therapy in the management of necrotizing fasciitis. Am J Surg. 2005;189(4):462–6. 9. Maguina P, Palmieri T, Greenhalgh D. Split thickness skin grafting for recreation of the scrotum following Fournier’s gangrene. Burns. 2003;29:857–62. 10. Lee S, Rah D, Lee W. Penoscrotal reconstruction with gracilis muscle flap and internal pudendal artery perforator flap transposition. Urology. 2012;79:1390–6. 11. Chen S, Fu J, Wang C, Lee T, Chen S. Fournier gangrene: a review of 41 patients and strategies for reconstruction. Ann Plast Surg. 2010;64:765–9.

Part XIX Trauma

Hypotension and Blunt Abdominal Trauma

150

Cheyenne C. Sonntag and Steven R. Allen

Algorithmic Approach

crystalloid solution given. Patients will often have IV access and fluids initiated in the field A. On patient arrival, a brief history provided by by EMS, and this volume should be considtransporting EMS may identify blunt mechaered. If hypotension does not correct with nism. The first steps in evaluation of patients crystalloid bolus, early transition to blood with blunt traumatic injury is the primary surproducts is warranted. vey (ABCs) to identify and intervene for life-­ C. In the setting of persistent hypotension, it is threatening conditions [1]. The airway is inappropriate to transport the patient for comassessed for patency, with maintenance of puted tomography (CT) scan, and other diagspinal precautions. Bilateral chest is ausculnostic modalities must be considered to tated for presence of breath sounds, oxygen evaluate for internal hemorrhage. For abdomsaturation obtained, chest wall inspected, and inal evaluation, these include diagnostic perioxygen therapy initiated. Interventions such toneal aspirate (DPA), diagnostic peritoneal as obtaining definitive airway and needle lavage (DPL), and focused assessment sonogdecompression are performed as indicated if raphy in trauma (FAST) and are equally life-threatening condition is found during airappropriate and dependent on provider/instiway and breathing assessment. tution capabilities. Thoracic and pelvic B. In continuation of the primary survey, circutrauma are elsewhere covered. latory assessment consists of blood pressure, D. DPA is considered positive if gross blood is heart rate evaluation, and assessment of found on aspiration (10 mL); DPL is positive peripheral pulses. Sources of large external if microscopic analysis reveals >100 K/mm3 blood loss are controlled. Two large-bore IVs red blood cells and >500 K/mm3 white blood should be obtained preferentially and, in cells or lavage shows bile or particulate matpatients found to be hemodynamically unstater [2, 3]. It should be remembered that false-­ ble, a bolus of 1–2 liters of warm isotonic positive DPL may occur in the setting of pelvic fractures, when retroperitoneal hematoma may unintentionally be sampled [3]. C. C. Sonntag Positive DPA/DPL in a hemodynamically Department of Surgery, Penn State Milton S. Hershey Medical Center, Hershey, PA, USA unstable patient warrants emergent operative exploration. S. R. Allen (*) Department of Surgery, Penn State Health Milton E. Exploratory laparotomy is indicated in S. Hershey Medical Center, Hershey, PA, USA patients who are hemodynamically unstable e-mail: [email protected]

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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 evaluated. 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 hypotension 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 hemodynamic instability

No

Continue primary survey

YES

C

· Transfuse blood products · DPA/DPL or FAST

DPA positive?

FAST positive?

· aspirate 10mL gross blood or DPL positive?

E

· RBC>100 K/mm3 · WBO >500 K/mm3 · Bile or particulates

G

No

· Continue resuscitation · Investigate other sources of shock

Algorithm 150.1

YES

No

F

D · Continue resuscitation · Investigate other sources of shock · Consider DPA/DPL

YES

Exploratory laparotomy

618

References 1. Initial Assessment and Management. Advanced trauma life support ATLS: student course manual. 9th ed. Chicago: American College of Surgeons; 2012. p. 6–13. 2. Root HD, Hauser CW, McKinley CR, Lafave JW, Mendiola RP Jr. Diagnostic peritoneal lavage. Surgery. 1965;57:633–7. 3. Hoff WS, Holevar M, Nagy KK, Patterson L, Young JS, Arrillaga A, et al. Practice management guidelines

C. C. Sonntag and S. R. Allen for the evaluation of blunt abdominal trauma: the East practice management guidelines work group. J Trauma. 2002;53(3):602–15. 4. Branney SW, Wolfe RE, Moore EE, Albert NP, Heinig M, Mestek M, et al. Quantitative sensitivity of ultrasound in detecting free intraperitoneal fluid. J Trauma. 1995;39(2):375–80.5. 5. Carter JW, Falco MH, Chopko MS, Flynn WJ Jr, Wiles Iii CE, Guo WA. Do we really rely on fast for decision-making in the management of blunt abdominal trauma? Injury. 2015;46(5):817–21.

Traumatic Brain Injury

151

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 computed tomography (CT) scan should be obtained to rule out a more significant brain injury. It is common for patients with moderate or severe TBI to present with a lucid interval, 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: [email protected]

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 discharged with instructions on symptoms which would prompt a return visit. If there are concerns for the patient despite a normal exam, 12–24 h of continued observation prior to discharge 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 condition, 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, assuming 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.

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­ yperventilation can be considered in the H acute setting, maintaining PaCO2 between 30 and 35 mm Hg. Patients also need to be adequately resuscitated, and the patient should also be properly assessed for any sources of ongoing bleeding which may lead to a hypovolemic state. It is critical to avoid hypotension (systolic blood pressure  1500 mL, then the versus endovascular management of aortic patient should go to the OR for immediate thorainjury. With flail chest, sternal fracture, and cotomy). A pericardial effusion can be managed severe pulmonary contusions, there should in the emergency department (ED) with pericarbe a low threshold for intubating the patient diocentesis, although we recommend going to the if they are in respiratory distress. OR for subxiphoid pericardial window if these Management for these conditions is mostly resources are available. If the patient loses vital conservative (i.e., mechanical ventilation, signs, consider an ED thoracotomy (see separate pain control, and aggressive pulmonary Algorithm). A high degree of suspicion for intra-­ toilet). Rib plating for flail chest or multithoracic or intra-abdominal injury should be ple rib fractures will be dictated by existing maintained if scapula fracture, flail chest, sternal institutional protocols, as there are no confracture, or posterior sternoclavicular dislocation clusive guidelines at this time. • Mild to moderate injuries include rib fractures, mild pulmonary contusions, soft tisN. R. Manley · G. O. Maish III (*) Department of Surgery, University of Tennessee sue injury, thoracic spine fractures, and Health Science Center, Memphis, TN, USA clavicle fractures. Rib fractures and mild e-mail: [email protected]

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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 orthopedic 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 survey. 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 initially 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 specific 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—including 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

B

A Stable

Unstable

Chest CT Angiography

Continued Resuscitation

Severe Injury Manage per etiology

Mild or Moderate Injury

Responds

Manage per etiology

Abbreviations: ACLS: Advanced cardiac life support; ATLS: Advanced trauma life support; CXR: Chest x-ray; ED: Emergency department; FAST: Focused assessment with sonography in trauma; HTX: Hemothorax; OR: Operating room; PTX: Pneumothorax; VS: Vital signs

No response

· Reassess for life-threatening injury · Consider Blunt Cardiac Injury · ACLS

Algorithm 155.1

Suggested Reading American College of Surgeons. Advanced trauma life support. 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 guideline 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

rib fractures after blunt trauma: a practice management 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 management of chest wall trauma in adults. Up to Date [Internet]. 2016 Sep [cited 2017 Aug 14]. Available from: https://www.uptodate.com/contents/initialevaluation-and-management-of-chest-wall-traumain-adults. Simon B, Ebert J, Bokhari F, Capella J, Emhoff T, Hayward T, et  al. Management of pulmonary contusion and flail chest: an Eastern Association for the Surgery of Trauma practice management guideline. J Trauma Acute Care Surg. 2012;73(5 Suppl 4):S351–61.

Blunt Cardiac Injury

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Algorithmic Approach

B. In the patient with abnormal EKG and normal troponin, consult cardiology for further workAny patient presenting to the emergency departup. Consider cardiac ECHO.  If injury is ­ ment (ED) with blunt trauma to the anterior chest found, manage per specific etiology and conshould be worked up for blunt cardiac injury sider ICU admission for cardiac monitoring. (BCI). In addition to routine trauma labs (e.g., Continue full trauma work-up as indicated. In CBC, BMP, lactate, PT/INR, PTT, ABG) and the patient with abnormal troponin and norimaging (e.g., portable chest), a 12-lead EKG mal EKG, consult cardiology for further should be done, and cardiac troponins should be work-up. Again, consider cardiac ECHO.  If sent to assess baseline level. It is also important injury is found, manage per specific etiology to obtain a thorough past medical history (PMH) and consider ICU admission for cardiac monif possible to put the patient’s current injuries into itoring. Continue with full trauma work-up as context. Pertinent PMH to BCI includes any pre-­ appropriate. existing cardiac abnormality (e.g., murmur or C. In the hemodynamically unstable patient, folpacemaker), current medications (especially carlow ATLS protocols in the trauma bay and diac meds and anticoagulants), previous myocarensure ABCs are secure. Even if BCI is high dial infarction, previous cardiac catheterizations on the differential diagnosis for instability, and any stents placed, baseline functional status, assume tachycardia is secondary to hemorand any past cardiac surgeries (e.g., coronary rhage until proven otherwise. Any arrhythartery bypass surgery [CABG]). Always consider mias should be managed with ACLS myocardial infarction as the inciting event that protocols. Echocardiogram should be done to led to the trauma, especially in the elderly. assess for structural defects; if any valve, septum, or ventricular wall injuries are found, A. In the patient with normal EKG and normal cardiothoracic surgery should be consulted troponin, blunt cardiac injury (BCI) is effecimmediately for possible operative interventively ruled out. Continue with trauma worktion. Consider inserting a pulmonary artery ­up per chief complaint and mechanism of catheter (PAC) to guide fluid resuscitation injury. when cardiac abnormalities are present, as it is important to avoid fluid overload in these patients. Once trauma work-up is complete, N. R. Manley · G. O. Maish III (*) Department of Surgery, University of Tennessee these patients require ICU admission, conHealth Science Center, Memphis, TN, USA tinuous telemetry, and close observation. e-mail: [email protected]

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N. R. Manley and G. O. Maish III

638 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.

A

Normal EKG and Troponin

· No BCI · Continue trauma work up

B

Abnormal EKG or abnormal troponin; hemodynamically stable

· Cardiology consult · Consider ECHO · Specific management per etiology[1]

C

Hemodynamically unstable

· ATLS & ACLS · ICU admit · Cardiology consult · ECHO · Consider PAC · Specific 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

Suggested Reading American College of Surgeons. Advanced trauma life support. 9th ed. Chicago: American College of Surgeons; 2012. 336 p. American Heart Association. Advanced cardiac life Support. Dallas: American Heart Association; 2015. 183 p.

639 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 practice management guide. J Trauma Acute Care Surg. 2012;73(5 Suppl 4):S301–6. Legome E, Kadish H. Cardiac injury from blunt trauma. Up to Date [Internet]. 2017 Jul [cited 2017 Aug 13]. Available from: http://www.uptodate.com/contents/ cardiac-injury-from-blunt-trauma.

Deceleration Injury: Blunt Aortic Injury

157

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 following algorithm should be followed in the stable patient. B. Initial management of any trauma patient presenting to the trauma bay should follow advanced trauma life support (ATLS) protocols. It is especially important in patients with a high degree of suspicion for blunt aortic 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 portable chest x-ray. Common features indicating 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 paravertebral 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: [email protected]

enough, a CT of the chest with contrast should be obtained. D. If an aortic injury is found on CT, urgent vascular and/or thoracic surgery consultation is recommended, 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 nitroprusside 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 aortic injury are possible, although current recommendations favor the endovascular approach unless the patient is hemodynamically unstable and the patient has other obvious injuries requiring operative exploration. Aortic injuries based on CT findings and general management guidelines are as follows: • Type I: Intimal tear. Typically managed conservatively with heart rate (48  h [3]. The patient should also be prepped for resuscitative endovascular balloon R. M. Staszak · L. J. Laufenberg (*) occlusion of the aorta (REBOA), if this is Department of Surgery, Division of Trauma, Acute Care, and Critical Care Surgery, Penn State Milton available at your institution. S. Hershey Medical Center, Hershey, PA, USA e-mail: [email protected]

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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 hemorrhage 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 control with preperitoneal packing, external fixation, 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 combination 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 rectal 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, arteriography, 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 operative and nonoperative management, with weight bearing as tolerated. Orthopedic surgery should be involved early in the stabilization 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: -Activate MTP -CXR & Pelvis, Pelvic binder (if amendable) -Femoral Arterial catheter for possible REBOA

C

CT scan of abd/pelvis with signs of bleeding from the pelvis or major pelvic injury? Yes

FAST

D

Positive

E

Negative

-To operating room: Control intra-abdominal hemorrhage -Control any pelvic hemorrhage (pelvic fixation, preperitoneal packing, arteriography, REBOA)

ICU admission follow CBC & exam

Algorithm 166.1

G

-Obtain immediate surgical/ortho consultation - Pelvic arteriography or other intervention

-Control extra-abdominal hemorrhage -Control pelvic hemorrhage - Pelvic stabilization/fixation -Preperitoneal packing if uncontrolled bleeding Consider Pelvic arteriography, REBOA

F

No

Admission with serial re-examinations orthopedics consultation as indicated

ICU admission follow CBC & exam

* REBOA –Resuscitative endovascular balloon occlusion of the aorta

682

References 1. Coccolini F, et al. Pelvic trauma: WSES classification and guidelines. World J Emerg Surg. 2017;12(5):1–18. 2. Mattox KL, Moore EE, Feliciano DV. Trauma: pelvis. 7th ed. New York: McGraw-Hill; 2013. p. 655–68. 3. Fiechtl J, et  al. Pelvic trauma: initial evaluation and management. In: Post T, editor. UpToDate.

R. M. Staszak and L. J. Laufenberg [Internet]. Waltham, MA: UpToDate; 2017. Available from: https://www.uptodate.com/contents/ pelvic-trauma-initial-evaluation-and-management. 4. Cullinane DC, et al. Eastern Association for the surgery of trauma practice management guidelines for hemorrhage in pelvic fractures – update and systemic review. J Trauma. 2011;71(6):1850–68.

Bladder Injuries

167

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 compressive or shear forces. An appropriate mechanism 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 pelvic fractures, blunt trauma to the lower abdomen, 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 following 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: [email protected]

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 urethra injury by exam or retrograde urethrogram 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, followed 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 provide 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 limited to the perivesical space are often associated 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].

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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 cystotomy 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 peritoneal surface has been disrupted with concomitant urinary extravasation. These bladder injuries often occur when blunt traumatic 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 ureteral 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, usually 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 Urine for gross blood (r/o urethral trauma before placing a Foley)

B

Consult urology

Complex injury

No Gross blood or significant concern for Bladder injury?

Treat other injuries

F

G

Intraperitoneal bladder injury

OR for repair –2 layered closure –Foley 5–10 days

H

Yes CT cystogram or cystoscopy

No injury

I

C

Extraperitoneal bladder injury

Foley 10–14 days

D

E

Repeat cystogram prior to removing foley

Algorithm 167.1

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 ruptures. J Urol. 1987;138(4:743–5.

3. Carroll PR, McAninch JW.  Major bladder trauma: mechanisms of injury and a unified method of diagnosis and repair. J Urol. 1983;132:254. 4. Peng MY, Parisky YR, Cornwell EE, et al. CT cystography 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.

168

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 secondary 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 uncommon due to protection from bony pelvis but can be seen with severe pelvic fractures [2]. Penetrating injuries can result from transpelvic gunshot wounds, perineal impalement, iatrogenic processes, foreign body insertion, or sex-related injuries [3]. B. The patient’s physical exam findings (abdominal 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: [email protected]

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 immediate management of the patient, so performance 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 versus extraperitoneal. If there are any concerning 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 discontinuity [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 considered the gold standard for detection and

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688

localization of rectal injuries [8–10]. This will serve to determine if the injury is intraperitoneal or extraperitoneal. If the injury is to the intraperitoneal portion of the rectum, then further 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 contamination. 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 primary repair only [4, 14]. F. Any rectal injury that is either inaccessible or more severe should undergo proximal diversion. If the injury is nondestructive (25% circumference

E F

Injury is partial thickness and easily accessible

Fecal diversion with colostomy, pre-sacral drainage, distal rectal washout

Injury is full thickness, not easily accessible, /=30 mmHg or delta pressure of /=30mmHg or delta P−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 ameliorate the edema. A failed cuff-leak test does not always lead to failed extubation particularly when inappropriately sized tube was used. D. Diligence must be observed prior to endotracheal extubation especially if intubation was noted to be difficult. Caution must be taken in extubating patient with obstructive sleep apnea, maxillofacial trauma, generalized edema, postoperative procedure like thyroid and ENT surgeries, and cervical spine procedures. Informing the anesthesia or surgical team prior to extubating a previously difficult intubation patient is not unreasonable. Reintubation has been associated with higher mortality (see table in Algorithm 172.2).

A. P. Santos

716

Criteria for Extubation:

A

1. 2. 3. 4. 5.

Patient is awake and can support airway Adequate respiratory drive and muscle strength Adequate oxygenation and ventilation Passed spontaneous breathing trial (+) Cough reflex and able to clear secretions

Indication for the intubation resolved?

Do not Extubate Re-assess again

No

Yes

B

Spontaneous Breathing Trial for 30 minutes or more

Do not Extubate No

Re-assess again

Yes

Yes

C

IV Steroids

Cuff Leak? No

Re-assess again

172  Intubation and Extubation

717 Yes

Previous Difficult Intubation?

No

Prepare to extubate

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

References 1. 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):832–9. 2. Jaber S, Jung B, Corne P, et  al. An intervention to decrease complications related to endotracheal intubation 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 randomized trial. Can J Anaesth. 2012 Nov;59(11):1032–9.

4. Neumar RW, Otto CW, Link M, et  al. Part 8: adult 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 placement: 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 extubation 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 undertaken for patients with moderate-to-­ A. If one should have a patient developing new-­ severe ARDS including the use of neuroonset or worsening respiratory compromise muscular blockade agents [7] and prone within 1  week of exposure to relevant risk positioning [8]. factors, one should be aware that the patient E. Measurement of driving pressure [9] and could be developing ARDS [1]. This syntrans-pulmonary pressure [10] may impede drome is underrecognized in 40% of all cases injury to the lung in the form of volutrauma, [2] and has a mortality rate of greater than barotrauma, atelectrauma, and biotrauma. 40% in moderate-to-severe disease [3]. F. Recruitment maneuvers to open collapsed B. Once you suspect ARDS, apply the criteria alveoli [11] and utilization of a directed fluid cited in the Berlin definition of ARDS [1]. management strategy for specific subphenoRecognition of a patient with ARDS and stagtypes of ARDS [12] may benefit certain ing (mild, moderate, severe) of the syndrome ARDS patients. clarifies the mortality risk and drives treat- G. To optimize care of the ARDS patient, the ment efforts maximizing survival. (see table ABCDEF [13] bundle must be employed. in Algorithm 173.1) H. Presently, there is no compelling evidence to C. Patients meeting ARDS criteria must have support the routine use of extracorporeal lung protective strategies initiated. These membrane oxygenation [14], high-frequency strategies include low tidal volume ventilaoscillatory ventilation [15], inhaled nitric tion, elevated positive end-expiratory presoxide [16], or glucocorticoids [17] in the sure (PEEP), and diminished plateau treatment of ARDS patients. pressures [4]. PEEP strategy should be determined by the ARDS stage [5, 6].

D. A. Galvan (*) Geisinger Holy Spirit Hospital, Harrisburg, PA, USA e-mail: [email protected] © 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_173

719

D. A. Galvan

720

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:

A

Is this ARDS?

Pneumonia Non-pulmonary sepsis Aspiration of gastric contents Major trauma Pulmonary contusions Pancreatitis Inhalational injury Severe burns Non-cardiogenic shock Drug overdose Multiple transfusions or transfusionassociated acute lung injury Pulmonary vasculitis Drowning

The Berlin Definition of Acute Respiratory Distress Syndrome Acute Respiratory Distress Syndrome Within 1 week of a known clinical insult or new or worsening respiratory symptoms

Timing Chest imaginga Origin of edema

B

Oxygenationb Mild

Bilateral opacities—not fully explained by effusions, lobar/lung collapse, or nodules 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

20 mmHg < PaO2/FIO2 ≤300 mmHg with PEEP or CPAP ≥ 5 cmH2OC 100 mmHg < PaO2/FIO2 ≤ 200 mmHg with PEEP ≥ 5 cmH2O Moderate 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)

C

Begin lung protective strategies including low tidal volume ventilation (4-6 mL/kg predicted body weight), elevated PEEP while keeping plateau pressures ≤ 30 cm H2O. Utilize low PEEP for mild ARDS and high PEEP for moderate-to-severe ARDS.

D

Utilizing appropriate sedation, begin a continuous infusion of Cisatracurium for 48 hours. Then initiate proning of the patient for at least 16 consecutive hours per day until desired improvement in oxygenation is achieved.

E

Initiate measurement of driving pressure and transpulmonary pressure as described in the referenced articles.

F

Utilize recruitment maneuvers; obtain plasma levels of IL-8, bicarbonate and 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.

G

Delirium should be assessed utilizing numerical rating scales, prevented and managed. Delirium leads to prolonged mechanical ventilation, increased 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)

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References 1. Ranieri VM, Rubenfeld GD, Thompson BT, et  al. The ARDS definition task force. Acute respiratory distress syndrome: the Berlin definition. JAMA. 2012;307(23):2526–33. 2. Bellani G, Laffey JG, Pham T, LUNG SAFE Investigators; ESICM Trials Group, et  al. Epidemiology, patterns of care, and mortality for patients with acute respiratory distress syndrome in intensive care units in 50 countries. JAMA. 2016;315(8):788–800. 3. Villar J, Blanco J, Kacmarek RM. Current incidence and outcome of the acute respiratory distress syndrome. Curr Opin Crit Care. 2016;22(1):1–6. 4. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342(18):1301–8. 5. Briel M, Meade M, Mercat A, et al. Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome systematic review and meta-analysis. JAMA. 2010;303(9):865–73. 6. Chiumello D, Cressoni M, Carlesso E, et al. Bedside selection of positive end-expiratory pressure in mild, moderate and severe acute respiratory distress syndrome. Crit Care Med. 2013;42(2):1–13. 7. Papazian L, Forel JM, Gacouin A, ACURASYS Study Investigators, et al. Neuromuscular blockers in early acute respiratory distress syndrome. N Engl J Med. 2010;363(12):1107–16. 8. Guérin C, Reignier J, Richard JC, PROSEVA Study Group, et  al. Prone positioning in severe

D. A. Galvan acute respiratory distress syndrome. N Engl J Med. 2013;368(23):2159–68. 9. Amato MB, Meade MO, Slutsky AS, et  al. Driving pressure and survival in acute respiratory distress syndrome. N Engl J Med. 2015;372(8):747–55. 10. Talmor D, Sarge T, Malhotra A, et al. Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med. 2008;359(20):2095–104. 11. Constantin JM, Godet T, Jabaudon M, Bazin JE, Futier E.  Recruitment maneuvers in acute respiratory distress syndrome. Ann Transl Med. 2017;5(14):290–5. 12. Famous KR, Delucchi K, Ware LB, et al. Acute respiratory distress syndrome subphenotypes respond differently to randomized fluid management strategy. Am J Respir Crit Care Med. 2017;195:331–8. 13. Marra A, Ely EW, Pandharipande PP, Patel MB. The ABCDEF bundle in critical care. Crit Care Clin. 2017;33(2):225–43. 14. Abrams D, Brodie D. Extracorporeal membrane oxygenation for adult respiratory failure 2017 update. Chest. 2017;152(3):639–49. 15. Meade MO, Young D, Hanna S, et  al. Severity of hypoxemia and effect of high-frequency oscillatory ventilation in acute respiratory distress syndrome. Am J Respir Crit Care Med. 2017;196(6):727–33. 16. Gebistorf F, Karam O, Wetterslev J, Afshari A.  Inhaled nitric oxide for ARDS in children and adults. Cochrane Database Syst Rev. 2016;(6). Art. No.:CD002787. 17. The National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. Efficacy and safety of corticosteroids for persistent acute respiratory distress syndrome. N Engl J Med. 2006;354(16):1671–84.

Management of Sepsis

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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 resuscitation and vasopressor requirement to maintain MAP >65  mmHg [1]. The first step in evaluation of a patient with sepsis is the history and physical. Questions regarding the onset of infection and concern for organ dysfunction are essential. Findings may include altered mental status, tachycardia, hypotension, 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, elevated CRP, hypotension, elevated mixed venous oxygen saturations, and elevated cardiac index [2]. B. Signs of organ dysfunction include acute hypoxemia, acute oliguria, increase in creatinine, 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: [email protected]

perfusion, elevated lactate, and decreased capillary refill or mottling [2]. C. Establish IV access and start fluid resuscitation. 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 resuscitation. Patients requiring surgical exploration or intervention for emergent source control should be identified with management as soon as medically possible after diagnosis [1]. D. Initial resuscitation for sepsis-induced hypoperfusion 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 passive leg raise or fluid challenge [3–5]. E. Vasopressors may be used for patients in septic shock with hypotension refractory to adequate 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 duration of 7–10 days, though longer courses may

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be appropriate with slow clinical response, bacteremia, undrainable source of infection, immunologic deficiencies, and certain bacterial, viral, and fungal infections [1, 6]. G. Supplemental oxygen or mechanical ventilation may be required for patients with sepsis. A large trial of pressure- and volume-limited strategy showed 9% absolute decrease in mortality 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 blockade should be avoided in patients without ARDS [1]. I. Continue supportive intensive care unit therapies including glucose control and deep vein thrombosis prophylaxis. Blood product administration is appropriate in symptomatic patients with hemoglobin 38.3°C or < 36.0°C, HR >100, RR > 20, WBC > 12,000 or < 4,000 or > 10% bands, hypotension altered mental status, edema or positive fluid balance, hyperglycemia in absence of diabetes, infection

B

Findings: signs of organ dysfunction (sepsis), SBP 65 mmHg, lactate > 2 mmol/L (septic shock)

C

Trend vital signs, frequent physical exams, cardiac and hemodynamic monitoring, pulse oximetry, obtain labs including cultures, ScVO2, and lactate, obtain arterial and venous access and give fluid bolus

D

Initial resuscitation & fluid therapy Administer 30 mL/kg crystalloid for hypotension or lactate within the first 4–6 hours. Reassess volume status and tissue perfusion

E

Vasoactive medications Use vasopressors for hypotension that does not respond to IV fluid resuscitation to maintain a mean arterial pressure (MAP) ≥65 mmHg

F

Antimicrobial therapy & source control Start broad-spectrum IV antibiotics as soon as possible within 1 hr of identifying sepsis. Deescalate when culture data is available. Pursue source control or surgical intervention as soon as possible

G

Supplemental O2 or mechanical ventilation Ventilate with pressure and volume limited ventilation such as 6 mL/kg tidal volumes in the setting of ARDS/ALI and plateau pressure ≤ 30 cm H2O in patient with sepsis-induced ARDS

H

Sedation & analgesia Appropriate sedation and analgesia must be maintained if neuromuscular blockade is used in sepsis, avoid NMBA in patients without ARDS due to risk of prolonged blockade

I

Supportive management Glucose control, DVT prophylaxis, blood product administration, goals of care, communication of prognosis

4 mmol/L

Algorithm 174.1

References 1. Rhodes A, et al. Surviving sepsis campaign: international 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.

4. Yealy DM, Kellum JA, Huang DT, et al. A randomized 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 traditional 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

175

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Algorithmic Approach A. Shock can be described as a failure of the circulatory system to adequately deliver blood, oxygen, and nutrients to vital organs, preferentially 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 established first. This includes securing an airway through intubation if necessary, establishing IV access, and administering an initial intravenous fluid bolus while considering the etiology 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 resuscitation, whereas those with hemorrhagic shock, sepsis, or infarction of the right ventricle often require larger volumes for fluid resuscitation. Patients with massive hemorrhage will require blood products. Patient with shock may require vasopressors and inotropes in addition to resuscitation, and hemodynamic monitoring should be established J. Engelbart · L. J. Garcia (*) Department of Surgery, University of Iowa Hospitals and Clinics, Iowa City, IA, USA e-mail: [email protected]

with central venous access, pulmonary artery catheters, and arterial lines. Occasionally echocardiograms are necessary for visualization. Necessary laboratory studies and imaging may include basic metabolic panel (BMP), complete blood count (CBC), coagulation 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

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should be administered epinephrine. Sepsis presents with hypotension, confusion, hyperventilation, 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 urinary output, lactate clearance, and venous saturations. D. Hypovolemic shock occurs as a result of large fluid losses such as with trauma, burns, hemorrhage, vomiting, or diarrhea. In hemodynamically unstable trauma patients, they are considered to be bleeding unless proven otherwise. A focused assessment with sonography 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 resuscitation, direct pressor, and emergent surgical control of bleeding. E. Obstructive shock often presents in the setting of cardiac tamponade, pulmonary embolism, 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 congestive heart failure. Treatment includes coronary revascularization, intra-aortic balloon pump, surgical valve repair, or following advanced cardiac life support (ACLS) protocols in the case of unstable arrhythmias.

175  Management of Shock

729

A

Focused clinical history and examination of patient with shock

B

Initial stabilization, secure the airway if necessary, establish 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

Hypovolemic shock

Hemorrhagic shock – Volume resuscitation, 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

Suggested Reading Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2016. Crit Care Med. 2017;45:486–552.

Van Diepen S, Katz JN, Albert NM, et al. Contemporary 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

176

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 hemoglobin 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 operation, cancer patients requiring therapy, massive blood loss or anemia in the setting of pregnancy and childbirth, hereditary disorders like hemophilia and thalassemia, critical illness, and severe burn victims. B. In the setting of acute hemorrhage with hypovolemia, 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: [email protected]

include orthostatic hypotension or tachycardia not responsive to fluid replacement, myocardial 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 erythropoiesis (malignancies, chemotherapy, other drugs suppressing bone marrow, renal disorders, nutritional deficiencies). No definite triggers have been defined so the decision to transfuse is considered on an individual basis guided by symptoms or functional impairment [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  20 mmHg with or without an abdominal perfusion pressure (APP = MAP – IAP)  10 mmHg) and is associated with new or progressing organ dysfunction and failure that can be attributed to elevated IAP

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[2, 5, 6]. ACS is better defined without E. Abdominal decompression with delayed s­pecified pressure thresholds as no specific c­ losure may be attempted with IAP >20 mmHg IAP threshold can consistently be used to and organ dysfunction not responding to medidiagnose ACS [5]. cal treatment. There is a risk of hypotension D. Supportive management and temporizing leading to pulseless electrical activity (PEA) measures for ACS include drainage of intraarrest from reperfusion and sudden decrease in luminal contents with nasogastric and rectal systemic vascular resistance. Even with temdecompression; removal of intra-abdominal porary closure there remains risk of recurrent ascites or hematomas; reduction of intra-­ abdominal compartment syndrome [1, 2, 8]. abdominal volume by avoiding positive fluid F. Temporary abdominal closure techniques balance after initial resuscitation and diureinclude negative pressure systems including sis; improving abdominal wall compliance towel- and sponge-based techniques (vacuum-­ with analgesia, sedation, and paralysis; assisted closure), patch closure, silo closure, or decreasing head elevation; escharotomy in skin-only closure. If primary approximation is burn victims; and removal of constrictive not able to be achieved upon return to the operbinders or dressings. Vasopressors may be ating room, other adjunctive techniques may used to maintain an abdominal perfusion be used to facilitate primary closure or approxpressure  >  60  mmHg. IAP should be meaimate the fascia closer to midline. If no sured at least every 4 h while patient is critiimprovement, functional closure or a planned cally ill or with elevated IAP [1, 2, 7]. ventral hernia may need to be attempted.

177  Abdominal Compartment Syndrome

A

B

C

D

737

Patient has two or more risk factors or in the presence of organ failure with clinical suspicion for ACS

Assess intraabdominal pressure by measuring the bladder pressure

IAP > 20 mmHg

IAP < 20 mmHg

Supportive management (sedation, analgesia, paralysis, paracentesis, nasogastric decompression)

No

Yes

No response

Surgical management (abdominal decompression)

E Close monitoring

Recurrence Temporary abdominal closure

F Improvement

Advance fascial edges towards midline No improvement Functional closure Planned ventral hernia

Algorithm 177.1

Organ dysfunction

Return to OR

No

Abdominal closure Yes

Primary fascial closure

738

References 1. Rogers WK, Garcia L.  Intra-abdominal hypertension, abdominal compartment syndrome, and the open abdomen. Chest. Forthcoming 2017. https://doi. org/10.1016/j.chest.2017.07.023. 2. Kirkpatrick AW, et  al. Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med. 2013;39:1190–206. 3. Vidal MG, et  al. Incidence and clinical effects of intra-abdominal hypertension in critically ill patients. Crit Care Med. 2008;36:1823–31.

J. Engelbart and L. J. Garcia 4. Van Mook WN, et  al. Abdominal compartment ­syndrome. Lancet. 2002;360:1502. 5. Malbrain ML, et  al. Results from the international conference of experts on intra-abdominal hypertension and abdominal compartment syndrome. I. Definitions. Intensive Care Med. 2006;32:1722–32. 6. Sugrue M. Abdominal compartment syndrome. Curr Opin Crit Care. 2005;11:333–8. 7. Bailey J, et  al. Abdominal compartment syndrome. Crit Care. 2000;4:23–9. 8. Chang MC, et  al. Effects of abdominal decompression on cardiopulmonary function and visceral perfusion in patients with intra-abdominal hypertension. J Trauma. 1998;44:440–5.

Acute Renal Failure

178

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: [email protected] R. J. King (*) Department of Surgery, SUNY Upstate Medical University, Syracuse, NY, USA e-mail: [email protected]

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 differentiate etiology, a clinician should first rule out common post-renal causes with renal ultrasound. Urinalysis in addition to urine electrolytes 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 vascular compromise and decreased renal perfusion 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

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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  300 μmol/L), and (7) uremic complications (encephalopathy, pericarditis, 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 Life-threatening fluid or electrolyte abnormalities?

T 37.6 C, HR 103, RR 19, BP 110/82 Labs: elevated crt, electrolytes

Yes AKI etiology?

B

Compartment syndrome

Urgent dialysis

Renal ultrasound Check Foley catheter

Post-renal

Obtain UA & urine electrolytes

Renal

Patient reassessment

Nephrology consult

C Pre-renal

Yes

D Responsive to fluid challenge?

No

Mixed etiology: pre-renal & renal

F

Renal replacement therapy

E Fluid resuscitation

Consider adjunct measures to assess volume status

Stable? Yes

Hemodialysis

Algorithm 178.1

No

CVVH

742

References 1. Koza Y.  Acute kidney injury: Current concepts and new insights. J Inj Violence Res. 2016;8(1):58–62. 2. Kellum JA, Lameire N.  Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Crit Care. 2013;17(1):204–19.

K. A. Iles and R. J. King 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 X, Arulkumaran N, et  al. What is the impact of the fluid challenge technique on diagnosis of fluid responsiveness? A systematic review and meta-analysis. Crit Care. 2017;21(1):207.

Postoperative Pulmonary Emboli

179

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 factors in addition to recent behavioral changes and health risks should guide work-up and evaluation. Presenting symptoms for pulmonary 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 secondary 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: [email protected] R. J. King (*) Department of Surgery, SUNY Upstate Medical University, Syracuse, NY, USA e-mail: [email protected]

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 thrombectomy. Stable patients can undergo further diagnostic evaluation based on clinical suspicion and availability of resources. C. The Wells prediction scoring system is commonly employed to categorize patient risk for thrombus formation. This scoring stratification is often used to predict need for chemoprophylaxis but can also guide clinical suspicion when pulmonary embolus is suspected. Patients with moderate to high probability 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 superior sensitivity [2]. D. Angiography is definitive imaging, although now CT angiography has high sensitivity and

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specificity for PE, especially in hemodynamically significant PE.  Common radiologic findings include filling defects in pulmonary vasculature on CTA +/− evidence of pulmonary infarction. V/Q scanning will often show mismatched segment perfusion defects. E. Treatment for pulmonary embolism is dependent on anticoagulation contraindications and patient stability. Treatment consists of therapeutic anticoagulation to prevent clot propagation. 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 system (CNS) interventions may need temporary IVC filter placement. Routine placement of IVC filters in submassive PE and proximal deep vein thrombosis (DVT) is not supported by evidence;

K. A. Iles and R. J. King

however, retrievable IVC filter insertion should be ­performed if anticoagulation is contraindicated or temporary cessation of anticoagulant is required in 1 month [3]. IVC filters should be removed within the recommended time scale in order to limit associated complications of IVC filter placement and retrieval. The incidence of confirmed hospitalacquired 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 thromboprophylaxis, intermittent pneumatic compression 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   6.5), urine Na, K, and there is depletion of hydrochloric acid (HCl) HCO3 are elevated, with depressed Cl. As the and extracellular fluid, producing a hypochlokidneys attempt to correct the strong iron difremic hypokalemic metabolic alkalosis with ference, urine becomes paradoxically acidic an increased strong ion difference. Persistent (pH  3.5 mmol/L. B. Confirm metabolic alkalosis with arterial blood gas and calculate plasma strong ion dif- E. If indicated, reduce gastric HCl secretion with H2 blockers or proton pump inhibitors. Limit alkalotic solutions as much as possible R. S. Schoaps · S. W. Hazard III (*) (e.g., solutions containing HCO3, citrate, and Department of Anesthesiology and Perioperative Medicine, Penn State Hershey Medical Center, lactate). Hershey, PA, USA e-mail: [email protected]

© 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_188

779

R. S. Schoaps and S. W. Hazard III

780

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.

A

History & physical exam Vomiting? Gastric outlet obstruction? Fistula?

B

Arterial blood gas, serum electrolytes Calculate strong ion difference

C

Urine pH & electrolytes pH < 5.5, UNa < 10, UK < 20, UCl < 10, UHCO3 < 15

D

Volume Expansion with NSS (losses + 100mL/h) KCl replacement to K > 3.5

E

Reduce gastric HCl secretion (H2-blocker, PPI) Limit administration of alkalotic solutions

F

Goal of intravascular euvolemia Trend labs to normal plasma values and follow urine pH

G

Treat underlying etiology

Algorithm 188.1

References 1. Seifter JL.  Integration of acid-base and electrolyte disorders. N Engl J Med. 2014;371(19):1821–31.

2. Luke RG, Galla JH. It is chloride depletion a­ lkalosis, not contraction alkalosis. J Am Soc Nephrol. 2012;23(2):204–7.

Part XXII Hernia

189

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, defecation, or lifting), exercise, or prolonged periods of standing. The patient may or may not complain of symptoms of pain or discomfort. 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 sensitivity and specificity of 74.5% and 96.3%, respectively [1]. The groin area should be observed for evidence of bulging or asymmetry with coughing. Then, the tip of the examiner’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: [email protected]

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 ultrasound reach upwards of 97.6% and 99.8%, respectively, it is highly operator dependent [2]. When there is clinical uncertainty, computed tomography (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 diagnoses for groin bulge or discomfort should be pursued. D. Once the diagnosis of inguinal hernia is established, either by physical exam, imaging, 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 hernia. 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

© 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

783

784

work such as white blood cell count and lactate 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 strangulated, 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 (laparoscopic 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 laparoscopic 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 laparoscopic or open pre-peritoneal repair given the higher risk of concurrent femoral hernia. K. The open anterior tension-free mesh technique (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 spermatic 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 circumstances where there is a contraindication for mesh placement (strangulated hernia with bowel ischemia and perforation or contaminated field or patient refusal). Options for tissue 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 running sutures. In specialized centers, its efficacy is similar to mesh-based repairs. M. The open posterior approach uses a transverse skin incision above the traditional anterior incision. The preperitoneal space may be entered using either a transinguinal preperitoneal (TIPP) or trans-rectus sheath extraperitoneal (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) technique, 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 peritoneum. 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 entering 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 dropping 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 anastomosis through the inguinal incisions but there should be a low threshold for converting to a midline incision. An open preperitoneal (posterior) approach may also be used. The advantage of this incision is ability to convert to laparotomy without creating a separate incision. Finally, if surgical expertise is available, a laparoscopic or hybrid laparoscopic approach may be used to address the bowel. Due to concern for infection, mesh is not recommended in the repair of strangulated 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.

Q. L. Hu and D. C. Chen

786

A

Groin bulge Pain/vague discomfort

B

Perform a physical examination

No

Palpable bulge or defect? Yes

D E

Asymptomatic inguinal hernia

No

Yes

Symptomatic?

Inguinal hernia on imaging?

Yes Watchful waiting

C

Imaging

No No inguinal hernia. Consider other differential diagnoses.

Symptomatic inguinal hernia

F Reducible?

G

H

Reducible

Elective/urgent repair

Incarcerated

Yes

Manually reducible?

Laparoscopic/robotic approach

TEP

O

TAPP

K Algorithm 189.1

No

Emergent repair

I

P

Operative approach depends on surgeon expertise and surgeon/patient preference

J

N

Strangulated

Open approach

Anterior approach

Mesh-based repair

Posterior approach

Tissue-based repair

L

M

189  Inguinal Hernia

References 1. van den Berg JC, de Valois JC, Go PM, Rosenbusch G. Detection of groin hernia with physical examination, ultrasound, and MRI compared with laparoscopic findings. Investig Radiol. 1999;34(12):739–43. 2. Niebuhr H, Konig A, Pawlak M, Sailer M, Kockerling F, Reinpold W.  Groin hernia diagnostics: dynamic inguinal ultrasound (DIUS). Langenbeck’s Arch Surg. 2017;402(7):1039–45.

787 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 A. Prospective evaluation of 6895 groin hernia repairs in women. Br J Surg. 2005;92(12):1553–8. 5. McCormack K, Scott NW, Go PM, Ross S, Grant AM. Laparoscopic techniques versus open techniques for inguinal hernia repair. Cochrane Database Syst Rev. 2003;(1):CD001785.

Recurrent Inguinal Hernia

190

Q. Lina Hu and David C. Chen

Algorithmic Approach A. Inguinal hernia recurrence rates are reportedly 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 inguinal hernia is a thorough history. The patient may present with a groin bulge at the site of a prior hernia repair. More commonly, the presenting symptom of a recurrent inguinal hernia 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 genetics (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: [email protected]

However, in the recurrent inguinal hernia, physical exam may not always be diagnostic. C. When the physical exam findings are equivocal, 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 tomography (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 diagnoses should be pursued. It is especially important to differentiate chronic groin pain from recurrence. D. Once the diagnosis of recurrent inguinal hernia 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 recurrence rates and the risk of strangulation is low, watchful waiting is a reasonable treatment approach in the asymptomatic or minimally symptomatic patient [2]. F. For symptomatic inguinal hernias, the next step is to establish the reducibility of the hernia. If the mass is incarcerated, it is important

© 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

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 strangulated, manual reduction may be attempted. If the hernia cannot be reduced manually or there is evidence of strangulation, then emergent repair is indicated. The approach to emergent repair is similar to that of the emergent 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 operative 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 recommended. For open posterior repairs, either transinguinal preperitoneal (TIPP) or trans-­ rectus sheath extra-peritoneal (TREPP) technique 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 hernia on the contralateral side, a Stoppa repair through a lower midline or Pfannenstiel incision is advisable to address both sides simultaneously. 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 transabdominal preperitoneal (TAPP) technique may be used [4]. In TEP, a specialized balloon is passed along the posterior rectus sheath and is used to dissect the preperitoneal space. The hernia 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. 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 surgeon expertise, either an open posterior (TIPP, TREPP, or Stoppa repair) or laparoscopic 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 advisable for the redo operation. M. If surgical expertise is available, it is reasonable to attempt the redo operation laparoscopically through a transabdominal preperitoneal (TAPP) approach. The potential advantage of this technique is the ability 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

A

Groin bulge/pain/discomfort at site of prior inguinal hernia repair

B

Perform a physical examination

No

Palpable bulge or defect?

Asymptomatic recurrent inguinal hernia

No

Yes

Yes

D

C

Imaging

Inguinal hernia on imaging?

Symptomatic?

No

Yes Symptomatic recurrent inguinal hernia

No inguinal hernia. Consider other differential diagnoses.

F E

Watchful waiting

Reducible? Signs of strangulation?

Incarcerated/strangulated

Reducible

Elective repair

Manual reduction Emergent repair

G

H

Prior repair technique?

Prior tissue repair

I

Prior mesh-based repair

Open anterior or posterior approach Laparoscopic approach

K

J

Prior anterior approach

Prior posterior/laparoscopic approach

Open posterior or laparoscopic approach

Open anterior approach

L

TAPP

M

Algorithm 190.1

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.

3. Pisanu A, Podda M, Saba A, Porceddu G, Uccheddu A. Meta-analysis and review of prospective randomized 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.

191

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 discomfort. Femoral hernias are relatively uncommon and account for 3–4% of all hernias [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 hernias. 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 protrude through the femoral canal and then slide up over the inguinal ligament, making it difficult 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: [email protected]

C. Imaging can be especially helpful in identifying 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 resonance 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 diagnoses should be pursued. D. Femoral hernias are often diagnosed intraoperatively when patients are taken to the operating room for a small bowel obstruction or concurrent inguinal hernia. If found intraoperatively, it is advisable to repair the hernia concurrently. E. All femoral hernias should be repaired due to the high risk of incarceration and strangulation [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.

© 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

793

794

Q. L. Hu and D. C. Chen

G. Either a totally extraperitoneal (TEP) or triangular extension is included to ensure transabdominal preperitoneal (TAPP) techproper coverage of the femoral canal and nique may be used for the repair of a femoral secured to the inguinal ligament, ilioinguinal hernia. In TEP, a specialized balloon is passed tract, lacunar ligament, and Cooper’s along the posterior rectus sheath and is used ligament. to dissect the preperitoneal space. The hernia K . In an open posterior preperitoneal approach, sac is reduced and a prosthetic mesh is used a transinguinal preperitoneal (TIPP) or tranto cover the entire myopectineal orifice. The srectus preperitoneal repair (TREPP) may be TAPP technique is performed in the same used to place a mesh prosthetic into the premanner except that the peritoneal cavity is peritoneal space to cover the entire myopecfirst entered and then the peritoneum is tineal orifice including the femoral canal. For incised to enter the preperitoneal space. This large, complicated, or bilateral defects, a approach is advantageous as it allows for Stoppa repair or giant prosthetic reinforcevisual inspection of the bowel to assess for ment of visceral sac (GPRVS) may be perviability. As in the open approach, if there is formed though a lower midline or Pfannenstiel suspicion for bowel compromise, the peritoincision. A large synthetic mesh is placed in neal cavity should be entered (if using TEP the preperitoneal space to the cover the entire technique) to assess bowel viability and permyopectineal orifices bilaterally, including form bowel resection if necessary. both the femoral and inguinal areas. If there is H. If the bowel is necrotic and surgical expertise concern for bowel compromise on visual is available, the bowel resection may be perinspection, the peritoneal cavity may be formed laparoscopically. Due to concern for entered for bowel resection. infection, a synthetic mesh is not advisable in L. If bowel compromise is suspected, then an the setting of strangulation, perforation, gross open anterior or abdominal approach is contamination, or bowel resection. In this advised. In the setting of strangulation, perscenario, a tissue repair or delayed mesh-­ foration, gross contamination, or bowel based repair at a later date is advised. resection, a McVay (Cooper’s ligament) I. There are many options for open femoral herrepair is preferred as it obliterates the femonia repairs. If the diagnosis is made preoperaral space without the need for mesh. In this tively and strangulation is not suspected, the technique, a relaxing incision is made to repair may be performed from either an anterelieve tension in the suture line. Then, the rior or posterior approach. transversus abdominis aponeurosis is J. From the anterior approach, a femoral modiapproximated to Cooper’s ligament medial fied Lichtenstein technique may be used. This to the femoral canal and iliopubic tract lattechnique follows the traditional Lichtenstein eral to the canal with interrupted nonabsorbtechnique, except that an additional lateral able sutures.

191  Femoral Hernia

795

A

Groin bulge Pain/vague discomfort

B

Perform a physical examination

C Palpable bulge below inguinal ligament?

No

Imaging

Yes

D

Intraoperative diagnosis

Yes

Femoral hernia

E

Femoral hernia on imaging?

Operative repair

No

No femoral hernia. Consider other Operative approach depends on surgeon expertise and differential diagnoses. surgeon/patient preference

F

Laparoscopic approach

Open approach

Bowel viable?

Viable bowel

G

TEP

Bowel viable?

Viable bowel

Necrotic bowel

TAPP

H

I

Laparoscopic bowel resection and delayed repair

Anterior approach

J

Femoral Modified Lichtenstein

K

Posterior approach

Necrotic bowel

Open anterior or abdominal approach

TIPP, TREPP, Stoppa repair

L

McVay repair

Algorithm 191.1

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

Hernias Abdominal Wall Surg. 2015;19(3):513–6. 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

192

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: [email protected]

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 hernia or if clinical suspicion is high, computed tomography (CT) is considered the gold standard 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 diagnosis, and, thus, whenever an obturator hernia is discovered, operative repair is strongly recommended [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 synthetic mesh is placed in the preperitoneal space to cover the obturator orifice as well as the rest of the myopectineal orifice, including

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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 posterior 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 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. It is important 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 obturator orifice. As in the open approach, if there is suspicion for bowel compromise, the peritoneal 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 transabdominal 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 hernia 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 peritoneum. 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 entering 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 hernia defect may be suture repaired in two layers [4]. Alternatively, a biologic mesh may be used or the defect may be reinforced with adjacent tissues such as periosteal flaps, bladder wall, uterine fundus, or ligaments [2]. If a laparoscopic approach was used, then a laparoscopic 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

A

Proximal thigh mass Groin/medial thigh pain Small bowel obstruction

B

Perform a physical examination

C

Imaging

Obturator hernia on imaging?

No

No obturator hernia. Consider other differential diagnoses.

Yes

D

Obturator hernia

Intraoperative diagnosis

E

Operative repair

Preoperative diagnosis? Strangulation?

F

G

Preoperative diagnosis AND Strangulation not suspected

Stoppa repair

Laparoscopic repair

K

H

Intraoperative diagnosis OR Strangulation suspected

I

Abdominal approach

J

Viable bowel

Open posterior Laparoscopic repair repair

Algorithm 192.1

Necrotic bowel

Open tissue repair

L

Laparoscopic repair

800

References 1. Stamatiou D, Skandalakis LJ, Zoras O, Mirilas P.  Obturator hernia revisited: surgical anatomy, embryology, diagnosis, and technique of repair. Am Surg. 2011;77(9):1147–57.

Q. L. Hu and D. C. Chen 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 E.  Obturator hernia: a case report and review of the literature. Int J Surg Case Rep. 2013;4(10):889–92. 4. Shipkov CD, Uchikov AP, Grigoriadis E. The obturator hernia: difficult to diagnose, easy to repair. Hernia J Hernias Abdominal Wall Surgery. 2004;8(2):155–7.

Ventral Hernia Repair

193

Justin A. Doble and Eric M. Pauli

Algorithmic Approach

D. Operative approach to defect closure is based upon surgeon expertise/preference but modiA. Initial evaluation for any ventral hernia fied based on patient risk factors that will perrequires complete medical history, physical mit (or preclude) a minimally invasive examination, and radiologic assessment approach, the presence (or absence) of old (ultrasound [US] or computed tomography mesh, and the potential need for a component [CT] scan). Modification of patient-specific separation [2]. risk factors (including smoking cessation, E. For patients with risk factors and 10–20 cm reduction in immunosuppression, improved defects, a minimally invasive operation glycemic control, and weight loss/obesity reduces wound complications at the expense surgery) has been shown to reduce complicaof fascial closure difficulties (e.g., component tions and recurrence. separation may be needed). An open opera B. Multiple hernia staging systems exist, includtion facilitates defect closure but at a greater ing the Ventral Hernia Working Group clasrisk of surgical site infections. We prefer a sification, European Hernia Society robotic repair with transversus abdominus classification, and Hernia, Patient, Wound release or an open retrorectus repair depend(HPW) staging system. Here, we utilize the ing on patient candidacy for a minimally HPW staging system as it provides a TNM-­ invasive herniorrhaphy [3, 4]. like (Tumor Node Metastasis) approach help- F. The presence of a contaminated wound ful for patient management and operative (ostomy, fistula, concomitant organ resection, decision-making [1]. or inadvertent enterotomy) is the predomi C. Fascial defect closure is preferred for most nant consideration for stage III hernia. Wound patients as it may provide a more durable contamination decreases the likelihood of a repair and reduce the risks of both short- and safely performed definitive repair in a single long-term complications. However, closure procedure. Thus, attempts to downstage herof the hernia defect in a geriatric population nia with a staged operative approach can be or patients with comorbid diseases may considered. exceed the risk-to-benefit ratio. G. In a contaminated field, options for temporary repair include suture repair (if possible passed on defect size) or bridge repair using a J. A. Doble · E. M. Pauli (*) Department of Surgery, Penn State Milton S. Hershey biologic or a bioabsorbable mesh. Although Medical Center, Hershey, PA, USA bridged repairs have a high recurrence rate, e-mail: [email protected]

© 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

801

J. A. Doble and E. M. Pauli

802

controlling wound contamination first permits definitive repair during a second operation. This controlled/planned failure approach permits downstaging of wound class. H. Mesh choice in the setting of potential bacterial 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 bioA

logic mesh in select contaminated circumstances; 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.

H&P; abdominal imaging (CT/US)

1. 2. 3. 4.

Yes

Risk reduction possible? No

B

Stage I

Smoking cessation Reduce immunosuppression Lower HbA1c Weight loss/obesity surgery

Stage hernia

Stage II

20 cm

Contamination or adhesions?

Fascia closable?

No

MIS repair

Yes

Yes

E

Medium weight mesh

Open retrorectus

F

No Bridged repair w/ heavy mesh

ICU evaluation and monitoring if needed

Medium defect 10–20 cm

TAR

H

I

EO

G MIS w/ sublay mesh

Open repair w/ sublay mesh

MIS or open EO ± retrorectus mesh: onlay, sublay, or ‘sandwich’

Algorithm 196.1

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 extraperitoneal (eTEP) technique for laparoscopic

retromuscular hernia repair. Surg Endosc. 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 reinforcement. 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

197

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 recommendations 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, hypertension, hyperlipidemia, obesity-hypoventilation syndrome, nonalcoholic fatty liver disease, pseudotumor cerebri, gastroesophageal reflux disease, asthma, venous stasis disease, stress urinary incontinence, debilitating arthritis,

impaired quality of life, and disqualification from other surgeries resulting from obesity (e.g., joint replacement, organ transplantation, and ventral hernia repair) [4]. D. Patients generally excluded from bariatric surgery include those with reversible disorders that cause obesity, active drug or alcohol abuse, poorly controlled psychiatric conditions, current pregnancy, history of active suicide 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 multidisciplinary adolescent weight loss surgery program with appropriate pediatric specialties 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].

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: [email protected] © 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

819

J. S. Kim and A. M. Rogers

820 Algorithm 197.1

Patient has obesity

Does the patient live in the US?

A No

Yes

B

See local guidelines Does the patient have a BMI > 35? No Yes Seek medical weight management BMI 35–39.9

Yes

No

Does the patient have significant weight-related problems?

BMI > 40

Any contraindications? Yes

D

No

E

Recommend bariatric surgery

C

References 1. Burguera B, Agusti A, Arner P, et al. Critical assessment 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 surgery 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.

4. Mechanick JI, Youdim A, Jones DB, et  al. Clinical practice guidelines for the perioperative nutritional, metabolic, and nonsurgical support of the bariatric 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 bariatric/metabolic surgery. Ann Gastroenterol Surg. 2017;1:171–9.

Work-Up of Abdominal Pain in the Bariatric Patient

198

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 quality, location, and timing of the pain and associated 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, complications may arise specific to the patient’s procedure 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 hernia) may also occur after any of these [1]. C. For any AGB patient with abdominal pain, nausea, or vomiting, the band should be completely deflated prior to pursuing a diagnostic work-up because of the risk of gastric ischemia 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: [email protected]

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 tomography (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 generally helpful in the examination of post-­ bariatric anatomy; use of intravenous contrast is optional, depending on suspected diagnoses 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 obstruction 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 bariatric surgery (e.g., gastroesophageal motility

© 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

821

S. S. McGuire and A. M. Rogers

822

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 disease), abdominal CT scan (intestinal obstruction), 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 · Establish operative date, procedure type, and postoperative course · Obtain vital signs and blood work. If febrile, work up for infection.

A

B

Early postoperative setting:

Consider complications specific to procedure: · RYGB: strictures, leaks, and ulcers · AGB: band malfunction/malposition · BPD/DS: leaks Rule-out missed bowel perforation.

Later postoperative setting (>30 days)

F Patients may present with intestinal obstruction after any procedure, marginal ulcers with or without associated strictures after RYGB, dumping syndrome after RYGB, gallstone disease, nutritional deficiencies, and gastrointestinal problems unrelated to bariatric surgery.

C For AGB patients, deflate the band prior to work-up. UGI swallow study is the test of choice.

E

D

Obtain abdominal and pelvic CTscan to exclude closed loop bowel obstruction, bowel perforation, or gastric prolapse when UGI is not available. Use of oral contrast is preferred.

G

Exploratory laparotomy or laparoscopy is indicated when internal hernia, perforated marginal ulcer, intussusception, adhesive bowel obstruction, or symptomatic gastric prolapse through a band are suspected.

Follow-up care

Algorithm 198.1

Depending on history, symptoms, and physical exam, work-up can include abdominal ultrasound and/or nuclear scan, abdominal CT scan, stool specimen, upper or lower endoscopy, or contrast studies.

198  Work-Up of Abdominal Pain in the Bariatric Patient

References 1. Lee CW, Kelly JJ, Wassef WY.  Complications of bariatric surgery. Curr Opin Gastroenterol. 2007; 23(6):636–43. 2. Mechanick JI, Youdim A, Jones DB, et  al. Clinical practice guidelines for the perioperative nutritional,

823 metabolic, and nonsurgical support of the bariatric surgery patient—2013 update: cosponsored by American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic & Bariatric Surgery. Surg Obes Relat Dis. 2013;9:159–91.

Internal Hernia: Diagnosis and Treatment

199

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 associated with strangulation [1]. Patients who have undergone gastric bypass or the duodenal switch procedure are at risk for internal hernia bowel obstructions because of new mesenteric 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 guarding. If the hernia is spontaneously reducible, symptoms may be vague and can include recurrent central abdominal pain and nausea.

B. Because of altered anatomy, internal hernia bowel obstructions in post-bariatric patients cannot be definitively diagnosed with plain abdominal radiographs [2]. Contrast computed 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 correction is unsuccessful or when such skills are unavailable [4].

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: [email protected] © 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

825

B. LaBarge and A. M. Rogers

826

Post-bariatric patient with acute or recurrent central abdominal pain, +/– nausea and vomiting

A

B

Internal hernia

CT scan with oral, +/– i.v. contrast

Normal/Nondiagnostic

Symptoms persist

C

Exploration

Other findings

Symptoms improve

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

References 1. Salar O, El-Sharkawy AM, Singh R, et  al. Internal hernias: a brief review. Hernia. 2013;17(3):373–7.

2. Martin L, Merkle E, Thompson W. Review of internal 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 management 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 of this algorithm. A. Marginal ulcer (MU), which occurs at or near B. If upper GI symptoms are present in post-­ the intestinal side of a gastrojejunal anastoRYGB patients, an upper endoscopy should mosis, is a common complication of Roux-­ be the first diagnostic step [3]. Endoscopic en-­Y gastric bypass (RYGB) surgery, seen in findings may include normal anatomy, MU up to 16% of patients. Most MUs are seen alone, MU with associated anastomotic stricwithin 1  year after RYGB [1]. Early MU is ture, MU with exposed staples or sutures, or likely due to technical issues such as anastoMU with gastro-gastric fistula [4]. If MU is motic tension, ischemia, or type of staples or present with or without associated findings, sutures used but may be related to patient facbiopsy for Helicobacter pylori (H. pylori) tors such as diabetes or hypertension. Later testing should be performed [5]. presentations of MUs may be associated with C. Management of uncomplicated MUs includes smoking, alcohol use, steroid or nonsteroidal 3 months of proton pump inhibitor (PPI) +/− anti-inflammatory drug (NSAID) use, or sucralfate. Cessation of smoking and steroid larger pouch size [2]. Patients with MUs or chronic NSAID use should be implecommonly present with upper gastrointestimented if applicable [2]. If H. pylori testing is nal (GI) symptoms including abdominal pain, positive, the patient should be treated with nausea, vomiting, dysphagia, and hematemeappropriate antibiotic therapy in addition [5]. sis. Fever may also be present [3]. History If anastomotic stricture is identified, then and physical exam are the first steps in the endoscopic balloon or Bougie dilation of the diagnosis of MU. It is important to note that stricture should be performed [5]. If exposed 28–61% of patients report no prior symptoms staples or sutures are identified, they should and may present with massive bleeding or be removed and associated ulceration should perforation of the MU [2]. Emergent treatbe treated as above [3]. If gastro-gastric fistula is identified in addition to MU, then elective interventions to close the fistula are Y. Tian appropriate. Penn State Health Milton S. Hershey Medical Center, Hershey, PA, USA D. If MU symptoms persist or worsen after 3  months of treatment, or in the setting of A. M. Rogers (*) Department of Surgery, Penn State Milton S. Hershey bleeding or perforation, then surgical interMedical Center, Hershey, PA, USA vention may be necessary. e-mail: [email protected]

© 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_200

827

Y. Tian and A. M. Rogers

828

History and Physical Exam: Epigastric abdominal pain, nausea, vomiting, dysphagia, hematemesis +/-fever after RYGB surgery

A

Further work-up

Normal postRYGB anatomy

B

Obtain upper endoscopy

What does the upper endoscopy show?

MU with Stricture

Gastro-gastric fistula with marginal ulcer Marginal ulcer

C

Treat MU and consider closure of fistula

Cessation of smoking and NSAID use if applicable

Endoscopic balloon dilation; initiate 3 mo therapy with PPI, +/- sucralfate

Check H. pylori biopsy result

H. pylori positive?

No Initiate 3 months of medical therapy with PPI +/Sucralfate

Are symptoms persisting or worsening?

Algorithm 200.1

Yes

Initiate 3 mo medical therapy with PPI, +/Sucralfate, and eradicate H pylori

200  Marginal Ulcer: Diagnosis and Treatment

829 Yes

D

No

Repeat endoscopy

MU present?

Continue medical therapy for another 3 months and discontinue if asymptomatic No

Yes Consider surgical intervention to resect and reconstruct GJ anastomosis

Follow-up Care

Algorithm 200.1 (continued)

References 1. Steinemann DC, Bueter M, Schiesser M, et  al. Management of anastomotic ulcers after roux-en-Y gastric bypass: results of an international surgery. Obes Surg. 2014;24:741–6. 2. Coblijn UK, Lagarde SM, de Castro SMM.  Symptomatic marginal ulcer disease after roux-en-Y gastric bypass: incidence, risk factors and management. Obes Surg. 2015;25:805–11.

3. Racu C, Mehran A. Marginal ulcers after roux-en-Y gastric bypass: pain for the patient…pain for the surgeon. Bariatric Times. 2010;7(1):23–5. 4. Nguyen NT, Hinojosa MW, Gray J, Fayad C. Reoperation for marginal ulceration. Surg Endosc. 2007;21:1919–21. 5. Chaves LCL, Borges IKLC, de Souza MDG, et  al. Inflammatory disorders associated with helicobacter pylori in the roux-en-Y gastric pouch. Arq Bras Cir Dig. 2016;29(Suppl 1):31–4.

Ventral Hernia Repair in Bariatric Patients

201

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: [email protected]

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 infection and recurrence [1, 2]. As a result, it is important to determine whether hernia repair can be delayed, what the safest and most effective surgical approach would be, and whether the patient qualifies for weight loss surgery. C. If a ventral hernia is known prior to bariatric surgery, the surgeon has three options: (1) perform planned bariatric surgery and defer hernia repair to a later time; (2) perform 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 performing bariatric surgery prior to ventral hernia repair. In setting of open ventral hernia in the obese patient, the incidence of complications (surgical site infection (SSI), recurrence, cardiovascular, pulmonary) has been directly correlated to the rise in BMI [1, 3]. An evaluation of BMI and ventral hernia demonstrated that patients with a BMI  >  40  kg/ m2 had a 2.89 times greater chance of h­ aving

© 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

A. Shah and S. Docimo Jr.

a ­ complication compared to a group with BMI  40 kg/m2

Weight loss prior to ventral hernia repair: surgical or medicinal

Ventral hernia repair after adequate weight loss

BMI < 40 kg/m2

Concomitant hernia and bariatric surgery

Concomitant hernia and bariatric surgery: fascial closure with mesh

C

D

E

201  Ventral Hernia Repair in Bariatric Patients

References 1. Veljkovic R, Protic M, Gluhovic A, et al. Prospective clinical trial of factors predicting the early development of incisional hernia after midline laparotomy. J Am Coll Surg. 2010;210:210–9. 2. Fischer JP, Basta MN, Mirzabeigi MN, et al. A risk model and cost analysis of incisional hernia after

elective abdominal surgery based on 12,373 cases. The case for targeted prophylactic intervention. Ann Surg. 2016;263:1010–7. 3. Flancbaum L, Choban PS.  Surgical implications of obesity. Annu Rev Med. 1998;49:215–34. 4. Pernar LIM, Pernar CH, Dieffenbach BV, Brooks DC, Smink DS, Tavakkoli A. What is the BMI threshold for open ventral hernia repair? Surg Endosc. 2017;31(3):1311–7.

Acute Leak Following Bariatric Surgery: Endoscopic Stent Management

202

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, ­ tachypnea, and possibly hypotension. A leukocytosis 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 therapeutic 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 gastrectomy 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 ischemia 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: [email protected]

sis within the gastric sleeve causing an increase of proximal intraluminal pressure [7]. The optimal diagnostic modality is a contrast computed 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 treatment paradigm to follow. If a patient demonstrates septic shock or peritonitis, intraoperative management with surgical exploration should be the first line of treatment. If the patient is stable, leaks in the proximal or midportion 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 resolution 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

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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 anastomosis 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 underwent stent placement for gastrojejunal leaks notes complete closure in 30 cases on contrast studies [14].

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].

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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 · Resuscitation and operative intervention

Patient Stable?

B

C

Yes

· Demonstration of a Leak within the sleeve or gastro-jejunal anastomosis

· CT Scan with PO/IV Contrast · Localize Leak if possible · Evaluate for an abscess

Yes

· CT guided drainage

· Abscess? No

· Endoscopic placement of a selfexpanding covered metal stent

· UGI to evaluate for leak occlusion

· Continued Leak · Leak is occluded

E · Endoscopic re-positioning or placement of a second stent

· Difficult removal due to mucosal hyperplasia during initial removal

· Any change in clinical status warrants evaluation of stent position with an UGI or X-ray

· Remove in 2 weeks.

· Argon plasma coagulation of hyperplastic mucosa and immediate removal of stent · Stent-in-stent with removalin 2 weeks of both stents

Algorithm 202.1

D

838

References 1. Whitlock KA, Gill RS, Ali T, et al. Early outcomes of roux-en-Y gastric bypass in a publically funded obesity program. ISRN Obes. 2013;2013:296597. 2. van Rutte PW, Smulders JF, de Zoete JP, et  al. Outcome of sleeve gastrectomy as a primary bariatric procedure. Br J Surg. 2014;101(6):661–8. 3. Weiner RA, El-Sayes IA, Theodoridou S, et  al. Early post operative complications: incidence, management, and impact on length of hospital stay. A retrospective comparison between laparoscopic gastric bypass and sleeve gastrectomy. Obes Surg. 2013;23(12):2004–12. 4. Andrade JE, Martinez JM. Management of postsurgical leaks and fistulae. In: Thompson C, Ryan MB, editors. Bariatric endoscopy. New York: Springer; 2013. p. 91–101. 5. Aurora AR, Khaitan L, Saber AA. Sleeve gastrectomy and the risk of leak: a systematic analysis of 4,888 patients. Surg Endosc. 2012;26(6):1509–15. 6. Sakran N, Goitein D, Raziel A, Keidar A, Beglaibter N, Grinbaum R, et  al. Gastric leaks after sleeve gastrectomy: a multicenter experience with 2,834 patients. Surg Endosc. 2013;27(1):240–5. 7. Kim J, Azagury D, Eisenberg D, DeMaria E, Campos GM. ASMBS position statement on prevention, detection, and treatment of gastrointestinal leak after gastric bypass and sleeve gastrectomy, including the roles of imaging, surgical exploration, and nonoperative management. Surg Obes Relat Dis. 2015;11(4):739–48. 8. Prathanvanich P, Chand B.  Laparoscopic sleeve gastrectomy: management of complications. In: Brethauer SA, Schauer PR, Schirmer BD, editors. Minimally invasive bariatric surgery. 2nd ed. New York: Springer; 2015. p. 151–71. 9. de Aretxabala X, Leon J, Wiedmaier G, Turu I, Ovalle C, Maluenda F, Gonzalez C, Humphrey J, Hurtado M, Benavides C.  Gastric leak after sleeve gastrectomy: analysis of its management. Obes Surg. 2011;21:1232–7.

S. Docimo Jr. 10. Martin-Malagon A, Rodriguez-Ballester L, Arteaga-­ Gonzalez I.  Total gastrectomy for failed treatment with endotherapy of chronic gastrocutaneous fistula after sleeve gastrectomy. Surg Obes Relat Dis. 2011;7:240–2. 11. El Mourad H, Himpens J, Verhofstadt J. Stent treatment for fistula after obesity surgery: results in 47 consecutive patients. Surg Endosc. 2013;27:808–16. 12. Lo Menzo E, Szomstein S, Rosenthal RJ. Laparoscopic gastric bypass: management of complications. In: Brethauer SA, Schauer PR, Schirmer BD, editors. Minimally invasive bariatric surgery. 2nd ed. New York: Springer; 2015. p. 261–9. 13. Bingham J, Shawhan R, Parker R, Wigboldy J, Sohn V. Computed tomography scan versus upper gastrointestinal fluoroscopy for diagnosis of staple line leak following bariatric surgery. Am J Surg. 2015;209(5):810–4. 14. Salinas A, Baptista A, Santiago E, Antor M, Salinas H. Self-expandable metal stents to treat gastric leaks. Surg Obes Relat Dis. 2006;2:570–2. 15. Puli SR, Spofford IS, Thompson CC.  Use of self-­ expandable stents in the treatment of bariatric surgery leaks: a systematic review and meta-analysis. Gastrointest Endosc. 2012;75(2):287–93. 16. Ross AS, Kozarek RA. Esophageal stents: indications and placement techniques. Self-expandable stents in GI tract. In: Kozarek R, Baron T, Song H, editors. Self-expandable stents in the gastrointestinal tract. New York: Springer; 2013. p. 129–40. 17. Eisendrath P, Cremer M, Himpens J, et al. Endotherapy including temporary stenting of fistulas of the upper gastrointestinal tract after laparoscopic bariatric surgery. Endoscopy. 2007;39:625–30. 18. Efthimiou E, Stein L, Szego P, et al. Stent migration causing alimentary limb obstruction necessitating laparotomy and surgical stent extraction. Surg Obes Relat Dis. 2009;5:375–7. 19. Aiolfi A, Bona D, Ceriani C, Porro M, Bonavina L.  Stent-in-stent, a safe and effective technique to remove fully embedded esophageal metal stents: case series and literature review. Endosc Int Open. 2015;3(4):E296–9.

Vitamin and Micronutrient Deficiencies After Bariatric Surgery

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Algorithmic Approach A preoperative assessment of micronutrients prior to bariatric surgery demonstrated deficiencies of zinc (24.6%), vitamin B12 (18.1%), magnesium (6.9%), phosphorous (4.7%), folic acid (3.4%), and vitamin D (25.4%) [1]. These minerals are cofactors vital to functions of appetite, metabolism, nutrient absorption, glucose homeostasis, 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 consideration 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 laboratory evaluation for micronutrient derangements. 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: [email protected]

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 encephalopathy 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, malabsorption, 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

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and induction of hepcidin, which blocks iron absorption proteins [9], making iron deficiency prevalent prior to surgery. Iron deficiency has been noted in 10% of sleeve gastrectomy patients [5]. Symptoms of deficiency include cravings for ice, pallor, lethargy, koilonychias, and anemia [8]. Total iron-binding capacity or serum transferrin receptors are better measures of iron deficiency 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 supplementation [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 calcium in the small intestines [11, 12]. Calcium deficiency can lead to low bone density, osteoporosis, 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 transfers. These enzymes include cytochrome c

S. Docimo Jr.

oxidase (electron transport chain), superoxide dismutase (antioxidant), amine oxidases (synthesis of neurotransmitter norepinephrine), and lysyl oxidase (involved in collagen crosslinking) [cousin RJ, allied health]. Severe deficiency of copper may present as unsteady gait, extremity numbness, parenthesis, 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.

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A patient undergoing bariatric surgery or presenting with acute symptomatology not explained by an anatomical abnormality

A · Any preoperative micronutrient and vitamin deficiencies should be replaced · A history and physical examination is utilized to narrow the possible micronutrient deficiency

B

· Visual disturbance, ataxia, peripheral neuropathy, memory loss, confusion

Thiamin deficiency

C

· Parathesias of limbs, macrocytic anemia

D

· Fatigue, headache, diarrhea, palpatations

E

· Pallor, lethargy, koilonychias, anemia, craving for ice

F

· Low bone density, osteoporosis, muscle contractions, spasms

Calcium & vitamin D deficiency

G

· Unsteady gait, extremity numbness, parathesiasis, paralysis

Copper deficiency

H

· Hair loss, poor wound healing, change in taste perception

Zinc deficiency

I

Algorithm 203.1

· Treat all acute deficiencies with replacement · Maintenancewith daily vitamin use

Vitamin B12 deficiency

Folic Acid deficiency

Draw blood samples

Iron deficiency

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References 1. Ernst B, Thurnheer M, Schmid SM, Schultes B. Evidence for the necessity to systematically assess micronutrient status prior to bariatric surgery. Obes Surg. 2009;19(1):66–73. 2. Allied Health Sciences Section Ad Hoc Nutrition Committee, Aills L, Blankenship J, Buffington C, Furtado M, Parrott J. ASMBS allied health nutritional guidelines for the surgical weight loss patient. Surg Obes Relat Dis. 2008;4(5 Suppl):S73–108. 3. Bloomberg RD, Fleishman A, Nalle JE, Herron DM, Kini S.  Nutritional deficiencies following bariatric surgery: what have we learned? Obes Surg. 2005;15(2):145–54. Review. 4. Schweiger C, Weiss R, Keidar A. Effect of different bariatric operations on food intolerance and quality of eating. Obes Surg. 2010;20:1393–9. 5. Himpens J, Dapri G, Cadière GB. A prospective, randomized study between laparoscopic gastric banding and laparoscopic isolated sleeve gastrectomy: results after 1 and 3 years. Obes Surg. 2006;16(11):1450–6. 6. Kaplan LM.  Pharmacological therapies for obesity. Gastroenterol Clin N Am. 2005;34:91–104. 7. Charney P, Malone A, editors. ADA pocket guide to nutrition assessment. Chicago: American Dietetic Association; 2004. 8. Malinowski SS.  Nutritional and metabolic complications of bariatric surgery. Am J Med Sci. 2006;331:219–25.

S. Docimo Jr. 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 Vitam Nutr Res. 2010;80:263–70. 10. Zimmermann MB, Hurrell RF. Nutritional iron deficiency. Lancet. 2007;370:511–24. Hoffman HNI, Phyliky RL, Fleming CR. Zinc-induced copper deficiency. Gastroenterology. 1988;94:508–12. 11. Wood RJ.  Calcium and phosphorus. In: Stipanuk MH, editor. Bio- chemical and physiological aspects of human nutrition. Philadelphia: Elsevier; 2000. p. 643–70. 12. Weaver CM, Fleet JC. Vitamin D requirements: current and future. Am J Clin Nutr. 2004;80:S1735–9. 13. Mechanick JI, Youdim A, Jones DB, Garvey WT, Hurley DL, McMahon MM, Heinberg LJ, Kushner R, Adams TD, Shikora S, et  al. Clinical practice guidelines for the perioperative nutritional, metabolic, and nonsurgical support of the bariatric surgery patient-2013 update: cosponsored by American Association of Clinical Endocrinologists, The Obesity Society, and American Society for Metabolic and Bariatric Surgery. Obesity (Silver Spring). 2013;21(Suppl 1):S1–27. 14. Cousins RJ, Blanchard RK, Moore JB, Cui L, Green CL, Liuzzi JP, Cao J, Bobo JA.  Regulation of zinc metabolism and genomic outcomes. J Nutr. 2003;133:S1521–6.

Part XXIV Pregnancy and General Surgery

Pregnancy and Cholelithiasis

204

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 gallstone formation due to the hormonal effects of estrogen and progesterone that increase cholesterol secretion and decrease soluble bile acid secretion. Additionally, progesterone also decreases smooth muscle contractility and slows gallbladder emptying. Up to 30% of pregnant women have biliary sludge, which develops into gallstones, on ultrasound. Risk factors for cholelithiasis include obesity, multiparity, and increasing gestational 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 postpartum year [2, 3]. B. Gallstones cause biliary colic, acute cholecystitis, gallstone pancreatitis, choledocholithiasis, 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: [email protected]

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 evaluation as appropriate for gestational age per obstetrics. C. Ultrasound has 95–98% accuracy in diagnosing cholelithiasis [2, 5]. Findings of cholecystitis are thickened gallbladder wall (>3–5 mm) or edema, presence of gallstones, pericholecystic fluid, and a sonographic Murphy’s sign [1, 5]. Other imaging that may be useful for the diagnosis and treatment of small or extrahepatic stones includes endoscopic retrograde cholangiopancreatography (ERCP), which has minimal radiation exposure (300 mrad) in an acceptable range for pregnancy after the first trimester [1]. Non-contrast

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magnetic resonance cholangiopancreatograspectrum antibiotics for patients with sysphy (MRCP) may also be considered in comtemic signs [1, 4–6]. plex cases. E. Lu et  al. demonstrated that if conservative D. Surgical intervention via laparoscopic or management is chosen for gallstone disease open cholecystectomy (see algorithm for in pregnancy, there is a 38% chance of sub“Cholecystectomy of the Pregnant Patient”) optimal outcome, with a 34% risk of relapse is clearly indicated for obstructive jaundice, and increased severity of disease at relapse acute cholecystitis failing medical manage[6]. Although there is a higher risk for prement (approximately one-fourth of patients term contractions with operative managewith cholecystitis), gallstone pancreatitis, ment, there is a higher rate of preterm or suspected peritonitis [3, 6]. The appropridelivery, induction of labor for symptoms, ate management of symptomatic cholelithiand cesarean delivery with non-operative asis and biliary colic is less clear, particularly management. Consideration for definitive since there is a hesitancy to operate on pregsurgical management of gallstone disease nant patients [2, 6]. Conservative manageduring pregnancy, especially in the first and ment includes intravenous hydration, bowel second trimesters, has further been supported rest, and pain management, with broad-­ by other authors [1].

204  Pregnancy and Cholelithiasis

847

A

History: Pregnant Right upper quadrant pain +/– nausea/vomiting/fever

B

Obtain vital signs, blood work, and perform a physical examination 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

D

Thickened gallbladder wall or edema Gallstones Pericholecystic fluid Sonographic Murphy’s sign

Obstructive jaundice Gallstone pancreatitis Peritonitis

Immediate cholecystectomy (open or laparoscopic)

E

Algorithm 204.1

No gross abnormalities: consider ERCP or MRCP to evaluate/treat small stones or extrahepatic stones

Biliary colic Acute cholecystitis

Conservative management: IVF, bowel rest, narcotics +/– antibiotics

Symptoms worsen or recur

Symptoms improve: plan postpartum followup

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References 1. Gilo NB, Amini D, Landy HJ.  Appendicitis and cholecystitis in pregnancy. Clin Obstet Gynecol. 2009;52(4):586–96. 2. Williamson C, Mackillop L, Heneghan MA. Diseases of the liver, biliary system, and pancreas. In: Creasy 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 complications in pregnancy. Am J Surg. 2008;196(4):599–608.

J. M. Pauli 4. Sharp HT. The acute abdomen during pregnancy. Clin Obstet Gynecol. 2002;45(2):405–13. 5. Diegelmann L. Nonobstetric abdominal pain and surgical emergencies in pregnancy. Emerg Med Clin N Am. 2012;30:885–901. 6. Lu EK, Curet MJ, El-Sayed YY, Kirkwood KS. Medical versus surgical management of biliary tract disease in pregnancy. Am J Surg. 2004;188:755–9.

Pregnancy and Appendicitis

205

Emily Smith and Jaimey M. Pauli

Algorithmic Approach A. Evaluation of possible appendicitis in pregnancy begins with a thorough history and physical examination. Right lower quadrant pain, even in pregnancy, is still the most common presenting symptom (regardless of gestational 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 examination are the foundation of diagnosis; however, 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 considered 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: [email protected]

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 imaging modality. Unfortunately, ultrasound accuracy may be operator dependent, and as gestational age increases, the appendix is frequently not visualized [5]. MRI without gadolinium 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 (operation within 24 h of presentation) is associated with better outcomes [9]. Unlike non-­ pregnant appendicitis, conservative management with antibiotics is not currently considered appropriate [8]. More extensive studies in support of conservative management 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 insufflation, a Hassan/open entry should be considered [11]. Other considerations are to use a

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midline incision if peritonitis is suspected and to keep intraabdominal pressures